Hypertension Flashcards

1
Q

two types of hypertension

A

primary and secondary

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2
Q

factors of primary hypertension

A

family, race, obesity, stress, smoking, lifestyle, high fat diet

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3
Q

factors of secondary hypertension

A

renal disease, pregnancy, drug induced, cushing

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4
Q

stage 1 hypertension BP

A

130-139 / 80-89

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5
Q

stage 2 hypertension BP

A

> 140 / >90

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6
Q

elevated BP

A

120-129 / <80

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7
Q

hypertensive crisis

A

> 180 / > 110

stroke or MI can occur

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8
Q

what can hypertension lead to

A

heart failure, cerebral hemorrhage- stroke, kidney failure

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9
Q

how does body control BP

A

adrenergic NS
broreceptors
EPI and NE increase BP
RAAS

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10
Q

non drug therapy for hypertension

A
decrease sodium and fat
weight reduction
moderate alcohol
increase physical activity
avoid tobacco
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11
Q

rules with ions in kidneys

A

where Na goes H2O follow
if Na goes in K goes out
if H goes in Na goes out
if Cl goes in Na follows

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12
Q

5 parts of nephron

A
glomerulus
PCT
LOH
DCT
collecting duct
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13
Q

processes of urine production

A

filtration
reabsorption
secretion

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14
Q

functions of kidneys

A

water/electrolyte/acid-base balance

rids of excess waste in urine

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15
Q

where does filtration occur

A

glomerulus

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16
Q

when does tubule reabsorption occur

A

ions go from tubules to blood supply or vascular system

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17
Q

when does tubular secretin occur

A

ions go from blood supply to tubules

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18
Q

what happens at proximal and distal site

A

H ions secreted causing sodium and water to be reabsorbed

19
Q

what happens at loop of henle

A

Cl ions reabsorbed and sodium and water follow

20
Q

what happens at distal tubule site

A

aldosterone released to control K levels

Na and water reabsorbed K secreted, can cause hypokalemia

21
Q

collecting duct

A

ADH maintains water balance causing increase in blood volume

22
Q

collecting duct

A

if depleted ADH: pt can use vasopressin (DDAVP): mimics ADH

23
Q

MOA of thiazide and thiazide like diuretics

A

inhibit hydrogen secretion

24
Q

types of diuretics

A

thiazide
thiazide-like
loop
potassium sparing

25
MOA of loop diuretics
prevent Cl and Na reabsorption
26
MOA of potassium sparing diuretics
block aldosterone receptor
27
patient teaching of diuretics
``` overdose can be life threatening taking as prescribed helps control HBP syncope can be experienced monitor pulse if taking with glycoside orthostatic hypotension can result log daily weight ```
28
side effects of thiazide diuretics
hypokalemia causing: | leg cramps, muscle weakness, constipation, arrhythmias, lethargy, decreased alertness
29
patient teaching of thiazide diuretics
eat high in potassium can cause hypercalcemia, hyperlipidemia, hyperglycemia, hypericemia report to MD: increased HR
30
types of sympatholytics
BB (-olols) centrally acting aplha 2 adrenergic agonists peripheral alpha 1 blockers
31
RAAS
decrease in renal perfusion to kidneys increase of renin from juxtagolmerular cells of kidney angiotensionogen, angiotensin 1, ACE, angiotensin 2
32
what does the RAAS cause
increase in aldosterone release increase in NA reabosrption and water volume increase in blood volume
33
goal of RAAS
increase BP
34
what do all ACE inhibitors end in
pril
35
what do ACE inhibitor do
prevent angiotenin 1 to convert to angiotensin 2 decrease aldosterone release decrease sodium reabsorption and water can cause hyperkalemia
36
goal of ACE inhibitors
decrease BP
37
bradykinin
vasodilator | kininase
38
increase in bradykinin causes
vasodialtion
39
3 side effects of ACE inhibitors
hyperkalemia, coughing, angioedema
40
what do all angiotensin 2 receptor antagonist (ATII) drugs end in
sartan
41
MOA of (ATII) receptor antagonists
block AT II receptor | causing decrease in aldosterone release and vasodilation
42
hypotension symptoms
dizziness, light head, sweat, syncope
43
treatment of hypotension
lay down, elevate legs, oxygen, fluids