Cardiology

Question 1

GTN

Mechanism of action

Answer 1

cause release of NO from smooth muscle which increase cGMP which in turn causes relaxation of muscle.

Question 2

Pharmacodynamics of GTN

Answer 2

vein respond at a lower drug concentration then art.
venodilation, reduced venous return, reduced LVEDV(reduced preload) reduced LV wall tension, reduced o2 consumption. reduced cardiac output in normal person, incr in pathological.
coronary art dil- relieves spasm
arterial dilation causes headache also reduced after load
GTN also relaxes Bronchial SM(APO) + GI SM
Decrease Platelet Aggregation

Question 3

Toxicity of GTN

Answer 3

Hypotension
Reflex tachycardia
Headache
Tolerance

Question 4

B-Blocker- Pharmacokinetics

Answer 4

well absorbed orally
Low bioavailability
undergoes first pass metabolism hence oral dose more than IV
Lipid soluble- High VD
half life Metoprolol 3-6 hours, Atenolol 6-9 hours
Metabolized by liver
Excreted by Kidney

Question 5

B-Blocker- effects

Answer 5

CVS- Negative inotopic and chronotropic
         Slows AV conduction
         unopposed alpha effect lead to inc vascular resistance 
Resp- Bronchospasm
Eyes- Decreased IO pressure

Question 6

B-Blocker-Toxicity

Answer 6

Hypotension, Bradycardia
Bronchospasm
Sedation, seizures

Question 7

Osmotic diuretics-MOA

Answer 7

Filtered freely from glomeruli, not reabsorbed. Causes water retention in the permeable sections of nephron PCT +Descending LOH

Question 8

Mannitol- Clinical use

             Toxicity

Answer 8

Raised ICP
Diuresis in Rhabdomyolysis

Hypernatremia, extracellular volume expansion

Question 9

Acetazolamide-MOA

Answer 9

Carbonic anhydrase inhibitor
causing depression of bicrbonate reabsorption in thr prox tubule
causing reduced synthesis of bicarbonate synthesis in the ciliary body

Question 10

Acetazolamide-Toxicity

Answer 10

Metabolic acidosis
glucoma
hepatic encephalopathy in cirrohsis pt
neurological toxicity in Renal Failure
renal stones

Question 11

Digoxin MOA

Answer 11

inhibit NaK ATPase pump-Inc Na inside cell swapped for Ca

Plus Inc ECF K

Question 12

Digoxin Cardiac effect

Autonomic effect

Answer 12

Inc contractility
IncK brief prolongation of AP
followed by Shortening AP due to Ca
toxic doses leads to depolarising afterpotientials leading to ECTOPIC/VT/VF

vagal stimulation enhanced parasympthathetic effect

Question 13

Digoxin Toxicity

Answer 13

toxic doses leads to depolarising afterpotientials leading to ECTOPIC/VT/VF

GIT NVD
CNS disorientation hallucination
Hyperkalemia

Question 14

salicylate toxicity

Answer 14

salicylism-dec hearing vertigo tinnitus
GIt disturbance including gastritis bleeding
CNS-coma
Metabolic acidosis
Resp alkalosis