Anti Diuretics

Front 1

Pre- htn is considered what? Htn is anything over that-- stage 1 and stage 2 possible for Htn. With Diabetes htn is anything above___

Back 1

1. 120-139 and 80-89
2. >130 or >80

Front 2

Essential htn affects what percentage of htn pts?
What diseases cause secondary htn?

Back 2

1. 90-95%- ppl think this is due to disregulation of RAAS and salt probs
2. renal artery stenosis, pheochromocytoma, primary hyperaldosteronism, coarctation of the aorta

Front 3

BP is proportional to ____ and is inversely proprtional to ____. Where is the largest site of systemic vasc resistance? What is the major site of capacitance?

Back 3

1. blood flow
2. systemic vascular resistance
3. pre cap arterioles
4. post cap venules

Front 4

CO ___ with increasing HR and with increasing stroke volume. Stroke volume increases when there is increased ___ return which increases ventricular filling pressure.

Back 4

1. increases
2. venous

Front 5

Name factors that affect vascular resistance.

Back 5

1. length and diameter of vessel
- MOST imp is vessel diameter of small arterioles
- vascular tone is degree of constriction relative to maximally dilated state-- has intrinsic and extrinsic influences-- intrinsic is myogenic and endothelial factors like NO and endothelin, extrinsic are nervous syst, RAAS, and ANP

2. vascular network org- parallel versus in series
3. physical characteristics of blood--i.e. viscosity
4. extravascular mechanical forces-- muscle contraction

Front 6

ANS (sympathetic and parasympathetic) controlled by _____. What part of brain is ANS controller in? The ___ receives input from systemic and central receptors-- name some sites of input

Back 6

1. medulla
2. NTS
3. baroreceptors and hypothalamus

Front 7

The NTS has what type of effect on the sympathetic nervous system?

Back 7

Inhibitory

Front 8

Where are sympathetic adrenergic nerves along vascularity? What vessels receive no innervation? Vasoconstriction is mediated by what type of adrenoreceptors?

Back 8

- In adventitia of blood vessels
- capillaries
- alpha receptors

Front 9

Baroreceptors are part of a reflex arc with autonomic ganglia which then will send out _____ in response to low bp.

Back 9

1. sympathetic stimulation

Front 10

NE has main effect at ____ receptors. Epi at higher concentrations bind to _____ and ____ receptors and produce vasoconstriction. Muscarinic innervation in which vessels so that vasodilation can occur?

Back 10

1. alpha 1
2. alpha 1 and 2-- EPI
3. coronary vessels-- Ach mediated so can prevent ischemia

Front 11

What substance is the major determinant of EC vol? The primary derangement in htn is inability of kidney to regulate sodium balance so that ___ xs is maintained. In pts with essential htn have ___ alteration in ability to handle sodium

Back 11

1. NaCl
2. sodium xs
3. renal- theory that essential htn due to inherited inability to excrete sodium

Front 12

How is essential htn inherited? Which proteins are involved? Is there an association of obesity w/ htn? Insulin increases or decreases sodium reabsorption as well as higher sympathetic activity?

Back 12

1. multiple alleles
2. sodium transporter function
3. yes
4. increases sodium reabsorption

Front 13

What is pressure natriuresis?

Back 13

When bp increases there is more renal bp which then causes more natriuresis and diuresis b/c higher GFR. When blood vol decreases then excretion becomes normal.

Front 14

How much sodium is resorbed in the PCT, in loop at TAL, in DCT, and how much at collecting duct?

Back 14

1. PCT- 65-70%-- CA inhibitors
2. Loop TAL- 25%-- loop diuretics
3. DCT- 5%-- thiazides= Ca+2 sparing
4. collecting duct-- 1-2%- K+ sparing diuretics including aldosterone antagonists and ADH antagonists

Front 15

What is the main channel effected by the CA inhibitors? Where is this in the nephron?

Back 15

1. Na/H+ exchanger- the gradient is lost b/c with CA, H+ (and HCO3-)not made into CO2 leading to a bunch of H+ around so NA/H exchanger has no driving force and Na+ is NOT resorbed- is more commonly used for glaucoma not as a diuretic
2. in PCT

Front 16

In loop of henle water is resorbed so that more concentrated urine can be formed. Which transporter do loop diuretics work?

Back 16

Loop diuretics inhibit the NA/K/2Cl- cotransporter in Thick AL (TAL)-- resorption. Also creates positive potential in lumen for Ca+2 and Mg+2 interepithelial resorption

Front 17

In the DCT which diuretics work and on what channel?

Back 17

Thiazide diuretics inhibit resorption via the Na+/Cl- cotransporter. Advantage of thiazide diuretics is little chance of downstream resorption

Front 18

Where does aldosterone work, what channel does it work on? What is MOA of diuretics at this point? What other type of diuretic could work at collecting duct?

Back 18

1. In the distal segment of DCT
2. Aldosterone will cause incerased resorption of Na+ and more excretion of K+ and H+
3. aldosterone antagonists will inhibit on the Na+/K+-H+antiporter, so Na+ lost and K+ and H+ will be saved
4. ADH blockers-lithium

Front 19

After 6-8 wks on diuretics what happens to CO? What will happen to the PVR?

Back 19

1. bodys sodium stores decrease
2. body vol may decrease
3, BUT THEN CO will revert to normal and peripheral vsc resistance will decline
4. Na contribs to vasc resistance by increasing vessel stiffness and neural activity

Front 20

Acetazolamide, methazolamide, sulfanilamide, and dichlorophenamide--Class, MOA, PK

Back 20

Class: CA Inhibitors
MOA: CA inhibitors will inhibit CA in PCT and stop Na/H+ exchanger
PK: Increases pH of urine, secreted by renal blood flow into PCT area

Front 21

Acetozolamide, methazolamide, dichlorphenamide- Use, Tox, CI

Back 21

Use: CA inhibitors are not used as diuretics that much instead used for glaucoma, respiring in mountains- b/c this causes resp alkalosis, metabolic alkalosis (b/c H+ is saved- Na/H+ exchanger is blocked and Na+ lost and H+ saved)
Tox: metabolic acidosis, renal stones b/c calcium stones are insoluble in alkaline pH, K+ wasting, allergy to sulfas- rash

Front 22

Furosemide, bumentanide and torsedmide, and ethacrynic acid- Class, MOA, PK

Back 22

Class: Loop diuretics
MOA: Inhibits Na+/K+/2Cl- cotransporter at the TAL of the loop. Stimulates renin release DIRECTLY via macula densa, increases systemic venous capacitance
PK: must get into urine to work (organic acid secretion- competes with uric acid secretion), bound to plasma proteins, NSAIDS and probenicid compete for same site, induces renal PG synth

Front 23

Furosemide, bumentanide, and torsemide and ethacrynic acid- Use, Tox, CI

Back 23

Use: Edema (ACUTE), htn (esp if reduced renal function), hypercalcemia treatment, and acute renal failure (helps to prevent oliguria in renal failure)
Tox: OTOTOXICITY, ion disregulation-- hypocalcemia, hypomagnesimia, HYPERuricemia. Increas LDL and decrease HDL. Allergic rxn b/c are sulfa drugs (except ethacrynic acid)
CI: osteoporosis

Front 24

Hydrochlorothiazide, metolazone, chlorothiazide, indapamide- Class, MOA, PK

Back 24

Class: Thiazide diuretics
MOA: Inhibits Na/Cl symport in DCT, this is last place to make dilute urine. Enhances Ca+2 reabsorption in PCT and DCT. Mg+2 excretion increased
PK: secreted by organic ACID transport sys in prox tubule (uric acid--gout), NSAIDs, probenicid competition

Front 25

Hydrochlorothiazide, metolaxone, chlorothiazide, and indapamide- Use, Tox, CI

Back 25

Use: Htn, edema, osteoporosis, decreases stone formation, nephrogenic diabetes insipidius (helps decrease Aqp load)
Tox: decrease glucose tolerance, increase LDL, hyponatremia, allergic rxns (ass with sulfas), rare weakness, fatigue, and impotence

Front 26

Chlorothiazide- special b/c

Back 26

ONLY IV THIAZIDE diuretic

Front 27

indapamide special b/c

Back 27

biliary excretion so shouldnt use with liver failure

Front 28

Metolazone special thiazide diuretic b/c

Back 28

still effective at lower GFR

Front 29

Spironolactone, eplerenone- Class, MOA, Pk

Back 29

Class: aldosterone antagonists
MOA: block ald receptors in CD, inhibit Na+/K+/H+ anti port which is what aldosterone regulate- more Na+ excreted and less H+ and K+ excreted- which is why aldosterone antagonists are K+ sparing
PK: secreted by organic BASE transport sys in proximal tubule-- does NOT interfere with probenecid

Front 30

Spironolactone, eplerenone- Use, Tox, CI

Back 30

Use: combined with other diuretics to prevent hypokalemia, if hyperaldosteronism, DOC for cirrhosis pts
Tox: life threatening hyperkalemia, met acidosis in cirrhotic pts b/c less H+ excretn, steroid symptoms- gynecomastia, impotence, decreased libido, hirsutism, and menstral irregularities
CI: renal failure, hyperkalemia, NEVER use with OTHER K+ sparing diuretics OR ACE INHIBITORS!

Front 31

Lithium- MOA, Class

Back 31

- ADH antagonist, inhibits action of ADH by reducing formation of cAMP in response to ADH

Front 32

Mannitol, Glycerin- Class, MOA, Tox, Use

Back 32

Use: Cerebral edema and glaucoma by inducing water to leave cells
Class: osmotic diuretics
MOA: freely filtered at glomerulus w/o resorption--increases osmolality of plasma and tubular fluid, causes water retention in proxc tubules and descending limb (where water is freely filtered)

Front 33

Amiloride and Triamterene- Class, MOA, PK,

Back 33

Class: K+ sparing diuretic, work at principal cells of distal part of DCT and collecting duct
MOA: block Na+/K+ antiporter so that Na+ is excreted more and K+ is saved more
PK: secreted by organic base secretory mech
Tox: life threatening hyperkalemia
Use: in COMBO with other diuretics, CF, liddles syndrome