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Pharmacology > Chronic Kidney Disease (Exam 2) > Flashcards

Chronic Kidney Disease (Exam 2) Flashcards

1
Q

Carbonic Anhydrase Inhibitors examples

A

Acetazolamide
Methazolamide
Dorzolamide
Indisulam
Topiramate
Benzthiazide

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2
Q

Loop Diuretics examples

A

Furosemide
Bumetanide
Torsemide
Ethacrynic Acid

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3
Q

Thiazide Diuretics

A

Chlorthalidone
Indapamide
Metolazone
Bendroflumethiazide
Hydrochlorothiazide
Chlorothiazide

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4
Q

Loop Agents + Thiazide Osmotic Diuretics

A

Mannitol

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5
Q

K+ Sparing Diuretics

A

Amiloride
Triamterene
Eplerenone
Spironolactone

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6
Q

Carbonic Anhydrase Inhibitors on NaCl

A

Increases +

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7
Q

Carbonic Anhydrase Inhibitors on NaHCO3

A

Increases +++

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8
Q

Carbonic Anhydrase Inhibitors on K+

A

Increases +

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9
Q

Carbonic Anhydrase Inhibitors on Body pH

A

Acidosis

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10
Q

Loop Diuretics on NaCl

A

Increases ++++

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11
Q

Loop Diuretics on NaHCO3

A

No change

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12
Q

Loop Diuretics on K+

A

Increases +

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13
Q

Loop Diuretics on Body pH

A

Alkalosis

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14
Q

Thiazide Diuretics on NaCl

A

Increases ++

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15
Q

Thiazide Diuretics on NaHCO3

A

Increases +

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16
Q

Thiazide Diuretics on K+

A

Increases +

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17
Q

Thiazide Diuretics on Body pH

A

Alkalosis

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18
Q

Loop Agents + Thiazide Osmotic Diuretics on NaCl

A

Increases +++++

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19
Q

Loop Agents + Thiazide Osmotic Diuretics on NaHCO3

A

Increases +

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20
Q

Loop Agents + Thiazide Osmotic Diuretics on K+

A

Increases ++

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21
Q

Loop Agents + Thiazide Osmotic Diuretics on Body pH

A

Alkalosis

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22
Q

K+ sparing agents on NaCl

A

Increases +

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23
Q

K+ sparing agents on NaHCO3

A

Questionable increase

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24
Q

K+ sparing agents on K+

A

Decreases -

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25
Q

K+ sparing agents on Body pH

A

Acidosis

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26
Q

What do carbonic anhydrase inhibitors treat?

A

Edema
Epilepsy
Glaucoma

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27
Q

How do CAIs work for gluacoma?

A

Control fluid secretion

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28
Q

How do CAIs work for edema?

A

Promotion of diuresis in instances of abnormal fluid retention

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29
Q

Carbonic anhydrase diuretic effect is due to

A

Action in the kidney on reversible reaction involving hydration of carbon dioxide and dehydration of carbonic acid

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30
Q

Net result of reversible reaction in kidneys

A

Loss of HCO3 ion, which carries out Na+, water, and K+
Alkalinization of urine and promotion of diuresis

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31
Q

What does furosemide (FUR) treat?

A

Hypertension
Edema
Congestive Heart Failure
Liver Cirrhosis
Renal Disease

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32
Q

Furosemide MOA

A

Inhibits absorption of Na+ + Cl- in PCTs, DCTs, and loop of Henle. Action on DCT is independent of inhibitory effect on CA and aldosterone

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33
Q

Where is furosemide metabolized?

A

Kidneys and liver
Bound to plasma proteins, albumin

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34
Q

What are the major metabolites of furosemide?

A

FUR-glucuronide (Pharmacologically active)
Saluamine

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35
Q

Bioavailability of FUR in fasted

A

~60-64%

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36
Q

Terminal 1/2-life of FUR

A

2 hours

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37
Q

Excretion of FUR is greatest via

A

IV injection

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38
Q

FUR in elderly patients

A

Binding to albumin may be reduced and is excreted unchanged in urine
Initial diuretic effect declines

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39
Q

Hydrochlorothiazide (HCTZ) MOA

A

Acts directly on kidneys and promotes diuresis by inhibiting Na+/Cl- cotransporter located in DCT of nephron

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40
Q

How do thiazides work?

A

Increase excretion of Na+ and Cl- in equal amounts, which decreases extracellular fluid and plasma volume –> reduces BP

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41
Q

Natriuresis (water loss) causes

A

secondary loss of K+ and bicarbonate but retains Ca+

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42
Q

Plasma half-life of HCTZ in fasted

A

2.5 hours

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43
Q

At maximal therapeutic dosages all thiazides are

A

approximately equal in diuretic potency (weak diuretic)

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44
Q

K+ sparing agents MOA

A

Inhibition of sodium reabsorption at DCT, cortical collecting tubule decreasing net negative potential of tubular lumen. Reduces K+ and H+ secretion and excretion

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45
Q

What does Ami treat?

A

Pyrizine compound that treats hypertension and congestive heart failure

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46
Q

Amiloride HCl possesses

A

weak natriuretic, diuretic, and antihypertensive activity

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47
Q

Amiloride in presence of thiazide or loop diuretic

A

Decreases enhanced urinary excretion of magnesium

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48
Q

Is Ami an aldosterone antagonist?

A

No stupid fuck

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49
Q

What are aldosterone antagonists?

A

Spironolactone
Eplerenone

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50
Q

Where is Ami metabolized?

A

idk but NOT the liver
Excreted unchanged by kidneys

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51
Q

Hepatorenal syndrome and Ami

A

Ami accumulation likely

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52
Q

Ami effect on GFR and renal blood flow

A

Very little

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53
Q

Prototypical ADH agonists

A

Antidiuretic hormone (ADH)
Desmopressin

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54
Q

ADH and Desmopression are

A

Peptides and must be given parenterally

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55
Q

ADH antagonists

A

Conivaptan
Tolvaptan
Demeclocycline
Lithium - not rlly used for this

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56
Q

ADH MOA

A

Facilitates water reabsorption from collecting tubule by activation of V2 receptors

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57
Q

Activation of V2 receptors stimulates

A

Adenylyl cyclase via Gs
Increases cAMP

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58
Q

Increased cAMP from ADH causes

A

Insertion of additional aquaporin AQP2 water channels

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59
Q

Conivaptan

A

ADH inhibitor at V1a and V2 receptors

60
Q

Tolvaptan

A

More selective V2 blocker with little V1 affinity

61
Q

Demeclocycline and Lithium

A

Inhibit action of ADH at some point distal to generation of cAMP and interfere with insertion of water channels

62
Q

ADH and desmopressin will

A

reduce urine volume and increase concentration

63
Q

Which disease is ADH and desmopression useful in?

A

PITUITARY diabetes insipidus
no value in nephrogenic form

64
Q

Nephrogenic diabetes insipidus

A

Use salt restriction, water restriction, thiazides, loop diuretics

65
Q

Syndrome of inappropriate ADH secretion (SIADH)

A

Causes hyponatremia

66
Q

How to treat SIADH

A

Demeclocycline
Conivaptan
Tolvaptan
Lithium

67
Q

Chronic Kidney Disease

A

Irreversible decrease in number of function nephrons resulting in progressive and permanent deterioration of renal function

68
Q

Kidney damage of > 3 months defined as

A

-Structural/functional abnormality
-With/Without decreased GFR
-Manifested by pathogenic abnormalities or markers of disease
-Abnormalities in composition of blood or urine

69
Q

GFR of CKD

A

< 60mL/min/1.73 m2

70
Q

Predisposing factors of CKD

A

Diabetes mellitus
Hypertension
CV disease
Family history of ESRD

71
Q

Biomarkers of kidney function

A

Serum creatinine
GFR
Albumin
Proteinuria
BUN

72
Q

REN-related kidney disease

A

Mutation in REN gene !!!
leads to production of abnormal protein toxic to cells that normally produce renin

73
Q

Polycystic kidney disease

A

Mutations in PKD1, PKD2, PKHD1 genes !!!
lead to cysts in kidneys that interfere with filtering waste products

74
Q

Uromodulin-associated kidney disease

A

Mutations in UMOD gene !!! leads to damage of kidney tubules

75
Q

Medullary cystic kidney disease type 1

A

Mutations in MUC1 gene !!! leads to production of altered protein decreasing mucin 1 and normal kidney development

76
Q

Kidney stones

A

Dehydration and calcium deficiency lead to formation of stones

77
Q

Fabry Disease

A

Mutations in GLA gene !!! lead to absence of alpha-galactosidase A activity and buildup of globotriaosylceramine (wtf)

78
Q

Dent Disease

A

Mutations in CLCN5 or OCRL gene !!! leads to disruption of reabsorption of proximal tubules

79
Q

GFR

A

volume of plasma ultra-filtrate presented to nephrons per unit time during process of urine formation

80
Q

Stage 1 CKD (G1)

A

Normal
>90 GFR

80
Q

Calculate NFP

A

GBHP-CHP-BCOP

81
Q

Stage 2 CKD (G2)

A

Mildly decreased
60-89 GFR

82
Q

Stage 3 CKD (G3a)

A

Mildly-Moderate decrease
45-59 GFR

83
Q

Stage 3 CKD (G3b)

A

Mildly-Moderate decrease
30-44 GFR

84
Q

Stage 4 CKD (G4)

A

Severely decreased
15-29 GFR

85
Q

Stage 5 CKD (G5)

A

Kidney failure
<15 GFR

86
Q

Quantification of Proteinuria

A

AER (mg/24hr)
PER (mg/24hr)
ACR (mg/g)
PCR (mg/g)
Protein reagent strip

87
Q

Other complications of CKD

A

Amyloidosis
Blood and immune disorders
Endocrine
GI
Protein-energy wasting
Neurologic

88
Q

What is eGFR?

A

Estimated glomerular filtration rate

89
Q

What stage do you start ACE/ARB therapy for CKD?

A

> 60 eGFR + microalbumin <30
Stage 2/3 CKD

90
Q

Primary cause of anemia in CKD patients

A

Decreased production of EPO

91
Q

Iron deficiency medications for CKD

A

ESA:
-Epoetin alfa
-Epoetin beta
-Darbepoetin alfa or placebo

92
Q

hepcidin is very common in what stage of CKD?

93
Q

hepcidin

A

a hormone produced by the liver that regulates iron
directly binds to ferroprotein
an inflammatory marker

94
Q

hepcidin is _______ in iron deficiency and ________ by transfusion induced iron and inflammatory diseases

A

decreased or absent

increased

95
Q

hepcidin has high correlation with

A

serum ferritin levels

96
Q

high iron means

low iron means

inflammation or infection means

A

high hepcidin

low hepcidin

high hepcidin

97
Q

hepcidin is produced primarily by

98
Q

what is required by most CKD patients receiving ESA

A

iron supplementation

99
Q

iron is absorbed in

A

the duodenum

100
Q

IV iron preparations

A

Iron dextran
Sodium ferric gluconate
iron sucrose
ferumoxytol

101
Q

FGF-23

A

regulates phosphate concentration in plasma
phophatonin hormone
elevated in CKD to promote renal phosphate excretion

102
Q

CKD mineral and bone disorders

A

biochemical abnormalities
bone abnormalities
soft tissue and vascular calcification

103
Q

how much calcium is found in the bone?
as a component of what?

A

99%
hydroxyapatite

104
Q

calcium is important for

A

signal transduction

105
Q

dietary calcium is determined by

A

the needs for bone development and maintenance

106
Q

concentration of calcium is regulated by

A

interactions between the PTH
various forms of Vitamin D
calcitonin

107
Q

phosphate binding agent drugs

A

calcium carbonate
calcium acetate
sevelamer carbonate
lanthanum carbonate
aluminum hydroxide

108
Q

calcimimetics

A

Cinacalcet (Sensipar) and etelcalcetide (Parsabiv)
enhance the sensitivity of PT to Ca in the blood

109
Q

goal of calcimimetic therapy

A

decrease PTH
reduces risk of 2nd hyperparathyroidism

110
Q

two types of calcimimetics

A

Type 1 - agonists NOT USED CLINICALLY
Type 2 - allosteric activators (cinacalcet)

111
Q

MOA of calcimimetics

A

enhances the sensitivity of PTH calcium sensing receptor to the concentration of blood (ionized calcium)
indirectly activates Ca receptors
CaSR more responsive to calcium

112
Q

when the PT gland senses a higher ionized calcium,

A

the CaSR decreases the secretion of PTH

113
Q

Vitamin D

A

group of lipophilic pre hormones
converted to biologically active metabolites that function as hormones

114
Q

Vitamin D maintains plasma Ca by

A

increases Ca absorption in SI
decrease Ca renal excretion
mobilize Ca from bone vitamin D

115
Q

two sources of vitamin D

A

dietary ergocalciferol - plants
cholecalciferol - skin

116
Q

nutritional vitamin D

A

ergocalciferol - D2
cholecalciferol - D3

117
Q

active vitamin D

A

calcitrol - D3

118
Q

Vitamin D analogs

A

paricalcitol - D2
doxercalciferol - D2

119
Q

Cholecalciferol is generated in the ______ from __________ by the action of ________

A

skin

7-dehydrocholesterol

UV irradiation

120
Q

role of phosphate

A

constituent of nucleic acids and ATP

excretion of H ions from the kidney

121
Q

Hyperphosphatemia can cause

A

osteomalacia

122
Q

calcitriol

A

regulates phosphate deposition in the bone as hydroxyapatite

123
Q

PTH increases

A

phosphate excretion

124
Q

FGF-23 (bone derived fibroblast growth factor-23) binds to

A

FGF receptor

125
Q

regulators of FGF-23

A

hyperphosphatemia
oral Pi loading
calcitriol
PTH

126
Q

FGF-23 is synthesized and secreted in

A

osteoblasts

127
Q

FGF-23 in the kidneys directly

A

inhibits intestinal Pi absorption

128
Q

FGF023 lowers

A

serum calcitriol

129
Q

calcitriol stimulates

130
Q

increase in FGF23 activity leads to

A

increase kidney excretion of phosphate and down regulates sodium reabsorption

131
Q

ACEI and ARB adverse drug reactions

A

decrease angiotensin II effects and vasodilation –> drop in BP
dec in GFR
inc in serum K

132
Q

the combo of an ACE inhibitor or ARB with a diuretic is effective in _________.

Why?

A

lowering BP

primarily dilate afferent and efferent arterioles
relieve glomerular pressure
protective towards kidneys

133
Q

chronic metabolic acidosis

A

increase skeletal muscle breakdown
decrease albumin synthesis
muscle weakness
release of Ca and PO4 from bone (worsens bone health)

134
Q

activation of complement pathway for chronic metabolic acidosis

A

promotes tubule-interstitial injury

135
Q

Rx to slow progression of chronic metabolic acidosis

A

bicarbonate supplementation

136
Q

Cystatin C

A

0.53-0.95 mg/L
biomarker for early detection of AKI
increases as GFR decreases in AKI and CKD
serves as an alternative to sCr for estimating GFR

137
Q

RRT for asymptomatic patients, GFR can become

A

5-9 ml/min

138
Q

indications for RRT

A

severe metabolic acidosis
hyperkalemia
pericarditis
encephalopathy
intractable volume overload
failure to thrive/malnutrition
peripheral neuropathy
intractable GI symptoms

139
Q

compensatory renal hypertrophy

A

upon removal of one kidney, the other enlarges and increases in function
dominant contributor to growth

140
Q

two mechanisms of compensatory renal hypertrophy

A

increased activity by the remaining kidney via hypertrophy
release of a kidney specific factor in response to unilateral nephrectomy that initiates CRH

141
Q

compensatory hypertrophy can only take place if

A

some portion of the original structure is left to react to the loss

142
Q

Compensatory renal cell proliferation

A

kidney mass goes down, remaining renal tissue undergoes compensatory growth

143
Q

compensatory renal cell proliferation is associated with

A

increase in size of the kidney tubules
increase in size of the glomeruli
increase in single nephron glomerular filtration rate

144
Q

nephrons are unable to

A

divide!!!!!!!!!!

Pharmacology (18 decks)

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