Chronic Kidney Disease (Exam 2) Flashcards
1
Q
Carbonic Anhydrase Inhibitors examples
A
Acetazolamide
Methazolamide
Dorzolamide
Indisulam
Topiramate
Benzthiazide
2
Q
Loop Diuretics examples
A
Furosemide
Bumetanide
Torsemide
Ethacrynic Acid
3
Q
Thiazide Diuretics
A
Chlorthalidone
Indapamide
Metolazone
Bendroflumethiazide
Hydrochlorothiazide
Chlorothiazide
4
Q
Loop Agents + Thiazide Osmotic Diuretics
A
Mannitol
5
Q
K+ Sparing Diuretics
A
Amiloride
Triamterene
Eplerenone
Spironolactone
6
Q
Carbonic Anhydrase Inhibitors on NaCl
A
Increases +
7
Q
Carbonic Anhydrase Inhibitors on NaHCO3
A
Increases +++
8
Q
Carbonic Anhydrase Inhibitors on K+
A
Increases +
9
Q
Carbonic Anhydrase Inhibitors on Body pH
A
Acidosis
10
Q
Loop Diuretics on NaCl
A
Increases ++++
11
Q
Loop Diuretics on NaHCO3
A
No change
12
Q
Loop Diuretics on K+
A
Increases +
13
Q
Loop Diuretics on Body pH
A
Alkalosis
14
Q
Thiazide Diuretics on NaCl
A
Increases ++
15
Q
Thiazide Diuretics on NaHCO3
A
Increases +
16
Q
Thiazide Diuretics on K+
A
Increases +
17
Q
Thiazide Diuretics on Body pH
A
Alkalosis
18
Q
Loop Agents + Thiazide Osmotic Diuretics on NaCl
A
Increases +++++
19
Q
Loop Agents + Thiazide Osmotic Diuretics on NaHCO3
A
Increases +
20
Q
Loop Agents + Thiazide Osmotic Diuretics on K+
A
Increases ++
21
Q
Loop Agents + Thiazide Osmotic Diuretics on Body pH
A
Alkalosis
22
Q
K+ sparing agents on NaCl
A
Increases +
23
Q
K+ sparing agents on NaHCO3
A
Questionable increase
24
Q
K+ sparing agents on K+
A
Decreases -
25
K+ sparing agents on Body pH
Acidosis
26
What do carbonic anhydrase inhibitors treat?
Edema
Epilepsy
Glaucoma
27
How do CAIs work for gluacoma?
Control fluid secretion
28
How do CAIs work for edema?
Promotion of diuresis in instances of abnormal fluid retention
29
Carbonic anhydrase diuretic effect is due to
Action in the kidney on reversible reaction involving hydration of carbon dioxide and dehydration of carbonic acid
30
Net result of reversible reaction in kidneys
Loss of HCO3 ion, which carries out Na+, water, and K+
Alkalinization of urine and promotion of diuresis
31
What does furosemide (FUR) treat?
Hypertension
Edema
Congestive Heart Failure
Liver Cirrhosis
Renal Disease
32
Furosemide MOA
Inhibits absorption of Na+ + Cl- in PCTs, DCTs, and loop of Henle. Action on DCT is independent of inhibitory effect on CA and aldosterone
33
Where is furosemide metabolized?
Kidneys and liver
Bound to plasma proteins, albumin
34
What are the major metabolites of furosemide?
FUR-glucuronide (Pharmacologically active)
Saluamine
35
Bioavailability of FUR in fasted
~60-64%
36
Terminal 1/2-life of FUR
2 hours
37
Excretion of FUR is greatest via
IV injection
38
FUR in elderly patients
Binding to albumin may be reduced and is excreted unchanged in urine
Initial diuretic effect declines
39
Hydrochlorothiazide (HCTZ) MOA
Acts directly on kidneys and promotes diuresis by inhibiting Na+/Cl- cotransporter located in DCT of nephron
40
How do thiazides work?
Increase excretion of Na+ and Cl- in equal amounts, which decreases extracellular fluid and plasma volume --> reduces BP
41
Natriuresis (water loss) causes
secondary loss of K+ and bicarbonate but retains Ca+
42
Plasma half-life of HCTZ in fasted
2.5 hours
43
At maximal therapeutic dosages all thiazides are
approximately equal in diuretic potency (weak diuretic)
44
K+ sparing agents MOA
Inhibition of sodium reabsorption at DCT, cortical collecting tubule decreasing net negative potential of tubular lumen. Reduces K+ and H+ secretion and excretion
45
What does Ami treat?
Pyrizine compound that treats hypertension and congestive heart failure
46
Amiloride HCl possesses
weak natriuretic, diuretic, and antihypertensive activity
47
Amiloride in presence of thiazide or loop diuretic
Decreases enhanced urinary excretion of magnesium
48
Is Ami an aldosterone antagonist?
No stupid fuck
49
What are aldosterone antagonists?
Spironolactone
Eplerenone
50
Where is Ami metabolized?
idk but NOT the liver
Excreted unchanged by kidneys
51
Hepatorenal syndrome and Ami
Ami accumulation likely
52
Ami effect on GFR and renal blood flow
Very little
53
Prototypical ADH agonists
Antidiuretic hormone (ADH)
Desmopressin
54
ADH and Desmopression are
Peptides and must be given parenterally
55
ADH antagonists
Conivaptan
Tolvaptan
Demeclocycline
Lithium - not rlly used for this
56
ADH MOA
Facilitates water reabsorption from collecting tubule by activation of V2 receptors
57
Activation of V2 receptors stimulates
Adenylyl cyclase via Gs
Increases cAMP
58
Increased cAMP from ADH causes
Insertion of additional aquaporin AQP2 water channels
59
Conivaptan
ADH inhibitor at V1a and V2 receptors
60
Tolvaptan
More selective V2 blocker with little V1 affinity
61
Demeclocycline and Lithium
Inhibit action of ADH at some point distal to generation of cAMP and interfere with insertion of water channels
62
ADH and desmopressin will
reduce urine volume and increase concentration
63
Which disease is ADH and desmopression useful in?
PITUITARY diabetes insipidus
no value in nephrogenic form
64
Nephrogenic diabetes insipidus
Use salt restriction, water restriction, thiazides, loop diuretics
65
Syndrome of inappropriate ADH secretion (SIADH)
Causes hyponatremia
66
How to treat SIADH
Demeclocycline
Conivaptan
Tolvaptan
Lithium
67
Chronic Kidney Disease
Irreversible decrease in number of function nephrons resulting in progressive and permanent deterioration of renal function
68
Kidney damage of > 3 months defined as
-Structural/functional abnormality
-With/Without decreased GFR
-Manifested by pathogenic abnormalities or markers of disease
-Abnormalities in composition of blood or urine
69
GFR of CKD
< 60mL/min/1.73 m2
70
Predisposing factors of CKD
Diabetes mellitus
Hypertension
CV disease
Family history of ESRD
71
Biomarkers of kidney function
Serum creatinine
GFR
Albumin
Proteinuria
BUN
72
REN-related kidney disease
Mutation in REN gene !!!
leads to production of abnormal protein toxic to cells that normally produce renin
73
Polycystic kidney disease
Mutations in PKD1, PKD2, PKHD1 genes !!!
lead to cysts in kidneys that interfere with filtering waste products
74
Uromodulin-associated kidney disease
Mutations in UMOD gene !!! leads to damage of kidney tubules
75
Medullary cystic kidney disease type 1
Mutations in MUC1 gene !!! leads to production of altered protein decreasing mucin 1 and normal kidney development
76
Kidney stones
Dehydration and calcium deficiency lead to formation of stones
77
Fabry Disease
Mutations in GLA gene !!! lead to absence of alpha-galactosidase A activity and buildup of globotriaosylceramine (wtf)
78
Dent Disease
Mutations in CLCN5 or OCRL gene !!! leads to disruption of reabsorption of proximal tubules
79
GFR
volume of plasma ultra-filtrate presented to nephrons per unit time during process of urine formation
80
Stage 1 CKD (G1)
Normal
>90 GFR
80
Calculate NFP
GBHP-CHP-BCOP
81
Stage 2 CKD (G2)
Mildly decreased
60-89 GFR
82
Stage 3 CKD (G3a)
Mildly-Moderate decrease
45-59 GFR
83
Stage 3 CKD (G3b)
Mildly-Moderate decrease
30-44 GFR
84
Stage 4 CKD (G4)
Severely decreased
15-29 GFR
85
Stage 5 CKD (G5)
Kidney failure
<15 GFR
86
Quantification of Proteinuria
AER (mg/24hr)
PER (mg/24hr)
ACR (mg/g)
PCR (mg/g)
Protein reagent strip
87
Other complications of CKD
Amyloidosis
Blood and immune disorders
Endocrine
GI
Protein-energy wasting
Neurologic
88
What is eGFR?
Estimated glomerular filtration rate
89
What stage do you start ACE/ARB therapy for CKD?
>60 eGFR + microalbumin <30
Stage 2/3 CKD
90
Primary cause of anemia in CKD patients
Decreased production of EPO
91
Iron deficiency medications for CKD
ESA:
-Epoetin alfa
-Epoetin beta
-Darbepoetin alfa or placebo
92
hepcidin is very common in what stage of CKD?
stage 5
93
hepcidin
a hormone produced by the liver that regulates iron
directly binds to ferroprotein
an inflammatory marker
94
hepcidin is _______ in iron deficiency and ________ by transfusion induced iron and inflammatory diseases
decreased or absent
increased
95
hepcidin has high correlation with
serum ferritin levels
96
high iron means
low iron means
inflammation or infection means
high hepcidin
low hepcidin
high hepcidin
97
hepcidin is produced primarily by
the liver
98
what is required by most CKD patients receiving ESA
iron supplementation
99
iron is absorbed in
the duodenum
100
IV iron preparations
Iron dextran
Sodium ferric gluconate
iron sucrose
ferumoxytol
101
FGF-23
regulates phosphate concentration in plasma
phophatonin hormone
elevated in CKD to promote renal phosphate excretion
102
CKD mineral and bone disorders
biochemical abnormalities
bone abnormalities
soft tissue and vascular calcification
103
how much calcium is found in the bone?
as a component of what?
99%
hydroxyapatite
104
calcium is important for
signal transduction
105
dietary calcium is determined by
the needs for bone development and maintenance
106
concentration of calcium is regulated by
interactions between the PTH
various forms of Vitamin D
calcitonin
107
phosphate binding agent drugs
calcium carbonate
calcium acetate
sevelamer carbonate
lanthanum carbonate
aluminum hydroxide
108
calcimimetics
Cinacalcet (Sensipar) and etelcalcetide (Parsabiv)
enhance the sensitivity of PT to Ca in the blood
109
goal of calcimimetic therapy
decrease PTH
reduces risk of 2nd hyperparathyroidism
110
two types of calcimimetics
Type 1 - agonists NOT USED CLINICALLY
Type 2 - allosteric activators (cinacalcet)
111
MOA of calcimimetics
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
when the PT gland senses a higher ionized calcium,
the CaSR decreases the secretion of PTH
113
Vitamin D
group of lipophilic pre hormones
converted to biologically active metabolites that function as hormones
114
Vitamin D maintains plasma Ca by
increases Ca absorption in SI
decrease Ca renal excretion
mobilize Ca from bone vitamin D
115
two sources of vitamin D
dietary ergocalciferol - plants
cholecalciferol - skin
116
nutritional vitamin D
ergocalciferol - D2
cholecalciferol - D3
117
active vitamin D
calcitrol - D3
118
Vitamin D analogs
paricalcitol - D2
doxercalciferol - D2
119
Cholecalciferol is generated in the ______ from __________ by the action of ________
skin
7-dehydrocholesterol
UV irradiation
120
role of phosphate
constituent of nucleic acids and ATP
excretion of H ions from the kidney
121
Hyperphosphatemia can cause
osteomalacia
122
calcitriol
regulates phosphate deposition in the bone as hydroxyapatite
123
PTH increases
phosphate excretion
124
FGF-23 (bone derived fibroblast growth factor-23) binds to
FGF receptor
125
regulators of FGF-23
hyperphosphatemia
oral Pi loading
calcitriol
PTH
126
FGF-23 is synthesized and secreted in
osteoblasts
127
FGF-23 in the kidneys directly
inhibits intestinal Pi absorption
128
FGF023 lowers
serum calcitriol
129
calcitriol stimulates
FGF-23
130
increase in FGF23 activity leads to
increase kidney excretion of phosphate and down regulates sodium reabsorption
131
ACEI and ARB adverse drug reactions
decrease angiotensin II effects and vasodilation --> drop in BP
dec in GFR
inc in serum K
132
the combo of an ACE inhibitor or ARB with a diuretic is effective in _________.
Why?
lowering BP
primarily dilate afferent and efferent arterioles
relieve glomerular pressure
protective towards kidneys
133
chronic metabolic acidosis
increase skeletal muscle breakdown
decrease albumin synthesis
muscle weakness
release of Ca and PO4 from bone (worsens bone health)
134
activation of complement pathway for chronic metabolic acidosis
promotes tubule-interstitial injury
135
Rx to slow progression of chronic metabolic acidosis
bicarbonate supplementation
136
Cystatin C
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
RRT for asymptomatic patients, GFR can become
5-9 ml/min
138
indications for RRT
severe metabolic acidosis
hyperkalemia
pericarditis
encephalopathy
intractable volume overload
failure to thrive/malnutrition
peripheral neuropathy
intractable GI symptoms
139
compensatory renal hypertrophy
upon removal of one kidney, the other enlarges and increases in function
dominant contributor to growth
140
two mechanisms of compensatory renal hypertrophy
increased activity by the remaining kidney via hypertrophy
release of a kidney specific factor in response to unilateral nephrectomy that initiates CRH
141
compensatory hypertrophy can only take place if
some portion of the original structure is left to react to the loss
142
Compensatory renal cell proliferation
kidney mass goes down, remaining renal tissue undergoes compensatory growth
143
compensatory renal cell proliferation is associated with
increase in size of the kidney tubules
increase in size of the glomeruli
increase in single nephron glomerular filtration rate
144
nephrons are unable to
divide!!!!!!!!!!
