Purified cardiac glycoside extracted from foxglove plant, Digitalis lanata.
Only inotrpic drug given orally.
Widely used in treatment of,
Atrial fibrillation.
Atrial flutter.
CHF uncontrolled by other medication.
ACTION:
Increases myocardial contractility.
Reduces heart rate.
Decreases AV conduction.
CHANGES IN ECG:
Inversion of T-wave.
Increased PR interval.
Shortening of QT interval (Systole duration shortened).
Depression of ST segment.
PHARMACOKINETICS:
70 to 80% oral digoxin dose absorbed.
Mainly in proximal part of small intestine.
20 to 30% binds to serum albumin.
Extensively distributed in tissues.
High concentrations – Heart & kidneys.
Skeletal muscles – Largest digoxin storage.
t1/2 elimination – (26 -45 hrs).
Excreted by kidneys.
DOSE:
Digoxin dose in child – 0.04-0.06 mg/kg
Theurapetic level: 0.5-1.5 ng/ml.
Toxic level > 2.4 ng/ml.
Digoxin dose altered in old age, renal disease & hypercalcemia.
INDICATION:
Congestive Heart Failure
Tachyarrhythmias
Atrial Fibrillation
Atrial Flutter
Acute MI
Paroximalatrial tachycardia
CONTRAINDICATION:
Hypersensitivity
Uncontrolled Ventricular Arrhythmias
AV block
Constrictive Pericarditis
Idiopathic Hypertrophic Subaortic Stenosis
DRUG INTERACTION:
Diuretics, amphotericin B & corticosteroids:
Cause hypokalemia.
Can precipitate digitalis-induced arrhythmias.
Quinidine:
Reduces digoxin binding to tissue proteins & it’s renal and biliary clearance.
T Plasma concentration of digoxin toxicity can occur.
Cholestyramine, sucralfate, neomycin, sulfasalazine, antacids and kaolin-pectin:
Reduce digoxin absorption.
ADVERSE EFFECT:
Dizziness (4.9%)
Mental disturbances (4.1%)
Diarrhoea (3.2%)
Headache (3.2%)
Nausea (3.2%)
Vomiting (1.6%)
Maculopapular rash (1.6%)
Anorexia
Cardiac dysrhythmia – Characteristic associated with digitalis intoxication.
Ventricular premature beats.
Bigeminy.
Ventricular tachycardia.
Rarely ventricular fibrillation.
AV block.
Nonparoxysmal atrial tachycardia with variable AV block.
If arrhythmia in children –
Should consider toxicity.
DIGOXIN TOXICITY:
Features:
Generally unwell & lethargy.
Nausea & vomiting.
Confusion.
Yellow-green vision.
Arrhythmias (e.g. AV block, bradycardia)
Dizziness.
Precipitating factors:
Renal disease
Hypokalaemia
Hypomagnesemia
Hypoalbuminemia
Hypothermia
Hypothyroidism
Hypercalcemia.
Hypernatremia
Acidosis.
Myocardial ischaemia.
Partial AV block.
Drugs:
Amiodarone.
Quinidine.
Verapamil.
Spironolactone.
Furosemide.
Hydrochlorothiazide – Compete with DCT secretion, hence reducing excretion.
Management
Digibind.
Correct ventricular arrhythmia by lignocaine.
Bradyarrhythmias by propanolol.
Atrial tachyarrhythmias by atropine.
Phenytoin.
Monitor K+
Exam Question
Digoxin toxicity may result from the concurrent administration of digoxin with Amiodarone, quinidine, verapamil, spironolactone, Furosemide, Hydrochlorothiazide.
Digoxin toxicity is increased by Renal impairment, Hypercalcemia hypokalemia & Hypomagnesemia
Digoxin induced arrhythmia shows Paroxysmal Atrial Tachycardia with variable AV block, Ventricular Bigeminy & May be used to treat Atrial Fibrillation
Most effective method of treatment of Digitalis toxicity is Digoxin Antibody – Digibind.
Dose of digoxin is altered in Old age,Renal disease & Hypercalcemia
Therapeutic plasma level of digoxin is 0.5-1.5 ng/ml
Half-Life of Digoxin is 40 hrs(26-45hrs)
Diuretics, amphotericin B, corticosteroids, Quinidine, Cholestyramine, sucralfate, neomycin, sulfasalazine, antacids and kaolin-pectin are the drugs showing interaction with digoxin.
Interaction occurring when quinidine and digoxin are given together – Quinidine decreases excretion of digoxin
Interaction occurring when quinidine and digoxin are given together – Quinidine displaces digoxin from protein binding sites & decreases excretion
Digoxin is contraindicated in Hypertrophic obstructive cardiomyopathy.
Digoxin is useful in Complete heart-block with CHF.
Digoxin induced arrhythmia can be treated with Lignocaine
Dose of digoxin in child 0.04-0.06 mg/kg
Atrial Fibrillation is treated by digoxin
Digoxin is distributed in heart, kidney & skeletal muscles.
On changing maintenance dose of digoxin the new steady state plasma digoxin concentration would be achieved in approximately 1 week.
Don’t Forget to Solve all the previous Year Question asked on Digoxin
Q. 1 A patient with normal renal function has received a daily maintenance dose of digoxin for 2 weeks, if the dosage is changed, the new steady state plasma digoxinconcentration would be achieved in approximately
A
2days
B
lweek
C
2 weeks
D
4 weeks
Q. 1 A patient with normal renal function has received a daily maintenance dose of digoxin for 2 weeks, if the dosage is changed, the new steady state plasma digoxinconcentration would be achieved in approximately
A
2days
B
lweek
C
2 weeks
D
4 weeks
Ans.
B
Explanation:
The time required to establish a new steady-state plasma drug concentration when maintenance doses are changed is approximately four half-lives, the same amount of time required to establish the initial steadystate level. Because the half-life of digoxin is approximately 1.6 days, the time required to reach a new steady state is approximately 7 days. Digitoxin has a much longer half-life of approximately 7 days and the time required to reach steady state with digitoxin is approximately 4 weeks. The time required to reach steady state is independent of dose or dosage interval
Q. 2 A 50 years old man is admitted to the hospital with acute myocardial infarction. After 12 hours he becomes hypotensive and oliguric. He is lying comfortably on his back, B.P. is 90/60 mmHg, heart rate is 60 BPM and JVP is 15 cm H2O. The heart sounds are regular without gallop, murmur or rub and the lungs are clear on auscultation. The next step should be to give:
A
Intravenous Furosemide
B
Intravenous Fluids
C
Digoxin & Dopamine
D
Norepinephrine and Intraaortic Balloon Pump
Q. 2 A 50 years old man is admitted to the hospital with acute myocardial infarction. After 12 hours he becomes hypotensive and oliguric. He is lying comfortably on his back, B.P. is 90/60 mmHg, heart rate is 60 BPM and JVP is 15 cm H2O. The heart sounds are regular without gallop, murmur or rub and the lungs are clear on auscultation. The next step should be to give:
A
Intravenous Furosemide
B
Intravenous Fluids
C
Digoxin & Dopamine
D
Norepinephrine and Intraaortic Balloon Pump
Ans.
C
Explanation:
This patient probably has an inferior wall myocardial infarction complicated by right ventricular involvement.
TheCardiac output is probably depressed because of low left heart filling pressure secondary to right ventricular infarction. The initial treatment should be to administer fluids intravenously.
Q. 3 Digoxin toxicity may result from the concurrent administration of digoxin with all of the following drugs EXCEPT.
A
Quinidine
B
Hydrochlorothiazide
C
Triamterene
D
Furosemide
Q. 3 Digoxin toxicity may result from the concurrent administration of digoxin with all of the following drugs EXCEPT.
A
Quinidine
B
Hydrochlorothiazide
C
Triamterene
D
Furosemide
Ans.
C
Explanation:
Triamterene is a potassium-sparing diuretic that may protect against diuretic-induced digoxin toxicity. Dioxin toxicity may be caused by drugs that increase serum digoxin levels or increase the binding of dioxin to its receptor, the sodium potassium adenosine tri phosphatase (ATPase). Quinidine decreases digoxin volume of distribution and clearance. Verapamil also decreases the clearance of digoxin. Both drugs may thereby increase serum digoxin levels and precipitate digoxin toxicity. Diuretics(e.g.hydrochlorothiazide, furosemide) may cause hypokalemia and hypomagnesemia, both of which may predispose to cardiac arrhythmias. Furthermore, hypokalemia increases dioxin binding to sodium potassium ATPase.
Q. 4
Digoxin toxicity is precipitated by all except :
A
>Electrolyte disturbance
B
>Acute myocardial infarction
C
>Hepatic disease
D
>Renal disease
Q. 4
Digoxin toxicity is precipitated by all except :
A
>Electrolyte disturbance
B
>Acute myocardial infarction
C
>Hepatic disease
D
>Renal disease
Ans.
C
Explanation:
Hepatic disease [Ref. K.D.T. 5th/e p 462, 463]
Digoxin toxicity is enhanced by renal failure as it is excreted through kidneys where as digitoxin toxicity is enhanced by liver failure because it is eliminated by hepatic metabolism.
Other factors precipitating Digitalis toxicity
Advanced age
Acute myocardial infarction or ischemia
Hypoxemia
Hypomagnesemia
Renal insufficiency
Hypercalceinia
Electrical cardioversion
Hypothyroidism
Hypokalemia (most common precipitating cause of digitalis intoxication. This often occurs in patients with heart failure as a result of diuretic therapy and secondary hyperaldosteronism).
ALSO REMEMBER
The administration of following drugs raises the serum concentration of Digoxin by reducing both the renal and nonrenal elimination of digoxin and by reducing its volume of distribution.
– Quinidine
– Verapamil
– Amiodarone
– Propafenone
Q. 5
Which of the following does not contribute to Digoxin toxicity:
A
Hyperkalemia
B
Hypercalcemia
C
Renal failure
D
Hypomagnesemia
Q. 5
Which of the following does not contribute to Digoxin toxicity:
A
Hyperkalemia
B
Hypercalcemia
C
Renal failure
D
Hypomagnesemia
Ans.
A
Explanation:
Ans:A.)Hyperkalemia
Digoxin toxicity
Symptoms include vomiting, loss of appetite, confusion, blurred vision, changes in color perception, and decreased energy.
Potential complications include an irregular heartbeat, which can be either too fast or too slow.
Toxicity may occur over a short period of time following an overdose or gradually during long-term treatment.
Risk factors include low potassium, low magnesium, and high calcium.
The most common precipitating cause of digitalis intoxication is depletion of potassium stores, which occurs often in patients with heart failure as a result of diuretic therapy and secondary hyperaldosteronism.
Digoxin toxicity increases in individuals who have kidney impairment
Diagnosis
Serum digoxin level
Therapeutic levels are 0.6-1.3 to 2.6 ng/mL.
Electrolytes
In acute toxicity, hyperkalemia is common
Chronic toxicity is often accompanied by hypokalemia and hypomagnesemia
Electrocardiography
Digoxin toxicity may cause almost any dysrhythmia
Classically, dysrhythmias associated with increased automaticity and decreased AV conduction occur
Sinus bradycardia and AV conduction blocks are the most common ECG changes in the pediatric population, while ventricular ectopy is more common in adults
Nonparoxysmal atrial tachycardia with heart block and bidirectional ventricular tachycardia are particularly characteristic of severe digitalis toxicity
Management
Supportive care of digitalis toxicity includes the following:
Hydration with IV fluids
Oxygenation and support of ventilatory function
Discontinuation of the drug, and, sometimes, the correction of electrolyte imbalances
GI decontamination
Activated charcoal is indicated for acute overdose or accidental ingestion
Binding resins (eg, cholestyramine) may bind enterohepatically-recycled digoxin
Treatment of electrolyte imbalance
For hyperkalemia, use insulin plus glucose, and sodium bicarbonate if the patient is acidotic
Treatment with digoxin Fab fragments is indicated for a K + level greater than 5 mEq/L
Hemodialysis may be necessary for uncontrolled hyperkalemia
Correct hypokalemia (usually in chronic intoxication)
Concomitant hypomagnesemia may result in refractory hypokalemia
Q. 6
All of the following statements about Digoxin induced arrhythmia’s are true, except:
A
Bi ventricular Tachycardia
B
Paroxysmal Atrial Tachycardia with variable AV block
C
Ventricular Bigeminy
D
May be used to treat Atrial Fibrillation
Q. 6
All of the following statements about Digoxin induced arrhythmia’s are true, except:
A
Bi ventricular Tachycardia
B
Paroxysmal Atrial Tachycardia with variable AV block
C
Ventricular Bigeminy
D
May be used to treat Atrial Fibrillation
Ans.
A
Explanation:
The most frequent disturbances of cardiac rhythm associated with digitalis intoxication are ventricular premature beats, bigeminy, ventricular tachycardia and rarely ventricular fibrillation. AV block and nonparoxysmal atrial tachycardia with variable AV block are characteristic of intoxication.
Ref: Harrison’s 16th Edition, Page 1375
Q. 7
Most effective method of treatment of Digitalis toxicity is?
A
Hemodialysis
B
Cardioversion
C
Digoxin Antibody
D
Atropine
Q. 7
Most effective method of treatment of Digitalis toxicity is?
A
Hemodialysis
B
Cardioversion
C
Digoxin Antibody
D
Atropine
Ans.
C
Explanation:
Ans. is ‘c’ i.e., Digoxin Antibody
Q. 8
Dose of digoxin is NOT altered in ‑
A
Old age
B
Hepatic disease
C
Renal disease
D
Hypercalcemia
Q. 8
Dose of digoxin is NOT altered in ‑
A
Old age
B
Hepatic disease
C
Renal disease
D
Hypercalcemia
Ans.
B
Explanation:
Ans. is ‘b’ i.e., Hepatic disease
o Make it clear once and for all that Digitalis is the parent compound. Digitalis is applied as a collective term for the whole group and has come to mean a cardiac glycoside.
o Digoxin and digitoxin are two of the many types of cardiac glycoside.
o Digoxin is a polar glycoside, and is excreted by kidney, does not undergo hepatic metabolism. So dose need not be altered in hepatic disease.
o Digitoxin undergoes hepatic metabolism and its dose has to be altered in hepatic disease.
Q. 9
Digoxin can accumulate to toxic levels in patients with-
A
Renal insufficiency
B
Chronic hepatitis
C
Advanced cirrhosis
D
Chronic pancreatitis
Q. 9
Digoxin can accumulate to toxic levels in patients with-
A
Renal insufficiency
B
Chronic hepatitis
C
Advanced cirrhosis
D
Chronic pancreatitis
Ans.
A
Explanation:
Ans. is ‘a’ i.e., Renal insufficiency
Q. 10
Therapeutic plasma level of digoxin –
A
0.1-0.3 ng/ml
B
0.8-1.5 ng/ml
C
1.2 to 2 ng/ml
D
> 2.4 ng/ml
Q. 10
Therapeutic plasma level of digoxin –
A
0.1-0.3 ng/ml
B
0.8-1.5 ng/ml
C
1.2 to 2 ng/ml
D
> 2.4 ng/ml
Ans.
B
Explanation:
Ans. is `b’ i.e., 0.8-1.5 ng/ml
o Therapeutic concentration of digitoxin is 15-30 ng/ml and of digoxin is 0.5-1.4 ng/ml
Q. 11
TY2 of digoxin is –
A
24 hrs
B
40 hrs
C
48 hrs
D
60 hrs
Q. 11
TY2 of digoxin is –
A
24 hrs
B
40 hrs
C
48 hrs
D
60 hrs
Ans.
B
Explanation:
Ans. is ‘b’ i.e., 40 hrs.
o T1/2 of digoxin —> 40 hrs
o T’/2 of digitoxin —>5-7 days
Q. 12
The following drugs have significant drug interaction with digoxin, except –
A
Cholestyramine
B
Thiazide diuretics
C
Quinidine
D
Amlodipine
Q. 12
The following drugs have significant drug interaction with digoxin, except –
A
Cholestyramine
B
Thiazide diuretics
C
Quinidine
D
Amlodipine
Ans.
D
Explanation:
Ans. is `d’ i.e., Amlodipine
Diuretics, amphotericin B’ and corticosteroids cause hypokalemia can precipitate digitalis induced arrhythmias.
Quinidine reduces binding of digoxin to tissue proteins as well as its renal and biliary clearance T Plasma concentration of digoxin toxicity can occur.
Cholestyramine, sucralfate, neomycin, sulfasalazine, antacids and kaolin-pectin reduce absorption of digoxin.
Q. 13
Interaction occurring when quinidine and digoxin are given together –
A
Quinidine decreases excretion of digoxin
B
Quinidine displaces digoxin from protein binding sites
C
Increases the metabolism of digoxin
D
a and b
Q. 13
Interaction occurring when quinidine and digoxin are given together –
A
Quinidine decreases excretion of digoxin
B
Quinidine displaces digoxin from protein binding sites
C
Increases the metabolism of digoxin
D
a and b
Ans.
D
Explanation:
Ans. is ‘a’ i.e.,Quinine decreases excretion of digoxin; ‘b’ i.e., Quinine displaces digoxin from protein binding sites
o Quinidine reduces binding of digoxin to tissue proteins as well as its renal and biliary clearance by inhibiting efflux transporter P – glycoprotein —> plasma concentration is doubled —> toxicity can occur.
Q. 14
The dose of Digoxin should be reduced when given along with –
A
Quinidine
B
Rifampicin
C
Indomethacin
D
Antacids
Q. 14
The dose of Digoxin should be reduced when given along with –
A
Quinidine
B
Rifampicin
C
Indomethacin
D
Antacids
Ans.
A
Explanation:
Ans. is ‘a’ i.e., Quinidine
Quinidine reduces binding of digoxin to tissue proteins as well as its renal/biliary clearance.
Its plasma concentration is then doubled and toxicity may occur if dose is not reduced.
Q. 15
Digoxin is contraindicated in –
A
Supraventricular tachycardia
B
Atrial fibrillation
C
Congestive heart failure
D
Hypertrophic obstructive cardiomyopathy
Q. 15
Digoxin is contraindicated in –
A
Supraventricular tachycardia
B
Atrial fibrillation
C
Congestive heart failure
D
Hypertrophic obstructive cardiomyopathy
Ans.
D
Explanation:
Ans. is ‘d’ i.e., Hypertrophic obstructive cardiomyopathy
Digitalis is contraindicated in
o HOCM – By increasing the contractility it decreases the size of ventricle —> obstruction.
o Partia1A-V block – Digitalis increases ERP of A-V node —> A.V. conduction —> may convert partial block into complete block.
o WPW syndrome – Digitalis slows the conduction in the normal AV bundle and accelerates it in the aberrant pathway —> increase chances of reentry —> ventricular fibrillation may occur.
o Ventricular tachycardia – Digitalis decreases the refractory period of ventricle muscle ventricular fibrillation may occur.
Q. 16
Digoxin is useful in –
A
Atrial fibrillation in thyrotoxicosis
B
Complete heart-block with CHF
C
Ventricular tachycardia
D
Myocarditis
Q. 16
Digoxin is useful in –
A
Atrial fibrillation in thyrotoxicosis
B
Complete heart-block with CHF
C
Ventricular tachycardia
D
Myocarditis
Ans.
B
Explanation:
Ans. is ‘b’ i.e., Complete heart-block with CHF
Digitalis has depressant action on AV node -4 it delayes the conduction through AV node by increased ERP.
If partial block is present, digitals may convert it into complete block.
But, if complete block is already present, digitalis cannot worsen the condition (as conduction is blocked to maximum block, i.e., complete heart block).
So, in this condition digitalis can be used for heart failure.
About other options
In thyrotoxicosis and myocarditis there is reduced responsiveness and patient becomes more prone for digitalis induced arrhythmias.
Digitalis is contraindicated in ventricular tachycardia as ventricular fibrillation may be precipitated.
Q. 17
Best used in digoxin induced arrhythmia-
A
Phenytoin
B
Lignocaine
C
Quinidine
D
Procainamide
Q. 17
Best used in digoxin induced arrhythmia-
A
Phenytoin
B
Lignocaine
C
Quinidine
D
Procainamide
Ans.
B
Explanation:
Ans. is ‘b’ i.e., Lignocaine
o Lignocaine is DOC for digitalis induced ventricular arrhythmias. o Phenytoin is an alternative.
Q. 18
Dose of digoxin in a child as mg/kg is –
A
0.02-0.04
B
0.03-0.05
C
0.04-0.06
D
0.06-0.08
Q. 18
Dose of digoxin in a child as mg/kg is –
A
0.02-0.04
B
0.03-0.05
C
0.04-0.06
D
0.06-0.08
Ans.
C
Explanation:
Ans. is ‘c’ i.e., 0.04 – 0.06
o Premature and neonates —-> 0.04 mg/kg
o 1 months to 1 year —> 0.08 mg/kg
o Between 1 to 3 years —-> 0.06 mg/kg
o Above 3 years —-> 0.04 mg/kg
Q. 19
Digoxin toxicity is enhanced by all, except:
A
Quinidine
B
Hypokalemia
C
Hypomagnesemia
D
Hepatic dysfunction
Q. 19
Digoxin toxicity is enhanced by all, except:
A
Quinidine
B
Hypokalemia
C
Hypomagnesemia
D
Hepatic dysfunction
Ans.
D
Explanation:
Answer is D (Hepatic dysfunction)
Digoxin toxicity is enhanced by renal failure as it is excreted through kidneys where as digitoxin toxicity is enhanced by liver failure because it is eliminated by hepatic metabolism. Hepatic dysfunction does not affect digoxin elemination.
The administration of following drugs raises the serum concentration of digoxin : (by reducing both the renal and nonrenal elimination of digoxin and by reducing its volume of distribution)
Quinidine Q
Verapamil
Amiodarone
Propufenone°
Q. 20
Treatment of digoxin over dose includes administration of all of the following except :
A
Potassium
B
Lignocaine
C
Phenyton
D
Hemodialysis
Q. 20
Treatment of digoxin over dose includes administration of all of the following except :
A
Potassium
B
Lignocaine
C
Phenyton
D
Hemodialysis
Ans.
D
Explanation:
Answer is D (Hemodialysis)
Hemodialysis has no role in treatment of digoxin overdose.
Management of digitalis overdose includes:
Withdrawl of drug e
Potassiume: administer cautiously and by oral route whenever possible if hypokalemia is present. Potassium must not be employed in the presence of A-V block or hyperkalemia
Phenyloin//3 blocker or Lidocaine e :Lidocaine is effective in treatment of digitalis induced ventricular tachyarrhythmias.
Cardiac pacemaker : may be required in digitalis induced A-V block
Electrical conversion : may be life saving in digitalis induced ventricular fibrillation
FAB fragments/digitalis antibodies e :are potentially life saving in severe intoxication.
Hemodialysis is not useful in poisonings due to:
Digoxin Q
Kerosene Q
Benzodiazepines Q
Organophosphates Q
Q. 21
Drug distribution in tissue true is all except ‑
A
Chloroquine – eye
B
Ephedrine – bone
C
Digoxin – skeletal muscle
D
Minocycline – adipose tissue
Q. 21
Drug distribution in tissue true is all except ‑
A
Chloroquine – eye
B
Ephedrine – bone
C
Digoxin – skeletal muscle
D
Minocycline – adipose tissue
Ans.
B
Explanation:
Ans. is ‘b’ i.e., Ephedrine – bone
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Nitrates decrease myocardial oxygen consumption by direct reduction of myocardial oxygen consumption, dilation of capacitance vessels & decreasing heart size.
Long-term nitrate usage decreases its own effect due to SH group in enzyme.
NTG is given by sublingual route because of hepatic first-pass metabolism.
Treatment of stable angina include nitrates & CCBs.
DOC in an acute attack of Prinzmetal’s angina is Nitrates.
Aggravation of angina symptoms is seen in Idiopathic hypertrophic subaortic stenosis on administering nitrates.
Best time to administer long-term nitrates for nocturnal angina is evening.
GTN can be used as “Transdermal patch”.
Tachycardia due to nitrates with angina pectoris is blocked by Beta-blocker.
Don’t Forget to Solve all the previous Year Question asked on Glyceryl Trinitrate
Nitroglycerine relaxes all types of smooth muscle irrespective of the state of the preexisting muscle tone.
The most prominent action is exerted on the vascular smooth muscle.
– Apart .from vascular smooth muscle nitrates also cause relaxation of the smooth muscles of the bronchi, gastrointestinal tract (including biliary system) and genitourinary tract.
Nitrates are rapidly denitrated in the smooth muscle to release nitric oxide which activates cytosolic guanyl cyclase which in turn increases CGMP that leads to vasodilation
Effect of nitrate on cardiovascular system
Enzymes activates
Nitrates –4 NO —> Gyanylcyclase 1′ CGMP Vasodilation
Nitrates cause relaxation of all the components of vascular system from large arteries to veins, arterioles and
capillaries.
Veins respond at the lowest concentrations and arteries at slightly higher one (Veins express greater amount of the enzyme that generates NO )from organic nitrates).
The primary direct result of an effective dose of nitroglycerine is marked relaxation of veins with increased venous capacitance and decreased ventricular preload. This leads to reduction in pulmonary vascular pressure and heart
size.
Effect of nitrates on coronary circulation
‘• In normal subjects without coronary disease
– Nitroglycerine can induce a significant if transient increase in total coronary blood flow.
In patients with angina due to atherosclerosis
– There is no evidence that total coronary .flow is increased in patients with angina due to atherosclerotic obstructive
coronary artery disease.
However, in these patients
– Nitrates cause redistribution of coronary blood flow from normal to ischemic regions which may play role in
therapeutic effect.
There are two types of vessels in coronary circulation :Larger conducting arteries
They run epicardially and send perforating branches to deeper tissue.
Smaller resistance vessels
These are the perforating branches of larger conducting arteries.
These arterioles supply blood to endocardium. If there is ischemia in any region of endocardium the perforating vessels of those region are dilated due to autoregulation (hypoxia causes vasodilation).
This pattern of action favours more blood flow towards the ischaemic zone as the smaller endocardial vessels are already dilated as a result of hypoxia / ischaemia.
Nitrates in heart failure
Nitrates afford relief by causing venous pooling of blood.
– Nitrates reduce venous return (preload) decreasesend diastolic volume –4 improvement in left ventricular function by Laplace law regression of pulmonary congestion.
Nitrates are used in cyanide poisoning
Cyanide poisoning results from complexing of cytochrome iron by the CV ion.
– Methemoglobin has a very affinity for CN ion.
– Methemoglobin combines with CN to form cyamnethemoglobin which is rapidly excreted by the body.
It is a well known fact that Nitrates generate generate Methemoglobin when they combine with Hb. – Thus administration of nitrates will generate large amount of methemoglobin.
– Due to its high offinity.for cyanide, methemoglobin combines with cyanide .forming cyanmethemoglobin. – This will regenerate active cytochrome.
– However this may again dissociate to release cyanide.
– The cynamethemoglobin can be further detoxified by the intravenous administration of sodium thiosulfate. This results in formation of thiocyanate ion a less toxic ion that is readily excreted.
Biliary colic
Esophageal spasm
Sublingual GIN promptly relieves pain. Nitrates taken before a meal facilitate feeding in esophageal achalasia by reducing esophageal tone.
Also remember these important properties of Nitrates.
Oral availability of Nitrates is low
The liver contains a high capacity organic nitrate reductase that removes nitrate groups in a stepwise _fashion from the parent molecule and ultimately inactivates the drug.
Therefore oral bioavailability of the traditional organic nitrates e.g. nitroglycerine and isosorbidedinitrate is very low.
For this reason sublingual route is preferred for nitrates. Nitroglycerine and isosorbide dintrate are both absorbed effectively by this route and reach therapeutic blood levels within a few minutes.
Nitrates develop tolerance
With continued exposure smooth muscles develop tolerance to nitrates.
The mechanism by which tolerance develops are not completely understood. As noted above diminished release of
nitric oxide resulting from depletion of tissue thiol compounds may be partly responsible ,for tolerance to nitrates.
Some student argue that cyanide poisoning should be the answer because nitrites not nitrates are used in cyanide poisoning but we are not convinced.
All the standard books group them together and do not differentiate between nitrates or nitrites. More so
Nitrates have’nt found wide clinical use in Renal colic
– None of the standard text books mention use of nitrates in renal colic.
– Both Goodman Gilman and KDT says that unlike its consistent effect on muscles of biliary tract, the action
of nitrates on ureteric muscles is variable therefore it has not found application in renal colic.
– None of the studies and research papers convincingly state that nitrates should be used in renal colic.
Nitrates have been anecdotally used only in uruguay to treat renal colic.
A trial was conducted based on this but it did’nt come out with conclusive results.
– It states that large trials and studies should be undertaken before nitrates before nitrates use is begun clinically.
Q. 2
Role of nitrates in congestive cardiac failure is due to‑
A
Direct inotropic action
B
Decrease preload
C
Decrease afterload
D
Coronary vasodilatation
Q. 2
Role of nitrates in congestive cardiac failure is due to‑
A
Direct inotropic action
B
Decrease preload
C
Decrease afterload
D
Coronary vasodilatation
Ans.
B
Explanation:
Ans. is ‘b’ i.e., Decrease preload
Q. 3
Nitrates decrease myocardial oxygen consumption by all of the following mechanisms except –
A
By increasing the left ventricular end diastolic pressure
B
By direct reduction of oxygen consumption of the myocardial cell
C
By dilation of the capacitance vessels
D
By decreasing the size of heart
Q. 3
Nitrates decrease myocardial oxygen consumption by all of the following mechanisms except –
A
By increasing the left ventricular end diastolic pressure
B
By direct reduction of oxygen consumption of the myocardial cell
C
By dilation of the capacitance vessels
D
By decreasing the size of heart
Ans.
A
Explanation:
Ans. is ‘a’ i.e., By increasing the left ventricular end diastolic pressure
o Nitratets dilate veins (capacitance) vessels and decrease venous return (preload) o This results in decreased end diastolic pressure and left ventricular size (not increased), which ultimately leads to decreased oxygen consumption.
Q. 4
Not true about nitroglycerine is that –
A
Causes AV conduction delay
B
Causes tolerance
C
Caused reflex tachycardia
D
Caused hypotension
Q. 4
Not true about nitroglycerine is that –
A
Causes AV conduction delay
B
Causes tolerance
C
Caused reflex tachycardia
D
Caused hypotension
Ans.
A
Explanation:
Ans. is ‘a’ i.e., Causes AV conduction delay
Nitroglycerine and other nitrates have no effect on A-V conduction. About other options o Tolerance can develop if nitrates are continuously present in the body. o Nitrates can cause reflex tachycardia and hypotension.
Q. 5
Nitroglycerine causes all except –
A
Hypotension and bradycardia
B
Methemoglobinemia
C
Hypotension and tachycardia
D
Vasodilatation
Q. 5
Nitroglycerine causes all except –
A
Hypotension and bradycardia
B
Methemoglobinemia
C
Hypotension and tachycardia
D
Vasodilatation
Ans.
A
Explanation:
Ans. is ‘a’ i.e., Hypotension and bradycardia
Nitrates effect on BP & HR o Nitrates cause vasodilatation that results in:
Hypotension
Reflex tachycardia (not bradycardia)
o Due to hypotension (caused by vasodilatation) there is reflex sympathetic stimulation –> stimulation of β1 receptor on heart –> tachycardia.
Q. 6
Long term use of nitrates lead to decreased effect because of –
A
Development of resistance
B
SH group in the enzyme
C
Decreased oral absorption
D
Increased resistance
Q. 6
Long term use of nitrates lead to decreased effect because of –
A
Development of resistance
B
SH group in the enzyme
C
Decreased oral absorption
D
Increased resistance
Ans.
B
Explanation:
Ans. is ‘b’ i.e., SH groups in the enzyme
o Tolerance develops to hemodynamic and antiischaemic effects of nitrates if they are continuously present in the body. No significant tolerance develops when nitrates are used intermittently. However; significant tolerance develops when nitrates are used continuously. This mechanism of nitrate tolerance is not well understood. The mechanism proposed is —> “Reduced ability to generate NO due to depletion of cellular SH radicals”.
Q. 7
Glyceryl trinitrate is given by sublingual route because of-
A
Short t1/2 in plasma
B
Hepatic first pass metabolism
C
Lower bioavailability by oral route
D
Extensive protein binding
Q. 7
Glyceryl trinitrate is given by sublingual route because of-
A
Short t1/2 in plasma
B
Hepatic first pass metabolism
C
Lower bioavailability by oral route
D
Extensive protein binding
Ans.
B
Explanation:
Ans. is ‘b’ i.e., Hepatic first pass metabolism
o This question is tricky one as option b & c literally have the same meaning, i.e. any drug with high hepatic first pass metabolism will have lower oral bioavailability.
o But, we use sublingual nitroglycerine to produce immediate relief of symptoms in angina By sublingual route there is direct absortiption into systemic circulation bypassing liver.
“The sublingual route is used when terminating an attack or aborting an imminent one is the aim. The tablet may be crushed under the teeth and spread over buccal mucosa. It acts within 1-2 min because of direct absorption into systemic circulation (bypassing liver where almost 90% is metabolized)”
Q. 8
Nitrates are not used in –
A
CCF
B
Esophageal spasm
C
Renal colic
D
Cyanide poisoning
Q. 8
Nitrates are not used in –
A
CCF
B
Esophageal spasm
C
Renal colic
D
Cyanide poisoning
Ans.
C
Explanation:
Ans. is ‘c’ i.e., Renal colic
Uses of nitrates
Angina pectoris
MI
CHF and acute LVF —> nitroglycerine i.v. can be used Act by decreasing preload (LV filling pressure).
Biliary colic and esophageal spasm (achalasia cardia)
Acute coronary syndrome (unstable angina and non-ST segment elevation Ml).
Cyanide poisoning
Q. 9
Treatment of stable angina include –
A
Nitrates
B
CCBs
C
Streptokinase
D
a and b
Q. 9
Treatment of stable angina include –
A
Nitrates
B
CCBs
C
Streptokinase
D
a and b
Ans.
D
Explanation:
Ans. is ‘a’ i.e., Nitrates & ‘b’ i.e., CCBs
Q. 10
Agent of first choice in an acute attack of Prinzmetal’s angina is –
A
Diltiazem
B
Nitrates
C
Propranolol
D
Verapamile
Q. 10
Agent of first choice in an acute attack of Prinzmetal’s angina is –
o Nitroglycerin is considered the drug of choice for the patient with variant angina.
o Prazosin a selective a-blocker may also be used because it prevents a mediated vasospasm.
o β-blocker’s are contraindicated because they cause constriction of coronary artery due to unopposed a mediated vasoconstriction.
Prevention of variant angina
o In contrast Nitrates are not used for the prevention of variant angina because of delevelopment of tolerance.
o CCBs are the DOC for prevention.
Q. 11
Agent of first choice in an acute attack of Prinzmetal’s angina is:
A
Diltiazem
B
Nitrates
C
Propranolol
D
Verapamil
Q. 11
Agent of first choice in an acute attack of Prinzmetal’s angina is:
A
Diltiazem
B
Nitrates
C
Propranolol
D
Verapamil
Ans.
B
Explanation:
Answer is B (Nitrates)
“Sublingual nitroglycerine is the drug of choice” — CMDT
Nitrates decrease arteriolar and venous tone, reduce preload and afterload, and reduce the oxygen demand of the heart. Nitrates may also improve myocardial blood flow by dilating collateral channels in the presence of increased vasomotor tone, or coronary stenosis.
Q. 12
Aggravation of symptoms of angina in a patient when given nitrates is seen in :
A
Aortic regurgitation
B
Mitral regurgitation
C
Single left coronary artery stenosis
D
Idiopathic hypertrophic subaortic stenosis
Q. 12
Aggravation of symptoms of angina in a patient when given nitrates is seen in :
A
Aortic regurgitation
B
Mitral regurgitation
C
Single left coronary artery stenosis
D
Idiopathic hypertrophic subaortic stenosis
Ans.
D
Explanation:
Answer is D (Idiopathic Hypertrophic Sub Aortic Stenosis):
Idiopathic hypertrophic subaortic stenosis (HOCM) is a dynamic outflow obstruction which is increased by any mechanism decreasing the preload. Nitrates decrease the preload, & the volume of blood in LV & thereby increase the dynamic obstruction & symptoms of angina.
Q. 13
A 35-year-old farmer consulted a local medical practitioner for recurrent attacks of chest pain. His elder brother had similar complaints and had died suddenly at the age of 40 years. The farmer was advised to take nitroglycerine sublingually at the time of pain. However, the patient finds that the intensity of pain is increased by nitroglycerine. Most probably, he is suffering from :
A
Subacute bacterial endocarditis involving the aortic valve.
B
Hypertrophic obstructive cardiomyopathy.
C
Degenerative mitral regurgitation
D
Chronic Type A dissection of aorta.
Q. 13
A 35-year-old farmer consulted a local medical practitioner for recurrent attacks of chest pain. His elder brother had similar complaints and had died suddenly at the age of 40 years. The farmer was advised to take nitroglycerine sublingually at the time of pain. However, the patient finds that the intensity of pain is increased by nitroglycerine. Most probably, he is suffering from :
A
Subacute bacterial endocarditis involving the aortic valve.
B
Hypertrophic obstructive cardiomyopathy.
C
Degenerative mitral regurgitation
D
Chronic Type A dissection of aorta.
Ans.
B
Explanation:
Answer is B (Hypertrophic obstructive cardiomyopathy)
Family history of the disease and aggravation of symptoms with the intake of Nitroglycerine (Nitrates) nugget the diagnosis of Hypertrophic obstructive cardiomyopathy.
Q. 14
Best time to administer long term nitrates for nocturnal angina:
September 2011
A
Early morning
B
Noon
C
Evening
D
Late night
Q. 14
Best time to administer long term nitrates for nocturnal angina:
September 2011
A
Early morning
B
Noon
C
Evening
D
Late night
Ans.
C
Explanation:
Ans. C: Evening
If nocturnal angina is a predominant symptom, long term nitrates can be given at the end of the day
Nitrates:
They cause vasodilation, flushing, headache, dizziness, met-hemoglobinemia
Decreases preload and afterload
Decreases myocardial oxygen consumption
Causes reflex tachycardia, hypotension
Long acting nitrates are not used chronically as tolerance develops
*Shortest acting NITRITE: Amyl nitrite
Shortest acting nitrate: Nitroglycerine
Longest acting nitrate: Penta-erythritol-nitrate
Q. 15
Transdermal patch is not used for following drug‑
A
GTN
B
Fentanyl
C
Nicotine
D
Naloxone
Q. 15
Transdermal patch is not used for following drug‑
A
GTN
B
Fentanyl
C
Nicotine
D
Naloxone
Ans.
D
Explanation:
Ans. is `d’ i.e., Naloxone
Q. 16
Tachycardia due to nitrates in a patient with angina pectoris is blocked by‑
A
Digoxin
B
Dobutamine
C
Beta blocker
D
Calcium channel blocker
Q. 16
Tachycardia due to nitrates in a patient with angina pectoris is blocked by‑
A
Digoxin
B
Dobutamine
C
Beta blocker
D
Calcium channel blocker
Ans.
C
Explanation:
Ans. is ‘c’ i.e., Beta blocker
Use of beta blocker and long acting nitrate combination is rational in classical angina because :
Tachycardia due to nitrate is blocked by beta blocker
The tendency of beta blocker to cause ventricular dilatation is countered by nitrate
The tendency of beta blocker to reduce the total coronary flow is opposed by nitrate
Q. 17
All of the following statements about antianginal action of nitrates are true except‑
A
L Myocardial 02 consumption
B
Both pre and after load
C
I Total coronary flow
D
Cause favourable redistribution of coronary flow
Q. 17
All of the following statements about antianginal action of nitrates are true except‑
A
L Myocardial 02 consumption
B
Both pre and after load
C
I Total coronary flow
D
Cause favourable redistribution of coronary flow
Ans.
C
Explanation:
Ans. is ‘c’ i.e., 1‘ Total coronary flow
Pharmacological actions of nitrates
The only major action is direct nonspecific smooth muscle relaxation. The most prominant action is exerted on vascular smooth muscles.
Preload reduction – Nitrates dilate veins more than arteries decreased venous return (preload) → decreased end diastolic size and pressure → decreased O2 consumption.
Afterload reduction – Nitrates also produce some arteriolar dilatation → slightly decreased total peripheral resistance (afterload).
Redistribution of coronary flow –
There are two types of vessels in coronary circulation.
Larger conducting arteries which run epicardially and send perforating branching to deeper tissue (endocardium).
Smaller resistance arterioles – These are the perforating branches of larger conducting arteries. These arterioles supply blood to endocardium. Ischemia causes dilatation of these vessles by autoregulatory mechanism.
Nitrates preferentially dilate bigger conducting vessels. This pattern of action cause favourable redistribution of blood to ischemic zone because the smaller resistance vessels in ischemic zone are dilated by autoregulatory mechanism, while smaller resistance vessels in non ischemic zone are not dilated → blood supply of ischemic zone is increased.
Nitrates do not appreciably increase total coronary flow in angina patients.
The dilator effect on larger coronary vessels is the principal action of nitrates benefiting variant angina by counteracting coronary spasm.
In classical angina, primary effect is to reduce cardiac wark.
Other smooth muscles – Nitrates cause relaxation of bronchi, biliary tract, esophagus → can be used in biliary colic and esophageal spasm.
Mechanism of action
Organic nitrates are rapidly denitrated enzymatically in the smooth muscle cell to release nitric oxide (NO) which activates cytosolic guanyl cyclase → rcGMP →Vasodilatation.
Veins express greater amount of the enzyme that generates NO from organic nitrates than arteries – Account for the predominant venodilatory effect.
Remember
The NO generated from nitrates activates cGMP production in platelets as well mild antiaggregatory effect.
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Massive engorgement, congestion and tortuosity of retinal veins
Whole fundus is full of hemorrhages giving a tomato splash appearance or blood and thunder appearance
Cotton wool spots
Marked macular hemorrhage
and edema
Late stages:
Marked sheathing around veins
Collaterals around the disc
Neovascularization at the disc (NVD) or at the periphery (NVE)
Mar
ked pigmentary changes in the macula & CME
COMPLICATIONS:
Rubeosis iridis
Neovascular glaucoma within 3 months (90 or 100 days glaucoma)
Vitreous hemorrhage
Proli
ferative retinopathy
TREATMENT:–
Panretinal photocoagulation (PRP)
CRAO( CENTRAL RETINAL ARTERIAL OCCLUSION)
ETIOLOGY
EMBOLI FROM CAROTID ARTERY
VALVULAR HEART DISEASES
THROMBUS FROM ARTERIO SCLEROSIS
HYPERTENSION
ARTERITIS.
ORBITAL MUCORMYCOSIS
SYMPTOMS:
PAINLESS SUDDEN UNILATERAL LOSS OF VISION
SIGNS:
LARGER ARTERIES THREAD LIKE AND ARTERIOLES ARE INVISIBLE.
VEINS NORMAL .
FEW HOURS THE RETINAL LOSES ITS TRANSPARENCY AND BECOME MILKY WHITE.
NEOVASCULAR GLAUCOMA
CHERRY RED SPOT
CATTLE TRACK APPEARANCE.
TREATMENT:
DIGITAL MASSAGE.
IV ACETAZOLAMIDE.
5% CO2 AND 95% O2 MIXTURE OF 10 MIN.
PARACENTSIS.
RETROBULBAR INJECTION OF ACETYLCHOLINE.
ANTI COAGULANTS.
Exam Question
Cattle track appearance in fundoscopy is due to CRAO
Sudden loss of vision is seen in CRAO & CRVO
Central Retinal Venous Occlusion (CRVO) from Ocular Ischemic Syndrome can be differentiated on the basis of Tortuous Retinal Vein,Retinal Artery Pressure, Ophthalmodynamometry
Cherry red spot on the macula in Fundus examination of a patient presenting with loss of vision is seen in CRAO
Rubeosis iridis is seen in CRVO
CRAO may be seen in Orbital mucormycosis
Neovascular glaucoma can occur in both CRAO & CRVO
CRAO REF: Elsevier Comprehensive Guide, page 628 Common fundoscopy findings:
Condition
Finding
Optic disc coloboma
Morning glory appearance
CRAO
Cattle track appearance
CRVO
Blood and thunder fundus
Chloroquine toxicity
Bull’s eye maculopathy
Quinine toxicity
Cherry red spot
Retinitis pigmentosa
Waxy pallor of optic disc
Bone spicule pigmentation
Congenital syphilis/ Rubella
Salt and pepper fundus
Sickle cell anemia
Rising sun sign
CMV retinitis
Mozzarella pizza fundus
AIDS
Cotton wool spots
Q. 2
Sudden loss of vision is seen in following, except:
A
CRAO
B
CRVO
C
Optic neuritis
D
Papilledema
Q. 2
Sudden loss of vision is seen in following, except:
A
CRAO
B
CRVO
C
Optic neuritis
D
Papilledema
Ans.
D
Explanation:
Papilledema (choked disk) is usually a symptom of increased intracranial pressure caused by a mass, such as a brain tumor. The increased pressure is transmitted to the optic disk through the extension of the subarachnoid space around the optic nerve. Papilledema caused by a sudden increase in intracranial pressure develops within 24 to 48 hours. Visual acuity is not affected in papilledema, although the blind spot may be enlarged.
Ref :Chang D.F. (2011). Chapter 2. Ophthalmologic Examination. In P. Riordan-Eva, E.T. Cunningham, Jr. (Eds), Vaughan & Asbury’s General Ophthalmology, 18e.
Q. 3
All of the following may be used to differentiate Central Retinal Venous Occlusion (CRVO) from Ocular Ischemic Syndrome due to, except:
A
Dilated Retinal Vein
B
Tortuous Retinal Vein
C
Retinal Artery Pressure
D
Ophthalmodynamometry
Q. 3
All of the following may be used to differentiate Central Retinal Venous Occlusion (CRVO) from Ocular Ischemic Syndrome due to, except:
A
Dilated Retinal Vein
B
Tortuous Retinal Vein
C
Retinal Artery Pressure
D
Ophthalmodynamometry
Ans.
A
Explanation:
Central Retinal Vein Occlusion and Ocular Ischemic Syndrome due to carotid artery stenosis are both associated with Dilated Retinal veins and hence this feature cannot be used to distinguish these conditions.
Ref: Ophthalmology By Yanoff, 3rd Edition, Page 625; Ocular Therapeutics Handbook: A Clinical Manual, 2nd Edition, Page 86
Q. 4
Fundus examination of a patient presenting with loss of vision revealed a Cherry red spot on the macula. What is he most likely suffering from?
A
Retinitis pigmentosa
B
Retinoblastoma
C
CRAO
D
CRVO
Q. 4
Fundus examination of a patient presenting with loss of vision revealed a Cherry red spot on the macula. What is he most likely suffering from?
A
Retinitis pigmentosa
B
Retinoblastoma
C
CRAO
D
CRVO
Ans.
C
Explanation:
Cherry red spot on the retina is seen in central retinal artery occlusion. Other retinal signs in this condition includes retinal oedema and segmentation of blood column in the retinal vein (cattle tracking sign). Patients often presents with sudden painless loss of vision.
Reference: Comprehensive Ophthalmology By A K Khurana, 4th Edition, Page 255.
Q. 5
Rubeosis iridis is NOT COMMONLY seen in:
A
CRVO
B
CRAO
C
Diabetic retinopathy
D
Neovascularization
Q. 5
Rubeosis iridis is NOT COMMONLY seen in:
A
CRVO
B
CRAO
C
Diabetic retinopathy
D
Neovascularization
Ans.
B
Explanation:
Rubeosis iridis or neovascularization of iris is a medical condition of the iris in which new blood vessels are found on the surface of the iris. It is associated with conditions which cause ischemia of the retina. Conditions commonly associated with rubeosis iridis are central retinal vein occlusion, proliferative diabetic retinopathy, ocular ischemic syndrome, ocular surgery complication and chronic retinal detachment. Rubeosis iridis may also be associated with CRAO but is less common than with CRVO.
Ischemic diseases of the retina causes the release of VEGF which in turn stimulate angiogenesis. They can be seen on the iris, and it can also grow into the angle of the eye resulting in an increase in intra ocular pressure.
Ref: Glaucoma Surgery edited by Ashok Garg, page 350, Ocular Angiogenesis: Diseases, Mechanisms, and Therapeutics edited by Joyce Tombrain-Tink, PAGE 128.
Q. 6
Cherry red spot is seen in all of the following conditions, EXCEPT:
A
CRAO
B
Tay Sach’s disease
C
Niemman pick’s disease
D
Central retinal vein occlusion
Q. 6
Cherry red spot is seen in all of the following conditions, EXCEPT:
A
CRAO
B
Tay Sach’s disease
C
Niemman pick’s disease
D
Central retinal vein occlusion
Ans.
D
Explanation:
Cherry red spots of the macula are produced when ganglion cells filled with lipid degenerate thereby exposing the vascular choroidal tissue behind these cells. Central retinal vein occlusion is not associated with cherry red spot. In CRVO retina appears congested with large areas of flame hemorrhages.
Conditions associated with cherry red spot:
Central retinal artery occlusion
Tay sachs disease
Farber’s disease
Sandhoff’s disease
Neimann Pick disease
Goldberg’s syndrome
Gaucher’s disease
Gangliosidase GM1 type 2
Hurler’s syndrome
Ref: Ophthalmology edited by Myron Yanoff, 3rd edn page 590
Q. 7
All of the following conditions exhibit cherry red spot on retina, EXCEPT:
A
CRAO
B
Tay Sach’s disease
C
Niemann pick’s disease
D
Central retinal vein occlusion
Q. 7
All of the following conditions exhibit cherry red spot on retina, EXCEPT:
A
CRAO
B
Tay Sach’s disease
C
Niemann pick’s disease
D
Central retinal vein occlusion
Ans.
D
Explanation:
Conditions diseases displaying a cherry-red macular spot:
Central retinal artery occlusion
Commotio retinae (Berlin’s edema)
GM1 gangliosidosis
GM2 gangliosidosis (Tay-Sachs and Sandhoff type)
Sialidosis
Niemann-Pick disease types A to D (not E and F); ring may be diffuse and indistinct
Farber lipogranulomatosis
Metachromatic leukodystrophy
Neuronal ceroid lipofuscinosis, late infantile form (“bull’s-eye” maculopathy, not true cherry-red spot)
Ref: Ropper A.H., Samuels M.A. (2009). Chapter 37. Inherited Metabolic Diseases of the Nervous System. In A.H. Ropper, M.A. Samuels (Eds), Adams and Victor’s Principles of Neurology, 9e.
Q. 8
Cherry red spot is seen in the fundus of patients with all of the following conditions, EXCEPT:
A
CRAO
B
Tay Sach’s disease
C
Niemman pick’s disease
D
Central retinal vein occlusion
Q. 8
Cherry red spot is seen in the fundus of patients with all of the following conditions, EXCEPT:
A
CRAO
B
Tay Sach’s disease
C
Niemman pick’s disease
D
Central retinal vein occlusion
Ans.
D
Explanation:
Central retinal vein occlusion is characterized by diffuse retinal hemorrhages in all quadrants and dilated and tortuous retinal veins. There can be few scattered retinal hemorrhages with a few cotton wool spots to very extensive retinal hemorrhage throughout the fundus.
Conditions with cherry red spots are:
Central retinal artery occlusion
Tay Sach’s disease
Niemann pick’s disease
Gaucher’s disease
Faber’s disease
Hurler’s syndrome
Ref: Ophthalmology edited by Myron Yanoff, page 590 , Atlas of Fundus Fluorescein Angiography By Pukhraj Rishi chapter 27.
Q. 9
Cherry red spot on retina is seen in A/E
A
CRAO
B
CRVO
C
Nieman-pick diseases
D
Tay-sach’s disease
Q. 9
Cherry red spot on retina is seen in A/E
A
CRAO
B
CRVO
C
Nieman-pick diseases
D
Tay-sach’s disease
Ans.
B
Explanation:
B i.e. CRVO
Q. 10
CRAO may be seen in
A
Diabetes mellitus
B
CMV retinitis
C
Panophthalmitis
D
Orbital mucormycosis
Q. 10
CRAO may be seen in
A
Diabetes mellitus
B
CMV retinitis
C
Panophthalmitis
D
Orbital mucormycosis
Ans.
D
Explanation:
D i.e. Orbital mucormycosis
– Most of central retinal artery obstruction (CRAO) are caused by atherosclerotic thrombus formation at or just proximal to the lamina cribrosaQ (-80%) followed by emboli (20%). Inflammation in form of vasculitis (eg varicella infection), optic neuritis or even orbital disease (eg mucormycosis)Q, local trauma and radiation may also cause CRAO.
Vascular tropism/ invasion is the hallmark of orbital mucomycosis. This along with thrombosis b/o inflammatory process results in CRAO.
In CRAOQ, when obstruction to blood flow is not complete, the flow may be partially restored in the course of a few days in which case gentle pressure upon the globe may break up the column of venous blood (in retinal veins)Q into red beads separated by clear interspaces. The beads move in jerky fashion sometimes in normal direction of blood flow & sometimes in the opposite direction – The “Cattle Truck Appearance”. Central retinal artery occlusion characteristically presents with sudden (not gradual) painless loss of vision, cherry red spotQ and cattle truck appearanceQ of retinal veins (usually).
Q. 11
All of the following may be used to differentiate Central Retinal Venous Occlusion (CRVO) from Ocular Ischemic Syndrome due to Carotid Artery Stenosis, Except:
A
Dilated Retinal Vein
B
Tortuous Retinal Vein
C
Retinal Artery Pressure
D
Opthalmodynamometry
Q. 11
All of the following may be used to differentiate Central Retinal Venous Occlusion (CRVO) from Ocular Ischemic Syndrome due to Carotid Artery Stenosis, Except:
A
Dilated Retinal Vein
B
Tortuous Retinal Vein
C
Retinal Artery Pressure
D
Opthalmodynamometry
Ans.
A
Explanation:
A i.e. Dilated Retinal Vein
Central Retinal Vein Occlusion and Ocular Ischemic Syndrome due to carotid artery stenosis are both associated with dilated retinal veins and hence this feature cannot be used to distinguish these conditions. However, ophthalmic artery pressure (measured by ophthalmo dynamometry) and retinal artery pressure is usually normal in CRVO and decreased (low) in carotid artery obstruction. And to differentiate both conditions other features include presence of swollen optic disc & tortuous retinal veins in CRVOQ. Ophthalmodynamometry is a non invasive method of estimating ophthalmic artery pressure.
Features
Ocular Ishemic Syndrome
(Carotid Artery Obstruction)
CRVO (Non Ischaemic)
(Central Retinal Vein Obstruction)
Definition
Ocular Ischemic Syndrome is a condition
with variable spectrum of sign and
symptoms resulting from chronic ocular
hypoperfusion usually secondary to
severe carotid artery obstruction.
Pathogenesis of this syndrome is
decreased arterial inflow on a chronic
basis
CRVO is an ocular syndromes with
ocular signs and symptoms resulting
from an occlusion of the central
retinal vein
– Ischemic : Complete obstruction (20‑
25% of cases)
– Non ischaemic : Incomplete
obstruction (70-75% of cases)
Laterality
Unilateral (80%)
Unilateral
Age (years)
50-80
50-80
Fundus
signs
Veins
Dilated, nontortuous
Dilated, tortuous
Optic disc
Normal
Swollen
Retinal artery
perfusion pressure
Decreased
Normal
Retinal
hemorrhages
Mild
Mild to severe
Microaneurysms
Mid-periphery
Variable
Hard exhudates
Absent unless in association with diabetes
Rare
Fluorescein
Angiography
Choroidal filling
Delayed, patchy
Normal
Arteriovenous
transit time
Prolonged
Prolonged
Retinal vessel
staining
Prominent arterial staining
Prominent venous staining
Ophthalmodynamometry
(non invasive)
Ophthalmic artery pressure is usually
lowQ
Ophthalmic artery pressure is usually
normal or elevated
Q. 12
Rubeosis iridis is not seen in:
A
CRVO
B
CRAO
C
Diabetic retinopathy
D
Neovascularization
Q. 12
Rubeosis iridis is not seen in:
A
CRVO
B
CRAO
C
Diabetic retinopathy
D
Neovascularization
Ans.
B
Explanation:
B i.e. CRAO
Q. 13
Painless sudden visual loss is seen in all except
A
CRAO
B
Retinal detachment
C
Vitreous hemorrhage
D
Angle closure glaucoma
Q. 13
Painless sudden visual loss is seen in all except
A
CRAO
B
Retinal detachment
C
Vitreous hemorrhage
D
Angle closure glaucoma
Ans.
D
Explanation:
D i.e. Angle closure glaucoma
Angle closure glaucoma is a cause of painful, not painless loss of visionS2
Q. 14
Rubeosis iridis is not seen in:
A
CRVO
B
CRAO
C
Diabetic retinopathy
D
Neovascularization
Q. 14
Rubeosis iridis is not seen in:
A
CRVO
B
CRAO
C
Diabetic retinopathy
D
Neovascularization
Ans.
B
Explanation:
B i.e.CRAO
Q. 15
Neovascular glaucoma can occur in all except:
A
Diabetes mellitus
B
Hypertension
C
CRAO
D
CRVO
Q. 15
Neovascular glaucoma can occur in all except:
A
Diabetes mellitus
B
Hypertension
C
CRAO
D
CRVO
Ans.
B
Explanation:
Ans. Hypertension
Q. 16
Vitreous haemorrhage is seen in all except:
A
Coat’s disease
B
Eales’ disease
C
CRVO
D
CRAO
Q. 16
Vitreous haemorrhage is seen in all except:
A
Coat’s disease
B
Eales’ disease
C
CRVO
D
CRAO
Ans.
D
Explanation:
Ans. CRAO
Q. 17
All of the following may be used to differentiate central retinal venous occlusion (CRVO) from ocular ischemic syndrome due to carotidartery stenosis, except:
A
Dilated retinal vein
B
Tortuous retinal vein
C
Retinal artery pressure
D
Ophthalmodynamometry
Q. 17
All of the following may be used to differentiate central retinal venous occlusion (CRVO) from ocular ischemic syndrome due to carotidartery stenosis, except:
A
Dilated retinal vein
B
Tortuous retinal vein
C
Retinal artery pressure
D
Ophthalmodynamometry
Ans.
A
Explanation:
Ans. Dilated retinal vein
Q. 18
Neovascular glaucoma is caused by:
A
CRVO
B
CRAO
C
Diabetes mellitus
D
All of the above
Q. 18
Neovascular glaucoma is caused by:
A
CRVO
B
CRAO
C
Diabetes mellitus
D
All of the above
Ans.
D
Explanation:
Ans. D: All of the above
Although NVG primarily effects the front part of the eye (anterior chamber), its cause usually is associated with a lack of oxygen to the retina in the posterior region (vitreous chamber).
The technical term for this lack of oxygen is retinal hypoxia.
Conditions leading to retinal hypoxia include diabetic retinopathy and central retinal vein occlusion (CRVO).
These two diseases account for about two-thirds of all NVG cases.
The predisposing condition for diabetic retinopathy obviously is diabetes.
With respect to CRVO, predisposing conditions include elevated intraocular pressure and systemic hypertension (high blood pressure).
The remaining one-third of NVG cases has less-common causes. Among these are:
Central retinal artery occlusion (CRAO)
Carotid artery obstructive disease
Rhegmatogenous retinal detachment (a tear in the retina with fluid accumulating underneath that can further separate the pigment layer from other layers).
Choroidal melanoma beneath a retinal detachment.
Sickle-cell retinopathy
Carotid-cavernous fistula
A causative condition for NVG that is not associated with retinal hypoxia, is chronic anterior uveitis (irritation of the middle layer of the eye).
Q. 19
Hundred day glaucoma is associated with:
A
Neovascular glaucoma
B
CRAO
C
CRVO
D
Steroid-related glaucoma
Q. 19
Hundred day glaucoma is associated with:
A
Neovascular glaucoma
B
CRAO
C
CRVO
D
Steroid-related glaucoma
Ans.
C
Explanation:
Ans. C: CRVO
Occurrence of neovascular glaucoma in many patients with CRVO is observed in a span of three months, or 100 days, from the onset of occlusion.
Diabetes is a primary risk factor for CRVO, along with elevated blood cholesterol, and high blood pressure.
CRVO is an acute event
Q. 20
Cherry red spot is seen in:
September 2010March 2013
A
CRVO
B
CRAO
C
Eale’s disease
D
Retinitis pigmentosa
Q. 20
Cherry red spot is seen in:
September 2010March 2013
A
CRVO
B
CRAO
C
Eale’s disease
D
Retinitis pigmentosa
Ans.
B
Explanation:
Ans. B: CRAO
The cherry red spot is seen in central retinal artery occlusion, appearing several hours after the blockage of the retinal artery occurs.
The cherry red spot is seen because the macula receives its blood supply from the choroid artery while the surrounding retina is pale due to retinal artery infarction.
It is also seen in several other conditions, classically Tay-Sachs Disease, but also in Niemarm-Pick Disease, Sandhoff disease, and mucolipidosis.
Q. 21
Following are the causes of painless sudden onset of loss of vision except ‑
A
Acute congestive glaucoma
B
Vitreous hemorrhage
C
CRAO
D
Central serous retinopathy
Q. 21
Following are the causes of painless sudden onset of loss of vision except ‑
A
Acute congestive glaucoma
B
Vitreous hemorrhage
C
CRAO
D
Central serous retinopathy
Ans.
A
Explanation:
Ans. is ‘a’ i.e., Acute congestive glaucoma
Acute congestive glaucoma causes sudden painful loss of vision.
Q. 22
Which of the following is an ocular emergency ‑
A
CRAO
B
Optic neuritis
C
Acute congestive glaucoma
D
All of the above
Q. 22
Which of the following is an ocular emergency ‑
A
CRAO
B
Optic neuritis
C
Acute congestive glaucoma
D
All of the above
Ans.
D
Explanation:
Ans. is ‘d’ i.e., All of the above
Ocular emergencies include those conditions that result in acute, severe pain in association with sudden vision loss, or that may lead to vision loss if left untreated; and traumatic conditions that affect globe or adnexa.
Comon ophthalmic emergencies are :-
Acute congestive glaucoma
Ruptured globe
Ulcerative or traumatic corneal diseases
Optic neuritis
Hyphema
Endophthalmitis
Acute blindness
Orbital cellulitis
Eyelid or conjunctival laceration
Central retinal arterial occlusion (CRAG)
Anterior lens subluxation
Retinal detachment
Q. 23
A 56 year-old female presents with sudden onset loss of vision in her right eye. She a past medical history of hypertension, hyperlipidema and medication-controlled diabetes mellitus type 2. Her medications include aspirin, ramipril, atorvastation and metformin. On examination she has 6/60 vision in her right eye.Fundoscopic picture is given in the image.What is the most probable diagnosis?
A
CRAO
B
CRVO
C
Diabetic retinopathy
D
Hypertensive retinopathy
Q. 23
A 56 year-old female presents with sudden onset loss of vision in her right eye. She a past medical history of hypertension, hyperlipidema and medication-controlled diabetes mellitus type 2. Her medications include aspirin, ramipril, atorvastation and metformin. On examination she has 6/60 vision in her right eye.Fundoscopic picture is given in the image.What is the most probable diagnosis?
A
CRAO
B
CRVO
C
Diabetic retinopathy
D
Hypertensive retinopathy
Ans.
B
Explanation:
Ans:B.) CRVO
‘Blood and thunder’ retinal appearance is shown in the image.
Central retinal vein occlusion (CRVO)
Predisposing factors:
glaucoma
old age
hypertension
diabetes mellitus
hypercoagulable state
atherosclerosis (vein is compressed by adjacent artery)
retrobular compressive lesions (e.g. thyroid disease, orbital tumour)
vasculitis
Examination:
Visual acuity — variable depending on severity and duration since onset
A Marcus-Gunn pupil may be present if ischemic CRVO (relative afferent pupillary defect = RAPD)
A 40 year old male develops excessive hyperventilation.
ABG reveals pH- 7.5, PCO2 24 mmHg, PO2 88 mm of Hg.
Treatment is :
A
Respiratory alkalosis
B
Metabolic alkalosis
C
Respiratory acidosis
D
Metabolic acidosis
Q. 4
A 40 year old male develops excessive hyperventilation.
ABG reveals pH- 7.5, PCO2 24 mmHg, PO2 88 mm of Hg.
Treatment is :
A
Respiratory alkalosis
B
Metabolic alkalosis
C
Respiratory acidosis
D
Metabolic acidosis
Ans.
A
Explanation:
Answer A (Respiratory alkalosis)
There is alkalosis (pH = 7.5) and CO2 is low (alkalosis).
Change in CO2 is in keeping with change in pH and thus the primary cause is respiratory.
The acid base disturbance is thus primary respiratory alkalosis.
Q. 5
An ABG analysis shows : pH 7.2, raised pCO2, decreased HCO3; diagnosis is :
A
Respiratory acidosis
B
Compensated metabolic acidosis
C
Respiratory and metabolic acidosis
D
Respiratory alkalosis
Q. 5
An ABG analysis shows : pH 7.2, raised pCO2, decreased HCO3; diagnosis is :
A
Respiratory acidosis
B
Compensated metabolic acidosis
C
Respiratory and metabolic acidosis
D
Respiratory alkalosis
Ans.
C
Explanation:
Answer is C (Respiratory and metabolic acidosis)
The acid base disorder is therefore both respiratory and metabolic acidosis.
There is acidosis (pH < 7.35).
Raised PCO2 (acidosis) indicates that change in CO2 is in keeping with change in pH.
The respiratory component is therefore primary.
Decreased HCO3 (acidosis) indicates that change in HCO3 is also primary.
The acid base disorder is therefore both respiratory and metabolic acidosis.
Q. 6
A 40 year old male develops excessive hyperventilation. ABG reveals pH- 7.5, PCO2 24 mmHg, PO2 88 mm of Hg. Treatment is :
A
Respiratory alkalosis
B
Metabolic alkalosis
C
Respiratory acidosis
D
Metabolic acidosis
Q. 6
A 40 year old male develops excessive hyperventilation. ABG reveals pH- 7.5, PCO2 24 mmHg, PO2 88 mm of Hg. Treatment is :
A
Respiratory alkalosis
B
Metabolic alkalosis
C
Respiratory acidosis
D
Metabolic acidosis
Ans.
A
Explanation:
Answer A (Respiratory alkalosis) :
There is alkalosis (pH = 7.5) and CO2 is low (alkalosis). Change in CO2 is inkeeping with change in pH and thus the primary cause is respiratory. The acid base disturbance is thus primary respiratory alkalosis.
Q. 7
ABG analysis of a patient on ventilator,shows decreased pCO2, normal pO2, pH 7.5; diagnosis is:
A
Respiratory acidosis
B
Metabolic alkalosis
C
Resp alkalosis
D
Metabolic acidosis
Q. 7
ABG analysis of a patient on ventilator,shows decreased pCO2, normal pO2, pH 7.5; diagnosis is:
A
Respiratory acidosis
B
Metabolic alkalosis
C
Resp alkalosis
D
Metabolic acidosis
Ans.
C
Explanation:
Answer is C (Respiratory akalosis) :
There is alkalosis (pH = 7.5) and CO2 is low (alkalosis). Change in CO2 is inkeeping with change in pH and thus the primary cause is respiratory. The acid base disturbance is thus primary respiratory alkalosis.
Q. 8
An ABG analysis shows : pH 7.2, raised pCO2, decreased HCO3;diagnosis is :
A
Respiratory acidosis
B
Compensated metabolic acidosis
C
Respiratory and metabolic acidosis
D
Respiratory alkalosis
Q. 8
An ABG analysis shows : pH 7.2, raised pCO2, decreased HCO3;diagnosis is :
A
Respiratory acidosis
B
Compensated metabolic acidosis
C
Respiratory and metabolic acidosis
D
Respiratory alkalosis
Ans.
C
Explanation:
Answer is C (Respiratory and metabolic acidosis)
lhe acid base disorder is therefore both respiratory and metabolic acidosis.
There is acidosis (pH < 7.35).
Raised PCO2 (acidosis) indicates that change in CO2 is in keeping with change in p1-1. The respiratory component is therefore primary.
Decreased HCO3 (acidosis) indicates that change in HCO3 is also primary .
The acid base disorder is therefore both respiratory and metabolic acidosis.
Q. 9
A female patient after injury comes to casualty. Her ABG shows low pH, pCO2 high, bicarbonate normal. The diagnosis is:
A
Respiratory alkalosis
B
Respiratory acidosis
C
Metabolic acidosis
D
Metabolic alkalosis
Q. 9
A female patient after injury comes to casualty. Her ABG shows low pH, pCO2 high, bicarbonate normal. The diagnosis is:
A
Respiratory alkalosis
B
Respiratory acidosis
C
Metabolic acidosis
D
Metabolic alkalosis
Ans.
B
Explanation:
Answer is B (Respiratory acidosis)
The acid base disorder is respiratory acidosis.
There is acidosis (pH : low)
Raised pCO2 (acidosis) indicates that the change in CO2 is therefore primary
Normal bicarbonate indicates that there is no alteration in the metabolic component
The acid base disorder therefore is Respiratory acidosis.
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Which of the following inhibits aldosterone synthesis in the adrenal cortex?
A
Adrenocorticotropin (ACTH)
B
Atrial natriuretic peptide (ANP)
C
Angiotensin I
D
Angiotensin II
Q. 1
Which of the following inhibits aldosterone synthesis in the adrenal cortex?
A
Adrenocorticotropin (ACTH)
B
Atrial natriuretic peptide (ANP)
C
Angiotensin I
D
Angiotensin II
Ans.
B
Explanation:
Atrial natriuretic peptide (ANP) inhibits the synthesis of aldosterone in the adrenal cortex. ANP is secreted by atrial cardiocytes and it stimulates the excretion of Na+, accompanied by an increase in water excretion. The inhibitory effect on aldosterone synthesis is partially responsible for the physiological effects of ANP, however other mechanisms (e.g. increase in glomerular filtration rate) are also important in the natriuretic action of ANP. Adrenocorticotropin (ACTH), angiotensin II, and the increase of plasma K+ level are the major physiological stimuli of aldosterone biosynthesis. Angiotensin I, the prohormone form of angiotensin II does not influence directly the aldosterone synthesis in the adrenal cortex.
Ref: Molina P.E. (2013). Chapter 10. Endocrine Integration of Energy and Electrolyte Balance. In P.E. Molina (Ed), Endocrine Physiology, 4e.
Q. 2
Cyclic GMP act on :
A
Insulin
B
Thyroxin
C
Atrial natriuretic peptide
D
Growth harmone
Q. 2
Cyclic GMP act on :
A
Insulin
B
Thyroxin
C
Atrial natriuretic peptide
D
Growth harmone
Ans.
C
Explanation:
C i.e. Atrial natriuretic peptide
Q. 3
ANF is mediated by (ANF: Atrial natriuretic factor):
A
Inositol phosphate
B
DAG
C
CyAMP
D
CyGMP
Q. 3
ANF is mediated by (ANF: Atrial natriuretic factor):
A
Inositol phosphate
B
DAG
C
CyAMP
D
CyGMP
Ans.
D
Explanation:
D i.e. CyGMP
Q. 4
ANP acts at the:
September 2009
A
Proximal tubule
B
Distal tubule
C
Collecting tubule
D
Henle loop
Q. 4
ANP acts at the:
September 2009
A
Proximal tubule
B
Distal tubule
C
Collecting tubule
D
Henle loop
Ans.
C
Explanation:
Ans. C: Collecting tubule
ANP act on the collecting tubule and duct to increase Na+ excretion.
It produce this effect by dilating afferent arterioles and relaxing mesangial cells. Both of these actions increase glomerular filtration. In addition, it act on the renal tubules to inhibit Na+ reabsorption. Other actions include an increase in capillary permeability, leading to extravasation of fluid and a decline in blood pressure. In addition, it relax vascular smooth muscle in arterioles and venules. These peptides also inhibit renin secretion and counteract the pressor effects of catecholamines and angiotensin II.
In the brain, ANP is present in neurons, and an ANP-containing neural pathway projects from the anteromedial part of the hypothalamus to the areas in the lower brainstem that are concerned with neural regulation of the cardiovascular system. In general, the effects of ANP in the brain are opposite to those of angiotensin II, and ANP-containing neural circuits appear to be involved in lowering blood pressure and promoting natriuresis.
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