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Pharm Fall '24 > Test 3 - Diuretics (10/7 & 10/14) > Flashcards

Test 3 - Diuretics (10/7 & 10/14) Flashcards

1
Q

What is the function of the kidney?

A

Filter the blood and get rid of waste products (especially ammonia..makes it into urea and is excreted)

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2
Q

How many nephrons does a kidney have?

A

800,000 to 1,000,000

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3
Q

What are the 3 principle activities of nephrons in producing urine?

A
  1. filtration
  2. reabsorption
  3. secretion
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4
Q

Where in the nephron is filtration taking place?

A

Renal corpuscle (Glomerulus)

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5
Q

How much of our urine volume is total filtrate volume

A

1%

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6
Q

Where in the nephron is reabsorption taking place?

A

Peritubular capillaries on the proximal tubule

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7
Q

Where in the nephron is secretion taking place?

A

Distal tubule

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8
Q

List the segments of the nephron

A
  1. Renal corpuscle
    -glomerulus
    -bowmans capsule
  2. renal tubule
    -proximal convoluted tubule
    -loop of henle
    -distal convoluted tubule
  3. collecting ducts (not technically part of the nephron)
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9
Q

What is the blood component of the renal corpuscle?

A

Glomerulus. afferent arteriole brings blood in, efferent takes blood out

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10
Q

What is the function of the glomerulus. what are the cells called

A

has a layer of cells called podocytes and they provide the filtration of blood through capillaries. (only found in the cortex)

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11
Q

What is the function of Bowmans capsule?

A

structure that surrounds the glomerulus, catches the secretions from the glomerulus

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12
Q

Function of the proximal convolutes tubule? What transporter is found here?

A

reabsorbs about 80% of the glomerular filtrate back into the blood.
NHE3.

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13
Q

Proximal tubule targets for diuretics

A

Targeting NaCl and NaHCO3 reabsorption

-Carbonic anhydrase inhibitors
-Caffeine

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14
Q

What are the four different parts of the loop of henle

A
  1. thick descending limb
  2. thin descending limb
  3. thin ascending limb
  4. thick ascending limb
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15
Q

What part of the nephron goes down into the medula?

A

The bottom part of the loop of henle

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16
Q

Function of descending loop of henle

A

water reabsorption due to hypertonic medullary interstitium

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17
Q

Function of ascending loop of henle

A

driving out NaCl via NKCC2

NaKATPase then pumps Na into interstitum

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18
Q

What happens to Mg and Ca in the ascending loop of henle

A

if there is extra K in the nephron it will go down its concentration gradient to the lumen, that positive charge will push Mg and Ca to interstitium

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19
Q

what is the osmolality at the bottom of the loop of henle

A

1200

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20
Q

The ascending loop of henle is _____ to water

A

impermeable

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21
Q

pump found at distal convoluted tubule

A

NCC

very little water movement (we are balanced)

low amount of Na absorption via NCC (NaCl goes from lumen to DCT)

active Ca reabsorption (from lumen to DCT) by parathyroid

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22
Q

function of collecting tubule. is it part of nephron?

A

Na and H2O can be reabsorbed. and K can be secreted

not part of nephron but still target for diuretics

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23
Q

In the collecting tubule the _____ reabsorption is being based on the activity of aldosterone

A

Na

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24
Q

What happens to the charge in the lumen if we have increased activity of ENaC in the collecting tubule

A

builds up negative charge because we have more Na in than K out. so Cl will leave through paracellular route

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25
Q

describe ENaC and aldosterone in the collecting tubule if we have hypotension

A

aldosterone (from adrenal cortex) increases activity of ENaC.

adds more Na into collecting tubule which is then pumped out to interstitum via NaKATP

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26
Q

What is the vasa recta?

A

Capillary system that is around the ascending and descending loop of henle.

For osmolality changes, reabsorbing ions that will be taken up into the medulla as opposed to the cortex

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27
Q

Location of macula densa and juxtaglomerular apparatus

A

Located at the end of the distal convoluted tubule by the glomerulus.

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28
Q

What does the macula densa do?

A

monitors the osmolality and volume of the fluid in the distal tubule. transmits the info to juxtaglomerular cells

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29
Q

Where are the juxtaglomerula located?

A

They are a thin layer of cells that line the afferent arteriole

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30
Q

what could cause the juxtaglomerular cells to relax

A

if there isn’t enough fluid or Na coming through the macula densa it can release NO and that will relax the juxtaglomerular

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31
Q

What does the Juxtaglomerular do?

A

can activate the RAAS system in response to the changes sensed by macula densa. Can also regulate blood flow into the glomerulus by changing size of afferent arteriole.

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32
Q

True/false. We have glomeruli in the medulla

A

false. only in the cortex

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33
Q

How do the kidneys regulate GFR?

A

Directly controlled by the juxtaglomerular apparatus.

  1. Renal Autoregulation (regulated by the kidney itself)
  2. neural regulation (activation of sympathetic NS..release epi/noreip)
  3. hormonal regulation (endocrine hormones, epi)
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34
Q

How do the kidneys regulate glomerular filtration rate through neural regulation?

A

activation of SNS. Release epi and norepi. act at juxtaglomerular cells, increase renin secretion.

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35
Q

How do the kidneys regulate glomerular filtration rate through renal autoregulation?

A
  1. Increase BP sensed by macula densa and that info sent to JGA
  2. JGA will decrease secretion of NO
  3. arteriole constricts

-some stimulus disrupts homeostasis by increasing GFR (go from sitting to standing that will increase BP)

-The change is sensed by the macula densa cells of JGA

-macula densa sends the input that we have too high of an input

-output from Juxtaglomerular apparatus- decreased secretion of nitric oxide

-afferent arteriole constricts, decreasing blood flow through glomerulus

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36
Q

Function of NHE3 and carbonic anhydrase (only urine side)

A

NHE3 is the start of the cycle. its is a transporter (Na in; H out)

Once cycled via NHE3, H that was pumped out is combined with HCO3 to form H2CO3.

Carbonic anhydrase will break down H2CO3 to form CO2 and H2O

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37
Q

What happens in the proximal convoluted tubule after NHE3 and carbonic anhydrase made H2O and CO2 in the urine?

A

CO2 uses simple diffusion back into the proximal convoluted tubule, combines with carbonic anhydrase again to form H2CO3 and then be broken down to H and HCO3.

HCO3 is transported to the blood to buffer

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38
Q

What does NHE3 and carbonic acid have to do with Na and bicarb reabsorption?

A

The NHE3 pump puts Na into the proximal convoluted tubule from lumen where it is pumped out to the interstitium via Na/K/ATPase.

HCO3 is pumped to the interstitium following a full cycle.

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39
Q

Describe how the osmolality of the kidney medulla affects water movement

A

Countercurrent mechanism.
In the PCT, water follows Na to keep osmolality constant.

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40
Q

List the 5 major types of diuretics.

A
  1. Carbonic anhydrase inhibitors
  2. Loop diretics
  3. Thiazides
  4. Potassium Sparing diuretics
  5. Osmotic Diuretics
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41
Q

Carbonic Anhydrase Inhibitor: Site of action. med example

A

Primarily block Na and HCO3 reabsorption in proximal convoluted tubule. (more Na and HCO3 staying in the lumen)

more Na in lumen = more water bc it follows Na.

Acetazolamide.

42
Q

Carbonic anhydrase inhibitor: urinary electrolytes

A

Urine: NaCl (+), NaHCO3 (+++), K (+)

43
Q

Carbonic Anhydrase Inhibitor: main effect.

A

Major effect is bicarbonate diuresis (Sodium bicarb is excreted in large amounts..nothing for H to bind to) Can lead to metabolic acidosis.

Also K+ depletion, toxicity

44
Q

When is Acetazolamide used as a diuretic. What kind of diuretic is this?

A

Only if edema is accompanies by significant metabolic alkalosis. it is a carbonic anhydrase inhibitor

45
Q

Other uses of acetazolamide

A

acute mountain sickness

glaucoma, alkalinization of urine, edema with alkalosis

46
Q

osmolality. what should it be?

A

the number of dissolved particles in solution. 300mOsm/kg

47
Q

is osmolality higher in the cortex or medulla?

A

medulla. bc all the extra Na before it is reabsorbed

48
Q

in the proximal tubule, water reabsorption must equal _____ to keep osmotic gradient equal

A

Na

49
Q

What is the part of the PCT where we have secretion of larger substances into urine? what kind of substances are secreted

A

Straight segment.
drugs

50
Q

Effects of mannitol compared to other diuretics. uses. side effects.

A

osmotic diuretic mainly used to reduce intracranial pressure.

can cause extracellular volume expansion (causing hyponatremia and pulmonary edema).

Toxicity: N/V, headache

51
Q

Where does mannitol work primarily?

A

Proximal convoluted tubule

52
Q

mannitol toxicity

A

N/V
headache

53
Q

Mannitos is an ______ solute. as water follows Na, mannitol concentration ______

A

impermeable.
increases.

54
Q

If we increase concentrations of mannitol we ______ osmolality

A

increase

55
Q

what parts of the nephron will be affected by mannitol?

A

mainly PCT but works throughout entire nephron

56
Q

Furosemide is a ___

A

Loop diuretic

57
Q

Where do loop diuretics work

A

thick ascending limb

58
Q

Loop diuretics: MOA

A

MOA: Block the NakCC2 pump. Selectively inhibits NaCl reabsorption in the thick ascending limb.

more Na in urine = more water in urine

59
Q

loop diuretics can cause ______ (alkalosis/acidosis)

A

alkalosis

60
Q

what is the most efficacious diuretic

A

loop diuretic

61
Q

what happens to Mg and Ca with loop diuretics

A

we lose it in the urine since we stopped the NACC2 pump the K isnt leaving the nephron to the lumen so its not being driven out.

62
Q

Loop diuretics: urinary electrolytes

A

Urine electrolytes: NaCl (++++), K (+), Mg and Ca

63
Q

Loop diuretics: main side effect

A

Toxicity: most are sulfonamide, avoid in pt with sulfa allergies.

64
Q

What loop diuretic would we use in a patient with a sulfa allergy?

A

ethacrynic acid

65
Q

Thiazide MOA

A

Block NCC channel (inhibiting NaCl to come into nephron). keeping more Na in urine = more water

Some inhibition of carbonic anhydrase activity

66
Q

All thiazides can be given ______

A

orally

67
Q

Hydrochlorothiazide is a ___

A

Thiazide diuretic

68
Q

Thiazide urine electrolytes

A

NaCl (++)
NaHCO3 (+)
K (+)

69
Q

Thiazide side effects

A

Sulfa allergy. (its a sulfonamide).

70
Q

What happens if we combine thiazides and loop diuretics

A

since they have targets at different parts of the nephron we can have greater effects.

shit ton of fluids moved

71
Q

What do we have in regards to ion movement in the collecting tubule with no diuretics

A

Na into tubule
K into lumen

more negative charge in lumen will push Cl to interstitum (paracellular route)

72
Q

ion movement in collecting tubule with K wasting diuretics (Furosemide, thiazides)

A

Lots of Na into tubule
lots of K to lumen

still net negative, Cl leaving

73
Q

ion movement in collecting tubule when acetazolamide is given

A

Huge net negative charge in lumen bc of the bicarb build up.

means LOTs of K out to lumen bc its moving towards the negative.

LOTS of K wasting

74
Q

Define potassium wasting

A

diuretics that increase the amount of K lost in the urine

75
Q

Mechanism of K and HCO3 wasting in the collecting tubule following Acetazolamide administration

A

Lots of HCO3 in the urine which means negative charge and thats why we have lots of K wasting. (more so)

76
Q

Spironolactone MOA

A

Antagonize effects of aldosterone therefore inhibiting ENaC so more Na in lumen.

K sparing diuretic

77
Q

Amiloride MOA

A

inhibition of Na flux through ion channels in collecting tubule.

K sparing diuretic

78
Q

primary clinical indications for K sparing diuretics

A

Mineralocorticoid excess (something wrong in the adrenal cortex and they are producing extra aldosterone)
Ex.
-Conns syndrome
-Ectopic ACTH production (pituitary gland tumor)

79
Q

Secondary clinical indication for using K sparing diuretic

A

-CHF
-nephrotic syndrome
-use of other diuretics that are K wasting

80
Q

contraindications for K sparing diuretics

A

-pt taking K
-pt on drugs affecting K
-liver disease impairs metabolism

81
Q

K sparing diuretic toxicity

A

hyperkalemia

-increased w renal disease
-most common if k sparing agent is solo diuretic

82
Q

what is the hormone at the collecting duct

A

ADH (vasopressin)

83
Q

what does ADH do at collecting duct

A

increases blood volume, increasing blood pressure

  1. binds to receptor
  2. activates cAMP
  3. AQP gets migrated to surface of lumen
  4. causes water to go from lumen to interstitum

water cant move without the AQP.

84
Q

what happens if there is no production of ADH

A

urine is very diluted bc there is no movement of water.

85
Q

when would we give an ADH agonist? what med?

A

when we want to increase BP. vasopressin

86
Q

when would we give ADH antagonist? what med?

A

Hypertension. Conivaptan

87
Q

2 drugs that reduce K loss during Na diuresis

A

Conivaptan: ADH antagonist

Spironolactone: block aldosterone receptor

88
Q

what parts of the nephron are freely permeable to water

A

PCT and descending loop

89
Q

Osmotic Diuretic MOA.

A

Keeps the osmolality high throughout entire nephron so water doesn’t leave

Increase urinary flow by retaining water throughout nephron.

90
Q

Absorption for mannitol

A

suppppper poor. Cant ingest it so its injected

91
Q

when does glomerular filtration occur with osmotic diuretics?

A

within 30-60 min after administration

92
Q

Uses for mannitol. what kind of diuretic is this

A

osmotic diuretic.

  1. reduce ICP
  2. promote removal of renal toxins
    -acute hemolysis
    -after use of radiocontrast agents
93
Q

pharmacodynamics of osmotic diuretics

A

counter osmotic force.
result is
-increase urine volume
-reduces Na reabsorption

(lose H2O and Na in urine)

94
Q

clinical indications for osmotic diuretics

A

-increases urine output
-reduces ICP

95
Q

How long does it take to reduce ICP following administration of an osmotic diuretic

A

60-90 min after administration

96
Q

Osmotic diuretic toxicity in vasculature system

A

extracellular volume expansion

nephron isn’t leaky to it but vascular system is so its distributed to extracellular compartments.

can lead to acute pulmonary edema and hyponatremia prior to dieresis

97
Q

osmotic diuretic toxicity in nephron

A

High or extended use
1. dehydration
2. hypernatremia
3. hyperkalemia

  1. in pt with renal failure - hyponatremia
98
Q

what can happen to mannitol during administration

A

can crystalize, use in-line filter

99
Q

most common reason for diuretic use is _____ or _____.

A

peripheral or pulmonary edema

100
Q

What would be non edematous states that diuretics are used? (6)

A
  1. HTN (decrease by 10-15mmHg)
  2. renal stones
  3. rhabdomyolysis (osmotic sweeping out nephron)
  4. hypercalcemia
  5. urinary casts
  6. diabetes insipidus
101
Q

Why would we use diuretics for neohrogenic diabetes insipidus

A

These patients have insufficient ADH (pouring out dilute urine)

102
Q

what diuretic would we use for diabetes insipidus? what are the 6 steps on how this works?

A

thiazide.

  1. decrease tubular Na reabsorption
  2. increase urinary excretion of Na
  3. overall decrease EC volume
  4. increase proximal tubule Na and H2O reabsorption
  5. decrease distal delivery of Na and H2O
  6. decrease urinary output overall.

Pharm Fall '24 (7 decks)

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