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Digoxin

Digoxin


DIGOXIN:

  • 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:

Diureticsamphotericin 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

Digoxin

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 digoxin concentration 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 digoxin concentration 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.

Reduced tolerance to digoxin may be seen in :

  • Advanced age Q
  • Acute myocardial infarction Q / ischaemia / hypoxemia
  • Magnesium depletion
  • Hypercalcemia Q
  • Hypothyroidism e
  • Renal insufficiency Q
  • Electrical cardioversion.

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



Glyceryl Trinitrate

Glyceryl Trinitrate


NITRATES:

  • Prodrugs that are sources of nitric oxide (NO).

Drugs include: 

  • Glyceryl trinitrate (Nitroglycerin/NTG).
  • Isosorbide mononitrate.
  • Isosorbide dinitrate

MECHANISM OF ACTION:

  • Organic nitrates forms reactive gaseous free radical NO & it’s related NO-containing compounds.

NO activates guanylyl cyclase:

  • Increases cellular cyclic GMP level, activates PKG, & modulates cyclic nucleotide phosphodiesterases activity.
ADMINISTRATION
  • NTG given by sublingual route because of hepatic first pass metabolism
  • Transdermal patch can be used for GTN.
AVAILABLE DRUGS:
  • Pentaerythritol tetranitrate – Longest acting by inhalation route.
  • Amyl nitrate – Shortest acting drug.

ACTION:

  • Promote relaxation of vascular smooth muscle.
  • Bronchial smooth muscle relaxed irrespective of preexisting tone.
  • Relaxes ureteral & uterine smooth muscle.
  • Muscles of biliary tract, including gallbladder, biliary ducts, & sphincter of Oddi – Effectively relaxed.
  • Smooth muscle of GI tract, including oesophagus – Relaxed & decreases spontaneous motility.

Low concentrations of NTG:

  • Dilates veins more than arterioles
  • Decreases venous return.
  • Reduces left & right ventricular chamber size.
  • Systemic arterial pressure may fall slightly.

Higher doses of NTG:

  • Further venous pooling.
  • Decreases arteriolar resistance, blood pressure & cardiac output
  • Results in pallor, weakness, dizziness, & activation of compensatory sympathetic reflexes.

Reduces myocardial O2 demand 

  • Decreases preload & afterload.
  • Dilates coronary arteries & increases coronary blood flow.
  • Limits platelet aggregation/adhesion.
  • Long-term use of nitrates leads to tolerance (decreased efficiency).
  • Due to its SH group in enzyme.
  • Not seen with sublingual route.
  • Melosidomine – Emerging non-tolerant drug.

USES:

  • Stable angina pectoris
  • CCF
  • Unstable angina pectoris and NSTEMI
  • Acute myocardial infarction
  • Prinzmetal angina
  • Portal hypertension
  • Asthma  and as a diuretic (obsolete)
  • Cyanide poisoning – Mainly Amyl nitrate & sodium nitrate
  • Oesophagal Spasm.
  • DOSE:

NITROGLYCERINE DOSE:

ROUTE DOSE DURATION
Sublingual 0.3-0.6 to 1.5mg 10 min
spray 0.4mg 10min
Ointment

2%6×6″ 15x15cm

7.5 to 40mg

7hrs
Transdermal 0.2-0.8mg/hr every 12hr 8-12hr intermittent 
Oral sustained release 2.5-13mg  4-8 hrs
Intravenous  5-200mcg/min 7-8 hrs

ADVERSE EFFECT:

  • Headache.
  • Transient episodes of dizziness.
  • Weakness.
  • Manifestations of postural hypotension.

High doses of organic nitrates causes:

  • Postural hypotension.
  • Facial flushing.
  • Tachycardia (blocked by beta blocker).
  • Prolonged therapy causes endothelial dysfunction
  • Vasodilatation.

Methemoglobinemia – 

  • Nitrates convert hemoglobin to methhemoglobin.
  • High affinity for cyanide ions.
  • Aggravation of angina symptoms in Idiopathic hypertrophic subaortic stenosis, on nitrate administration.

INTERACTION:

With Phosphodiesterase V inhibitors:

  • Sildenafil & Vardenafil potentiates nitrates action.
  • May result in dangerous hypotension.
  • Due to excess cGMP by nitrates.
Exam Question
 
  • CCF, oesophageal spasm & cyanide poisoning can be treated by Nitrates 
  • Nitroglycerine causes methemoglobinemia, vasodilatation, hypotension & tachycardia.
  • Nitrates act in CCF by decreasing preload.
  • 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

Glyceryl Trinitrate

GLYCERYL TRINITRATE

Q. 1

Nitrates are not used in 

 A

CCF

 B

Esophageal spasm

 C

Renal Colic

 D

Cyanide poisoning

Q. 1

Nitrates are not used in 

 A

CCF

 B

Esophageal spasm

 C

Renal Colic

 D

Cyanide poisoning

Ans. C

Explanation:

Renal colic [Ref: KDT 6th/e p. 524-530]

The main pharmacological action of Nitrates

  • 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).

 Nitrates preferentially dilates larger conducting vessels.

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) decreases end 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:

  1. Hypotension
  2. 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

  1. Angina pectoris
  2. MI
  3. CHF and acute LVF —> nitroglycerine i.v. can be used Act by decreasing preload (LV filling pressure).
  4. Biliary colic and esophageal spasm (achalasia cardia)
  5. Acute coronary syndrome (unstable angina and non-ST segment elevation Ml).
  6. 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 –

 A

Diltiazem

 B

Nitrates

 C

Propranolol

 D

Verapamile

Ans. B

Explanation:

Ans. is ‘b’ i.e., Nitrates

Treatment of variant angina

Drugs are :

1.       Nitrates

2.       Calcium channel blockers (verapamil, diltiazem)

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 :

  1. Tachycardia due to nitrate is blocked by beta blocker
  2. The tendency of beta blocker to cause ventricular dilatation is countered by nitrate
  3. 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.
  1. Larger conducting arteries which run epicardially and send perforating branching to deeper tissue (endocardium).
  2. 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.


Crvo & Crao

Crvo & Crao


CRVO (CENTRAL RETINAL VEINOUS OCCLUSION)

Classification

Central retinal vein occlusion

  1. Non ischemic CRVO (venous stasis retinopathy)
  2. Isch
  3. emic CRVO (hemorrhagic retinopathy)

Non-ischemic CRVO

  • Most common type
  • Mild to moderate visual loss
  • No RAPD
  • Fundus examination

Early stages:

  1. Mild venous congestion & tortuosity
  2. Few superficial flame shaped hemorrhages,
  3. Mild papilledema
  4. Mild
  5. or no macular edema

Late stages (after 6-9 months):

  1. Sheathing around the main veins
  2. Cilioretinal collaterals around the disc
  3. C
  4. ystoid macular edema
  • 50% cases resolve spontaneously with normal vision
  • In the rest, visual loss is due to cystoid macular edema (CME)
  • Intravitreal triamcinolone acetonide is given for CME

Ischemic CRVO

  • Acute complete occlusion of central retinal vein
  • Marked sudden visual loss
  • Relative afferent pupillary defect (RAPD) — present
  • Visual field defects
  • Reduced amplitude of b-wave in ERG
  • Fundus examination

Early stages:

  1. Massive engorgement, congestion and tortuosity of retinal veins
  2. Whole fundus is full of hemorrhages giving a tomato splash appearance or blood and thunder appearance
  3. Cotton wool spots 
  4. Marked macular hemorrhage
  5. and edema

Late stages:

  1. Marked sheathing around veins 
  2. Collaterals around the disc
  3. Neovascularization at the disc (NVD) or at the periphery (NVE)
  4. Mar
  5. ked pigmentary changes in the macula & CME

COMPLICATIONS:

  1. Rubeosis iridis
  2. Neovascular glaucoma within 3 months (90 or 100 days glaucoma)
  3. Vitreous hemorrhage
  4. Proli
  5. 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
  • Vitreous haemorrhage is seen in CRVO
  • Hundred day glaucoma is associated with CRVO
  • CRVO & CRAO ‘ blood & thunder ‘ appearance of retina
Don’t Forget to Solve all the previous Year Question asked on Crvo & Crao

Crvo & Crao

CRVO & CRAO

Q. 1

Cattle track appearance in fundoscopy is due to?

 A CRAO
 B

CRVO

 C Retinitis pigmentosa
 D

Diabetic retinopathy

Q. 1

Cattle track appearance in fundoscopy is due to?

 A CRAO
 B

CRVO

 C Retinitis pigmentosa
 D

Diabetic retinopathy

Ans. A

Explanation:

 

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 2010 March 2013

 A

CRVO

 B

CRAO

 C

Eale’s disease

 D

Retinitis pigmentosa

Q. 20

Cherry red spot is seen in:           

September 2010 March 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 :-

  1. Acute congestive glaucoma
  2. Ruptured globe
  3. Ulcerative or traumatic corneal diseases
  4. Optic neuritis
  5. Hyphema
  6. Endophthalmitis
  7. Acute blindness
  8. Orbital cellulitis
  9. Eyelid or conjunctival laceration
  10. Central retinal arterial occlusion (CRAG)
  11. Anterior lens subluxation
  12. 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)
  • Red reflex — may be abnormal
  • Fundoscopy — large areas of hemorrhage:
  • non-ischemic CRVO —
    dilated tortuous veins, retinal hemorrhages, cotton wool spots, retinal edema, disc swelling.
  • ischemic CRVO (more severe) —
    classic ‘blood and thunder’ appearance from widespread hemorrhages that obscure most fundal details. Neovascularisation.



Q. 24

Regarding assesment & management of crvo & crao which statement is incorrect?

 A

In both condition visual loss can be abrupt

 B

 ‘ blood & thunder ‘ appearance of retina

 C

Emergent referral to opthalmology is indicated in both crvo & crao 

 D

No evidence to suggest emergent therapies such as pulse massage of eyeball & intravenous acetazolamide are effective

Q. 24

Regarding assesment & management of crvo & crao which statement is incorrect?

 A

In both condition visual loss can be abrupt

 B

 ‘ blood & thunder ‘ appearance of retina

 C

Emergent referral to opthalmology is indicated in both crvo & crao 

 D

No evidence to suggest emergent therapies such as pulse massage of eyeball & intravenous acetazolamide are effective

Ans. C

Explanation:

C: Emergent referral to opthalmology is indicated in both crvo & crao 

  • In both CRAO & CRVO unilateral visual loss is abrupt & painless. 
  • In CRVO visual loss is present when patient wakes up in morning from blurred vision to complete loss.
  • Optic disc & diffuse retinal hemorrhages can occur in CRVO due to venous stasis edema hence term  blood & thunder used.
  • Unaffected fundus appear normal
  • Immediate referral to opthalmolgist is indicated for CRAO but there is no specific treatment for crvo & patient can visit within few days
  • Medical therapies can be used in ED for CRAO

Q. 25

Regarding CRAo which is true?

 A

Atherosclerosis in carotid arteries & emboli originating in heart are 2 most common cause

 B

Relative afferent pupillary defect is absent

 C

Local intraarterial  thrombolysis has proven benefit

 D

Majority of patient will recover to gain good visual acuity

Q. 25

Regarding CRAo which is true?

 A

Atherosclerosis in carotid arteries & emboli originating in heart are 2 most common cause

 B

Relative afferent pupillary defect is absent

 C

Local intraarterial  thrombolysis has proven benefit

 D

Majority of patient will recover to gain good visual acuity

Ans. A

Explanation:

A;Atherosclerosis in carotid arteries & emboli originating in heart are 2 most common cause



Atrial Blood Gas

Atrial Blood Gas


NORMAL ABG VALUE:

    pH

    PaO2

    PaCO2

    HCO3-

 Base excess

    SaO2

 7.35 – 7.45

80 – 90 mm/Hg

35 – 45 mm/Hg

22-26 mEq/L

+2

95 – 100% 

INDICATIONS:

  • Cardiac Failure
  • Renal or Hepatic Failure
  • Mechanical ventilation
  • Diabetic Ketoacidosis
  • Respiratory Failure Or Dysfunction.
  • Sepsis and burns
  • Poisoning
  • Cardiopulmonary surgery
  • Cardiac pulmonary exercise testing
  • Oxygen administration

CONTRAINDICATIONS:

  • Patients on anticoagulant & those with coagulopathies.
  • Obstructing thrombus in the artery.
  • Patients with poor collateral flow

 PROCEDURE OF ABG ANALYSIS:

  • Use of Intraarterial cannula in major surgery for Sample for ABG

Arterial puncture sites:

  • Wrist :most common site used.
  • Radial artery
  • Brachial artery
  • Femoral artery
  • Dorsalispedis artery

COMPLICATIONS:

  • Hematoma
  • Hemorrhage
  • Arteriospasm
  • Nosocomial  Bacteraemia
  • Distal  Ischemia
  • Numbness of Hand
  • Sepsis
  • Infection of health care worker.

UNCOMPENSATED ABG VALUES

 

pH

PaCO2

HCO3

Respiratory acidosis

↓    

↑ 

Normal

Respiratory  alkalosis

 ↑  ↓

Normal

Metabolic

acidosis

 ↓

Normal

Metabolic

alkalosis

 ↑

Normal

 

   ph

 < 7.35

 7.35-7.45

> 7.45

 Acidosis

 Normal or Compensated

 Alkalosis

 

PaCO2

 < 35  35 -45 > 45
  • Tends toward alkalosis
  • Causes high pH
  • Neutralizes low pH
 Normal or Compensated
  • Tends toward acidosis
  • Causes low pH
  • Neutralizes high pH

 

High pH

Low pH

 Alkalosis

Acidosis

 High PaCO2

Low PaCO2

High PaCO2

Low PaCO2

 Metabolic

Respiratory

Respiratory

Metabolic

 
Exam Question
 
  • In Respiratory and metabolic acidosis ABG analysis show: pH 7.2,↑ PaC02, ↓HC03
  • Reading of ABG analysis as ↓ PaCO2, Normal PaO2 and pH 7.5 shows Respiratory alkalosis
  • Use of Intraarterial cannula in major surgery for Sample for ABG
  • ABG revealing pH- 7.5, PCO2 24 mmHg, PO2 88 mm of Hg with excessive hyperventilation treated for  Respiratory alkalosis
Don’t Forget to Solve all the previous Year Question asked on Atrial Blood Gas

Atrial Blood Gas

Atrial Blood Gas

Q. 1

In which of the following condition does an ABG analysis show: pH 7.2,↑ PaC02, ↓HC03:

 A

Respiratory and metabolic acidosis

 B

Respiratory acidosis

 C

Compensated metabolic acidosis

 D

Respiratory alkalosis

Q. 1

In which of the following condition does an ABG analysis show: pH 7.2,↑ PaC02, ↓HC03:

 A

Respiratory and metabolic acidosis

 B

Respiratory acidosis

 C

Compensated metabolic acidosis

 D

Respiratory alkalosis

Ans. A

Explanation:

The ABG analysis given in the question points to a mixed acid-base disorder, Respiratory acidosis-Metabolic acidosis.
In this condition there is a high or normal anion-gap metabolic acidosis; prevailing PaCO2 above predicted value.
This is seen in conditions like severe pnuemonia, pulmonary edema.
The given Blood Gas analysis profile cannot be explained by either metabolic or respiratory alkalosis alone, even with or without compensation.
 
Ref: Renal and Electrolyte Disorder By Robert.W.Schrier, Page 133 ; Harrison’s Internal Medicine, 18th Edition, Pages 364, 371, 372

Q. 2

A patient put on ventilator shows a reading of ABG analysis as ↓ PaCO2, Normal PaO2 and pH 7.5, what is the likely diagnosis?

 A

Respiratory acidosis

 B

Metabolic alkalosis

 C

Metabolic acidosis

 D

Respiratory alkalosis

Q. 2

A patient put on ventilator shows a reading of ABG analysis as ↓ PaCO2, Normal PaO2 and pH 7.5, what is the likely diagnosis?

 A

Respiratory acidosis

 B

Metabolic alkalosis

 C

Metabolic acidosis

 D

Respiratory alkalosis

Ans. D

Explanation:

The ABG analysis reading in this patient clearly favours for respiratory alkalosis.

 
In respiratory alkalosis:
 
? ↓PaCO2
? ↑ HCO3/PaCO2 ratio
? ↑pH
? the plasma K is often reduced and Cl increased
 
Respiratory alkalosis is commonly seen in anesthetized or mechanically ventilated patient.
 
Ref: Harrison’s Internal Medicine, 18th Edition, Pages 363-372

Q. 3

Use of Intraarterial cannula in major surgery : 

 A

Measurement of direct intra arterial BP

 B

Sample for ABG

 C

Drug injection

 D

All

Q. 3

Use of Intraarterial cannula in major surgery : 

 A

Measurement of direct intra arterial BP

 B

Sample for ABG

 C

Drug injection

 D

All

Ans. D

Explanation:

D. i.e. All


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

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.


Atrial Natriuretic Peptide

Atrial Natriuretic Peptide


ATRIAL NATRIURETIC PEPTIDE

Introduction:

  • A type of peptide hormone causing natriuresis (Increased Naexcretion)
  • Present as granules in atrial muscle cells.
  • Cyclic GMP act on Atrial natriuretic peptide
Regulation of secretion:
  • Released in response to increased plasma Na+ concentration & raised BP.

MAJOR PHYSIOLOGICAL EFFECTS:

  • Mainly acts on Kidney & Blood vessels 
  • Effects of ANP are physiologically antagonistic to angiotensin II

1. Causes natriuresis (Increased Na+ excretion) by

  • Increasing GFR 
  • Relaxing mesangial cells of glomerulus
  • Reducing Na+ reabsorption from distal tubule & collecting ducts.

2. Reduces secretion of renin, aldosterone & ADH.

  • Inhibit ADH-stimulated water reabsorption across collecting ducts.
  • By inhibiting synthesis of aldosterone in the adrenal cortex

3. Reduces BP by,

  • Decreasing total peripheral resistance.
  • Enhancing urinary excretion of NaCl & water.
  • Increasing capillary permeability.

4. Powerful Vasodilator

  • Relaxes vascular smooth muscle in arterioles & venules.
  • Lowers BP.
Specific effects of ANP:
1. Role of ANP in delaying onset of cardiac compensation:
  • Secretion increases on stretching of atrial walls.

Heart failure –

  • Circulating ANP levels increases 5-10 folds
  • Direct effect on kidney on NaCl & water hemostasis 
  • Prevents extreme congestive symptoms during cardiac failure.

2. Biomarker:

  • Used as biomarkers for CVs diseases such as stroke, MI, coronary artery disease & heart failure.
Exam Question
 

ATRIAL NATRIURETIC PEPTIDE

  • ANP causing natriuresis (Increased Naexcretion), by increasing GFR & reducing Na+ reabsorption from distal tubule & collecting ducts.
  • Cyclic GMP act on Atrial natriuretic peptide.
  • Effects of ANP are physiologically antagonistic to angiotensin II, mainly acts on kidney & blood vessels.
  • Reduces secretion of renin, aldosterone & ADH, inhibit ADH-stimulated water reabsorption across collecting ducts.
  • ANP is “Powerful vasodilator” relaxes vascular smooth muscle in arterioles & venules, lowering BP.
Don’t Forget to Solve all the previous Year Question asked on Atrial Natriuretic Peptide

Atrial Natriuretic Peptide

ATRIAL NATRIURETIC PEPTIDE

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

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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