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Pathophysiology II > week 2: blood pressure & valvular ht dz > Flashcards

week 2: blood pressure & valvular ht dz Flashcards

1
Q

______ is the measure of force exerted against the walls of arteries as heart pumps blood to the body

A

blood pressure

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2
Q

____ is consistent elevation of systemic arterial blood pressure

A

hypertension

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3
Q

true or false:

hypertension is caused by increases in cardiac output or total peripheral resistance, or both

A

true

cardiac output - increased by any condition that increases heart rate or stroke volume

peripheral resistance - increased by any factor that increases blood viscosity or reduces vessel diameter (vasoconstrict.)

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4
Q

which pathophysiologic mechanisms mediate the effects of htn?

  1. sympathetic NS
  2. renin angiotensin aldosterone system (RAAS)
  3. natriuretic peptides
A

all!

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5
Q

do inflammation, endothelial dysfunction, obesity related hormones and insulin resistance also contribute to increased peripheral resistance and increased blood volume?

A

yes!

they are all modifiable, too.

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6
Q

true or false

ppl with htn tend to secrete less salt in their urine?

A

true

bc of a shift in the pressure natriuresis relationship

(increased vascular volume related to decrease in renal excretion of salt)

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7
Q

how does the SNS affect HTN?

A

overactivity of the sns can result from increased production of catecholamines (epinephrine and norepinephrine) or from increased receptor activity from these neurotransmitters.
increased sns activity causes increased heart rate and systemic vasoconstriction, thus raising blood pressure

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8
Q

what are the organs that are involved with the RAAS ?

A

kidney
liver
lung
adrenals
heart

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9
Q

overactivity of what system contributes to salt and water retention and increases vascular resistance?

A

RAAS

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10
Q

4 stimuli that activate RAAS

A
  1. low blood volume
  2. low blood sodium
  3. sympathetic stimulation
  4. low blood pressure
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11
Q

flow of RAAS

A

renin is released from kidney to regulate the blood pressure during decreased bp, decreased na delivery, sympathetic stimulation

renin acts on angiotensinogen which is released by liver and converts in to angiotensin I

angiotensin I travels in blood to lungs
lungs convert angiotensin I into II by enzyme called ACE

angiotensin II travels through blood to adrenals. acts on adrenals and adrenals produce aldosterone

aldosterone then goes back to kidney to retain sodium and water until there is correct blood volume, also acts on heart (pumping blood - constriction) and arteries (constricting so blood pressure increases)

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12
Q

overactive RAAS causes ____

A

high blood pressure
bc there will be more blood volume

–based on sodium and water

more vascular resistance

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13
Q

high levels of angiotensin II contribute to:

A

endothelial dysfunction
insulin resistance
dyslipidemia (altered levels of cholesterol)
platelet aggregation

assoc with end organ effects of htn : atherosclerosis, renal dz, cardiac hypertrophy

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14
Q

two medications that oppose activity of RAAS, reduce blood pressure, protect against target organ damage

A

ACE and ARB

ACE block angiotensin I from converting into angiotensin II

ARB block the angiotensin I receptor sites

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15
Q

what is natriuresis?

A

sodium excretion in the urine
through action of kidneys

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16
Q

natriuresis requires which minerals?

A

potassium, calcium, magnesium

17
Q

how is natriuresis connected to htn?

A

salt retention leads to water retention and increased blood volume,
which contributes to an increase in blood pressure

18
Q

does increasing dietary intake of potassium, calcium, and magnesium enhance natriuretic peptide fx?

A

yes!
it improves body’s ability to remove salt

19
Q

how does endothelial inflammation contribute to htn?

A

endothelial injury and tissue ischemia result in the release of vasoactive inflammatory cytokines

(cytokines - messengers)

chronic inflammation contributes to vascular remodeling and smooth muscle cxn

decreased production of vasodilators (nitric oxide) and increased production of vasoconstrictors (endothelin) occurs

20
Q

how does diabetes and obesity affect htn?

A

obesity causes changes in adipokines (leptin and adiponectin) and is assoc w increased activity of sns and raas.

obesity is linked to inflammation, small artery remodeling, endothelial dysfunction, and insulin resistance and increased risk for cardiovascular complications from htn

21
Q

true or false

insulin resistance is not common in hypertension

A

FALSE

insulin resistance is assoc w decreased endothelial release of nitric oxide and other vasodilators. causes renal salt/water retention. assoc with overactive sns and raas

22
Q

true or false

chronic hypertension damages the walls of systemic blood vessels

A

true

once fibrosis (thickening/scarring) occurs, reduced blood flow and dysfunction of other organs perfused by these affected vessels in inevitable (kd, brain, ht, extremities, eyes)

23
Q

cardiovascular complications include:

A

atherosclerosis
left ventricular hypertrophy
angina pectoris
congestive ht failure (left heart)
CAD
MI
sudden death

24
Q

___ is when there is deposition of collagen in the heart muscle which causes it to become thickened, scarred, and less able to relax during diastole leading to diastolic heart failure

A

myocardial hypertrophy

25
Q

what is an early sign of impending renal dysfunction and significantly increased risk for cardiovascular events?

A

microalbuminuria (small amounts of protein in urine)

26
Q

complications of htn

A

vascular complications
retina specific complications
cerebrovascular complications

27
Q

hypertension is the most prevalent risk factor for ____

A

stroke

28
Q

what type of stroke?

blood clot stops flow of blood to an area of the brain

A

ischemic stroke

29
Q

what type of stroke?

weakened/diseased blood vessels rupture and blood leaks into brain tissue

A

hemorrhagic stroke

most commonly assoc w htn

30
Q

what is an antihypertensive med used for patients with mild/mod htn and normal cardiac/renal fx
that has side effect of Hypokalemia (low potassium)

(muscle crams, impaired diabetes control, increased LDL/HDL? )

A

thiazide diuretic

31
Q

what is an antihypertensive med used for patients to reduce blood volume and is often used with other diuretics?

used in patients to correct hypokalemia and to avoid potassium depletion

A

potassium sparing diuretic

32
Q

what is an antihypertensive med used for patients with a shorter duration of action than thiazide or potassium sparing diuretics and used when urgent diuresis is required? used for swelling/edema especially around the heart

side effects: dehydration, hypokalemia, impaired diabetes ctrl, lipid profile alterations

A

loop diuretics

33
Q

what is an antihypertensive med used to decrease myocardial contractility and heart rate by blocking the release of epinephrine and norepinephrine?

side effects: mild to moderate chronic fatigue, low exercise tolerance, sexual dysfunction in men is common

A

beta-blockers

SNS driven htn

relax musculature

34
Q

what is an antihypertensive med that interferes with renin/angiotensin cascade mechanism, inhibits production of angiotensin II and decreases total peripheral resistance

side effects: dry cough,

A

ACE inhibitors

(ens in -pril)

35
Q

what is an antihypertensive med used to inhibit Ca2+ influx into vascular smooth muscle, relax peripheral arteriole smooth muscle and thereby decrease total peripheral resistance

used in patients with ischemic heart dz, CPD, diabetes mellitus, angina

side effects: constipation, dizziness, palpitations, fatigue, flushing, HA, n, rash

A

calcium channel blockers

relax musculature

36
Q

_______ means a decrease in systolic and diastolic blood pressure on standing

A

orthostatic (postural) hypotension

systolic = -20
diastolic = -10
within three minutes of standing up

37
Q

changes in the mitral leaflet tissue aka

A

mitral valve prolapse

38
Q

what is the most common cause of severe Aortic Valva Regurgitation (AR)

A

rheumatic heart disease (from strep throat or scarlet fever)

39
Q

Aortic Valve stenosis =?

A

left venticle adapts to obstruction by increasing wall thickness while maintaining normal LV chamber size
hypertrophy is a compensatory mechanism to normalize LV wall stress

Pathophysiology II (3 decks)

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