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MED SCI > Pharmacology > Flashcards

Pharmacology Flashcards

0
Q

Why are thiazide diuretics less effective than loop diuretics?

A

Only ~5% of filtered sodium goes through the DCT, therefore only a small fraction left to be reabsorbed.

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1
Q

Where do thiazide diuretics work on?

A

Distal convoluted tubule

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2
Q

Give an examples of thiazide diuretics

A

Hydrochlorothiazide

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3
Q

What are CCD acting diuretics? And how do they work?

A

Acts on cortical collecting duct

Promote sodium excretion

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4
Q

What is drug is dobutamine?

A

An beta 1 adrenergic receptor agonist (selective)

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5
Q

What is dobutamine used for?

A

Used to treat acute heart failure, following myocardial infarction or cardiac surgery.
Given intravenously

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6
Q

What is dopamine used for, and why?

A

Acute heart failure

  • Increases tissue adrenaline levels
  • Stimulates ??? 1 adrenergic receptors?
  • Increases renal perfusion by stimulating dopamine receptors in the renal vasculature.
  • Given intravenously
  • May be given in low doses with dobutamine in cardiogenic shock
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7
Q

What drugs are used for acute heart failure?

A

Dobutamine and dopamine

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8
Q

What groups of drugs are used for chronic heart failure? (4) Why are they used?

A

Diuretics - improve oxygenation, remove oedema from lungs

RAAS blockers - reduce blood pressure elevations (ACE inhibitors - keep sodium down
ARAs (angiotensin receptor antagonists) - similar to beta ACEis)

Beta blockers - reduce sympathetic drive

Cardiac glycosides - help inotropic action

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9
Q

What are the four sites of salt and water reabsorption (in relation to kidney)

A
  1. Proximal convoluted tubule
  2. Loop of Henle (loop diuretics)
  3. Early Distal convoluted tubule (thiazides)
  4. Cortical Collection Duct diuretics
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10
Q

Give an example of a loop diuretic (and where does it work?)

A

Furosemide (Lasix) - thick ascending limb

Na/K/2Cl Co-transporter is blocked.

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11
Q

What is spironolactone?

A

Specific competitive antagonist of aldosterone

Aldosterone can cause cardiac fibrosis so is good to treat heart failure

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12
Q

What is Aldactone?

A

It is a spironolactone that is potassium sparing

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13
Q

What’s a side effect of loop and thiazide diuretics? Why does it happen? What is the risk from the side effect?

A

Increases potassium excretion and hence hypokalemia. Sodium reabsorption is blocked, more sodium to CCD activates RAAS, hence excrete sodium.

Hypokalemia - risk of arrhythmia, increased toxicity of cardiac glycosides (slow k)

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14
Q

Briefly describe the RAS system

A

Renin converts angiogensinogen into angiotensin I. Angiotensin I converts into Angiotensin II through ACE (angiotensin converting enzyme, found in lungs). Angiotensin II reacts with ATI receptor to vasoconstrict and raise blood pressure, act on CNS and act on the aldosterone: fluid electrolyte balance, and is pro-inflammatory and pro-fibrotic. ATII receptor activation antagonises ATI effects

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15
Q

What is ACE? Where is it found? How does it do its action?

A

Angiotensin converting enzyme
Ubiquitous apparently, but famously in lungs
Converts ATI into ATII via cleaving,

16
Q

What are some examples of ACE inhibitors? How do we remember?

A

Ramipril
Enalapril

If suffixes end with -pril

17
Q

What are ACEi used for and why?

A

Used as hypertensives, also used for congestive heart failure!!!
Should be used when diuretics are used because diuretics increase compensatory RAAS by causing salt loss. ACEi block effects of increased RAAS.
Reduce after load, reduce sodium retention, reduce cardiac fibrosis (as aldosterone reduced)

18
Q

Mechanism of ACE inhibitors

A
  1. Block angiotensin II formation; no vasoconstriction so blood level cannot rise, and bradykinin levels rise.
  2. Aldosterone production downstream is also reduced, promoting sodium and water loss, and potassium retention (avoiding hypokalemia)
19
Q

What are some side effects of ACE inhibitors? (2) when is its use contraindicated?

A
  • hypotension
  • cough
  • adverse effects on renal development and function in foetus and newborns
  • don’t use to treat hypertension in pregnancy
20
Q

What are the two angiotensin receptors and their main actions?

A

AT1-R : most biological actions of angiotensin occurs through this receptor. Pro-fibrotic

AT2-R : unknown function, inhibitory effects

21
Q

What are Angiotensin receptor blocking drugs? (ARAs?) what are its actions why it’s used

A

Peptide analogues of angiotensin that block the AT1-R

Similar actions to ACE inhibitors but don’t have cough side effect

22
Q

What are examples of ARAs? How do we remember?

A

Saralasin (competitive antagonist)

Lasartan, Valsartan (-sartan suffixes)

23
Q

Cardiac glycosides e.g digoxin

What is it used for? Actions? Adverse effects?

A

Digoxin is most commonly used cardiac glycosides with a long plasma half life, excreted by kidneys. Narrow therapeutic range

Glycosides reduce AV node conduction and reduces atrial fibrillation

Adverse effects: arrhythmias at higher doses, AV block and ectopic foci

24
Q

Mechanism of action for cardiac glycosides digoxin

A

inhibits Na/K exchange, which increase intercellular [Na+], decreased Na/Ca exchange leaving more extracellular [Ca++] and hence more Ca++ stored in SR. Hence increased contraction during depolarisation.

25
Q

What are class I anti-arrhythmia drugs? What are their sub classes?

A

Sodium blockers.
Subclasses are classified according to time taken to recover from the block.
1a. 1b. And 1c.

26
Q

For sub class 1a anti arrhythmic drugs what are examples and how fast is recovery time?

A

Quinidine, procaineamide, disopyramide

TRecovery = 1-10 seconds

27
Q

For sub class 1b anti- arrhythmic drugs what are examples and how fast is recovery time? Significance of 1b?

A 
Lignocaine, lidocaine 
- T recovery <1s
- most important
- used for ventricular arrhythmias 
(IV infusion)
28
Q

For sub class 1c anti-arrhythmic drugs what are examples and how fast is recovery time? Significance?

A

Flecainide and Encainide

  • Long recovery time (>10s) but quick acting and fewer side effects. Can use in young AF.
  • Slowing of conduction in normal tissue at normal rates
  • suppress ventricular ectopic beats
  • long acting
29
Q

What are class 2 anti arrhythmic drugs? Examples? Mechanisms? Effects and risks?

A

Beta blockers (beta adrenoceptor antagonists)
E.g. Propranolol, metoprolol, atenolol, timolol
- blocks sympathetic effects

  • reduce mortality post Mi
  • prevent SNS induced arrhythmias
  • but can cause asthma, negative inotropic effects and fatigue
30
Q

What are class 3 anti arrhythmic drugs? Examples? Mechanisms? Effects and risks?

A

K-channel blockers

E.g. Amiodarone (convert AF to sinus rhythm)

  • increase AP duration
  • side effects includes torsade de points (PVT.)

E.g. Sotalol; defitilide (maintain sinus rhythm)

  • non selective b blocker
  • prolongs QT interval and AP
  • but can provoke VA including PVT
31
Q

What are class 4 anti arrhythmic drugs? Examples? Mechanisms? Effects and risks?

A

Calcium channel blockers

E.g. Verapamil, diltiazem

  • block calcium entry via prevent opening of L-type calcium channels
  • inhibit calcium entry caused by Depolarisation
  • used in paroxysmal supra ventricular tachycardia
  • used in AF
32
Q

Mechanism of Adenosine **UNFINISHED

A
  • Inhibition of Ca-channels via inhibit adenylate cyclase
  • hyper polarisation via Opening K channels
  • reduction in HR via —
33
Q

What are four fibrinolytic agents currently available in Australia?

A

Streptokinase (SK), and tissue specific agents: alteplase, reteplase, and tenecteplase (-teplase)

34
Q

In which situations are fibrin specific agents (-teplase) used over streptokinase (SK)? Why?

A
  • Fibrin specific agents reduce mortality compared to SK in patients with STEMI who present within 6 hours of symptom onset.
  • These agents also lack the significant acute side effects of hypotension and allergy called by SK
  • Second Gen fibrin specific agents can be given as single or double bolus - easy use
35
Q

In which situations would streptokinase be used over fibrin specific agents?

A

Steptokinase may be associated with lower incidence of intracranial haemorrhage, particularly in the elderly.

36
Q

Why is streptokinase use avoided in Aboriginal Australians?

A

There is evidence SK is less effective because high levels of skin infection (thus streptococcal antibodies), particularly remote populations

MED SCI (2 decks)

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