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Primary Pharmacology > Cardiovascular Pharmacology > Flashcards

Cardiovascular Pharmacology Flashcards

1
Q

Examples of class one antiarrhythmics
Effect on phase o slope ,ap, repolarisation

A

Ia quinadine, some, longer, longer
Ib lidocaine, little, shorter, shorter
Ic flecanide, marked slowing, none, none

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2
Q

What is the pharmacological difference between the vw 1a/b/c drugs

A

A - half way between b and c
B - shorter association with receptors than duration of cardiac cycle so blocks myofibrils from premature contractions. Bind preferentially to refractory channels so selective for ischaemic myocardium
C - longer association with receptors so blocks cycle to cycle generally reducing excitability effective for re-entry type rhythms

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3
Q

Which class 1 antiarrhythmics effect QT

A

A lengthens, b shortens

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4
Q

Which class 1 antiarrhythmics effect pr and qrs

A

Class c lengthens both significantly, class a to a small extent

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5
Q

What is the effect of beta blockade on cardiac cycle
Why

A

Slows and lengthens phase 4 depolarisation
Ap is shortened and refractory period prolonged
Mediated by blockage of Gs activated slow l type calcium channels

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6
Q

What is the effect of class III antiarrhythmics
Examples

A

Amiodarone, bretylium, sotalol
Prolong repolarisation and thus the action potential and increase the effective refractory period

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7
Q

Cautions for sotalol use

A

Hypokalaemia
When other qt prolonging agents used
As with other beta blockers asthma etc

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8
Q

What phase of the ap do class iV antiarrhythmics effect

A

Phases 2 and 3 (reduces)

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9
Q

Effects of adenosine receptor activation

A

A1 - inhibits av node, reduce heart rate, reduce atrial contractility, anti hypertensive, decreased cerebral excitability, renal vasoconstriction, bronchoconstriction,
A2a- vasodilation, inhibition of platelet aggregation
A2b - anti inflammatory
A3 - cardioprotection

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10
Q

How do a1 receptors result in cardiac slowing

A

Gs link to k channels (same as opened by m2 receptors)

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11
Q

Adenosine half life

A

10 seconds

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12
Q

Structure of a cardiac glycoside

A

Steroid nucleus,
lactose ring - pharmacologically active
carbohydrate unit - makes it soluble

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13
Q

Mechanism of action of cardiac glycosides

A

Reversible bind to cardiac NaKATPase
Results in more sodium and less k intracellular
Less naca pump activity thus more ca in the cell

Causes positive inotropy,
Direct slowing at av node and increased vagal tone also causing slowing

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14
Q

Elimination of cardiac glycosides

A

Slow! Highly bound to cardiac muscle
Most excreted unchanged in urine however digoxin metabolised hepatically

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15
Q

Side effects of cardiac glycosides

A

Exacerbated by k loss
Heart block
Arrhythmia
Fatigue
Nausea
Anorexia
Confusion
Neuralgia
Gynaecomastia

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16
Q

How is mg stored in the body

A

53% in bone
27% in muscle
0.3% in plasmaa

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17
Q

Physiological effects of magnesium

A

Cofactor in 300 enzyme systems
Neuronal activity
Neurotransmitter release
Adenylel cyclase and ip3 regulation

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18
Q

Uses of mg as a med

A

Replacement of deficit
Tx of eclampsia and pre eclampsia
Treatment of dysrhthmia
Inhibition of prem labour
Cardioplegia (arresting heart in cardiac surgery)
Prevention of hypertensive response to intubation
Treatment of asthma
Reduction of catecholamine release in phaeochromocytoma surgery

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19
Q

What type of calcium channel do ccbs work on

A

L type voltage gated

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20
Q

Groups of ccbs and examples with broad characteristics

A

Papaverines - verapamil - mainly effect cardiac muscle inhibiting ca entry in phase 2/3 of AP (with decreased contractility and slower av node conduction)
Benzothiapines - diltiazem - both cardiac and smooth muscle with moderate effect on vascular system (dilatation) and cardiac output.
Dihydropyridines - amlodipine, nifedipine - mainly act at smooth muscle effecting vascular tone

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21
Q

How do ccbs effect SVR and CO

A

Reduce it by causing vasodilatation (mainly arterial)
Slight negative inotropy
Combination of above mean lower preload and afterload so less myocardial work

22
Q

What are selective phosphodiesterase inhibitors

A

Only inhibit pde3 which is in myocardial and vascular smooth muscle
General pde inhibitors inhibit all 5 isoenzymes (eg theophylline)
Sildenafil inhibits pde5

23
Q

Classifications and Examples of selective pde3 inhibitor

A

Bipyridines - milrinone
Imidazolines - enoximone

24
Q

How do selective pde3 inhibitors work

A

Inhibit pde3 which is responsible for cAMP breakdown
Increase in cAMP in myocardial and vascular smooth muscle
Phosphorylation of protein kinases in the cell
In heart Increased influx of calcium through slow calcium channels by increased number and duration of opening and increased reuptake of calcium
Increased ca and thus increased contraction and improved relaxation
In vasculature phosphorylation if myosin light chain kinase reducing affinity of calmodulin and dephosphorylates the myosin - causes relaxation and vasodilation

25
Q

Clinical effects of pde3 inhibitors

A

Improved heart contractility Without increasing oxygen utilisation
Reduced pre and after load
Reduced coronary vascular resistance
Some bronchodilation

26
Q

How does milrinone present
Clinical administration and effects

A

Yellow solution of lactate salt
Loading dose then infusion
May cause hypotension because of vasodilation

27
Q

Milirinone elimination

A

80% unchanged in urine thus renal failure can have large impact on effect (including renal effects of heart failure)

28
Q

Issues with use of enoximone

A

Reduces refractoriness of atrium and av and ventricle so may cause ectopics and VT
Hypotension

29
Q

Metabolism of enoximone

A

Hepatic
T1/2 4 hrs

30
Q

Effects of angiotensin 2, what sort of molecule is it

A

Vasoconstriction
Release of aldosterone resulting in na and water conservation

An octopeptide

31
Q

What type of molecule is ace

A

A carboxypeptidase

32
Q

What dose ace do

A

Ang 1 to 2
Inactivates bradykinin

33
Q

Types of angiotensin II receptor
What do ARBS block

A

AT1 - GRPC - triggers vasoconstriction and aldosterone secretion
AT2 - anti proliferation at endothelial cells
ARBS block AT1

34
Q

How does furosemide work

A

Acts on thick ascending limb of loop
Interferes with sodium and chloride reabsorption
Thus more water excreted due to higher osmotic pressure
Also cause vasodilation - also increases renal blood flow without effecting gfr meaning distal tubule protein more dilute thus lower osmotic pressure
Overall decreased gradient so less waster reabsorption

35
Q

How are the vascular effects of furosemide mediated I

A

Interference with prostaglandin e2 and i2 degradation

36
Q

Why do loop diuretics cause hypokalaemia and alklalaemia

A

More filtrate and na to DCT so more na/k exchange pump action
Also more hydrogen ions secreted in exchange for k

37
Q

How do loop diuretics enter tubules
Why
How are they excreted

A

Highly protein bound so not readily filtered at glomerulus
Actively secreted into pct
Excreted in urine

38
Q

How do thiazide diuretics work?

A

Act on luminal membrane pumps of DCT inhibiting na Cl reabsorption

39
Q

What secretion is increased with thiazides

A

Magnesium
Potassium
Sodium

40
Q

What secretion is reduced with thiazides

A

Calcium and uric acid

41
Q

Effect of thiazides on diabetics

A

Hyperglycaemia

42
Q

How do potassium sparing diuretics work
Examples

A

Spironolactone, amiloride
Spironolactone inhibits nak exchange pump in DCT
Amiloride interferes with na channels o which effect of aldosterone is mediated

43
Q

Efficacy of loop diuretics, thiazides and k sparing diuretics at causing na and water excretion

A

25, 10 and 5% respectively

44
Q

Examples of osmotic diuretics
Mechanism

A

Mannitol, urea
Freely filtered but not reabosorbable in tubule

45
Q

What is amiodarones structure

A

An iodinated benzofuran derivative

46
Q

Bioavailability and protein binding of amiodarne
T1/2

A

22-86%
97%;protein bound
54 days

47
Q

What visual changes result from amiodarone

A

Benign reversible corneal micro deposits

48
Q

Side effects of amiodarone

A

Peripheral neuropathy
Nightmares
Tremor
Ataxia
Av block
Alveolitis
Pulmonary fibrosis
Thyroid issues

49
Q

Effect of amiodarone on thyroid function

A

Blocks t2 to thyroid. Conversion thus may cause hyo or hyper thyroid is

50
Q

Why is amiodarones half life so long

A

Highly lipid soluble and highly tissue bound

51
Q

Bioavailability of digoxin
Protein binding

A

75%
25%

Primary Pharmacology (18 decks)

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