Test 3

Question 1

How does bradykinin produce vasodilation?

Answer 1

Stimulate the release of NO and prastacyclins for potent vasodilation

Question 2

Which is the main mineralcorticoid?

Answer 2

Aldosterone

Question 3

Which is the post potent vasocontrictor?

Answer 3

Angiotension II

Question 4

Endogenous vasoconstrictor?

Answer 4

Endothelin 1

Question 5

What does ADH cause?

Answer 5

Only H20 retention. No Na retention

Question 6

How does spironolactone affect K and Na levels?

Answer 6

K retention and Na excretion

Question 7

What does aldosterone do?

Answer 7

Na retention that leads to concomitant H20 retention
Also does K excretion

Question 8

Explain how NO causes smooth muscle relaxation?

Answer 8

NO combines with the heme group of soluble gunaylyl cyclase which converts GTP to cGMP which leads to vasodilation

Question 9

What two types of meds might you need to add with hydralazine?

Answer 9

beta blocker and diuretic (hydrochlorothiazide) to counteract the compensatory tachycardia and water retention.

Question 10

clinical results of B2 stimulation?

Answer 10

smooth muscle relaxation. I.e. lungs and vascular smooth muscle

Question 11

How do ACE-I affect renin levels?

Answer 11

increase it

Question 12

What does Aliskiren (tekturna) do?

Answer 12

reduce plasma renin activity by 50-80%. Can increase renin levels up to 10x.

Question 13

Are ACE-I safe in a pt with ischemic heart disease?

Answer 13

yes because they don’t cause reflex sympathetic activation.

Question 14

How do ACE-I affect pt with CKD?

Answer 14

diminish proteinuria and stabilize renal function.

Question 15

How do ACE-I affect DM incidence in patients with high cardiovascular risk?

Answer 15

reduce incidence of DM

Question 16

Are ACE-I venous or arterial?

Answer 16

both

Question 17

How much do ACE-I decrease BP?

Answer 17

less than 10mmHg

Question 18

What meds should you avoid with ACE-I?

Answer 18

NSAIDs - block bradykinin mediated vasodilation
K supplements. Lead to hyperkalemia
K sparing diuretics.

Question 19

clinical effects of NO?

Answer 19

relax vascular smooth muscle
inhibit platlet aggregation
inhibit leukocyte-endothelial interactions
directly prevent Na and H2O reabsorption in the kidneys

Question 20

Name a phenylalkylamine

Answer 20

verapamil

Question 21

name a benzothiazepine

Answer 21

diltiazem

Question 22

Do CCB have high or low first pass effect?

Answer 22

high

Question 23

Is orthostatic hypotension a concern in CCB?

Answer 23

Not as much as it is with nitrates.

Question 24

Which CCB has greatest affinity for cerebral vascular bed?

Answer 24

Nicardipine

Question 25

Verapamil increases levels of what other medication>

Answer 25

Digoxin

Question 26

How do alpha 2 receptors work in neurons?

Answer 26

inhibit adenylyl cyclase activity, which decreases ca ions influx into cell which decreases exocytosis of vessicle containing NE. Also decrease cAMP???

Question 27

Name the newer relatively selective alpha 1 antagonists

Answer 27

Prazosin Terazosin Doxazosin Trimazosin

Question 28

Name the older non selective alpha blockers

Answer 28

phentolamine phenoxybenzamine

Question 29

Describe how alpha 1 receptors in smooth muscle work

Answer 29

Gq linked proteins that activate smooth muscle contraction through IP3 pathway and increased Ca

Question 30

Describe how alpha 2 receptors in smooth muscle cause contraction?

Answer 30

alpha 2 are Gi proteins and binding decreases intracellular cAMP > smooth muscle contraction

Question 31

do alpha blockers affect arteries or veins more?

Answer 31

arteries because arteries are under greater sympathetic tone

Question 32

Which alpha blockers cause more more reflex tachycardia?

Answer 32

non selective alpha blockers

Question 33

How do beta agonists work in the vascular smooth muscle?

Answer 33

ATP > cAMP > de-phosphorylation of myosin light chain kinase.

Question 34

How do beta agonists work in the heart?

Answer 34

beta receptor stimulates adenylyl cyclase which converts ATP to cAMP. cAMP activates PKA which stimulates Ca influx into cell which causes increased contraction.

Question 35

What three things make up myocardial oxygen demand?

Answer 35

wall tension heart rate contractility

Question 36

4 ways we can relax vascuar smooth muscle?

Answer 36

decrease intracellular calcium increase cGMP increase cAMP hyper polarize (stabilize) cell membrane

Question 37

explain the role of calcium as it relates to myosin light chain?

Answer 37

calcium combines with calmodulin complex and activates the enzyme myosin light chain kinase which is what phosphorylates myosin light chains. Once phophorylated, MLCs can couple with actin to produce contraction.

Question 38

how do beta blockers affect L type calcium chanels in vascular cardiac cells?

Answer 38

they block cAMP from activating PKA to phosphorylate the Ca chanel which would cause an increase in calcium influx. so we end up with less calcium influx

Question 39

How does cAMP cause smooth muscle relaxation?

Answer 39

phosphorylates (inactivates) myosin light chain kinase

Question 40

how does cGMP cause vascular smooth muscle relaxation?

Answer 40

it dephosphorylates (inactivates) myosin light chain

Question 41

What is stongest predictor of ischemia under GA?

Answer 41

tachycardia

Question 42

Number 1 treatment for effort angina?

Answer 42

beta blockers

Question 43

What increases with the use of a PDE inhibitor?

Answer 43

cGMP

Question 44

Explain how NTG is processed by the body

Answer 44

denitrated by enzymes glutathiube S-transferase and mitochondrial aldehyde dehydrogenase

Question 45

do you get tachypylaxis with nitro vasodilators?

Answer 45

yes