Renal Flashcards

1
Q

What do the pronephros and mesonephros become?

A
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2
Q

What parts of the kidney are the metanephros? and when does it first appear?

and the ureteric bud?

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3
Q

Duplex collecting mechanism?

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4
Q

Posterior urethral mechanism?

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5
Q
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6
Q

Horseshoe kidney

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7
Q

Unilateral renal agenesis mechanism?

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8
Q

Potter sequence

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9
Q

Multi

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10
Q

Clearance equation?

and if Cx<gfr></gfr>

<p>Cx&gt;GFR?</p>

<p>equal?</p>

</gfr>

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11
Q

1 using inulin and #2 using forces

GFR equations

normal GFR is?

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12
Q

Course of the ureter? arises from? travels under? over the? and under the?

3 places for constriction?

A
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13
Q

Fluid compartments

Plasma volume can be measured using?

ECF measured using?

normal plasma osmolality?

Normal HCT?

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14
Q

How do we measure RPF?

equation?

Plasma volume?

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15
Q

Filtration fraction equation?

Normal FF?

Filtered load equation?

Prostaglandins do what?

AG2 does what?

A
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16
Q

Glomerular filtration barrier composed of what 3 things?

Charge barrier b/c all 3 layers contain?

Size barrier b/c?

A
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17
Q

Formula for Excretion rate?

So reasborption rate?

Formula for FeNa

A
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18
Q

Early DCT reasorbs? impermeable to? makes urine?

PTH effect?

how much sodium reabsorbed?

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19
Q
A

Effects on GFR, RPF, FF?

Afferent arteriole constriction?

efferent constriction?

incraesed plasma protein?

decreased plasma protein?

ureter constriction

dehydration

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20
Q

ANP/BNP

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21
Q

Renin

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22
Q

EPO released by what cells in respons to?

Calciferol converted by what cells in kidney?

Prostaglandins secrete how and do what to afferent?

Dopamin secreted by? promotes?

A
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23
Q
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24
Q
A
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25
Q

Gittlemans

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26
Q

Barrter?

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27
Q

AT2 limits?

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28
Q

Syndrome of apparent mineralocorticoid excess

In cells containing these receptors, what converts what?

inheritd how?

causes what to potassium? metabolic ______?

Treat with?

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29
Q

loop of henle

Descending?

ascending?

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30
Q

collecting duct?

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31
Q

Liddle

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32
Q

ADH

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33
Q

Aldosterone

A
34
Q

PCT

A
35
Q

Glucose transport

A
36
Q

Fanconi

A
37
Q

Relative concentrations

Which ones are secreted more than water?

and less?

A
38
Q

JG appartus

A
39
Q

Alkalosis causes for resp and metabolic

A
40
Q

HardASS

A
41
Q

Resp Acidosis causes

A
42
Q

Mudpiles stands for?

and Anion gap is?

A
43
Q

Symptoms when sodium is low? high?

Potassium low? high? (include ECK findings)

A
44
Q

What shifts potassium into the cell?

and out of the cell? DO LABSS

A
45
Q

Autosomal dominant polycystic kidney

A
46
Q

AG2 effects on kidney?

PTH?

ANP?

Aldosterone?

ADH?

A
47
Q

Symptoms when calcium low?high?

magnesium low? high?

A
48
Q

Symptoms when phosphate low? high?

A
49
Q

Renal tubular acidosis types? which part of kidney affected?

A
50
Q

Types of casts

RBC?

WBC?

Fatty?

Granular (muddy brown)?

waxy?

hyaline?

hematuria with no casts?

A
51
Q

Minimal change disease

A

Etiology: most common nephrotic syndrome in children, 15% in adults, idiopathic usually but can be seen in hodgkins and renal cell carcinoma

Labs: serum: low albumin, normal creatinine

Normal BP, Edema

Podocyte injury - effacement -protein goes between slits. No immune deposition. Normal LM, no IF, EM shows above.

52
Q

Membranous nephropathy

A

idiopathic or secondary to SLE, HepB, syphilis, malaria, captopril, lithium, mercury, gold, penicillamine (Wilson’s)

Domes and Spikes

Sub-EPIthelial

53
Q

Focal Segmental

A

also secondary to HIV, morbid obesity, chronic reflux nephropathy, heroin use, malignancies, congenital renal agenesis, renal ablation nephropathy, glomerulonephritis

Pathogenesis of secondary is due to reduction in renal mass, compensatory hypertrophy and hyperfiltration of remaining glomeruli to maintain GFR, intraglomerular hypertension–injury

54
Q

IgA nephropathy

A

Associated with hepatic cirrhosis, gluten enteropathy, HIV infection, minimal change disease, membranous, wegeners, ankylosing spondylitis, small cell cancer

55
Q

Post-Strep GN

A

Post Strep -preceded by pharyngitis (7-10 days) or impetigo (3 weeks)

Elevated ASO or anti-DNAase B, LOW CMPLEMENT. Don’t biopsy, do supportive therapy (b/c most likely outcome is resolution)

Complexes start subendo-but are rapidly cleared within a few days-hematuria resolves in this time.

EM: see Humps subepithelial —proteinuria persists for weeks

LM: Global and diffuse hypercellularity

CX: RPGN (Type 2)

56
Q

Renin, Aldosterone, Ca levels in

Bartter

Gittleman

Liddle, SAME

SIADH

Conn’s

Reninoma

A
57
Q

Amyloid deposition in kidney

A
58
Q

Diabetic nephropathy

A
59
Q

Diffuse cortical necrosis

A
60
Q
A
61
Q

Membranoproliferative GN

Type 1

Type 2

A

Type 1: Cryoglobulinemia (Hep C), Hep B, lupus, parasitic infections, endocarditis

(Cryoglobulinemia - IgM made against the virus Hep C precipitating within vessels in extremities.Cx: digital gangrene)

Leads to activation of classical complement pathway- low levels of C1/C4

Deposits are subendothelial made of C1q/C4/IgG

LM: Tram-track- double contour- splitting of basement membrane

Type 2: Idiopathic - worse prognosis- in children -dense deposit disease

Deposits found along basement membrane -made of C3 (very low C3 levels-activation of alternative complement pathway)- also has C3 nephritic factor

62
Q

Alport

A
63
Q

Diffuse proliferative GN

Often due to?

LM shows?

IF type?

A
64
Q

Auto recessive polycystic kidney

A
65
Q

UTI most common order?

A
66
Q

Pyelonephritis

Acute?

Risk factors? tx? Cx?

Chronic? tubules can resemble?

A
67
Q

Renal Cell Carcinoma

A

Tobacco smoking, obesity, HTN, cadmium, long standing dialysis

only 5% inherited -Von-Hippel-Lindau (CH3), autosomal dominant renal cell

Sporadic papillary, - trisomy 7, 17 loss of Y, activated/mutated MET

Hereditary papillary- trisomy 7, mutated/activated MET

Sporadic & hereditary clear cell- deletions on chromosome 3, loss of VHL

68
Q

Urine osmolality if prerenal, instrinsic and postrenal?

Urine Na?

FeNa?

Serum BUN/Cr?

Causes of each?

A
69
Q

Transitional cell carcinoma

A

Common- p53, rb, p16 genes

Males more than females, smoking (2X), analgesic abuse (phenacetin), cyclophosphamide, naphthylamine, rubber products

70
Q

Renal Osteodystrophy

A

See completely throughout the bone (tunneling of bone) - iron and aluminum accumulate in bone to prevent further bone deposition

Also involves decreased BMP7–increased RANKL–FGF-23 (increased phosphate- contributing to secondary hyperparathyroid)

71
Q

Consequences of renal failure

MAD HUNGER

A
72
Q

Wilms tumor

A

2 tumor suppressor genes short arm chromosome 11 - see triphasic pattern (blastema, stroma, epithelial)

73
Q

Acute tubular necrosis

most common cause

3 stages?

Can be from? and which impact which part of neprhon?

A
74
Q

Acute interstitial nephritis. Often due to?

less commonly due to?

Symptoms? 5 P’s

A
75
Q

Renal Oncocytoma

A
76
Q

AD Tubulointerstitial kidney disease

A
77
Q

Simple vs complex renal cysts

A
78
Q

Renal papillary necrosis causes?

presents with?

may be triggered by?

A
79
Q

Stress?

Urgency?

Overflow?

A
80
Q

Hydronephrosis

Distention of? usualy caused by?

what becomes elevated when?

A
81
Q

Sqaumous cell carcinoma caused by?

presnts with?

A
82
Q

Rapidly progressive also called?

IF Type 1?

type 2?

type 3?

A