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
2nd line management of HTN
A+C or A+D C+A or C+D
26
3rd line management of HTN
A+C+D
27
4th line management of HTN
if K <4.5 - spiro If K >4.5 - Alpha or beta blocker
28
pathophysiology of HOCM
autosomal dominant defect in gene encoding contractile proteins LVH causes decreased compliance and decreased CO septal hypertrophy causes LV outflow obstruction
29
which specific genes can be affected in HOCM
beta-myosin heavy chain protein myosin binding protein C
30
How does HOCM present
mostly asymptomatic exertional SOB angina syncope often following exercise sudden death
31
HOCM examination findings
jerky pulse, double apex beat ESM Pansytolic murmur
32
Investigation HOCM
ECHO: MR SAM ASH - MR - systolic arterior motion of anterior mitral valve leaflets asymmetric hypertrophyBo
33
Biopsy HOCM
myofibrillar hypertrophy with chaotic and disorganised myocytes and fibrosisHOCM
34
HOCM management
Amiodarone Beta blockers Cardioversion Dual chamber pacemaker Endocarditis prophylaxis
35
Meds CI in HOCM
nitrates, ACE I, inotropes