Pharmacology Flashcards

1
Q

Heparin MOA

A

activates anti-thrombin III

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2
Q

Clopi MOA

A

P2Y12 inhibitor

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3
Q

Abciximab MOA

A

glycoprotein IIb/IIIa inhibitor

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4
Q

Dabigatran MOA

A

direct thrombin inhibitor

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5
Q

Rivaroxaban MOA

A

direct factor X inhibitor

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6
Q

Amiodarone MOA

A

Blocks K+ channels

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7
Q

furosemide site of action

A

ascending loop of henle

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8
Q

Furosemide MOA

A

inhibits the Na-K-Cl cotransporter in the thick ascending limb of the loop of Henle

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9
Q

ACE inhibitor MOA

A

inhibits conversion of angiotensin I to angiontensin II

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10
Q

Where are ACE inhibitors activated?

A

Liver

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11
Q

Common SE of ACE Inhibitors?

A

cough, angioedema, High K+

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12
Q

Can you give ACE inhibitors in pregnancy?

A

No

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13
Q

Beta Blockers MOA

A

Bind to beta-adrenoreceptors which prevents adrenaline/noradrenaline binding. This inhibits sympathetic effects

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14
Q

Beta blockers SE

A

bronchospasms, cold peripheries, fatigue, erectile dysfunction

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15
Q

Beta blockers CI

A

asthma, sick sinus syndrome, verapamil

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16
Q

Ivabradine SE

A

visual effects, particular luminous phenomena, are common
headache
bradycardia, heart block

17
Q

Nicorandil MOA

A

potassium-channel activator with vasodilation through activation of guanylyl cyclase which results in increase cGMP

18
Q

Nicorandil SE

A

headache
flushing
skin, mucosal and eye ulceration
gastrointestinal ulcers including anal ulceration

19
Q

Renal causes of secondary hypertension

A

glomerulonephritis, pyelonephritis, PCKD

20
Q

Endocrine causes of secondary hypertension

A

primary hyperaldosteronism
Cushings, Liddles

21
Q

Drug causes of secondary hypertension

A

Steroids, COCP, NSAIDS

22
Q

What normally happens to BP during pregnancy?

A

Decreases until 20-24 weeks then increases back to pre-pregnancy level

23
Q

What is considered HTN in pregnancy

A

140/90 or an increase of 30/15

24
Q

1st line management of HTN

A

<55/T2DM: ACE inhibitor or ARB
>55 or A/AC: CCB

25
Q

2nd line management of HTN

A

A+C or A+D
C+A or C+D

26
Q

3rd line management of HTN

A

A+C+D

27
Q

4th line management of HTN

A

if K <4.5 - spiro
If K >4.5 - Alpha or beta blocker

28
Q

pathophysiology of HOCM

A

autosomal dominant
defect in gene encoding contractile proteins
LVH causes decreased compliance and decreased CO
septal hypertrophy causes LV outflow obstruction

29
Q

which specific genes can be affected in HOCM

A

beta-myosin heavy chain protein
myosin binding protein C

30
Q

How does HOCM present

A

mostly asymptomatic
exertional SOB
angina
syncope often following exercise
sudden death

31
Q

HOCM examination findings

A

jerky pulse, double apex beat
ESM
Pansytolic murmur

32
Q

Investigation HOCM

A

ECHO: MR SAM ASH
- MR
- systolic arterior motion of anterior mitral valve leaflets
asymmetric hypertrophyBo

33
Q

Biopsy HOCM

A

myofibrillar hypertrophy with chaotic and disorganised myocytes and fibrosisHOCM

34
Q

HOCM management

A

Amiodarone
Beta blockers
Cardioversion
Dual chamber pacemaker
Endocarditis prophylaxis

35
Q

Meds CI in HOCM

A

nitrates, ACE I, inotropes