hypertension Flashcards

1
Q

what is hypertension?

A

persistently elevated blood pressure (>140/90)

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2
Q

BP=

A

cardiac output (CO) x peripheral resistance (PR)

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3
Q

at rest, cardiac output is

A

STABLE but PR fluctuates for varying reasons

changes in PR occur from vasoconstriction and vasodilation

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4
Q

changes in cardiac output affect the body

A

systemically

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5
Q

systole=

A

PUMPING phase (around 120 mmHg)

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6
Q

diastole=

A

RESTING phase (around 80 mmHg)

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7
Q

4 control mechanisms of BP?

A

baroreceptors
vascular autoregulation
renin angiotensin-aldosterone system (RAAS)
fluid volume regulation

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8
Q

baroreceptors?

A

located centerly in aorta and carotid arteries

  • detect changes in PRESSURE
  • feed info to NS
  • HOMEOSTATIC mechanisms engage to return pressure to original state
  • located in TUNICA EXTERNA/ADVENTITA
  • SENSORY NEURON excited by stretch of vessel—> AP—> CNS—> stimulation of vascular smooth muscle—> constrict or dilate—> alter PR—>alter BP
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9
Q

what is vascular autoregulation?

A

blood vessels constrict and dilate in response to many changes in the body (like pH, pO2)

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10
Q

what is the renin-angiotensin-alodsterone system (RAAS)

A

homeostatic mechanism triggered by DECREASED BP

it INCREASES THE BP to NORMAL RANGE

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11
Q

point form explain RAAS

A

-juxtaglomerular cells (kidneys) release RENIN, liver releases -
angiotensinogen —> angiotensin
-angiotensin I circulates until ACE is made by pulmonary capillaries
-ACE converts angiotensin I- II
-angiotensin II: stimulates thirst,constricts efferent arteriole to increase pressure, stimulates release of: aldosterone (from adrenal cortex), antidiuretic hormone (from posterior pituitary gland) BOTH promote H20 and Na retention—> INCREASE BP

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12
Q

what is fluid volume regulation?

A

kidney: excretes and retains fluid to maintain BV and BP
- OPERATES together with RAAS
- RAAS only occurs when there is DECREASED BP

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13
Q

when is BP highest?

A

in the morning! BP varies on circadian rhythm

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14
Q

when is BP lowest?

A

between 2 and 5am

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15
Q

mild htn?

A

140-159/ 90-99

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16
Q

moderate htn?

A

160-179/100-109

17
Q

severe htn?

A

> 180/>110

18
Q

what is primary hypertension?

A

> 140/90, idiopathic (unknown cause)

  • 1 or 4 control mechanisms is defective
  • may be multifactoral
  • most cases
19
Q

what is systolic hypertension?

A

systolic >140, diastolic remains normal, less than 90
occurs mostly after age 50
peripheral resistance in vessels increases d/t some degree of atherosclerostic change, change in elasticity of vessels

20
Q

white coat hypertension?

A

CLINICAL setting hypertension

21
Q

malignant hypertension?

A

ACUTE EMERG, diastolic exceeds 120

22
Q

gestational hypertension?

A

during pregnancy

most women return to normal after

23
Q

what is secondary hypertension?

A

not second phase of primary, develops because of underlying problem
-etiology is identifiable, usually due to renal disease
kidneys receive blood to filter and perfuse renal tissue
-significant part of CO goes to kidney, if excretion/reabsorption not balanced, BP affected
-decreased renal perfusion—> RAAS activated

24
Q

what is renovascular hypertension?

A

a FORM of secondary

-increased BP caused by kidneys responding to narrowed/blocked arteries supplying kidneys

25
Q

manifestations of hypertension?

A

“silent killer” because can be asymptomatic
-elevated BP, measure regularly to find this out!
later manifestations:
-fatigue, palpitations, morning headaches, blurred vision, dizziness
-can result in multi organ failure

26
Q

first thing for treatment of hypertension?

A

LIFESTYLE modifications

  • DIET (DASH)
  • EXERCISE
  • WEIGHT CONTROL
  • OTHERS—> less alcohol, waist circumference, sodium consumption, smoking, stress management
27
Q

first line of pharmacologic hypertension?

A

diuretics! monotherapy—> promotes diuresis (increase voiding, excrete fluid, decrease blood volume)

28
Q

if first line doesnt work, then what?

A

calcium channel blockers (calcium aids contraction of muscle, by blocking decrease contraction and vessels cannot constrict)
angiotensin II receptor blocker (angiotensin II must bind to receptor to be activated, but this blocks it so vasodilation–> decreased BP
ACE inhibitor, angiotensin cannot convert to II, no vasoconstriction—> decreased BP