Kidney Flashcards

1
Q

Causes of ATN=Broad causes

A

Pre-renal (sepsis, hypovolemia-dehydration)

Toxic

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2
Q

6 Toxins cause ATN

A
  1. Contrast
  2. Meds.
  3. Ca oxalate from ethylene glycol poisoning
  4. Urate crystal/stones
  5. Myoglobinuria
  6. Hemoglobinuria
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3
Q

Meds. cause ATN

A

“ATN”=

  1. AG
  2. NSAIDs
  3. amphoTericin B
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4
Q

Myoglobinuria caused by

A

Crush injury

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5
Q

Urate crystals/stones caused by

A

Tumor lysis syndrome–uric acid stones

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6
Q

Hemoglobinuria caused by

A

blood transfusion

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7
Q

RBC casts

A

Glomerulonephritis, malignant hypertension.

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8
Q

WBC casts

A

Tubulointerstitial inflammation, acute pyelonephritis, transplant rejection.

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9
Q

Fatty casts (“oval fat bodies”)

A

Nephrotic syndrome. Associated with “Maltese cross” sign.

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10
Q

Granular (“muddy brown”) casts

A

Acute tubular necrosis.

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11
Q

Waxy casts

A

End-stage renal disease/chronic renal failure.

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12
Q

Generalized reabsorptive defect in PCT.

A

Fanconi syndrome

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13
Q
May result in
metabolic acidosis (proximal renal tubular acidosis).
A

Fanconi syndrome

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14
Q

Associated withexcretion of nearly all amino acids, glucose, HCO3 , and PO4 .

A

Fanconi syndrome

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15
Q

Presents similarly to chronic loop diuretic use.

A

Bartter syndrome

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16
Q

Reabsorptive defect in thick ascending loop of Henle. Autosomal recessive. Affects Na+/K+/2Cl– cotransporter.

A

Bartter syndrome

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17
Q

Reabsorptive defect of NaCl in DCT.

A

Gitelman syndrome

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18
Q

Similar to using lifelong thiazide diuretics.

A

Gitelman syndrome

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19
Q

Gain of function mutationŽinc.Na+ reabsorption in collecting tubules (inc.activity of epithelial Na+ channel).

A

Liddle syndrome

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20
Q

Presents like hyperaldosteronism, but aldosterone is nearly undetectable.

A

Liddle syndrome

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21
Q

Liddle syndrome tx.

A

Amiloride

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22
Q

Potter sequence facial anomalies

A

low-set ears and
retrognathia,
flattened nose

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23
Q

Potter sequence (syndrome) 6 sxs (Mnemonic)

A

limb deformities,
facial anomalies,
compression of chest and
pulmonary hypoplasia

"POTTER" sequence associated with: Pulmonary hypoplasia 
Oligohydramnios (trigger) 
Twisted face
Twisted skin 
Extremity defects 
Renal failure (in utero)
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24
Q

pulmonary hypoplasia in potter seq due to

A

lack of amniotic fluid aspiration into fetal lungsŽpulmonary hypoplasia

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25
(cause of death). in Potter sequence
pulmonary hypoplasia
26
Cause of Potter seq.
"Babies who can’t “Pee” in utero develop Potter" =kidney problems ARPKD, obstructive uropathy (eg, posterior urethral valves), bilateral renal agenesis, chronic placental insufficiency.
27
AT II Effect on kidney BV's
constrict efferent arteriole
28
ACEi effect on kidney BV's
dilate efferent arteriole (inhibits efferent a. constriction by AT II), so decr. GFR but decr. BP by inhib. Aldosterone release
29
Ions re-absorbed in PCT
Na+, glucose, aa, K+, Cl-, uric acid, H2O, Phosphate, Bicarb.
30
Ions secreted in PCT
H+
31
ATII action on PCT: reabsorbs what 3 and secretes what 1 ion?
Bicarb., H2O & Na+ reabsorption and H+ excretion=Contraction ALKalosis
32
Thick ascending loop reabsorbs?
Na+/K+/Cl- & Mg2+/Ca2+
33
PTH acts on what part of kidney?
1. PCT--decr. Phosphate re-absorb 2. DCT--reabsorbs Ca2+ 3. Converts inactive vitD to active (vitD allows Phosphate and Ca2+ absorption in gut)
34
Contraction alkalosis occurs due to what hormone?
ATII
35
Acetazolamide MOA
Carbonic Anhydrase inhibitor--lose Bicarb. and H2o in urine
36
Mannitol SE
pulmonary edema
37
Acetazolamide 2 uses
1. Glaucoma | 2. make urine basic
38
Mannitol MOA
=a sugar, incr. blood & urine osmolarity
39
Mannitol Used for?
Brain & Eye pressure
40
Carbonic Anhydrase
Converts bicarb. to H2O--water reabsorbed in kidney
41
Acetazolamide SE
"ACID"azolamide of blood causes ACIDosis"
42
Thick ascending reabsorbs which ions?
Na+/K+/Cl- & Mg2+/Ca2+
43
DCT reabsorbs which ions?
Na+/Cl- & Ca2+ via PTH
44
Collecting Tubule reabsorbs which ions? secretes which?
reabsorbs: Na+/H2O (ADH) secretes: K+/H+
45
Amiloride/Triamterene action in kidney?
blocks Na+ channels (ENaC)
46
4 K+-sparing diuretics
"The K+ STAEys" 1. Spironolactone 2. Eplerenone 3. Amiloride 4. Triamterene
47
Thiazide MOA
blocks Na+/Cl- reabsorption in DCT, incr. Ca2+ excretion, activates RAAS
48
SE's Thiazides
"HyperGLUC" ``` Hypo-K+ (activated RAAS) Metabolic ALKALosis (activated RAAS) ``` Hypo-Na+ (blocks Na+/Cl- transporter) Hyper-Glyc-emia Hyper-Lipid-emia Hyper-Uricemia Hyper-Ca2+
49
3 Thiazides
1. HCTZ 2. Chlorthalidone 3. Metolazone
50
3 Loops
1. Furosemide 2. Bumetanide 3. Torsemide
51
Loops MOA
Inhibit Na+/K+/Cl- transporter, increase Ca2+ excretion
52
Loops SE's
"OHH DAANG!" Ototoxicity Hypo-K+ Hypo-Mg2+ ``` Dehydrate Alkalosis Allergy (to Sulfa) Nephritis (interstitial) Gout ```
53
Ethacrynic Acid MOA
inhibits Na+/K+/Cl- transporter like Loops
54
Ethacrynic Acid Use
diuretic in those allergic to sulfa drugs
55
Ethacrynic Acid SE
Ototoxic ("Loop earrings hurt your ears")
56
Sulfa diuretics
Loops and Thiazides
57
Spironolactone cause gynecomastia because
Testosterone antagonist
58
Thiazides and Loops both have what effect on pH? Why?
ALKalosis b/c RAAS activated
59
Medication that decreases ATII
ACEi
60
ACE 2 functions?
1. Converts AT I to AT II | 2. Breaks down Bradykinin
61
ACEi SE's
"Catopril's CATCHH" ``` Cough Angioedema Teratogen Creatinine incr. (b/c decr. AT II cause GFR decr.) Hyper-K+ Hypo-tension ```
62
How ACEi effects fetus?
Need AT II to for kidney development--> orelse causes baby oligo-hydramnios
63
Don't use ACEi in what dz,?
BLT RAS--because decr. GFR more
64
ARB MOA?
Blocks AT II receptor
65
Difference between ACEi & ARB?
ARB not incr. BRadykinin
66
ARB SE
Same as ACEi except increased Bradykinin effects (from CATCHH to TCHH)
67
Bradykinin cause edema because?
increase BV permeability
68
AlisKiren MOA
inhibits renin
69
Aliskiren contra-indicated in?
Already taking ACEi/ARB
70
Angiotensinogen is released from what part of the body?
Liver
71
Renin role
Converts Angiotensinogen to AT I
72
What Macula densa does if detects low Na+ in DCT?
Renin secretion
73
ANP and BNP are released from where?
From Atria (ANP) and Ventricles (BNP)
74
ANP/BNP effect on GFR?
Increase: dilate afferent and constrict efferent arterioles & Na+ loss w/o reabsorb
75
AHD activated by?
Low blood volume
76
ANP release in response to?
Increased Atrial pressure
77
inactive and active vitD form
Calciferol= 25-OH D3 --> 1,25-(OH)2 D3
78
PTH release in response to which 3 stimuli?
1. low blood Ca2+ 2. high blood Phosphate 3. decreased active VitD (1,25-[OH]2 D3) in blood
79
ADH released in response to which 2 stimuli?
1. increased blood osmolarity | 2. decreased blood volume
80
6 effects of AT II
1. vaso-Constrict= increased BP 2. constrict efferent a.=incr. GFR 3. Aldo. 4. ADH (from posterior pituitary) 5. Contraction alkalosis 6. Thirst (stim. HypoThalamus)