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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
Q

(cause of death). in Potter sequence

A

pulmonary hypoplasia

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26
Q

Cause of Potter seq.

A

“Babies who can’t “Pee” in utero develop Potter”

=kidney problems
ARPKD, obstructive uropathy (eg, posterior urethral valves), bilateral renal agenesis, chronic placental insufficiency.

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27
Q

AT II Effect on kidney BV’s

A

constrict efferent arteriole

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28
Q

ACEi effect on kidney BV’s

A

dilate efferent arteriole (inhibits efferent a. constriction by AT II), so decr. GFR but decr. BP by inhib. Aldosterone release

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29
Q

Ions re-absorbed in PCT

A

Na+, glucose, aa, K+, Cl-, uric acid, H2O, Phosphate, Bicarb.

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30
Q

Ions secreted in PCT

A

H+

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31
Q

ATII action on PCT: reabsorbs what 3 and secretes what 1 ion?

A

Bicarb., H2O & Na+ reabsorption and H+ excretion=Contraction ALKalosis

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32
Q

Thick ascending loop reabsorbs?

A

Na+/K+/Cl- & Mg2+/Ca2+

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33
Q

PTH acts on what part of kidney?

A
  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
Q

Contraction alkalosis occurs due to what hormone?

35
Q

Acetazolamide MOA

A

Carbonic Anhydrase inhibitor–lose Bicarb. and H2o in urine

36
Q

Mannitol SE

A

pulmonary edema

37
Q

Acetazolamide 2 uses

A
  1. Glaucoma

2. make urine basic

38
Q

Mannitol MOA

A

=a sugar, incr. blood & urine osmolarity

39
Q

Mannitol Used for?

A

Brain & Eye pressure

40
Q

Carbonic Anhydrase

A

Converts bicarb. to H2O–water reabsorbed in kidney

41
Q

Acetazolamide SE

A

“ACID”azolamide of blood causes ACIDosis”

42
Q

Thick ascending reabsorbs which ions?

A

Na+/K+/Cl- & Mg2+/Ca2+

43
Q

DCT reabsorbs which ions?

A

Na+/Cl- & Ca2+ via PTH

44
Q

Collecting Tubule reabsorbs which ions? secretes which?

A

reabsorbs: Na+/H2O (ADH)
secretes: K+/H+

45
Q

Amiloride/Triamterene action in kidney?

A

blocks Na+ channels (ENaC)

46
Q

4 K+-sparing diuretics

A

“The K+ STAEys”

  1. Spironolactone
  2. Eplerenone
  3. Amiloride
  4. Triamterene
47
Q

Thiazide MOA

A

blocks Na+/Cl- reabsorption in DCT,
incr. Ca2+ excretion,
activates RAAS

48
Q

SE’s Thiazides

A

“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
Q

3 Thiazides

A
  1. HCTZ
  2. Chlorthalidone
  3. Metolazone
50
Q

3 Loops

A
  1. Furosemide
  2. Bumetanide
  3. Torsemide
51
Q

Loops MOA

A

Inhibit Na+/K+/Cl- transporter, increase Ca2+ excretion

52
Q

Loops SE’s

A

“OHH DAANG!”
Ototoxicity
Hypo-K+
Hypo-Mg2+

Dehydrate
Alkalosis
Allergy (to Sulfa)
Nephritis (interstitial)
Gout
53
Q

Ethacrynic Acid MOA

A

inhibits Na+/K+/Cl- transporter like Loops

54
Q

Ethacrynic Acid Use

A

diuretic in those allergic to sulfa drugs

55
Q

Ethacrynic Acid SE

A

Ototoxic (“Loop earrings hurt your ears”)

56
Q

Sulfa diuretics

A

Loops and Thiazides

57
Q

Spironolactone cause gynecomastia because

A

Testosterone antagonist

58
Q

Thiazides and Loops both have what effect on pH? Why?

A

ALKalosis b/c RAAS activated

59
Q

Medication that decreases ATII

60
Q

ACE 2 functions?

A
  1. Converts AT I to AT II

2. Breaks down Bradykinin

61
Q

ACEi SE’s

A

“Catopril’s CATCHH”

Cough
Angioedema
Teratogen
Creatinine incr. (b/c decr. AT II cause GFR decr.)
Hyper-K+
Hypo-tension
62
Q

How ACEi effects fetus?

A

Need AT II to for kidney development–> orelse causes baby oligo-hydramnios

63
Q

Don’t use ACEi in what dz,?

A

BLT RAS–because decr. GFR more

64
Q

ARB MOA?

A

Blocks AT II receptor

65
Q

Difference between ACEi & ARB?

A

ARB not incr. BRadykinin

66
Q

ARB SE

A

Same as ACEi except increased Bradykinin effects (from CATCHH to TCHH)

67
Q

Bradykinin cause edema because?

A

increase BV permeability

68
Q

AlisKiren MOA

A

inhibits renin

69
Q

Aliskiren contra-indicated in?

A

Already taking ACEi/ARB

70
Q

Angiotensinogen is released from what part of the body?

71
Q

Renin role

A

Converts Angiotensinogen to AT I

72
Q

What Macula densa does if detects low Na+ in DCT?

A

Renin secretion

73
Q

ANP and BNP are released from where?

A

From Atria (ANP) and Ventricles (BNP)

74
Q

ANP/BNP effect on GFR?

A

Increase: dilate afferent and constrict efferent arterioles
&
Na+ loss w/o reabsorb

75
Q

AHD activated by?

A

Low blood volume

76
Q

ANP release in response to?

A

Increased Atrial pressure

77
Q

inactive and active vitD form

A

Calciferol= 25-OH D3 –> 1,25-(OH)2 D3

78
Q

PTH release in response to which 3 stimuli?

A
  1. low blood Ca2+
  2. high blood Phosphate
  3. decreased active VitD (1,25-[OH]2 D3) in blood
79
Q

ADH released in response to which 2 stimuli?

A
  1. increased blood osmolarity

2. decreased blood volume

80
Q

6 effects of AT II

A
  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)

Facts (16 decks)

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