Module 13 - Part 2

Question 1

______ are the mainstay of therapy for HTN.

Answer 1

diuretics

Question 2

What are the three main classes of diuretics?

Answer 2

Loop diuretics
Thiazide diuretics
potassium sparing diuretics/aldosterone antagonists

Question 3

Diuretics work by blocking ______ and ________ ion reabsorption from the nephron of the kidney.

Answer 3

sodium

chloride

Question 4

By preventing the reabsorption of Na+ and Cl-, diuretics make an osmotic pressure within the tubule that prevents the _____ of _______.

Answer 4

reabsorption of water

Question 5

Diuretics produce more _______ decreases in BP at sites of ____ sodium reabsorption.

Answer 5

effective

high

Question 6

______ diuretics produce the largest decrease in BP since 20% of sodium is reabsorbed at its site of action.

Answer 6

Loop diuretics (the most effective diuretics available

Question 7

Mechanism of action of loop diuretics?

Answer 7

They act by blocking sodium and chloride ion reabsorption in the thick ascending limb of the LoH

Question 8

Loop diuretics are usually reserved for situations that required rapid loss of fluid such as? (3)

Answer 8

Edema
Severe HTN that does not respond to milder diuretics
Severe renal failure

Question 9

What are the adverse effects of Loop diuretics?

Answer 9

Hypokalemia
Hyponatremia
Dehydration
Hypotension

Question 10

Low potassium levels in the blood, may also cause fatal ______ ________.

Answer 10

Hypokalemia

may cause fatal cardiac dysrhythmias

Question 11

Why does hypokalemia occur as an adverse effect when taking loop diuretics if they decrease sodium reabsorption?

Answer 11

The transporter responsible for reabsorbing Na+ and Cl- also transports K+ into the blood, which is why hypokalemia occurs

Question 12

Most commonly used class of drugs to treat HTN

Answer 12

Thiazide diuretics

Question 13

Thiazide diuretics act by two main mechanisms, what are these?

Answer 13

Blocking sodium chloride ion reabsoprtion in the distal tubule
Decreasing vascular resistance (unknown mechanism)

Question 14

For many hypertensive patients, thiazide diuretics alone _____ enough to control BP.

Answer 14

are

Question 15

Adverse effects of thiazide diuretics?

Answer 15

Hypokalemia - may cause fatal cardiac dysrhythmias
Dehydration
Hyponatremia

Question 16

Potassium sparring diuretics are also called this.

Answer 16

Aldosterone antagonists

Question 17

Aldosterone Antagonists/Potassium sparing diuretics mechanism of action?

Answer 17

Act by inhibiting aldosterone receptors in the collecting duct
Blocking these receptors causes increased sodium excretion and potassium retention

Question 18

What is the main use of potassium sparing diuretics?

Answer 18

Main use is in combination with thiazide and loop diuretics to counteract hypokalemia side effect

Question 19

Potassium sparring diuretics should not be used with these.

Answer 19

Ace inhibitors or renin in inhibitors

Question 20

What is the primary side effect of potassium sparring diuretics?

Answer 20

Hyperkalemia - may result in fatal dysrhythmias

Question 21

Beta blockers are effective at treating HTN and they do this through two distinct mechanisms, what are these?

Answer 21

Blocking cardiac beta 1 receptors

Blocking beta 1 receptors on juxtaglomerular cells

Question 22

What does blocking beta 1 receptors do?

Answer 22

Blocks catecholamine (e.g. epinephrine) binding to beta 1 receptors, decreasing CO and thus BP

Question 23

What does blocking beta 1 receptors on juxtaglomerular cells do?

Answer 23

Beta blockers decrease renin release and therefore decrease RAAS mediated vasoconstriction

Question 24

Beta blockers all have this suffix.

Answer 24

“olol”

Question 25

What are the beta blocker classes?

Answer 25

1st generation (non-selective) and 2nd generation beta blockers (selective)

Question 26

Inhibit both beta 1 (heart and juxtaglomerular cells) and beta 2 (lung) receptors

Answer 26

1st generation beta blockers

Question 27

1st generation beta blocker use can be problematic in what instances?

Answer 27

If patients have asthma or other lung disorders

Question 28

Produce selective blockage of beta 1 receptors

Answer 28

2nd generation beta blockers

Question 29

What are the adverse effects of 2nd generation beta blockers?

Answer 29

Bradycardia, decreased CO, heart failure rare, rebound hypertension/cardiac excitation is withdrawn abruptly

Question 30

How can rebound hypertension/cardiac excitation be avoided?

Answer 30

By tapering the dose of beta blockers slowly over 10-14 days

Question 31

What additional adverse effects do non-selective beta blockers have?

Answer 31

Bronchoconstriction | inhibition of hepatic and muscle glycogenolysis

Question 32

The inhibition of hepatic and muscle glycogenolysis can be dangerous to which types of patients?

Answer 32

Patients with diabetes if they accidentally take too much insulin

Question 33

How do ACE inhibitors decrease BP?

Answer 33

Decrease angiotensin II production | Inhibit the breakdown of bradykinin

Question 34

Decreased angiotensin II causes what?

Answer 34

Decreased PVR and total blood volume, thus CO

Question 35

Inhibiting the breakdown of bradykinin has what effect?

Answer 35

Elevated bradykinin leads to vasodilation

Question 36

ACE inhibitors have this suffix.

Answer 36

"ipril"

Question 37

What are the ACE inhibitor side effects related to decreased angiotensin II?

Answer 37

1st dose hypotension | Hyperkalemia

Question 38

Due to 1st dose hypotension with ACEI's, what is done?

Answer 38

first few doses should be low

Question 39

Why is hyperkalemia a side effect of ACE inhibitor use?

Answer 39

Decreased angiotensin II means decreased aldosterone release, thus decreased sodium reabsorption and thus greater potassium reasborption -- should avoid use with potassium sparing diuretics

Question 40

What are the side effects related to increased bradykinin?

Answer 40

Persistent cough | Angioedema

Question 41

Use of certain _______ may decrease the effects of ACE inhibitors.

Answer 41

NSAIDs

Question 42

Similar action to ACE inhibitors, but the mechanism differs.

Answer 42

Angiotensin receptor blockers (ARBs)

Question 43

Mechanism of action of ARBs.

Answer 43

Block the binding of angiotensin II to the AT1 receptor (do not block its synthesis), this causes vasodilation and decreased aldosterone release from the adrenal cortex

Question 44

ARBs have this suffix.

Answer 44

"sartan"

Question 45

What are the side effects of ARBs?

Answer 45

Although we would expect the sides to match up with ACE inhibitors, there is no hyperkalemia, or persistent cough, and the incidence of angioedema is much lower

Question 46

What is the mechanism of action of direct renin inhibitors?

Answer 46

Bind to renin and block the conversion of angiotensinogen to angiotensin I This is the rate limiting step of the RAAS pathway, and thus the entire pathway is affected.

Question 47

What are the adverse effects associated with DRIs?

Answer 47

Hyperkalemia Very low incidence of persistent cough and angioedema Diarrhea

Question 48

DRIs should never be used with these.

Answer 48

Potassium sparing diuretics

Question 49

How do calcium channel blockers decrease BP?

Answer 49

Block the entry of calcium into the heart cells and smooth muscle cells, therefore decreasing contraction

Question 50

What are the two categories of calcium channel blockers?

Answer 50

Dihydropyridine calcium channel blockers | Non-dihydropyridine calcium channel blockers

Question 51

At therapdeutic doses, dihydropyridine calcium channel blockers do not affect this.

Answer 51

The heart - effect exclusive to smooth muscle around arteries

Question 52

What is the suffix of dihydropyridine calcium channel blockers?

Answer 52

"dipine"

Question 53

What are adverse effects of dihydropyridine calcium channel blockers?

Answer 53

flushing, dizziness, headache, peripheral edema, reflex tachycardia, rash

Question 54

What is the difference between dihydropyridine calcium channel blockers and non-dihydropyridine calcium channel blockers?

Answer 54

The non-hydridopyrimidine counterparts also block calcium channels in the heart and thus also decrease CO.

Question 55

What are the adverse effects of non-dihydropyridine calcium channel blockers?

Answer 55

constipation, dizziness, flushing, headache, edema, may compromise cardiac function and should be used with caution in patients with cardiac failure

Question 56

What is the mechanism of action of centrally acting alpha 2 agonists?

Answer 56

bind to and activate alpha 2 receptors in the brainstem --> activation of these receptors decreases sympathetic outflow to the heart and blood vessels, thereby decreasing CO and peripheral resistance

Question 57

What are adverse effects of centrally acting alpha 2 agonists?

Answer 57

drowsiness, dry mouth, rebound HTN if withdrawn abruptly

Question 58

The target BP that most patients should achieve is less than this.

Answer 58

140/90 torr

Question 59

Patients with diabetes or chronic kidney disease should achieve a blood pressure less than this.

Answer 59

130/80 torr

Question 60

In patients with severe renal disease, ______ diuretics are ineffective so _____ diuretics should be used.

Answer 60

thiazide | loop