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Cardio block > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

what are the classes of antidysrhythmics

  • what is used to treat bradycardia
A 
class 1 - na+ channel blockers
class 2 - beta blockers
class 3 - k+ channel inhibitors
class 4 - ca2+ channel blockers

“nice boys kick cats”

brady cardia - muscR blockers (rarer)

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2
Q

class 1 antidysrhythmics - what are they

how do they work

examples
- what is their effect on the effective refractory period

A

Na+ channel blockers

  • decrease the phase 0 slope
  • decrease the peak of ventricular action potential

they all have different effects on ERP

class 1a - quinidine - ↑ERP

class 1b - lignocaine - ↓ERP 
- clinical use = topical anaesthetic, very narrow therapeutic range if IV (only use in emergency)

class 1c 0 flecainide - no effect on ERP

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3
Q

class 2 antidysrhythmics - what are they

how do they work

effects

adverse effects

examples

A

class 2 - beta blockers

block the stimulation by the SNS on cardiac electrical activity

also stabilises the membrane in Purkinje fibres (similar to class I - can block Na+)

effects

  • ↓sinus rate
  • ↓conduction velocity
  • ↓aberrant pacemaker activity

adverse effects

  • hypotension
  • bradycardia
  • can’t increase HR to meet extra demand
  • bronchoconstriction

examples - “olols”

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4
Q

class 3 antidysrhythmics - what are they

how do they work

what do they increase risk of?

examples

A

K+ channel inhibitors

  • stop the efflux of K+ (phase 3)- prolong the cardiac action potential
  • ↓incidence of re-entry

increase risk of triggered events (in refractory period)

example: amiodarone (also blocks sodium, calcium)

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5
Q

class 4 antidysrhythmics - what are they

how do they work

examples

A

calcium channel blockers

mechanism

  • preferentially acts on SA/AV nodes
  • decreases Ca2+ entry for action potential activation
  • slow phase 0

example - varapamil (cardio-selective)

  • preferentially acts on SA/AV nodes
  • treats atrial tachy
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6
Q

Hypertension - risk factors

Treatment

A 
Smoking
Diet
Weight
Stress
Sex - male
Age

Treatment

  • lifestyle modification - smoking, diet, weight, stress
  • drugs
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7
Q

describe the cardiac cycle

A

Split into diastole (filling) and systole (ejection)

1) AV valves are open, semilunar valves are closed
- passive filling of the ventricles
- atrial contraction
- end with EDV in the ventricles

2) Isovolumetric contraction
- AV valves close as intraventricular P > atrial
- ventricular P < aortic P
- volume remains constant because all valves closed

6) rapid filling - AV valves open
- ventricle P still falling because muscle is still relaxing
- rapid flow in by bood

7) reduced filling - less compliant, pressures are rising

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8
Q

how much volume is EDV of LV normally

A

~120ml

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9
Q

what sounds is sometimes heart that signifies atrial contraction?

A

4th heart sound

  • reduced ventricle compliance
  • eg ventricular hypertrophyt
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10
Q

Heart sounds

  • 1st
  • 2nd
  • 3rd
  • 4th
A

1st = closure of AV valves

2nd = closure of aortic/pulm valves

3rd = (sometimes - normal in kids) - during rapid filling, indicates ventricular dilatation

4th (sometimes) - atrial contraction

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11
Q

described jugular wave form

A

2 positive waves seen with each beat

  • a wave - reflect atrial contraction
  • v wave - reflex atrial venous filling (happening at same time as ventricular contraction)
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12
Q

raised JVP indicates

A

jvp reflects right atrium pressure

  • resistance to right atrial emptying

eg. - pulmonary hyptertension
- fluid overload
- RVF
- bradycardia
- tricuspid stenosis/regurgitation

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13
Q

ECG

  • what electrical events does it measure?
  • configuration of the leads
  • what do the different waves mean
A

12 leads
6 - precordial (V1, V2, V3, V4, V5 and V6)
6 - limb

up = depolarisatin
down = repolarisation

p wave - atrial depolarisation
pr interval - time for electrical impulse to travel through atria, cross AV node
qrs wave - ventricular depolarisation
t wave - ventricular repolarisation

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14
Q

approach to reading ecg

A
  1. examine rate
  2. examine rhythm
  3. examine axis, intervals, segments
  4. examine everything else
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15
Q

examining rhythm on ecg

A

sinus rhythm = p wave on lead II is upright

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16
Q

electrical conduction through heart

A

1) spontaneous depolarisation at sinus node (high in right atrium)
2) wave of depolarsiation spreads through RA and across intra-atrial septum into LA
3) atria + ventricles are separated by electrically inert fibrous ring - only conduction is through AV node

AV node delays signal for a short time

4) wave of depolarisation spreads down interventricular septum (via bundle of his + right and left bundle branches) into ventricles + down purkinje fibres

depolarise and contract from apex up

17
Q

intrinsic beats

  • SA node
  • AV node
  • ventricles
A

SA - 100
AV - 50 bpm
ventricles - 30

18
Q

What is AV block?

What are the types? what do you see on ECG

A

impaired transmission from the AV node to the rest of the heart

First degree - slow conduction through AV junction

  • elongated PR interval
  • causes: MI, some drugs

Second degree - sometimes no contraction of ventricle at all
type 1 - get a gradual prolongation of PR interval, until you skip a ventricle contraction all together
type 2 - get PR intervals are constant, until a nonconducted p wave occurs - get a ratio of p:qrs

Third degree - total AV block
- just see p waves - no qrs

19
Q

What is Stokes-Adam syndrome?

A

collapse into unconsciousness due to complete AV block

return to consciousness as purkinje kicks into gear

20
Q

Digoxin (cardiac glycosides)

  • mechanism
  • why is it not used much
  • when is toxicity increased
  • main use
A

increase contractility by increasing intracellular Ca2+ (more ca released from SR with each ap - more contractility)

Mechanism
- inhibits Na+/K+ ATP-ase = increase intracellular [Na2+]
- Na+ is exchanged wtih Ca2+ as well (pump calcium out, sodium in)
- high intracellular Na2+ -> less calcium is being pumped out
=> increase Ca2+

Problems

  • narrow therapeutic index + low selectivity
  • targets are widely distributed - may block AV conduction; and increase ectopic pacemaker activity -> risk of ventricular arrhythmia

side effects:

  • nausea, vom, diarrhoea, anorexia, confusion, drowsiness
  • ventricular dysrhythmias
  • AV block

Increased toxicity with

  • low K+ (be careful with diuretics) (K+ competes for target site)
  • high Ca2+ (decrease gradient for Ca efflux)
  • renal impairment

main use = AF (increase vagal outflow to reduce AV conduction rate)

21
Q

Which ionotropes can be used in acute heart failure?
how do they work
adverse effects

A

Acute = emergency = use IV for acute HF and cardiogenic shock

1) Beta-adrenoceptor agonists
= adrenaline, noradrenaline - activate a- and b-adrenoceptors - increase contractility
= dobutamine - selective for b1

adverse effects

  • increase O2 demand
  • risk of arrhythmia
  • only SR - chronic overactivation of b1-adrenoceptors occurs in chronic HF -> reduced sensitivity to these

2) Phosphodiesterase inhibitors (PDE)
= amrinone

works through reducing phosphorylation of b1-adrenoceptors - less reduced sensitivity to agonists/sympathetic drive

22
Q

what happens to b1-adrenoceptors in chronic heart failure?

A

because there is chronic overstimulation by the SNS - b1 adrenoceptors are downregulated

+ there is impaired b1-adrenoceptor coupling (this can be improved by PDE inhibitors)

=> over time the cardiac cells become less sensitive to stimulation by SNS and b1-adrenoceptor agonists

23
Q

Diuretics - what are they

what are their classes

A

drugs that increase Na+ and water excretion

  • decrease Na+ and Cl- into blood
  • secondary H2O secretion

Classes:

  1. Loop diuretics
  2. Thiazide diuretics
  3. Potassium sparing diuretics
  4. Osmotic diuretics
24
Q

Osmotic diuretics - how do they work
- where is their main effect

examples

clinical uses

A

Pharmacologically inert - exert osmotic effects

  • are filtered but not reabsorbed, stay in lumen
  • reduce passive water reabsorption
  • main effect is in water-permeable parts of nephron
  • prox tubume
  • desc. loop of henle
  • collecting tubules

eg. mannitol - small sugar molecule (polar - not reabsorbed)

clinical uses:

  • decrease fluid load - ↑ICP, ↑inctraoc pressure
  • prevent acute renal failure (if can’t play around with Na+)
25
Q

which are the most powerful diuretics and why

A

loop diuretics
act on thick ascending limb of loop ofhenle
result in excretion of 15-20% of Na+ in filtrate = torrential urine flow

-> double effect of local reduced osmotic pressure and distal effects in distal tubule

26
Q

Loop diuretics

  • where do they act
  • how do they work
  • adverse effects
  • clinical uses
  • example
A

act in thick ascending limb of loop of Henle

mechanism

  • inhibit Na+/K+/2Cl- carrier into cells (from lumen)
  • Na+ stays in lumen, water excreted

distal effects

  • increased Na+ in the distal tubule
  • less water reabsorbed again (where is normally reabsorbed)

adverse effects

  • hypokalaemia = need supplement (Na+ is more concentrated in distal tubule - so want to increase Na+ reabsorption there - to reabsorb Na+ - secrete K+ (Na/K ATP-ase) ))
  • metabolic alkalosis
  • hypovolaemia + hypotensio in elderly

clinical uses

  • hypertension
  • salt, water overload (acute pulm oedema, chronic HF, ascites, renal failure)

example - frusemide

27
Q

Thiazide diuretics

  • where do they act
  • how do they work
  • adverse effects
  • clinical uses
  • example
A

distal convoluted tubule

mechanism

  • inhibit Na+/Cl transporter
  • Na+ stays in lumen - water goes wtih

adverse effects

  • hypokalaemia - take supplement (Na+ is more concentrated in distal tubule - so want to increase Na+ reabsorption there - to reabsorb Na+ - secrete K+ (Na/K ATP-ase) )-
  • increased plasma uric acid - gout

clinical use

  • hypertension
  • severe resistant oedema (in combo w/loop)

examples

  • true thiazides: bendrofluazide, hydrochlorothiazide
  • thiazide-like - indapamide
28
Q

Potassium-sparing diuretics

  • where do they act
  • when are they used
  • example
A 
act distally (where there is limited reabsorption of na+) => their diuretic effect is limited 
- collecting tubule + ducts

mainly used to prevent K+ loss (coadminister with K+ losing diuretics)

exammples: 2 groups
- spironolactone
- triamterene + amiloride

29
Q

spironolactone

  • how it works as diuretic
  • where does it work
  • adverse effects
  • clinical uses
  • example
A

aldosterone receptor antagonist (complex can’t bind DNA - can’t stimulate synth of Na/K channels)

aldosterone - normally stimulates synthesis of Na/K channel on basolateral membrane -> gradient for Na+ to flow through
- also activates Na+ channel on apical surface

spironolactone - block this, K+ stays in intersititium

woirks in collecting ducts/tubules

adverse effects

  • hyperkalaemia if used alone
  • GI upset

clinical use

  • with loop/thiazide diuretic
  • heart failure
  • hyperaldosteronism
30
Q

Triamterene and amiloride

  • how it works as diuretic
  • where does it work
A

Block luminal sodium channels in collecting ducts/tubules
- less reabsorption of Na+
=> by proxy less exchange for K+ at the basolateral surface -> less loss of K+

31
Q

How do Angiotensin receptor antagonists work in treating hypertension?
What is their suffix

side effects

A

“sartans”

  • block AT1 receptors
  • > reduce vasoconstriction
  • > reduce aldosterone
  • > reduce cardiac hypertrophy
  • > reduce sympathetic activity -> more so than ACE inhibitors

side effects
- hyperkalaemia

32
Q

How do beta-blockers work in treating hypertension?

A

Block effects of sympathetic activity on kidney + heart (b1 adrenoceptors)

kidney
- decreased renin release -> decreased downstream effects of AngII/aldosteronne

heart
- decrease CO (rate, contractility)

33
Q

which beta adrenoceptors are present in kidney, heart

A

both b1

34
Q

adverse effects of beta blockers and why do they occur

A

cold extremities (reflex a-adrenoceptor constriction to decreased CO + blocking b2 receptors in peripheries)

fatigue
- cant increase HR

dreams, insomnia

bronchoconstriction (contraindicated in asthma)

35
Q

why are beta blockers contraindicated in diabetes

A

diabetics use HR to signal blood sugar level requirements

=> beta blockers can cause hypoglycaemia

36
Q

Calcium channel blockers + hypertension - how do they work, which ones are better for hypertension

A

block L-type ca2+ channels in myocardium + vasculature

dihydropyridines - considered vascular selective
- block constriction - reduce vascular resistance

37
Q

How do diuretics work in treatment of hypertension?

A
  • increase Na+ and water excretion by decreasing their reabsorption into blood stream
  • > reduce preload

Cardio block (6 decks)

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