SOMERSET FAMILY MEDICINE CLINICAL MODULE ‘The Bread and Butter of Family Medicine’
DR NEIL JADDOU M.D BOARD CERTIFIED AND PROFESSOR OF FAMILY MEDICINESomerset Family Medicine
36950 Ryan RdSterling Heights
MI 48310
WELCOME!
Page | 1
Welcome to Dr Neil Jaddou’s Externship Program!
This is a brief manual to “The Bread and Butter of Family
Medicine’. In this manual, the most common
pathologies are discussed. Not only will you will have a better understanding of their presentation,
you will also learn the latest recommended guidelines on how to treat
them.
Enjoy!
CONTENT
1 . HYPERTENSION --------------------------------------PG 3-14
2 . DIABETES DISORDERS -----------------------------PG 15-20
3 . BLOOD CHOLESTEROL AND ATHEROSCLEROTIC
CADIOVASCULAR DISEASEPG ------------------------PG21 -28
4 . ANTIBIOTICS- -----------------------------------------PG 29-35
5 . ASTHMA--------------------------------------------------PG 36-43
6 . THYROID DISORDERS -----------------------------PG 44-50
7 . GOUT -----------------------------------------------------PG 51-55
8 . ALLERGIC RHINITIS -------------------------------PG 56-57
9 . MIGRANE-----------------------------------------------PG 58-75
10. SKIN RASH----------------------------------------------PG 76-85
11. PAIN MANAGEMENT-------------------------------PG 86-90
12. CONSTIPATION--------------------------------------PG 91-95
13. SMOKING CESSATION-----------------------------PG 96-103
Page | 2
Somerset Family Medicine Clinical Module
Bread & Butter of Family Medicine:Hypertension
Prevelance: Most common chronic condition. Over 60% of elderly have HTN, more common and more severe in African Americans.Without treatment approximately many will die of CAD, CHF, CVA and renal failure.Etiology: Majority caused by unknown reason or hereditary, Essential or Idiopathic HTN (90-95%), while 5-10% of cases are due to other causes Secondary causes: Hyperthyroidism, hyperaldosteronism, pheochromocytoma (epin and norepinephrine, Cushing, sleep apnea and renal artery stenosis.Meds that increase BP: pseudoephedrine, OCP, NSAIDS, opiates, cocaine and energy drinks.
CLINICAL PRESENTATION:Usually asymptomatic (silent killer) discovered during routine medical care, but severe HTN may present with headache, dizziness, SOB or blurred vision.
COMPLICATIONS OF CHRONIC HYPERTENSION:1.Left Ventricular Dysfunction: Due to increased afterload, the left ventricle has to accommodate by increasing its diameters concentrically leading to Concentric left ventricular hypertrophy which can be detected on EKG, on the long run, the hypertrophied LV becomes stiff and Diastolic failure occurs which manifests as S4, eventually Systolic dysfunction ensues if HTN is not controlled.
2. Vascular disease: HTN accelerates atherosclerosis and is considered the most common risk factor for ischemic heart disease, and is a risk factor for both ischemic and hemorrhagic strokes.
3. Hypertensive Retinopathy & NephropathyLeading to eye problems and renal failure.
DIAGNOSTIC TESTS: UA, EKG, Metabolic panel, Lipid panel.Routine tests for hypertension cases are:
Treatment: JNC guidelines vs standard of care, you may or may not follow guidelines but you must follow standard of care. Erectile dysfunction: Beta blocker and Diuretics (although others may as well)IF risks eliminated, consider tapering off. i.e., patient looses 30lb etc
NONPHARMICOLOGICAL MEASURES• Follow DASH diet (low fat, low salt, fruit & veg, grains, lean meat, fish, chicken) • Exercise
Page | 3
• stress and anger management (Relaxation techniques)• Weight loss (10-15% wt)• smoking cessation, limit alcohol intake, decrease excess caffeine such as energy drinks.
Q/What is the most effective lifestyle modification for hypertension?Answer: Weight loss
If lifestyle modifications have no effect over 3-6 months, initiate medicaltherapy:
Pharmacology:
Use a thiazide diuretic, such as hydrochlorothiazide or chlorthalidone.• In diabetics, however, use ACEI/ARB as the first-line therapy.About 70 percent of patients will be controlled with a diuretic alone. If pressurecontrol is not achieved with a diuretic alone, add a second drug:• Beta blocker (atenolol, metoprolol)• ACE inhibitor• Angiotensin receptor blocker (ARB)• Calcium channel blocker (CCB)About 90-95 percent of patients should achieve control with the use of 2 medications.If 2 drugs do not work, add a third drug and investigate for causesof secondary hypertension.
Page | 4
CLASS MOA NAMES Indications Adverse Effects
Loop Diuretic (-ide)
Thiazide Diuretics
Sulfonamide loop diuretic. Inhibits co-transportsystem (Na+, K+, 2 CJ-) of thick ascendinglimb of loop of Henle.Stimulates PGE release (vasodilatory effecton afferent arteriole)
Thiazide diuretic. Inhibits NaCl reabsorption inearly distal tubule, reducing diluting capacityof the nephron (weak diuretic); increases Ca2+ excretion.
Lasix (Furosemide)( 20, 40 mg)Ethacrynic acid (25-50 mg) (used in case of Sulfa Allergy.
Hydrochlorothiazide (12.5, 25, 50 mg)
Edematous states (CHF, cirrhosis, nephroticsyndrome, pulmonary edema), hypertension,hypercalcemia.
Ototoxicity, Hypokalemia, Dehydration, Allergy(sulfa), Nephritis (interstitial), Gout.
Page | 5
ACE-Inhibitor(-pril)
inhibit angiotensin-converting enzyme thereby decreasing angiotensin II, a potent vasoconstrictor.
Lisinopril ( 10, 20, 40 mg)EnalaprilCaptoprilRamipril
Use in diabetic to prevent kidney damage; Hypertension, CHF, Prevent unfavorable heart remodelingas a result of chronic hypertension and IHD
Avoid in bilateral renal artery stenosis.Cough, Angioedema, Teratogen (fetal renal agenesis),decreases creatinine clearance (GFR)Hyperkalemia, and Hypotension
ARB(-sartan)
Blocks binding of angiotensin to a receptor
Losartan (12.5mg, 25mg, 50mg, 100mg)Valsartan ( 20 mg, 40 mg, 80 mg)Candesartan ( 4 mg, 8 mg, 16 mg, 32 mg)
Angiotensin II receptor haveeffects similar to ACE inhibitors but do not increase bradykinin, therefore there is no cough or angioedema.
Beta Blocker(-lol)
Decrease heart rate and contractility by blocking b- adrenergic
Atenolol (25 mg, 50 mg, 100 mg)Metoprolol (25 mg, 50 mg, 100 mg)Propranolol ( 10
Atenolol, Carvedilol and Metoprolol decrease mortality
Impotence, exacerbation of asthma,cardiovascular adverse
Page | 6
receptors thereby decreasing the CO; decrease renin secretion (clue tob1-receptor blockade on JGA cells)
mg, 20 mg, 40 mg, 80 mg)
in CHF; 1st line for Rx of angina and MI; class II antiarrythmic with negative chromotropic effect, used in SVT
effects (bradycardia, AVblock, CHF), CNS adverse effects (seizures,sedation, sleep alterations); use with caution indiabetics
Calcium Channel Blockers
Block voltage-dependent L-type calcium channel s of cardiac and smooth muscle and therebyreduce muscle contractility.
Amlodipine ( 2.5 mg, 5 mg, 10 mg)Diltiazem ( 30 mg) Verapamil ( 120 mg, 180 mg, 240 mg)
Heart-verapamil > diltiazem > amlodipine = nifedipine (verapam il = ventricle) .Vascular smooth muscle -amlodipine = nifedipine > diltiazem > verapamil.
Cardiac depression, AV block, peripheral edema, flushing, dizziness, and constipation.
Alpha BlockersCentral
Vasodilation through alpha blockade.
Prazosin,( 1mg, 2 mg, 5 mg, 10 mg)Terazosin ,( 1mg, 2 mg, 5 mg, 10 mg) ,
Used for HTN with BPH.
1st-close orthostatic hypotension, dizziness,
Page | 7
Blocks alpha receptors at the bladder neck promoting bladder emptying.
Doxazosin ( 1mg, 2 mg, 4 mg, 8 mg)Tamsulosin ( 0.4 mg, 0.8 mg, 1.2 mg)
headacheSedation, t serum cholesterol
Vasodilators
Smooth muscle relaxation via guanylyl cyclase pathways, Vasodilates arterioles > veins, and decreases afterload.
Hydralazine ( 25 mg, 50 mg, 100 mg)
First-line therapy for hypertension in pregnancy.Severe hypertension, CHF
Compensatory tachycardia (contra indicated in angina/CAD ),( co administered with b blocker) , fluid retention, headache,angina. Lupus-like syndrome.
Indications for Specific Medications:
Coronary artery disease Beta blocker
Congestive heart failure Beta blocker, ACE, or ARBMigraine Beta blocker, CCB
Hyperthyroidism Beta blockerOsteoporosis Thiazide
Depression No beta blockersAsthma No beta blockers
Pregnancy Alpha methyldopa, HydralazineBPH Alpha blockers
Page | 8
Diabetes ACE/ARBAfrican American CCB
JNC 8 Summary of Recommendations:1.In the general population aged ≥60 years, initiate pharmacologic
treatment to lower blood pressure (BP) at systolic blood pressure (SBP) ≥150 mm Hg or diastolic blood pressure (DBP) ≥90 mm Hg and treat to a goal SBP <150 mm Hg and goal DBP <90 mm Hg.
2.In the general population <60 years, initiate pharmacologic treatment to lower BP at DBP ≥90 mm Hg and treat to a goal DBP <90 mm Hg.
3.In the general population <60 years, initiate pharmacologic treatment to lower BP at SBP ≥140 mm Hg and treat to a goal SBP <140 mm Hg.
4.In the population aged ≥18 years with chronic kidney disease (CKD), initiate pharmacologic treatment to lower BP at SBP ≥140 mm Hg or DBP ≥90 mm Hg and treat to goal SBP <140 mm Hg and goal DBP <90 mm Hg.
5.In the population aged ≥18 years with diabetes, initiate pharmacologic treatment to lower BP at SBP ≥140 mm Hg or DBP ≥90 mm Hg and treat to a goal SBP <140 mm Hg and goal DBP <90 mm Hg.
6.In the general nonblack population, including those with diabetes, initial antihypertensive treatment should include a thiazide-type diuretic, calcium channel blocker (CCB), angiotensin-converting enzyme inhibitor (ACEI), or angiotensin receptor blocker (ARB).
7.In the general black population, including those with diabetes, initial antihypertensive treatment should include a thiazide-type diuretic or CCB.
8.In the population aged ≥18 years with CKD, initial (or add-on) antihypertensive treatment should include an ACEI or ARB to improve kidney outcomes. This applies to all CKD patients with hypertension regardless of race or diabetes status.
9.The main objective of hypertension treatment is to attain and maintain goal BP. If goal BP is not reached within a month of treatment, increase the dose of the initial drug or add a second drug from one of the classes in recommendation 6 (thiazide-type
Page | 9
diuretic, CCB, ACEI, or ARB). The clinician should continue to assess BP and adjust the treatment regimen until goal BP is reached. If goal BP cannot be reached with 2 drugs, add and titrate a third drug from the list provided. Do not use an ACEI and an ARB together in the same patient. If goal BP cannot be reached using only the drugs in recommendation 6 because of a contraindication or the need to use more than 3 drugs to reach goal BP, antihypertensive drugs from other classes can be used. Referral to a hypertension specialist may be indicated for patients in whom goal BP cannot be attained using the above strategy or for the management of complicated patients for whom additional clinical consultation is needed.
Secondary Hypertension:
Investigate for secondary hypertension if you see the following:
• Young(< 30) or old(> 60) patient
• Failure to control pressure with 2 medications.
HTN Urgency: ≥180/120 mmHg without evidence of end organ damage
HTN Emergency: ≥180/120 mmHg with symptoms or evidence of end organ damage (papilledema, chest pain, acute kidney injury, encephalopathy, focal neurological deficit). These patients should be immediately sent to the ER
BOARD PEARLS:
• # Drug of choice for hyertensive emergency in pregnancy - hydrazine (S/E : coronary steel syndrome)
• # Eplerenone is a pottasium sparing diuretic but it does not cause gynecomastia.
• # 1st choice of drugs in African American with HTN – CCB(amlodipine)
• # ACE inhibitors and ARB’s are C/I in pregnant woman.
Page | 10
• # Drug of choice for patients with HTN with asthma- amlodipine
• # Drug of choice patients HTN with COPD/angina/supraventricular tachycardia with angina - verapamil.
• # Hydrochlorothiazide increases calcium and parathyroid hormone.
#S/E of ACE Inhibitors mnemonic: CAPTOPRIL. C : Cough A : Angioedema P : prodrug(All ACE inhibitors are prodrugs except Captopril and lisinopril) T : taste alterans(Dysguesea) O: Orthostatic hypotension. P : Pregnancy C/I R : Renal stenosis C/I I : Increase potassium L : Lowers angiotensin II production.
• # Drug of choice for HTN with BPH – Tamsulosin. It does not cause orthostatic hypotention.
• # Alpha blockers are C/I in patient with cataract surgery as it leads to Floppy iris syndrome
• # Causes of secondary HTN mnemonic (CHAPS) C: Cushings syndrome H : Hyperaldosteronism(CONN’s Syndrome) A : Aortic coarctation P : Pheochromocytoma S : Stenosis of renal arteries.
Clinical Vignettes
Page | 11
1.A 45 Yo male presented for routine physical exam, he has no complaints, his Vital signs are as follows: BP 155/90 , HR: 60, Temp: 98, Resp: 13Which of the following is the best next step in management?a. Initiate Lisinoprilb. Initiate a diureticc. Repeat in 2 wksd. Doppler U/S of the kidneys
2.A 32 Y/O male presented for routine health care exam with mild weakness of lower extremities, polydipsia and polyuria, he denied any other complaints, his vital signs are BP: 135/95 , HR: 76, Temp 97.1 , Respiration: 12, His chemistry profile is as follows:
Na: 141K: 2.8Cl: 105Ca: 9.5Blood Glucose: 76
Which of the following is the best next step in management?a. Repeat the BP measurement in 2 weeksb. Initiate HCTZc. Measure Aldosterone/ Renin Ratiod. Initiate lifestyle changes.
3.A 55 YO male with type 2 DM presented with HTN on more 3 readings, he was initiated on Lisinopril 10 mg 1 wk. ago, his GFR had been decreased from 90 ml/min at that time to 81 ml/min , which of the following is the best next step in management?
a.Switch to Candesartan 4mgb.Switch to a diureticc.Initiate Dialysisd.Continue treatment with Lisinopril
4. You are seeing a 45-year-old diabetic woman who reports bilaterallower extremity peripheral edema. In addition to diabetes, she has hypertensionand depression. Which of the following medications is the likelycause of her edema?
a.Fluoxetine
Page | 12
b.Metforminc.Glyburided.Hydralazine
e. Hydrochlorothiazide
5. A 52 YO male patient with HTN presents for complete physical examination, he is taking Amlodipine 10 mg/d, he eats a well balance healthy diet and exercises regularly, but he complains of leg swelling in the last 3 months, physical examination confirms bilateral pitting edema, His cardiac exam is unrevealing, his EKG is normal and His vital signs : BP 130/82, HR: 88, Temp : 97.2 , Respiration: 12His blood work is as follows:Na: 140K: 4.1Cl: 104CO2: 30Anion Gap: 7Glucose: 78BUN: 20Creatinine: 0.8Ca: 9.1Albumin: 4.3Globulin: 2.9ALP: 90ALT: 30AST: 35Bilirubin total: 0.6GFR: 110
Which of the following is the best explanation of these findings:a.Congestive Heart Failure
b. Drug side effects c. Renal failure d. Liver Injury e. lymphatic obstruction
6 .A 58 YO male presented to the ER with acute chest pain, he was diagnosed with ST elevation myocardial infarction and was discharged 10 days later on medications.Two years later he was found dead in his apartment without obvious reason.
Page | 13
The autopsy showed dilated ventricular chambers of the heart with increased cardiac diameters. Which of the following would prevent the subsequent complication if given before?
a.Atenolol 100 mgb.Aspirin 81 mgc.Captopril 50 mgd.HCTZ 12.5 mge.Simvastatin 20 mg
7. A 1hr neonate born to a 33 YO female presented with respiratory distress immediately after birth, examination revealed a flattened nose, recessed chin, prominent epicanthal folds, and low-set abnormal ears, his mother has oligohydramnios during her pregnancy, which of the following scenario is likely during the pregnancy?
a.Diabetes treated with metforminb.HTN treated with alpha methyl dopa.c.DVT treated with Coumadind.Infection treated with tetracycline.e.HTN treated with Lisinopril.
8. You have diagnosed a 35-year-old African American man with hypertension.Lifestyle modifications helped reduce his blood pressure, but he wasstill above goal. You chose to start hydrochlorothiazide, 25 mg daily. Thishelped his blood pressure, but it is still 142/94 mm Hg. Which of the followingis the best approach to take in this situation? a. Increase his hydrochlorothiazide to 50 mg/d b. Change to a loop diuretic c. Change to an ACE inhibitor d. Change to a β-blocker e. Add an ACE inhibitor.
9.A 58 YO male presented to the ER with headache and confusion for 3 hr, his past medical history is significant for HTN, his vital signs : BP 118/110, HR: 90, Temp 98, Respiration: 12, physical exams shows increased DTRs, which of the following is the best treatment ?
Page | 14
a.Sublingual Nifedipineb.IV labetalolc.Oral Atenolold.IV furosemide.
10. You are caring for a 45-year-old man with hypertension, gastroesophagealreflux, and depression. His medication list includes hydrochlorothiazide,verapamil, atenolol, omeprazole, and bupropion. He iscomplaining of difficulty with ejaculation. Which of the following medicationsis the most likely cause of this problem?a. Hydrochlorothiazideb. Verapamilc. Atenolold. Omeprazolee. Fluoxetine
11. A 47-year-old man with a history of hypertension presents to the EDcomplaining of continuous left-sided chest pain that began while snortingcocaine 1 hour ago. The patient states he never experienced chest pain inthe past when using cocaine. His BP is 170/90 mm Hg, HR is 101 beats perminute, RR is 18 breaths per minute, and oxygen saturation is 98% onroom air. The patient states that the only medication he takes is alprazolamto “calm his nerves.” Which of the following medications is contraindicatedin this patient?a. Metoprololb. Diltiazemc. Aspirind. Lorazepame. Nitroglycerin
Page | 15
Answers:1. c2. c3. d4. d5. b6. c7. e8. E9. B10. A11.A
Somerset Family Medicine Clinical Module
Bread & Butter of Family Medicine:
DIABETES
Clinical Pearls:
Normal fasting blood glucose (FBS) 60-99 mg/dL
Page | 16
• Diabetes defined by any one of four criteria below:o FBS of ≥ 126 mg/dL on two occasionso RBS of > 200 mg/dL with classic symptoms of DM (polyuria, polydipsia,
polyphagia)o Hemoglobin A1c ≥ 6.5%o Oral glucose tolerance test (OGTT): 2 hours post-prandial of ≥ 200
mg/dL (NOT USED in Office practices except in pregnancy)• Pre-diabetes:
o FBS 100-125 mg/dLo RBS of 140-199 mg/dL with classic symptoms of DM (polyuria,
polydipsia, polyphagia)o Hemoglobin A1c 5.7 to 6.4%o Oral glucose tolerance test (OGTT): 2 hours post-prandial of 140 to 199
mg/dL (NOT USED in Office practices except in pregnancy)• GOAL of Hgb A1C in diabetic is < 7%• Foot exam every visit for neuropathy, arterial insufficiency, and ulcers. Use the
10 g foot microfilament to check for peripheral neuropathy at least once a year• UA for microalbumin yearly• Eye exam yearly for retinopathy
o Proliferative retinopathy = neovascularization or vitreal hemorrhageso Diabetic retinopathy can be prevented with tight glycemic controlo Treatment of diabetic proliferative retinopathy is with laser
photocoagulation. Intraocular injections with vascular endothelial growth factor (VEGF) inhibitors prevent further progression of diabetic retinopathy. Examples of VEGF inhibitors are bevacizumab and ranibuzimab
o Diabetic Nephropathy=characterized by glomerular hyper filtration followed by microalbuminuria. preventive measures include ACE or angiotensin receptor blockers (ARB) and BP/glucose control.
• Hgb A1c twice a year for glycemic-controlled patients and quarterly for uncontrolled
• Initial management of Type 2 diabetes is with diet, weight loss and exercise • Treatment of HTN in diabetes in non-African Americans should include thiazide
diuretics, ACE-Is (or ARBs), or CCBs. (JNC 8)• Treatment of HTN in diabetes in African Americans should include thiazide
diuretics or CCBs. (JNC 8)• Pharmacological treatment for BP in diabetes should start at a BP of 140/90
mm Hg (JNC 8) in the general population (JNC 8)• Goal of LDL-cholesterol in diabetes is < 100 mg/dL. Use statins.• Goal of LDL-cholesterol in diabetes and CAD is < 70 mg/dL. Use statins.• Encourage smoking cessation in those with diabetes with cardiovascular
disease including those with peripheral artery disease• First line pharmacological treatment of diabetes is with metformin unless
contraindicated (see table).o Add sulfonylureas or basal insulin (with or without preprandial insulin)
if blood glucose is not well controlled with metformin. o Other oral agents may be used as first line treatment if there are
contraindications to the use of metformin
Prevention:
Page | 17
Diabetes can often be prevented by following.- Maintain Normal body weight.- Physical exercise, and following a healthy diet.- Diet rich in whole grains and fiber.- Choosing good fats, such as Polyunsaturated fats found in nuts, vegetable oils, and
fish.- Limiting sugary beverages and eating less red meat.
CLASS MOA NAMES Clinical Info CAUTION
Biguanides Decreases hepatic glucose production, decreases intestinal absorption,
Metformin(Glucophage)500-1000mg BID-TID (also comes in 850)2550mg QD
First line agent Avoid situations that increase risk of lactic acidosis: renal insufficiency, radio-contrast agents,Caution with CHF,Causes Megaloblastic Anaemia
Sulfonylureas Stimulates insulin secretion from beta cells in pancreas
Glipizide (Glucotrol XL) 2.5-10mg QD (dosage >10m max 20mgGlyburide (Diabeta, Glynase, Micronase) 2.5-5mg QD, max 20/dGlimepiride(Amaryl)
Take 30 min before meals
Reduce drug clearance in renal failure
Causes Hypoglycemia, weight gain and SIADH
Thiazolidinediones Decreases insulin resistance in the periphery and liver
Pioglitazone (Actos) 15-45mg QD
Monitor serum transaminase when starting
Contraindicated for liver disease and symptomatic heart failure
May cause or exacerbate CHF and MI, bladder cancer
Dipepidyl peptidase-4 inhibitor
Enhance incretin hormones
Januvia (Sitagliptin) 100mg QDSaxagliptin
Possible increased risk of pancreatitis
Nausea, skin rashes, increased risk of infections
Page | 18
Glucagon-like peptide-1 receptor agonists - act as incretin which increase insulin
Mimics the enhancement of glucose dependent insulin secretion
Byetta (Exenatide), Victoza (Liraglutide) shots
Both promote weight loss,
Amylinomimetics (pramlintide). Acts as a synthetic analogue of amylin
Amylin is an endogenous pancreatic hormone that helps to slow gastric emptying, suppress glucagon, and regulate appetite
Symlin, SymlinPen 120, SymlinPen 60. Given subcutaneously.
Nausea, vomiting. Hypoglycemia
Meglitinides ↑ insulin secretion from pancreatic β cells
Repaglinide (Prandin), Nateglinide (Starlix)
Similar to sulfonylureas
Weight gain, hypoglycemia
Insulin Binds to insulin receptors
Short: Regular or apidra before each meal (sliding scale)
Intermediate: NPH
Long (24hr): Glargine (Lantus), (Levimir)Once QHS
May be used in combo with oral agentsUsed when oral agents fail
Levemir or glargine (Lantus)Start with 10 U SC QHS then increase by 1 U daily until FPG <100
Board Pearls:
- Insulin is safe to use in Gestational Diabetes.- Microalbuminuria Cannot be detected on routine UA protein dipstick.- Afrezza (Inhalable Insulin) was approved by the FDA for general sale in June 2014.- Coronary artery bypass should be performed in a diabetic patient even if there is only
two vessel coronary disease.
Page | 19
- Hyper osmolar nonketotic coma(HONK) is a syndrome that occurs predominantly in patients with type 2 diabetes and is characterized by severe hyperglycemia in the absence of significant ketosis.
- the SOMOGYI effect is rebound hyperglycemia in the morning because of counter regulatory hormone release after an episode of hypoglycemia in the middle of the night.
- Frozen Shoulder is the most common risk factor In DM.It is an idiopathic condition, symptoms are Loss of active and passive shoulder rotation with severe pain.
Practice Questions:
1. A 49-year-old woman presents to her physician’s office with a long-standing history of polydipsia, polyuria, central obesity, and hyperlipidemia. She is currently taking metformin, a sulfonylureas, and an ACE inhibitor. ACE inhibitors are most beneficial in preventing or slowing the progression of which of the follow- ing diabetic complications? a. Diabetic ketoacidosisb. Diabetic nephropathyc. Diabetic neuropathyd. Diabetic retinopathye. Peripheral vascular disease
2. A 42-year-old man with a long-standing history of diabetes mellitus type 1 presents to his physician for his yearly checkup. On examination, the physician notes decreased sensation in both of his feet. Although he insists other- wise, the physician suspects that he has not been adequately monitoring and controlling his blood glucose level. Which of the following tests would be best for letting the physician know how well the patient’s blood glucose has been controlled over the past 3 months? a. Dilated eye examinationb. Fasting blood glucose level c. Hemoglobin A1Cd. Microalbumin Screeninge. Random blood glucose level
3. Diabetic neuropathies are diagnosed using all of the following except? a.Nerve conduction studies or electromyography b.Ultrasound c. Foot examinations
Page | 20
d. Minnesota Mutiphasic Personality inventory (MMPI)
4. Which of the following regimens offers the best blood glucose control for persons with type 1 diabetes? a. A single anti-diabetes drugs b. Once daily insulin injections c. A combination of oral anti-diabetic medications d. Three or four injections per day of different types of insulin.
5. Which of the following diabetes drugs acts by decreasing the amount of glucose produced by the liver? a. Sulfonylureas b. Meglitinides c. Biguanides d. Alpha-glucosidase inhibitors
6. Proliferative retinopathy is often treated using: a. Tonometry b. Fluorescein angiogram c. Antibiotics d. Laser surgery
Answers:
1. The answer is B. ACE inhibitors such as captopril have been shown to decrease blood pressure and prevent and slow the progression of diabetic nephropathy in patients with diabetes. It is believed that ACE inhibitors play a renoprotective role by reducing glomerular filtration rate and reducing macro- proteinuria.
2. The answer is C. When hemoglobin is exposed to increased levels of glucose circulating in the blood, a higher percentage of glucose binds to the hemoglobin. This glycosylated hemoglobin can be measured with the HbA1c
blood test. Target HbA1C levels for diabetics are
7.0% to 6.5% in diabetic patients. Because the average lifetime of an RBC is 120 days, this test is best for determining average blood glucose levels over the previous 3–4 months.
Page | 21
3. The answer is D. Nerve conduction studies assess transmission of electrical signals through nerves and electromyography evaluates nerve transmission to muscles. Ultrasound can assess the responsivity and function of internal organs that may be compromised by neurological damage. Foot exams help to assess peripheral neuropathy and to ensure the integrity of skin. The MMPI is a psychological test and is not used to assess diabetic neuropathy.
4. The answer is D. Because persons with type 1 diabetes do not produce insulin, they require insulin and cannot be treated with oral anti-diabetic drugs. Several injections of insulin per day, calibrated to respond to measured blood glucose levels, offer the best blood glucose control and may prevent or postpone the retinal, renal, and neurological complications of diabetes.
5. The answer is C. Biguanides, such as metformin, lower blood glucose by reducing the amount of glucose produced by the liver. Sulfonylureas and Meglitinides stimulate the beta cells of the pancreas to produce more insulin. Alpha-glucosidase inhibitors block the breakdown of starches and some sugars, which helps to reduce blood glucose levels.
6. The answer is D. Scatter laser treatment is used to shrink abnormal blood vessels in an effort to preserve vision. When there is significant bleeding in the eye, it is removed in a procedure known as vitrectomy. Tonometry is a diagnostic test that measures pressure inside the eye. A
fluorescein angiogram is a diagnostic test that traces the flow of dye through the blood vessels in
the retina; it is used to detect macular edema. Somerset Family Medicine Clinical Module
Bread & Butter of Family Medicine:
Blood Cholesterol and Atherosclerotic Cardiovascular Disease (ASCVD)
Introduction
In the United States, atherosclerotic cardiovascular disease (ASCVD) is the leading cause of:
• Death
• Decreased quality of life, and
• Medical cost
The Adult Treatment Panel (ATP) IV was first released by the National Heart, Lung, and Blood Institute (NHLBI) in 2008. The panel used evidence from randomized control trials including meta-analyses to update the 2001 ATP III guidelines. In November 2013, the American College of Cardiology and American Heart Association (ACC/AHA) released the “Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Disease (ASCVD) in Adults.”
Page | 22
The guideline addressed the goals of low density lipoprotein cholesterol (LDL-C) and non-high density lipoprotein cholesterol (HDL-C) in both secondary and primary prevention, as well as the efficacy and safety of cholesterol lowering medications. One major shift from ATP III to the current guideline is that the 2013 ACC/AHA recommendation does not favor treating hyperlipidemia to specific target goal.
Treatment Recommendation
ACC/AHA highly recommends lifestyle modification as being critical to health promotion and ASCVD risk reduction, both prior to and in concert with the use of cholesterol loweringdrug therapies. Measures include:
• Adhering to a heart healthy diet• Regular exercise habits• Avoidance of tobacco product• Maintenance of a healthy weight
According to the guideline, there are four 4 major statin benefit groups:
1. Individuals with clinical ASCVD2. Individuals with primary elevations of LDL–C >190 mg/dL3. Individuals with diabetes aged 40 to 75 years with LDL–C 70 to189 mg/dL and
without clinical ASCVD4. Individuals without clinical ASCVD or diabetes with LDL–C 70 to189 mg/dL and
estimated 10-year ASCVD risk >7.5%
Clinical ASCVD is defined by the inclusion criteria for the secondary prevention statin RCTs (acutecoronary syndromes, or a history of MI, stable or unstable angina, coronary or other arterialrevascularization, stroke, TIA, or peripheral arterial disease presumed to be of atherosclerotic origin).
Statins for Treatment of ASCVD$
Statin Therapy* Daily Dose
High Intensity# Moderate Intensity## Low Intensity###
Page | 23
▪ Atorvastatin (Lipitor) (40†)-80 mg 10 (20) mg -
▪ Rosuvastatin (Crestor) 20 (40) mg (5) 10 mg -
▪ Simvastatin (Zocor) - 20-40 mg‡ 10 mg
▪ Pravastatin (Pravachol) - 40 (80) mg 10-20 mg
▪ Lovastatin - 40 mg 20 mg
▪ Fluvastatin - 80 mg XL 20-40 mg
▪ Fluvastatin - 40 mg (twice daily) -
▪ Pitavastatin - 2-4 mg 1 mg
Specific statins and doses are noted in bold that were evaluated in RCTs (17,18,46-48,64-67,69-78) included in CQ1,CQ2 and the CTT 2010 meta-analysis included in CQ3 (20). All of these RCTs demonstrated a reduction in majorcardiovascular events. Statins and doses that are approved by the U.S. FDA but were not tested in the RCTs reviewedare listed in italics.*Individual responses to statin therapy varied in the RCTs and should be expected to vary in clinical practice. Theremight be a biologic basis for a less-than-average response.#Daily dose lowers LDL–C on average, by approximately ≥50%##Daily dose lowers LDL–C on average, by approximately 30% to <50%###Daily dose lowers LDL–C on average, by approximately <30%†Evidence from 1 RCT only: down-titration if unable to tolerate atorvastatin 80 mg in IDEAL (47).‡Although simvastatin 80 mg was evaluated in RCTs, initiation of simvastatin 80 mg or titration to 80 mg is notrecommended by the FDA due to the increased risk of myopathy, including rhabdomyolysis.
XL – Extended release
$Adapted from Table 5 of Guideline
Recommendations of the Panel are summarized below&:
✓ Healthy lifestyle habits should be encouraged for all persons.✓ The appropriate intensity of statin therapy should be initiated or continued:
1. Clinical ASCVD‡a. Persons aged ≥75 y with no safety concerns: high-intensity statin (class I, level A)b. Persons aged <75 y or with safety concerns: moderate-intensity statin (class I, level A)
2. Primary prevention: primary LDL-C level _190 mg/dLa. Rule out secondary causes of hypercholesterolemiab. Persons aged ≥21 y: high-intensity statin (class I, level B)
Page | 24
c. Achieve ≥50% reduction in LDL-C level (class IIa, level B)d. May consider LDL-C–lowering non-statin therapy to further reduce LDL-C levels (class IIb, level C)
3. Primary prevention: persons with diabetes aged 40–75 y with an LDL-C level of 70–189 mg/dL
a. Moderate-intensity statin (class I, level A)b. Consider high-intensity statin when 10-y ASCVD risk is ≥7.5% (class IIa, level B)
4. Primary prevention: persons aged 40–75 y without diabetes with an LDL-C level of 70–189 mg/dL
a. Estimate 10-y ASCVD risk (risk calculator based on Pooled Cohort Equations recommended)§ in those not receiving a statin; estimate risk every 4–6 y (class I, level B)b. To determine whether to initiate a statin, engage in clinician–patient discussion of potential for ASCVD risk reduction, adverse effects, drug–drug interactions, and patient preferences (class IIa, level C). Reemphasize healthy lifestyle habits and address other risk factors. If statin therapy is chosen:
i. Persons with ≥7.5% 10-y ASCVD risk: moderate- or high-intensity statin (class I, level A)ii. Persons with 5% to < 7.5% 10-y ASCVD risk: consider moderate-intensity statin (class IIa, level B)iii. Other factors may be considered_: LDL-C level ≥160 mg/dL, family history of premature ASCVD, lifetime ASCVD risk, high-sensitivity C-reactive protein level of ≥2.0 mg/L, coronary artery calcification score ≥300 Agatston units, or ankle–brachial index <0.9 (class IIb, level C)
5. Primary prevention when LDL-C level is <190 mg/dL and person is aged <40 y or >75 y or has <5% 10-y ASCVD risk
a. Statin therapy may be considered in selected persons|| (class IIb, level C)6. Statin initiation is not routinely recommended for persons with NYHA class II–IV heart failure or those who are receiving maintenance hemodialysis.
✓ Regularly monitor adherence to lifestyle and drug therapy with lipid and safety assessments. Nonstatin therapy can be considered in selected persons.
Assess adherence, response to therapy, and adverse effects within 4–12 wk after statin initiation or change in therapy (class I, level A)
a. Measure fasting lipid panel (class I, level A)b. Do not routinely monitor hepatic function with ALT levels or muscle injury with CK levels unless patient is symptomatic (class IIa, level C).c. Screen and treat type 2 diabetes mellitus according to current practice guidelines. Healthy lifestyle habits should be encouraged to prevent progression to diabetes (class I, level B).d. Anticipated therapeutic response: approximately ≥50% reduction in LDL-C level from baseline for high-intensity statin and 30% to <50% for moderate-intensity statin (class IIa, level B)
i. Insufficient evidence from RCTs for LDL-C or non–HDL-C treatment goals
Page | 25
ii. For guidance in persons with unknown baseline LDL-C level, a level of <100 mg/dL was observed in RCTs about high-intensity statin therapy.
e. Less-than-anticipated therapeutic response:i. Reinforce improved adherence to lifestyle and drug therapy (class I, level A)ii. Evaluate for secondary causes of hypercholesterolemia if indicated¶ (class I, level A)iii. Increase statin intensity, or if patient is receiving maximally tolerated statin intensity, consider addition of non-statin therapy shown in RCT to reduce ASCVD events in selected high-risk persons** (class IIb, level C)
f. Regularly monitor adherence to lifestyle and drug therapy every 3–12 months once statin adherence has been established. Continue to assess adherence for optimum ASCVD risk reduction and safety (class I, level A)
✓ In persons unable to tolerate the recommended intensity of statin therapy, use the maximally tolerated intensity of statin.
If there are muscle or other symptoms, establish their relationship to statin therapy (class IIa, level B)
a. Obtain a history of muscle symptoms before initiating statin therapy.b. If muscle or other symptoms develop during statin therapy, discontinue the statin.c. Once mild to moderate muscle or other symptoms resolve, re-challenge with the same dose of statin or lower; if muscle symptoms recur, discontinue statin and re-challenge with progressively lower doses of the same or a different statin.d. If muscle symptoms persist > 2 months after statin discontinuation,
consider other conditions that may increase the risk for muscle symptoms
ConclusionIn summary the main areas addressed by the Panel are enumerated below
Page | 26ALT = alanine aminotransferase; ASCVD = atherosclerotic cardiovascular disease; CK = creatine kinase; HDL-C = high-density lipoprotein cholesterol; LDL-C =low-density lipoprotein cholesterol; NYHA = New York Heart Association; RCT = randomized, controlled trial.* Adapted from reference 2. Reprinted with permission.† For information about class and level, please see appendix 1.‡ Clinical ASCVD is defined as acute coronary syndromes or a history of myocardial infarction, stable angina, coronary or other arterial revascularization, stroke, transientischemic attack, or peripheral arterial disease presumed to be of atherosclerotic origin.§ Estimated 10-y “hard” ASCVD risk includes first occurrence of nonfatal myocardial infarction, death from coronary heart disease, and nonfatal and fatal stroke as used inthe Pooled Cohort Equations on the basis of age, sex, smoking status, total cholesterol level, HDL-C level, systolic blood pressure, and the use of antihypertensive therapy.|| Other factors that may influence ASCVD risk include primary LDL-C level _160 mg/dL or other evidence of genetic hyperlipidemias; family history of premature ASCVDwith onset before age 55 y in a first-degree male relative or before age 65 y in a first-degree female relative; high-sensitivity C-reactive protein level of ≥2 mg/L; coronary
▪ Encourage adherence to a healthy lifestyle ▪ Statin therapy is recommended for adults in groups demonstrated to benefit (see introduction)▪ Statins have an acceptable margin of safety when used in properly selected individuals and
appropriately monitored▪ Engage in a clinician–patient discussion before initiating statin therapy, especially for primary
prevention in patients with lower ASCVD risk▪ Use the newly developed pooled cohort equations for estimating 10-year ASCVD risk (This is
available in medical applications such as Epocrates and Omnio). The equation considers:o Age (years)o Gender (Male/Female)o Race (White/African American)o Total cholesterol (mg/dL)o HDL level (mg/dL)o Systolic BP (mmHg)o Is SBP treated or untreated (T or U)o Current smoker (Yes/No)o Diabetic (Yes/No)
▪ Initiate the appropriate intensity of statin therapy▪ Evidence is inadequate to support treatment to specific LDL-C or Non–HDL-C goals ▪ Regularly monitor patients for adherence to lifestyle and statin therapy
References
Stone NJ, Robinson J, Lichtenstein AH, Bairey Merz CN, Lloyd-Jones DM, Blum CB, et al. 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2013. [PMID: 24239923]
Stone NJ, Robinson JG, Lichtenstein AH, Lloyd-Jones DM, Goff D, Smith SC Jr, et al. Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Disease Risk in Adults: Synopsis of the 2013 ACC/AHA Cholesterol Guideline. Ann Intern Med. 2014.
BOARD PEARLS :
# ATP III GUIDELINES FOR RISK SATISFICATION OF DYSLIPIDEMIA :
RISK CATEGORY LDL Goal LDL TO START LIFESTYLE MODIFICATION
LDL TO CONSIDER DRUG THERAPY
CAD or CAD risk equivalents å
< 100 mg/dl ( or < 70) > 100 mg/dl > 100 mg/dl
2+ risk factors ∫ < 300 mg/dl > 130 mg/dl > 130 mg/dl
0 - 1 risk factor ∫ < 160 mg/dl > 160 mg/dl > 190 mg/dl
Page | 27
ALT = alanine aminotransferase; ASCVD = atherosclerotic cardiovascular disease; CK = creatine kinase; HDL-C = high-density lipoprotein cholesterol; LDL-C =low-density lipoprotein cholesterol; NYHA = New York Heart Association; RCT = randomized, controlled trial.* Adapted from reference 2. Reprinted with permission.† For information about class and level, please see appendix 1.‡ Clinical ASCVD is defined as acute coronary syndromes or a history of myocardial infarction, stable angina, coronary or other arterial revascularization, stroke, transientischemic attack, or peripheral arterial disease presumed to be of atherosclerotic origin.§ Estimated 10-y “hard” ASCVD risk includes first occurrence of nonfatal myocardial infarction, death from coronary heart disease, and nonfatal and fatal stroke as used inthe Pooled Cohort Equations on the basis of age, sex, smoking status, total cholesterol level, HDL-C level, systolic blood pressure, and the use of antihypertensive therapy.|| Other factors that may influence ASCVD risk include primary LDL-C level _160 mg/dL or other evidence of genetic hyperlipidemias; family history of premature ASCVDwith onset before age 55 y in a first-degree male relative or before age 65 y in a first-degree female relative; high-sensitivity C-reactive protein level of ≥2 mg/L; coronary
å : CAD risk equivalents include symptomatic carotid artery disease, peripheral arterial disease, AAA and diabetes.
∫ : Risk factors include cigarette smoking, hypertension,low HDL(<40 mg/dl), a family history of premature CAD and age (men > 45 years; women > 55 years). An HDL >60 mg/dl counts as a “negative” risk factor and removes 1 risk factor from the total score.
# LIPID LOWERING AGENTS :
CLASS Examples MOA Effect on lipid Profile
Side effects
HMG- CoA Reductase inhibitor(statins)
Atorvastatin,Simvastatin,Lovastatin, Pravastatin,Rosuvastatin.
Inhibit the rate-limiting step in cholesterol synthesis.
lowers LDL, lowers Triglycerides
Increase LFTs, Myositis, Warfarin potentiation.
Lipoprotein lipase stimulators (fibrates)
Gemfibrozil increase lipoprotein lipase,leading to increase VLDL and triglyceride catabolism.
lowers triglycerides , lowers HDL.
GI upset, Cholelithiasis, myositis, increase LFTs.
Cholesterol absorption inhibitors
Ezetimide(zetia) lowers absorption of cholesterol at the small intestine brush border.
lowers LDL Diarrhea, abdominal pain. can cause angioedema
Niacin Niaspan lowers fatty acid release from adipose tissue, lowers hepatic synthesis of LDL
Increase HDL, Lowers LDL
Skin flushing(can be prevented with ASA), paresthesias, pruritus, GI upset, increase LFTs
Bile acid resins Cholestyramine, colestipol, colesevelam.
Bind intestinal bile acids, leading to decrease bile acid stores and increase catabolism of LDL from plasma.
lowers LDL Constipation, GI upset, LFT abnormalities, myalgias. can lower absorption of other drugs from small intestine.
# Indications for CABG are GNEMONIC(UnLimiTeD):
Page | 28
U : Unable to perform PCI(diffuse disease)
L : Left main coronary artery
T : Triple-vessel disease
D : Depressed ventricular function.
# Drug that increases the elasticity of RBC : Pentoxyphilline
# Heparin induced thrombocytopenia treatment : Direct thrombin inhibitors(Hirudin, lepirudin, bivalirudin)
1. A 52-year-old white male is being considered for pharmacologic treatment of hyperlipidemia because of an LDL cholesterol level of 180 mg/dL. Before beginning medication for his hyperlipidemia, he should be screened for: (check one)A. Hyperthyroidism B. Hypothyroidism C. Addison’s disease D. Cushing’s disease E. Pernicious anemia
Answer:
1.B
Page | 29
Somerset Family Medicine Clinical Module
Bread & Butter of Family Medicine: “Walking Into The Exam Room & The Board”
ANTIBIOTICSIf you over prescribe can cause c. dificil colitis (psudomembreneous colitis),
MRSA,candida, (can give diflucon 150mg)
Sore Throat: Majority of ST are caused by virus, ST can potentially be strep if you
have the following:
- ST, HA, fever, stomach pain, dysphagia, “swallowing glass or razer blade” body
pain, no cough
- May have nausea and vomiting, Phyryngeal exudate (white spot on tonsils)
- Beefy red throat, Petachie on posterior palate
- Anterior submandibular LN. (post. LN highly suggestive of Mono (infectious
mono. Especially if patient is very fatigue) Some patient may have both. Do not
give Amoxil in mono they may get a rash. To test for mono, do blood test called
monospot. To test for Strep, do rapid strep. Sometime some doctors order strep
culture.
URI: Majority are cold virus
- Duration, can last 5-10d sometime longer.
- Clear runny nose, post nasal drip, sneezing, bodyache, tired, fever, ST, HA
Page | 30
- Cough, mainly dry. If sputum of the cough is yellow or green does not always
mean bacterial. Do not prescribe Abx, some are allergic rhinitis. Above you can
prescribe non-sedating antihistamine such as Claritin and herbal medicine such
as vitamin C, fluids, rest etc
Acute Sinusitis ; Sever sinus tenderness, headache, teeth pain, frontal sinus pain,
sometimes worse with position. You may prescribe abx.
OM: if ear drum is red give abx. In Europe they do not prescribe abx for om. They give
supportive RX of Ibuprofen and possible eardrops such Aurlgan ear drop for pain.
Otitis externa : if turgate is painful, ear canal swollen and eardrum is normal can give
cortisporing ear drops. If sever can also give oral abx.
Acute Bronchitis : Majority is virus. However in smokers/asthmatics or COPD can
potentially turn into pneumonia. So treat with Abx for above patients, possible inhaler (or
nebulizer) could be steroid inhalers or po steroids as well depending on breathing
status, may give cough syrup with codine (do not drive), or may send to ER. Others can
treat with cough syrup alone.
Pneumonia : to be safe send to ER. However some can be treated with Rocephin shot
plus z-pack or levaquin. Do not treat anyone with pneumonia as an outpatient who is
SOB (low pulse ox) or pediatrics or elderly.
Laryngitis: Caused by virus use honey and tea, Tylenol or Ibuprofen if needed.
( hoarsness case, ddx)
Tuberculosi s : Hemoptysis, (ddx), Malaria:
H. Pylori : Causing gastritis and PUD, Nobel prize, RX with triple therapy of
PPI/Abx/Abx , bismuth (black stool/tongue)
Traverler ’ s diarrhea : Cipro/Bismuth Watery diarrhea, Giardia/Cholera
Hemmorrhagic colitis/Food poisoning: Bloody diarrhea: E. coli: O157:H7,
Page | 31
Gastro-enteritis: BRATY diet, if not better get fecal leukocytes, c.dificil antibody, stool
culture ova/parasite
Pinworms : fecal/oral, Dx with Scothch tape “tape test” in am, anal itching/wt loss , Rx:
treat ALL family mebendazole
Scabies : Trails burrowing mites are linear/s-shaped tracks accompanied by rows of
pimple-like insect bites. Elemite cream
Clinical Vignettes
1. A 27-year-old male presents with what he thinks is a sinus infection. He has a 2-day history of right maxillary pain associated with nasal congestion and clear rhinorrhea. The only significant findings on examination are a low-grade fever and subjective tenderness with palpation over the right maxillary sinus. Which one of the following treatments is most supported by current evidence? (check one)A. Antihistamines B. Oral decongestants C. Topical vasoconstrictor sprays D. Oral analgesics E. Nasal lavage
2. A 30-year-old white male complains of several weeks of nasal stuffiness, purulent nasal discharge, and facial pain. He does not respond to a 3-day course of trimethoprim/sulfamethoxazole (Bactrim, Septra). Follow-up treatment with 2 weeks of amoxicillin/clavulanate (Augmentin) is similarly ineffective. Of the following diagnostic options, which one is most appropriate at this time? (check one)A. Pulmonary function testing B. Coronal CT of the sinuses C. Culture and sensitivity testing of the discharge D. Erythrocyte sedimentation rate
Page | 32
3. A 32-year-old African-American female presents with a 3-day history of fever, cough, and shortness of breath. She has been healthy otherwise, except for a sinus infection 2 months ago treated with amoxicillin. She does not appear toxic. A chest radiograph reveals an infiltrate in the right lower lobe, consistent with pneumonia. Which one of the following would be the best choice for antibiotic treatment? (check one)A. High-dose amoxicillin B. Azithromycin (Zithromax) C. Doxycycline D. Levofloxacin (Levaquin) E. Cefuroxime axetil (Ceftin)
4. A 7-year-old male presents with a 3-day history of sore throat, hoarseness, fever to 100 degrees (38 degrees C), and cough. Examination reveals injection of his tonsils, no exudates, and no abnormal breath sounds. Which one of the following would be most appropriate? (check one)A. Recommend symptomatic treatment B. Perform a rapid antigen test for streptococcal pharyngitis C. Treat empirically for streptococcal pharyngitis D. Perform a throat culture for streptococcal pharyngitis E. Perform an office test for mononucleosis
5. An 18-year-old male presents with a sore throat, adenopathy, and fatigue. He has no evidence of airway compromise. A heterophil antibody test is positive for infectious mononucleosis.
Appropriate management includes which one of the following? (check one)A. A corticosteroid B. An antihistamine C. An antiviral agent D. Strict bed rest E. Avoidance of contact sports1.
Page | 33
6. The treatment of choice for a 4-month-old infant with suspected pertussis is: (check one)A. Supportive care (respiratory, fluids) only B. Ceftriaxone (Rocephin) C. Ampicillin D. Gentamicin (Garamycin) E. Erythromycin
Answers:1. C 2.B 3.D 4.A 5.E 6.B
Antibiotic Adult Dose
Pediatric Dose
Comments
Amoxicillin (Amoxil) (a form of PCN)1st line, Inhibit Cell wallAugmentin (amoxil + Clav. acid)
500mg TID x 7-10 dAlso comes in 250mg
125mg/5ml TID x 7-10 d250mg/5ml TID x 7 -10d30-50mg/kg/day
Not if allergic to PCN.
Cephalexin (Keflex)1st line, inhibit cell wall1st gen. cephalosporin
500mg TID x 7-10 dAlso comes in 250mgBest for skin infection
125mg/5ml TID x 7-10 d250mg/5ml TID x 7-10 d30-50mg/kg/day
If allergic to PCN may be allergic to Keflex (5%). give if rash, aphylactic Dont GIVE
Erythromycin, Macrolide 1st lineInterfere with protein synthesis
500mg TID x 7-10 d
125mg/5ml TID x 7 days250mg/5ml TID x 7 days30-50mg/kg/day
Give if allergic to PCN. SE: GI
Azithromycin (Zithromax) (macrolide)2nd line: Z-pack
Z-pack 2 today and one day 2-5
10mg/kg QD x 1 day +5mg/kg QD x4 days100mg/5ml,
Every patient wants z-pack. Atypical pneumonia caused by Mycoplasma, Treat Chlymedia
Page | 34
200mg/5ml
Ciprofloxacin (Cipro)2nd lineQuinolones/Inhibit DNA
500mg BID x 3-5 dFor UTI in elderly 7d
For age >18Levaquine forpneumonia
Risk tendinitis/tendon rupture,. Treat divertics
Ceftriaxone (Rocephin)2nd line, IM 3rd gen. cephlo, cell wall
Used of sever infection and pneumonia, used to treat GC
Trimethoprim/Sulfamethoxazole (Bactrim-DS)2nd line, Sulfonamid
Bactrim DS 3-5d UTI 7 day in elderly
In children bactrim liquid
MRSA treatmentNot for pregnant women or allergic to sulfa drugs.
Metronidazole (Flagyl) 500mg TID x 5-7 d
Treat c-diff., bacteria vaginosis, and trichemonas, Not for pregnant women. Can Not Drink ETOH. Diverticulitis
Doxycycline (Vibramycin, tetracycline)2nd line
100mg PO BID
>12 years Acne. MRSA, if allergic to Sulfa. bronchitis Not for pregnant women. Treat Chlymedia
Nitrofurantoin (Macrobid) 100mg BID x 7 days
UTI treatment for pregnant women.
Acyclovir and Valtrex, antivirals Look up dosing
Valtrex very expensive
Treat Shingles and genital herps
Bacroban cream or ointment Minor skin infection, Impitigo
Sulfasulamide (Bleph-10) opth slnTobramyocing op slon. Erythr oint
Eye infections
BOARD PEARLS :
# Amoxicillin used for treatment of lyme disease.
# Erythromycin +Theophylline leads to Theophylline toxicity.Treatment for theophylline toxicity is beta blockers.
# Azithromycin is the drug of choice for atypical pneumonia, rheumatic fever and prophylaxis of MAC.
# Ciprofloxacin is the drug of choice for Anthrax,Typhoid fever in OPD,Prophylaxis of meningococcal meningitis.
Page | 35
# Ciprofloxacin causes Seizures and Phototoxicity.
# Acyclovir +Valcyclovir is used for treatment of H.Simplex.
# MRSA outpatient we use Bactrim-DS , if inpatient we use Vancomycin.
# linezolid(Zyvox,vivox) is also used to treat MRSA if they are allergic to clindamycin, it is very expensive so not used often.
# patient with Anaphylaxis treatment order CPR(if patient is not responsive)àepinephrine injectionàIV fluidsàantihistamines and steroids given.
# Augmentin is a penicillin resistant penicillin.
# Alendronate(anti osteoporosis) helps to prevent hip fracture.
# Pentoxyfylline is used for treatment of venous ulcers if patient is unable to tolerate compression therapy.
# Indomethacin not prescribed for older patients due to its propensity to produce more CNS adverse effects than other NSAIDS.
# Sulfonamides side effects : GNEMONIC (ABC RASH) A : aplastic anemia B :bilirubin displace(kernicterus in meningitis) C : crystalluria R : rash(most common side effect) A : acetylation S : SLE H : hemolysis(G6PD deficiency).
# Primigravida with pregnancy with vomiting and nausea treatment is Doxylamine and Vitamin B6
# Metronidazole is also used to treat Pseudomembranous colitis and Amoebiasis. It is contraindicated for pregnant woman.
# Doxycycline is the only tetracycline that is safe in kidney disease patients.
Page | 36
Somerset Family Medicine Clinical Module
Bread & Butter of Family Medicine:
ASTHMAAsthma is a chronic pulmonary disease characterized by inflammation, hypersecretion and bronchospasm of airways.Diagnostic evaluation: history and physical exam are crucial for the diagnosis.
Remember: not all wheezes are asthma, not all asthma wheezes! Peak flow testing can provide additional evidence of airway obstruction and support clinical impression. Airway obstruction exists when peak flow is less than 80% of predicted. When diagnosis is still uncertain, complete pulmonary function testing can be obtained:
- Allergy testing (skin test, blood test, in vitro-specific IgE antibody test)- Chest x-ray to exclude alternatives, hyperinflation seen- Arterial blood gas(mild hypoxia & respiratory alkalosis)- Bronchial provocation (methacholine challenge) if spirometry is normal
or near normal- Sinus x-ray or CT scan- GERD evaluation- CBC with eosinophils, total IgE, sputum exam- spirometry/PFTs -decrease FEV1/FEV, increase RV,increase TLC(PFTs
may be normal or exacerbations)
In 2-23% of adults with asthma, and rarely in children with asthma, aspirin (acetylsalicylic acid) and non-steroidal anti-inflammatory drugs (NSAIDs) cause asthma exacerbations. ASA triad (Samter ’ s triad): hypersensitivity to aspirin, chronic rhinosinusitis and nasal polyps, and severe bronchial asthma.
Lung volume measurements in diagnosis of asthma(PFTs): Test Normal Mild Moderate Severe
Page | 37
FEV1(% of FEC) >75 60 - 75 40 - 60 <40
RV(% of predicted) 80-120 120 - 150 150 - 175 >200
Here are the key messages from the EPR-3 (Expert Panel Report) Asthma Guidelines.1) Inhaled corticosteroids are the most effective anti-inflammatory medication for long
term management of persistent asthma. 2) Write asthma action plan for every patient3) Initial assessment of asthma severity4) Review of the level of asthma control (impairment and risk) at all follow up visits
2) 5) Periodic, follow up visits (at least every 6 months)6) Assessment of exposure and sensitivity to allergens and irritants and
3) recommendation to reduce relevant exposures. 7) Asthma education by a qualified health professional.9) Education regarding the danger of over-use of short-acting beta-agonists.
Classification of Asthma Severity
Components of Severity
Intermittent Persistent Mild Persistent Moderate or Severe
Symptoms Less or 2 days per week
More 2 days per week, but not daily
daily
Nighttime awakenings
Less or 2 times per month
3 to 4 times per month
More than once per week
Short-acting beta agonist use for symptom control (not prevention of exercise-induced bronchospasm)
Less or 2 days per week
More than 2 days per week, but not more than once per day
Daily
Interference with normal activity
none Minor limitation Some or extremely limitation
Page | 38
Lung function Normal FEV1 between exacerbation; FEV1 more than 80%of predicted; FEV1/FVC normal
FEV1 more or equal 80 % of predicted;FEV1/FVC normal
FEV1 more than 60 but less 80 % (M) or less than 60% (S);FEV1/FVC reduced 5%
Classification of Asthma Control
Stepwise Approach for Asthma Management
Step Preferred treatment Alternative treatment
1 (intermittent asthma) Inhaled short-acting Beta2 agonist, as needed Albuterol (Proair) Salbutamol (Ventolin)
2 (persistent asthma: mild, moderate and severe)
Low-dose inhaled corticosteroids Beclomethasone (Q-var)
Cromolyn, leukotriene receptor antagonist Singulair, nedocromil, theophylline
3 Low-dose inhaled corticosteroids plus long-acting inhaled Beta2 agonistSalmeterol (Serevent) or Medium-dose inhaled corticosteroids
Low-dose inhaled corticosteroid plus on the of the following – Singulair, theophylline or Zileuton (Zyflo)
4 Medium-dose inhaled corticosteroids plus long-acting inhaled beta2 agonistAdv-air (Fluticasone plus salmeterol)
Medium-dose inhaled corticosteroid plus one of the following – Singulair theophylline or Zileuton
Page | 39
Consult with asthma specialist if step 4 is required, consider consultation at step 3. Step 5 and 6 are not pictured as it is for asthma specialist. Each step: Patient education, environmental control, management of comorbidities.Step 2-4: consider subcutaneous allergen immunotherapy for patients who have allergic asthma.Quick-relief medication for all patients: Inhaled short-acting beta2 agonist as needed: up to 3 treatments at 20-minute intervals. Short course of oral corticosteroids may be needed.Use of inhaled short-acting beta2 agonist 2 or more days a week for symptom relief (not for exercise-induced asthma) indicated inadequate control and the need to step up treatment.If step-up needed, first check adherence, environmental control, comorbid conditions.
Step down is possible if asthma is well controlled at least three months. DRUG MOA S/E
BETA 2 Agonists albuterol/salbutamolTerbutaline :short acting.Relaxes bronchial smooth muscle.D.O.C for pregancy with acute asthma attack.Salmeterol and formeterol : long acting agent for prophylaxis.formeterol(fast acting, used in acute attack & prophylaxis.
TremorsTachycardiaTolerance
Corticosteriods Inhaled corticosteroids are 1st line treatment for long-term control of asthmaBeclomethasone, prednisone: inhibit the synthesis of virtually all
loss of potassiumobesitypuffiness of face(moon face)coughsore throat
Page | 40
cytokines.
muscarinic antagonists Ipratropium and Tiotropium: competitively blocks muscarinic receptors, pretending bronchoconstriction.D.O.C in labour with acute attack of asthma.
drowsiness, blurred vision, dry mouth, heat intolerance, flushing, decreased sweating, difficulty urinating, abdominal cramping, constipation, rapid heart beat, confusion, memory problems, and glaucoma
methylxanthines Theophylline:causes bronchodilation by inhibiting phosphodiesterase,thereby decreasing cAMP hydrolysis and increasing cAMP levels.Is a zero order kinetics.cant be given as inhalation.
cardiotoxicityneurotoxicitytheophylline+ciprofloxacin/erythromycin : inhibit metabolism of theophylline and leads to toxicity.
cromolyn prevents the release of vasoactive mediators from mast cells.useful for exercise-induced bronchospasm. effective only for prophylaxis of asthma ; not effective during an acute attack. toxicity is rare.
Coughingnauseathroat irritationchest tightness
anti leukotrines zileuton: A 5-lipoxygenase pathway inhibitor. blocks conversion of arachidonic acid to leukotrienes.Monterlukast , Zafirleukast: blocks leukotriene receptors.
headache;stomach pain, heartburn, upset stomach, nausea, diarrhea;tooth pain;tired feeling;fever, stuffy nose, sore throat, cough, hoarseness; ormild rash.
Page | 41
Mast cell stabilizers Nedocromil,sodium cromoglycate ,ketotifen used only for prophylaxis and not used for treatment.
headache ,cough,throat irritation and abdominal pain.
stop antigen - antibody reaction
Omalizumab(Xolair): antibody against anti IgE antibody (monoclonal antibody against IgE)Used for prophylaxis.
tightness in your chest, trouble breathing,hives or skin rash,feeling anxious or light-headed, fainting,warmth or tingling under your skin,swelling of your face, lips, tongue, or throat.
Board pearls:
# beta 2 agonists + steroids : decrease pottasium in asthma patients.
# meds for asthma exacerbation (mnemonic): ASTHMA
A - albuterol
s - steroids(Beclomethasone and predisone)
T - Theophylline
H - humidified o2
M - monterleukast , magnesium
A - anticholinergics( Ipratropium and Tiotropium)
# Corticosteroids inhaled in rush & can lead to thrush
# asthma should be suspected in children with multiple episodes of CROUP & URIs associated with dyspnea.
Clinical Vignettes
Page | 42
ASTHMA MANAGEMENT WITH DRUGS
1. A 22-year-old competitive cross-country skier presents with a complaint of not being able to perform as well as she expects. She has been training hard, but says she seems to get short of breath more quickly than she should. She also coughs frequently while exercising. A review of systems is otherwise negative. Her family history is negative for cardiac or pulmonary diseases. Her physical examination is completely normal, and pulmonary function tests obtained before and after bronchodilator use are normal. After you discuss your findings with the patient, she acknowledges that her expectations may be too high, but can think of no other cause for her problem. Which one of the following would be the next reasonable step? (check one)A. An echocardiogram to look for cardiomyopathy or valvular dysfunction B. Counseling regarding competition stress and athlete burnout syndrome C. A sports medicine consultation to evaluate her training regimen D. A trial of inhaled albuterol (Proventil) for exercise-induced bronchospasm
2. A 24-year-old female with a past history of asthma presents to the emergency department with an asthma exacerbation. Treatment with an inhaled bronchodilator and ipratropium (Atrovent) does not lead to significant improvement, and she is admitted to the hospital for ongoing management. On examination she is afebrile, her respiratory rate is 24/min, her pulse rate is 92 beats/min, and oxygen saturation is 92% on room air. She has diffuse bilateral inspiratory and expiratory wheezes with mild intercostal retractions. Which one of the following should be considered in the acute management of this patient? (check one)A. Chest physical therapy B. Inhaled fluticasone/salmeterol (Advair) C. Oral azithromycin (Zithromax)
Page | 43
D. Oral prednisone E. Oral theophylline
3. A 6-year-old male is brought in for evaluation by his mother, who is concerned that he may have asthma. She reports that he coughs about 3 days out of the week and has a nighttime cough approximately 1 night per week. There is a family history of eczema and allergic rhinitis. Which one of the following would be the preferred initial treatment for this patient? (check one)A. A leukotriene receptor antagonist such as montelukast (Singulair) B. A low-dose inhaled corticosteroid such as budesonide (Pulmicort Turbuhaler) C. A long-acting beta-agonist such as salmeterol (Serevent) D. A mast-cell stabilizer such as cromolyn sodium (Intal)
4. When prescribing an inhaled corticosteroid for control of asthma, the risk of oral candidiasis can be decreased by: (check one)A. using a valved holding chamber B. limiting use of the inhaled corticosteroid to once daily C. adding nasal fluticasone propionate (Flonase) D. adding montelukast (Singulair) E. adding salmeterol (Serevent)
Answers:
1.D 2.D 3.B 4.A
Somerset Family Medicine Clinical Module
Page | 44
Bread & Butter of Family Medicine: THYROID DISEASE
Epidemiology:- Hypothyroidism: 4-6% of the population, Primary congenital hypothyroidism – 1/3,000 infants-Hyperthyroidism:2-3% of the population-Age – onset is 40s-50s for both hypo- and hyperthyroidism-Sex – M<F, 1:5-8 for both types
Indications for Testing: Symptoms of hyper- or hypothyroidism, Family history of autoimmune thyroiditis, Goiter on physical exam
Testing of Thyroid FunctionTFTs include, TSH, T4,T3■ TSH measurement: The single best test for assessing thyroid function.High TSH levels lead to 1° hypothyroidism; low TSH levels lead to thyrotoxicosis.■ Radioactive iodine uptake (RAIU) and scan: Determines the level of iodineuptake by the thyroid. Useful in differentiating thyrotoxic states, buthas a limited role in determining malignancy.
Diagnosis TSH T4 T3 Causes
1° hyperthyroidism
Low High High Graves’ disease, toxic multinodular goiter, toxic adenoma, amiodarone,molar pregnancy, postpartumthyrotoxicosis, postviral thyroiditis.
1° hypothyroidism
High Low Low Hashimoto’s thyroiditis, hypothyroidphase of thyroiditis, iatrogenicfactors (radioactive iodine thyroidablation, excision with inadequatesupplementation, external radiation,lithium, or amiodarone), iodine
Page | 45
defi ciency, infi ltrative disease.
■ Total T4 measurement: Not an adequate screening test. Ninety-nine percent, of circulating T4 is bound to thyroxine-binding globulin (TBG). Total T4 levels can be altered by changes in levels of binding proteins.■ T3 resin uptake (T3RU): Used with total T4 or T3 to correct for changes,in TBG levels (e.g., the free thyroxine index = total T4 × T3RU).■ Free T4 measurement: The preferred screening test for thyroid hormone levels; more useful for nstable thyroid states.
HyperthyroidismRefers to causes of thyrotoxicosis (↑ levels of T3/T4 due to any cause) in which, the thyroid overproduces thyroid hormone, including Graves’ disease, toxic, multinodular goiter (also called Plummer’s disease), and toxic adenomas.
HISTORY/PE■ Presents with weight loss, heat intolerance, nervousness, palpitations, ↑bowel frequency, insomnia, and menstrual abnormalities.■ Exam reveals warm, moist skin, goiter, sinus tachycardia or atrial fibrillation, fine tremor, lid lag, and hyperactive refl exes. Exophthalmos, pretibial myxedema, and thyroid bruits are seen only in Graves’ disease DIAGNOSISThe initial test of choice is serum TSH level, followed by T4 levels and, rarely,T3 (unless TSH is low and free T4 is not elevated).
TREATMENT• 1°therapy is radioactive 131I thyroid ablation; antithyroid drugs (methimazole or
propylthiouracil) may also be used if radioactive iodine is not indicated. Thyroidectomy is rarely indicated.
• Give propranolol for adrenergic symptoms while awaiting the resolution of hyperthyroidism.
• Administer levothyroxine to prevent hypothyroidism in patients who have undergone ablation or surgery.
HypothyroidismHashimoto’s thyroiditis is the most common cause of hypothyroidism. Anti-TPO antibodies are _. The second most common cause is iatrogenic. Myxedema coma refers to severe hypothyroidism with ↓ mentalstatus, hypothermia, and other parasympathetic symptoms. Mortality is 30–60%.HISTORY/PEPresents with weakness, fatigue, cold intolerance, constipation, weight gain, depression, menstrual irregularities, and hoarseness. Exam may reveal dry, cold, puffy skin accompanied by edema, bradycardia, and delayed relaxation of DTRs.TREATMENT
• Uncomplicated hypothyroidism (e.g., Hashimoto’s disease): Administer levothyroxine.
Page | 46
• Myxedema coma: Treat with IV levothyroxine and IV hydrocortisone (if adrenal insufficiency has not been excluded).
Thyroiditis:Inflammation of the thyroid gland. Common subtypes include subacute granulomatous, radiation-induced, autoimmune (lymphocytic, chronic, or Hashimoto), postpartum, and drug-induced (e.g., amiodarone) HISTORY/PEThe subacute form presents with a tender thyroid accompanied by malaise and URI symptoms. Other forms are associated with painless goiter.DIAGNOSISThyroid dysfunction (typically thyrotoxicosis followed by hypothyroidism), with ↓ uptake on RAIU during the thyrotoxic phase.TREATMENT
• β-blockers for hyperthyroidism; levothyroxine for hypothyroidism.• Subacute thyroiditis is usually self-limited; treat with NSAIDs or with oral
corticosteroids for severe cases.
Thyroid Neoplasms : Thyroid nodules are very common and show an ↑ incidence with age. Most are benign.HISTORY/PE-Usually asymptomatic on initial presentation.-Hyperfunctioning nodules present with hyperthyroidism and local symptoms, (dysphagia, dyspnea, cough, choking sensation) and are associated with a _ family history (especially medullary thyroid cancer).- ↑ risk of malignancy is associated with a history of neck irradiation, “cold” nodules on radionuclide scan, male sex, age < 20 or > 70, firm and fixed solitary nodules, a _ family history (especially medullary thyroid cancer), and rapidly growing nodules with hoarseness.-Medullary thyroid carcinoma is associated with multiple endocrine neoplasia (MEN) type 2 and familial medullary thyroid cancer.DIAGNOSIS- The best method of assessing a nodule for malignancy is fi ne-needle aspiration (FNA), which has high sensitivity and moderate specificity.- TFTs (TSH to exclude hyperfunction).- Ultrasound determines if the nodule is solid or cystic; a radioactive scan determines whether it is hot or cold (cancers are usually cold and solid). Hot nodules are never cancerous and should not be biopsied.
• Type • character Prognosis
• Papillary • Represents 75–80% of thyroid
• cancers. The female-to-male ratio is
• 3:1. Slow growing;
• Ninety percent of patients survive 10
years or more after diagnosis; the• prognosis is worse in
Page | 47
• Type • character Prognosis
found in thyroid• hormone–producing
cells.
elderly patients• or those with large
tumors.
• Follicular • Accounts for 17% of thyroid
• cancers; found in thyroid hormone–
• producing cells
• Ninety percent of patients survive 10
• years or longer after diagnosis; the
• prognosis is worse in elderly patients
• or those with large tumors
• Medullary • Responsible for 6–8% of thyroid
• cancers; found in calcitoninproducing
• C cells; the prognosis• is related to degree of
vascular• invasion.
• Eighty percent of patients survive at
• least 10 years after surgery.
• Anaplastic • Accounts for 2% of thyroid
• cancers; rapidly enlarges and
• metastasizes.
• Ten percent of patients survive for
• > 3 years.
BOARD PEARLS:
# sodium iodine ,pottasium iodide and lugol’s iodide are fast acting antithyroid drugs A/K/A thyroid constipating drugs.These are the drug of choice for thyroid storm.
# Euthyroid sick syndrome: TSH-normal , T3 very low, caused due to MOF,sepsis,shutdown metabolism to conserve energy,supress conversion of free T4 to T3. it is normal and there is no treatment.
# TBG levels are tested to find out if thyroid hormones levels are endogenously produced or endogenously produced.
# THYROID STROM : TREAT urgently with IV propranalol,propylthiouracil and corticosteroids.high dose potassium iodide SSKI is also used.
# Bone loss is seen with hyperthyroidism.
Page | 48
# Hypothyroid and PKU could present as delayed walking in children, mental retardation and global developmental delay.
BOARD PEARLS FOR THYROID NEOPLASMS :
# PAPILLARY CARCINOMA : it is the slow growing and spreads via lymphatics. MNEMONIC 5P’s P : papillae (branching) P : palpable lymph nodes P : pupil nuclei (orphan annie nuclei) P : psammoma bodies with in lesions P : positive prognosis.
# FOLLICULAR CARCINOMA : Spreads hematogenously with distant metastasis to lung and bone.Hurtle cells are seen in both papillary and follicular carcinomas but mostly seen in follicular carcinoma.
# MEDULLARY CARCINOMAS : Arise from parafollicular cells of the thyroid.medullary carcinoma is the only cancer with an elevated CALCITONIN level .medullary carcinoma : DNA testing is the most effective screening test.
# ANAPLASTIC CARCINOMA : Highly malignant with rapid and painful enlargement. spreads by direct extension.# Cold nodules on RAI scan should be biopsy.
# Hyperfunctioning thyroid nodules are not malignant
Clinical Vignettes
1. An asymptomatic 55-year-old male visits a health fair, where he has a panel of blood tests done. He brings the results to you because he is concerned about the TSH level of 12.0 µU/mL (N 0.45-4.5). His free T4 level is normal. Which one of the following is most likely to be
Page | 49
associated with this finding? (check one)A. Atrial fibrillation B. Reduced bone density C. Systolic heart failure D. Elevated LDL cholesterol E. Type 2 diabetes mellitus
2. A 67-year-old female presents with progressive weakness, dry skin, lethargy, slow speech, and eyelid edema. Of the following medications currently taken by this patient, which one is most likely to be causing her symptoms? (check one)A. Donepezil (Aricept) B. Lithium C. Lisinopril (Prinivil, Zestril) D. Alendronate (Fosamax) E. Glyburide (DiaBeta, Micronase)
3. A 54-year-old female takes levothyroxine (Synthroid), 0.125 mg/day, for central hypothyroidism secondary to a pituitary adenoma. The nurse practitioner in your office orders a TSH level, which is found to be 0.1 mIU/mL (N 0.5-5.0). Which one of the following would you recommend? (check one)A. Decrease the dosage of levothyroxine B. Increase the dosage of levothyroxine C. Order a free T4 level D. Order a TRH stimulation test E. Repeat the TSH level in 3 months
4. In a patient with a solitary thyroid nodule, which one of the following is associated with a higher incidence of malignancy? (check one)A. Hoarseness B. Hyperthyroidism C. Female gender D. A nodule size of 2 cm E. A freely movable nodule
Page | 50
5. A small child with failure to thrive is found to have a bone age that is markedly delayed relative to height age and chronologic age. The most likely etiology is: (check one)A. Cystic fibrosis B. Hypothyroidism C. Down syndrome D. Fetal alcohol syndrome E. Gonadal dysgenesis
6. Chronic excess thyroid hormone replacement over a number of years in postmenopausal women can lead to: (check one)A. Diffuse nontoxic goiter B. Osteoarthritis C. Osteoporosis D. Hyperparathyroidism
7. A woman presents in the postpartum period with palpitations, irritability, and heat intolerance. Radioactive iodine uptake is low. Which one of the following statements is correct? (check one)A. She has Graves disease. B. She will likely have an elevated thyroid-stimulating hormone level and a high triiodothyronine-to-thyroxine ratio. C. She should be treated with a thiourea. D. She should be treated with propranolol.
Answers:1. D 2.B 3.D 4.A 5.B 6.C 7.D
Page | 51
Somerset Family Medicine Clinical Module
Bread & Butter of Family Medicine: GOUT
❖ What is it?➢ Group of disorders related to hyperuricemia➢ Crystal-induced arthropathy caused by monosodium urate crystal deposition in tissue
resulting in acute and chronic arthritis, soft tissue masses/nodules called tophi (classically on earlobe, but can be on fingers, toes, prepatellar bursa, olecranon), urate nephropathy, and uric acid nephrolithiasis
Gout is caused by monosodium urate monohydrate crystals; pseudogout is caused by calcium pyrophosphate (CPP) crystals and is more accurately termed calcium pyrophosphate disease (CPPD). Epidemiology
➢ Common - Prevalence: 6 per 1,000 men; 1 per 1,000 women❖ Risk factors
➢ Hyperuricemia (Odds ratio: 32 times more likely than those with normal serum uric acid)➢ Male gender ➢ EtOH ingestion (beer and liquor > wine)➢ Metabolic syndrome, and separately, obesity, HTN, diabetes, dyslipidemia, and renal
insufficiency➢ Diet rich in purines (e.g., meats, liver, kidney, shellfish, anchovies, sardines) or high-
fructose corn syrup (e.g., soda beverages); dehydrationMedications that can cause hyperuricemia via underexcretion (e.g., thiazide diuretics,
➢ niacin) and overproduction (e.g., chemo causing high turnover of cells)➢ Family hx especially with genetic conditions like Lesch-Nyhan Syndrome (deficiency in
hypoxanthine-guanine-phosphoribosyltransferase resulting in overproduction of uric acid)
❖ Diagnosis➢ Hx of rapid onset of severe pain, usually beginning in early morning with 1 or 2 joints +/-
fever▪ Affected joint is inflamed (red, hot, swollen, and exquisitely tender)▪ Up to 75% are monoarticular▪ First metarsotarsophalangeal joint involved in ~50% of initial attacks (called
Podagra)▪ Untreated attacks last up to 3 weeks with absence of inflammation between attacks
(unless chronic or tophaceous phase has occurred)▪ Can have renal colic 2/2 uric acid renal stones
➢ Best initial test?▪ Arthrocentesis of affect joint to evaluate for crystals and rule out septic arthritis
• Synovial fluid analysis ♦ Urate crystals (negatively birefringent)♦ WBC usually 2,000-50,000/mm3 (neutrophil-predominant); for infxn, WBC
>50K♦ Should always check gram stain and cx to rule out infxn (which can coexist)
▪ In clinical practice, a presumptive dx can be made with classic Podagra + hyperuricemia
Page | 52
if there is fluid in the joint,it needs analysis immediately .➢ Other labs
▪ CBC can show neutrophil-predominant leukocytosis; check Cr for renal insufficiency▪ Elevated serum uric acid level (may be normal during 15% of acute attacks due to
precipitation in tissue)▪ UA, 24-hr urinary uric acid▪ X-ray may show “punched-out” erosions (for recurrent/chronic gout); urate stones
are radiolucent and thus invisible on x-ray▪ Biopsy of soft tissue nodule or synovial membrane (rarely done if other labs not
helpful)❖ Other less common complications urate crystals deposit in other organs
➢ Nerve or spinal cord impingement by urate deposition➢ Eye involvement including keratitis and anterior uveitis
❖ Treatment for Acute Gout – discontinue any meds (e.g., diuretics) that may contribute
Class MOA Names Clinical Info Caution
NSAIDs,except aspirin (which can alter uric acid lvl and intensify acute attacks)
Inhibits COX pathway, reducing prostaglandin and thromboxane synthesis
Indomethacin 50mg po TIDNaproxen 750mg po x1, then 250mg q8h or 500mg BID
First-lineTaper to lowest effective dose; give with food if GI upset
Renal insufficiency, PUD, liver disease
Lifestyle modification
Avoid EtOH, diets high in purines and high-fructose corn syrup
First line
Colchicine Concentrates in PMN cells and inhibits microtubule polymerization, preventing neutrophil activity
Colchicine 1.2mg po x1, then 0.6mg 1hr later
Second lineEffective if given within first 24 hrs of attack
GI side effects (n/v/diarrhea), bone marrow suppression(neutropenia);If renal impairment with CrCl<30, cannot give til 2 weeks later
Steroids Anti-inflammatory effects via multiple pathways
IV/po systemic corticosteroids(e.g., prednisone 40mg po x1-3 days, then tapered over 2 wks)Intra-articular
Second lineSystemic given with multiple jts; intra-articular with single or few jts
Rule out septic joint, caution with diabetes, HTN, PUD, glaucoma, etc.
Adrenocorti-cotropic hormone (ACTH)
Induces patient’s own adrenal corticosteroid production
ACTH 25 USP units SC for acute small-joint monoarticular gout; 40 USP units IM/IV for larger joints or polyarticular gout
Second line Hypersensitivity reaction
Page | 53
Combination therapy
NSAIDs + Colchicine
Steroids + Colchicine
NSAIDs + steroids
First line for severe attacks involving multiple large jointsThird line if others not effective
Treatment for Chronic Gout ➢ Indications: >2 attacks per year, tophi present, or radiographic evidence of joint damage➢ Goal serum uric acid <6➢ Do NOT start until 2-3 wks after acute attack has resolved, because acute changes in
serum uric acid level can intensify and prolong an acute attack➢ If Pt is already on chronic therapy during an acute attack, okay to continue meds.
Class MOA Names Clinical Info Caution
Xanthine oxidase inhibitors
Inhibits xanthine oxidase, which usually converts hypoxanthine into uric acid (from purine metabolism)
Allopurinol 100mg po daily, adjust q2-4wks until goal serum uric acid lvl
Febuxostat 40mg po daily, titrate to 80mg daily
First-lineCo-prescribe with colchicine 0.5-1mg/d OR low-dose NSAIDs on initiation of treatment to prevent rebound acute attacks
Allopurinol: monitor for renal insufficiency and hypersensitivity rxn (rash, hepatitis, interstitial nephritis)
Lifestyle modification
Avoid EtOH, diets high in purines and high-fructose corn syrup.Increase fluid intake.
First line
Uricosuric agentsGiven only if pt is underexcretor (i.e. 24-hr urinary uric acid <800)
Inhibit tubular reabsorption of uric acid
Probenecid 250mg po BID and titrate qMonthly until goal
Sulfinpyrazone 50mg po BID and titrate qMonthly until goal
Second line-Only given if normal renal fxn without h/o renal stones-Also co-prescribe with colchicine or low-dose NSAIDs as above
Increase risk of stone formation and renal failure
Can alkalinize urine with potassium citrate supplementation to decrease urate stone formation (also counsel to increase fluid intake)
Page | 54
Other agents with modest uricosuric effects
Inhibit tubular reabsorption of uric acid
FenofibrateLosartanAmlodipine
Third line
Uricase Breaks down uric acid to allantoin, which is inactive and readily excreted by the kidneys
Rasburicase IVPegloticase IV(uricase enzyme is obtained by recombinant DNA Therapy as uricase is absent in humans)
Third lineExpensive and rarely used for gout; used mainly in tumor lysis syndrome
Hypersensitivity reactions
BOARD PEARLS :
# Patients with gout should take low protein diet as increase protein results in increase uric acid .
# Gout crystals appear yellow when parallel to the condenser.
# Colchicine is most effective drug used for resistant gout. S/E :-myopathy and GI disorders.
# Colchicine inhibits neutrophil chemotaxis.
# Gout significantly increased the risk of preeclampsia, preterm birth, cesarean delivery, low birth weight, and small-for-gestational age infants.There are currently five drugs that can be used to treat gout during pregnancy: allopurinol (Zyloprim), colchicine (Colcrys), febuxostat (Uloric), pegloticase (Krystexxa), and probenecid.
# Causes of hyperurcemia: *increase cell turnover(hemolysis,blast crisis,tumor lysis,myelodysplasia,psoriasis) *cyclosporine *lead poisoning *salicylates *starvation *dehydration
# Pseudogout: pt. has a history of hemochromatosis and hyperparathyroidism.
# punched out lesions with overhanging cortical bone(RAT BITE erosions) are seen in advanced gout.
# Culture of joint fluid is positive in only 50% or less of gonococcal arthritis.
# The basic test to run on synovial fluid are the 3 Cs(cell count,crystals and cultures) and the gram strain.
Page | 55
Joint aspiration is done because in monoarticular i.e septic arthritis it must be ruled out because it leads to bone erosions with in a day.
# Synovial Fluid Analysis:
DISEASE WBC’s Crystals/polarization
Non Inflammatory Disease Osteoarthritis
<2,000 Negative
Inflammatory DiseaseRheumatoid arthritis(Gout & Pseudogout)
5,000 - 50,000Acute gout: needle shaped uric acid crystal,-ve birefringent.Pseudogout: rhomboid shape uric acid crystals,+ve birefringent
Septic arthritis >50,000 -ve gram stain and culture usually negative for GC and absent crystals.
There are few exceptions to the above:septic arthritis may sometimes present with <50,000WBC/mm3 in the joint aspiration if antibodies are given before the joint aspiration.
Somerset Family Medicine Clinical Module
Bread & Butter of Family Medicine:
ALLERGIC RHINITISAllergic rhinitis and asthma often coexist and more than half of the asthma cases can be attributed to seasonal allergies. In some cases allergic rhinitis and asthma may be thought of as manifestation of the same disease.
Treatment:
LIFESTYLE AND AVOIDING ALLERGENSThe best treatment is to avoid the pollens that cause your symptoms. It may be impossible to avoid all pollen. But you can often take steps to reduce your exposure.
Page | 56
Antihistamins: 1st generation (Diphenhydramine), 2nd generation (Loratadine, fexofenadine, cetirizine);
1. Decongestants: symptomatic relieve, for short period of time. Do not use Afrin (oxymetazoline nasal) for more than 3 days – it causes rebound congestion. Saline nasal spray and irrigation with special device “neti (or nutty) pot”
2. Corticosteroid Nasal Spray: the most effective treatment and first-line therapy for the long-term management of mild to moderate persistent symptoms (Flonase, Nasonex)
3. Leukotriene inhibitors: useful in both asthma and allergic rhinitis (Singulair, Accolate)
4. Oral corticosteroids: only for severe allergy and at the lowest dose for short period of time
5. Desensitization therapy: injections weekly or biweekly
6. Ophthalmic symptoms: OTC – Zaditor (ketotifen ophthalmic), Naphcon, Cromolyn ophthalmic. Prescription – Patanol. Avoid Visine!!!
BOARD PEARLS :
Page | 57
Symptoms:Symptoms that occur shortly after you come into contact with the substance you are allergic to may include:Itchy nose, mouth, eyes, throat, skin, or any areaProblems with smellRunny noseSneezingWatery eyes “red eyes”
Symptoms that may develop later include:Stuffy nose (nasal congestion)Coughing(non productive)Clogged ears and decreased sense of smellSore throatDark circles under the eyes,conjunctivitisPuffiness under the eyesFatigue and irritabilityHeadache
Exams and Tests:
The health care provider will perform a physical exam and ask about your symptoms. You will be asked whether your symptoms vary by time of day or season, and exposure to pets or other allergens.
Allergy testing may reveal the pollen or other substances that trigger your symptoms. Skin testing is the most common method of allergy testing.
If your doctor determines you cannot have skin testing, special blood tests may help with the diagnosis. These tests, known as IgE RAST tests, can measure the levels of allergy-related substances.
A complete blood count (CBC) test called the eosinophil count may also help diagnose allergies.
Page | 58
Somerset Family Medicine Clinical Module
Bread & Butter of Family Medicine: MIGRAINE
What is Migraine?• Its Neurovascular disease categorized as a primary headache disorder according to
International Headache Society (IHS)• It is the second most common cause of headache after tension headache• The pain of migraine occurs when excited brain cells trigger the trigeminal nerve to
release chemicals that irritate and cause swelling of blood vessels on the surface of the brain. These swollen blood vessels send pain signals to the brainstem, an area of the brain that processes pain information. The pain of migraine is a referred pain that is typically felt around the eye or temple area. Pain can also occur in the face, sinus, jaw or neck area. Once the attack is full-blown, many people will be sensitive to anything touching their head. Activities such as combing their hair or shaving may be painful or unpleasant.
• It is usually episodic headache disorder characterized by combinations of neurologic, gastrointestinal, and autonomic changes.
• Migraine is recurrent, often life-long, and characterized by attacks.
Epidemiology
• Migraine is an extraordinarily common disease that affects 36 million men, women and children in the United States.
• Nearly 1 in 4 U.S. households includes someone with migraine.• Amazingly, over 10% of the population - including children - suffers from migraine.
That's more than diabetes and asthma combined!• About 18% of American women and 6% of men suffer from migraine (F>M).• Migraine is most common during the peak productive years, between the ages of 25 and
55.• Migraine ranks in the top 20 of the world's most disabling medical illnesses.
Risk Factor• Family history. Migraine tends to run in families. If one parent suffers from migraine,
there is a 40% chance a child will suffer. If both parents suffer, the chance rises to 90%.• Age. Migraines can happen at any age but most often begins at puberty and most affects
aged between 35 and 45 years• Sex. In childhood, boys are affected more than girls, but after adolescence, when estrogen
influence begins in young girls, the risk of migraine and its severity rises in females.
Page | 59
• Hormonal changes. More severe and more frequent attacks often result from fluctuations in estrogen levels and decrease after menopause.
Triggered factor: Specific Lifestyle Factors Lifestyle triggers can vary from person to person. Some reported triggers include
• Caffeine withdrawal• Changes in hormone levels during a woman's menstrual cycle or with the use of birth
control pills• Changes in sleep patterns• Drinking alcohol• Exercise or other physical stress• Loud noises or bright lights• Missed meals• Odors or perfumes• Smoking or exposure to smoke• Stress and anxiety
Migraines can also be triggered by certain foods. Most common are:• Baked goods• Chocolate• Dairy foods• Foods with monosodium glutamate (MSG)• Foods with tyramine, which includes red wine, aged cheese, smoked fish, chicken livers,
figs, and certain beans• Fruits (avocado, banana, citrus fruit)• Meats containing nitrates (bacon, hot dogs, salami, cured meats)• Onions• Peanuts and other nuts and seeds• Processed, fermented, pickled, or marinated foods
Phases of Migraine. Migraine is divided into four phases, all of which may be present during the attack:
• Premonitory symptoms occur up to 24 hours prior to developing a migraine. These include food cravings, unexplained mood changes (depression or euphoria), uncontrollable yawning, fluid retention, or increased urination.
• Aura. Some people will see flashing or bright lights or what looks like heat waves immediately prior to or during the migraine, while others may experience muscle weakness or the sensation of being touched or grabbed.
Page | 60
• Headache. A migraine usually starts gradually and builds in intensity. It is possible to have migraine without a headache.
• Postdrome (following the headache). Individuals are often exhausted or confused following a migraine. The postdrome period may last up to a day before people feel healthy.
Migraine Headaches Are Classified? Classification Of Migraine Headache According to The International Headache Society (IHS).
International Headache SocietyInternational Classification Headache Disorders –II
Code Types of Migraine Headache1.1 Migraine without Aura1.2 Migraine with Aura 1.2.1 Typical Aura with Migraine Headache 1.2.2 Typical Aura with non-migraine headache 1.2.3 Typical aura without headache 1.2.4. Familial Hemiplegic Migraine 1.2.5 Sporadic Hemiplegic Migraine 1.2.6. Basilar-type Migraine 1.3 Childhood periodic Syndromes that are commonly precursors of migraine 1.3.1 Cyclical Vomiting 1.3.2 Abdominal Migraine 1.3.3 Benign Paroxysmal Vertigo of Childhood1.4 Retinal Migraine1.5 Complications of Migraine 1.5.1 Chronic Migraine 1.5.2 Status Migrainosus 1.5.3 Persistent aura without infarction 1.5.4 Migrainous infarction 1.5.5 Migraine-triggered seizure1.6 Probable Migraine 1.6.1 Probable Migraine without Aura 1.6.2 Probable Migraine with Aura 1.6.3 Probable Chronic Migraine
Diagnoses
Page | 61
• It is based on the headache’s characteristics and associated symptoms. The International Headache Society (IHS) diagnostic criteria for headache disorders provide definitions for six subtypes of migraine
Table 1.1. Diagnostic Criteria For Migraine Without Aura (Common Migraine)
A. At least 5 attacks fulfilling criteria B-D
B. Headache attack last 4 to 72 hours (untreated or unsuccessfully treated)
C. Headache has at least two of the following Characteristics: 1. Unilateral location 2. Pulsating Quality 3. Moderate or severity intensity 4. Aggravation by routine physical activity (i.e. walking or climbing stairs)
D. During headache at least one of the following: 1. Nausea &/or Vomiting 2. Photophobia or phonophobia
E. Not attributed to another disorder.
Table 1.2. Diagnostic Criteria for Migraine With Aura (Classic Migraine)
A. At least 2 attacks fulfilling criteria B-D
B. Aura consisting of at least 1 of the following but no motor weakness: 1. Fully reversible visual symptoms including positive features (eg. Flickering lights or Spots or lines) &/or negative features (ie vision loss) 2. Fully reversible sensory symptoms including positive features(ie pins and needles) &/or negative features( ie numbness) 3. Fully reversible dyphasic speech disturbances
C. At least 2 of the following: 1. Homonymous visual symptoms &/or unilateral sensory symptoms 2. At least one aura symptom develops gradually over ≥ 5 minutes 3. Each symptoms lasts ≥ 5 minutes or ≤ 60 minutes
D. Headache fulfilling criteria B-D for migraine without aura begins during the aura or follows aura within 60 minutes
Page | 62
E. Not attributed to another disorder
Table 1.2.1 & 1.2.2. of Migraine has same Diagnostic Criteria as in Table 1.2 (Migraine with Aura)
Table 1.2.3. Diagnostic Criteria for Typical Aura Without Headache
A. At least 2 attacks fulfilling criteria B-D
B. Aura consisting of at least 1 of the following, with or without speech but no motor weakness: 1. Fully reversible visual symptoms including positive features (eg. Flickering lights or Spots or lines) &/or negative features (ie vision loss) 2. Fully reversible sensory symptoms including positive features(ie pins and needles) &/or negative features( ie numbness) 3. Fully reversible dyphasic speech disturbances
C. At least 2 of the following: 1. Homonymous visual symptoms &/or unilateral sensory symptoms 2. At least one aura symptom develops gradually over ≥ 5 minutes 3. Each symptoms lasts ≥ 5 minutes or ≤ 60 minutes
D. Headache does not occur during aura nor follow aura within 60 minutes
E. Not attributed to another disorder
NOTE: Additional loss or blurring of central vision may occur.
Table 1.2.4. Diagnostic Criteria for Familial Hemiplegic Migraine (FHM)
A. Migraine with aura including motor weakness and at least first- or Second-degree Relative has migraine aura including motor weakness
B. At least 2 attacks fulfilling criteria C and D
Page | 63
C. Aura consisting of fully reversible motor weakness and at least one of the following: 1. Fully reversible visual symptoms including positive features(eg flickering lights, Spots or lines) &/or negative features(ie loss of vision) 2. Fully reversible sensory symptoms including positive features( eg pins & needles) &/or negative symptoms( ie numbness) 3. Fully reversible dysphasic speech disturbances
D. At least two of the following : 1. At least one aura symptom develops gradually over ≥ 5 minutes and/or different Aura symptoms occur in succession over ≥ 5 minutes 2. Each aura symptoms last ≥5 minutes and <24 hours 3. Headache fulfilling criteria B-D for Migraine without aura begins during aura or Follows onset of aura within 60 minutes.
E. At least one first-or second-degree relative has had attacks fulfilling these criteria B-F.
F. Not attributed to another disorder
Table 1.2.5. Diagnostic Criteria For Sporadic Hemiplegic Migraine
A. Migraine with aura including motor weakness but NO first-or second-degree Relative Has aura including motor weakness.
B-F. Same as in Table 1.2.4 Familial Hemiplegic Migraine (FHM).
Table 1.2.6. Diagnostic Criteria For Basilar Migraine
A. Migraine with aura symptoms clearly originating from the brainstem and/or from both Hemispheres simultaneously affected, but no motor weakness
B. At least 2 attacks fulfilling criteria C-E
Page | 64
C. Aura consisting of at least two of the following fully reversible symptoms but no Motor weakness
• Dysarthria• Vertigo• Tinnitus• Hypacusia• Diplopia• Visual Symptoms simultaneously in both temporal & nasal fields of both eyes• Ataxia• Decrease level of consciousness• Simultaneously bilateral paresthesiasis
D. At least one of the following: 1. At least one aura symptom develops gradually over ≥ 5 minutes and/or different Aura symptoms occur in succession over ≥ 5 minutes 2. Each aura symptoms lasts ≥ 5 minutes and ≥ 60 minutes
E. Headache fulfilling criteria B-E for Migraine without aura begins during the aura or Follows aura within 60 minutes
F. Not attributes to another disorder
Table 1.3-1.3.1. Childhood periodic Syndromes that are commonly precursors of Migraine: Diagnostic Criteria for Cyclic Vomiting
A. Recurrent Episodic attacks, usually stereotypical in the individual patient, of intense Vomiting and intense Nausea. Attacks associated w/ Pallor & lethargy. There is Complete resolution of symptoms between attacks.
B. At least 5 attacks fulfilling criteria C and D
C. Episodic attacks, stereotypical in the individual patient, of intense Nausea and Vomiting last from 1 hours to 5 days
D. Vomiting during attacks occurs at least 4 times/ hr for at least 1 hr.
E. Symptoms-free between attacks
F. Not attributes to another disorder.
NOTE: In particular, H/P examination do not show signs of Gastrointestinal Disease
Table 1.3.2. Diagnostic Criteria for Abdominal Migraine
Page | 65
A. An Idiopathic Recurrent disorder seen mainly in children and characterized by Episodic midline abd pain manifesting in attacks lasting 1-72 hours with Normality between episodes. The pain is of moderate to severe intensity and asso. w/ Vasomotor symptoms, N & V.
B. At least 5 attacks fulfilling criteria C-E
C. Attacks of Abd pain lasting 1-72 hrs (untreated or unsuccessfully treated)
D. Abd Pain has all of the following characteristic:• Midline location, periumbilical or poorly localized• Dull or “just sore” quality• Moderate or severe intensity
E. During Abd pain at least 2 of the following:• Anorexia• Nausea• Vomiting• Pallor
F. Not attributed to another disorder
NOTE: In H&P, do not show any signs of GI or renal disease. Pain is severe enough to interfere with daily activities. The pallor is often accompanied by dark shadow under eyes. In few patients flushing is predominant vasomotor phenomenon. MOST children with Abd migraine will develop migraine headache later in life.
Table 1.3.3. Diagnostic Criteria for Benign Positional Vertigo of Childhood
A. Heterogeneous Disorder is characterized by recurrent brief episodic attack of vertigo Occurring without warning and resolving spontaneously in otherwise healthy children
B. At least 5 attacks fulfilling criteria C
C. Multiple episodes of severe vertigo, occurring without warning & resolving Spontaneously after minutes to hour
D. Normal Neurological examination, audiometric &vestibular functions between attacks
E. Normal Electroencephlogram
NOTE: Often asso w/ Nystagmus or vomiting, unilateral throbbing headache may occur in some attacks.
Page | 66
Table 1.4 Diagnostic Criteria For Retinal Migraine
A. Repeated attacks of monocular visual disturbance, including scintillations, scotomata, Or blindness, associated with Migraine headache
B. At least 2 attacks fulfilling criteria C & D
C. Fully reversible monocular positive and/or negative visual phenomenon (eg scintillations, scotomata or blindness) confirmed by examination during an attack Or ( after proper instruction) by the patient’s drawing of a monocular field defect during attack
D. Headache fulfilling criteria B-D for Migraine without aura begins during visual Symptoms or follow them within 60 minutes
E. Normal Ophthalmological examination between attacks
F. Not attributed to another disorder
Table 1.5-1.5.1. Complications of Migraine: Diag Crit for Chronic Migraine
A. Migraine headache occurring on 15 or more days per month for more than 3 months In the absence of medication overuse
B. Headache Fulfilling criteria C & D for Migraine without aura on ≥15 days /month for >3 months
C. Not attributed to another disorder
Table 1.5.2. Diagnostic Criteria for Status Migrainosus
A. A debilitating migraine attack last for more than 72 hours
B. The present attack in a patient with Migraine without aura is typical of previous Attacks except for its durationC. Headache has both of the following features: 1. Unremitting for >72 hours 2. Severe intensity
D. Not attributed to another disorder
Page | 67
Table 1.5.3. Diagnostic Criteria for Persistent aura without infarction
A. Aura symptoms persist for more than 1 week without radiographic evidence of infarction
B. The present attack in a patient with Migraine with aura is typical of previous attacks Except that one or more aura symptoms persists for > 1 week
C. Not attribute to another disorder
Table 1.5.4. Diagnostic Criteria for Migrainous Infarction
A. One or more Migrainous aura symptoms associated with an Ischemic brain lesion in Appropriate territory demonstrated by neuroimaging
B. The present attack in a patient with Migraine with aura is typical of previous attacks Except that one or more aura symptoms persists for >60 minutes
C. Neuroimaging demonstrates ischemic infarction in a relevant area
D. Not attributed to another disorder
Table 1.5.5. Diagnostic Criteria for Migraine-triggered Seizure
A. A seizure triggered by a migraine aura
B. Migraine fulfilling criteria for Migraine with aura
C. A seizure fulfilling diagnostic criteria for one type of epileptic attack occurs during or Within 1 hour after a migraine aura
Table 1.6-1.6.1-1.6.2 Probable Migraine: Diag Crit for Prob Mig Without Aura & With Aura
A. Definition: Attacks and/or headaches missing one of the features needed to fulfill all Criteria for a disorder.
B. Attacks fulfilling all but one of criteria A-D for Migraine without aura
Page | 68
C. Not attributed to another disorder
Table 1.6.3 Diagnostic Criteria for Probable Chronic Migriane
A. Same as Table 1.5.1 Chronic Migraine
Treatments
Tx of Acute MigraineDrugs Trade/Brand Name Dosage
Simple Analgesic
Acetaminophen, aspirin, caffeine
Excedrin Migraine 2 tabs or caps q6h (max 8 per day)
NSAIDS
Naproxen Aleve, Anaprox, generic 220-550mg PO bid
Ibuprofen Advil, Motrin, Nuprin, generic
400mg PO q3-4h
Tolfenamic acid Clotam Rapid 200mg PO. May repeat x1 after 1-2 h
5-HT1 Agonist
Oral
Ergotamine Ergomar One 2mg sublingual tab at onset & q1/2h (max 3 per day, 5 per week)
Ergotamine 1 mg,caffeine 100mg
Ercaf Wigraine 1 or 2 tab at onset, then 1 tab q1/2h (max 6 per day, 10 per week)
Naratriptan Amerge 2.5mg tab at onset, may repeat once after 4h
Rizatriptan Maxalt 5-10mg tab at onset, may
Page | 69
Maxalt-MLT repeat after 2h (max 30mg/dl)
Sumatriptan Imitrex 50-100mg tab at onset; may repeat after 2h (max 200mg/dl)
Frovatriptan Frova 2.5mg tab at onset, may repeat after 2h(max 5mg/dl)
Almotriptan Axert 12.5mg tab at onset, may repeat after 2h(max 25mg/dl)
Eletriptan Relpax 40 or 80mg
Zolmitriptan ZomigZomig Rapimelt
2.5mg tab at onset, may repeat after 2h(max 10mg/dl)
Nasal
Dihydroergotamine Migraine Nasal Spray 1 spray(0.5mg) is administered, followed in 15min by a second spray
Sumitriptan Imitrex Nasal Spry 5-20 intranasal spary as 4 sprays of 5mg or a single 20mg spray (may repeat once after 2 h, not to exceed a dose of 40mg/dl)
Zolmitriptan Zomig 5mg intranasal spray as one spray( may repeat once after 2h, not to exceed a dose of 10mg/dl)
Parenteral
Dihydroergotamine DHE-45 1mg IV, IM or SC at onset & q1h (max 3mg/dl, 6mg per week)
Sumatriptan Imitrex injection 6mg SC at onset(may repeat once after 1 h for max of 2 doses in 24h)
Dopamine Antagonists
Oral
Metoclopramide Reglan, 5-10mg/d
Page | 70
Prochlorperazide Compazine 1-25mg/d
Parenteral
Chlorpromazine 0.1mg/kg IV at 2mg/min; max 35mg/d
Metoclopramide Reglan 10mg IV
Prochlorperazine Compazine 10mg IV
Other
Oral
Actaminophen, 325mg, plus dichloralphenazone 100mg, plus isometheptene, 65mg
Midrin, Duradin 2 caps at onset followed by 1 cap q1h(max 5 capsules)
Nasal
Butorphanol Stadol 1mg(1 spray in nostril), may repeat if necessary in 1-2h
Parenteral
Narcotics Multiple preparation and dosage
Clinical Stratification of Acute Specific Migraine TreatmentsClinical Situation Treatment Options
Failed NSAIDS/ Analgesics First Tier• Sumatriptan 50mg or 100mg PO• Almotriptan 12.5mg PO• Rizatriptan 10mg PO• Eletriptan 40mg PO• Zolmitriptan 2.5mg PO
Slower Effect/better tolerability• Naratriptan 2.5mg PO• Frovatriptan 2.5mg PO
Infrequent Headache• Ergotamine 1-2mg PO• Dihydroergotamine nasal spray 2mg
Page | 71
Early Nausea or difficulties taking tablets • Zolmitriptan 5mg nasal spray• Sumatriptan 20mg nasal spray• Rizatriptan 10mg MLT wafer
Headache recurrence • Ergotamine 2mg(most effective PR/usually with Caeffeine)
• Naratriptan 2.5 mg PO• Almotriptan 12.5mg PO• Eletriptan 40mg
Tolerating acute treatments poorly • Naratriptan 2.5 mg• Almotriptan 12.5mg
Early vomiting • Zolmitriptan 5mg Nasal Spray• Sumitriptan 25mg PR• Sumitriptan 6mg SC
Menses-related Headache Prevention• Ergotamine PO at night• Estrogen Patches
Treatment• Triptans• Dihydroergotamine nasal spray
Very Rapidly developing symptoms • Zolmitriptan 5mg Nasal Spray• Sumatriptan 6mg SC• Dihydroergotamine 1mg IM
Preventive Treatments in MigraineDrug Dose Selected Side Effects
Pizotifen 0.5-2 mg qd • Weight Gain• Drowsiness
Beta blocker
Propanolol 40-120 mg BID • Reduced energy• Tiredness• Postural Symptoms• Contraindicated in
Asthma
Tricyclics
Amitriptyline 10-75mg at night Drowsiness
Dothiepin 25-75mg at night
Page | 72
Nortriptyline 25-75mg at night Note: Some pt many only need a total dose of 10mg, although1-1.5mg/kg body weight is required
Anticonvulsants
Topiramate 25-200mg/dl • Paresthesias• Cognitive
Symptoms• Weight loss• Glaucoma• Caution with
nephrolithiasis
Valproate 400-600 mg BID • Drowsiness• Weight gain• Tremor• Hair loss• Fetal abnormalities• Hematologic or liver
abnormalaties
Gabapentin 900-3600 mg qd • Dizziness• Sedation
Serotonergic drugs
Methysergide 1-4mg dq • Drowsiness• Leg cramps• Hair loss• Retroperitoneal
Fibrosis
Flunarizine 5-15mg qd • Drowsiness• Weight gain• Depression• Parkinsonism
Natural treatments for migraine include riboflavin (vitamin B2), magnesium, coenzyme Q10, and butterbur.
Board Pearls:
- Withdrawal from Decongestants can Precipitate Migraines.
Page | 73
- Cortical spreading depression (CSD) a main culprit behind migraine attacks.
- Genetic mutations leads to defective NA+ and CA++ channels which are linked to migraine.- A migraine lasting longer than 72 hours is termed Status Migrainous.
- Rx acute attacks of migraines : Rizatriptan
- Rx for acute attack of migraines lasting longer than 48 hours or that are frequently recurrent : Ergotamine
- Migraine is most common in women and has a strong genetic component.
Difference between sinus headache and migraine: Parameters Sinus headache Migrane
Face pain + —
Infection + —
Upper Respiratory Problems + —
Fever, purulent discharge and post nasal drip
+ —
Pale or Pink nasal mucosa + + /—
Significant sinus fluid levels + —
References
World Health Organizationhttp://www.who.int/mediacentre/factsheets/fs277/en/
American Migraine Foundationhttp://americanmigrainefoundation.org
Migraine Research Foundationhttp://migrainereserachfoundation.org
International Headache Society http://www.ihs-headache.org/ Kasper DL, Braunwald E, Fauci AS, Hauser SL, Longo DL, Jameson JL, Loscalzo J. 18 ed. Harrison's principles of internal medicine: Headache. New York, NY: McGraw-Hill; 2012:118,119,121.New York, NY.
Page | 74
Somerset Family Medicine Clinical Module
Bread & Butter of Family Medicine: Skin Rash
Page | 75
Type of Skin Rashes
Clinical presentation Treatments
Acne vulgaris • Caused by hormonal imbalance.• Contributing organism: Propionibacterium
acnes.• Closed comedones are white and open
comedones are black. The discharge although purulent, is odorless.
• Rashes can appear as pustules and cysts that can erupt and release free fatty acids, causing further irritation.
• Mild acne: Use topical antibacterial such as benzoyl peroxide. If ineffective, add topical antibiotics such as clindamycin or erythromycin.
• Moderate acne: Add topical vitamin A derivatives such as tretinoin, adaphalene to topical antibiotics as mentioned above.If ineffective, use oral antibiotics such as minocycline or doxycycline.
• Severe acne: Add oral vitamin A, such as isotretinoin to oral antibiotics as mentioned above.
Dandruff (seborrheic dermatitis)
• Caused by Malassezia furfur.• An over secretion of sebaceous material and a
hypersensitivity reaction to a superficial fungal organism underlie seborrheic dermatitis.
• Scaly, yellowish, greasy dermatitis found on a red base on the scalp, eyebrows, and in the nasolabial fold.
• Common association with Parkinson disease and AIDS.
• Wash scalp with Selenium Sulfide shampoo or ketoconazole shampoo daily.
• Rub in betamethasone or fluocinonide solution one to two times a day into the affected area for itchy skin if moderate or severe dandruff.
Eczema(Atopic dermatitis: Type I IgE-mediated hypersensitivity reaction)
• Inflammatory dermatoses characterized by pruritus.
• In children: Dry skin and eczema on cheeks and extensor and flexural surfaces.
• In adults: dry skin and eczema on hands, eyelids, elbows, and knees.
• Acute eczema: weeping, erythematous rash with vesicles.
• Chronic eczema: dry, thickened skin (hyperkeratosis) caused by continual scratching.
• Emollients provide moisture to the skin and help prevent further water loss.
• Use topical steroids for mild to moderate eczema. For the face use only low-potency hydrocortisone such as Hydrocortisone (DermAid cream/soft cream). For other sites, medium potency corticosteroids such as Clobetasone butyrate (Eumovate cream), triamcinolone or high potency corticosteroids such as Betamethasone dipropionate (Diprosone OV cream/ointment) are recommended.
• Oral corticosteroids such as prednisone are often used in the short term management of severe eczema.
• Use antihistamines such as claritine to control the itching.
Page | 76
Herpes zoster • Herpes zoster is caused by the reactivation of a latent VZV infection.
• It is characterized by a prodrome of pain and dysesthesia in a dermatomal pattern, followed by an eruption of grouped vesicles on an erythematous base.
• It most commonly occurs in older individuals.
• Use acyclovir 800 mg 5x/daily for 7 to 10 days or valacyclovir 1000 mg 3x/daily for 7 days.
• Use pain medication depending on the degree of pain: Acetaminophen, acetaminophen-hydrocodone, gabapentin or tricyclic antidepressants are recommended.
Impetigo • Bacterial infection of the skin caused by Streptococcus pyogenes and Staph. Aureus (bullous impetigo).
• Starts as maculopapules and rapidly progresses to vesicular pustular lesions or bullae.
• Superficial, pustular skin infection, seen mainly in children, with oozing, crusting, and draining of the lesions (honey colored lesions).
• Can progress to cellulitis, acute glomerulonephritis.
• It is highly contagious.
• Use topical antibacterial such as mupirocin (bactroban) or retapamulin for mild cases of impetigo.
• In adults: Use oral first gen. cephalosporin such as Cephalexin (Keflex) 250 mg to 1000mg , 4x/day for 7 to 14 days
• In children, the dose can range from 25 mg to 100 mg /kg/day, 3-4x/day for 7 to 10 days.
• For Penicillin-allergic patients: UseMacrolides such as clarithromycin (Biaxin) or azythromycin (Z-pack)
• For MRSA: TMP/SMZ (bactrim).• If allergic to sulfa drugs, use doxycycline or
clindamycin (cleocin)
Pityriasis rosea • Transient, pruritic, erythematous, salmon-colored eruption that starts out as a single lesion (herald patch) and then disseminates.
• Can look like secondary syphilis, except that it spares the palms and soles.
• Lesions on the back appear in a pattern like a Christmas tree.
• Use topical steroids such as triamcinolone.
Poison Ivy (contact dermatitis: type IV hypersensitivity reaction)
• A rash from poison ivy, poison oak or poison sumac is caused by Urushiol, an oil substance found in the sap of these plants.
• The rash is very itchy and can be characterized by red streaks, hives, small or large blisters or crusting skin (after blisters burst).
• No skin to skin spread.
• Most rashes go away w/o treatments in about 1 to 3 weeks. However, some treatments are recommended based on the severity.
• For mild rash: Use calamine lotion (Local anesthetic).
• For moderate rash: Use cortisone cream such as triamcinolone 0.1% or clobetasone butyrate.
• For severe rash: Use oral prednisone fr 10-14 days.
• Use local antihistamines such as Benadryl cream or oral antihistamines such as Claritin to control the itching.
Page | 77
Psoriasis • Etiology is unknown.• Well-demarcated, flat, elevated, salmon-
colored plaques covered by adherent white to silver-colored scales.
• Rash common on the extensor surface of the elbows and knees, lower back and pitting of the nails.
• Salicylic acid can be used to remove heaped-up collections of scaly material.
• If localized disease, use topical steroids such as triamcinolone (Kenalog cream 0.1%).
• To avoid the long term use of steroids which can cause skin atrophy, substitute with topical vitamin D (calcipotriene) and vitamin A derivatives.
Rosacea (adult acne)
• Inflammatory reaction of the pilosebaceous units of facial skin.
• Characterized by pustules and flushing of the cheeks which causes enlargement of the nose (rhinophyma).
• Exacerbated by drinking alcohol, eating spicy foods, and stress.
• Mild disease: Use topical metronidazole gel (Metro gel 0.75%, 1 %), Metro cream or Metro lotion 0.75%. A thin film of metronidazole gel should be rubbed on affected areas once or twice daily.
• Severe disease: Use oral antibiotics such as tetracycline (sumycin), doxycycline (oracea). Add isotretinoin if ineffective.Note:Side effects of doxycycline: phototoxicity, discoloration of the milk teeth and enamel hypoplasia. Decrease dose in liver dysfunction.
Scabies • Parasitic infection caused by mites, sarcoptes scabiei. It is characterized by superficial burrows, intense pruritus and secondary infections.
• Rashes are found in web spaces between fingers and toes, at elbows or near the genitals. The infection often does not affect the scalp
• Transmitted through skin-to-skin contact
• Apply Elimite (Permethrin cream) from the neck down, usually before bedtime and leave it for about 8 to 14 hours; then washed off in the morning.
• If the infection is Permethrin-resistant, Benzyl benzoate is suggested.
• For patients with AIDS, the combination of Permethrin and Ivermectin is recommended.
• One application is often sufficient for mild infections.
Tinea capitis • Superficial fungal infection of the scalp• Circular or ring patches of hair loss (alopecia)• One or more lesion present on the body
surface, typically annular with an elevated red, scaly border, tendency for central clearing.
• Patient may have a history of exposure to a cat or dog.
• Use oral terbinafine (Lamisil) for 4 to 8 weeks.
Page | 78
Tinea cruris (jock itch)
• It is a fungal infection of the groin.• Sweat is important in pathogenesis.• The rash begins in the groin fold, usually on
both sides. The area may enlarge and other sores may develop. The rash has sharply defined borders that may blister and ooze.
• Use topical antifungal medication from azole type such as miconazole (Monistat), clotrimazole (lotrimin) or from allylamine type such as terbinafine 1% cream (Lamisil) once daily for 7 days
• Minimizing damp conditions can help treat and prevent the rash.
• Steroids (such as 1% triamcinolone cream) may be combined with the anti-fungal drug to help prevent further irritation.
Tinea unguium (nail; onychomycosis)
• Dermatophyte infection affecting the nails.• The nail is raised and the nail plate is white,
thick, and crumbly.• The nail is frequently discolored.
• Oral therapy includes terbinafine (Lamisil) or itroconazole. At least 6 weeks for fingernails and 12 weeks for toenails.
Note:Terbinafine is hepatotoxic. Check liver function periodically.
Tinea versicolor • Caused by the malassezia fungus.• Skin infection characterized by multiple,
brown (hyper pigmented), or white (hypo pigmented) scaling macular lesions that tend to coalesce. Found on chest, abdomen, neck or face.
• Diagnostic: skin scrapings examined with KOH under a microscope: spaghetti (short hyphae) and meatballs (yeast).
• Use oral antifungal medications; 400 mg of ketoconazole (best treatment) or fluconazole in a single dose, or ketoconazole 200 g daily for 7 days.
• Use topical antifungal medication containing 2.5 % selenium sulfide if the rash is localized.
• Use Ketoconazole (Nizoral ointment and shampoo): it is normally applied to dry skin and washed off after 10 minutes, repeated daily for 2 weeks.
• Terbinafine (Lamisil cream) can also be used.Note:The skin may remain discolored for several weeks or months following treatment.
Note:
Oral Vitamin A derivatives are extremely teratogenic (craniofacial, central nervous system, and cardiovascular defects). Do a pregnancy test first. Only treat patients on suitable hormonal and barrier birth control. Isotretinoin causes hyperlipidemia
Class of topical steroids:
Class 1 Very potent or superpotent (up to 600 times as potent as hydrocortisone)
• Clobetasol propionate (Dermol™ cream/ointment/scalp lotion)
• Betamethasone dipropionate (Diprosone™ OV cream/ointment)
Page | 79
Class 2 Potent (100-150 times as potent as hydrocortisone)
• Betamethasone valerate (Beta™ cream/ointment/scalp solution, Betnovate™ lotion/C cream/C
ointment, Fucicort™ cream)
• Methylprednisolone aceponate (Advantan™ cream/ointment)
Class 3 Moderate (2-25 times as potent as hydrocortisone)
• Clobetasone butyrate (Eumovate™ cream)
• Triamcinolone acetonide (Aristocort™ cream/ointment, Viaderm KC™ cream/ointment,
Kenacomb™ ear drops)
Class 4 Mild
• Hydrocortisone (DermAid™ cream/soft cream)
Vehicles of topical steroids
• Lotions are easy to apply
• Creams rub in well
• Ointments may be most effective for dry lesions
• Gels and solutions are useful in hairy areas or for a drying effect
sedating antihistamines Non-sedating antihistamines
Diphenhydramine (Benadryl) Cetirizine (Zyrtec)
Promethazine (Phenergan) Fexofenadine (Allegra)
Hydroxyzine (Atarax, Vistaril) Loratadine (Claritin)
Cyproheptadine (Perlactin) Desloratadine (Clarinex)
Clemastine (Tavist)
Page | 80
Impetigo
Page | 81
Herpes zooster
Page | 82
Psoriasis
Page | 83
Scabies
Page | 84
Tinea cruris
Page | 85
Tinea capitis
Acne VulgarisPage | 86
Pityriasis Rosea
Page | 87
Seborrheic dermatitis
Page | 88
Clinical vignettes
1. A 17 year-old boy comes to the physician because of a 4-year history of facial lesions. He says that some lesions begin as painful “bumps”, whereas others look like “pimples” and large pores. His medical history is
2. unremarkable and he takes no medications. He drinks occasionally on weekends. He denies illicit drug use. He is sexually active and he uses condoms consistently. His temperature is 36.9C (98.4 F). The examination shows open and closed comedones. Numerous deep inflammatory nodules and ice pick-like scarring. What is the most appropriate pharmacotherapy for this patient’s condition?
A. Oral acitretin
B. Oral isotetinoin
C. Oral minocycline
D. Oral prednisone
E. Oral spironolactone
F. Topical tazarotene/benzoyl peroxide.
3. A 32 y o woman comes to the physician because of a red rash on her cheeks, nose, and forehead for 1 year. She has had facial flushing and redness and occasionally small pimples. She states that the rash is worsened by sun exposure and drinking hot beverages. She has had dryness and stinging in her eyes for the past 3 months. Her medical history is unremarkable and she takes no medications. Temp. 36.8 C (98.2) and BP 115/70. Examination shows mild erythema and telangiectasias over the malar cheeks, nasal sidewalls, and forehead; there are few pustules. The lid margins are erythematous with mild crusting. Which of the following is the most likely diagnosis?
A. Acne vulgaris
B. Dermatomyositis
C. Rosacea
D. Sjoegren syndrome
E. Systemic lupus erythematosus
4. A 40 yo woman comes to the physician because of a 1-month history of a progressive, light-colored rash on her chest that has been spreading rapidly. Her medical history is unremarkable and she takes no medications. She recently started working as a cook in a local fast-food restaurant. Her husband and 2 school-aged children are in good health. Before that, she was a homemaker. Temp36.8 C (98.2 F), BP 114/76, Pulse 74/min, and respirations 14/min. Examination shows well demarcated, slightly scaly hypopigmented patches. The remainder of the examination shows no abnormalities.
Which of the following is the most appropriate next step in management?
Page | 89
A. Monospot test
B. Potassium hydroxide preparation
C. Skin biopsy
D. Skin culture
E. Tzanck smear
5. A 20 yo college student comes to student health services because of an itchy rash for 6 days that began as a large red mark and then spread to her back, upper arms, and thighs. She had a sore throat 2 weeks ago that lasted 4 days. She denies fever, vaginal discharge, abdominal pain, back pain, or joint pain. Current medications include OCP. She is sexually active and she and her partner use condoms inconsistently. Examination shows multiple pink oval patches on the back, proximal upper extremities, and proximal lower extremities. There is no lymphadenopathy. Which of the following is the most likely diagnosis?
A. Acute HIV reaction
B. Herpes zoster
C. Lyme disease
D. Pityriasis rosea
E. Pityriasis versicolor
F. Secondary syphilis
6. A 71 yo man comes to the physician because of a 2 days history of painful rash. He has had no fevers, chills, or weight loss. His past medical history is unremarkable. He lives with his cousin who has AIDS. Temp 37.2 C (99.0 F). Examination shows an eruption of grouped vesicles on an erythematous base in the TH5 dermatomal distribution. There is no lymphadenopathy. Lab studies show Hb 14, MCV 90 , leucocyte count 11.500, platelet count 350.000. Which of the following is the most appropriate pharmacotherapy?
A. Amitriptyline and gabapentin
B. Dexamethasone
C. Emtricitabine, tenofovir, and efavirenz
D. Ganciclovir
E. Valacyclovir
7. A 14 yo girl is brought to dermatologist by her mother because of acne. The girl reports worsening of the lesions despite usage of an over-the-counter topical acne treatment. Examination shows open and closed comedones, especially on the forehead. In addition, there are some comedones and many papules and large pustules on the chin, in the nasolabial folds, and on the cheeks. There are a few lesions on the upper back, but none seen on the chest or deltoid regions. Which of the following is the most appropriate pharmacotherapy?
A. Isotretinoin
Page | 90
B. Oral doxycycline plus topical retinoid
C. Topical azelaic acid
D. Topical benzoyl peroxide plus clindamycin gel.
E. Topical adapalene
8. A previously healthy 17-year-old girl comes to the physician because of a 1-week history of itching and progressive rash. She has no history of skin problems or associated symptoms. She takes no medications. Her sister with whom she shares a room had similar symptoms during the previous week. The patient's temperature is 36.8°C (98.2°F). There are multiple 2- to 5-mm erythematous papules over the trunk, especially at the waistline, and over the , hands, and fingers. There is no lymphadenopathy or hepatosplenomegaly. Which of the following is the most likely causal organism?
A. Epstein-Barr virus
B. Group A streptococcus
C. Measles virus
D. Sarcoptes scabiei
E. Zoster virus
9. A 6-year-old girl is brought to the physician because of a 1-month history of a recurrent pruritic rash on her arms. She was born at term and has been healthy except for an episode of bronchiolitis 6 months ago treated with albuterol. The examination shows a dry skin and eczema on the flexor surface of the elbows bilaterally. Which of the following is the most appropriate next step in management?
A. Coal tar therapy
B. Oral antibiotic therapy
C. Topical antibiotic therapy
D. Topical corticosteroid therapy
E. Vitamin supplementation
9. A 56 yo man has had a painful weeping rash on the right side of the forehead for 2 days. He underwent chemotherapy for non-Hodgkin lymphoma 1 year ago. His temperature is 36.7°C (98°F), pulse is 80/min, and blood pressure is 138/76 mm Hg. Examination shows no other abnormalities. Which of the following is the most likely diagnosis?
A. Herpes zoster
B. Impetigo
C. Pyoderma gangrenosum
D. Syphilis
E. Systemic lupus erythematosus
Page | 91
10 . The first line of treatment recommended for contact of crusted scabies is:
A. Permethrin
B. Lindane
C. Ivermectin
D. Benzoyl benzoate
11. Seborrheic dermatitis (dandruff) is commonly associated with two diseases. Which one?
12. Is the poison ivy rash contagious between people?
Yes or No.
13. What kind of topical steroids do you prescribe for eczema of the face?
A. Low potency
B. Medium potency
C. High potency
14. Give an example of a low potency, medium potency and high potency hydrocortisone?
15. Give two side effects of doxycycline.
16. What should the physician do before prescribing oral vitamin A derivatives such as isotretinoin?
17. What should you do as a physician before prescribing terbinafine to a patient?
18. What is the 1st and 2nd line treatment of a super infection of impetigo with community acquired MRSA?
19. In which patients should you avoid sulfa drugs?
20. Give one side effect of acyclovir. How do you prevent it?
Answers:
1.B
2.C
3.B
4.D
5.E
6.B
7.D
8.D
Page | 92
9.A
10.A
11. Parkinson disease and AIDS
12.No.
13.A
14. Hydrocortisone (DermAid cream), Clobetasone butyrate (Eumovate™ cream) , Betamethasone dipropionate (Diprosone cream/ointment.
15. Photosensitivity and discoloration of milk teeth.
16. Exclude pregnancy by doing a pregnancy test. PT should be on table hormonal and barrier birth control.
17. Check liver function.
18. 1st line Bactrim. 2nd line: doxycycline.
19. Sulfa drugs allergy, G6PD deficiency
20. Crystalluria (crystal nephropathy). Full hydration.
Page | 93
Somerset Family Medicine Clinical Module
Bread & Butter of Family Medicine:
Pain Management
IntroductionPain is one of the most common patient complaints in family medicine. It is very difficult to control effectively because it is highly subjective and multidimensional. The different types of pain are: • Nociceptive/somatic Pain: linked to tissue damage and the resulting inflammation.
• Neuropathic Pain: results from a lesion or disease of the somatosensory system. It can persist even after healing, and is lancinating, shock-like, and burning.
• Central Sensitization: alteration to the CNS processing of sensation, leading to amplification of pain signals (mechanisms poorly understood)
• Psychogenic Pain: compounded by mental states of anxiety, depression, maladaptive coping mechanisms, excessive stress, and influence of social support systems.
• Idiopathic Pain: no identifiable etiology.Unfortunately, a patient’s complaint of pain is likely a combination of all of the above factors.
HistoryThe history is the most valuable tool for evaluation because the patient’s self report has been proven to
be the most reliable indicator of pain. Be sure to ask thorough questions regarding onset, provoking/palliating factors, quality, radiation, severity, timing, and associated symptoms. Severity can be difficult to gauge, as all patients handle and interpret pain differently. There are three common scales:1. Visual Analog Scale 2. Numeric Rating Scale: Either ask to rate from 1-10, 10 being worst pain you can imagine, or if they would say their pain is mild, moderate, or severe. 3. Wong-Baker FACES Pain Rating Scale
An important clinical distinction to be made is if the pain is acute or chronic. Chronic pain is pain not associated with cancer or other medical conditions that persists more than 3-6 months, pain lasting 1 month longer than the acute illness or injury, or pain recurring in intervals of months to years [1]. Acute pain could require more investigation to rule out injuries, while chronic pain often requires more consideration of compounding factors (especially psychiatric issues).
Physical ExaminationObservation: There are nonverbal cues for pain such as jaw clenching, pacing/restlessness, immobility, guarding, and wincing. Vital Signs: Patients may be hypertensive, tachycardic, and tachypneic.
Page | 94
Examination: Evaluate for warmth, tenderness to palpation, range of motion restriction, and misalignment in the area of the pain. Pay close attention to changes in sensation, asymmetric reflexes, or poor motor function. Perform any special tests indicated [straight leg raise for low back pain, Anterior Drawer Test for ACL, McMurray’s for meniscus, Tinel’s/Phalen’s for carpal tunnel, etc.]
Diagnostic StudiesX-ray: Least expensive imaging study, can rule out fractures and evaluate joint space changes associated with arthritis.MRI: Ordered with high suspicion of ligament/tendon tear, intervertebral disc damage, radiculopathy; or in the case of pain refractory to treatment attempts. (CT if MRI is contraindicated)
Conservative TherapiesThere are various non-pharmacologic ways of relieving pain. Patients should attempt these instead of or in conjunction with their medications.
1. PRICE- Protect, Rest, Ice, Compress (tape, ACE bandages), Elevate.2. Stretching/Exercise/Weight Loss **No complete bed rest with back pain!**3. Physical Therapy 4. Massage 5. Psychiatric eval.6. Thermo-therapies: Alternating hot and cold patches, warm baths, hot tubs. 7. Chiropractors, Osteopathic Manipulative Medicine Specialists
Patches Caspaicin, Lidoderm, Salonpa, IcyHot
Creams Caspaicin, Volteran gel, BenGay
Joint Supplements Help preserve cartilage. Glucosamine Chondroitin, Osteo Bi-Flex
Pharmacologic ManagementPain medication is a slippery slope, and prescribers need to be extremely cautious with regard to max doses of harmful medications and their risk of dependence/addiction. A rule of thumb is to start with low initial doses and increase slowly, perpetually offering conservative options for pain relief.
The World Health Organization developed a ladder for the management of pain. Their steps are:1. Start with non-opioid +/- adjuvant medication (anti-anxiety or muscle relaxers).2. If pain persists or increases, use weak opioid (hydrocodone) +/- non-opioid, +/- adjuvant.3. If pain still worsening, use stronger opioid (morphine), +/- non-opioid, +/- adjuvant.
Medication Mechanism of Action
Dosing Info Adverse Effects Use with Caution
Steroids[Medrol Dosepak]
Decreases transcription of inflammatory
mediators
6-4mg pills day 1, 5 on day 2, 4 on
day 3, 3 on day 4, 2 on day 5, and 1 on
day 6.
Acne, adrenal suppression,
hyperglycemia, osteoporosis
Side effects likely occur with long-
term use
Page | 95
NSAIDs[Ibuprofen, Naproxen,
Motrin, Advil]
Reversible inhibition of COX
1 and 2
Adult: 10mg/kg dose, max dose
800mg, q 6-8 hr. max 2,400mg/day
PED: 4-10 mg/kg/dose q 6-8
hours.
GI discomfort/bleeds, cardiovascular
thrombotic events
Renal impairment, GERD/PUD/history
of GI bleeds, atherosclerotic
disease
Aspirin (NSAID)Irreversible
Inhibition of COX 1 and 2
325-1,000mg q4-6hrs with max of
4g/day
Same as above, Contraindicated in children [Reye’s Syndrome], except in
Kawasaki’s Dz.
Celebrex[Celecoxib]
Selective COX-2 inhibition
200mg/day
Less GI issues but higher
cardiovascular risk (stroke/MI)
Atherosclerotic disease, afib,
hypercoagulable state
Tylenol[Acetaminophen]
Decreases CNS production of
prostaglandins, anti-pyretic
effects on hypothalamus
ADULT: 325-650mg q 4-6hrs
with max of 4,000mg [FDA].
PED: 10-15mg/kg/dose with max 2,600mg.
Hepatotoxicity
Drinkers, liver disease. If a patient
drinks, decrease max dose to
3,000mg/day.
Tramadol[Ultram]
Antagonizes opioid receptors
and blocks serotonin and NE
reuptake
50-100mg q4-6 hours, 400mg
max/day.
Flushing, dizziness, HA, constipation,
nausea
Contraindicated with acute alcohol or
opioid intoxication
Flexeril[Cyclobenzaprine]
Muscle Relaxant related to tricyclic
antidepressants
5mg-10mg up to t.i.d.
Drowsiness, dry mouth
CHF, arrhythmias, hyperthyroidism
Valium[Diazepam]
Muscle Relaxant, binds to GABA
receptors to increase release
2-10mg b.i.d.-q.i.d. Dependence, withdrawal
seizures, respiratory dpn.
Depression, substance abuse,
respiratory disorders
Opioids[Norco]
Antagonizes opioid receptors
in CNS to decrease synaptic
transmission of pain signals
5-10mg of hydrocodone with
325 acetaminophen q4-6hrs (max
4,000mg acetaminophen)
Constipation, nausea/vomiting,
itching, respiratory depression,
DEPENDENCE.
Liver disease/drinkers, substance abuse,
hypoventilated states.
INJECTIONS
Toradol [Ketorolac] NSAID; IM 60mg single dose C/I epidural or intrathecal
Kenalog [Triamcinolone]Steroid; Intra-articular. 40mg
large joint, 30mg medium, 10mg small.
Long-term and frequent injections can result in osteonecrosis.
Page | 96
Headache Management
Medication Mechanism Dosing Adverse Effects Caution
NSAIDs[Ibuprofen, Naproxen,
Motrin, Advil]
Reversible inhibition of COX 1
and 2
Adult: 10mg/kg dose, max dose
800mg, q 6-8 hr. max 2,400mg/day
PED: 4-10 mg/kg/dose q 6-8
hours.
GI discomfort/bleeds
, cardiovascular thrombotic events
Renal impairment, GERD/PUD/histor
y of GI bleeds, atherosclerotic
disease
Excedrin Migraine
Anti-inflammatory and
vasoconstrictor
250mg Acetaminophen, 250mg Aspirin,
65mg Caffeine per tablet.
GI discomfort/bleeds
, hepatotoxicity
Renal impairment, GERD/PUD/histor
y of GI bleeds, atherosclerotic
disease
Imitrex[Sumatriptan]
Serotonin receptor agonist,
cause vasoconstriction
in cranial arteries
25, 50, or 100mg tablet at onset of
headache. No relief in 2 hours,
take a second tablet.
Chest pain/tightness, coronary artery spasm, nausea
Uncontrolled HTN, CAD
Inderal[Propranolol]
Migraine prophylaxis.
Nonselective B blockade
80mg/day and increase q three weeks to 160-
240mg/day divided q 6-8hr.
Bradycardia, hypotension,
masks hypoglycemia,
depression
Heart block, diabetics
(especially on insulin),
depression
Medical Marijuana: Uses- Chronic and severe pain, anti-nausea, appetite stimulant. Most often used for late
stage cancer. THC binds to cannabinoid receptors to alter signaling with neurotransmitters. Physicians apply
for licensure through their state’s program. In Michigan, it is the Medical Marijuana Program at
[http://www.michigan.gov/lara/0,4601,7-154-35299_63294_63303_51869---,00.html]. Patients undergo full
evaluation by licensed physician and then apply for their registration cards.
References
Page | 97
1. Bickley, L., & Szilagyi, P. (2013). Bates' guide to physical examination and history-taking (11th ed.).
Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. 2. uptodate.com 3.
http://www.who.int/cancer/palliative/painladder/en/,
Somerset Family Medicine Clinical ModulePage | 98
Bread & Butter of Family Medicine: CONSTIPATION
- Less than 3 bowel movements a week or hard, dry, or small, difficult to pass stoolCauses
- Diet low in fiber, and not enough liquids - Lack of physical activity- Medications- Neurological (spinal cord injury, Parkinson’s etc) and metabolic disorders- GI tract (adhesions, tumors, celiac, diverticulosis, colon polyps)
Management Medication categories of treatment:
- Bulking laxatives (psyllium=Metamucil, methylcellulose=Citrucel, polycarbophil=FiberCon)
- Osmotic laxatives (magnesium hydroxide=Exlax, Milk of Magnesium, polyethylene glycol= Miralax, Peg for bowel prep, and Lactulose)
- Stimulant laxatives (sennosides= Senokot, Senexon, and bisacodyl=Dulcolax, Correctol)
- Surfactant laxatives (docusate sodium=Colace, Philips, docusate calcium, mineral oil, and fleets oil enema)
- Chloride channel activator (lubiprostone or Amitiza)Medication mechanism of action include:Bulking laxatives: Metamucil, Citrucel (First-line therapy)
Bulk laxatives bind to fecal content and pull water to the stool. Bulk forming holds water in the stool. (not useful when patients on opioids, avoid if patient has celiac disease or gluten intolerance due to wheat dextrin products). More bloating occurs. May take up to 3 days to work.Osmotic laxatives: Miralax and Lactulose. (Second-line therapy)
Increased concentration of solutes creates osmotic pressure by drawing fluid from a less concentrated gradient to a more concentrated gradient, thus increases osmotic pressure to stimulate intestinal motility. Research shows Miralax more effective than lactulose. Osmotic laxatives have less bloating
Stimulant laxatives: Senokot, Dulcolax (Third-line therapy)Increase peristalsis through direct effects on the smooth muscle and simultaneously promote fluid accumulation in the colon. Avoid for long-term use as they have short-term usefulness.
Surfactant laxatives: (stool softener) Colace, Philips, and mineral oil (Third-line therapy)Reduces surface tension of the liquid contents of the bowel, therefore allowing
water and fat to enter and soften. Only prevents constipation, but do not treat it. Chloride channel activator: Amitiza
Derived from prostaglandin. Works by enhancing chloride-rich intestinal fluid without altering serum sodium and potassium concentration. The activation of chloride in the intestines pulls water into the lumen of intestine.
Page | 99
The drug is poorly absorbed systemically and appears to act locally on the intestines, improving stool consistency and motility. No studies to compare efficacy of Amitiza to other medications.
Lifestyle modificationsDiet and nutrition management 20-35 grams of fiber a day (no refined or processed foods)Drinking plenty of liquids (water, vegetable juice, & fruit juice)
Examples of Foods That Have Fiber
Beans, cereals, and breads Fiber
½ cup of beans (navy, pinto, kidney, etc.), cooked 6.2–9.6 grams
½ cup of shredded wheat, ready-to-eat cereal 2.7–3.8 grams
cup of 100% bran, ready-to-eat cereal⅓ 9.1 grams
1 small oat bran muffin 3.0 grams
1 whole-wheat English muffin 4.4 grams
Fruits
1 small apple, with skin 3.6 grams
1 medium pear, with skin 5.5 grams
½ cup of raspberries 4.0 grams
½ cup of stewed prunes 3.8 grams
Vegetables
½ cup of winter squash, cooked 2.9 grams
1 medium sweet potato, baked in skin 3.8 grams
½ cup of green peas, cooked 3.5–4.4 grams
1 small potato, baked, with skin 3.0 grams
½ cup of mixed vegetables, cooked 4.0 grams
½ cup of broccoli, cooked 2.6–2.8 grams
½ cup of greens (spinach, collards, turnip greens), cooked 2.5–3.5 grams
Physical activity
“Physical activity appears to be unrelated to the risk of constipation in employed adults, but higher physical activity was associated with improved quality of life. Recommendations to increase physical activity may not
Page | 100
alter symptoms of constipation but may improve overall well-being.” (American Journal of Gastroenterology, 2005)
Constipation quiz1. Which describes constipation?
A. Irregular motions B. Less than one stool per day C. Less than three bowel movements per week or difficult and painful defecation with
incomplete evacuation D. Blood in stool
2. Which lifestyle causes of constipation?
A. Lack of fiber in diet B. Lack of exercise C. Lack of fluids in diet D. All of the above
3. Which disease has constipation as its clinical feature?A. Interstitial nephritis B. Rheumatic fever C. Irritable bowel syndrome D. Onchocercosis
4. Which drug causes constipation as a side effect?A. Antidepressants B. Aluminum containing antacids C. Diuretics D. All of the above
5. Which metabolic disease leads to secondary constipation?A. Rickets and OsteomalaciaB. Hypothyroidism C. Hyperthyroidism D. Hyperparathyroidism
6. True or false, prolonged laxative use may predispose towards constipation? True
False
7. Constipation is a clinical feature in which of the following diseases?A. Systemic Scleroderma B. Q fever C. Scarlet fever D. Chickenpox
Page | 101
8. Which of the following neurological disorders has constipation as its clinical feature?A. Parkinson's disease B. Chagas disease C. Multiple sclerosisD. All of the above
9. Stool bulking agents may be beneficial in the treatment of constipation in irritable bowel disorder. True False
10. Which of the following is useful in the diagnosis of constipation?A. Barium enema B. SigmoidoscopyC. Thyroid function test D. All of the above
Constipation quiz answers
Page | 102
1. Which describes constipation?A. Irregular motions B. Less than one stool per day C. Less than three bowel movements per week or difficult and painful defecation with
incomplete evacuation D. Blood in stool
2. Which lifestyle causes of constipation?
A. Lack of fiber in diet B. Lack of exercise C. Lack of fluids in diet D. All of the above
3. Which disease has constipation as its clinical feature?A. Interstitial nephritis B. Rheumatic fever C. Irritable bowel syndrome (bowel dysfunction with abdominal pain with characterized by
disturbed bowel movement such as diarrhea, alone or alternating)D. Onchocercosis
4. Which drug causes constipation as a side effect?A. Antidepressants B. Aluminum containing antacids C. Diuretics D. All of the above
5. Which metabolic disease leads to secondary constipation?A. Rickets and OsteomalaciaB. Hypothyroidism C. Hyperthyroidism D. Hyperparathyroidism
6. True or false, prolonged laxative use may predispose towards constipation? True (due to degeneration of mesenteric plexus of colon. Increase constipation in
spite of taking larger doses of laxatives.
False
7. Constipation is a clinical feature in which of the following diseases?A. Systemic Scleroderma (due to number of GI signs & symptoms such as nausea, vomiting,
gaseous distention) B. Q fever C. Scarlet fever D. Chickenpox
Page | 103
8. Which of the following neurological disorders has constipation as its clinical feature?A. Parkinson’s diseaseB. Chagas disease C. Multiple sclerosis D. All of the above
9. Stool bulking agents may be beneficial in the treatment of constipation in irritable bowel disorder.
True
False
10. Which of the following is useful in the diagnosis of constipation?A. Barium enema B. SigmoidoscopyC. Thyroid function test D. All of the above
Somerset Family Medicine Clinical Module
Bread & Butter of Family Medicine:Page | 104
Smoking Cessation
Smoking cessation is a leading preventable cause of mortality. Tobacco use can lead to tobacco/nicotine dependence and serious health problems. Nicotine dependence is the most common form of chemical dependence in the United States. Quitting smoking is difficult and may require several attempts.
Assessment of use and exposure: The United States Preventive Health Services guidelines recommend that tobacco use status of every patient treated in a healthcare setting be assessed and documented at every visit. This practice has been shown to increase the likelihood of smoking-related discussions between patients and physicians and to increase the smoking cessation rates.
Nicotine withdrawal syndrome : Nicotine is a potent psychoactive drug that can cause physical dependence and tolerance. In the absence of nicotine, a smoker develops cravings for cigarettes and symptoms of nicotine withdrawal syndrome. These symptoms include:
1. Dysphoric or depressed mood2. Insomnia3. Irritability,frustration or anger4. Anxiety5. Difficulty concentration6. Restlessness7. Increased appetite or weight gain
Clinical trials have found that behavioural therapy along with pharmacotherapy has the best results for smoking cessation.
Choice of treatmentIn general, clinicians should offer patients both behavioural and pharmacologic therapy as these treatments in combination have been found to have higher abstinence rates.
Types of treatment:Behavioural counselling: Behavioural counselling can be provided in a variety of formats, including direct parent-physician encounters, via telephone,
Page | 105
computer programs, text messaging, or group based therapy. A simple five step program called the 5 A’s (ask,advise,assess,assist,arrange) that operationalizes the elements of brief counselling programs for office practice are effective for increasing the abstinence rates.
Five "A's" for assessing for tobacco use and addressing smoking cessation
Interventio
n
Technique
Ask Implement an officewide system that ensures that, for every patient at every clinic visit, tobacco-use status is queried and documented. Repeated assessment is not necessary in
the case of the adult who has never used tobacco or has not used tobacco for many years, and for whom this information is clearly documented in the medical record.
Advise
Strongly urge all tobacco users to quit in a clear, strong, personalized manner.
Advice should be:
Clear - "I think it is important for you to quit smoking now and I can help you." "Cutting down while you are ill is not enough."
Strong - "As your clinician, I need you to know that quitting smoking is the most important thing you can do to protect your health now and in the future. The clinic staff and I will help you."
Personalized - Tie tobacco use to current health/illness, and/or its social and economic costs, motivation level/readiness to quit, and/or the impact of tobacco use on children and others in the
household.
Assess
Determine the patient's willingness to quit smoking within the next 30 days:
If the patient is willing to make a quit attempt at this time, provide assistance.
If the patient will participate in an intensive treatment, deliver such a treatment or refer to an intensive intervention.
If the patient clearly states he or she is unwilling to make a quit attempt at this time, provide a motivational intervention.
Page | 106
If the patient is a member of a special population (eg, adolescent, pregnant smoker), provide additional information specific to that population.
Assist Provide aid for the patient to quit. These actions are summarized in the accompanying table.
Arrang
e
Schedule follow-up contact, either in person or by telephone. Follow-up contact should occur soon after the quit date, preferably during the first week. A second follow-up contact is recommended within the first month. Schedule further follow-up contacts as indicated.
Congratulate success during each follow-up. If tobacco use has occurred, review circumstances and elicit recommitment to total abstinence. Remind the patient that a lapse can be used as a learning experience. Identify problems already encountered and anticipate challenges in the immediate future. Assess pharmacotherapy use and problems. Consider
use or referral to more intensive treatment.
Adapted from: Fiore MC, Jaen C, Baker T, et al. Treating tobacco use and dependence: 2008 update. Clinical Practice Guideline. Rockville, MD: US Department of Health and Human Services. Public Health Service. 2008.Graphic 74402 Version 7.0
Five "R's" to motivate smokers unwilling to quit
Interventio
n
Technique
Relevance
Encourage the patient to indicate why quitting is personally relevant, being as specific as possible. Motivational information has the greatest impact if it is relevant to a patient's
disease status or risk, family or social situation (eg, having children in the home), health concerns, age, gender, and other important patient characteristics (eg, prior quitting
experience, personal barriers to cessation).
Risks Ask the patient to identify potential negative consequences of tobacco use. The clinician may suggest and highlight those that seem most relevant to the patient. The clinician should emphasize that smoking low-tar/low-nicotine cigarettes or use of other forms of
tobacco (eg, smokeless tobacco, cigars, and pipes) will not eliminate these risks.
Page | 107
Examples of risks are:
Acute risks - Shortness of breath, exacerbation of asthma, harm to pregnancy, impotence, infertility, and increased serum carbon monoxide.
Long-term risks - Heart attacks and strokes, lung and other cancers (larynx, oral cavity, pharynx, esophagus, pancreas, bladder, cervix), chronic obstructive pulmonary diseases (chronic bronchitis
and emphysema), long-term disability, and need for extended care.
Environmental risks - Increased risk of lung cancer and heart disease in spouses; higher rates of smoking in children of tobacco users; increased risk for low birth weight, Sudden Infant Death
Syndrome, asthma, middle ear disease, and respiratory infections in children of smokers.
Reward
s
Ask the patient to identify potential benefits of stopping tobacco use. The clinician may suggest and highlight those that seem most relevant to the patient.
Examples of rewards include:
Improved health
Food will taste better
Improved sense of smell
Save money
Page | 108
Feel better about yourself
Home, car, clothing, breath will smell better
Can stop worrying about quitting
Set a good example for and have healthier babies and children
Not worry about exposing others to smoke
Feel better physically and perform better in physical activities
Reduced wrinkling/aging of skin
Roadblocks
Ask the patient to identify barriers or impediments to quitting and note elements of treatment (problemsolving, pharmacotherapy) that could address barriers.
Typical barriers might include:
Withdrawal symptoms
Fear of failure
Page | 109
Weight gain
Lack of support
Depression
Enjoyment of tobacco
Repetiti
on
The motivational intervention should be repeated every time an unmotivated patient visits the clinic setting. Tobacco users who have failed in previous quit attempts should be told
that most people make repeated quit attempts before they are successful.
Adapted from: Fiore MC, Jaen C, Baker T, et al. Treating tobacco use and dependence: 2008 update. Clinical Practice Guideline. Rockville, MD: US Department of Health and Human Services. Public Health Service. 2008.Graphic 70628 Version 5.0
Pharmacologic therapy: Aims at reducing the symptoms of nicotine withdrawal, thereby making it easier for the smoker to stop the habitual use of smokers.
Drug-nicotine replacement therapy
dose and duration
efficacy and safety and side effects
Nicotine transdermal patchSmokers > 10 cigarettes per day
21 mg/day for 6 weeks, followed by 14 mg/day
Insomnia and vivid dreams are reported as side effects when the patch is left overnight.
Page | 110
smokers<45 kgs or <10 cigarettes per day
for two weeks, finishing with 7 mg/day for two weeks.
14 mg/kg per 14 days followed by 7 mg/day for two weeks
Nicotine Gum
Smokers >25 cigarettes
lighter smoker
4 mg per day
2 mg per day
Nausea, vomiting,abdominal pain, headache,sore jaw
Nicotine Lozenge
Smokers who smoke within 30 min after awakeninglighter smokers
4 mg per day
2 mg per day
Mouth irritation, ulcers
Nicotine sublingual tablet 4 or 2 mg depending on nicotine dependence
Nicotine inhaler 6 to 16 cartridges per day for the first 6-12 weeks, followed by gradual reduction of dose over the next 6 to 12 weeks.
Irritation of mouth and gums.
Nicotine nasal spray 1-2 sprays for recommended for maximum of 3 months
Nicotine mouth spray 1-2 sprays when the cravings occur
Bupropion Started 1 week before the start of the quit date.150 mg/day for 3 days,
Insomnia, agitation,dry mouth and headache.
Page | 111
followed by 150 mg/day twice a day thereafter for 7-12 weeks.
Varenicline 0.5 mg for 3 days,followed by 0.5 mg for twice daily for four days, and then 1 mg daily for 12 weeks
suicidal ideation,depression,increase in cardiovascular events in patients with CVD
Combined nicotine therapy
Nicotine patch + short acting-NRT product (gum,spray or inhaler)
more efficacious than single agent
Finally, for the patients who are not ready to quit smoking, it is the duty of the clinicians to assess the patient’s perspective (the risks and benefits of continuing to smoke) in order to help the smoker to begin to think about quitting.
REFERENCES
http://wwwuptodate.com.www.webmd.com
Page | 112
ENDOF
CLINICALMODULE
Page | 113
