(PTU) drug for hyperthyroid stop TH synthesis agranulocytosis, GI upset, Iiver Damage (especially PTU), Rashes 1/2 life of T4 is... a week 1st line tx in mild-mod dz H2 blockers 2 Ways of increasing FLUID volume? ADH/Aldosterone are 2 ways our body maintains homeostasis in fluid volume. ADH-sent by pituitary to make kidneys reabsorb H20 in the collecting ducts Aldosterone-sensed by the kidneys-release of renin-converts angiotensin 1 to 2-angiotensin 2 allows aldosterone to act on the kidneys to increase Na reabsorption and K depletion 4 H2 receptor antagonists -tidine -cimetidine - inhibits many cytochrome P450 enzymes and thus can interfere w/ hepatic metabolism; not recommended during pregnancy or nursing. also has antiadrenergic effects -- >gynecomastia -ranitidine -famotidine -nizatidine *reversibly and competitively inhibit the binding of HISTAMINE to H2 receptors, resulting in suppression of gastric acid secretion *they also indirectly decrease gastrin and acetylcholine-induced gastric acid secretion -peak plasma levels achieved w/in 1-3 hours **benefits: CHEAPER, with the exception of cimetidine, safe for preg. and adverse effects better studied
Transcript
(PTU) drug for hyperthyroid stop TH synthesisagranulocytosis, GI upset, Iiver Damage
(especially PTU), Rashes
1/2 life of T4 is... a week
1st line tx in mild-mod dz H2 blockers
2 Ways of increasing FLUID volume?
ADH/Aldosterone are 2 ways our body maintains homeostasis influid volume.
ADH-sent by pituitary to make kidneys reabsorb H20 in thecollecting ducts Aldosterone-sensed by the kidneys-release of renin-convertsangiotensin 1 to 2-angiotensin 2 allows aldosterone to act on thekidneys to increase Na reabsorption and K depletion
4 H2 receptor antagonists -tidine
-cimetidine - inhibits many cytochrome P450 enzymes and thus can interfere w/ hepaticmetabolism; not recommended during pregnancy or nursing. also has antiadrenergic effects -->gynecomastia-ranitidine-famotidine-nizatidine*reversibly and competitively inhibit the binding of HISTAMINE to H2 receptors, resulting insuppression of gastric acid secretion*they also indirectly decrease gastrin and acetylcholine-induced gastric acid secretion-peak plasma levels achieved w/in 1-3 hours**benefits: CHEAPER, with the exception of cimetidine, safe for preg. and adverse effects betterstudied
5-10 mLLEVOTHYROXINE SHOULD BE
CRUSHED FOR PATIENTS WITHDIFFICULTY SWALLOWING AND PLACE
IN HOW MANY ML OF WATER?
75-125 mcg/day Maintenance dose for levothyroxine?
Ablation• Performed w/radioactive iodine (131)• Initially increase symptoms• Results in chronic hypOthyroidism• Lifelong TH supplement
Aciphex (rabeprazole) dose? PPI----20mg po q daily
AcipHex (rabeprazole): _ PUD/GERD* PO; 20mg/day
actions decrease amount of acid produced bystomach
Addison's
When glucocorticoids are in use, especially in higher dose andlong term therapy-the adrenal glands shrink/atrophyIf we taper clients off glucocorticoids, then adrenal glands return tonormal function.If we suddenly stop the glucocorticoids, we have Addison's Crisis,the client will start losing there blood pressure, have renal failure,be very tired and lethargic, have nausea and vomiting, asthenia(lack of strength), they will die without getting a dose ofglucocorticoids
Adrenal GlandsSit on top of the kidneys.Inner Medulla- Epi/NorepinephrineOuter Cortex - Glucocorticoids (sugars),Mineralocorticoids (salts),gonadocorticoids (sex)
Adverse effects of PPI's are: not common
Adverse effects of PPIs
-headache, nausea, disturbed bowel function, abdominal pain-the large increase in gastrin secretion ---> can induce ECL cellsand parietal cells to hyperplasia -->carcinoid tumors ??? (notobserved in humans)
-may affect effectiveness of clopidogrel (anti-platelet agent)because CYP2C19 metabolizes PPIs as well as activates clopidogrel:this enzyme has various polymorphisms and is responsible for thevariation in clearance rate of PPIs
Adverse reactions
CNS side effects include confusion anddizziness. Cardiovascular side effectsinclude edema, chest pain, and irregularheartbeat. Irritation, pain, redness orbruising may occur at injection site.Bleeding, angioedema, rash, and hives.
Afrin
SE = use for 3-5 days only or could have Rebound congestion (worse than before), insomniaContraindicated = Heart disease, diabetes, HTNNursing Implications = Rebound congestion, taper use one nare @ a time.CNS stimulation (nervous, uneasy, aggitated)Vasoconstriction (avoid with CAD/HTN)Administer = lay on side, lateral, head low on sideEffective? Breathe, sleep, no agitation, no HTN, no chest pain, no nasal congestion
**Oral decongestants = work body wide, no rebound congestion, slower (SE = insomnia, anxiety)
Amiodarone (Cordarone/Pacerone)Class III antidysrhythmicPotassium channel blockerVentricular and Atrial Arrhythmias-especially with heart failureIV onset or PO onset looks to be 2-3 days to 1-3 weeksHalf life can be greater than 100 daysCheck K and MG levels prior to starting therapySide Effects: Fibrosis of lungs, destruction of thyroid, Photosensitivity-Smurfs,Liver destruction, N/V, Hypotension, Blindness, very hard on the stomach-GIDistressCan increase serum digoxin levels by 70%, Increase warfarin levels, Increasephenytoion (Dilantin), Stop BB and CCB?
amphojel dose 600mg po TID or QID
Antacids ...
Anti-Diuretic Hormone Drugs
ADHVassopressin (pitressin) Half-life 2-8 hoursDesmopressin (DDAVP) Half-life 20 hoursPromotes water reabsorption by the kidneys, vasoconstriction, and increased clotting factorVIII-used with hemophilia and von Willebrand's Disease, off label use-bedwetting in childrenSide Effects: Fluid Overload (reabsorbed too much water)-monitor for edema, hypertension,pounding headache, sleepiness. Myocardial Ischemia from vasoconstrictionmonitor: EKG and blood pressure, chest pain, dyspnea, diaphoresisCategory X for PregnancyDo not use in clients with CAD, Decreased Peripheral Circulation, and Chronic Nephritis
Aspirin (ASA)
Increased risk for GI bleeding (coffee ground emesis,black tarry stool)Increase Prothrombin time (PT/INR) ...stop a weekbefore surgery due to platelet life of 7 days Enteric coated = prevent GI bleed/upsetToxicity = tinnitus, humming, dizzy, bad balance,nauseaCaution = with heparin, lovenox, coumadin, Nsaids
Aspirin (ASA)
Non-opioidnon-steroidalanti-inflammatoryantipyreticBlood thinnerAspirin = binds to Cox 1/Cox 2 (stops plateletaggregation, gi upset, tinnitus, HA, sweating)
Atrovent
Inhaled anticholinergic work well on COPD/brochospasmallergen induced/exercise induced asthmaVery little absorbed from lungs, few systemic effects, dry nasalmucosa, dry mouth, hoarsenessRinse mouth (for nasty taste), peanut allergy (don't use)Anticholinergic = dry mouth, urine retention (suck on candies/sipliquids)Usually 2 puffs/dose
Decrease inflammation of nasal passageFew systemic effects unless swallowed in
large amounts
Beconase (inhaled)
Supress inflammation, decrease mucous, promote Beta 2 response(dilation of the bronchi)Anti-inflammatory for Asthma, COPD, allergic rhinitis, inhaledcorticosteroidSE = hoarse, dry mouth, changes in tasteMUST rinse mouth after/spit the water out --> Can cause OralCandidiasisOral Candidiasis = fungal yeaste, look for white spots in themouth.
Beconase (nasal)
SE = Nasal irritation, nosebleed, it maskssigns of infectionsLicorice = potentiate effectsAssess = signs of oral fungal infection,alternate nares, hoarseness, changes in voiceInterventions = blow nose before meds!!
Benadryl
SE = drowsy(excitation in kids)anticholinergic(dry mouth, urinary retention, gi upset)ACUTE toxicity (flushed face, fever, tachy, dry mouth, dilated pupils, mildhypotension)Contraindicated--> BPH, glaucoma, 3rd trimester, breastfeeding, newborn,bowel obstruction, CNS depressants/alcohol INC effectsToxicity = induce vomiting, remove anti-histamine, activated charcoal, tylenolfor fever, ice packs, send them to ERMAOI's = hypertensive crisis
Effectiveness? No Rhinitus (runny, itchy nose), no Uticaria (no itching, noallergic reactions)
Benadryl (diphenhydramine)
H1 receptor antagonist (1st Generation)antihistamine/makes you sleepyTreats: N/V, allergic reactionsEffects #1 = dry mouthIM --> Z track, deep injectionAntihistamines = prevent release of histamine byblocking H1 receptor sites on the mast cells in nasalcavity.
Benefits of PPI last: 3 - 5 days after therapy is stopped
Beta blockers/olol's
Beta-Adrenergic BlockersMetoprolol/Lopressor ENDING OLOLBeta Blockers are use with heart failure, hypertension, angina and with myocardial infarctions.Action = Blocks Beta-Receptors in the heart causing...Decreases = HR, force of contraction, Rate of atrioventricular (AV) conductionSE = Bradycardia, lethargy, GI disturbance, congestive heart failure, decrease BP, depression
The beta blockers stop sympathetic nervous system stimulation of the heart. Does not allow the heart rate and blood pressureto rise with stress thus lowering the oxygen demand of the heart. It is very heart protective!Will slow the heart rate and lower the blood pressureCan have beta 2 blockage with larger doses-will constrict the bronchioles-watch for clients with known COPD, Asthma
Nursing InterventionsCheck pulse-needs to be 60 or aboveCheck blood pressure-if hypotensive do not give (Systolic below 100 is a good rule of thumb I go by)Monitor for sexual dysfunction-impotence for men-a good reason for non-complianceDrowsiness/Fatigue-operating heavy machinery, driving could put client at riskInsomnia-Contraindicated with Heart Blocks, Bradycardia, Worsening Heart FailureIncreases Hypoglycemic effect of Insulin-monitor blood sugars and for hypoglycemia, may need to lower insulin dosageBeta Blockers have to be weaned slowly to prevent rebound hypertension and tachycardia-if a client wants to stop his beta-blocker they need to contract their physician
Metamucildecrease the absorption and effects ofWarfarin, Digoxin and Aspirin. Do notgive to patients with: GI obstructions,fecal impaction or abdominal pain andN/VMonitor elevated serum glucose
caffeine effect? 1) decrease LES pressure2) increase acidity
3) makes GABA less effective
Calcium & aluminum AA side effects? 1) constipation2) precipitate stone (Ca ones)
Blocks calcium channels in the myocardial and vascular smooth muscles, decreases the contraction of smooth muscle-relaxes the arteries-vasodilation. Blocking of calcium channels in the SA and AV node-Slows conduction through the SAand AV node. Decreases the force of contraction slows heart rate
Grapefruit juice may increase absorption of nifedipine
Side Effects: Relaxes smooth muscle and cardiac muscle-HeadacheDizziness-Take lying, sitting and standing B/P, educate client to sit and stand slowlyPeripheral edema-assess for edema, monitor for worsening (diuretic)FlushingReflex tachycardia-monitor for elevated heart rate (may need a BB)Constipation-increase fibers and fluids (if not restricted) stool softenerFatigue-Due to low heart rate-monitor EKG, pulse rate and rhythmWeakness-Monitor B/P and Heart RateImpotence and sexual dysfunction-Discuss possibility with client-have client to call and not just to stop medicationsHepatotoxicity-ALT, AST, ALK PHOS, BilirubinMI-Monitor for chest pain, dyspnea, increases fatigue, weaknessCHF-Monitor for chest pain, dyspnea, edema, increasing weight, decreasing output, increasing HR and B/PAngioedema-edema in face, throat, trouble swallowing, trouble breathing, thickened tongueGrapefruit juice may increase absorption of nifedipine
Acute ToxicityWith an overdose or overmedicatedGastric lavageMonitor EKG-bradycardia-widening QRS, hypotensionNorepinephrine to treat hypotension and decreased cardiac contractilityAtropine or Isoproterenol-Bradycardia and Cardiac Blocks
Verapamil (Calan, Covera, Isoptin Verelan)Class IV antidysrhythmicCalcium channel blockerInhibits the flow of calcium ions both into the myocardia cells and the vascular smooth muscle, slow the conductions velocityand stabilizes dysrhythmias. Lowers the blood pressure, reduces cardiac workload and lowers the blood pressure. Dilatesthe coronary arteries-anti-anginalSide Effects: Headache, constipation, hypotension, edema, bradycardia
-to tx H. pylori associated ulcers, hemorrhagic ulcers,AND to allow continued use of NSAIDs in a patientw/ a known peptic ulcer*they also contribute to the eradication of theH. Pylori infection*
-clot formation is impaired in acidic environments -so increasing pH allows for clotting of ulcers
Contraindications Known hypersensitivity to the medication,pork products, or heparin.
Cortef
Naturally occurring glucocorticoids (hydrocortisone andcortisone), which also have salt-retaining properties, are used asreplacement therapy in adrenocortical deficiency states. Theirsynthetic analogs are primarily used for their potent anti-inflammatory effects in disorders of many organ systems.Glucocorticoids cause profound and varied metabolic effects. Inaddition, they modify the body's immune responses to diversestimuli.
Cortef (hydrocortisone) side effects
Immune --> susceptible to infection and signs of infection will bemaskedPUD-Give w/food, Give prophylactic H2 or PPI do NOT give with NSAIDSMonitor: abd pain, coffee ground emesis, tarry stools, feverOsteoporosis-Have client take Ca/vit D, walkPsychoses-monitor for irritability, nervousness, mood changesbefore increasing to hallucinations/suicidal ideation,
Anti-inflammatory drugsMust taper them off Inhibits --> Making of prostaglandins, suppress histamines, stops some functions ofphagocytes/lympocytes (so, when infection happens they're aren't enough WBC to fight offinfection)SE = suppress adrenal glands --> Addison's crisis...hyperglycemia, mood changes, cataracts,PUD, electrolyte inbalance, osteoporosis, mask infections.Long-term = Cushing's syndrome
Glucocorticoids = inhaled, oral, IVEnd in -oneWe give all 3 types for Asthma/COPD
Sickest = IV, then PO, then inhaled glucocorticoid
Corticosteroids
Corticosteroids produced in the adrenal cortex. Corticosteroids: stress response, immune response, regulation ofinflammation, carbohydrate metabolism, protein catabolism, bloodelectrolyte levels, behavior.
Glucocorticoids: Cortisol. Control carbohydrate, fat protein metabolism,anti-inflammatory by preventing phospholipid release, decreasingeosinophil action and a number of other mechanisms.Mineralocorticoids: Aldosterone. Control electrolyte/water levels, mainlyby promoting sodium retention in the kidney.
Cortisol
When people are under stress, levels of cortisol hormone rise. Chronicstress can result in chronically high levels of cortisol, which can lead tosymptoms like weight gain, memory problems, high blood pressure, andother health problems. The stress release of cortisol is designed to enablethe flight or fight response with a quick burst of energy, but whenpeople are in a state of constant high stress, levels of the hormone neverhave a chance to fall back down to normal levels. This is one reason whytreatments for chronic stress include exercises and activities that aredesigned to reduce stress levels, allowing production of this hormone toslow down.
Coumadin
Warfarin/CoumadinWarfarin inhibits the action of Vitamin K, and without adequate Vitamin K the synthesis ofclotting factors 2, 7, 9, and 10 is diminishedINR/PTWarfarin takes 2-3 days to achieve therapeutic effect-99% of warfarin is bound to plasmaproteins and unavailable to produce effectsVitamin K is the antidote-green leafy veggies Aquamephyton-works within 6 hoursNormal INR therapeutic range is 2-3Normal INR for everyone who is not taking an anticoagulant is around 1Category X for pregnancyAvoid alcohol, diuretics, SSRI's, Antidepressants, Steroids, Antibiotics, Vaccines, Some Vitamins,Amiodarone-all can potentiate warfarinBleeding-
Cushing
Too much glucocorticoids for a long timeSigns Adrenal atrophy, osteoporosis, hypertension,increased risk of infections, delayed wound healing,acne, peptic ulcers, general obesity, redistribution offat around the face-Moon Face-shoulders, and neck-Buffalo Hump. Mood and personality changedHigh mortality rate from the complications such ashypertension from sodium and water retention
DDAVP (desmopressin)Prevents or controls thirst and frequent urination caused bydiabetes insipidus and certain brain injuries.Works on posterior pituitary....Treatment for: diabetes insipidus,bedwetting(nocturia), brain injuries, hemophilia A w/ some factorVIII productionnasally, IV, oral/subling tabup to 20 hours
Deficient knowledge R/T medicationregimen
Potential nursing diagnoses for pt. takingSynthroid?
Desmopressin (DDAVP): used forTreatment for: diabetes insipidus,
bedwetting(nocturia), brain injuries,hemophilia A w/ some factor VIII
production
Desmopressin acetate (DDAVP): availableas
nasally, IV, oral/subling tab
Desmopressin acetate (DDAVP): durationof action
up to 20 hours
Desmopressin acetate (DDAVP): is an antidiuretic hormone, works by limitingthe amount of water that is eliminated in
the urine.
Desmopressin acetate (DDAVP): works onthe
posterior pituitary
Detecting H.pylori-C-urea breath test (based on organismsproduction of urease)*urease converts C-urea to CO2 that isdetected in the breath
Dexilan (dexlansoprazole) dose? PPI.......-30 mg q daily-60 mg q daily if more erosive
Diabetes Insipidus (DI) No Antidiuretic Hormone = large amt offluid lost. You will see DI = w/head
injuries & lung cancer.
Diabetics: 14% take insulin only57% take oral medications only
14% take a combo of both.
Digoxin
Cardiac GlycosideDigoxin/Digitek, Lanoxin, Lanoxicaps (Dig)Increases the contractility of the heart muscle - Inotropic effect-Increases cardiac outputAlso Suppresses the SA node and slows conduction through the AV nodeHalf-life is 3-4 daysGreat Drug-real side effectsDigoxin SE =DysrhythmiasToxicity 0.5-1.8 normal levelSigns of toxicity-halos around objects, Nausea/Vomiting/Anorexia, blurred vision, fatigueBradycardia-must take an apical pulse for one full minute, must be 60 or above to give digoxinGive with caution with pediatric and geriatric patients due to inadequate renal or hepatic metabolic enzymesHyperkalemia can reduce effects of digoxinDigoxin and Beta Blockers can really lower the pulseGive with caution with renal failure-digoxin excreted via the kidneysDIGIBIND IS THE ANTIDOTE FOR DIGOXIN TOXICITYDigoxin Decreases automaticity of the SA nose and slows conduction through the AV nodeAtrial dysrhythmiasAll the side effects and warnings are still important
Dose and administration
*Adult: STEMI: single IV bolus of 30mg plus1mg/kg SQ dose followed by 1mg/kg SQevery 12 hours (Max 100mg)NSTEMI: 1mg/kg SQ every 12 hours inconjunction with oral aspirin therapy (100-325mg daily)Ped: 1mg/kg SQ
Drug interactions Interacts with NSAIDs, warfarin, and anti-platelet agents.
Drug Interactions: Protein binding Anticonvulsants, Estrogen, increasesWarfarin
Drugs that PPI interfere with? drugs that need acid environ. forabsorption (ex. iron)
Duration of action onset: 3-5 hourspeak: 3-5 hoursduration: varies
duration of action 2 hours
EXAM 1 DRUGS!!!! ...........
EXAM 2 DRUGS!!!!!!!!!!!! ..........
EXAM 3 DRUGS .......
furosemide/lasix (-ide)
...Loop Diuretics-prevents Na/Cl reabsorption, thus Na leaves the body, water follows Na and K follows thewaterFurosemide/Lasix, Bumex/Bumetanide, Torsemide/DemadexWork on the entire Loop of Henle-large volumes of water, Na, and K are removedWorks in renal failureHypovolemic and hypokalemia very commonNursing interventionsKnow your potassium level prior to administrationAssess Lung Sounds, Weight, I/O, Edema, SaO2, RR, Blood Pressure, K Level prior to administration, assessall of these post administration, especially K Level and Lung Sounds, Sao2, I/O. If you urine bag is not twiceas full 30 minutes post IV Lasix administration, check your IV site. If your client without a Foley has notcalled to urinate within an hour of giving po Lasix, check your clientWarn your client to get up slowly after taking Lasix, watch for orthostatic hypotensionLasix does have sulfa as a base componentMay not be used with anuria, hepatic comaUse with extreme caution with electrolyte depletionLow K with Digoxin can equal lethal Dysrhythmias, know your potassium level-has a digoxin level been ran
GI TractH2 activation of parietal cells --> gastric
Used with diet and exercise to control blood sugar in patients with type 2diabetes. May be used alone or with other medicines.starting dose of GLUCOPHAGE (metformin hydrochloride) Tablets is 500 mgtwice a day or 850 mg once a day, given with meals. Dosage increases shouldbe made in increments of 500 mg weekly or 850 mg every 2 weeks, up to atotal of 2000 mg per day. The purpose of both insulin and metformin is to lower blood glucose levels.Insulin injections replace the insulin your body can no longer make when thecells in the pancreas cease to function. Metformin is an oral hypoglycemic,which lowers blood glucose levels by decreasing the liver's output of glucose.Metformin also increases insulin sensitivity, and improves not only bloodglucose levels but also lipid levels and often results in weight loss.
goal of antacid
1) symptom relief2) lifestyle modification needed-raise head of bed-limit caffeine-stop smoking-weight loss-diet (increase fiber)
goal of tx w/ H2 & PPI relieve sx & heal ulcers
H. pylori
-gram negative, spiral, found in gastric antrum, orally transmittedcorkscrews through the gastric mucus layer** H. Pylori = inflammation/epithelial cell damage
increased GASTRIN/dec SOMATOSTATIN
**its is able to live in such an acidic environment b/c of itsproduction of UREASEUrease = converts urea to ammonia (ammonia buffers the H+ &creates an alkaline cloud around the h.pylori)
H. pylori - risk recurrent ulcer (60-85% vs 5-10% if cured)
H. pylori - treatment**
PPI + 2 of the following antibiotics--Clarithromycin--Metronidazole--Amoxicillin
One week treatment: 90% cure rate
Two weeks of PPI + 1 antibiotic (typically clarithromycin): 10-20% lower cure rate
MHD notes:--Tetracycline can be 1 of the 2 antibiotics--Bismuth salts, doxycycline, and metronidazole for 14 days is cheap and effective
H1 distribution Smooth muscleEndothelium
H2 blocker---Prototype Drug? Zantac
H2 Blockers (-tidine) Ranitidine
H2 blockers uses...(-tidine) 1) GERD2) PUD
3) hypersecretory conditions (ZE)
H2 blockers-how long to work? 30 min.
H2 distribution Gastric mucosaCardiac muscle
Vascular SM
H2 receptor antag - therapeutic use?
Peptic ulcer disease PUDGastric acid hypersecretionInhibit stimulated acid secretionNocturnal acidity (useful when added toproton pump therapy to control "nocturnalacid breakthrough")**
H2 receptor antag that can cause:gynecomastia (male breasts)/galactorrhea
(milk leakage)
CimetidineDue to decreased estrogen metabolism
(cyt p450 inhibition)
H2 receptor antag- MOA (mechanism ofaction)
Reduce gastric acid secretion
H2 receptor antag- pharmacokinetics
Absorption: well absorbed after oraladministrationPeak plasma concentrations reached in 1-2 hoursT1/2: 1-3 hoursSome hepatic biotransformation (cimetidine hasthe greatest)Mostly excreted unchanged by the kidney
H2 receptor antagonists - drug names
ClimetidineFamotidineNizatidineRanitidine
Note: these drugs have different structuresand therefore different side effects
Naturally found in the liver and lining of blood vesselsProlong coagulation timeIV immediate onset, Sub Q 1 hourDestroyed by gastric enzymesWeight basedaPTT (PTT also, but in the hospital we use the aPTT)Sub QThrombocytopenia occurs in 30% of clientProtamine Sulfate is the antidote, 1 mg for every100 units ofheparin, works for Lovenox also
HistaminesIncrease capillary permeabilityIncrease BloodIncrease runny noseBrocho-constriction (try to keep out theallergens/dust)
How do NSAID cause gastric epith celldamage?
they are weak acids...they becometrapped....and cause damage
how do they work-weak bases that neutralize HCl acid -raise pH which inactivates pepsin-increase Lower Esophageal Sphinctertone, which decreases reflux-does NOT coat stomach lining
how long does it take for blood to cleartract
72 hours
How long once PPI's are stopped to returnto normal gastric level??
3-5 days
How soon when taken on empty stomach 20-40 min.
Hydrocortisone
Hydrocortisone belongs to the family of medications known ascorticosteroids. It is used to treat many different conditions. Itworks by reducing swelling, inflammation, and irritation or as areplacement when the body does not make enough cortisol.Hydrocortisone is more commonly used to treat allergic reactions,some skin conditions, severe asthma, lupus, and arthritis.It can also be used to treat steroid deficiency in the body, certainblood disorders, certain types of cancer, multiple sclerosis, andulcerative colitis.
HYPERglycemia
3-P'sPolyuria-frequent urinationPolyphagia-hungerPolydipsia- thirstGlycosuria-high sugar in the urineWeight loss-even though their sugar is high, they aren't getting nutrients intothe cellFatigueKetones- in the urine/breath--gives off ketones (fruity Smell to the breath)No nutrients to the cell, burning fat for energy Rapid, Deep Respirations (blowing off the ketones)Dry Skin (Dehydrated from peeing too much)
Hyperthyroidism: During pregnancy? PTU preferred in first trimester/Tapazolelater in pregnancy
mo when stable)Labs: Symptoms, wt., pulse, Free T4, TSH,
CDC Tests
HYPERthyroidism? Synthroid toxicity/overdose
HYPOglycemia
Blood sugar is low, usually below 70 (70-110 is considered normal range)The brain is not getting sugar, it needs sugar to keep functioningFirst signs are neuro in natureSweatingTremorsIrritabilityBlurred visionDiaphoretic (sweating)HeadacheLightheadednessAnxiousDecreased LOC NauseaPalenessAnd whatever else your patient states is a sign of their hypoglycemia. If your patient states they arehypoglycemic, believe them
Hypothyroid pregnancy? increase dose
if PPI is uneffective q daily? PPI BID for 8-12 wks
IndicationsUsed to inhibit clot formation in ACSincluding STEMI, NSTEMI, and unstableangina. Also used to prevent pulmonaryembolism and DVT in patients predisposedto such problems.
Insomnia Give synthroid before breakfast toprevent____.
Insulin
Is a polypeptide hormone that controls thestorage and metabolism of carbohydrates,proteins, and fats. This activity occursprimarily in the liver, in muscle, ind inadipose tissues after binding of the insulinmolecules to receptor sites on cellular plasmamembranes
Insulin (never given PO)
Available in 1922 (1922-1980's Insulin from Pork or Beef pancreas)Insulin must be available when glucose is in the bloodControl of Diet-when and what is eatenControl of ExerciseDuring IllnessNever PO-GI Juices destroys the insulinVial in use @ room temp (extra vial in refrigerator)
Recombinant DNA (rDNA) now is used almost exclusivelyMost effective, fewer allergies, lower incidence of resistance
Insulin VS Metformin Treatments?Mechanisms
Oral hypoglycemics are used only in Type 2 diabetes, because Type1 diabetics make little or no insulin, so reducing the glucose levelsproduced by the liver won't reduce blood glucose levels. Withoutinsulin, glucose can't enter cells and remains in the bloodstream.While all Type 1 diabetics take insulin, some Type 2 diabetics alsoneed insulin in addition or instead of oral hypoglycemics such asmetformin. Insulin, which must be injected, comes in several formsand doses, and can have rapid or slow onset.
Insulin VS MetforminTreatments?....Benefits
Both metformin and insulin help to normalize blood glucose levels.Keeping blood glucose levels as close to normal levels as possiblelimits the damage high blood glucose imposes on every bloodvessel and organ of the body. High blood glucose levels lead to poorcirculation, heart problems, vision problems, nerve damage,susceptibility to infection and kidney damage. While damageoccurs earlier in Type 1 diabetics, Type 2 diabetics can alsoexperience complications.
Insulin VS MetforminTreatments?....Considerations
For Type 1 diabetics, insulin is the onlymedication choice. For Type 2 diabetics,medical practitioners generally start with anoral hypoglycemic such as metformin andadd insulin only when oral hypoglycemicscan't stabilize blood glucose levels.
Insulin VS Metformin Treatments?....SideEffects
Diarrhea, the most common side effect of metformin, improves ifmetformin is taken with food. Liver failure and increased acidity,acidosis, occur rarely, The Merck Manuals Online Medical Librarystates. Insulin must be carefully calibrated or blood glucose levelsmay drop too low, a condition called hypoglycemia. Taking insulinwithout eating or taking too much insulin for the amount of foodeaten can cause hypoglycemia. Symptoms of hypoglycemia includeweakness, shakiness, sweating, lightheadedness and confusion;coma and death can result in severe cases.
Insulins (dec blood sugar)
Interaction w/Cortef (othercorticosteroids)
NSAID's/alcohol-may increase chance of GI BleedOral Anticoagulants may inc/dec anticoagulationUse with diuretic, increase K depletionMonitor? EKG/K levelsVaccines? May reduce the antibody response tovaccine
Intermediate Acting = NPHHumulin N
NPHOnset 1-2 hoursPeak 6-14 hours
Duration 16-24 hours
IV/PO Synthroid Routes?
IV/PO dose IV = 200, 500 mcg vialTab = 25-300 mcg
Lab monitoring in stable patients? Follow up: 6-12 moNeed for hormone decreases with age
Lantas -->long-acting insulinTreats diabetes mellitus. Insulin is ahormone that helps get sugar from theblood to the muscles, where it is used forenergy. This type of insulin usually workslonger than regular insulin.
length of tx for hypersecretory or erosiveconditions
LOW Initial dose of geriatric/cardiac pt. takingsynthroid?
Maalox 30mL QID
maalox dose 30 mL---QID
Magnesium AA Side effect? diarrhea
max. effect occurs? taken 1 hour after meals
Mechanism of action Deactivates thrombin. Also prevents theconversion of fribrinogen and fribrin.
Med interactions w/glucocorticoids
NSAID's and Alcohol-may increase chance of GIBleedOral Anticoagulants may increase or deceaseanticoagulationUse with diuretic, may increase K depletion-monitor EKG and K levelsVaccines-may reduce the antibody response tovaccine
Mineralocorticoids
Aldosterone-95% of the mineralocorticoids secreted by the adrenalsAldosterone regulates plasma volume: Na REABSORPTION & KEXCRETION by the tubules. 1. Plasma volume falls2. Kidney senses this and release renin3. Renin allows angiotensin 1 -->angiotensin 2. 4. Angiotensin 2 causes aldosterone secretion5. Allowing sodium reabsorption/potassium depletion (remember,WATER follows salt!)
moderate s/s are... s/s several times a week or daily
MOM (milk of mag) dose 15-30 mL---QID
monitor check electrolytes periodically
Monitor blood/urine glucose in what kindof patient's taking Synthroid?
Diabetic
Monitor: Ht., wt, psychomotordevelopment.
When a child is taking Synthroid.
MORE side effects: H2 or PPI? H2
Morphine
PO, SQ, IM, Rectal, IV epi, Intrathecal
Must have RR of 12 or higher!!!!Don't use = premature infants, demerol w/renal failure, with head injuries (LOC is too hard toaccess)Precautions = asthma, emphasema, older, babies, respiratory depression, pregnancy, labor,obesity, IBD, enlarged prostate, liver/renal disease--prolonged accumulation of drug)Anticholinergic agent--Benadryl, will increase effects of constipation/urinary retentionMAOI = high fever/comaAnti-hypertensive meds = hypotensive effectNursing administration = assess pain, docoument, 1-10 scaleOral = 45 - hr laterIV = 30 mintes laterCancer? give fixed schedule, around the clock, PRNAddicted? Taper off over 3 days!!!
Morphine (opioid)
Opioid agonistTX of moderate/severe painInduces pleasureActivates Mu receptors (analgesia, sedation, resp. depression, euphoria)Activates Kappa Receptors (analgesia, sedation, decreased GI motility)Attaches to receptors in CNS & alters perception & response to pain.Complications = respiratory depression, constipation, orthostatichypotenstion, urinary retention, cough supression (cough hourly), sedation,biliary colic (spasm of sphincter of Oddi--use meperidine), emesisOverdose? Coma, respiratory depression, pinpoint pupilsMonitor -->Breath sounds, vitals, Narcan, mechanical ventilation
Most commonly reported adverse effectsof PPI's are:
- headache- abd pain- diarrhea
- N/V
The most widely used antacids aremixtures of ____ and ____
-aluminum hydroxide (can cause constipation)-magnesium hydroxide (can cause diarrhea)*so when taken together you can avoid thosesymptoms
-OH combines w/ H+ to form water-metals form salts with bicarbonate
Mucomyst Antidote for tylenolEffectiveness?? Liver enzymes are
normal/no enlargement)
Mucosal protective agents - drug names SucralfateColloidal bismuth (Pepto-Bismol)
Mylanta
This medication works only on existing acid in the stomach. It does notprevent acid production. It may be used alone or with other medicationsthat lower acid production (e.g., H2 blockers such ascimetidine/ranitidine and proton pump inhibitors such as omeprazole).This medication can cause nausea, constipation, diarrhea, or headacheby mouth, usually after meals and at bedtimehis product may react withother medications (e.g., digoxin, iron, tetracycline antibiotics, quinoloneantibiotics such as ciprofloxacin), preventing them from being fullyabsorbed by your body.
Mylanta
This medication is used to treat thesymptoms of too much stomach acid such asstomach upset, heartburn, and acidindigestion. Aluminum and magnesiumantacids work quickly to lower the acid inthe stomach. Liquid antacids usually workfaster/better than tablets or capsules.
Myxedema Coma SEVERE HypOthyroidism= mental, cold, low HR
Myxedema TX? (mistaken for adrenaldysfunction at times)
1. Synthroid by IV2. Glucocorticoids (dec stress on body
when metabolism goes up)3. Management/treat causative factors
Narcan
SE = tachycardia, tachypnea, ventricula arrhythmia, pulmonary edemaAbstinence syndrome = cramping, HTN, vomiting (by stoppingmorphine effect, we can induce withdrawal quickly)Caution = history of heart failure/pulm edema (the HTN/teachycardiacan induce heart failure by increasing workload of the heart) Contraindicated = with opioid dependency (immediate withdrawal)Titrate dosage = relieve pain, reverse respiratory depression (if youdon't titrate it can cause sudden onset of pain/withdrawal)Rapid Infusion = HTN, tachycardia, N/V
Narcan (naloxone)Opioid antagonistTreats Overdose = competes w/opioid receptorsDon't give with pregnancy(Rebound resp depression, abstinence syndrome, titrate dosage, rapid infusion) IV, IM, SQ, NOT ORALLY1/2 LIFE = 60-90 MINUTES1/2 LIFE of opioid = 3-4 hoursCan lead to rebound respiratory depressionRespirations = Monitor for 4 hours after giving it
Nexium (esomeprazole) dose? PPI---20-40mg po q daily
Nitroglycerin/Nitrostat, Nitro-Bid, Nitro-DurNitrates form nitric acid which is a relaxes smooth muscle and dilates venous and arterial blood vesselsOpen veins-blood pools in the legs-not as much blood returning to the heart-reduces preloadOpen arteries-heart does not have to work as hard to pump blood out of the heart-reduces afterloadOpens the coronary arteries and helps supply blood to the heart tissue
Can be given sublingually, orally, topically, IV, buccalCan be for acute or long term useNitroglycerin dilates any artery and vein-including yours if you touch it while administering it-WEAR GLOVESNitroglycerin IV needs a glass bottle and covered from light-some hospitals still use special tubing (nitro is absorbed in thetubing)Short term-nitrostat-sublingually-1 tablet every 5 minutes x 3 for relief of chest pain-still having chest pain call911/physicianLong-term nitro-dur will last for up to 14 hours in the body
Side Effects:Headache-dilates the cerebral arteries-do not give with head trauma or increased intracranial pressureHypotension and reflex tachycardia-do not give with hypotension, monitor blood pressure and HR when administeringHypotension-correct hypervolemia prior to giving nitroglycerinDO NOT GIVE WITH VIAGRA, LEVITRA, OR CIALIS (nitroglycerin and Viagra increase nitric acid and relaxation of thesmooth muscles-can kill a client with hypotension with a combination of these drugs)
nonpharms1) balanced meals at regular intervals2) avoid foods that exacerbate sx3) high fiber diet 4) avoid caffeine & alcohol5) stop smoking
NPH -->intermediate-acting
Often used in combination with a shorter-actinginsulin. NPH insulin is a man-made insulin product isthe same as human insulin. It replaces the insulinthat your body would normally make. It is an insulin(isophane). It starts to work more slowly but lastslonger than regular insulin. Helps blood sugar(glucose) get into cells so your body can use it forenergy.
NSAIDS (Ibuprofen)
Analgesic, anti-inflammatory, antipyretic, antiprostaglandinSodium based = may increase BP/heart failure, causes UlcersSE = N/V, GI bleeding, heartburn, epigastric pain, GI ulcer, renal impairment,bruising, blood in urineCaution = with MI's and bypass patient's.No more than 3,200 Mg/day (it can kill the kidneys/especially w/long termuse)
AntipyreticAnalgesisWork on Cox 1/Cox 2Take with FOODStop production of prostaglandinsCan cause --> kidney toxicityNSAIDS = N/V, gi bleed, platelet aggregation, kidneytoxicity possible)
Nurse can increase gastrin level while onPPI to around what range
Nursing considerations 2 Monitor for signs of water intoxication-headache, confusion, pounding headache,
edema, hypertension, sleepiness
Nursing considerations 3 Extravasation of IV vasopression can leadto Gangrene
Nursing considerations 4 Effectiveness-normal urine output,without signs of fluid overload
Nursing considerations for ADH meds Monitor vital signs, I/O, specific gravity,daily weights, Electrolytes,
Nursing Interventions?
1) check stools/vomit for blood2) LFT (Liver enzyme tests, formerly called liver function tests(LFTs), are a group of blood tests that detect inflammation anddamage to the liver. They can also check how well the liver isworking. Liver enzyme testing includes ALT, AST, alkalinephosphatase; true liver function tests (LFTs) include PT, INR,albumin, and bilirubin)3) BUN/crea4) don't crush or chew PPI's
ORAL, IV systemic glucocorticoids
Suppresses the adrenal glandsMust taper them off the dose or.....Can send them into Addison's CrisisAddison's = Low BP, no energy, bone loss, increase blood sugar, muscle weakness, PUD (huge issue), takewith food/no NSAIDS, sore throat.Sodium Retention = hypokalemia (weak muscle/cramps)Give Ca with Vitamin DWATCH for edema, weight gain, HTNInflammation = Defense brought on by injury, toxic chemicals, heat, microorganisms, cell death, allergenresponse.Sighs = swell, pain, warmth, rednessAcute = 1-2 weeksChronic = Lupus, RA
Who responds to inflammation? Mast cells, Bradykins, leukotrines, histamines, prostaglandins.
Other drugs - Misoprostol Blocks binding of prostaglandins toparietal cell receptor --> decreased acid
secretion
Other drugs - Pirezepine Blocks binding of Ach to M3 receptors -->decreased acid secretion
Painful subacute thyroiditis Acute = thyroid is destroyed inHashimotos
Acute then goes down to hypOthyroidism
PCA pumps
4 hour dose limitSet machine for how many mg/hour.Encourage = use before activities Assess client = LOC, RR, BP, HREducate = it's very hard to OD on pumpsNursing Intervention = check IV line patency, ask to change PCAto oral med if they're feeling betterNursing Prejudices = assess their pain, respirations must be 12+Pain 1-4 = PO medsPain 5-10 = IV meds
pepcid dose 20mg BID or 40mg po Q HS
Peptic Ulcera break in the lining of thestomach/duodenumcause: IMBALANCE b/wprotective/damaging factors2 COMMON factors = H. pylori & NSAIDs
Irreversibly alter the plasma membrane of platelets, alters the ability of platelets to aggregateTiclid and Plavix are given orallyTiclid can cause Agranulocytosis-only used when someone is allergic to PlavixGlycoprotein is an enzyme necessary for platelet aggregation, IV only, Very expensive used with MI's Strokes, and PTCA's
Clopidogrel (Plavix) Antiplatelet drugADP receptor blockerInhibits ADP binding to its receptor's-irreversible and will be with the platelet for their lifespan (5-7 days)Used for MI's, CVA's, PAD/PVD, Unstable Angina, PTCA's-first 6 months post ptca'sBleeding is a problem
PO dose ---> IV? cut in 1/2
PPI ....1/2 life? LONG = (72 hours)
PPI uses... (-prazole)1) GERD2) PUD
3) hypersecretory conditions4) H. pylori
PPI with longer 1/2 life? Nexium (esomeprazole)
PPI' s heal 90% gastric ulcers w/in : 6 - 8 weeks
PPI's (-prazole) Omeprazole
PPI's are effective at: reducing gastric acid secretions
PPI's are used for: short term control, PUD, GERD
PPI's heal 90% of duodenal ulcers w/in: 4 weeks
PPI's mechanism -prazole
-block the parietal cell H+/K+ ATPase (proton pump)-superior to H2 receptor antagonist*OMEPRAZOLE -prototypealso: esomeprazole, rabeprazole, lansoprazole, dexlansoprazole, pantoprazole-all are PRODRUGS that require activation in an acidic env. --> converted toSULFENAMIDE (active form) which reacts with a cysteine residue on theH+/K+ ATPase-->irreversible inhibition of the proton pump-for acid production to resume it takes ~18 hours before new H+/K+ ATPasecan be produced**there site of action is in the parietal cell canaliculus (this is why intravenousadministration is useful to bypass the acidic stomach and duodenum)
PPI's usually taken? during the day
PPIs - drug interactions
Decrease the metabolism and clearance of:--Bendodiazepines--Warfarin--Phenytoin
Reduce absorption of:--Ketoconazole
Increase the absorption of:--Digoxin
PPIs - drug namesOmeprazole (children, GERD)Lansoprazole (NSAID ulcers)
RabeprazolePantoprazoleEsomeprazole
PPIs - Drug of choice (DOC) for... Zollinger-Ellison syndrome (g acidsecreting tumor)
GERD (Gastricesophageal Reflux Disease)
PPIs - MOA (mech of action)
Irreversibly inhibit the gastric parietal cell protonpump H/K ATPase (Note: the prolonged duration ofaction reflects the covalent modification of the pump,rather than prolonged serum half life)**A single daily dose can effectively inhibit 95% ofgastric acid secretionProdrugs - activated in an acidic environment
PPIs - use with H2 antagonists?Should not be given simultaneouslybecause the H2 antagonist reduces theefficacy of the PPIUsually the PPI is taken during the dayand the H2 antagonist is taken at night
PPIs- adverse reactions
Few and generally mild
DiarrheaHeadache
DrowsinessMuscle painConstipation
Prednisone (ORAL glucocorticoid)
Anti-inflammatory corticosteroidGlucocorticoids = inhibits making of prostaglandins, suppress histamine, stops some functionsof phagocytes/lympocytesShort-term use only/taper them offauto-immune disease = long-term use
Fever = signs of inflammation/natural defense to neutralize foreign organismsProlonged fever in children = febrile seizuresProlonged fever in adults = breakdown body tissue, delirium/comaObscure causes of fever --> SSRI (serotonin syndrome), Thorazie, Anesthetics (malignanthyperthermia), immunodilators, cytotoxic drugs, chemotherapy, neutropenic agents
prego cat none
Prevacid (lansoprazole) dose PPI---15 mg q daily x 8 weeks
Prevacid (lansoprazole) in h. pylori? 30 mg BID x 2weeks + 2 antibiotics
Prevacid (lansoprazole):- PUD- combo w/antibiotics for H. Pylori* PO; 15-60mg/day-- Prevacid combines (lansoprazole)w/amoxicillin/clarithromycin
Pril/ace inhibitors
Enalapril/Vasotec PRIL-is the ending for ace'sReduces Angiotensin 2 and aldosterone levelsPrevents Angiotensin 1 from converting to Angiotensin 2 in the lungs-leaves the Angiotensin 1 hanging in the lungs-createsirritation-coughVasodilation-mostly arteriole (decreases afterload)Excretion of sodium and water-retention of K (decreases preload)Treats hypertension and heart failureDo not take 2nd and 3rd Trimester of pregnancy
SE = Angioedema-allergic reaction-swelling of tongue, throat-stop taking and notify mdHyperkalemia-monitor for widening and slowing of pulse/qrs, weakness, fatigue, avoid high K foods, AVOID SALTSUBSTITUTES-usually very high in K, avoid potassium sparing diuretics, sport drinks are high in K alsoOrthostatic Hypotension-teach client to sit and stand slowly, enact fall precautionsNeutropenia/Agranulocytosis-monitor CBC-WBC count, reoccurring infectionsRenal Insufficiency-Monitor weight, edema, I/O, BUN, Cr, and GFRHepatic Insufficiency-Monitor AST, ALT, ALK PHOS, BilirubinCough-Cough lozenges, hard candy, increase fluid intake, sleep with HOB elevated, antihistamines
ACE Inhibitors
Discussed these medications with hypertension
Arb's-Angiotensin receptor blockers, sartan'sNo Cough, same effects and side effects as Ace's-just not as potent
Prilosec (omeprazole) dose PPI --20 mg q daily or 20 mg BID
Prilosec (omeprazole) tx w/ h. pylori -40 mg q daily x 2 weeks -then 20 mg w daily x 2 weeks + antibiotic
Prilosec (omeprazole):- PUD/GERD
- often used in combo w/- antibiotics for H. Pylori
* 20-60mg 1 -2 daily
Protonix (pantoprazole) dose 40 mg po q daily x 8-16 weeks
Protonix (pantoprazole): - mainly for GERD- IV form avail
* PO; 40mg/day
Proventil
SE = HA, irritate throat, tremor, nervousness, tachycardiaCaution = HTN, cardiac, heart failure, seizuresPatients = keep log of attacks/frequency/what triggers themLungs = lotsa blood supply/large surface area, making them a quickonset (we don't give PO)Use = asthma control, prevent exercise induced asthmaEffective? Clear breath sounds--NO wheezing/rhonchi, respiratory rate@ baseline, SaO2 @ baseline 90%
Note = Long-acting are combined w/corticosteroids. Get bronchi openand the corticosteroid can get in there easier when it's dilated!
Proventil
Beta 2 adrenergic agonistBrochodilatorQuick-acting rescue inhaler (5 minutes)Use before exercise to preventBronchoconstrictionUse beta 2 agonist inhaler beforeglucocorticoid
pt. education with tablets? chew & take w/ full glass of water
PTU
Treats Graves' disease andhyperthyroidism (too much thyroidhormone from the thyroid gland) inpatients who have already been treatedwith other medicines (such asmethimazole) that did not work well.
Quadruple therapy for H. pylori-tetracycline
-metronidazole*both broad spectrum antibiotics
-PPI-bismuth (for coating and eradication)
Receptors
Norepinephrine-Adrenergic (adrenergic comes from the wordadrenalin)Alpha 1-all sympathetic target organs except the heart-constrict theblood vessels and dilation of pupilsAlpha 2-Presynaptic adrenergic nerve terminal-inhibits the releaseof norepinephrineBeta 1-Heart and Kidneys (BETA 1-ONE HEART)-increased heartrate and force of contraction, release of reninBeta 2-All sympathetic target organs-inhibits smooth muscle(BETA 2-TWO LUNGS)
Reg -->short actingHumulin® R U-100 is a polypeptidehormone structurally identical to humaninsulin synthesized through rDNA technologyin a special non-disease-producinglaboratory strain of Escherichia coli bacteria
Regular Insulin = Fast Acting
Humulin R, Novolin R/Insulin RegularOnset 30-60 minutesPeak 2-6 hoursDuration 6-10 hoursTHIS IS THE ONLY Insulin That Can BeGiven IV
Role of H2 receptor in acid secretion
ECL cell stimulation by gastrin or Ach -->histamine release --> H2 receptoractivation on parietal cells --> ACactivation --> cAMP production --> proteinkinase activation --> acid secretion byproton pump (K in; H out)
s/s1) Headache
2) nausea3) irritability4) weakness
Sartan's/angiotension blockers/arb's...
Arb's-Angiotensin receptor blockers,sartan's
No Cough, same effects and side effects asAce's-just not as potent
SE of bismuth
dark stool (When Helicobacter pylori isimplicated, bismuth acts as an antimicrobialagent, suppressing the organism but noteliminating it. In recent studies, bismuthcompounds have been used with conventionalantibiotics, producing elimination of theorganism, histological improvement)
Should you use PPI & H2 together? NO
Side effects of Synthroid Insomnia, irritable, nervous, arrhythmia,tachycardia, wt loss, cardiovascular
collapse.
Special considerationsDo not use in patients with active majorbleeding or thrombocytopenia. Use withcaution in the elderly or any patient withincreased risk of bleeding.
Statins (Lipitor)
HMG-CoA reductace inhibitor-(liver is where the cholesterol is made, it is where the HMG-CoA work)
LDL/Cholesterol is reducedGive with food to reduce GI symptomsLipitor can be taken at anytime, most of the class of this medication needs to be taken at bedtime-cholesterolis made by the liver at nightUp to 30 days to achieve full affect
Side Effects:GI-constipation, bloating, gas, nauseaLiver-monitor enzymes-alt, ast, alk phas, bilirubin, jaundice, enlarged liver-ascitesRhabdomyolysis-muscle destruction-CK elevation-muscle pain-MD has to be notified. Renal failure is very common with Rhabdomyolysis-need to make sure urine output is 30 ml or greater anhourNo grapefruit juiceThe statins are hard on the liver-you need to make sure other drugs the client is on is not hard on the liver-Amiodarone and Nizoral are two drugs that come immediately to my mind
Thyroid Therapy Partial hair loss may be experienced inkids taking __ ___.
Thyrotoxicosis --> THYROID STORM!!!!
Exaggerated signs/symptoms ofHYPERTHYROIDISMFever, mental, precipitated by illnessManagement? (Tapazole & PTU)Potassium Iodide, KI = stops release of thyroidhormonePropranolol = treat peripheral effects (lowers BP,angina, irregular Hbeat, migraines, tremors)
Too little cortisol? (Addison's disease)
What Causes Addison's Disease?Result from a problem with the adrenal glands themselves (primary adrenal insufficiency).Autoimmune disease accounts for 70% of Addison's disease. This occurs when the body's immune system mistakenly attacks the adrenal glands. Thisautoimmune assault destroys the outer layer of the glands.When glucocorticoids are in use, especially in higher dose and long term therapy-the adrenalglands shrink/atrophyIf we taper clients off glucocorticoids, then adrenal glands return to normal function.If we suddenly stop the glucocorticoids, we have Addison's Crisis, the client will start losing thereblood pressure, have renal failure, be very tired and lethargic, have nausea and vomiting,asthenia (lack of strength), they will die without getting a dose of glucocorticoids
Too much cortisol? (Cushing's syndrome)
Body is exposed to high levels of the hormone cortisol for a long time. Themost common cause of Cushing syndrome, sometimes calledhypercortisolism, is the use of oral corticosteroid medication. The conditioncan also occur when your body makes too much cortisol.Causes? pituitary adenoma, tumor: lungs, pancreas, thyroid or thymus gland. Signs: Adrenal atrophy, osteoporosis, hypertension, increased risk ofinfections, delayed wound healing, acne, peptic ulcers, general obesity,redistribution of fat around the face-Moon Face-shoulders, and neck-BuffaloHump. Mood/personality changedHigh mortality rate from the complications such as hypertension from sodiumand water retention
Toxic adenoma? benign tumors releasing TH
Toxic diffuse goiter (Graves' disease) Antibodies stimulate TSH receptorsNot TSH but acts like it
Treatment (tx) for severe PUD? PPI
Treatment (tx) in severe or erosive dz PPI q daily
Treatment: Synthroid overdose? Stop dose for 2-6 days
Triple therapy for H. pylori -amoxicillin-clarithromycin
-PPI
TSH is the best screening test for? Primary thyroid dysfunction (usuallyoutpatient)
tums/rolaid dose PRN
tx (treatment)? H2 blockers BID for 8-12 wks
Tx for HYPERglycemia 1. check sugar2. ketones in pee?
3. give insulin
Tx for HYPOglycemia (or brain cells willdie)
(HIGH SUGAR SNACK, THEN COMPLEX CARB)High sugar = coke, OJ, candy. Complex carb = peanut butter/crackers. (willstabilize sugar from falling after the high sugar snack)Unconscious? D50, sugar in the buccal area, orglucagon in a tube in buccal areaIn the hospital? get accu check 1st, then get sugarasap!
tx h. pylori H2 or PPI + antibiotics & sometimesBismuth
Vasopressin (pitressin)The antidiuretic action of vasopressin isascribed to increasing reabsorption ofwater by the renal tubules40u IVAdverse = cardiac ischemia/angina
What are glucocorticoids?1. Hypothalamus senses low glucocorticoid levels in the blood-2. Releases CRF (corticotropin releasing factor) to pituitary gland3. Pituitary releases ACTH (Adrenocorticotropic hormone)4. ACTH travels to adrenal cortex and tells it to releaseglucocorticoids5. Glucocorticoids support BP, GI functions, Mental Functions,Help control the immune response mechanisms
What can happen when AA are stopped? acid rebound
What can help balance the side effects? give them together
What if NO improvement in a week withH2 blockers??
increase dose or change to PPI
what if that happens maintenance tx needed (use lower dosethan initial tx)
WHAT is ADH?
ADH = maintain fluid balance, control BP, and cardiac output inyour body. Antidiuretic - holds fluidsDiuretics allow fluids to be lost through the kidneys
Hypothalamus sense if the plasma volume has decreased, if the Nalevel has risen (or the osmolality of the blood) and will send ADHto increase the amount of fluid retained by the kidneys.
what to use if signs/symptoms >2 hoursor occur at bedtime
H2 blockers
What will prevent complete absorption ofSynthroid?
Ca, Fe, Mg, Zinc
what's common when stop taking meds? relapse (80%)
When are H2 blockers given? early evening or after meals
when to take 1 hour after meals
When to take PPI's? 30 min. BEFORE meal
When to take Synthroid? MORNING/same time every day
when to take to avoid interaction w/ othermeds?
1 hour before/2 hours after other meds
which are more powerful (how) PPI (decrease acid to greater extent)
Which formulation has highest acid-neutralizing capacity?
1) gels2) suspensions
Which H2 blocker has lots of SE & druginteractions?
cimetidine (Tagamet)
why are there less SE w/ axid (H2)doesn't start the P450 system (P450=themajor enzymes involved in drugmetabolism and bioactivation, accountingfor about 75% of the total number ofdifferent metabolic reactions.)
Why do you need thyroid med? to replace/substitute diminished or absentthyroid function
why should you try not to use sodiumbicarbonate??
It increases Na = bad for fluid retention &CHF
Zantac (ranitidine) dose? Prototype H2 Blocker....150 mg BID/300mg @ night
Zollinger-Ellison syndrome Gastrin-secreting TUMOR of the non betacells of the endocrine pancreas
