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Pharm 3 Test 1 > Nephrology > Flashcards

Nephrology Flashcards

1
Q

Definition: Passive transport from plasma into the renal tubule

A

Filtration

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2
Q

Definition: when substances in tubule move to plasma

A

Reabsorption

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3
Q

Definition: active transport of substances from plasma into renal tubule

A

Secretion

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4
Q

Main process in glomerulus?

A

filtration

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5
Q

Drugs that work on glomerulus?

A

NONE

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6
Q

What is the first stop in the nephron?

A

glomerulus

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7
Q

What controls filtrate formation in the glomerulus?

A

BP

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8
Q

What is being formed in the glomerulus?

A

ultrafiltrate

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9
Q

What is contained in the ultrafiltrate at the level of the glomerulus?

A
  • Ions, small particles

- NOT proteins and RBCs

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10
Q

Main process in PCT?

A

reabsorption; some secretion

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11
Q

What is reabsorbed in the PCT/ percentages?

A

65% NaCl, K, Mg
85% nahco3
100% glu, AAs

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12
Q

What is secreted in the PCT?

A

organic acids and bases

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13
Q

Which meds work on the PCT?

A

CAIs

Adenosine antagonists

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14
Q

First site of reabsorption?

A

PCT

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15
Q

What is being reabsorbed and secreted in the LOH?

A

Reabsorption: 15-25% NaCl, K
-Ca, Mg

Secretion: Some K

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16
Q

Which meds work on the LOH?

A

Loop diuretics

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17
Q

What exact spot on the LOH do loops work?

A

thick ascending limb of LOH

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18
Q

What is being reabs and secreted in the DCT?

A

Reabs: 4-8% Na, Cl
Sec: Ca (parathyroid control)

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19
Q

What meds work on the DCT?

A

Thiazide diuretics

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20
Q

What is being reabs and secreted in the cortical collecting tubule?

A

Reabs: 2-5% Na
Sec: K* and H+

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21
Q

What meds work on the collecting tubule?

A

K sparing diuretics, adenosine antagonists

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22
Q

What is being reabs and secreted in the medullary collecting duct?

A

Reabs: water
Sec: NOTHING
**collecting duct= final conc of urine

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23
Q

What meds work on the collecting duct?

A

ADH antagonists

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24
Q

List the drugs that are carbonic anhydrase inhibitors

A

Acetazolamide (oral), dorzolamide, brinzolamide (topical)

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25
Q

MC CAI?

A

Acetazolamide

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26
Q

the oral CAI is?

A

Acetazolamide

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27
Q

Topical CAI is?

A

dorzolamide, brinzolamide

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28
Q

The topical CAIs are used in which body part?

A

eyes (ophthalmic drops)

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29
Q

CAIs MOA?

A

Inhibits carbonic anhydrase, which is responsible for dehydrating H2CO3; reduces aqueous humor production

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30
Q

Bicarb buffer system

A

H2CO3–>

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31
Q

CAIs main effect on the body?

A

reduce aqueous humor production

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32
Q

CAIs and acid/base concs in body?

A
  • H2CO3 (carbonic acid) which is a weak acid, is retained
  • Urine contains less H+
  • Blood contains more acid
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33
Q

CAIs ___ the pH of the urine

A

increase (more alkaline)

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34
Q

Indications of CAIs

A

*Glaucoma (main), urinary acidosis, metabolic alkalosis, acute mtn sickness, inc IOP post op cataract surgery, aspirin overdose

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35
Q

Absorption of CAIs?

A

absorbs well (oral and ocular)

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36
Q

Why are CAIs given in aspirin overdose?

A

aspirin is a weak acid and therefore will be excreted more quickly in alkaline urine

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37
Q

CAIs: onset, duration, peak

A

30 min, 12 hr, 2 hr

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38
Q

CAIs work on the… (part of nephron)

A

PCT

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39
Q

CAI ADRs

A

*drowsiness (MC), renal stones, K wasting, hypersensitivity rxn

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40
Q

CAI CIs

A

hepatic cirrhosis

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41
Q

Which dosage form of CAIs decreases systemic absorption, decreasing side effects?

A

ocular/topical (dorzolamide, brinzolamide)

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42
Q

What technique can be done to decrease systemic absorption of CAIs?

A

nasolacrimal duct block

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43
Q

How do you do the nasolacrimal duct block?

A

put drops in, close eyes, apply pressure to nasolacrimal ducts for 1-2 mins
-not guaranteed to completely prevent systemic absorption

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44
Q

Are CAIs usu used single or in combo?

A

BOTH! (combo w/ b-blockers)

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45
Q

What is H2CO3s conjugate base?

A

HCO3- (bicarbonate ion)

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46
Q

H2CO3 is a… (acid or base)

A

weak acid

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47
Q

Adenosine antagonists work on which parts of the nephron?

A

PCT, collecting tubule

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48
Q

Adenosine affects which parts of the nephron?

A

glomerulus, PCT, asc limb of LOH, collecting duct

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49
Q

Adenosine antagonists work how?

A

diuretic effects, work on coll tubule and PCT, work like caffeine

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50
Q

Name the Loop diuretics (4)

A

furosemide, torsemide, bumetanide, ethacrynic acid

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51
Q

MC loop used?

A

furosemide

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52
Q

MOA of loop diuretics?

A 
Inhibits Na 2Cl K transporter;inhibits their active transport
Stop ions (Na, K, Cl) from being reabsorbed, more are excreted into the urine along with H2O
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53
Q

Loops work on what part of nephron?

A

thick ascending limb of LOH

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54
Q

Indications of Loops?

A
  • *Edema (MC, very effective)- CHF
  • HTN (less used for this)
  • Hypercalcemia, hyperkalemia (gets rid of excess ions in the plasma)
  • Anion overdose (fluoride, bromide, iodide)
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55
Q

T or F, Loops are a high ceiling effect med?

A

True. (ceiling effect- near max diuretic effect; if you go over max, won’t be beneficial)

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56
Q

Loops in combo with what have bet combined effect/highest amount of Na blocking over time?

A

thiazides

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57
Q

Loops absorption

A

orally well absorbed

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58
Q

Loops available in these routes of administration:

A

oral, IV

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59
Q

What are the best drugs to diurese pts?

A

loops

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60
Q

Torsemide vs furosemide onset and duration?

A

T: o- 1 hr, d- 4-6 hrs (short onset, long duration)
F: o- 2-3 hrs, d: 2-3 hrs (longer onset, shorter duration)

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61
Q

Loops ADRs

A
  • hypo- mg, ca, k, na, cl
  • hyperuricemia
  • ototoxicity (if given w/ other ototoxic meds)
  • allergic rxn
  • increase Scr
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62
Q

Loops CIs

A
  • overuse in hepatic cirrhosis, renal failure (nephrotoxic, heart failure
  • sulfa allergies
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63
Q

best loop to give in sulfa allergic pt?

A

ethacrynic acid (no sulfa group)

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64
Q

Loop diuretic drug-drug interactions

A

NSAIDs- will decrease effectiveness of loops. Don’t stop NSAIDs, just find a balance

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65
Q

Furosemide PO:IV conversion

A

2:1 (ex 40 mg PO= 20 mg IV)

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66
Q

Torsemide PO:IV conversion

A

1:1

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67
Q

Bumetanide PO:IV conversion

A

1:1

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68
Q

Conversion btw loops (F:T:B)

A

40 mg furosemide= 20 mg torsemide= 1 mg bumetanide

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69
Q

most potent loop?

A

bumetanide

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70
Q

Are diff loops interchangeable?

A

yes, can switch from one to another at any time

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71
Q

List the thiazide diuretics

A

HCTZ, chlorothiazide

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72
Q

List the thiazide-like diuretics

A

metolazone, indapamide, chlorthalidone

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73
Q

Which drug class has a ceiling effect?

A

loop diuretics

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74
Q

MOA of thiazides?

A

Inhibit NaCl transporter, enhance Ca reabsorption; NaCl and water are excreted

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75
Q

Which part of nephron do thiazides work?

A

DCT

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76
Q

Thiazides indications

A

*HTN (MC), heart failure, nephrogenic DI, nephrolithiasis

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77
Q

Thiazides absorption

A

Slowly

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78
Q

Which thizide or thiazide like diuretic absorbs the slowest but has the longest duration of action?

A

chlorthalidone (thiazide-like)

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79
Q

MC used thiazide in practice?

A

HCTZ

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80
Q

Thiazides are weak or strong diuretics?

A

weak

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81
Q

Thiazides ADRs

A
  • hypo- Na, Cl, K,
  • hyper- uric acid, Ca, glucose, lipids
  • allergic rxn (sulfa)
  • photosensitivity
  • orthostatic hypotension (minimal)
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82
Q

Thiazides CIs

A

-Overuse in: hep cirrhosis, renal failure, CHF (dont give high doses)

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83
Q

Thiazides caution in pts with which allergy?

A

sulfa

84
Q

Thiazides may be ineffective in these pts

A

pts w/ CrCl less than 20 ml/min, EXCEPT metolazone (thiazide like)

85
Q

Only thiazide that is effective in pts w/ low CrCl?

A

metolazone (thiazide-like)

86
Q

Which thiazide diuretic is the only one that is available in IV form?

A

chlorothiazide (thiazide)

87
Q

What routes of admin are thiazides available in?

A

oral (most) and IV (chlorthiazide)

88
Q

What drug class are not structurally like thiazides, but contain a sulfonamide group and have the same MOA as thiazides?

A

thiazide-like diuretics

89
Q

List the K- sparing (aldosterone receptor blocker) diuretics

A

Spironolactone, eplerenone

90
Q

List the other K- sparing agents

A

Triamterene, amiloride

91
Q

K- sparing (aldosterone receptor blocker) diuretics MOA

A

block aldosterone receptors (antagonize mineralcorticoid receptors) in the collecting tubules, preventing aldosterone from binding; More K and H stays in plasma

92
Q

Where in the nephron do K- sparing (aldosterone receptor blocker) diuretics work?

A

cortical collecting tubule

93
Q

Indications for K- sparing (aldosterone receptor blocker) diuretics

A
  • hypokalemia prevention and tx

- Spironolactone: hyperaldosteronism, PCOS, hirsutism

94
Q

T or F? Spironolactone has a slow onset, duration, and peak?

A

True

95
Q

Does spironolactone take a while to reach therapeutic levels?

A

Yes- several days

96
Q

K sparing diuretics ADRs (all types)

A

hyperkalemia

97
Q

Spironolactone ADRs

A

gynecomastia, impotence, tumorogenic (animals)

98
Q

K sparing diuretics CIs (all types)

A

hyperkalemia, renal impairment, hepatic impairment

99
Q

Spironolactone CIs

A

Addison’s dz

100
Q

Eplerenone drug-drug interactions

A

-strong CYP3A4 agents- grapefruit, fluconazole, diltiazem (EPLERENONE ONLY)

101
Q

K sparing diuretics (other) MOA

A

inhibits JUST the Na ion channels in the collecting tubules

102
Q

Triamterene onset and duration

A

o- 2-3 hrs

d- 7-9 hrs

103
Q

Triamterene ADRs

A

kidney stones

104
Q

Which is more effective, triamterene or spironolactone?

A

spiro

105
Q

List the INDIRECT ADH antagonists

A

Lithium, demeclocycline

106
Q

List the DIRECT ADH antagonists

A

conivaptan, tolvaptan

107
Q

T or F? Li and Na are the same size

A

T

108
Q

INDIRECT ADH antagonists MOA?

A

unknown; DO NOT work on ADH receptors

109
Q

DIRECT ADH antagonists MOA?

A

inhibit vasopressin (ADH) receptors; ADH blocked and H2) is not retained

110
Q

ADH antagonists work on which part of the nephron?

A

collecting duct

111
Q

Are ADH antagonists used often?

A

No

112
Q

ADH antagonists (direct and indirect) indications

A

CHF, SIADH

113
Q

Direct ADH antagonists onset/peak/duration?

A

o- 2-4 hrs
p- 4-8 hrs
d- 24 hrs

114
Q

How often are direct ADH antagonists taken per day?

A

1x/day (bc they last 24 hrs)

115
Q

Direct ADH antagonists ADRs?

A

Nausea, dry mouth, thirst

116
Q

Direct ADH antagonists CIs?

A

hypovolemia, hyponatremia

117
Q

Direct ADH antagonists drug-drug interactions?

A

-strong CYP3A4 agents- grapefruit juice, fluconazole, diltiazem

118
Q

List the osmotic diuretics

A

Glycerol, mannitol

119
Q

Mannitol available forms?

A

PO, inhalation, IV

120
Q

Osmotic diuretics MOA?

A

increase osmotic pressure in the glomerulus, decreasing water and electrolyte reabsorption

121
Q

Osmotic diuretics indications?

A
  • cerebral edema (head injury)
  • acute glaucoma
  • bronchial hyperresponsiveness
122
Q

Describe the absorption, excretion, duration of osmotic diuretics?

A

poorly absorbed, quickly excreted, don’t last long

123
Q

Osmotic diuretics ADRs?

A
  • Glycerol (oral form)- N/V/Diarrhea
  • Mannitol- excess volume expansion, can cause HF, edema, pulm congestion (pulling water out of bloodstream into the tissues)
124
Q

Osmotic diuretics CIs

A

hypersensitivity

125
Q

How should you take oral osmotic diuretics?

A

mix w/ small amount of juice (OJ preferred), add ice, sip SLOWLY, small sips

126
Q

How should IV mannitol be infused?

A

SLOWLY

127
Q

Mannitol IV is indicated for what pt population?

A

inpts, esp head injury, edema

128
Q

Sulfonamide chemical structure?

A

SO2NH2

129
Q

How many chemical arrangements of sulfonamides are there?

A

3

130
Q

Can pts w/ sulfa abx allergy receive loop diuretics?

A

yes. caution. best=ethacrynic acid

131
Q

No cross sensitivity for sulfonamide allergic pts taking loops:

A

abx, other sulfonamide containing meds

132
Q

3 questions to ask pt when they say they have a med allergy?

A
  • what allergies?
  • what happens?
  • how long ago?
133
Q

Definition: Volume of plasma filtered across the glomerulus per unit of time

A

glomerular filtration rate (GFR)

134
Q

MC method for measuring kidney fn?

A

GFR

135
Q

The GFR reflects the number of..

A

functioning nephrons in the kidney

136
Q

GFR normal range

A

90-120 ml/min

137
Q

T or F? GFR is easy to measure directly

A

F

138
Q

Definition: endogenous byproduct of musc metabolism

A

serum creatinine

139
Q

how much of Cr is cleared by the kidneys? (%)

A

100%

140
Q

__% of Cr is cleared by glomerular filtration, and __% through tubular secretion

A

90%, 10%

141
Q

Scr is ____ (lower/higher) in elderly and paraplegics?

A

lower (less musc tone/mass)

142
Q

How do you DIRECTLY measure renal fn/creat?

A

24 hr urine collection

143
Q

How do you INDIRECTLY measure renal fn/creat?

A

calculation based on SCr

144
Q

Definition: rate at which the kidneys clear Cr from the blood

A

CrCl

145
Q

Name of the formula used to calculate CrCl

A

cockroft-gault formula

146
Q

when calculating crcl on females, what do you have to add to your calc?

A

multiply by 0.85

147
Q

If pts body weight is less than IBW, use the ___

A

actual body weight

148
Q

If pts body weight is 20% more than IBW, use the ____

A

adjusted body weight

149
Q

If pts weight is more than IBW, but less than 20% above it, use the ____

A

ideal body weight

150
Q

AKI clinical presentation

A

-inc Scr, dec GFR, accumulation of nitrogenous wastes, inability to regulate fluids/electrolytes/acid base balance, weight gain (edema), foamy urine, changes in urinary habits

151
Q

3 categories of AKI

A

Prerenal, intrinsic, postrenal (also functional?)

152
Q

AKI from hemodynamic changes without hypotension or structural damage

A

functional

153
Q

Decrease in renal perfusion

A

prerenal azotemia

154
Q

Structural damage inside the kidney

A

intrinsic

155
Q

obstruction of urine flow

A

postrenal

156
Q

Prerenal: urine sediment

A

normal

157
Q

Prerenal: urine RBCs

A

none

158
Q

Prerenal: urine WBCs

A

none

159
Q

Prerenal: urine Na

A

Less than 20

160
Q

Prerenal: urine/serum osmolarity

A

> 1.5 (highest of the 3)

161
Q

Prerenal: urine/scr

A

> 40:1 (highest)

162
Q

Prerenal: BUN/Scr

A

> 20 (highest)

163
Q

Intrinsic: urine sediment

A

casts, cellular debris

164
Q

Intrinsic: urine RBCs

A

2-4+ (most)

165
Q

Intrinsic: urine WBCs

A

2-4+ (most)

166
Q

Intrinsic: urine Na

A

> 40

167
Q

Intrinsic: urine/serum osmo

A

Less than 1.3

168
Q

Intrinsic: urine/Scr

A

Less than 20:1

169
Q

Intrinsic: BUN/Scr

A

15

170
Q

Postrenal: urine sediment

A

cellular debris

171
Q

Postrenal: urine RBCs

A

variable

172
Q

Postrenal: urine WBCs

A

1+ (middle)

173
Q

Postrenal: urine Na

A

> 40

174
Q

Postrenal: urine/serum osmo

A

Less than 1.5

175
Q

Postrenal: urine/Scr

A

Less than 20:1

176
Q

Postrenal: BUN/Scr

A

15

177
Q

Name the type of AKI caused by: hypovolemia

A

prerenal

178
Q

Name the type of AKI caused by: obstruction (upper-kidney, lower-bladder, prostate, catheter)

A

postrenal

179
Q

Name the type of AKI caused by: decreased cardiac output

A

prerenal

180
Q

Name the type of AKI caused by: radiocontrast dyes, APAP, cisplatin

A

intrinsic (acute tubular necrosis)

181
Q

Name the type of AKI caused by: rhabdomyolysis

A

intrinsic (acute tubular necrosis)

182
Q

Name the type of AKI caused by: decreased blood volume

A

prerenal

183
Q

Name the type of AKI caused by: infection

A

intrinsic

184
Q

Name the type of AKI caused by: ACE-I, NSAIDS

A

prerenal (impair renal perfusion)

185
Q

Name the type of AKI caused by: PCN, cephalosporins, sulfonamides, rifampin, phenytoin, furosemide, PPIs, NSAIDs

A

intrinsic (nephritis)

186
Q

How many stages of AKI/ARF are there?

A

3

187
Q

How are the stages classified (what are they based on?)

A

Scr and urine output

188
Q

Normal Scr value (men)

A

0.7-1.3 mg/dL

189
Q

Normal Scr value (women)

A

0.6-1.1 mg/dL

190
Q

What is used as the reference Scr?

A

lowest Scr recorded in the last 3 months

191
Q

What are the 3 urine output classifications?

A

non-oliguria (normal), oliguria, anuria

192
Q

non-oliguria numbers

A

adults >400 ml/day or >.5 ml/kg/hr

peds >1ml/kg/hr

193
Q

peds UO classified based on___

A

weight

194
Q

oliguria #s (adults)

A

A-less than 400 ml/ day or less than 0.5 ml/kg/hr for >6hrs

195
Q

Anuria #s (BOTH adults and peds)

A

Less than 50 mls/day

196
Q

Medication induced AKI: Which meds change renal hemodynamics by vasoconstricting the afferent arteriole?

A

NSAIDs, cyclosporine, tacrolimus, amphotericin B, radiocontrast agents, vasopressores

197
Q

Medication induced AKI: Which meds change renal hemodynamics by vasodilating the efferent arteriole?

A

ACEIs, ARBs, diltiazem, verapamil

198
Q

Medication induced AKI: Which meds cause direct toxicity to the renal tubules?

A

aminoglycosides, amphotericin B, radiocontrast agents, cisplatin/carboplatin (platinum chemotherapy agents)

199
Q

5 things that place pt at higher risk for AKI

A
  • hx CKD
  • increased age
  • comorbid conditions (DM)
  • dehydration
  • pt on AKI inducing medication
200
Q

Most important way to prevent AKI, esp when giving direct tubular toxic agents

A

adequate hydration, dilute toxic agents

201
Q

What steps do you need to take before giving a pt a radiocontrast agent?

A
  • administer oral or IV hydration for 6-12 hrs prior
  • Give NAC (N-acetylcysteine)- 4 doses PO
  • Use low or iso-osmolar agent
202
Q

Steps for tx of AKI (4)

A
  • Evaluate pt fluid status (hyper or hypovolemic)
  • ID cause of AKI (meds?)
  • Review meds for renal dose adjustments
  • Supportive therapy
203
Q

If AKI pt is hypervolemic, how would you tx?

A

diuretic or renal replacement therapy (dialysis)

204
Q

If AKI pt is hypovolemic, how would you tx?

A

fluids (crystalloid, colloid)

205
Q

If cause of AKI is medication elated, what do you do?

A
  • stop offending med

- start steroids (prednisone or methylprednisolone)

206
Q

What is included in supportive therapy for AKI pts?

A
  • dialysis

- adequate hydration

207
Q

T or F, there is a drug that has been proven to accelerate the recovery of renal failure

A

F- NONE; protection/prevention is key

Pharm 3 Test 1 (2 decks)

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