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Redew 208 > Pharmacology > Flashcards

Pharmacology Flashcards

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.
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2
Q

2- Enumerate four adverse effects of:
a. Nitrates.

A
  • Headache & Flush.
  • Tachycardia.
  • Tolerance.
  • Postural hypotension.
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3
Q

2- Enumerate four adverse effects of
b. CCB

A
  • Headache & Flush.
  • Hypotension.
  • Constipation.
  • Ankle edema.
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4
Q

2- Enumerate four adverse effects of c. Thiazide.

A
  • Hypovolemia.
  • Hyponatremia.
  • Hypokalemia.
  • Hypercalcemia.
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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.
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6
Q

2- Enumerate four adverse effects of e. Frusemide

A
  • Hypovolemia.
  • Hypokalemia.
  • Hypocalcemia.
  • Ototoxic.
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7
Q

Enumerate four adverse effects of f. ACEI.(Captopril)

A
  • Dry cough.
  • Angioedema.
  • First dose hypotension.
  • Bilateral renal artery stenosis.
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8
Q

Four disadvantages of Na nitroprusside

A
  • Large dose > Severe hypotension.
  • Sudden stop > Rebound hypertension.
  • Prolonged use in old age > Cyanosis & acidosis.
  • Teratogenic.
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9
Q

Four disadvantages of Heparin

A
  • Hemorrhage.
  • Hypersensitivity.
  • Hyperkalemia.
  • Heparin induced thrombocytopenia.
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10
Q

Enumerate four therapeutic uses of loop diuretic

A
  • Edema.
  • Acute renal failure.
  • Hypercalcemia.
  • Hypertension.
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11
Q

Enumerate four therapeutic uses of Beta blockers (propranolol)

A
  • Anxiety.
  • Tremors.
  • Migraine prophylaxis.
  • Glaucoma.
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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.
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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.
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14
Q

Mechanism of nicorandil as anti-anginal

A
  • Like nitrate > release nitric oxide.
  • Open K channels > hyperpolarization.
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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.
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16
Q

Mechanism of actions of statins

A
  • Inhibit HMG-COA reductase.
  • Decrease LDL level in plasma.
  • Depletion of intracellular cholesterol.
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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.
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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
Q

Digoxin toxicity treatment

A
  • Stop digitalis & K depleting diuretics.
  • Monitor digitalis plasma level & electrolytes.
  • Activated charcoal.
  • Purified fab fragments.
26
Q

Describe the mechanism of action of fibrates

A

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
Q

Explain why verapamil and nitrates is a favorable combination in treatment of angina

A

Nitrates cause coronary VD and veno dilation and decrease pre load

Verapamil cause coronary VD + arterio dilation and decrease after load

28
Q

Explain why Beta blocker should not be administered with verapamil

A

Since both are coronary VD and decrease HR, when combined they would cause severe cardiac inhibition

29
Q

Explain why the combination of spironolactone and ACEIs is not preferred

A

K retaining diuretics like spironolactone augments the hyperkalemic effects

30
Q

Explain why it is contraindicated to stop the administration of clonidine suddenly

A

If stopped suddenly, causes rebound hypertensive crisis

31
Q

Explain why Neprilysin inhibitor (sacubitril) must not be used with an ACEI

A

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
Q

Explain why verapmil should not be admistred with digitalis

A

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
Q

Nifedipine and nitrates is an unfavourable combination in treatment of angina

A

Since Nitrates causes coronary VD and Nifedipine causes potent arterio-dilation, it causes severe hypotension and tachycardia.

34
Q

Explain the Statins pleiotropic effects

A

Improved endothelial function
Reduced vascular inflammation
Reduced platelet aggregability
anti-thrombin actions

35
Q

Give reason most statins are taken at bed time

A

Because of diurnal rhythm of cholesterol synthesis

36
Q

Give reason ACEIs can produce dry cough

A

The dry irritant cough is due to increase of bradykinin and prostaglandins

37
Q

Explain the mechanism of action of Alpha methyl dopa

A

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
Q

Explain the adverse effects of statins

A

Increase liver enzymes
Myopathy
Rhabdomyolysis (break down of muscle fibers into blood stream)

39
Q

Compare Heparin and Warfarin in Mechanism, Antidote, Onset and Duration.

A

Heparin: potentiate effect of antithrombane III–> deactivates factor II and X. Protamine sulphate, Rapid, Short

Warfarin: Vitamin K antagonism, Vitamin K, Slow, Long

40
Q

What is the suffix of CCBs? Name the three most used

A

No suffix

Verapamil
Diltiazem
Nifedipine

41
Q

What are the suffix of Beta blockers?

A

-lol

Propranolol, Labetalol, Metoprolol, Bisoprolol and Carvedilol

42
Q

What is the suffix of ACEIs? Give the most famous one

A

-Pril

Captopril

43
Q

Fondaparinux mechanism of action

A

Binds antithrombin resulting in inactivation of factor Xa

44
Q

Explain the effect of noradrenaline on the heart and how to antagonize it

A

It causes reflex brady cardia due to increasing of BP leading to vagal stimulation which leads to bradycardia

It can be antagonized by atropine

Redew 208 (5 decks)

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