Case Study 500

Faculty of Medicine
MUST
2010

Kidney
Cases

General Medicine 500

Case Study
1- Kidney Cases
Case 1:
Female Patient 60 Years old, Presented with Severe Arthralgia & Proximal Interphalangeal Joint
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
Urine Protein +1
RBCs: Over 100

a-

Serum Creatinine 6ml/dl

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
Protein
Casts
Colour
RBCs
Acid
Hematuria

Surgical
Hematuria
No
No
Normal
Normal

Focal GN
Yes
Yes
Coca-cola
Dysmorphic

No

yes

2- 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 as
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 of
face, he has previous history of trauma of left leg few weeks before followed by fever & was
diagnosed as osteomyelitis, he was indicated for Antibiotics & Improved.
Urine Examination Shows:
Proteinuria +++
WBCs = 150
RBCs = more than 100
Red Cell Cast ++
Blood Urea = 100 mg/dl
Creatinine = 5 mg/dl
BP = 170/120

a-

What is the expected pathology?

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 Neck
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

a-

What is the expected pathology?

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 Nitrogen
BUN = 80, Serum Creatinine =3.2, She has not seem gone to a physician Since 10 years for
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 the
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 mostly
caused by Asprin i.e. Analgesic Nephropathy

______________________________________________________________________________

Case 7:
A Previous well 46 years old man, was admitted to the ICU with Pulmonary Oedema (Bubbling
Chest) & Acute Myocardial Infarction (Acute Left Ventricular Failure), Was Treated with Lasix &
improved markedly, Tests from Day 1 to Day 10 showed

BUN
Serum
Creatinine
Serum Na
Serum K
Serum Cl
Serum HCO3
Body Weight

Day 1
10

Day 10
100

1.0

4.2

140
4.4
102
26
76 KG

136
3.2
94
32
72 KG

Abnormal
Prerenal Disease
Normal Due to
Diuretics

Due to Diuretics

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 increase in
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. Azotemia?

Ischeamic 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

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 Surgically
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 was
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 Collapsing)
2- Minimal Change Disease
3- Diabetic Nephropathy
4-Membranous Nephropathy (Mainly in solid tumors as Lymphoma & Doesnt Cause
Impaired Kidney Function)

But Perihilar Focal Segmental Glomerulosclerosis is the most common as it occurs in

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 Diuretics
3- Captopril (Vasodilator - antihypertensive) as all blood is shifted to one kidney

Endocrine
Cases

2- Endocrinology Cases
Case 1:
30 years old male patient, single, works in Africa as a zoologist, non-smoker but alcoholic, he
has fever since 5 days with rigors which is more at night, one day before he felt right upper
abdominal discomfort relieves on lying on left side & worsen on drinking, 2 weeks before he
had diarrhea & now he has irritative cough (non-productive cough)
Examination:
Pt. looks ill
Fever 37.8 (low grade fever)
BP 130/80
Pulse 84 B/m Irregular

Palpable Liver
No spleenomegaly
Decrease air entry in right lung base
Tender Rt. Lower costal muscles & Rips

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-phrenic
Angle

a-

What is the Diagnosis?

Infective space occupying lesion most probably Hepatic Amoebic Abscess
Confirmed 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 history
of 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 she
ate her breakfast or had juice. Over the 810 months before presentation, the patient noted
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 was
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/dl.
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. Her
vital signs were significant only for mild hypertension 140/85 (not evident & very acceptable for
her age). Her physical and neurological exams were unremarkable. Her admission lab values
were significant for a glucose level of 36 mg/dl. She was completely asymptomatic upon
presentation and was thus placed on a fasting protocol.

a- What is your diagnosis?

The Most Probable Cause of Spontaneous Hypoglycemic Attacks is Increase
Level of Serum Insulin, Which is most Likely to be Insulinoma of the
Cells 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

mg/dl
70
110
126
Hypoglycemia Normal Fasting Blood Sugar Impaired Glucose Tolerance

200
DM

-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:
Its a peptide that is liberated from the langerhans cells of the pancreas due to
secretion endogenous pro-insulin yielding Insulin + C-peptide, its used as a screening
test for Insulinoma after exclusion of history of oral insulin synthesizers intake.
C-Peptide
Pro-Insulin

Insulin

b- What is the differential diagnosis?

123-

Factitious hypoglycemia
sulfonylurea drugs
The triad of hypoglycemia, high immunoreactive insulin levels, and suppressed plasma Cpeptide immunoreactivity is pathognomonic of exogenous origin. Insulin-induced hypoglycemia
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 endogenous

antibodies with insulin or the insulin receptor

5-

Nesidioblastosis is defined as hyperplasia of the islet cells causing hyperinsulinemic

hypoglycemia

678-

Noninsulinoma pancreatogenic hypoglycemia syndrome (NIPHS)

Familial persistent hyperinsulinemia
Other causes for hypoglycemia include liver disease, endocrine deficiencies,
extrapancreatic insulin-producing tumors (an insulin-secreting small-cell carcinoma of the cervix
recently has been described), and pentamidine-induced hypoglycemia.

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 insulin
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 of
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 80/60
mmHg. Because of her severe orthostatic hypotension, she could not stand up. Physical
examination revealed generalized hyperpigmentation and darkening with prominent gingival
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 range;
0.9-4 ng/ml) AntiGAD antibody was positive at 9 U/ml (normal range;0-1 U/ml) 1ry Type I
Diabetes Mellitus . Serum electrolyte levels were found within normal ranges Excludes Type I
Addisons Disease (Table 1).
The patient baseline cortisol level was low, while the serum ACTH level was high Type II
Addisons Disease (autoimmune) and aldosterone level was within normal ranges Normal Renin
Angiotensin System & Excludes Type 1 Addisons Disease.
Other laboratory investigations disclosed a low serum TSH level, with high free thyroid
hormone serum values. Thyroid Autoimmune Disease

NB: 1ry Addisons Disease: Due to Pansuprarenal Cortical Destruction (ex. Inflammation) leading to impaired
secretion of Aldosteron from Zona Glomerulosa & Glucocorticoids from Fasiculata.

2ry Addisons Disease: secondary to low ACTH low Glucocorticoids Normal Aldosteron

a- What is your diagnosis?

The Probable Causes of the previous signs are
1- Schmidts 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 Addisons Disease
c- Autoimmune Thyroid Disease (Thyroiditis Graves Disease)
d- Perinicous Anemia
e- Vitiligo
f- 1ry Hypogonadism
g- Myasthenia Gravis
h- Celiac Disease
2- Typical Presentation of 2ry Addisons Disease
a- Orthostatic Hypotension
Hypotension
Hypoglycemia
b- Hypoglycemia
Addisons
c- Areas of Hyperpigmentations
d- Low level of Serum Glucocorticoids
Disease
e- Normal level of Serum Aldosteron
f- History of Pregnancy
Hyperpigmentation
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, Chronic
7- 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:

1234-

16171819-

Loss
Loss
Loss
Loss

of
of
of
of

GH
LH-FSH
TSH
ACTH

WDHA Syndrome
Renal Failure Normal Urea Level
Type I Addisons Disease + Graves Disease
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-

2-

Laboratorial Studies:
a- CBC Anemia
b- TSH
c- ACTH Elevated - Differentiates Type I from Type II Addisons Disease
d- Serum Urea Renal Failure
Imaging
a- CT scan of the adrenal glands to exclude hemorrhage and fungal infections as
the cause of primary adrenal insufficiency

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

causes) is a possibility (rare)

c- thyroid imaging (uptake and/or scan) only in patients who are hyperthyroid;
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 diet.
b- If the patient is overweight, institute an 1800-calorie diabetic diet, preferably with low salt,
low cholesterol, and low saturated fat.
c- If Addison's disease is present, institute a high-sodium, low-potassium diet until electrolytes
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 their
life, depending on the severity of the presentation.
b- In type 1 diabetes mellitus, muscular exertion reduces the requirement for insulin, and either
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, Short
4th, 5th Metacarpal Bones

a- What is the differential diagnosis?

1- Pseudo Hypoparathyroidism

(low Ca, High P)

Its an Autosomal Dominant Disease with normal PTH & PTH receptors but the lesion is in
post receptor, With Short Stature, Calcifications of Basal Ganglia, Rounded Face (not Moon
Face) Short Metacarpals & Metatarsals

2- Pseudo-pseudo Hypoparathyroidism
Only Short Stature & 4
Hypoparathyroidism

th

3- Turner Syndrome

th

(normal Ca, P)

Short Metacarpals, Its a phenotype from Pseudo

(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 severe
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- Accochaurs Hand
c- Positive Signs:
1- +ve Trousseau Provocation Test
2- +ve Chvostek Sugn
3- +ve Erbs 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 the
past 3 months she has lost 8 kg, without changing her diet or activity, otherwise
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)
3- Tachycardia

2- Loss of Weight Inspite of Good Appetite

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 Analysis
3- 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 vascularity
of the gland. Inconvenient Dose Up to 3 Times/ Day
2- Carbimazole: used if the pt. has retrosternal extension
Starting 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
decision

b- Radioactive Iodine: absolutely forbidden in young female patients

2- Surgery: Subtotal Thyroidectomy + Replacement Therapy
GMED 501 Thyroid (Goiter)

Case 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 hospital 6
weeks ago where he was admitted after a car accident & spleenectomy was done,
Since that time he is on antidepressant as his fiance died in this accident his
past history showed an orthopedic operation 3 years ago
On Examination:
Jaundice
Cervical Lymphadenopathy
Chest (NAD) No Abnormality Detected
Heart (free)

Abdomen:
Scar of previous operation
Palpaple Tender Liver

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:

2-

Hepatitis A: IgG, IgM

Hepatitis B: Surface Antigen
Hepatitis C: Hepatitis C Antibodies
Cytomegalovirus

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

Case 8:
44 Years old male, lorry driver, smoker, has hypertension, treated by Nifedipine
(Adalat R) (Calcium Channel Blocker - Antihypertensive) 20 mg/twice/day, he complains of
muscle weakness, polyuria, muscle cramps, his past history is negative and no
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)
3
WBCs: 4000 / mm
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 6)
Urine: Normal
ECG: Sinus, Flat T-Wave

a- What is Your diagnosis?

Primary Hyperaldosteronism (Conns 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 (Conns 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

Case 9:
21 years old man is brought to the hospital at 5pm, he was found unconscious at
home in his flat by his girl friend she had last seen him at 8 pm in the evening
before they came home after Christmas shopping, when she came around next
afternoon she found him unconscious on the floor of the bathroom, there was no
signs of any trauma or any drugs, theres a family history of diabetes mellitus he
had been well previously with no medical history of diabetes, his girlfriend had
said that he had shown no signs of unusual mood on the previous day, he was
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