Renal Flashcards

1
Q

What activates RAAS?

A

decreased BP (JG cells), decreased Na delivery to DCT (MD cells), beta1 receptor stimulation

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2
Q

What are the 7 functions of AngII?

A

constrict vascular smooth muscle (AT1R), constrict efferent arteriole, aldosterone release, ADH release, increase Na/H exchange in PCT, hypT for thirst, decrease baroreceptor function (prevent reflex tach)

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3
Q

What is ANP?

A

relased in response to volume overload. Decreases RAAS activation. Relaxes vascular smooth muscle via cGMP

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4
Q

ADH

A

secreted from posterior pituitary. Regulates osmolarity

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5
Q

Aldosterone

A

Zona Glomerulosa, more ENaC and K+channel principle cells of CT. more proton pump in intercalated cells of CT

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6
Q

EPO

A

released by interstitial cells in peritubular capillary bed in response to hypoxia

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7
Q

1alpha hydroxylase

A

converts 25D to 1, 25D at the behest of PTH

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8
Q

Renin

A

secreted by JG cells if decreased pressure and increased sympathetic discharge (beta1)

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9
Q

Prostaglandins

A

paracrine secretion dilates AFFERENT arterioles to increase GFR (beware COX blockers)

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10
Q

What causes PTH release?

A

decreased plasma Ca++, increased plasma PO43-, or 1,25 D3

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11
Q

What causes K+ to leave cell (causing hyperK+)?

A

Digitalis, Hyperosmolarity, Insulin deficiency, cell lysis, acidosis, beta-antagonist

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12
Q

What causes K+ to enter cell (causing hypoK+)?

A

Hypoosmolarity, INSULIN, Alkalosis, beta-agonist (increases Na/K ATPase),

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13
Q

Low serum Na+

A

Nausea, malaise, stupor, coma

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14
Q

High serum Na+

A

Irritability stupor, coma

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15
Q

Low serum K+

A

U waves on ECG, flattened T waves, arrhythmias, muscle weakness

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16
Q

High serum K+

A

Wide QRS and peaky T. arrhythmias, muscle weakness

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17
Q

Low serum Ca++

A

Tetany, seizures (Chvostek or Trousseau)

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18
Q

High serum Ca++

A

Stones, bones, groans, psychiatric overtones (not necessarily calciuria)

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19
Q

Low serum Mg++

A

Tetany, arrhythmia

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20
Q

High serum Mg++

A

decreased DTRs, lethargy, bradycardia, hypotension, cardiac arrest, hypocalcemia

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21
Q

Low PO43-

A

Bone loss, osteomalacia

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22
Q

High PO43-

A

Renal stones, metastatic calcifications, hypocalcemia

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23
Q

Mannitol

A

Osmotic diuretic, used for drug overdose or elevated intracranial/ocular pressure: don’t give if pulmonary edema, dehydration, anuria or CHF

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24
Q

Acetazolamide

A

CA inhibitor (traps bicarb in tubule), Use for glaucoma, urinary alkalinization, Met. Alk., altitude sickness, pseudotumor cerebri: don’t use if hyperchloremic met. Acid., NH3 toxicity, sulfa allergy

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25
Q

Furosemide

A

Sulfonamide loop. (Blocks Na,K,2Cl in TAL): Ototoxicity, hypokalemia, dehydration, allergy (sulfa), interstitial nephritis, gout

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26
Q

Ehtacrynic acid

A

NONsulfonamide loop (Blocks Na,K, 2Cl in TAL): Ototoxicity, hypokalemia, dehydration, interstitial nephritis, gout

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27
Q

HCTZ

A

Blocks NaCl in early DCT: Causes hypokalemic met alk, hyponatremia, hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia, and sulfa allergy

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28
Q

What are the aldosterone-like K-sparing diuretics (CCT)?

A

Spironolactone and eplerenone: hyperkalemia, gynecomastia, antiandrogen

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29
Q

What are the ENaC blocking K-sparing diuretics (CCT)?

A

Triamterene and Amiloride:

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30
Q

Name some ACE inhibitors

A

Captopril, enalapril, lisinopril

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31
Q

What are ACE inhibitors used for?

A

HTN, CHF, proteinuria, diabetic renal disease

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32
Q

What are the toxicities of ACE inhibitors?

A

Cough, angioedema, teratogen(fetal malformations), Creatinine increase, hyperkalemia, Hypotension (never use in bilateral renal artery stenosis GFR will fall too much)

33
Q

RBC casts

A

glomerulonephrits, ischemia, malignant HTN

34
Q

WBC casts

A

Tubulointerstitial inflammation, acute pyelo, transplant rejection

35
Q

Fatty casts

A

Nephrotic syndrome

36
Q

Granular “muddy brown” casts

A

Acute tubular necrosis

37
Q

Waxy casts

A

ESRD

38
Q

Hyaline casts

A

nonspecific, can be normal

39
Q

Focal

A

less than 50% of glomeruli are involved

40
Q

Diffuse

A

greater than 50% of glomeruli are involved

41
Q

Proliferative

A

hypercellular glomeruli

42
Q

Membranous

A

Thickened GBM

43
Q

What are the diseases that cause nephritic syndrome?

A

Acute PSGN, RPGN, Berger’s IgA, Alport

44
Q

What are the diseases that cause nephrotic syndrome?

A

FSGS, Membranous nephropathy, minimal change, amyloidosis, diabetic glomerulonephropathy

45
Q

What diseases can cause either/or nephritic, nephrotic?

A

diffuse proliferative glomerulonephritis, membranoproliferative glomerulonephritis

46
Q

Define nephrotic

A

massive proteinuria (>3.5g/day) frothy urine, hyperlipidemia, fatty casts, edema. (associated with thromboembolism, ATIII loss in urine)

47
Q

Define Nephritic

A

Inflammatory process. Hematuria and RBC casts. Azotemia, oliguria, HTN (protein <3.5 mg/day)

48
Q

Calcium Stones

A

80%, calcium phosphate if alkaline, calcium oxalate if acidic; radiopaque, treat with thiazide and citrate

49
Q

What stones form with ethylene glycol or ascorbic acid abuse?

A

calcium oxalate

50
Q

Ammonium magnesium phosphate (struvite) stones

A

15% precips at alkaline pH (urease + proteus, staph, klebsiella)

51
Q

Uric acid stones

A

5% precips at acidic pH, RADIOLUSCENT. Treat by alkalinizing urine

52
Q

Cystine

A

1% precips at acidic pH, radiopaque, Hexagonal crytals treat by alkalinizing the urine

53
Q

WAGR

A

Wilm’s tumor, aniridia, genitourinary malformation, mental retardation: WT1 deletion chr. 11

54
Q

Transitional cell carcinoma: Pee SAC

A

Phenacetin, Smoking, Aniline dyes, Cyclophosphamide

55
Q

Renal osteodystrophy

A

no active vit. D, leads to hypocalcemia, and hyperphosphatemia. Increase in tissue calcifications while bones are robbed of calcium

56
Q

What is FeNa

A

Clearance of Na+/GFR

57
Q

What is the BUN/SerumCr in prerenal azotemia?

A

> 20:1

58
Q

What is a normal FF?

A

GFR/RPF=0.2

59
Q

What are the causes of increased K+ secretion in DCT?

A

High K+ diet, hyperaldosteronism, alkalosis, thiazides, loops, and luminal anions.

60
Q

How does PTH inhibit phosphate reabsorption?

A

Activates adenylate cyclase, generating cAMP, inhibitng Na+-phosphate cotransport. (increased phosphate AND cAMP in urine)

61
Q

Who competes for reabsorption in the TAL?

A

Mg++ and Ca++

62
Q

What is free water clearance, and what is it calculated for?

A

C(H20)= V - C(osm); estimates the ability of kidney to concentrate or dilute urine

63
Q

What drug could you give to make free water clearance zero?

A

loop diuretic (furosemide, ehtacrynic acid, bumetanide)

64
Q

What is the most important urinary buffer?

A

H2PO4-/HPO4-2. (titratable acid, pK is 6.8)

65
Q

Type 1 RTA

A

Collecting tubule can’t secrete H+ (urine pH is >5.5. Hypokalemia. Risk for calcium phosphate stones

66
Q

Type 2 RTA

A

PCT defect (HCO3- is not resorbed). Fanconi’s syndrome.urin pH <5.5

67
Q

Type 4 RTA

A

hypoaldosteronism (or functional hypoaldosteronism). Ammoniagenesis is impaired in PCT. Low urine pH

68
Q

FSGS

A

Most common nephrotic in adults. Associated with HIV, heroin, obesity, IFN treatment, CKD

69
Q

Membranous nephropathy

A

Thickened GBM, “spiked subepithelial deposits, IF is granular. Idiopathic, drugs, infections, SLE, tumors

70
Q

MCD

A

Most common nephrotic in kids. Responds to corticosteroids

71
Q

Amyloidosis

A

nephrotic. Think multiple myeloma, TB, RA

72
Q

MPGN

A

nephrotic or nephritic. Subendothelial tram-track. Type I think HBV or HCV. Type II think C3 nephritic factor

73
Q

Diabetic glomerulonephropathy

A

nephrotic. nonenzymatic glycosylation of GBM

74
Q

APSGN

A

nephritic. Subepithelial IC humps. Skin or throat

75
Q

RPGN (crescentic)

A

Goodpasture’s, Granulomatosis with polyangiitis, microscopic polyangiitis

76
Q

DPGN

A

nephrotic or nephritic SLE or MPGN (most common cause of death in SLE)

77
Q

Berger’s

A

IgA nephropathy (kidney HS) nephritic

78
Q

Alport

A

X-linked nephritic. Type IV collagen mutant. (Eyes, Ears and kidneys)