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Case Study 500
Faculty of MedicineMUST
2010
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Kidney
Cases
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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
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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
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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
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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
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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
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)
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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
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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
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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)
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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
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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
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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
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Endocrine
Cases
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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)
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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
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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
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-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
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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)
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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.
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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
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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.
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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
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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
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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
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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
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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
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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
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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
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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), ……
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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
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