Hypertension Flashcards

1
Q

RAAS system

A

Responds when BP serum sodium levels, or blood fluid levels are low by increasing BP

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2
Q

Angiotensinogen

A

Hormone in the blood that is released by the liver when BP is low

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3
Q

Renin

A

Enzyme released by the kidneys in response to angiotensinogen in the blood (decreased blood flow in the kidneys)

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4
Q

Angiotensin I

A

Created by reaction of angiotensinogen and renin, goes to the lungs and causes lungs to release ACE

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5
Q

ACE (angiotensin converting exyme)

A

Released by the lungs

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6
Q

Angiotensin II

A

ACE converts angiotensin I into angiotensin II and angiotensin II goes to the adrenal glands; also causes arterial vasoconstriction at the kidney level which increases BP

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7
Q

Aldosterone

A

Made when angiotensin II goes to the adrenal glands; increases sodium reabsorption which increases fluid and BP; decreases potassium thru urine excretion of K

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8
Q

Arginine vasopressin (ADH)

A

causes vasoconstrictor and water retention

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9
Q

Stress and BP

A

stress elevates angiotensin II–sets off RAAS

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10
Q

Arterial baroreceptors

A

in carotid sinus, aorta, L ventricle; sense BP and alter it by increasing HR; impacts vasodilation/constriction

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11
Q

Vasoautoregulation

A

helps keep consistent BP levels by altering resistance in BVs (based on MAP—mean arterial pressure)

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12
Q

Normal BP

A

Systolic under 120 AND diastolic under 80

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13
Q

Elevated BP

A

Systolic 120-129 AND diastolic under 80

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14
Q

HTN Stage 1

A

Systolic 130-139 OR diastolic 80-89

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15
Q

HTN Stage 2

A

Systolic 140+ OR diastolic 90+

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16
Q

HTN Stage 3

A

Systolic 180+ AND/OR diastolic 120+

17
Q

What is BP known as

A

The silent killer

18
Q

Primary HTN “essential HTN”

A

occurs w/o known cause; absence of underlying disease process; occurs because of interaction between genetics and environment, several neurohormonal effects

19
Q

Factors involved in primary HTN

A

Overactive SNS due to obesity, insulin resistance; RAAS, inflammatory interleukins circulating, endothelial dysfunction, natriuretic peptides

20
Q

Insulin resistance effect on BP

A

causes structural changes like permanent increase in peripheral vascular resistance

21
Q

Natriuretic peptides

A

Cause renal sodium excretion (water retention); increased BP and fluid volume in peptides that are malfunctioning

22
Q

Secondary HTN and causes

A

HTN with a known cause of underlying disease/dx like renal disease, adrenomedullary tumors (pheochromocytoma) which stimulate epinephrine, adrenocortical tumors which constantly secrete aldosterone and release angiotensin, and drugs (oral contraceptives, corticosteroids, antihistamines, cocaine, amphetamines)

23
Q

S/S of HTN

A

None

24
Q

When do you need to check BP immediately

A

End of organ damage

25
Q

Long term outcomes of BP

A

Increased L vent work, inc risk of heart attack, L vent hypertrophy bc of excess cardiac demand, accelerated atherosclerosis, inc risk of aortic aneurysm, end-stage renal disease (inc SNS, RAAS, dec blood flow), higher risk of stroke aneurysm, and hemorrhage, retinopathy, retinal sclerosis, inc retinal eye pressure, inc tissue death, gangrene, intermittent claudication

26
Q

Hypertensive crisis

A

complication of acute, uncontrolled BP; rapidly progressive HTN with systolic over 180 and/or diastolic over 120; often primary HTN; 2 types

27
Q

Hypertensive urgency

A

no s/s of end organ damage caused by anxiety, pain, abrupt withdrawal of meds; treated with oral agents to gradually decrease BP with time

28
Q

Hypertensive emergency

A

Leads to end organ damage; pt is symptomatic (headache, blurry vision); due to stroke, brain hemorrhage, chest pain, acute coronary; tx with IV meds in minutes to hours (even tho may cause future probs)

29
Q

Angiotensin II is a….

A

Powerful vasoconstrictor