165. A 20yo man complains of recent onset of itching which followed a viral infection.
There are
numerous wheals of all sizes on his skin particularly after he has scratched it. These can last up
to an hour. What is the most probable dx?
a. Uremia b. Urticaria
c. Psychogenic itching d. Atopic eczema
e. Primary biliary cirrhosis Ans. The key is B. Urticaria.
Urticaria Signs: wheals, rapid onset after taking drug ± association with angio-oedema /anaphylaxis. It can result from both immunological and non-immunological mechanisms.
Causes: Drugs:morphine & codeine cause direct mast cell degranulation; penicillins &
cefalosporins trigger IgE responses; NSAIDs; ACEi.
Clinical diagnosis. No investigations required.
Management:
Find the cause and avoid/treat it.
Antihistamines:
Non-sedating H1 antihistamines are the mainstay of treatment
In pregnancy chlorphenamine is often the first choice of antihistamine.
166. A 75yo lady who had mitral valve replacement 13 yrs ago has developed recurrent breathlessness. Her husband has noticed prominent pulsation in her neck. She
complains of
abdominal pain and ankle swelling. What is the most probable dx?
Ans. The key is D. Tricuspid regurgitation. [Points in favour: i) recurrent breathlessness – if the cause is LV dysfunction, ii) prominent pulsation in the neck – giant v waves, iii) abdominal pain – pain in liver on exertion, ankle swelling; These are features of tricuspid regurgitation. Reference:- OHCM, 9th edition, page- 142]
Pulmonary stenosis is mostly congenital. But it can be caused by rheumatic fever and in this case the patient could have developed rheumatic fever given his history of valve replacement. But there is no mention of abdominal pain in pulmonary stenosis so i guess that’s the differentiating point here.
Aortic regurgitation, mitral stenosis and regurgitation donot involve abdominal pain and ankle swelling. And the JVP will not be raised.
Tricuspid regurgitation
Causes: Functional (RV dilatation; eg due to pulmonary hypertension induced by LV failure); rheumatic fever; infective endocarditis (IV drug abuser); carcinoid syndrome;
congenital (eg ASD, AV canal, Ebstein’s anomaly, ie downward displacement of the tricuspid valve— drugs (eg ergot derived dopamine agonists,fenfluramine).
Symptoms: Fatigue; hepatic pain on exertion; ascites; oedema and also dyspnoea and orthopnoea if the cause is LV dysfunction.
Signs: Giant v waves and prominent y descent in JVP, RV heave; pansystolic murmur, heard best at lower sternal edge in inspiration; pulsatile hepatomegaly; jaundice; ascites.
Management: Treat underlying cause. Drugs: diuretics, digoxin, ACE-i. Valve replacement (~10% 30-day mortality).
.
167. A 45yo T1DM had an annual check up. Ophthalmoscopy showed dot and blot hemorrhage + hard exudate and multiple cotton wool spots. What is the next step in management?
a. Reassurance and annual screening only b. Urgent referral to ophthalmologist c. Laser therapy
d. Non-urgent referral to ophthalmologist e. Nothing can be done
Ans. The key is D. Non-urgent referral to ophthalmologist. [It is pre-proliferative retinopathy so non-urgent referral; If proliferative (with neovascularization) urgent referral].
Diabetic retinopathy Blindness is preventable. Annual retinal screening mandatory for all patients not already under ophthalmology care. Pre-symptomatic screening enables laser photocoagulation to be used, aimed to stop production of angiogenic factors from the ischaemic retina. Indications: maculopathy or proliferative retinopathy.
• Background retinopathy: Microaneurysms (dots), haemorrhages (blots) and
hard exudates (lipid deposits). Refer if near the macula, eg for intravitreal triamcinolone.
• Pre-proliferative retinopathy: Cotton-wool spots (eg infarcts), haemorrhages,
venous beading. These are signs of retinal ischaemia. Non urgent Refer to a specialist.
• Proliferative retinopathy: New vessels form. Needs urgent referral.
• Maculopathy: (hard to see in early stages). Suspect if acuity. Prompt laser, intra vitreal steroids or anti-angiogenic agents may be needed in macular oedema.
168. A 2m baby who has ambiguous genitalia presents to the ED with vomiting. Labs:
Na+=125mmol/L, K+=6mmol/L. What is the most likely dx?
a. Fragile X syndrome b. Turners syndrome c. Noonan syndrome
d. Congenital adrenal hyperplasia Q. 1. What is the key?
Q. 2. What are the points in favour?
Ans. 1. The key is D. Congenital adrenal hyperplasia
Ans. 2. Points in favour: i) ambiguous genitalia ii) salt wasting manifested as
hyponatremia and hyperkalemia (In mild forms of salt-wasting adrenal hyperplasia, salt wasting may not become apparent until an illness stresses the child). [here
hyperkalaemia inspite of vomiting is indicating the disease].
Congenital adrenal hyperplasia (From secretion of androgenic hormones deficiency of 21-hydroxylase, 11-hydroxylase, or 3--hydroxysteroid dehydrogenase).
Cortisol is inadequately produced, and the consequent rise in ACTH leads to adrenal hyperplasia and overproduction of androgenic cortisol precursors. CAH is a leading cause of male pseudohermaphroditism.
Signs: Vomiting, dehydration, and ambiguous genitalia. Girls may be masculinized.
Boys may seem normal at birth, but have precocious puberty, or ambiguous genitalia (androgens in 17-hydroxylase deficiency), or incomplete masculinization (hypospadias with cryptorchidism
from 3-hydroxysteroid dehydrogenase). Hyponatraemia and hyperkalaemia are common. Plasma hydroxyprogesterone Increased in 90%; Increased urinary 17-ketosteroids (not in 17-hydroxylase deficit).
Management of adrenocortical crisi: Urgent treatment is needed
0.9% saline IVI (3–5g Na+/day), glucose, fludrocortisone and hydrocortisone in neonate IV stat then maintanance dose.
CAH can lead to addison’s disease later in life due to delayed onset.
169. A 40yo man collapsed at home and died. The GPs report says he suffered from T2DM and
BMI=35. What is the most likely cause of death?
a. Myocardial Infarction
Q. 2. Why the patient’s death was unnoticed?
Ans. 1. The key is A. MI.
Ans. 2. In diabetics MI become painless when the patient develop autonomic neuropathy (till there is no autonomic neuropathy diabetic patients will feel MI pain). In this case the disease was unnoticed as it was a painless attack.
It is one of the complications of Diabetes.
Vascular disease Chief cause of death. MI is 4-fold commoner in DM and is more likely to be ‘silent’. Stroke is twice as common. Women are at high risk.
Address other risk factors—diet, smoking, hypertension. Suggest a statin (eg simvastatin 40mg
nocte) for all, even if no overt IHD, vascular disease or microalbuminuria. Fibrates are useful for triglycerides and reduced HDL. Aspirin 75mg reduces vascular events (if past stroke or MI) and is good as statin co-therapy (safe to use in diabetic retinopathy;
use in primary prevention is disappointing, at least at 100 mg/day.
170. A 38yo pt presented with tingling, numbness, paraesthesia, resp stridor and involuntary spasm of the upper extremities. She has undergone surgery for thyroid carcinoma a week ago. What is the most likely dx?
a. Thyroid storm
b. Hyperparathyroidism
c. Unilateral recurrent laryngeal nerve injury d. External laryngeal nerve injury
e. Hypocalcemia Q. 1. What is the key?
Q. 2. What is the cause of this condition?
Q. 3. Why there is respiratory stridor?
Ans. 1. The key is E. Hypocalcaemia.
Ans. 2. Hypocalcaemia may be due to accidental parathyroid gland removal during thyroidectomy.
Ans. 3. Laryngospasm is a feature in hypocalcaemia which may cause stridor.
Thyroid storm causes thyrotoxicosis (inc heart rate, palpitations, weight loss, tremors, heat intolerance etc) hyperparathyroidism causes hypercalcemia (bone pains, kidney stones, confusion, psychosis), nerve injuries only explain the stridor.
Causes of hypocalcemia:
Treatment
• Mild symptoms: give calcium 5mmol/6h PO, with daily plasma Ca2+ levels.
• In chronic kidney disease:May require alfacalcidol
• Severe symptoms: give 10mL of 10% calcium gluconate (2.25mmol) IV over 30min, and repeat as necessary. If due to respiratory alkalosis, correct the alkalosis
171. A 50yo chronic smoker came to OPD with complaint of chronic productive cough, SOB and
wheeze. Labs: CBC=increase in PCV. CXR >6ribs seen above the diaphragm in midclavicular line. ABG=pO2 decreased. What is the most likely dx?
a. Interstitial lung disease b. Wegener’s granulomatosis c. Ca bronchi
d. COPD e. Amyloidosis
Q. 1. What is the key?
Q. 2. What are the points in favour?
Ans. 1. The key is D. COPD.
Ans. 2. Points in favour: i) Age 50 yrs ii) Chronic smoker iii) Chronic productive cough, SOB and Wheeze iv) Raised PCV secondary to chronic hypoxaemia v) Low set diaphragm and widened horizontal ribs vi) Hypoxaemia on ABG.