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Block 9 Week 2 > Diuretics -Duan > Flashcards

Diuretics -Duan Flashcards

1
Q

What do kidneys regulate?

A
  • body fluid volume and osmolarity
  • electrolyte balance
  • acid-base balance
  • blood pressure
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2
Q

What do the kidneys secrete?

A
  • erythropoitin
  • 1,25-dihydroxy vitamin D3 (vitamin D activation)
  • renin-angiotensin-aldosterone
  • prostaglandin
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3
Q

What do the kidneys excrete?

A
  • Metabolic products
  • Foreign substances (pesticides, chemicals etc.)
  • Excess substance (water, etc)
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4
Q

T or F

The kidneys function in gluconeogenesis

A

T

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5
Q

What are the 2 major components of the kidney?

A

1) Glomerulus

2) Tubule system (sites of reabsorption, secretion, and excretion)

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6
Q

What is this:
a compact cluster of convoluted capillaries, site of filtration, functioning to remove certain substances from the blood before it flows into the convoluted tubule.

A

Glomerulus

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7
Q

What does the tubule system of the kidney do?

A

sites of reabsorption, secretion, and excretion

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8
Q

What is the renal corpuscle made up of?

A

Glomerulus and Bowman’s capsule

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9
Q

How do you get everything to filter within the glomerulus?

A

Glomerulus is very high pressure–> creating a pressure gradient that allows for (passive) filtration (starling forces of filtration)

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10
Q

The net filtration pressure= (favoring force- opposing force)
What is the favoring force?
What is the opposing force?

A

Favoring: Capillary blood pressure (BP)
Opposing: Blood colloid osmotic pressure (COP) and Capsule pressure (CP)

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11
Q

What is the glomerular filtration rate?

A

the volume of fluid filtered from the glomerular capillaries into the Bowman’s capsule per unit time (125 mL/min=180L/day)

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12
Q

What is the equation for GFR?

A

(Urine concentration X urine flow)/(plasma concentration)

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13
Q

Clinically, creatinine clearance or estimates of creatinine clearance based on the serum creatinin level are used to measure (blank)

A

GFR

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14
Q

What are the factors that alter filtration pressure and change GFR?

A
  • Increased RBF (vasodilators)-> increased GFR
  • Decreased plasma protein-> Increased GFR, Causes edema
  • Hemoorhage-> decreased capillary BP-> decreased GFR
  • Molecular weight
  • Charges of the molecule
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15
Q

How do you regulate GFR?

A

-renal autoregulation
-neural regulation
-hormonal regulation
(adjust renal BP and resulting blood flow)

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16
Q

What is this:

glomeruli in inner part of cortex and long loops of Henle which extend deeply into medulla

A

Juxtamedullary nephron

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17
Q

Blood flow through vasa recta in medulla is (fast/slow)

A

slow

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18
Q

Medullary interstitial fluid is (hypoosmotic/hyperosmotic)

A

hyperosmotic

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19
Q

The juxtamedullary nephron maintains (Blank) in addition to filtering blood and maintaining acid-base balance and concentrate urine

A

osmolality

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20
Q

What is this:

glomeruli in outer cortex and short loops of Henle that extend only short distance into medulla.

A

Cortical nephron

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21
Q

Blood through the the cortex is (fast/slow)

A

fast

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22
Q

The majority (70-80%) of nephrons are (blank).

A

cortical

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23
Q

Cortical interstitial fluid is isosomotic at (blank)

A

300 mOsm

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24
Q

Reabsorption is a (blank) process beginning with the active or passive extraction of substances from the tubular fluids into the renal interstitium (the CT that surrounds the nephrons). Then these sustances are transported from the interstitium into the (blank). These transport processes are driven by (blank, blank and blank)

A

2-step
bloodstream
Starling forces, passive diffusion, and active transport

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25
Q

In the proximal convoluted:

  • Tubule (PCT), reabsorption occurs when (blank) needs to be maintained.
  • (blank) ions are reabsorbed back into the bloodstream.
  • (blank, blank, and blank) are all actively transported into the blood
    (blank) percent organic solutes are reabsorbed

(blank and blank) are actively secreted from the blood into the tubule

A

pH (acid/base balance)

Biocarb

Glucose, AAs and K+ are all actively transported into the blood

70-80%

H+ and toxins

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26
Q

How does the Na+ H exchanger work?

A

puts sodium into the PCT and excretes hydrogen into the urine

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27
Q

What does carbonic anhydrase do?

A

makes Co2 and H20 into H2Co3

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28
Q

What is the descending limb of the loop of henle highly permeable to?

A

H20

does this via osmosis

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29
Q

The ascending limb of the loop of henle has (blank) permeability to H20 and is often called the (blank) segment

A

low

diluting

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30
Q

The ascending loop of henle is responsible for (blank) percent of H20 reabsorption BUT can increase to 50%

A

15%

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31
Q

The (blank) of the loop of henle allows for the passive and active transport of salts such as Na+ to move out of the tubules and be reabsorbed

A

thick ascending limb

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32
Q

How do you get Cl- out of the urine into the ascneding limb of the loop of henle and back into the blood stream?

A

NKCC2-> K/Cl- symport

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33
Q

What happens to most of the potassium in the tubules?

A

it goes into the lumen to get excreted as urine through potassium channels

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34
Q

How are Mg2+ and Calcium reabsorbed in the thick ascending limb?

A

via the paracellular shunt pathway

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35
Q

What is the main function of the loop of henle?

A

to create a concentration gradient in the medulla of the kidney by mean of a countercurrent multiplier system. So we can conserve water and ions :)

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36
Q

The loop of henle creates an area of (blank) deep in the medulla, near the collecting duct

A

high urea

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37
Q

How does the countercurrent multiplier system work?

A
  • filtrate entering the descending limb becomes progressively more concentrated as it loses H20
  • blood in the vasa recta removes water leaving the loop of henle
  • The ascending limb pumps out Na+, K+, Cl- and filtrate becomes hypo-osmotic
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38
Q

The Distal convoluted tubule (DCT) is (blank) to H20. What gets reabsorbed in the DCT?

A

relatively impermeable

NaCl (creating more dilute urine)

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39
Q

What are the 2 cell types present in the collecting tubule?

A

Principle cells and intercalated cells

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40
Q

Where does aldosterone affect the kidney? What does aldosterone do?

A

in the principle cells of the collecting tubule

affects the level of sodium and the final level of potassium in the urine

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41
Q

(blank) determines the expression of aquaporin channels that provide a physical pathway for water to pass through the principle cells in the collecting tubule

A

Vasopressin (ADH Antidiuretic hormone)

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42
Q

(blank) cells of the collecting tubule come in (blank) and (blank) varieties and participate in acid-base homeostasis

A

Intercalated

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43
Q

What do intercalated cells due?

A

put H+ into urine and Bicarb into blood-> i.e make urine acidic

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44
Q

In the collecting tubule, what drives the reabsorbtion of chloride into the blood and the efflux of potassium into the urine?

A

the Inward diffusion of sodium creating a gradient in the lumen

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45
Q

(blank) increases the activity of both apical Na+ channels and the Na+/K+ ATPase. What will this lead to?

A

Aldosterone

Sodium reabsorption and potassium secretion

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46
Q

(Blank) controls the water permeability of principal cells in this segment

A

Antidiuretic hormone (ADH, or vasopressin)

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47
Q

ADH regulates the insertion of (blank) into principal cells in the apical membrane

A

aquaporin-2 (AQP2)

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48
Q

What will your urine be like if you have low ADH?

A

dilute

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49
Q

How does vasopression (ADH) work?

A

ADH-> AC-> cAMP-> increased PKA activity-> phosphorylated proteins= water channels on apical membrane

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50
Q

Intercalated cells participate in acid-base homeostasis, how?

A

a-intercalated cells secrete acid and reabsorb bicarb

b-intercalated cells secrete bicarb and reabsorb acid

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51
Q

How do a-intercalated cells secrete acid?

reabsorb bicarb?

A

-via an apical H+ ATPase and H-/K+ exchanger

-

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52
Q

How do b-intercalated cells secrete bicarb?

How do they reabsorb acid?

A
  • Via pendrin a specialist apical Cl-/HCO3- exchanger

- Via a basal H+-ATPase

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53
Q

What is the equation for amount excreted?

A

Amount of solute excreted= (amount filtered) + (amount secreted) - (amount reabsorbed)

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54
Q

When there is excess water in the body and body fluid osmolarity is reduced, the kidney can exrete urine with an osmolarity as low as (blank).
Conversely, when there is a deficient of water and extracellular fluids osmolarity is high, the kidney can excrete urine with a concentration of about (blank) mOsm/liter.

A

50

1200 to 1400

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55
Q

What are the basic requirements for forming a concentrated or diluted urine?

A
  • controlled secretion of ADH
  • High osmolarity of renal medulla (so you can have a gradient to allow for water reabsorption in the presence of high ADH)
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56
Q

What happens to your urine if you add vasopression (ADH)?

A

it becomes more concentrated

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57
Q

All diuretics act on the (blank) surface EXCEPT for the (Blank)

A

luminal

Aldosterone antagonists

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58
Q

Where are osmotic diuretics filtered?

All other diuretics are not filtered there why?

A

glomerulus

Because they are bound to plasma proteins

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59
Q

Diuretics not filtered at the glomerulus are transported into the nephron by (blank) or (blank) transporters located in the proximal tubule

A

organic acid (A-) or organic base (C+)

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60
Q

What is the MOA of carbonic anhydrase inhibitors and how does it get into the lumen to work?

A
  • inhibits Carbonic Anhydrase in lumin and basolateral membrane (type IV) and cytoplasm (type II)
  • via organic acid transporter in PCT
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61
Q

What does carbonic anhydase do?

A

increased HCO3- excretion

increased Na+, K + (distally), H20 excretion

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62
Q

What will carbonic anhydrase do to your urine?

A

make it alkaline due to decreased urea and increased HCO3

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63
Q

How is carbonic anhydrase self-limiting in diuretic action?

A

it stops its diuretic action when metabolic acidosis occurs as HCO3- decreases

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64
Q

What are the non-diuretic uses of carbonic anhydrase inhibitors?

A

A Family GAME

  • Alkalinizing urine for excretion of weak acids
  • Familial hypokalemic periodic paralysis
  • Glaucoma (decrease aqueous humor formation)
  • Altitude (mountain) sickness (decreased CSF and pH)
  • Metabolic Alkalosis
  • Epilepsy (seldom used)
65
Q

What are the adverse effects of carbonic anhydrase?

A

A PACE

Acidosis (metabolic),
Potassium depletion (hypokalemia)
Allergic reactions (sulfonamide-based)
Calcium nephrolithiasis
Encephalopathy
(other: drowsiness, dizziness, parasthesia, bone marrow toxicity, skin rashes)
66
Q

What are the contraindications for carbonic anhydrase inhibitors?

A

patients with cirrhosis of the liver->Can lead to hepatic encephalopathy

This is due to the alkalization of urine causing retention of urea

67
Q

What are the four important osmotic diuretics?

A
  • Mannitol
  • Glycerin
  • Isosorbide
  • Urea
68
Q

Osmotic diuretics (mannitol, glycerin, isosorbide, urea) are (blank) filtered by the glomerulus. They undergo (blank) reabsorption.

A

freely

limited

69
Q

What is the mechanism of action of osmotic diuretics?

A

adding particles to increase water excretion therefore quantity of water retained is proportional to the quantity of solute administered

70
Q

Where do osmotic diuretics primarily act?

A

in the PCT and to a lesser extent in the ascending loop of henle

71
Q

What are the clinical uses of Osmotic diuretics?

A

(AAA ID)

  • Acute tubular necrosis
  • Anuria in hemolysis or rhabdomyolysis (prophylaxis)
  • Angle-closed glaucoma (reduce intraocular pressure)
  • Increased Intracranial pressure (used as the DOC)
  • Dialysis disequilibrium
72
Q

What are the adverse effects of osmotic diuretics?

A
  • dehydration
  • hypernatremia (serium Na concentration > 145 mEG/L)
  • If admin too rapidly IV, can cause cell dysfunction
73
Q

Diuretic access to the tubule lumen is decreased by…?

A

decreased renal blood flow (decreased GFR)

increase levels of compounds or drugs also transported by organic acid and base transporters

74
Q

What are examples of compounds/drugs that are ALSO transported by organic acids and bases thus inhibiting diuretic access to the tubule lumen?

A

alph-ketoglutarate catecholamines
uric acid
choline histamine antibiotics cimetidine probenecid

75
Q

Diuretics that act proximally are (blank) even though 70-80% of the filtered load is handled there. Why?

A

weak

their actions are counteracted by more distal reabsorption mechanisms

76
Q

Diuretics that act (blank) are weak because only 5-10% of the filtered load is involved.

A

distally

77
Q

Loop diuretics are strong because….?

A
  • an important transport mechanism is inhibited (Na+,K+,2Cl- co-transporter)
  • the affected site handles a large fraction of the filtered load (15-50%)
  • More distal mechanisms are not able to compensate
78
Q

Production of a concentrated urine requires a (blank)

A

hypertonic medulla

79
Q

Production of a dilute urine requires a (blank) by reabsorbing Na+ w/o H20.

A

hypotonic filtrate

80
Q

T or F

diuretics acting distal to the loop of henle (i.e thiazides) affect the concentration of urine

A

False, they affect dilution but not concentration

81
Q

Loop diuretics block the reabsorption of (blank) in the (blank). so it impairs both (blank and blank)

A
  • Na+ w/out water
  • ascending limb of henle
  • Concentration and dilution
82
Q

Diuretics are used to reduce (blank) by doing what? How?

A

ECF volume

decreasing total Na+ content through either reabsorbtion back into the plasma or secretion into the urine

83
Q

What do diuretics do to ECF?
Total Na+ retention?
Urine volume?
Urina Na+ content?

A

decrease ECF
decrease Na+ retention
increase urine volume
increase urine Na+ content

84
Q

What does the ending -Zolamide indicate?

A

Carbonic Anhydrase (CA) inhibitors

Zola eat Carbs

85
Q

What does the ending -thiazide indicate?

A

thiazide diuretics :)

86
Q

What does the ending -one indicate?

A

aldosterone antagonists

Aldoster-ONE
(except for chlorthaidone, thats a thiazide one)

87
Q

What does the ending

-semide indicate?

A

Loop or “high ceiling” diuretics

cuz loops are “semi”-circles

88
Q

What does the ending -azone indicate?

A

Thiazide related

cuz has 2 of the same letters as thiazide so it is related to it

89
Q

What are the carbonic anhydrase inhibitors (CA)?

A
  • acetazolamide
  • dorzolamide
  • dichlorphenamide
90
Q

What are the thiazide diuretics (Na+/Cl- symport inhibitors)?

A

hydrochlorothiazide

chlorothiazide

91
Q

What are the aldosterone antagonists?

A

Spironolactone

Epleronone

92
Q

What are the Na+ channel inhibitors?

A

Amiloride

Triamterene

93
Q

What are the ADH antagonists?

A

Lithium

Demeclocycline

94
Q

What are the thiazide related drugs?

A

Chlorthalidone
Indapamide
Metolazone
Quinethazone

95
Q

What are the loop or “high ceiling” diuretics (Na+ K 2Cl- symport inhibitors)?

A

Furosemide
Torsemide
Bunetanide
Ethacrynic acid

96
Q

What are the osmotic diuretics?

A
  • mannitol
  • glycerin
  • isosobide
  • urea
97
Q

What are the two types of K+ sparing diuretics?

A

Aldosterone antagonists

Na+ channel inhibitors

98
Q

What are the contraindications for Osmotic diuretics?

A

CHF

Severe renal disease

99
Q

There are 2 categories of loop diuretics, sulfonamide and non sulfonamide.
What are the sulfonamide derivatives?
What are the non-sulfonamide derivatives?

A

Furosemide
Torsemide
Bumetanide

Ethacrynic acid

100
Q

What is the mechanism of action of loop diuretics and how do they get where they need to go? What does this result in?

A
  • Reach the lumen via the organic acid transporter
  • NKCC2 innhibitos in the ascending limb of henle loop
  • Decrease hyperosmolarity in medulla
101
Q

What are the most effective diuretics and why?

A

Loop diuretics because the inhibit important transporter NKCC2 (this site handles a large fraction of the filtered load (15-50%)
More distal mechanisms are not able to compensate

102
Q

What are some other actions of Loop diuretics besides decreasing BV?

A
  • Increased loss of K+ and H+
  • decreased + potential
  • Increase excretion of Ca2+ and Mg2+ in urine
  • increased prostaglandins by inducing COX2 expression
  • increased excretion of acid and NH4+
103
Q

When you have high doses of furosemide (loop diuretic) and bumetamide (loop diuretic), what can happen?

A

-can inhibit CA and increase HCO3- excretion

104
Q

Loop diuretics can increase (blank) independent of diuretic activity

A

blood flow

105
Q

What loop diuretic increases renal blood flow?

A

furosemide

106
Q

What loop diuretics decrease pulmonary congestion in CHF?

A

Furosemide and ethacrynic acid

107
Q

Since loop diuretics bind to plasma proteins and access the tubule lumen via organic acid transporters, what happens if other compounds compete for these spots such as NSAIDs or Probenecid or in pnts with renal disease?

A

may have to increase the dose of the loop diuretic

108
Q

What are the clinical uses of loop or “high-ceiling” diuretics?

A
  1. edema-related

2. electrolyte or drug-related

109
Q

What are the edema related situations you should give loop diuretics for?

A
  • Emergency situations of acute pulmonary edema
  • CHF, acute renal failure, nephrotic syndrome, hepatic cirrhosis particularly when refractory to less efficacious diuretics
110
Q

What are the electrolyte or drug-related situations you should give loop diuretics for?

A
  • acute hypercalcemia
  • hyperkalemia
  • useful for anion overdose (Br-, Fl-, I-) in addition to saline
111
Q

What can torsemide do that is special?

A

can decrease BP without diuresis (useful for mild to moderate HTN)

112
Q

What are the adverse effects of loop diuretics?

A

-ototoxicity and transient deafness
-diabetogenic (furosemide and bumetanide)
-compete for binding to serum proteins with drugs, such as warfarin and clofibrate
-reduced clearance of Li+
-Due to competition for binding to organic acid transporter can have:
increased nephrotoxicity w/ cephalosporins
increased ototoxicity with aminoglycosides antibiotics
increased salicylate toxicity
-Hyperuricemia (due to increased reabsorption of uric acid in proximal tubule caused by decreased vascular volume)
-hypomagnesemia
-severe vascular volume decrease
-hyponatremia if pnt drinks too much water
-can increase LDL and TAG levels

113
Q

What are the contraindications for loop or “high-ceiling” diuretics?

A
  • severe Na+ and volume depletion

- hypersensitivity to sulfonamides (for sulfonamide-based loop diuretics)

114
Q

How do thiazide diuretics work? In what conditions are thiazide diuretics effective?

A
  • produce diuresis with increased Cl-.

- In both acidic and alkaline conditions

115
Q

High concentrations of some thiazides inhibit (blank) which lead to increased loss of (blank)

A

CA

HCO3-

116
Q

T or F
All thiazides have similar pharmacological actions but differ in duration of action, extent of CA inhibition, maximally effective dose, binding to serum proteins.

A

T

117
Q

Thiazide diuretics enter the nephron via the (blank). Also they compete with (blank) and can cause an increase in these levels.

A

organic acid transporter

Uric acid

118
Q

What is the mechanism of action of thiazides?

A

inhibit Na and Cl in urine (NCC) in the distale tubule-> which results in increase in Na+ and Cl- in urine

119
Q

The actions of thiazies depend partly on an increase in (blank) in the kidney

A

prostaglandinsq

120
Q

Are thiazide strong or weak diuretics and why?

A

weak because they work on the distal tubule where only 5% of filtered Na+ is reabsorbed where they act

121
Q

What are the effects of thiazide diuretics on calcium?

A

Increases Na+/Ca2+ exchange -> Increased reabsorption of Ca2+

122
Q

Thiazide diuretics cause less distortion of the (blank) since they cause a modest diuresis and affect the excretion of several ionic species.

A

ECF

123
Q

What are the clinical uses of thiazide diuretics?

A
  • Treat edema associated with CHF, hepatic cirrhosis, PMS
  • HTN (actions involve direct effects on vascular SM)
  • Ca2+ nephrolithiasis
  • Bromide intoxication
  • Diabetes insipidus
124
Q

What are the adverse effects of thiazide diuretics?

A
  • Increassed cholesterol (5-15% - transient) & LDL
  • Hypokalemia with prolonged therapy
  • Associated with arrhythmias
  • Hyperglycemia
  • Hypokalemic metabolic alkalosis
  • Hyperuricemia
  • Hyponatremia
125
Q

What are the contraindications of thiazide diuretics?

A
  • Patients hypersensitive to sulfonamides

- Effectiveness reduced by NSAIDs

126
Q

Whats the difference b/w thiazides and thiazide-like diuretics?

A

Chemically similar to thiazides but do not inhibit CA

127
Q

What is this:

  • A thiazide-like diuretic
  • anti-hypertensive actions independent of diuretic activity
  • used with loop diuretics in cases of renal failure
A

Indapamide

128
Q

What is this:

  • A thiazide-like diuretic
  • Efficacious & can be given in combination with a loop diuretic
  • Can be effective with renal insufficiency
A

Metolazone

129
Q

Why can you get hypokalemia with thiazide like diuretics?

Why is this important?

A

-K+ and H+ exchanged for Na+ in the distal nephron
-because hypokalemia can cause:
EKG abnormalities
Cardiac arrhythmias
Muscular weakness
Drowsiness
Confusion
Loss of sensation
Increased binding of cardiac glycosides

130
Q

What is an example of an aldosterone antagonist?

A

spironolactone (structural analog of aldosterone)

131
Q

What does spironolactone turn into after first pass in the liver? What does this do?

A

into canrenone which is an active metabolite
-Competitively blocks binding of aldosterone to its receptor
(aldosterone must be present for these drugs to be effective)

132
Q

What are the clinical uses of aldosterone antagonists?

A
  • Primary and secondary hyper-aldosteronism
  • Hypokalemia
  • Given with other diuretics used to treat hypertension & CHF
  • CHF
  • Cirrhosis of the liver & nephrotic syndrome
  • To avoid excessive loss of K+
133
Q

T or F

Spironolactone found to have significant benefit independent of its diuretic effects

A

T

134
Q

What are the adverse effects of Aldosterone Antagonists (potassium sparing diuretics)?

A
  • Hyperkalemia
  • Can increase serum Li+
  • Metabolism of cardiac glycosides
  • Reversible gynecomastia in males
  • Tumorigenic in rats
  • Hyperchloremic metabolic acidosis (due to decrease H+ secretion)
135
Q

What are some potassium sparing diuretics that are non-aldosterone antagonists?
How do they enter the nephron?

A
  • Triamterene, Amiloride

- Organic base transporter

136
Q

What is the mechanisms of action of triamterene,amiloride (non-aldosterone antagonists that are potassium sparing diuretics)?

A

Inhibits the sodium channel in principle cells (ENaC)

137
Q

What is the overall effect of non-aldosterone antagonists?

A

In the blood:

  • Increase Potassium
  • Decreased sodium
  • Increased NH4+
138
Q

What are the clinical uses of non aldosterone potassium sparing diuretics?

A
  • Used in combination with other diuretics to decrease K+ loss when treating edemas associated with CHF, cirrhosis of the liver, etc.
  • Amiloride has antihypertensive effects that are additive with those of the thiazides
139
Q

What are the adverse effects of non aldosterone potassium sparing diuretics?

A

Hyperkalemia

Decreased effects of cardiac glycosides

140
Q

What are the adverse effects of Triamterene?

A
  • Increase uric acid and increase chance of gout
  • inhibit dihydrofolate reductase and cause megaloblastic anemia if pnt has cirrhosis of liver
  • has a low solubility and can precipitate in urine and cause stones
141
Q

What are four edematous conditions?

A

CHF
Hepatic cirrhosis and ascites
Pulmonary edema
Cerebral edema

142
Q

How do you treat CHF?

A

thiazides, loop diuretics and aldosterone antagonists

143
Q

How do you treat Hepatic cirrhosis and ascites?

A

-treat with thiazide, loop and K+ sparing diuretics

144
Q

How do you treat pulmonary edema?

A

Treat aggressively with loop diuretics

145
Q

How do you treat cerebral edema?

A

Treat with osmotic diuretics for direct effects

146
Q

How do you treat nephrotic syndrome?
How do you treat acute renal failure?
How do you treat chronic renal failure?

A

w/ thiazide diuretics and decreased salt intake

use osmotic diuretics or loop diuretics

treat aggressively with loop diuretics

147
Q

How do you treat HTN?

A
  • Treat with decreased salt intake

- Add thiazides, can also add K+ sparing or loop diuretics

148
Q

How do you treat nephrolithiasis?

A
  • treat with thiazides to increase calcium reabsorption

- decrease salt intake

149
Q

How do you treat hypercalcemia?

A
  • treat with loop diuretics to increase calcium excretion

- add normal saline to prevent contraction of extracellular space, can add K+ sparing diuretics as needed

150
Q

How do you treat nephrogenic diabetes insipidus?

A

Treat with thiazide or loop diuretics to reduce plasma volume and contract the extracellular space

151
Q

What is diabetes inspidius and how do you treat it (any type)?

A

polyuria due to decrease ADH
-treat with thiazides or loop diuretics (paradoxically) which cause salt depletion and contraction of ECF-> which leads to proximal tubule reabsorption of Na+ and decrease volume of fluid reaching the distal tubule.

SO it works by creating a reflexive state to absorb water

152
Q

What are the 2 types of diabetes insipidus (DI)?

A
  • Central DI

- Nephrogenic DI

153
Q

What type of DI is this:

decreased ADH levels due to injury, tumors or infection

A

Central DI

154
Q

How do you treat central DI?

A 
arginine vasopressin (AVP=ADH)
Vasopressin analogs (desmopression and lypressin)
-chlorprpamide, a sulfonylurea, which increases actions of ADH
155
Q

What is nephrogenic DI?

A

decreased ADH responsiveness due to hypercalcemia, hypokalemia, post-obstructive renal failure, lithium

156
Q

What is the treatment for nephrogenic DI?

A

-ADD thiazides
-Amiloride (blocks Li)
-NSAIDs i.e indomethacin
(decrease prostaglandin synthesis-> increase response to ADH)

157
Q

What is SIADH?

A

syndrome of inappropriate secretion of ADH= too much ADH

158
Q

How do you treat SIADH?

A

loop diuretics (decrease ability to concentrate urine)
DEMECLOCYCLINE (cant use with liver dysfunction)
Vaptans
Lithium (not commonly used, it can damage kidneys)

159
Q

How does demeclocycline work?

A

a tetracycline that decreases actions of ADH

Block 9 Week 2 (7 decks)

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