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BSMS308 > 2. Cardiovascular drugs 1 > Flashcards

2. Cardiovascular drugs 1 Flashcards

1
Q

Pathophysiology of AF

A

chaotic electrical activity in the atria

Fibrosis and loss of atrial muscle related to:

  • inflammation
  • aging
  • genetics
  • chamber dilatation
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2
Q

AF risk factors

A 
hypertension
valvular heart disease, 
cardiomyopathy, 
previous cardiac surgery, 
congenital heart disease, coronary artery disease, 
pericarditis,
lung disease - PE, 
pneumonia, 
COPD, 
hyperthyroidism, 
alcohol
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3
Q

AF classification

A

Lone AF
Paroxysmal <7 days
Persistent >7 days
Permanent >7 days with our without cardioversion

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4
Q

AF clinical features

A 
asymptomatic
palpitations
SOB
chest pain
syncope
pre-syncope (light-headedness/dizziness)
heart failure
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5
Q

Atrial fibrillation treatment

A

Rate control
rhythm control
anticoagulation

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6
Q

Question to ask when someone presents with AF? and Treatment?

A

Are they compromised? (has the arrhythmia caused hypotension?)

If compromised - DC shock

If uncompromised - pharmacotherapy

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7
Q

AF treatment

A

<48 hours duration
-> attempt rhythm control

> 48 hours duration then attempt rate control

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8
Q

When is rate control preferred?

A

If more than 48 hours after AF onset

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9
Q

When is rhythm control preferred?

A 
If less than 48 hours after AF onset
for symptom improvement
in younger patients
Heart failure related to AF
Adequacy of rate control
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10
Q

Acute AF without heart failure

A

Rate control
1st line: beta blocker or CCB (diltiazem or verapramil)
2nd line: add digoxin

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11
Q

Acute AF with heart failure

A

Rate control
1st line: digoxin, amiodarone
2nd line: amiodarone

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12
Q

Permanent or paroxysmal AF

A

Rate control
1st line: beta blocker or CCB (diltiazem, verapamil)
2nd line: add digoxin

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13
Q

Acute cardioversion, normal heart

A

Rhythm control

Flecainide, sotalol

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14
Q

Acute cardioversion, abrnomal heart

A

rhythm control

amiodarone

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15
Q

Maintain sinus rhythm - normal heart

A

rhythm control

Flecainide, sotalol

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16
Q

Maintain sinus rhythm, abnormal heart

A

rhythm control

amiodarone

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17
Q

What do Beta-adrenergic agonists do?

A

Block B2 receptors leading to stimulation of Gi which inhibits AC which makes cAMP which phosphorylates Calcium channels and lets Ca2+ through Calcium receptors into the heart, causing contraction?? So basically causes this

Block B1,2 receptors, activating Gs which acts on AC to cause something to do with Calcium idk

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18
Q

Non-cardioselective Beta blockers

A

propanolol
Carvidelol
Sotalol

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19
Q

Cardioselective beta blockers

A 
atenolol
Bisoprolol
Esmelol
Metaprolol
Nebivolol
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20
Q

Vasodilatory

A

Labetalol

Carvedilol

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21
Q

Rate-limiting calcium channel blockers

A

verapamil

Diltiazem

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22
Q

Dihydropyridine calcium channel blockers (dipines)

A 
amlodipines
nifedipin
lercanidipine
nimodipine
felodipine
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23
Q

Anticoagulation: CHA2DS2 VaSC

A 
C- congestive heart failure = 1
H - hypertension =1
A2 - age >75 years =2
D - diabetes =1
S2 - previous stroke, TIA or thromboembolism =2
V - vascular disease =1
A - age 65 - 74 years =1
Sc = sex category (female gender) = 1

If CHA2DS2 VaSC is 2 or more, give warfarin or direct oral anticoagulent

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24
Q

When to give warfarin/direct oral anticoagulant?

A

When CHA2DS2 VaSC is 2 or more

25
Q

What to consider when giving anticoagulation?

A

Risk vs benefits - bleeding risk via HAS-BLED score

26
Q

HAS-BLED score?

A 
Bleeding risk
H- Hypertension =1
A- Abnormal renal/liver function = 1 point each
S- Stroke in past = 1
B- Bleeding history =1
L- Labile INRs =1
E- Elderly =1
D- drugs/alcohol concomitantly =1 point each
27
Q

AF other treatments

A

Radiofrequency catheter or cryo-ablation

Left atrial appendage occlusion (LAAO)

28
Q

Stroke classification

A

Ischaemic (blocked up)

Haemorrhagic (bleed out)

29
Q

Stroke treatment

A 
Fibrinolysis
Antithrombotics
-aspirin
-clopidogrel
-warfarin or DOACs
Lipid modification
Treat hypertension
30
Q

Lipid modification

A

For primary and secondary prevention
Exclude secondary cause of increased lipids e.g. excess alcohol, uncontrolled diabetes, hypothyroidism, liver disease and nephrotic syndrome

31
Q

When to refer to a lipid specialist?

A

Consider referral if:

  1. Total serum cholesterol >7.5mmol/l + family history of premature coronry artery disease
  2. Total serum cholesterol >9mmol/l
32
Q

Healthy/normal cholesterol levels

A 
Total 5 or below
HDL 1 or above
LDL 3 or below
Non-HDL 4or below
Triglycerides 2.3 or below
33
Q

Lipid modification - when to offer medicine for primary prevention

A

Offer atorvastatin for primary prevention of CVD to people who have:

  • 10% or greater 10 year risk of developing CVD
  • T1DM
  • CKD
34
Q

Lipid modification - secondary prevention of CVD

A

Atorvastatin for ANYONE who has had a stroke or MI regardless of cholesterol

35
Q

Ezetimibe

A

Monotherapy treats primary (heterozygous familial or non familial) hypercholesterolaemia in adults in whom initial statin therapy is contraindicated or not tolerated

Ezetimine coadministered w initial statin therapy might be appropriate

36
Q

Stroke - drug treatment (lipid lowering)

A

Nicotinic acid - stops FFA formation

Fibrates - oxidise DDas and stop VLDLs and promote formation of HDLs

Statins - inhibit HMG-CoA making cholesterol, and promote uptake of cholesterol to liver

Ezetimibe - inhibits dietary cholesterol absorption into blood

Resins - promote fats into the bile to be excreted?

37
Q

Proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9i)- Alirocumab, evolocumab

A

Alirocumab, evolocumab

bind to PCSK9, inhibiting the receptor binding to LDLRs on hepatocytes and causing their degradation which leads to more blood LDL-C levels,
so results in less LDL cholesterol in the blood

38
Q

Heart failure pathophysiology

A

Poor ventricular function/myocardial damage (e.g. post MI or dilated cardiomyopathy)

leads to decreased SV and CO

leads to neurohormonal response

leads to activation of sympathetic system and RAAS

result in vasoconstriction, increased sympathetic tone, angiotensin II, endothelins, impaired NO release -> sodium and fluid retention, increased vasopressin and aldosterone

leads to further stress on ventricular wall and dilatation (remodelling) leads to worsened ventricular functioning

leads to further heart failure

39
Q

Heart failure treatment aims

A

Relieve symptoms

Reduce mortality

40
Q

Heart failure treatment

A

Lifestyle - exercise, decrease alcohol, smoking cessation
Drugs
Devices
Surgery

41
Q

Heart failure treatments

A

Diuretics (improve symptoms)

ACEI (slightly improve symptoms, mostly reduce mortality)

Beta-blockers (improve symptoms and massively improve mortality)

Aldosterone antagonists (improve symptoms and reduce mortality)

ARBs (improve symptoms and reduce mortality)

Hydralazine/nitrates (improve symptoms and reduce mortality)

Digoxin (improve symptoms)

42
Q

Heart failure - diuretics

A

loop diuretics:
-furosemide

thiazides:
- bendroflumethiazide
- metolazone (thiazide-like)

K+ sparing:

  • spironolactone (mineralocorticoid receptor antagonists)
  • amiloride
43
Q

loop diuretics

A

Furosemide

act at Na/K/Cl symporter

44
Q

Thiazides

A

bendroflumethiazide
Metolazone (thiazide-like)

act at Na/Cl symporter

45
Q

K+ sparing

A

spironolactone and amiloride

act at epithelial Na channel

46
Q

heart failure - diuretics effect

A

provide symptom control
reduce cardiac preload
side effects

47
Q

Heart failure - ACE inhibitors

A

increase life expectancy vs placebo
Effect more marked in patients with more severe LV dysfunction
Benefit for all NYHA classes
Reduces risk of hospitalisation

48
Q

Heart failure - ACE inhibitors/ARBs mechanisms

A

ACE inhibitors inhibit ACE forming Angiotensin II from Angiotensin I, and bradykinin’s effect

ARB inhibit angiotensin receptors

Effects: vasoconstriction, salt and water retention, aldosterone secretion

49
Q

Heart failure - ACE inhibitors (…prils)

A 
Ramipril
Lisinopril
Enalapril
Perindopril
Captopril (not used as much due to short half-life)
50
Q

Heart failure - ARBs (…sartans)

A

losartan, candersartan, valsartan

Reduces mortality
Some data on QOL, symptom control
used in patients who can’t tolerace ACE-I

51
Q

Heart failure - beta blockers?

A

BB increase life expectancy vs placebo
All NYHA classes
Reduces hospitalisation
Low dose, titrate up, monitor HR, BP, clinical progression

52
Q

Heart failure - spironolactone

A

Patients w severe heart failure, NYHA III-IV
Increases life expectancy
Reduces hospital admission
low dose (12.5-25mg)

53
Q

Spironolactone mechanism

A

inhibits aldosterone secretion

54
Q

Chronic heart failure - treatment

A

Diuretics
ACE-i (ARBs)
Beta blockers
Spironolactone

55
Q

Chronic heart failure - other drugs

A

Ivabradine - use with or instead of BB if HR >75bpm

Hydralazine & nitrate - use if ACEi/ARB not tolerated or contraindicated or in people of African origin

Sacubitril(neprilysin inhibitor)/valsartan (ARB) - with NYHA class II to IV, a left ventricular ejection fraction of 35% or less and, who are already taking a stable dose of an ACE inhibitor or angiotensin receptor antagonist

56
Q

Chronic heart failure

A

inhibitors of sodium-glucose cotransporter 2 (SGLT2) - works at S1 segment proximal tubule - 90% of renal glucose reabsorption

diabetes drug but treats heart failure as a second result

57
Q

Acute heart failure - basic measures

A

Sit patient upright

High dose oxygen -> corrects hypoxia

58
Q

Acute heart failure - initial drug treament

A

IV loop diuretics - venodilation and diuresis

IV opiates/opioids (morphine) - reduce anxiety and preload (venodilatation)

IV, buccal or sublingual nitrates - reduce preload& afterload, ischaemia and pulmonary artery pressures

Continue beta blockers but DO NOT initiate!

BSMS308 (9 decks)

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