General Medicine 500 Case Study

7/28/2019 General Medicine 500 Case Study

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Case Study 500

Faculty of MedicineMUST

2010



Kidney

Cases



General Medicine 500

Case Study

1- Kidney Cases

Case 1:Female Patient 60 Years old, Presented with Severe Arthralgia & Proximal Interphalangeal

deformity, Urine Tests:

Proteinuria = 4 gm/dl

WBCs = 10-20

Red Cell Cast

a-

What is the expected pathology?Mixed (Nephritic + Nephrotic)

b- What is the Diffrential Diagnosis?Drug Induced Nephritis

Minimal Change Disease

Interstitial Nephropathy

_______________________________________________________________

Case 2:Male Patient 45 years old, Presented with Recurrent gross Hematuria with Influanza-like

Symptoms

BP was 130/80 Temprature 36.5

Normal Kidney function BUN 10 ml/dl Serum Creatinine 6ml/dl

Urine Protein +1 RBCs: Over 100

a- What is the expected pathology? Protein = Glomerular Disease

Age = 45 y

Influanza-like Symptoms = IgA Nephritic

Normal BP + Kidney Function = Focal Nephritis

Focal Proliferative Glomerulonephritis

b- What is the Final Diagnisis?

Messangio-proliferative Glomerulonephritis

Lesion is in Messengial Cells



c- What are other Investigations Required?

1- Macroscopic & Microscopic Examination of Urine to Exclude Surgical hematuria

SurgicalHematuria

Focal GN

Protein No Yes

Casts No Yes

Colour Normal Coca-colaRBCs Normal Dysmorphic

Acid

Hematuria No yes2- Ultrasound: Kidney Size (If Polycystic kidney is the cause)

3- Renal Biopsy

4- Serum IgA

d- What is the Possible Cause?

1- Age Category: Predisposing factor common in this Age

2- Influanza – like Symptoms: IgA

_________________________________________________________________________

Case 3:10 Years old Female, Presented with Acute onset Generalized Oedema of 10 days duration

BP 120/70

Urine Examination:

-Heavy Proteinuria 6 gm/24 hrs

-Benign Urine No sediment

-Blood Urea 20 mg

-Serum Creatinine .9 mg/dl

a- What is the expected pathology?

Young Age – Acute Onset – Heavy Proteinuria

Minimal Change Disease

b- What are other Investigations Required?

1- Protein Type (Selective or Non-Selective)

2- Renal Biopsy if the Case is Resistant to Corticosteroid Therapy

c- What is the Treatment You Advice?

Cyclosporine (Corticosteroid) 60mg (12tab 5mg) for 4 weeks followed by 40mg a

single morning dose on alternate days for 4 more weeks



Case 4:15 years old male, Presented with headache & oedema of the lower limbs & mild buffnes o

face, he has previous history of trauma of left leg few weeks before – followed by fever &

diagnosed as osteomyelitis, he was indicated for Antibiotics & Improved.

Urine Examination Shows:

Proteinuria +++

WBCs = 150

RBCs = more than 100Red Cell Cast ++

Blood Urea = 100 mg/dl

Creatinine = 5 mg/dl

BP = 170/120


Diffuse Proliferative Glomerulonephritis

b- What is the Possible Cause?

Membreno-Proliferative Glomerulonephritis Type I

(Only Type Caused by Osteomyelitis)

c- What is the Differential Diagnosis?

Lupus Nephritis Class IV (mixed)

_______________________________________________________________

Case 5:50 Years old male Patient, Presented With Repeated Vomiting, Anorexia, Nausea, Loss of

Weight & Asthenia (Easy Fatigability). He Has Past History of Diabetes 10 years &

Hypertension for last 3 years. By Examination there was Pallor, Healthy look, Congested N

Veins, mild oedema, BP 160/110. Investigations Showed:

a- Urine:

- Protein 1+

- WBCs = 3-5

- RBCs = 1-3

- Broad Casts ++

- Blood Urea = 200

- Serum Creatinine = 7 mg

- Serum Potassium = 7 ml eq

- Serum Uric Acid = 8 mg/dl

b- Abdominal Soar Showed Reduction of Kidney Size& loss of Delirium between cortex &

medulla & increased Echogenicity Grade III




Increased Echogenicity + Loss of Differentiation between Coterx & Medulla

Broad Casts Due to Broad Tubules

Chronic Interstitial Fibrosis

b- What is the Cause of GIT Upset?

Because of Uremia (the Patient is Uremic)

c- What is the possible Cause of Uremia?

Diabetes Mellitus

d- Why did the Hypertension appear after a long onset of

diabetes?Because Hypertension After a Long onset of Diabetes is a Character of a Renal

Disease

_________________________________________________________________________

Case 6:

During Evaluation for Hypertension, 50 Years old Woman found to had Blood Urea Nitroge

BUN = 80, Serum Creatinine =3.2, She has not seem gone to a physician Since 10 years

peptic ulcer, she has no history of renal disease, only had a Chronic Headache, Except for

Hypertension Everything is normal, Laboratorial Evaluation Revealed:

- Hemoglobin = 9.7 gm/dl Anemia

- Serum Na = 1.37 ml eq/lit (normal 1.34-1.45)- Serum K = 5.7 ml eq/lit (normal 3.5 – 5)

- Serum Cl = 114 (normal 96 - 106)

- Serum Hco3 = 14 (normal 23 – 30) Acidosis

Urine Examination Revealed:

- Protein +1 /24hrs = 1.0 gm/dl Parynchemal Disease (Glomerular – Interstitial – Nephrotic)

- RBCs = 3-5

- WBCs = 8-10

- No Casts No Glomerular Hypertrophy

- Creatinine Clearance = 20 ml/min Renal Failure

a- Does the Patient Has Acute or Chronic Renal Failure?

Chronic Renal Failure (End-Stage Renal Disease) & The Evidence is th

Anemia

b- What are other Investigations Required for Diagnosis?1-Creatinine / BUN Ration (normal 1/8) Denotes Preranal Elemant

2-Ultrasound to detect Kidney Size 7-8 cm (normal 11cm)



c- Which Type of Parynchemal Disease?

Glomerular or Interstitial, But Mainly Interstitial Due to History of Peptic Ulcer mo

caused by Asprin i.e. Analgesic Nephropathy

_________________________________________________________________________

Case 7:A Previous well 46 years old man, was admitted to the ICU with Pulmonary Oedema (Bubb

Chest) & Acute Myocardial Infarction (Acute Left Ventricular Failure), Was Treated with Lasix &

improved markedly, Tests from Day 1 to Day 10 showed

Abnormal

Prerenal Di

Normal Due

Diuretics

Due to Diure

Notes: 1- Difference Between Chronic Heart Failure & Acute Heart Failure

COP = SV (decrease in both) X HR (Increase in both to compensate)

BP = COP (decrease in both) X PR (Increase in Chronic)

(Increase in Acute but needs time which

means sudden drop of BP i.e. Shock)

2-Renal Failure Index: due to failure of kidney to excrete Creatinine so it will increas

blood causing failure to reabsorb sodium

3- Acute Renal Failure may be:

a- Ischeamic: with normal Osmolarity of Urine

b- Acute Tubular Necrosis: with low Osmolarity of urine due to failure of

concentration

a- What is the possible Diagnosis to Explain Pt. AzotemiaIscheamic Nephropathy Due to Sudden Drop of BP

b- What are Other Tests to Confirm?

Urine Creatinine (normal)

Urine Sodium (decrease in Ischemia)

c- What is the cause of Na – K reduction?

Due to excessive amounts of diuretics

Day 1 Day 10

BUN 10 100Serum

Creatinine1.0 4.2

Serum Na 140 136Serum K 4.4 3.2

Serum Cl 102 94Serum HCO3 26 32

Body Weight 76 KG 72 KG



Case 8:57 years old male, presented with increased oedema, urine analysis revealed ++++

Proteinuria (about 5.5 gm), but urine was otherwise normal, serum Creatinine was 2.8 mg

serum albumen was 3 gm, 20 years ago he has undergone left nephrectomy History of Surg

Curable Nephrotic Syndrome, 10 years ago he refused for insurance because of Proteinuria,

physical examination showed BP 150/90 & massive oedema, a large right thyroid nodule w

palpated during examination Mainly Malignant Metastasized to Kidney causing renal tumor formation

a- What is the Differential Diagnosis?

1- Focal Segmental Glomerulosclerosis (Perihilar – Glomerular tip – Collap

2- Minimal Change Disease

3- Diabetic Nephropathy

4-Membranous Nephropathy (Mainly in solid tumors as Lymphoma & Doesn’t

Impaired Kidney Function)

ut Perihilar Focal Segmental Glomerulosclerosis is the most common as it occu

case of glomerular overwork or ablation of one kidney

b- Should Renal Biopsy be Performed?

No, Because he has only 1 kidney for fear of Hemorrhage

c- What is the Treatment?

1- After Confirmation of Malignant Nodule (total Thyoridectomy)

2- Treatment of Nephrotic Syndrome by Diuretics3- Captopril (Vasodilator - antihypertensive) as all blood is shifted to one kidn



Endocrine

Cases



2- Endocrinology CasesCase 1:30 years old male patient, single, works in Africa as a zoologist, non-smoker but alcoholic

has fever since 5 days with rigors which is more at night, one day before he felt right upp

abdominal discomfort relieves on lying on left side & worsen on drinking, 2 weeks before h

had diarrhea & now he has irritative cough (non-productive cough)

Examination:

Pt. looks ill Palpable Liver

Fever 37.8 (low grade fever) No spleenomegaly

BP 130/80 Decrease air entry in right lung ba

Pulse 84 B/m Irregular Tender Rt. Lower costal muscles &

Investigations:

WBCs 16000/mm3 normal 4500 – 10000 per dl

Hb 11 gm% normal in males 13.5 – 15.5 gm/dl ESR 30 mm normal 0-15 mm in males 0-20 mm in females

FBS 90 mg% normal 70mg%

ALT 60 U/L normal 0-35 U/L but elevated 10 – 100 folds in Acute Viral Hepatitis

AST 52 U/L normal 0-35 U/L

Serum Alkaline Phosphatase 230 U/L normal 41 – 133 U/L

Chest X-Ray: Elevated Right Copula of the Diaphragm with obliteration of the Chondro-ph

Angle

a- What is the Diagnosis?

Infective space occupying lesion most probably Hepatic Amoebic AbsceConfirmed by Typical Presentation :

1- Right Hypochondrial Pain

2- Pleural Effusion due to venous pressure of Liver over Rt. Lung

3- Cough (Anshaugi Sauce-like Content of Abcess)

4- May open into Pericardium causing Pericardial Effusion (cause of death)

5- Rupture into Peritonium

6- Elevated Alkaline Phosphatase Because of Space Occupying lesion

b- Other Possible Causes?1- Ulcerative Colitis

2- Bacillary Dysentery

3- Viral Hepatitis

c- Further Investigations Required?1- Stools Analysis (Showing Cysts & Trophozoites)

2- Naked Eye Appearance of Stools (Bloody Stools)



3- Ultrasonography (Cheapest to detect lesion)

4- Sigmoidoscopy (to exclude other causes)

d- Treatment Required?Trophozoites: Metronidazole 750 mg for 1 day

Tenectazole 10 mg for 3 days

Amibazole 1000 mg – 2 tabs – single dose

Cyst: Diloxanidaformate

Aspiration: by Ultrasound guided Needle

_______________________________________________________________

Case 2:

75-year-old white woman who presented to her primary care physician with a 10-year hisof episodic confusion and somnolence . The episodes occurred about twice a year,

typically in the morning, just after waking. They lasted minutes and were relieved when s

ate her breakfast or had juice. Over the 8–10 months before presentation, the patient no

that the episodes were increasing in frequency as well as occurring throughout the day.

When she presented to her primary care doctor with the above complaints, the patient wa

reassured. As she was waiting for check-out, she developed confusion, a capillary blood

glucose test was performed, and she was noted to have a plasma glucose level of 28 mg/

She was given juice and her symptoms resolved after a few moments.

The patient was subsequently admitted to the hospital for further work up.

On exam, the patient was found to be a well-nourished woman in no apparent distress.

vital signs were significant only for mild hypertension 140/85 (not evident & very acceptable

her age). Her physical and neurological exams were unremarkable. Her admission lab va

were significant for a glucose level of 36 mg/dl. She was completely asymptomatic upo

presentation and was thus placed on a fasting protocol.

a- What is your diagnosis? The Most Probable Cause of Spontaneous Hypoglycemic Attacks is Incr

Level of Serum Insulin, Which is most Likely to be Insulinoma of theCells of the Pancreas

Confirmed by:

1- Age of the Patient

2- No History of Exogenous Insulin Intake

3- No History of Change in Dietary Habits

4- Low Serum Glucose



-Variant Glucose Levels

-Probable Causes of Hypoglycemia in this case:

1- Change of Dietary Habits

2- Decreased Glycogenolysis from Liver (defective glucose output)

3- Increase Level of Serum Insulin Due to:a- Exogenous Intake of Insulin (low C-Peptide)

b- Endogenous (elevated level of C-peptide)

- Oral Insulin Synthesizers as (as Meteglenides, Sulphonyluria)

- Insulin Secreting Tumors (as Insulinoma)

-What is C-peptide:It’s a peptide that is liberated from the β langerhans cells of the pancreas due to

secretion endogenous pro-insulin yielding Insulin + C-peptide, it’s used as a scree

test for Insulinoma after exclusion of history of oral insulin synthesizers intake.

b- What is the differential diagnosis?1- Factitious hypoglycemia

2- sulfonylurea drugs

3- The triad of hypoglycemia, high immunoreactive insulin levels, and suppressed plasma C

peptide immunoreactivity is pathognomonic of exogenous origin. Insulin-induced hypoglyce

can be detected by a ratio of insulin to C-peptide that is greater than 1.0

4- Autoimmune hypoglycemia is a rare disorder caused by the interaction of endogen

antibodies with insulin or the insulin receptor

5-

Nesidioblastosis is defined as hyperplasia of the islet cells causing hyperinsulinemichypoglycemia

6- Noninsulinoma pancreatogenic hypoglycemia syndrome (NIPHS)

7- Familial persistent hyperinsulinemia

8- Other causes for hypoglycemia include liver disease, endocrine deficiencies,

extrapancreatic insulin-producing tumors (an insulin-secreting small-cell carcinoma of the c

recently has been described), and pentamidine-induced hypoglycemia.

70 110 126 200mg

Hypoglycemia Normal Fasting Blood Sugar Impaired Glucose Tolerance DM

Pro-Insulin

C-Peptide

Insulin

http://emedicine.medscape.com/article/122122-overview




c- Give other investigations to be done to this patient?Fasting Blood Sugar + Serum C-peptide level

d- How would you treat this case?1- Medical:

- Diazoxide 3-8 mg/kg/d PO: Potassium channel activator – Vasodilator – Decrease insu

secretion

- Octreotide 200-300 mcg/d IV/SC: octapeptide that mimics natural somatostatin

pharmacologically potent inhibitor of growth hormone

2- Surgical: Whipple operation (pancreatectomy)

_________________________________________________________________________

Case 3:21 year old woman presented with weakness, fatigue, and widespread hyperpigmentation

the skin and oral mucosa (due to ACTH stimulation of melanocytic activity – MSH like Activity), two

months following delivery of her first child. She had no symptoms of nausea, vomiting or

diarrhea. She had a three-year history of type 1 diabetes mellitus and had been taking

mixtard insulin (Short acting + Intermediate Acting) twice daily. She complained of hypoglycemic attacks especially in the mornings. On admission, the

patient vital signs included a heart rate of 105 beats/min, and a blood pressure of 80/6

mmHg. Because of her severe orthostatic hypotension, she could not stand up. Physica

examination revealed generalized hyperpigmentation and darkening with prominent gin

and buccal mucosa

The thyroid gland was not palpable. Excluding Elevated level of TSH

Her HbA1c was 9% (normal is up to 9%) and fasting C peptide <0.5 ng/ml (normal ran

0.9-4 ng/ml) AntiGAD antibody was positive at 9 U/ml (normal range;0-1 U/ml) 1ry Type

Diabetes Mellitus . Serum electrolyte levels were found within normal ranges Excludes Type I

Addison’s Disease (Table 1).

The patient baseline cortisol level was low, while the serum ACTH level was high Type II

Addison’s Disease (autoimmune) and aldosterone level was within normal ranges Normal Renin

Angiotensin System & Excludes Type 1 Addison’s Disease.

Other laboratory investigations disclosed a low serum TSH level, with high free thyroid

hormone serum values. Thyroid Autoimmune Disease

B: 1ry Addison’s Disease: Due to Pansuprarenal Cortical Destruction (ex. Inflammation) leading to impaired

secretion of Aldosteron from Zona Glomerulosa & Glucocorticoids from Fasiculata.

http://en.wikipedia.org/wiki/Potassium_channel

http://en.wikipedia.org/wiki/Peptide

http://en.wikipedia.org/wiki/Somatostatin

http://en.wikipedia.org/wiki/Growth_hormone

http://en.wikipedia.org/wiki/Growth_hormone

http://en.wikipedia.org/wiki/Somatostatin

http://en.wikipedia.org/wiki/Peptide

http://en.wikipedia.org/wiki/Potassium_channel



2ry Addison’s Disease: secondary to low ACTH – low Glucocorticoids – Normal Aldosteron

a- What is your diagnosis?The Probable Causes of the previous signs are

1- Schmidt’s Syndrome (Polyglandular Deficiency Syndrome

Type I, II) Most Probable Diagnosis

2- Thyroidectomy

3- Infiltration by Amyloidosis (rare)

Confirmed by:

1- Typical Clinical Picture:

a- Type 1 DM

b- Type 2 Addison’s Disease

c- Autoimmune Thyroid Disease (Thyroiditis – Grave’s Disease)

d- Perinicous Anemia

e- Vitiligo

f- 1ry Hypogonadism

g- Myasthenia Gravis

h- Celiac Disease

2- Typical Presentation of 2ry Addison’s Disease

a- Orthostatic Hypotension

b- Hypoglycemia

c- Areas of Hyperpigmentations

d- Low level of Serum Glucocorticoids

e- Normal level of Serum Aldosteron

f- History of Pregnancy

g- Progressive weakness, fatigue, poor appetite, and weight loss

h- Syncopes

i- Myalgias and flaccid muscle paralysis may occur due to hyperkalemia

j- Muscle and joint pains

k- No History of GIT Troubles Excludes low Levels of Aldosteron

b- What is the differential diagnosis?1- Adrenal Crisis

2- Hypothyroidism

3- Celiac Sprue

4- Macrocytosis

5- Diabetes Mellitus, Type 1

6- Pancreatitis, Chronic7- DiGeorge Syndrome

8- Pernicious Anemia

9- Hemochromatosis

10- Polyglandular Autoimmune Syndrome, Type I

11- Hypoglycemia

12- Polyglandular Autoimmune Syndrome, Type III

13- Hyponatremia

14- Septic Shock

15- Panhypopituitarism (ex. Sheehan Syndrome) Charactaristic sequence of loss of function:

Addison’s

Disease

Hypoglycemia Hypot

Hyperpigmentation


































1- Loss of GH 2- Loss of LH-FSH 3- Loss of TSH 4- Loss of ACTH

16- WDHA Syndrome

17- Renal Failure Normal Urea Level

18- Type I Addison’s Disease + Grave’s Disease

19- TB of Suprarenal Gland

-What is ICA-GAD: Antibodies Attacking Insulin Secreting Cells in 1ry Type I

Autoimmune Diabetes Mellitus

c- Give other investigations to be done to this patient?1- Laboratorial Studies:

a- CBC Anemia

b- TSH

c- ACTH Elevated - Differentiates Type I from Type II Addison’s Disease d- Serum Urea Renal Failure

2- Imaging

a- CT scan of the adrenal glands to exclude hemorrhage and fungal infections

the cause of primary adrenal insufficiency

b- MRI of the pituitary if hypopituitarism (autoimmune hypophysitis vs oth

causes) is a possibility (rare)

c- thyroid imaging (uptake and/or scan) only in patients who are hyperthy

in Graves disease, it shows uniform distribution and high uptake

d- How would you treat this case?

1- Medications:a- Hydrocortisone: 20-240 mg PO

b- Levothyroxin: 12-25 mcg PO (Thyroid Hormone)

c- Propylthiouracil: 50-150 mg PO (Antithyroid Agent)

d- Methimazole: 5-15 mg PO (Antithyroid Agent)

e- Insulin: Titrate dose to maintain a premeal and bedtime glucose of 80-140 mg/dL f- Fludrocortisone: 0.1-0.2 mg qd PO

g- Vitamin B12 (Cyanocobalamine): 1 mg/mo IM – Nasal Spray

2- Diet:a- If the patient is diabetic and underweight, institute a 2000-calorie (minimum) diabetic d b- If the patient is overweight, institute an 1800-calorie diabetic diet, preferably with low s

low cholesterol, and low saturated fat.c- If Addison's disease is present, institute a high-sodium, low-potassium diet until electro

are controlled with mineralocorticoid therapy.d- If the patient has celiac disease, consult a dietician for a gluten-free diet.





3- Activity:a- Patients with polyglandular autoimmune syndrome type II can participate in all of their

regular activities. However, inform patients that their disease could unpredictably alter life, depending on the severity of the presentation.

b- In type 1 diabetes mellitus, muscular exertion reduces the requirement for insulin, and a snack must be provided or less insulin taken before the exercise. Where possible,consistency of diet and exercise will make control more consistent.

4- Consultation: Endocrinologist – Hematologist - Gastroenterologist

_______________________________________________________

Case 4:Female Patient, 15 Years old, presented with Short Stature, Rounded Face, Big Skull, Sho4th, 5th Metacarpal Bones

a- What is the differential diagnosis?1- Pseudo Hypoparathyroidism (low Ca, High P)

It’s an Autosomal Dominant Disease with normal PTH & PTH receptors but the lesion is

post receptor, With Short Stature, Calcifications of Basal Ganglia, Rounded Face (not Mo

Face) Short Metacarpals & Metatarsals 2- Pseudo-pseudo Hypoparathyroidism (normal Ca, P)

Only Short Stature & 4th 5th Short Metacarpals, It’s a phenotype from Pseudo

Hypoparathyroidism 3- Turner Syndrome (Short neck, Short Stature, Amenorrhea, Coactation of Aorta,

Gonadal Streaks, Breast Atrophy) 4- Familial – Racial

5- Cretinism

6- Precocius Puberty

7- Adrenogenital Syndrome

8- Acondroplasia (non-Proportional Dwarfism)

9- Pituitary Dwarfism (Proportional Dwarfism – Baby face)

10- Poverty

b- Give other investigations to be done to this patient?

Serum Calcium & Phosphorus



Case 5:Female Patient, 14 Years old, presented with coma, +ve history of convulsions after sever

stress, kussmaul respiration, carpopedal spasm

a- What is your diagnosis?Hypocalcemia (Tetany)

Confirmed by:

1- Kussmaul Respiration (Air Hunger) lead to Respiratory Alkalosis

2- Alkalosis Lead to Hypocalcemic Tetany

3- Typical Presentation of Tetany:

a- Carpopedal Spasm

b- Accochaur’s Hand

c- Positive Signs:

1- +ve Trousseau Provocation Test

2- +ve Chvostek Sugn

3- +ve Erb’s Test

b- Give other investigations to be done to this patient?Serum Calcium

_______________________________________________________________________

Case 6:37 Years old Female, healthy, complains of unintentional weight loss, over th

past 3 months she has lost 8 kg, without changing her diet or activity, other

she feels great, she has an excellent appetite, no GIT complains except for

occasionally loose stools, no fatigue no heat or cold intolerance

On Examination:

Pulse:108 Bpm – Regular (Tachycardia)

BP: 140/80 mmhg

Afebrile – Stairy Look (Thyrotoxic Look)

Fullness in Neck (Goiter)

Ejection Systolic Murmer at Apex

No Tremors

DD of Loss of Weight:

1- With loss of Appetite: Malignancy, TB, Depression, Auto immune Diseases

2- Without loss of Appetite: DM, Thyrotoxicosis, Parasitic Infestation, Depression, Malabsorption Syndrome

a- What is the most likely diagnosis?Thyrotoxicosis

Confirmed By:

1- Female (ratio 3:1) 2- Loss of Weight Inspite of Good Appetite

3- Tachycardia 4- Stairy Look 5- Fullness of Neck



Factors against the diagnosis:

No other manifestations of thyrotoxicosis as tremors, water hammer pulse, …….

Differential Diagnosis:

1- Diabetes Mellitus

a- Factors With: loss of weight + increased appetite

b- Factors against: no family history of DM, No other manifestations of DM

2- Parasitic infestation

b- How Would You Confirm?1- Thyroid Profile: to Confirm Thyroid

a- Free T3, T4, TSH

b- Neck Ultrasound

c- Technetium Scan

2- To Exclude Parasitic Infections

a- CBC

b- Stool Analysis

c- Urine Analysis3- Routine Investigations

a- Blood Sugar

b- Blood Chemistry

c- ECG

c- What are the options of treatment?

1- Medical:a- Drugs:

1- Propylthiouracil: used if the pt. has no retrosternal extension

because propylthiouracil increase the vascular

of the gland. Inconvenient Dose Up to 3 Times/ Day

2- Carbimazole: used if the pt. has retrosternal extensionStarting Dose: 45 mg/day (tab=5mg)

Maintenance Dose: 5-15 mg/day for 1.5 – 2 years duration

NB: Another Medical Try for should be given in case of recurrence for 2 years duration before making surgical

cision

b- Radioactive Iodine: absolutely forbidden in young female patients

2- Surgery: Subtotal Thyroidectomy + Replacement Therapy

Thyroid (GoGMED 501



ase 7:A young 28 years old male complains of nausea & feel unwell with nocturnal

sweats and weight loss since one week, he had been discharged from hospita

weeks ago where he was admitted after a car accident & spleenectomy was d

Since that time he is on antidepressant as his fiancée died in this accident his

past history showed an orthopedic operation 3 years ago

On Examination:

Jaundice Abdomen:

Cervical Lymphadenopathy Scar of previous operati

Chest (NAD) No Abnormality Detected Palpaple Tender Liver

Heart (free)

a- Suggest 3 possible causes for his jaundice?1- Blood borne Hepatitis:

Factors With: nausea, vomiting, enlarged tender liver, history of operation

Factors Against: Wieght loss, nocturnal sweat, no fever, large lymph nodes

2- Hodgkin Lymphoma:Factors With: Age, Loss of wight

Factors Against: Jaundice (except in cases of lymph nodes compression of porta hepatis)

3- Drug Induced Nephritis: (TCA) Most Likely Diagnosis

Factors With: Drug History of Tricyclic Antidepressants

b- Mention 4 most useful investigations.1- For Hepatitis:

Hepatitis Markers: Hepatitis A: IgG, IgM

Hepatitis B: Surface Antigen

Hepatitis C: Hepatitis C Antibodies

Cytomegalovirus

2- For Hodgkin Lymphoma:Lymph node or Liver Biopsy

3- Other Investigations

a- Paul-Bunnel Test for Infectious Mononucleosis

b- Bone marrow Biopsy for Leukemia

c- Serum Level of TCA



ase 8:44 Years old male, lorry driver, smoker, has hypertension, treated by Nifedip

(Adalat R) (Calcium Channel Blocker - Antihypertensive) 20 mg/twice/day, he complains o

muscle weakness, polyuria, muscle cramps, his past history is negative and n

family history of similar condition

On Examination:Pulse: 84 Bpm

BP: 170/96 mmhg (Hypertension)

JVP: Normal

Heart & Chest: Normal (In Case of Normal Systems, You Should Exclude Them From DD)

Fundus: Silver Wire Appearance (Long Standing Hypertension)

Investigations:

Hemoglobin: 13.4 gm/dl Na: 147 mmol/L (n=135-145)WBCs: 4000 / mm3 K: 2.2 mmol/L (n=3.5-5)

CHO3: 32 mmol/L (n=18-23) Urea: 3.9 mmol/L (1.2-7)

S.Creatinine: 84 mmol/L (n=up to 120) Glucose: 5.6 mmol/L (n= up to

Urine: Normal ECG: Sinus, Flat T-Wave

a- What is Your diagnosis?Primary Hyperaldosteronism (Conn’s Disease)

Confirmed By:

1- Hypokalemia

2- Muscle Weakness

3- Flat T-wave ECG

4- Hypertension

5- Fundus Vascular Changes

6- Alkalosis & Hypernatremia

Differential Diagnosis:

Famillial Periodic Paralysis:

Factors With: Sudden Paralysis, Hypo or Hyperkalemia Treated with IV Potassium

Causes of Hypokalemia:

1- Without Hypertension:

a- Diarrhea: Hypokalemia + Alkalosis

2- With Hypertension:

a- Thiaside Diuretics: Hypokalemia, muscle weakness + cramps

b- Primary Hyperaldosteronism (Conn’s Disease)

c- Secondary Hyperaldosteronism (Renovascular Disease)

d- Renal Tubular Acidosis (rare congenital condition)

e- Renal Artery Stenosis



b- What are Investigations needed + Treatment?1- Investigations:

a- Serum Levels of Aldosteron + Renin Levels

b- CT or MRI Abdomen

2- Treatment:

a- Medical:1- Urgent Potassium IV 20meq + 50cm3 Saline (Slow IV Drip)

2- Aldactone (Aldosteron Antagonist)

b- Surgical: Surgical Removal of Adenoma

ase 9:21 years old man is brought to the hospital at 5pm, he was found unconsciou

home in his flat by his girl friend she had last seen him at 8 pm in the evenin

before they came home after Christmas shopping, when she came around ne

afternoon she found him unconscious on the floor of the bathroom, there was

signs of any trauma or any drugs, there’s a family history of diabetes mellitu

had been well previously with no medical history of diabetes, his girlfriend ha

said that he had shown no signs of unusual mood on the previous day, he wa

anxious because he has midterm exams after 2 days

On Examination:

Pale

Pulse: 92 Bpm

BP: 114/74 mmhg

Respiratory Rate: 22/min

Normal CVS & RS

No response to verbal commands, Reflexes are Brisk (exaggerated) &

symmetrical, Planter Reflex if Flexor (-ve Babinski Sign - No Pyramidal Lesion) Fundus: Papillloedema (Increased ICT)

a- What is the most likely Diagnosis & immediate

Investigations needed?Causes of Coma:

1- Metabolic: DM, RF, ……

2- Neurological: Stroke, Infarction, sub arachnoid hemorrhage, ……

3- Drugs: Hypnotics, Paracetamol (Acetaminophen), ……



1- Metabolic:

a- Diabetic Ketoacidosis:Factors With: Family History, Pallor, Coma, Increased RR.

Factors Against: Brisky Reflexes, Tachycardia

b- Insulinoma:Factors With: Family History of DM, Hypoglycemia

Factors Against: Age

2- Neurological:

a- Subarachnoid Hemorrhage:Factors With: Sudden Onset Symptoms, Papilledema

Factors Against: -ve Babinski sign, No Pinpoint Pupil, No Neck Stiffness

b- Carbon Monoxide Poisoning: Most Likely Diagnosis Factors With: Bathroom, Tachycardia, Pallor, Papilledema, no Trauma, no Drugs

Factors Against: No Cherry Bright Red Coloration of the body

3- Drugs: Hyponitics, Sedatives, Paracetamol ….. No history of drug intake

Investigations Needed:

1- Metabolic Causes:

a- Blood Glucose

b- Insulin Level

2- Neurologic Causes:

a- Carboxy Hemoglobin level (ABG)

b- CT Scan Brain

3- Drug Causes:

a- Drug Monitoring

b- Liver Enzymes

Treatment:

1- Oxygen Mask for 2 Days

2- ABCs Resuscitation

Date post:	03-Apr-2018
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General Medicine 500 Case Study

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