Cology, Acei, Arb, Renin Inhibitors

Front 1

activities of the renin-angiotensin system

Back 1

bp regulation

secretio of aldosterone

renal blood flow

Na excretion

cns effects: enhance sns

ans

tissue-angiotensin system

Front 2

angiotensin work on these receptors

Back 2

AT 1-4

Front 3

ang 3 and 4 work on the --- receptors

Back 3

AT4

Front 4

ang 1-7 work on the --- receptors

Back 4

Mas-R

Front 5

Mas-R actions

Back 5

vasodilation

natriuresis

Front 6

at1 receptor actions

Back 6

vasoconstriction

aldosteroe

Na retention

Cell proliferation

Front 7

at2 actions

Back 7

vasodilation

aniproliferative

apoptosis

(almost opposite to at1. . . prominent role in fetal development)

Front 8

renin is a --- enzyme

Back 8

protease

Front 9

renin cleaves -- aa off antioteninogen to form inactive ---- --

Back 9

4

angiotensin 1

Front 10

what is renin synthesized as

Back 10

pre-prohormone

Front 11

renin is synthesized as pre-prohormone and processed to ------ which is inacitve

Back 11

pro-renin

Front 12

what synthesizes, stores and releases renin

Back 12

juxtaglomerular cells in the afferent arterioles

Front 13

t/f

juxtaglomerular cells in the efferent arterioles synthesizes, stores, and release renin

Back 13

afferent

Front 14

what controls the RAS system

Back 14

rate of release of kidneys

Front 15

secretion of renin controlled by

Back 15

renal baroreceptors

changes in NaCl in macula densa

SNS

Front 16

secretion of the renin controlled by renal -----, changes in --- in macula densa, and the sns system

Back 16

baroreceptors

NaCl

Front 17

renal baroreceptors responds to ------ of afferent arterioles

for example decreased perfusion, will lead to an increae in --- release

Back 17

stretch

renin

Front 18

macula densa responds to changes in Cl in the -- ----

Back 18

distal tubule

Front 19

--- Cl will stimulate renin release

Back 19

decrease

Front 20

what innervates juxtaglomerular cells

Back 20

SNS

Front 21

renal ---- --- controls release of renin

Back 21

nerve activity

Front 22

--- activation increases renin release

Back 22

sympathetic

Front 23

---receptors increase renin release

Back 23

beta 1

Front 24

--- receptors decrease renin release

Back 24

alpha 1

Front 25

which has a bigger role beta 1 or alpha 1

Back 25

beta 1

Front 26

ang 2 vasoconstricts thru which receptor

Back 26

AT2

Front 27

ang2 stimulates --- secretion

Back 27

aldosterone

Front 28

thru which receptors will ang 2 cause aldosterone secretion, renal vasoconstriciton, and increase sympathetic outflow by central action

Back 28

AT1

Front 29

what will inhibits renin release via neg feedback

Back 29

ang 2

Front 30

ang 2 increase ---- outflow by central action

Back 30

sympathetic

Front 31

ang 2 increase -- release by acting on the ---- receptors

Back 31

NE

presynaptic

Front 32

via what receptors does ang 2 increase ne

Back 32

AT1

Front 33

ang 2 stimulate ---, --, and ----- centrally

Back 33

thirst

Na appetite

ADH secretion

Front 34

what also regulates thirst

Back 34

cns

Front 35

ang 2 causes cell/tissue ---- and cardiac ----- after mi via what recetpors

Back 35

hypertrophy

remodeling

AT1

Front 36

t 1/2 of ang 2

Back 36

short

15-60 sec

Front 37

--- removes amino terminal aspartate to form ANG 3

Back 37

aminopeptidase

Front 38

t/f

ang 3 has limited activity

Back 38

t

Front 39

what cleaves ang 3 to inactive products

Back 39

angiotensinase

Front 40

ang 2 actions on bp

how

Back 40

10-25% effective on BP

increase aldosterone via AT1 and AT4

Front 41

ang 3 (3-8) increase aldosterone via -- and --- receptors

Back 41

AT1

AT 4

Front 42

ang 4 (3-8) works on --- and ----

it counteracts ang ----

Back 42

memory

learning

ang 2

Front 43

angiotensin (1-7) has opposite effects on ang ---

Back 43

ang 2

Front 44

overactive RAS can lead to:

Back 44

HTN

CHF


Diabetic nephropathy

myocardial remodeling post MI

Front 45

ace: dipeptdyl carboxypeptidase removes -- aa fromteh carboxy termnal of -----

Back 45

2

peptide

Front 46

t/f

ace selective for ang 1

Back 46

f

not selective

Front 47

ace inactivates -----, cleaves ---- and ----

Back 47

inactivates bradykinin

cleaves enkephalins

cleaves sub P

Front 48

where is ace found

esp?

Back 48

vascular endothelial cell

esp lungs

Front 49

why doesn't ace cleave ang 2

Back 49

due to proline

2nd to last aa

Front 50

ace is enzyme w/ -- binding domain

Back 50

Zn

Front 51

acei have a functional group that binds the --- at the active site of the enzyme

Back 51

An

Front 52

what the main difference in acei

Back 52

functional group that binds the Zn moiety

Front 53

which acei has a sulfhydryl group

Back 53

captropril

Front 54

which acei has a phosphyinly group

Back 54

fosinopril

Front 55

which acei has a carboxyl group

Back 55

all other inhibitors

Front 56

when acei bind to zinc what does this prevent

Back 56

ang 1 from bind and creating ang 2

Front 57

acei inhibit ---- vasoconstriction

Back 57

ang 2

Front 58

ace i inhibit --- vasoconstriction

Back 58

ang 2

renal

Front 59

acei prevents synthesis of ---- and ---- reabsorption

Back 59

aldosterone

Na

Front 60

acei inhibit --- metabolism

Back 60

bradykinin

so more bradykinin to vasodilate

Front 61

acei inhibit ang 2 mediated incease in -- release

Back 61

NE

both centrally and peripherally

Front 62

due to acei there will be a neg feedback to increase --- and ----

Back 62

ang 1

renin

Front 63

how are acei different, same

Back 63

different: t 1/2 and metabolism

same: MOA and effects

Front 64

prodrug esters of acei have to be activated in the --- to be active

Back 64

liver

Front 65

which acei don't have to be activated

Back 65

captopril

lisinopril

Front 66

active form eliminated thru

Back 66

kidneys

Front 67

which active form not eliminated thru kidneys

Back 67

fosinopril

Front 68

why is captopril no a q day med

Back 68

short t 1/2

Front 69

how is fosinopril eliminated

Back 69

balanced elimination btw liver and kidneys

Front 70

dosage form of enalaprilat

Back 70

iv

Front 71

why migh acei need bid dosing

Back 71

towards end of dosing interval may loose effectiveness

Front 72

w/ acei there's a --- dose response at low doses

higher doses --- dose response

Back 72

steep

flatter

if you double dose does not mean you'll double the effect

Front 73

how do acei tx htn

Back 73

decrease tpr: sbp and dbp

decrease L ventricular hypertrophy due to elevated bp

Front 74

who will be less effected by acei

less effective as MONOTHERAPY

Back 74

blacks

due to low renin, vol senisitive htn

Front 75

when used w/ ---- acei are equally effective in blacks and whites

Back 75

diureticq

Front 76

acei are the preferred antihtn in ----

Back 76

diabetics

Front 77

who should receive acei unless contraindicated

Back 77

LV dysfunction

Front 78

How do acei help w/ l ventricle dysfunction. . .chf

decrease -- remodeling and hypertrophy

decrease vascular ---- (afterload)

decrease ----, increase ------

Back 78

LV

resistance

preload

increase CO

Front 79

acei will delay or prevent the progression of -----

decrease the incidence of --- or hospitalization

Back 79

CHF

MI

Front 80

why use acei post mi

Back 80

decrease myocaridal remodeling following infarction

decrease overall mortality when given post mi

Front 81

whic dm pt gets acei

Back 81

thos wil at least 1 risk for cv disease

Front 82

acei given to pts at high risk for --- ---

Back 82

cv events

Front 83

acei given to pts w/ establised ------

Back 83

CAD

Front 84

diabetic nephropathy decrease ----- pressure and --- of w/in kidney

Back 84

glomerular

remodeling

Front 85

acei --- and ---- progression of renal disease in dm

Back 85

prevent

delay

Front 86

diabetic nephropathy slow progression of renal disease in other -----

Back 86

nephropatites

Front 87

dry cough w/ acei due to

Back 87

bradykinin and sub p accumulation in the lungs

Front 88

when do u see dry cough in acei

Back 88

from week 1 to 6 mo

Front 89

t/f

dry cough r/t to dose and specific agent

Back 89

f

not related

Front 90

dry cough mostly seen in men/women

Back 90

women

Front 91

t/f

always d/c acei if pt has a cough

Back 91

f

if bothersome

Front 92

hypo/hyper-kalemia seen w/ acei

Back 92

hyperkalemia

mainly seen w/ renal disease or w k sparing diuretics, supplements/salts

Front 93

when will the pt have hypotension w/ acei

Back 93

first dose

upwards titration

due to sudden wipe out of angiotensin

Front 94

when is hypotension most common

Back 94

in Na depletion

CHF

multi antiHTN meds

Front 95

why might acei cause renal fx impairment

Back 95

cuz renal bl flow might be dependent on ANG 2

acei will decrease ang 2 and decrease GFR

Front 96

how do you use acei w/ renal failure

Back 96

use cautiously, low doses move upward slowly

Front 97

acei should not be used w/ ---- and -----

Back 97

aortic stenosis

renal artery stenosis

Front 98

why shouldn't acei be uses w/ aortic stenosis and renal artery stenosis

Back 98

cuz bl flow around plaque might be dependent on the angiotensin

so it's removed. . .ischemia

Front 99

angioedema is rapid swelling of

Back 99

nose, throat, mouth, larynx, lips, and tongue

Front 100

when does angioedema develop

Back 100

w/in first week

Front 101

t/f

angioedema irreversible

Back 101

f

reversible if drug removed

Front 102

what might cause angioedema

Back 102

bradykinin accumulation

Front 103

when is acei ci in pregnancy

Back 103

2nd and 3rd trimesters

birth defects and fetal death

Front 104

which receptors are common in the fetus

Back 104

AT2

Front 105

pruritic skin rash most often w/ ---

Back 105

captopril

Front 106

--- disturbances is a se

Back 106

taste

binding of zinc drugs

Front 107

--- can decrease ace inhibitors effects

Back 107

NSAIDS

Front 108

how can nsaids decrease acei effects

Back 108

blocks bradykinin mediated relaxation due to PGs

Front 109

limiting factor of acei

Back 109

there are other pathways for ang 2 production:

trypsin

cathepsin

chymase

Front 110

to help w/ limiting factor of acei what do you do

Back 110

block the receptor

Front 111

which receptor expressed widely

Back 111

AT1

heart

endothelium vsm

kidney

Front 112

at2 expressed during ----

Back 112

development

limited in adults

Front 113

why a sustained blockade at AT1 receptors

Back 113

high affinity binding

slow dissociation

Front 114

actions of AT1 receptor blockade

Back 114

vasodilation

renal vasodilation

decrease aldosterone

decrease Na reabsorption

decrease NE (presynaptic)

decrease preload/afterload/vascular resistance

Front 115

which is better at reducing effects of ang 2 at AT1 receptor

Back 115

ARB's

Front 116

arb's indirectly activate ---- receptors by directly increasing -----

Back 116

AT2

ang2

(at2 vasodilates)

Front 117

disadvantae of arb

Back 117

don't inhibit breakdown of bradykinin

so bradykinin is broken down; this helped w/ vasodilation

Front 118

how are acei eliminated

arb's?

Back 118

acei: renal

arb: renal and bile

Front 119

15% of this arb is converted to 5-carboxycylic acid metabolite

Back 119

losartan

Front 120

at1 ---- at starting doses for most arb's

dose response -----

Back 120

saturated

nonlinear

so if you increase dose don't see much incease in effects

Front 121

why AT1 receptors saturated at starting doses

Back 121

cuz of high affinity

Front 122

which arb is the only fda approved med for HG

Back 122

valsartan

used when can't tolerate acei

Front 123

which is preferred for diabetic nephropathy

Back 123

arb's for renoprotection in type 2

Front 124

t/f

arb preffered for diabetic nephropathy for type 1 dm

Back 124

f

type 2

Front 125

for dm nephropaty which is give acei or arb for type 1

Back 125

acei

Front 126

initial use of arb worsens hf, but

Back 126

long term beneficial

Front 127

t/f

arb recommended for first line tx for simple MI

Back 127

f

not first line

Front 128

valsartan as effective as ----- in mi pts w/ --- ---- ---

Back 128

captopril

left ventricular dysfunction

Front 129

when do yu use arb in post mi

Back 129

when can't tolerate acei

Front 130

se of arb

----kalemia

Back 130

hyperkalemia

esp w/ renal disease or k sparing diuretics

Front 131

hypotension w/ --- ---- effect w/ arbs

Back 131

first dose

Front 132

why might there be impairment of renal fx w/ arb

Back 132

ang 2 important for renal fx

Front 133

when are arb ci in pregnancy

Back 133

2-3 trimester

Front 134

dosing for hf

Back 134

start low and titrate up

Front 135

arbs should not be used for

Back 135

aortic stenosis

renal artery stenosis

Front 136

t/f

arbs cause cough

Back 136

f

Front 137

direct renin inhibitor

Back 137

aliskiren

Front 138

aliskiren is --- active

dosing

Back 138

orally acitve

once daily

Front 139

what will decrease absorption by 71% of aliskiren

Back 139

high fat

Front 140

aliskiren has -- bioavailabilty

Back 140

low

Front 141

will aliskiren effect bradykinin levels

Back 141

no

Front 142

aliskiren mainly excreted ----- in the feces

Back 142

unchanged

Front 143

arbs used in combo w/ --- are more beneficial

Back 143

diuretics

Front 144

arbs --- effective in salt-sensitive form of htn

Back 144

less

so use diuretic

Front 145

which is better: aliskiren monotherapy or in combo

Back 145

in combo w/ hctz and valsartan

Front 146

se of aliskiren

Back 146

ha

dizziness

gi: diarrhea, dyspepsia

rash

angioedema: although less than acei

hyperkalemia: when in combe w/ valsartan, so monitor electrolytes

Front 147

over time there might be an increase in --- w/ renin inhibitors

Back 147

renin

Front 148

renin inhibitors have a --- dose response curve

Back 148

shallow

so double dose does not double the effect

renin inhibitors might lose effectiveness