Diuretics Flashcards

1
Q

nephron

A

functional unit of kindey

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2
Q

four regions of nephron

A

1) glomerulus

2) proximal convoluted tubule

3)loop of Henle

4) distal convoluted tubule

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3
Q

where does nephron fluid flow into

A

collecting ducts

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4
Q

upper portion of nephron is in

A

renal cortex

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5
Q

lower portion of nephron is located in

A

renal medulla

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6
Q

why are the nephron located different parts of the kidney (upper and lower)

A

allows different urine concentrations

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7
Q

kidneys main functions

A

1) cleansing ECF and maintenance of ECF volume and composition

2) maintenance of acid-base balance

3) excretion of metabolic waste and foreign substances (toxins, drugs, etc.)

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8
Q

filtration

A

small molecules in plasma undergo filtration
- large particles excluded

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9
Q

reabsorption

A

movement of fluids and molecules from nephron to peritubular capillaries

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10
Q

how do diuretics primarily work?>

A

interfering with reabsorption

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11
Q

active secretion (requires energy)

A

movement of fluids and molecules from peritubular capillaries back to nephron

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12
Q

what are the kidneys 2 pumps for active secretion?

A

1) transports organic acids

2) transports organic bases

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13
Q

Pathway of renal fluid through nephron

A

proximal convoluted tubule

loop of Henle

early distal convoluted tubule

distal convoluted tubule

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14
Q

percentages of sodium/chloride reabsorbed at specific sites

A

proximal convoluted tubule- 65%
- by the end of proximal tubule, Na/Cl only solutes that remain

ascending limb of Henle loop
20%
-not permeable to water
= osmolarity returns to orig. filtrate of 300mOsm/L

Early distal convoluted tubule
10%
-water follows passively

distal convoluted tubule and collecting tubule
1% - 5%

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15
Q

What important processes happen at late distal and collecting ducts?

A

1) exchange of sodium for potassium
- under influence of aldosterone

2) Determines final concentration of urine
- regulated by antidiuretic hormone

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16
Q

What does aldosterone stimulate?

A

stimulates linked process of sodium reabsorption and secretion of potassium

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17
Q

Basic mechanism of how diuretics work

A

Blockage of Sodium/ Chloride reabsorption
- creates increased osmotic pressure within nephron –> prevents passive reabsorption of water

  • diuretics cause both sodium/chloride and water to be retained in nephron
    –> excretion of both in urine
  • increase in urine flow directly related to AMOUNT of na/cl BLOCKED
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18
Q

where do drugs blocking na/cl in the nephron have the most profound diuresis

A

earliest in nephron (proximal, loop)

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19
Q

how much will diuretics increase urine output by?

A

1.8L for every 1 % blocked

20
Q

blocking a small amount of solute effect has a

A

profound effect on fluid and electrolyte composition in the body

21
Q

diuretics adverse impact on ECF

A
  • hypovolemia
    -acid/base imbalance
    -altered electrolyte levels
22
Q

how can effects be minimized while using diuretics

A

-use short acting diuretics
–> allow kidneys to function in a drug free manner between periods of diuresis

23
Q

Four classifications of diuretics include

A

1) Loop diuretics (furosemide)
2) Thiazide diuretics (hydrochlorothiazide)
3) Osmotic diuretics (mannitol)
4) Potassium-sparing diuretics (aldosterone antagonists and agonists)

24
Q

Loop Diuretics

A

Most effective

site of action: loop of Henle

25
Q

Loop Diuretic drug

A

Furosemide (fur-oh-semide)

26
Q

Furosemide mechanism

A

-Bind reversible to a carrier protein that stops it from reabsorbing NA/CL

  • potentially 20% of na/cl reabsorption can be blocked here
27
Q

Pharmakinetics of Furosemide

A

PO- diuresis within 60 min, lasts for 8 hrs
- use when rapid onset diuresis NOT REQUIRED

IV- within 5 min
-critical situations (pulmonary edema)

metabolism: hepatic
excretion: renal

28
Q

Adverse effects of Loop Diuretics

A

Hyponatremia, dehydration
- dry mouth, unuasual thirst, low urine output
- initiate therapy with low doses and monitor weight loss

Hypotension
- (1) from loss of water
- (2) relaxation of venous smooth muscle
- reduced venous return to heart –> monitor BP

Hypokalemia: low levels of Na
-if serum levels fall below 3.5 mEq/L fatal dysrhythmias may occur
- CONSUME K rich foods

Ototoxicity
- hearing impairment/ severity depends on different loop diuretics

29
Q

Loop Diuretic drug interactions

A

Dioxin: drug used for heart failure/ cardiac dysrhythmias
- loop diuretics cause hypokalemia
–> increases risk of ventricular dysthymias

Ototoxic: combined with furosemide should be avoided

30
Q

therapeutic uses of loop diuretics

A

hypertension

pulmonary edema

cardiac edema

31
Q

major difference between max diuresis with thiazides and loop diuretics is that

A

maximal diuresis is lower with thiazides

32
Q

Thiazide drug name

A

Hydrochlorothiazide (hydro-chlora-thi-a-zide)

33
Q

Mechanism of Thiazides

A

Blocks Na?Cl reabsorption in early segment of distal tubule
- only 10% reabsorbed her = change in urine flow is lower

34
Q

therapeutic uses of thiazides

A

FIRST choice for ESSENTIAL hypertensin
- can often by treated with thiazides alone

FIRST choice for EDEMA treatment associated with mild to moderate heart failure

35
Q

What responses do Potassium-Sparing Diuretics Ellicit

A

(1) MODEST increase in urine production

(2) Substantial Decrease in Potassium excretion

  • usually used in combination to counteract K loss
36
Q

Drug name for Potassium-Sparing Diuretics

A

Spironolactone (spira-no-lack-tone)

37
Q

Mechanism of Potassium- Sparring Diuretics

A

Blocks action of aldosterone in distal convoluted tubule and collecting duct

Aldosterone acts to increase na/cl reabsorption and increase secretion/excretion of K+

Inhibition of Aldosterone = increased reabsorption of potassium back into interstitial fluid

38
Q

Potassium- Sparring diuretics adverse effects

A

Hyperkalemia
- fatal dysrhythmias

Endocrine effects
- spironolactone is a steroid derivative
–> menstrual irregularities, impotence, deepening of voice
—> BLOCKS TESTOSTERONE/ ESTROGEN effects

39
Q

Therapeutic uses of potassium-sparring diuretics

A

hypertension and edema
- used with combination with other diuretics

COUNTERACT POTASSIUM-WASTING EFFECTS of other diuretics

HEART FAILURE- reduces mortality in sever heart failure patients

40
Q

Potassium- Sparring Diuretics drug interactions

A

don’t combine with ingestion of potassium supplements and other products high in potassium

41
Q

Mannitol

A

osmotic diuretic

42
Q

mechanism of action of mannitol

A

after IV admin. mannitol is filtered by glomerulus into nephron

  • undergoes minimal reabsorption

-creates an increased osmotic pressure in nephron

RESULTS - inhibits passive reabsorption of water

Degree of diuresis directly related to mannitol in tubular filtrate

43
Q

Pharmacokinetics of mannitol

A

IV- diuresis begins in 30-60 min
lasts 6-8 hours
excreted intact in urine

44
Q

Therapeutic uses of mannitol (2)

A

Prophylaxis of Renal failure
- if blood flow to kidney is decreased= great reduction in filtrate volume

  • low filtrate volume = most na/cl reabsorbed (water follows)
  • urine production ceases
  • kidney failure occurs
  • mannitol reduces risk because it is not reabsorbed in nephron
    –> preserves urine flow

Reduction of Intracranial pressure (ICP)
- mannitol’s presence in brain blood vessels (cannot pass through BBB)
- creates osmotic force that draws fluid from brain into blood
= reduction ICP

45
Q
A