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Ashland > HTN pathopharm (325E1) > Flashcards

HTN pathopharm (325E1) Flashcards

1
Q

what is the primary driver of BP

A

the sympathetic nervous system

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2
Q

what are the two ways RAAS affects BP

A

1) Na & H2O retention (fluid volume)
2) Vasoconstrictor & H2O retention (tighter/smaller passage)
how much volume is on board in blood vessels to keep normal BP

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3
Q

RAAS system

A

drop in BP and/or changes in Na levels -> release of angiotensinogen (A) by liver -> kidneys release renin which combines w/ A to make angiotensin 1 -> in the lung A1 is converted to A2 by ace -> A2 + adrenal glands release aldosterone to increase Na & H20 retention or combines w/ ADH to cause vasoconstriction

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4
Q

what is pathological reason for hypertension

A

chronic stress that stimulates RAAS so RAAS is constantly running, not just when it is actually needed to maintain or hypersensitivity to angiotensin 2 or high secretors of renin

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5
Q

other mechanisms that affect blood pressure

A

1) arterial baroreceptors: receptors in the heart that sense BP and can alter by altering HR
2) vascular auto-regulation: regulates based on mean arterial pressure (MAP) so alters the resistance (diameter) in the arterioles consistent BP at tissue level

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6
Q

blood pressure categories

A

normal: <120 & <80
elevated: 120-129 & <80
HTN 1: 130-139 or 80-89
HTN 2: 140+ or 90+
HTN crisis: >180 &/or >120

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7
Q

primary HTN

A

“no known cause”
complicated interactions of genetics, environment & several neurohormonal effects
SNS, RAAS, Natriuretic peptides

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8
Q

what causes an overactive SNS that then leaves to increased BP/HTN

A

systemic inflammation, endothelial disfunction, obesity related hormones, insulin resistance which leads to systemic vasoconstriction, overactive raas -> overtime remodels blood vessels & damages which leads to permeant increase of peripheral vascular resistance

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9
Q

natriuretic peptides

A

chemical and hormones that helps control renal sodium excretion interruptions in these can cause increased BP by holding onto more Na & H2O causing increased BP

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10
Q

risk factors for primary hypertension

A

-insulin resistance
-age: M >55, F>60
-smoking
-salt intake
-low activity
-stress
-obesity
-African Americans
-high Alc consumption
-hyper lip
-genetics

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11
Q

secondary hypertension

A

known cause -> treat underlying condition
-renal disorder: kidneys not sensing BP prop
-adrenomedullary tumors: constant secretion of aldosterone or release of angiotension
-adrenomedullary tumors: release epinephrine & stims SNS
-Drugs (meds)
-pregnancy

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12
Q

what medications can lead to secondary hypertension

A

-oral contraceptives
-corticosteroids
-antihistamines
-cocaine
-amphetamines

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13
Q

Signs and Symptoms of HTN

A

silent killer, usually no signs
look for end organ damage (chest pain, headache, visual changes, weakness/pain in extremeities)

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14
Q

what is HTN highly correlated with

A

CAD bc of high demand the left ventricle causing hypertrophy -> accelerates progression of atherosclerosis and increases risk for aortic aneurysm weakened vessel walls)

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15
Q

long term outcomes of HTN

A

-cardiac: CAD
-Kidneys: ESRD (inc raas & sns)
-brain: stroke/aneurysm/hemorrhage (dec blood flow & O2)
-eyes: retinopathy & blindness (leading cause, inc pressure)
-gangrene, intermittent claudication

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16
Q

HTN crisis

A

-rapidly progression htn
-occurs more common in primary htn
-2 types: urgency & emergency (more serious)

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17
Q

HTN crisis: urgency

A

-no S/s of end stage organ damage
-BP >180/120
-treat w/ oral agents & gradually reduce
-causes: anxiety, pain, abrupt withdrawal

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18
Q

HTN crisis: emergency

A

-uncontrolled BP that leads to end organ damage
-BP: >180/120
-S/s: headache, blurred vision, stroke, brain hem, chest pain, acute coronary syndrome, heart dysry
-aggressively lower BP in mins to hours w/ IV meds (labetalol)

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19
Q

classes of diuretics

A

-potassium sparing
-thiazide
-loop

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20
Q

how do diuretics lower BP

A

decreasing cardiac output by lowering stroke volume (block sodium & chloride reabsorption)

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21
Q

what is the first line management of HTN

A

thiazide diuretics

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22
Q

what is the thiazaide diuretic we will be tested on

A

hydrochlorothiazide

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23
Q

where do thiazide diuretics work

A

distal tubule

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24
Q

what are potassium rich you should eat when on a thiazide & loop diuretics

A

avocado, spinach, watermelon, banana, beans, tomatoes, sweet potatoes, beets

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25
Q

what should you monitor in a pt on hydrochlorothiazide & furosemide

A

potassium labs

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26
Q

what is the loop diuretic we will be tested on

A

furosemide

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27
Q

where do loop diuretics work

A

loop of henle

28
Q

what does loop diuretics cause

A

profound diuresis (so used for HTN & fluid overload)

29
Q

what can indicate kidney dysfunction

A

low urine output in a pt taking a loop diuretic

30
Q

normal K+ range

A

3.5-5

31
Q

what is the potassium sparing diuretics diuretic we will be tested on

A

spironolactone

32
Q

what diuretic is usually given with another class of diuretics

A

potassium sparing

33
Q

what should you monitor in a person taking spironolactone

A

+K because of hyperkalemia

34
Q

classes of sympatholytics

A

-alpha adrenergic blockers
-centrally acting alpha2 agonists
-beta adrenergic blockers

35
Q

what do sympatholytics all impact

A

the SNS (fight or flight response) which causes vasoconstriction which is usually good unless chronically wrongly activated then we need these drugs to turn it off

36
Q

what beta adrenergic blockers do we need to know for the exam

A

-metoprolol (selective)
-propranolol (non selective)
-carvedilol (alpha & beta)

37
Q

two types of beta receptors

A

-beta 1: found in the heart (cardioselective)
-beta 2: found in the lung (usually we do not want to block this)

38
Q

what pts should not take propranolol & carvedilol

A

pt’s with lung disease, asthma or COPD bc it is non selective and will block beta 2

39
Q

blocking beta 1 receptors does what

A

decrease heart rate and contractility

40
Q

increasing nitric oxide does what

A

causes vasodilation

41
Q

what can beta blockers mask

A

hypoglycemia bc it prevents tachycardia which is a main sign of low BG

42
Q

what happens if you do not wean a pt off of beta blockers

A

possible rebound HTN which causes critical rise in BP and puts pt at high risk for CV event/stroke/death

43
Q

when do we hold beta blockers

A

HR is less than 60 or systolic BP is less than 100

44
Q

what alpha 2 adrenergic antagonist do we need to know for the exam

A

clonidine

45
Q

what selective alpha 1 blocker do we need to know for the exam

A

doxazosin

46
Q

what are the classes of RAAS blockers

A

-ace inhibitors
-ARBs
-Renin inhibitors

47
Q

what conversion in RAAS do ace inhibitors stop

A

A1 to A2

48
Q

what conversion in RAAS do ARBs stop

A

A2 to aldosterone

49
Q

what ace inhibitors do we need to know for the exam

A

-captopril
-lisinopril

50
Q

what is a first line therapy for hypertension and heart failure

A

ace inhibitors

51
Q

what is the HTN drug of choice for pts w/ DM

A

ace inhibitors (captopril & lisinopril)

52
Q

what is the biggest complaint from pts to switch from an ace inhibitor

A

dry, nonproductive persistent cough

53
Q

what is the biggest fear when giving ACE inhibitors

A

angioedema -> rare but most common in African Americans, it is the swelling of your larynx

54
Q

what drugs can pregnant women not take

A

-ace inhibitors
-ARBs

55
Q

what should you monitor if a pt is on captopril or lisinopril

A

K+ level due to risk of hyperkalemia

56
Q

what angiotensin receptor blocker do we need to know for the exam

A

Iosartan

57
Q

what is the difference in angioedema risk between ARBs and ACE

A

ARBs do not have the racial disparity seen in ACE

58
Q

what renin inhibitor do we need to know for the exam

A

aliskiren

59
Q

what RAAS blockers cannot be given together

A

ACE and ARBs

60
Q

what calcium channel blockers do we need to know for the exam

A

-nifedipine (HTN)
-nicardipine (HTN)
-diltiazem (rhythm disturbances)
-verapamil (rhythm disturbances)

61
Q

what drug should be given for refractive hypertension in an IV

A

nicardipine

62
Q

who are calcium channel blockers best for

A

elderly and African Americans

63
Q

what vasodilators do we need to know for the exam

A

hydralazine

64
Q

PO hydralazine is usually seen

A

in combination w/ other anti HTN agents

65
Q

IV hydralazine is usually seen

A

in emergent settings or when PO cannot be tolerated

66
Q

why do we care about low potassium

A

K+ works on our heart and if low can cause cardiac rhythm problem

67
Q

MOA for all diuretics

A

-increased urinary output
-decreased circulating volume
-decreased arterial resistance

Ashland (157 decks)

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