Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

325 patho > mod 2 hypertension > Flashcards

mod 2 hypertension Flashcards

1
Q

renin angiotensin aldosterone system (RAAS)

A

RAAS- regulates long term BP and extracellular volume

angiotensionogen- released by LIVER from LOW BP and change BLOOD VOLUME (SODIUM)
- stimulates kidney to release RENIN
RENIN- converts angiotensinogen to ANGIOTENSIN 1
- ANGIOTENSIN 1 travels to LUNG and converts to ANGIOTENSIN II by ACE (angiotensin converting enzyme)
- ANGIOTENSIN II acts ADRENAL GLANDS release ALDOSTERONE (fluid retention)

ANGIOTENSIN II- potent vasoconstrictor
- causes NEPRHON to retain fluid and BP INCREASES

RAAS activated when:

  • Loss blood volume or drop BP
  • decrease renal perfusion
  • chronic stress
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

other mechanisms affect BP

A

arterial baroreceptors- receptors in carotid sinus, aorta, and l ventricle - ALTERS HR, vasodilation and vasoconstriction

vascular autoregulation- maintain tissue perfusion, regulates mean arterial pressure (MAP), resistance (diameter) arterioles
**helps consistent BP at tissues despite changes elsewhere

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

types hypertension- primary and secondary

A

categories

  • normal - less 120, less 80
  • elevated - 120-129, less 80
  • high BP (hypertension) stage 1- 130-139, 80-89
  • high BP stage 2- 140 higher, 90 higher
  • hypertensive crisis (consult dr immediately)- inc 180, incr 120
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

primary hypertension

A
  • essential hypertension, NO KNOWN CAUSES, idiopathic most common
    Why?- interactions genetics and environment - SNS, RAAS, natriuretic peptides

risk factors
- smoking, excess sodium intake, sedentary lifestyles, hyper-lipidemia, stress, family history, obesity, age > 60, african americans, high alcohol consumption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

secondary hypertension

A

KNOWN CAUSE associated

  • treat underlying condition
  • renal disorders, adrenocortical tumors, adrenomedullary tumors (pheochromocytoma), drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

hypertension causes

A

primary- excess salt, abnormal arteries, incr blood volume, genetic disorders, stress

secondary- health conditions, meds, rec drugs, pregnancy, hormone therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

S/S hypertension

A 
silent killer
must look at END-ORGAN damage
- chest pain- heart
- head ache- brain
- visual changes- eyes
- weakness/pain extremities- brain/stroke
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

long term outcomes hypertension

A

cardiac- inc l ventricle work
- hypertrophy, accelerated progress atherosclerosis, inc risk aortic aneurysm (weakened walls)

kidneys- primary cause end stage renal disease

brain- higher risk stroke, aneurysm, hemorrhage

eyes- retinopathy, blindness

lower extremities- gangrene, intermittent claudication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

hypertensive crisis

A

systolic >180 and diastolic >120
- occurs with PRIMARY hypertension

hypertensive urgency vs emergency

urgency- no S/S end organ damage, BP > 180/120, Tx w oral agents and GRADUALLY decr BP
- causes: anxiety, pain, abrupt withdrawal

  • emergency- lead to END ORGAN damage BP >180/120,
    S/S organ damage- headache, blurred vision, stroke, brain hemorrhage, chest pain, acute coronary syndrome, heart dysfunction
    **aggressively LOWER BP in mins to hrs (IV meds)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

hypertensive meds - gen diuretics (water pills) - remove excess sodium and water
MOA- incr urinary output, decr circulating volume, decr arterial resistance

A

Lower BP by decr CARDIAC OUTPUT - block sodium and chloride reabsorption
- can enhance effect other hypertensives
- least expensive
usually first line defense

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

hypokalemia = low K

loop and thiazide diuretics can cause

A

normal- 3.5-5
mild- 3-3.4
moderate- 2.5-2.9
severe- <2.5

decr K = cardiac arrythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

angiotensinogen

A

released by liver in response to low BP and low Na and blood volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

renin

A

released by kidney
stimulated by low fluid volume and low Na

  • causes liver to convert angiotensinogen to angiotensin 1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

angiotensin I

A

travels from liver to lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

ACE - angiotensin converting enzyme

A

converts angiotensin I to angiotensin II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

angiotensin II

A

acts on adrenal glands
releases aldosterone

angiotensin II potent VASOCONTRICTOR

increase BP

17
Q

aldosterone

A

from adrenal glands

causes increase Na, fluid retention, BP, and decrease K

18
Q

goal RAAS

A

to increase BP

19
Q

meds to treat hypertension

A 
diuretics
sympathetic nervous system blockers
beta blockers
calcium channel blockers
vasodilators
20
Q

diuretics (water pills) - 3 classes

  • potassium-sparing- mild
  • thiazide- mild
  • loop- moderate to profound
A

MOA

  • increase urinary output
  • decrease circulating volume
  • decrease arterial resistance

Results

  • lower BP by decreasing CARDIAC OUTPUT
  • – block sodium and chloride reabsorption
  • enhance effectiveness other hypertensives
  • least expensive
  • impacts stroke volume
    • usually 1st line therapy
21
Q

thiazide diuretics - 1st line management mild hypertension

A

Drugs

  • hydrochlorothiazide (HCTZ) - HydroDiuril
  • metolazone - Zaroxolyn

MOA

  • distal convoluted tubule inhibit reabsorption Na, K, Cl = decr cardiac output= water loss
  • relaxes arterioles = decre PVR

side effects

  • electrolyte and metabolic disturbances
  • HYPOKALEMIA (LOW K)
  • orthostatic hypotension, worsen renal insufficiency, hyper uricemia

nursing actions
- monitor K levels, K supplements, K enriched foods

22
Q

loop diuretics - also given in fluid overload

A

drugs

  • furosemide - Lasix
  • Bumetanide - Bumex
  • torsemide - Demadex

MOA

  • inhibit kidney reabsorb Na ** LOOP OF HENLE
  • kidney put more Na in urine = incr urine
  • decrease fluid in blood vessels = decr cardiac output
  • *PROFOUND DIURESIS

side effects

  • HYPOKALEMIA
  • dehydration, hypotension, ototoxicity

nursing considerations

  • monitor K levels, K supplements
    • if not have incr urine output, contact HCP
23
Q

potassium-sparing diuretics (aldosterone agonist)

A

drugs

  • spironolactone - Aldactone
  • triamterene - Dyerenium

MOA
- block action aldosterone (Na, H2O retention) = K retention and excretion Na and H2O

only provide small amount diuresis, given with combo hypertensives/diuretics to get lower chance of hypokalemia

side effects
HYPERKALEMIA
- deepened voice, impotence, irreg menstual cycles, gynecomastia, hirsutism

24
Q

sympatholytics 3 classes
Alpha-adrenergic blockers
centrally-acting alpha 2 agonists
beta adrenergic blockers

A

goal - SNS blockers cause PARASYMPATETIC response

- decreases vasoconstriction, decreases blood pressure by decreasing PVR - peripheral vascular resistance

25
Q

beta-adrenergic blockers (Beta-blockers

decr heart force, decr rate, decr renin seecretion

A

2 types - Beta-1 and Beta-2
Beta-1 receptors - found in HEART, cardioSELECTIVE beta receptors
Beta-2 - found in lungs
** OLOL = BETA BLOCKERS

Drugs:
metoprolol - selective Beta-1 blockers
propranolol - non-selective (Beta-1 & 2)
cardedivol - alpha and beta 
** pt with LUNG/RESPIRATORY issues, DO NOT USE PROPANOLOL OR CARDEDIVOL

MOA

  • incr nitric oxide = vasodilation
  • blocks stim beta-1 receptors = decr HR and heart contractility

use: many heart, but HTN

side effects

  • fatigue/lethargy
  • BRADYCARDIA, HYPOTENSION
  • mask hypoglycemia ** careful DM pts

rn considerations

  • wean when discontinue, **REBOUND HTN if abrupt discontinue= incr risk BP, CVA
  • **hold if <90 systolic and <50 HR
26
Q

alpha-2 adrenergic agonists (centrally acting sympathetic)

**not first line tx due to high side effect profile

A

drug

  • clondine- Catapress
  • methyldopa - Aldomet - most common for HTN pregnancy

MOA
decre sympathetic outflow resulting decr stim of adrenergic receptors (alpha & beta receptors) *** decr BP

side effect
- drowsiness, rebound HTN **may worsen preexisting LIVER disease

rn consideration
no discontinue abruptly, rebound HTN

27
Q

selective alpha-1 blockers

A

drug
- doxazosin - Cardura

MOA

  • selective alpha-1 blocker
    • VENOUS and ARTERIAL dilation
  • NOT first line tx

side effects
- hypotension, dizziness

**tamsulosin- Flomax also used to treat BPH

28
Q

RAAS Blockers

A
  • ace inhibitor
  • ARBs
  • renin inhibitor
29
Q

ace inhibitors
** -pril

1st line therapy hypertension and heart failure

A 
drug
captropril - Capoten
lisinopril- Zestril
enlapril- Vasotec
benazepril - Lotensin
ramipril- Altace

MOA

  • blocks angiotensin-converting enzyme (ACE)
  • inhibits prod angiotensin-2 (vasoconstrictor, inhibits alosterone secretion = less water retention
  • slows progression l ventricle hypertrophy w/HTN
  • *choice f/pt DM

side effects

  • first dose HTN
  • dry PERSISTENT cough, nonproductive
  • dizziness, rash, ANGIOEDEMA
  • *NOT FOR PREGNANT WOMEN

rn considerations

  • renal insufficiency, history renal disease
  • captopril can cause NEUTROPENIA
  • HYPERKALEMIA

-often given with thiazide diuretics

30
Q

ARBs- angiotensin receptor blockers

** - sartan

A

drug

  • losartan- Cozaar
  • eprosartan- Teveten
  • valsartan- Diovan
  • olmesartan- Benicar

MOA
blocks action angtiontensin-2 AFTER PRODUCED
- VASODILATION, incr Na and H2O excretion

indications
HTN, heart failure, stroke

side effects
well tolerated
- anioedema- not racially disparity like ACEi
**NOT FOR PREGNANT
-careful renal problems

**NEVER ACE AND ARB TOGETHER

31
Q

RENIN inhibitor - ACE and renin ok together

A

drug
aliskiren- Tekturna

MOA

  • direct inhibition of renin
  • vasodilation, decr blood volume, decr SNS, inhibit cardiac and vascular hypertrophy

side effects
well tolerated, GI discomfort, hyperkalemia when combined with ACEi

rn considerations
-long half life, NO PREGNANT

32
Q

CALCIUM channel blockers

-dipine

A

drugs
HTN
- nifedipine-Procardia
cardipine- Cardene

rhythmic disturbances

  • merapamil- Calan
  • diltiazem- Cardizem

MOA
- blocks Ca access to cells = decr contractility, decr conductibity of heart, decr O2 demand

indications
HTN and angina
- dilt and verapamil - arrythmias

side effects
-dec BP, bradycardia, may mask AV block, headache, GI discomfort, peripheral edema, orthostatic hypotension

rn considerations

  • best for elderly and African Americans
  • combo w diuretics for peripheral edema
33
Q

vasodilators

-alazine

A

drug
-hydralazine - Apresoline

MOA

  • causes relaxation smooth muscles ARTERIAL AND VENOUS muscles
  • decr SVR and PVR

indications - HTN

methods

  • PO with combo other antihypertensive
  • IV in emergency

side effects
HYPOTENSION
- dizziness, headache, tachycardia, edmea, dyspnea, GI

325 patho (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions