Pharmacology Flashcards
(44 cards)
1
Q
1- Enumerate six factors affecting action & dose of drugs
A
- Biological variation.
- Sex.
- Age.
- Weight & surface area.
- Route of administration.
- Time of administration.
2
Q
2- Enumerate four adverse effects of:
a. Nitrates.
A
- Headache & Flush.
- Tachycardia.
- Tolerance.
- Postural hypotension.
3
Q
2- Enumerate four adverse effects of
b. CCB
A
- Headache & Flush.
- Hypotension.
- Constipation.
- Ankle edema.
4
Q
2- Enumerate four adverse effects of c. Thiazide.
A
- Hypovolemia.
- Hyponatremia.
- Hypokalemia.
- Hypercalcemia.
5
Q
2- Enumerate four adverse effects of d. Spironolactone.
A
- Hyperkalemia.
- Weak diuretic & slow onset.
- Gynecomastia in males, menstrual disturbances in females.
- Decrease action of digitalis.
6
Q
2- Enumerate four adverse effects of e. Frusemide
A
- Hypovolemia.
- Hypokalemia.
- Hypocalcemia.
- Ototoxic.
7
Q
Enumerate four adverse effects of f. ACEI.(Captopril)
A
- Dry cough.
- Angioedema.
- First dose hypotension.
- Bilateral renal artery stenosis.
8
Q
Four disadvantages of Na nitroprusside
A
- Large dose > Severe hypotension.
- Sudden stop > Rebound hypertension.
- Prolonged use in old age > Cyanosis & acidosis.
- Teratogenic.
9
Q
Four disadvantages of Heparin
A
- Hemorrhage.
- Hypersensitivity.
- Hyperkalemia.
- Heparin induced thrombocytopenia.
10
Q
Enumerate four therapeutic uses of loop diuretic
A
- Edema.
- Acute renal failure.
- Hypercalcemia.
- Hypertension.
11
Q
Enumerate four therapeutic uses of Beta blockers (propranolol)
A
- Anxiety.
- Tremors.
- Migraine prophylaxis.
- Glaucoma.
12
Q
Mechanism of action of thiazide as antihypertensive
A
- Direct:
- Open K channels > Hyperpolarization.
- Depletion of Na & water from arterial wall.
- Prostaglandins play a role.
- Diuretic:
- Decrease blood volume.
13
Q
Mechanism of action of nitrates
A
- Release nitric oxide > activates guanylyl cyclase > increase cGMP
- Raised cGMP > reduce Ca entry > relaxation.
- Decrease platelet aggregation.
14
Q
Mechanism of nicorandil as anti-anginal
A
- Like nitrate > release nitric oxide.
- Open K channels > hyperpolarization.
15
Q
Mechanism of action of ACEI
A
- Inhibit conversion of angiotensin l to angiotensin ll
- Decrease vasoconstriction.
- Decrease aldosterone.
- Decrease sympathetic activity.
- Decrease hypertrophy & remodeling of heart.
16
Q
Mechanism of actions of statins
A
- Inhibit HMG-COA reductase.
- Decrease LDL level in plasma.
- Depletion of intracellular cholesterol.
17
Q
Mechanism of action of Digoxin as inotropic
A
- Inhibit Na/K ATPase enzyme > decrease intracellular K & increase
intracellular Na > increase intracellular Ca > increase Ca in cytosol >
increase binding to tropnin > +ve inotropic action.
18
Q
Give reason why Hyoscine better than atropine as preanesthetic medication
A
- No tachycardia.
- Strong antiemetic.
- Strong antisecretory.
- Strong stimulator to respiratory center.
- More CNS depressent.
19
Q
Explain propranolol used in stable not variant angina
A
- In stable angina > to decrease cardiac work & oxygen consumption.
- Not in variant angina > to avoid activity of unopposed alpha receptors.
20
Q
Explain why Beta Blockers + Nitrate is favorable combination.
A
- Nitrate > venodilator > decrease VR > decrease EDV > decrease
preload > reflex stimulation of sympathetic > tachycardia. - Beta blockers > decrease cardiac work & oxygen consumption >
prevent tachycardia induced by nitrates.
21
Q
Explain why Sacuibtril (Neprilysin inhibitor) should be combined with ARBs not ACEI.
A
Because both decrease breakdown of bradykinine lead to increase it’s level in plasma > increase risk of angioedema.
22
Q
Explain why Statins combined with Resin
A
To prevent compensatory increase in rate of biosynthesis cholesterol
induced by resins.
23
Q
Explain why LMW heparin replaced HMW heparin
A
- Adminstrated SC.
- Longer duration.
- No monitoring.
- Less frequent dose.
- Less thrombocytopenia.
- Less hemorrhage.
- More effective & safer.
24
Q
What are the factors of Digoxin toxicity
A
- Hypokalemia.
- Hypercalcemia.
- Hypothyroidism.
- Kidney disease.
25
Digoxin toxicity treatment
* Stop digitalis & K depleting diuretics.
* Monitor digitalis plasma level & electrolytes.
* Activated charcoal.
* Purified fab fragments.
26
Describe the mechanism of action of fibrates
They decrease hepatic triglyceride secretion and increase lipase activity.
They inhibit lipolysis in adipose tissue and decrease FFA supply to liver
They increase HDL
27
Explain why verapamil and nitrates is a favorable combination in treatment of angina
Nitrates cause coronary VD and veno dilation and decrease pre load
Verapamil cause coronary VD + arterio dilation and decrease after load
28
Explain why Beta blocker should not be administered with verapamil
Since both are coronary VD and decrease HR, when combined they would cause severe cardiac inhibition
29
Explain why the combination of spironolactone and ACEIs is not preferred
K retaining diuretics like spironolactone augments the hyperkalemic effects
30
Explain why it is contraindicated to stop the administration of clonidine suddenly
If stopped suddenly, causes rebound hypertensive crisis
31
Explain why Neprilysin inhibitor (sacubitril) must not be used with an ACEI
important substance broken down by neprilysin is bradykinin; neprilysin inhibition will also cause a build-up of bradykinin. Therefore, sacubitril cannot be used with an ACEI due to an increased risk of angioedema
32
Explain why verapmil should not be admistred with digitalis
Verapamil is a calcium channel blocker. Since digitalis increases the activation of Ca an Ca influx into the myocytes, Verapamil would cancel out that effect.
33
Nifedipine and nitrates is an unfavourable combination in treatment of angina
Since Nitrates causes coronary VD and Nifedipine causes potent arterio-dilation, it causes severe hypotension and tachycardia.
34
Explain the Statins pleiotropic effects
Improved endothelial function
Reduced vascular inflammation
Reduced platelet aggregability
anti-thrombin actions
35
Give reason most statins are taken at bed time
Because of diurnal rhythm of cholesterol synthesis
36
Give reason ACEIs can produce dry cough
The dry irritant cough is due to increase of bradykinin and prostaglandins
37
Explain the mechanism of action of Alpha methyl dopa
Stimulate a2 receptors in brain stem--> decrease sympathetic flow from CNS
Stimulate a2 receptors in the kidney ---> decrease release of rennin
Stimulate a2 receptors at the adrenergic nerve endings---> decrease NA release
38
Explain the adverse effects of statins
Increase liver enzymes
Myopathy
Rhabdomyolysis (break down of muscle fibers into blood stream)
39
Compare Heparin and Warfarin in Mechanism, Antidote, Onset and Duration.
Heparin: potentiate effect of antithrombane III--> deactivates factor II and X. Protamine sulphate, Rapid, Short
Warfarin: Vitamin K antagonism, Vitamin K, Slow, Long
40
What is the suffix of CCBs? Name the three most used
No suffix
Verapamil
Diltiazem
Nifedipine
41
What are the suffix of Beta blockers?
-lol
Propranolol, Labetalol, Metoprolol, Bisoprolol and Carvedilol
42
What is the suffix of ACEIs? Give the most famous one
-Pril
Captopril
43
Fondaparinux mechanism of action
Binds antithrombin resulting in inactivation of factor Xa
44
Explain the effect of noradrenaline on the heart and how to antagonize it
It causes reflex brady cardia due to increasing of BP leading to vagal stimulation which leads to bradycardia
It can be antagonized by atropine
