Practice of Medicine - homeopathy360
MCQ'S

Practice of Medicine

Q1. Wernicke’s encephalopathy is due to deficiency of (Bihar/Homoeo/MO/QP/2014):
a) Thiamine
b) Riboflavin
c) Pyridoxine
d) Niacin
Answer: (a)

Note Out of above given variables (a) Thiamine – is suggested.
Stem: Wernicke’s encephalopathy

Recall
A common condition in patients with long term alcoholism, resulting largely from thiamine deficiency and characterized by disturbances in ocular motility, pupillary alterations, nystagmus, and ataxia with tremors. An organic toxic psychosis is often an associated finding, and Korsakoff syndrome often coexists; the characteristic cellular pathology is found in several areas of the brain, particularly the mammillary bodies and regions adjacent to the third and fourth ventricles. Ref: http://medical-dictionary.thefreedictionary.com/Wernicke+encephalopathy

Review of variables
a) Thiamine:
Wernicke’s encephalopathy: Triad of Ophthalmoplegia, ataxia, confusion. Caused by a deficiency of Vitamin B1-Thiamine. Ref: Pg-485 and 868-23rd Ed, Gowalla
Thiamine is Vitamin B1; helps convert food into energy needed for healthy skin, hair, muscles, and brain. Deficiency causes Beriberi, Wernicke’s – Korsakoff syndrome. Triad of Wernicke encephalopathy consists of ophthalmoplegia, ataxia and confusion. Recommended daily amount: M: 1.2 mg, W: 1.1 mg. Food sources; eggs, fish, fruits, grains, kidneys, legumes, liver, meat, milk, nuts, poultry, seeds, vegetables, and yeast
b) Riboflavin:
Riboflavin deficiency causes angular stomatitis. Ref: Pg-868-23rd Ed, Gowalla
RIBOFLAVIN (vitamin B2)- Helps convert food into energy- needed for healthy skin, hair, blood, and brain. RDA: M: 1.3 mg, W: 1.1 mg. Food source-milk, yoghurt, cheese, whole and enriched grains and cereals, liver. Deficiency causes Angular stomatitis
c) Pyridoxine:
Pyridoxine deficiency:
1. Ch. convulsions in infant may be due to lack of pyridoxine.
2. Polyneuropathy – as a complication of isoniazid treatment of T.B. Ref: Pg-486 and 869-23rd Ed, Gowalla
VITAMIN B6 (pyridoxal, pyridoxine, pyridoxamine) aids in lowering homocysteine levels and may reduce the risk of heart disease. Helps convert tryptophan to niacin and serotonin, a neurotransmitter that plays key roles in sleep, appetite, and moods. Helps make red blood cells, influences cognitive abilities and immune function. RDA: 31–50: M: 1.3 mg, W: 1.3 mg 51+: M: 1.7 mg, W: 1.5 mg. Food source; Meat, fish, poultry, legumes, tofu and other soy products, potatoes, non-citrus fruits such as bananas and watermelons. Deficiency causes Glossitis, Cheliosis
d) Niacin:
Nicotinic acid (PP Factor)-Deficiency – Mental confusion. Pellagra. (Note: Requirement does not increase during pregnancy) Ref: Pg-486 and 868,869-23rd Ed, Gowalla
NIACIN (vitamin B3, nicotinic acid). Helps convert food into energy. Essential for healthy skin, blood cells, brain, and nervous system. RDA: M: 16 mg, W: 14 mg. Food source: meat, poultry, fish, fortified and whole grains, mushrooms, potatoes, peanut butter. Deficiency causes: Pellagra


Q2. The following diseases are transmitted by autosomal recessive genes (Bihar/Ayush/Homoeo/MO/ QP/2014):
a) Idiopathic haemochromatosis
b) Von Recklinghausen disease
c) Von Willebrand disease
d) Cystic fibrosis
Answer: Use your discretion

Note Out of the variables given above the most suitable choice suggested is (a) Idiopathic haemochromatosis and (d) Cystic fibrosis – is transmitted by autosomal recessive genes.

Review of variables
a) Idiopathic haemochromatosis (Autosomal Recessive)
The disease is inherited in an autosomal recessive pattern, which means both copies of the gene in each cell have mutations. Most often, the parents of an individual with an autosomal recessive condition each carry one copy of the mutated gene, but do not show signs and symptoms of the condition. Ref: http://www.medicineonline.com/articles/i/2/Idiopathic-Hemochromatosis/Hemochromatosis.html
b) Von Recklinghausen disease (Autosomal Dominant)
NF-1 was formerly known as von Recklinghausen disease after the researcher (Friedrich Daniel von Recklinghausen) who first documented the disorder. NF-1 is inherited in an autosomal dominant fashion, although it can also arise due to spontaneous mutation. Ref: http://en.wikipedia.org/wiki/Neurofibromatosis_type_I Ref: Pg-940-23rd Ed, Golwalla
c) Von Willebrand disease
(Autosomal Dominant)
Von Willebrand disease types I and II are inherited in an autosomal dominant pattern. Von Willebrand disease type III (and sometimes II) is inherited in an autosomal recessive pattern. The vWF gene is located on chromosome twelve (12p 13.2). It has 52 exons spanning 178kbp. Types 1 and 2 are inherited as autosomal dominant traits and type 3 is inherited as autosomal recessive. Occasionally type 2 also inherits recessively. Ref: http://en.wikipedia.org/wiki/Von_Willebrand_disease Ref: Pg-315-23rd Ed, Golwalla
d) Cystic fibrosis (Autosomal Recessive)

Cystic fibrosis (CF), also known as mucoviscidosis, is an autosomal recessive genetic disorder that affects mostly the lungs but also the pancreas, liver, and intestine. Difficulty in breathing is the most serious symptom and results from frequent lung infections. Other symptoms include sinus infections, poor growth, and infertility—affect other parts of the body. Ref: http://en.wikipedia.org/wiki/Cystic_fibrosis
Ref: Pg-940-23rd Ed, Golwalla


Q3. Atrial fibrillation is seen in all except (Bihar/AYUSH/Homoeo/MO/QP/2014):
a) Constrictive Pericarditis
b) Atrial Septal Defect (A.S.D.)
c) Ventricular Septal Defect (V.S.D.)
d) Mitral Stenosis
Answer: (c)

Note Out of above given variables (c) VSD-is suggested-for Atrial fibrillation seen in all except
Stem: Atrial fibrillation

Recall
A cardiac arrhythmia is marked by rapid randomized contractions of the atrial myocardium, causing a totally irregular, often rapid, ventricular rate. There is no synchronous atrial contraction and the ventricles beat irregularly. The heartbeat is irregular; the pulse is irregular in rhythm and amplitude.
Ref: http://medical-dictionary.thefreedictionary.com/atrial+fibrillation

Common causes of Atrial Fibrillation:

  1. CAD including Acute MI
  2. Valvular heart disease; Specially RHD
  3. Hypertension
  4. Sino-atrial disease
  5. Hyperthyroidism
  6. Alcohol
  7. Cardiomyopathy
  8. Congenital heart disease
  9. Chest infection
  10. Pulmonary embolism
  11. Pericardial disease
  12. Idiopathic

Ref: Pg-562, 20th Ed, Davidson’s

Review of variables
(a) Constrictive pericarditis:
Atrial fibrillation is seen in pericarditis; viral, post-cardiotomy and post-infraction.
Ref: Pg-194, 23rd Ed, Golwalla.
Constrictive pericarditis; Pulse small and rapid, pulsus paradoxus or atrial fibrillation may occur.
Ref: Pg-268, 23rd Ed, Golwalla.
(b) Atrial septal defect:
Atrial fibrillation is associated with Atrial septal defect.
Ref: Pg-194, 23rd Ed, Golwalla.
(c) Ventricular septal defect (V.S.D):
Atrial fibrillation not mentioned under VSD (Pg-201 & 202).
Ref: 2 Pg-201-202, 3rd Ed, Golwalla.
-Atrial fibrillation is not mentioned under VSD.
Ref: Pg-639, 20th Ed, Davidson’s
Ref: Pg-834, 6th Ed, Kumar and Clarke.
(d) Mitral stenosis:
Pregnant women with mitral stenosis are at increased risk for the development of atrial fibrillation and other tachyarrythmias. Medical management of severe mitral stenosis and atrial fibrillation with digoxin and beta-blockers is recommended. Balloon valvulotomy can be carried out during pregnancy. Ref: Harrison’s Principles of Internal Medicine 16th Ed


Q.5. Sudden onset of cough followed by increasing dyspnoea is characteristic of (Bihar/AYUSH/ Homoeo/MO/QP/2014):
a) Pleural effusion
b) Lobar pneumonia
c) Myocardial infarction
d) Pneumothorax
Answer: (d)

Note The choice among the above given variables suggested is (d) Pneumothorax –for sudden onset of cough followed by increasing dyspnoea.

Review of variables
(a)
Pleural effusion: Pleural effusion is an accumulation of exudative or transudate fluid in the pleural cavity. Onset is insidious with ill-defined health. Associated with pain, dyspnea, cough, loss of weight. About 500 ml fluid is required to produce physical signs.
Ref: Pg-156, 23rd Ed, Golwalla.
(b) Lobar pneumonia: Pneumonia is an accumulation of secretions and inflammatory cells in the alveolar spaces of lung due to infection. Symptoms include high fever, rigors, dyspnea, cough rusty sputum, pain with cough. Tachycardia, tachypnea, on auscultation are signs of consolidation.
Ref: Pg-112, 23rd Ed, Golwalla.
(c) Myocardial infarction: Acute MI is precipitated by – Physical exertion, emotional strain, heavy meal. Onset abrupt, pain in chest typical location and radiation, dyspnea, nausea and vomiting, anxiety, restlessness and features of shock.
Ref: Pg-234-235, 23rd Ed, Golwalla.
(d)  Pneumothorax: Pneumothorax is air in Pleural cavity. Primary spontaneous pneumothorax occurs in patients without clinical evidence of lung disease. Secondary spontaneous pneumothorax is related to parenchymal lung disease. Onset is sudden with feeling of something snapping in the chest, severe pain, increasing shortness of breath, cyanosis, restlessness, and shock. Hyper resonant chest with silence on the affected side.
Ref: Pg-151-152, 23rd Ed, Golwalla. Ref: Pg-733, 20th Ed, Davidson’s


Q.6. Seronegative Arthritis include (Bihar/AYUSH/Homoeo/MO/QP/2014):
a) Ankylosing spondylitis
b) Reiter’s arthritis
c) Psoriatic arthritis
d) All of the above
Answer: (d)

Note Out of above given variables (d) All of the above – is suggested for seronegative arthritis
Stem: Seronegative arthritis

Recall
The term ‘Seronegative’ incorporates a group of inflammatory joint disorders, which are distinct from Rheumatoid Arthritis, that are thought to share similar pathogenesis. They show considerable overlap and similarity of articular and extra-articular clinical features and striking genetic association with the histocompatibility antigen HLA-B27. These are as under:

  1. Ankylosing spondylitis
  2. Reactive arthritis, including Reiter’s syndrome
  3. Psoriatic arthropathy
  4. Arthritis associated with inflammatory bowel disease (Crohn’s disease, Ulcerative colitis)

Ref: Pg-1106, 20th Ed, Davidson’s.


Q.7. Characteristic ECG features of Hyperkalemia (Bihar/AYUSH/Homoeo/MO/QP/2014):
a) U waves
b) Narrow QRS Complex
c) Tall T Waves
d) Short PR Interval
Answer: (c)

Note The suggested choice among the above given variables is (c) Tall ‘T’ waves.
Stem: Characteristic ECG features of Hyperkalemia

Recall

Potassium excess (Hyperkalemia)
ECG features
include:
ECG features
a. With Serum
K > 5.5 mEq/l:

-Shortening of QT interval.
-Tall peaked T waves.
-Low P waves (Pg-577, 5th Ed, P.C. Das)
-Wide, tall and tented T waves
-Wide, flat or absent P waves
-Prolonged P-R interval
-Depressed S-T segment
-Widened QRS complex
 
b. With Serum
K > 6.5 mEq/l:

-Wide QRS complex
-Prolonged PR interval
-The disappearance of P waves
-Arrhythmias;
Nodal and ventricular
 
c. Final stages
(Extreme kalemia):

-QRS complex merges with T wave.
-A sine wave pattern with ventricular asystole or fibrillation
 
Ref: Hyperkalemia-Pg-875-876, 23rd Ed, Golwalla  

Q8. The early feature of Hypothyroidism is (Bihar/AYUSH/Homoeo/MO/QP/2014):
a) Low T3
b) Low T4
c) Increased TSH
d) High T4
Answer: (c)

Note The most suitable choice among the above given variables suggested is (c) Increased TSH
Stem: Early feature of Hypothyroidism

Recall
Early state of Hypothyroidism is termed as ‘subclinical’ Hypothyroidism. It is characterized by elevated TSH with normal serum T3.
Ref: Pg-370, 23rd Ed, Golwalla.

Extended information
Serum TSH is the investigation of choice, High TSH level confirms Primary hypothyroidism. A low free T4 level confirms the hypothyroid state.
Ref: Pg-1072, 6th Ed, Kumar and Clarke.
In the most common form of hypothyroidism, namely primary hypothyroidism resulting from an intrinsic disorder of thyroid gland, serum T4 is low and TSH elevated, usually in access of 20mU/l. Serum T3
concentrations do not discriminate reliably between euthyroid and hypothyroid patients and should not be measured.
In the rare secondary hypothyroidism there is atrophy of inherently normal thyroid gland caused by failure of TSH secretion in a patient with hypothalamic or anterior pituitary disease e.g., pituitary macroadenoma. Serum T4 is low but TSH may be low, normal or even slightly elevated.
Ref: Pg-750, 20th Ed, Davidson’s.


Q.9. Erythema nodosum can be caused by (Bihar/AYUSH/Homoeo/MO/QP/2014):
a) Sarcoidosis
b) Post Primary Tuberculosis
c) Streptococcal infection
d) Rheumatoid arthritis
Answer: Use your discretion.

Note Erythema nodosum can be caused by (a) Sarcoidosis and (b) Streptococcal infection.
Stem: Erythema nodosum:

Recall
An inflammatory reaction that occurs in deep fat cell in the skin and is characterized by the presence of tender, red, raised lumps or nodules that range in size from 1 to 5 centimeters and are most commonly located over the shins but occasionally on the arms or other areas.
It can be caused by a variety of conditions, and typically resolves spontaneously within 3–6 weeks. It is common in young people between 12–20 years of age.
(Ref: http://en.wikipedia.org/wiki/Erythema_nodosum)

Causes:

  1. Rheumatic fever
  2. Infections; streptococcal, tuberculosis (especially primary), toxoplasmosis, histoplasmosis, brucellosis, leprosy, blastomycosis, coccidioidomycosis, lymphogranuloma inguinale, psittacosis, rickettsial infection, cat scratch fever, tricophytosis.
  3. Inflammatory bowel disease.
  4. Sarcoidosis
  5. Immunological – Bechet’s disease
  6. Drugs; sulphonamides, oral contraceptives, barbiturates.

Ref: Pg-955, 23rd Ed, Golwalla

Note Erythema nodosum is not mentioned in cases of (b) Post-primary tuberculosis and (d) Rheumatoid arthritis.

Review of variables
a) Sarcoidosis
Erythema nodosum is seen in cases of Sarcoidosis. Ref: Pg-955, 23rd Ed, Golwalla
b) Post Primary Tuberculosis

Erythema nodosum is seen in cases of tuberculosis (especially primary). Ref: Pg-955, 23rd Ed, Golwalla Tuberculosis: Erythema nodosum is a companion of primary tuberculosis. Ref: Pg-189, 4th Ed, Illustrated Synopsis of Dermatology and Sexually Transmitted disease by Neena Khanna
c) Streptococcal infection

Erythema nodosum is seen in cases of Streptococcal infection. Ref: Pg-955, 23rd Ed, Golwalla
d) Rheumatoid arthritis

Erythema nodosum is not seen/ mentioned to be associated with cases of Rheumatoid arthritis. Ref: Pg-955, 23rd Ed, Golwalla Ref: Pg-539,540, 5th Ed, P.C. Das.


Q10. Kussmaul’s breathing is due to presence of (Bihar/AYUSH/Homoeo/MO/QP/2014):
a) Bicarbonates
b) H+ ions
c) Chloride ions
d) K+ ions
Answer: (b)

Note Out of above given variables (b) H+ ions-is suggested.
Stem: ‘Kussmaul’s breathing’

Recall
Kussmaul breathing is a deep and laboured breathing pattern often associated with severe metabolic acidosis, particularly diabetic ketoacidosis (DKA) but also kidney failure. It is a form of hyperventilation, which is any breathing pattern that reduces carbon dioxide in the blood due to increased rate or depth of respiration. In metabolic acidosis, breathing is first rapid and shallow [1] but as acidosis worsens, breathing gradually becomes deep, laboured and gasping. It is this latter type of breathing pattern that is referred to as Kussmaul breathing.
Ref: http://en.wikipedia.org/wiki/Kussmaul_breathing
Acidosis:
Metabolic acidosis can result either due to gain in acid, by loss of bicarbonates or failure to excrete acid when the pH becomes less than 7.36.
Clinical features:
When the fall in the bicarbonate is moderate (18mEq/l) there is mild degree of acidosis and it may be reverted back by compensatory over-breathing.
When the fall in plasma bicarbonate level is marked (15mEq/l) there may be tiredness, weakness, deep and rapid breathing called Kussmaul’ s respiration. This state cannot be compensated by breathing effect of lungs and is called decompensated metabolic acidosis.
When the plasma bicarbonate level falls below 10mEq/l severe metabolic acidosis results and patient usually becomes comatose.
Investigations:
-Plasma bicarbonate falls below 20mEq/l
-Serum PO4, K+ and Cl are raised
-Blood urea is elevated
-Serum calcium is low
-PCO2 is either normal or low
-Blood pH and urine pH fall markedly.
Ref: 582 and 583, 5th Ed, Textbook of Medicine by P.C. Das
Diabetic ketoacidosis:
Ketone bodies are strong organic acids that associate at physiological pH and generate a high concentration of H+ ions. This rapidly exceeds the body’s buffering capacity and leads to severe metabolic acidosis.
Ref: Pg-279. Essential Endocrinology and Diabetes, Includes Desktop Edition by Richard I. G. Holt, Neil A. Hanley

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