HTN Flashcards

1
Q

what is secondary HTN

A

caused by renal disease, sleep apnea, or adrenal disease

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2
Q

what is primary or essential HTN

A

what most people have

cause is unknown but attributed to risk factors

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3
Q

which systems have increased activity in HTN

A

sympathetic nervous system

Renin-angiotensin-aldosterone system

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4
Q

Describe how the RAAS system increases blood pressure

A

low blood pressure signals the liver to release angiotensinogen and renin which converts to angiotensin I. ACE then converts this to Angiotensin II which causes aldosterone secretion and vasoconstriction. aldosterone prompts increase Na and water reabsorption increasing blood volume.

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5
Q

how does an ACE inhibitor affect blood pressure

A

it prevents ACE from inactivating bradykinin (which causes vasodilation) and prevents the conversion of angiotensin I to angiotensin II

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6
Q

how does the sympathetic nervous system cause increased blood pressure

A

low blood pressure signals the brain to release Norepi which causes vasoconstriction by activating the alpha-1 receptors as well as increased HR and contractility by activating the beta 1 receptors

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7
Q

What do DHP CCBs affect?

A

SVR (systemic ventricular resistance)

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8
Q

what do non-dhp ccbs affect

A

contractility and heart rate

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9
Q

Normal blood pressure

A

<120/<80

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10
Q

top or bottom number: systolic

A

top

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11
Q

top or bottom number diastoli

A

bottom

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12
Q

HTN values

A

> /= 130/ >/= 80

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13
Q

what should sodium intake be reduced to for HTN management?

A

<1500mg/daily

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14
Q

when to start drug treatment

A

stage 2 HTN (>140/>90)
or
stage 1 HTN + ASCVD risk >/=10% or clinical CVD

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15
Q

First-line agents: non-black patients

A

thiazide, CCB, ACE inhibitor, ARB

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16
Q

First-line agents: black patient

A

thiazide or CCB

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17
Q

First-line agents: CKD (all races)

A

ACEi or ARB

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18
Q

First-line agents: diabetes with albuminuria

A

acei or arb

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19
Q

First-line agents: stage 2 HTN with readings >150/90

A

start 2 first-line agents

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20
Q

which first line agents should not be used in combo

A

acei and arbs

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21
Q

can you add a second agent before the first one is titrated to max?

A

Yes! actually works better and can prevent side effects

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22
Q

which htn drugs have a boxed warning for fetal toxicity when used in pregnancy

A

acei, arbs, and aliskiren

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23
Q

what is recommened in patients with a high risk of preclampsia

A

low dose aspirin daily after first trimester

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24
Q

when to treat chronic htn in a pregnant patient

A

if >/= 160/105

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25
Q

First-line agents: pregnant patient

A

labetalol and nifedipine ER

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26
Q

MOA thiazide diuretics

A

inhibit sodium reabsorption in the distal convoluted tubules, increasing excretion of sodium, cl, water, and K

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27
Q

thiazides CI

A

sulfonamide allergy

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28
Q

at what Crcl should thiazides not be used

A

CrCl < 30

29
Q

which thiazide is available IV

A

chlorothiazide

30
Q

which drug should not be used with thiazides due to increased risk of toxicity

A

lithium

31
Q

List of DHP CCBs

A

“-pine”

32
Q

MOA DHP CCBs

A

inhibit Ca from entering vascular smooth muscle and myocardial cells, causes peripheral arterial vasodilation

33
Q

Which side effects occur with CCBs due to peripheral vasodilation

A

reflex tachycardia/palpitations
headache
flushing
peripheral edema!

34
Q

Which CCB is preferred in HF

A

amlodipine

35
Q

CI Nicardipine

A

advanced aortic stenosis

36
Q

Non-DHP CCBs indication

A

control HR/arrhythmias

Afib

37
Q

MOA non-DHP CCBs

A

negative inotropic and chronotropic effects (decrease force of ventricular contractions and decrease HR)

38
Q

Side effects with non-DHP CCBs

A

edema, constipation, gingival hyperplasia

39
Q

CYP considerations with CCBs

A

CYP3A4 substrates

40
Q

If a patient experiences angioedema with an ACEi or ARB, can you try the other class?

A

NO

41
Q

ACEi/ARBs safe in pregnancy?

A

NO! Boxed warning

42
Q

hypo or hyperkallemia with ACEi?

A

hyperkalemia!

43
Q

why are K+ sparing diuretics used in combo with thiazides?

A

to combat K+ loss

44
Q

Which K+ sparing is non-selective?

A

spironolactone - also blocks androgen

45
Q

When are beta blockers recommended first line?

A

post-MI
ischemic heart disease
heart failure

46
Q

Which beta blockers are preferred in heart failure

A

metoprolol succinate
bisoprolol
carvedilol

47
Q

beta 1 selective beta blockers

A

atenolol
esmolol
metoprolol
nebivolol

48
Q

Non-selective beta blockers

A

propranolol
nadolol
carvediolol
labetalol

49
Q

CI beta blockers

A

hepatic impairment

50
Q

What type of beta blockers are preferred in bronchospastic disease

A

selective

51
Q

Why do we have to be cautious in diabetic patients on beta blockers

A

beta blockers can mask hypoglycemia

52
Q

metoprolol tartrate IV:PO dosing

A

1:2.5

53
Q

why does propranolol have more CNS effects

A

high lipid solubility = crosses BBB

54
Q

what can help with orthostatic hypotension in carvedilol

A

taking with food!

55
Q

alpha 2 adrenergic agonists list

A

clonidine

guanfacine

56
Q

MOA alpha 2 adreergics

A

stimulating these receptors reduces outflow of norepi which causes decreased SVR and HR

57
Q

which alpha 2 comes in a patch?

A

clonidine

*good for patients who can’t swallow

58
Q

which alpha 2 is commonly used in resistant HTn

A

clonidine

59
Q

which alpha 2 can be used in pregnancy

A

methyldopa

60
Q

methyldopa warnings

A

hemolytic anemia

hepatic necrosis

61
Q

list of direct vasodilators

A

hydralazine

62
Q

hydralazine CIs

A

mitral valvular rheumatic HD

CAD

63
Q

Alpha blocker list

A

-zosin

64
Q

role of alpha blockers

A

can be used in men with HTN and BPH

65
Q

HTN emergency or urgency - organ damage

A

emergency

66
Q

HTN emergency or urgency which one needs IV treatment

A

emergency

67
Q

How quickly do we need to decrease BP in emergency

A

NO MORE than 25% in first hour

68
Q

IV meds for HTN

A
chlorothiazide
diltiazem
enalaprilat 
esmolol
hydralazine 
labetalol 
metoprolol 
nicadipine 
propranolol
verapamil