Cruthirds

Question 0

Vasopressin

Answer 0

Increase water reabs
Increase BP
Vasoconstriction

Question 1

Aldosterone

Answer 1

Increase na+ and water reabs
Increase BP
Secretes k+

Question 2

Spiromolactone

Answer 2

Aldosterone antagonist 
Potassium sparing diuretic 
Decrease sodium and water reabs 
Decrease BP
Increase potassium

Question 3

Heart failure

Answer 3

Progressive clinical syndrome

Abnormality in the structure or function that impairs the ability of the ventricle to contract or eject blood

Question 4

In heart failure is the heart meeting the metabolic demand?

Answer 4

No bc cardiac output is low

Question 5

Heart failure compensation occurs when?

Answer 5

Sns and raas is activated

Question 6

SMS activation in heart failure

Answer 6

Activate beta 1 and alpha 1 causing increase co, increase hr, increase contraction, increase pressure, increase vasoconstriction, increase ne release

Question 7

Raas activation in heart failure

Answer 7

Ang 2 vasoconstrictor that increases map

Aldosterone increases sodium and water reabs increase bv, increase preload, increase FOC

Question 8

Digoxin is a ?

Answer 8

Cardiac glycoside

Question 9

What’s the critical component for contraction of all muscle cells?

Answer 9

Calcium

Question 10

Calcium role in cardiac myocytes

Answer 10

Tropinin C binds calcium which results in a conformational change exposing the actin binding site on the myosin filament allowing cross bridge formation

Question 11

Sodium movement is tied with what?

Answer 11

Calcium movement

Question 12

Scra pump

Answer 12

Moves calcium into scarp plasmid reticulum

Question 13

MOA of digoxin

Answer 13

Inhibits the sodium-potassium ATPase on cardiac myocytes

Increases sodium conc
Increases calcium in the cell

Question 14

Where does intracellular calcium get moved to?

Answer 14

Scarce plastic reticulum

Question 15

What will happen to heart failure patients on digoxin?

Answer 15

Increase contraction because more calcium In sarcoplasmic reticulum
Increases pumping ability
Beneficial for heart failure patients

Question 16

Digoxin acts in what type of manner?

Answer 16

Pns

Question 17

Digoxin and what binds near the same site on the sodium potassium ATPase pump?

Answer 17

Potassium

Question 18

Effect of potassium on digoxin activity

Answer 18

Increase potassium then decrease digoxin activity

Question 19

At therapeutic doses what is the effect that digoxin exhibits?

Answer 19

Vagiometic effect allowing digoxin to slow av node- good for a fib pts

Norm baroreceptor reflex is getting activated frequently, digoxin lowers the sensitivity so it’s not being constantly activated

Question 20

Clearance and secretion of digoxin

Answer 20

Cleared renally

Secreted by PGP

Question 21

Digoxin has good absorption where?

Answer 21

Gi tract

Question 22

Half life of digoxin

Answer 22

36 hrs

Question 23

Digoxin have a wide or narrow therapeutic range?

Answer 23

Narrow

Question 24

ADR of digoxin

Answer 24

``` N/v Vision disturbances(yellow and green halos) Av node block Ventricular arrhythmias Fatigue ```

Question 25

Drug interactions with Digoxin

Answer 25

Hyper or hypo kalemia Beta blockers and non-dhp cause decrease contractility Macrolide antibiotics- increase bioavailability Amiodarone, propane one, verapamil, spironolactone increase conc of drug

Question 26

MOA spironolactone

Answer 26

Potassium sparing Decrease bv Decrease BP Dis in vol overload

Question 27

Aldosterone in hf

Answer 27

If increase vol, increased aldosterone causes cardiac remodeling, nicreae collagen deposits and fibrosis occurs Inhibit pumping Increase stiffness and thickness of walls of heart

Question 28

Half life of spironolactone

Answer 28

7-20 hrs

Question 29

Protein binding of spironolactone

Answer 29

91-98%

Question 30

Pk of spironolactone

Answer 30

Food increases bioavailability | Hepatic metabolism to active metabolites

Question 31

ADR of spironolactone

Answer 31

N/v/d Gynecomastia Irregular menses Impotence

Question 32

Drug interactions with spironolactone

Answer 32

Acei and arbs and digoxin cause hyper kalemia

Question 33

Milrinone used for?

Answer 33

De compensated heart failure

Question 34

MOA of Milrinone

Answer 34

Inhibitor of pde3 | Inodilator

Question 35

Define Inodilator

Answer 35

Increase FOC, dilation

Question 36

Where are the effects of Milrinone present?

Answer 36

Cardiac and vascular smooth muscle

Question 37

If you inhibit PDE3 what happens to camp and amp

Answer 37

Blocks camp which inhibits amp

Question 38

Milrinone prevents block of camp to amp which enhances what effects?

Answer 38

Sns Includes beta1, beta2, and alpha1

Question 39

Onset of action of Milrinone

Answer 39

5-15 minutes

Question 40

Half life of Milrinone

Answer 40

2.5 hrs

Question 41

How is Milrinone cleared?

Answer 41

Active tubular secretion

Question 42

How is Milrinone admin?

Answer 42

Iv only

Question 43

ADR of Milrinone?

Answer 43

Hypotension Arrhythmias Thrombocytopenia

Question 44

Nesirtide is used in what?

Answer 44

Acute de compensated hf

Question 45

Nesiritide is what? Released when?

Answer 45

Recombinant bnp Released in response to vol overload

Question 46

Nesiritide results in what?

Answer 46

Natriuresis Diuresis Vasodilation

Question 47

MOA of Nesiritide

Answer 47

Binds Npr a Increases intracellular cGMP which increases natures is and diuresis including sm relaxation in venous and arterial systems Results in decrease in preload and decrease TPR

Question 48

Onset of action of Nesiritide

Answer 48

15 min

Question 49

Half life Nesiritide

Answer 49

18 minutes

Question 50

Elimination of Nesiritide

Answer 50

1 binds cell surface receptor NPR-C and cellular internalization and degradation 2 proteolytic cleavage by neutral endopeptidases 3 renal filtration

Question 51

ADR of Nesiritide

Answer 51

Hypotension | Gi upset

Question 52

Vasopressin treats?

Answer 52

Cardiac arrest

Question 53

Vasopressin is what?

Answer 53

Non- adrenergic peripheral vasoconstrictor which also increases blood flow to heart and brain

Question 54

MOA vasopressin

Answer 54

Binds v1 receptor activates ip3 mediated signaling which activated ip3 cascade results in vasoconstriction and water reabs

Question 55

Npr-a

Answer 55

Cell surface receptor that has intrinsic guanylyl Cyclades activity

Question 56

V1 receptor

Answer 56

Gq coupled receptor on vsm | When activated causes vasoconstriction

Question 57

Vasopressin can cause vasodilation where? How?

Answer 57

Where- cerebral and coronary vessels | How/why- MOA is calcium activates enos increases no, causes vsm relaxation

Question 58

Half life vasopressin, cleaved by?

Answer 58

17-35 min | Cleaved by proteases

Question 59

ADR vasopressin

Answer 59

N/v | Ab cramps

Question 60

ADH Antagonist treats?

Answer 60

Hf associated with hyper oil hyponatermia

Question 61

V2 receptor

Answer 61

Abso lateral side of collecting duct Activation of Gs coupled receptor leads to activation of adenylyl Cyclades resulting in increased camp and increased activity of pka which increases water perm across apical mem

Question 62

To.vaptan

Answer 62

Selective v2 antagonist Half life 12 hr 3a4 substrate Pgp substrate and inhibitor

Question 63

ADR of tolvaptan

Answer 63

``` Dry mouth Thirst Urinary freq Constipation Hyperglycemia ```

Question 64

Drug interactions with tolvaptan

Answer 64

CYP3a4 and pgp inhib or inducers | Digoxin may increase digoxin levels

Question 65

Conivaptan

Answer 65

V1a/v2 antagonist Iv Half life 5 to 8 hrs 3a4 substrate and inhibitor

Question 66

ADR conivaptan

Answer 66

Orthodtatic hypotension Fever Hypo kalemia Local injection site rxns

Question 67

Drug interactions with conivaptan

Answer 67

3a4 inhib/ inducers | Increase levels of simvastatin, digoxin, amlodipine, midazolam