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need to knows > Renal (FA + UWorld) > Flashcards

Renal (FA + UWorld) Flashcards

1
Q

where is PAH concentration the lowest?

A

Bowman’s capsule.
PAH is relatively low in plasma (= Bowman’s capsule bc freely filtered) PAH is actively secreted in the PCT, increasing its concentration

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2
Q

most common cause of obstructive unilateral hydronephrosis
most common cause of NONobstructive unilat hydronephrosis
most common cause of bilateral hydronephrosis

A

unilateral: reno-pelvic junction
non-obs: vesico-uretral reflux
bilateral: posterior urethral valves

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3
Q

describe the ureter’s positioning in relation to each:
internal iliac A
uterine vessels
ovarian/testicular vessels

A

Anterior to IIA
posterior to UA
medial to OA/TA

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4
Q

what does ADH do in the medullary collecting duct?

A

increase NH3 and water absorption, allowing for max concentrated urine

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5
Q

when in metabolic acidosis, what does the urine do to help?

A
  • it increases excretion of acid (so low urine pH, and presence of more acid buffers)
  • it increases bicarb reabsorption (so low bicarb in urine)
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6
Q

what increases as you go along PCT, what decreases?

A

increase: PAH, Inulin, Urea
decrease: glucose, AA, bicarb

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7
Q

plasma creatinine levels only start to rise after GFR gets how low?

A

as GFR gets LOWER than 60 Pcreat begins to rise, exponentially

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8
Q

ADH decreases clearance of what substance

A

UREA

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9
Q

what does metabolic acidosis do to pCO2 levels

A

compensatory resp alk causes pCO2 to be low

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10
Q

How does diabetes affect incontinence

A

due to neuropathy pt cant sense bladder is full. this leads to incomplete emptying, as well as overflowincontinence bc detrusor m is poorly innervated

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11
Q

large eosinophilic casts in urine?

A

MM

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12
Q

pt recieving chemotherapy gets oligouria, what happened?

A

tumor lysis syndrome– as tumor cells rapidly lyse their K+,PO43-, and uric acidis released into the system. When uric acid is in an acidic area (like the CD) it can precipitate into uric acid kidney stones

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13
Q

what are two common side effects of ACE inhibitors?

A

cough

hyperkalemia

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14
Q

alpha galactosidase A deficiency is known as

A

Fabry’s disease

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15
Q

PSGN is what type of HS?

A

TypeIII

immune complexes

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16
Q

what are the embryological derivatives of the kidney

A

pro-nephros– degenerates in week
mesonephros– part of genito-urinary tract- gives rise to uretric bud which makes ureters, calcixes, pelvis, CD
metanephros- when stimulated by ureteric bud, it makes the DCT to the glomerulus

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17
Q

what the last part of the kidney to canalize? most common site of obstruction?

A

ureteropelvic junction – causes hydronephrosis

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18
Q

Potter Sequence

A

oligohydramnios causes flat face and limb deformities due to compression

  • pulmonary hypoplasia is a common cause of death
    causes: bilateral renal agenesis, posterior urethral valves, obstructive uropathy, ARPKD
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19
Q

posterior urethral valves

A

membrane remnant in posterior urethra– hydronephrosis,and dilated/hypertrophy of bladder

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20
Q

what is the relation of ureters to vas deferens?

A

ureters pass UNDER vas deferens

remember also UNDER uterine artery

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21
Q

whats the breakdown of the body compartments?

A

60% of wt is TBW
40% of wt is ICF
20% of wt is ECF
in ECF.. 25%ECF is plasma

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22
Q

whats a normal osmolality

A

285-295 mOSm/kg H2O

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23
Q

whats the charge of the glomerulus?

A

neg.

so doesn’t let negative molecules in (like albumin)

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24
Q

name the three layers of the glomerulus?

A

(1) fenestrated capillary
(2) type IV collagen BM
(3) podocyte foot processes (epithelial layer)

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25
Q

renal clearance of X=

A

C(x)= ( [X in Urine] * rate of urine flow )/ ([X in plasma])

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26
Q

GFR=

A

( [Inulin in Urine] * rate of urine flow) / ([ Inulin in plasma])

if not Inulin, you can use creatinine, but remember that creatinine slightly overestimates GFR bc it is secreted a little

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27
Q

whats another way to measure GFR?

A

= ( Pg- Pb) - (Poncg - PoncB)

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28
Q

whats a normal GFR?

A

100 mL/min

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29
Q

RPF=

A

( [PAH in Urine] * rate of urine flow) / ([ PAH in plasma])

= (RBF) (1-HCT)

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30
Q

how do you calculate Filtration Fraction (FF)=

A

GFR/RPF

remember its rPf NOT RBF!!!

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31
Q

whats a normal filtration fraction

A

20%

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32
Q

how do you calculate filtered load??

A

Filtered Load of X= GFR * [X in plasma]

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33
Q

what do prostaglandins do at glomerulus?

what does angII do at glomerulus?

A

PDA, ACE
prostaglandins dilate Afferent arteriole
ang II constricts efferent arteriole

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34
Q

what does dehydration do to GFR, RPF, and FF

A

decrease GFR
reallllyyy decrease RPF
and b/c FF= GFR/RPF… FF will show an increase

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35
Q

how do you calculate the reabsorption rate of X

how do you calculate the secretion rate of X?

A

Filtered Load- Excretion rate

Excretion rate- Filtered load

36
Q

how do you calculate what FRACTION of X was excreted?

A

Fe(x)= ( [X in urine][P cr]) / ([urine Cr][X in plasma])

37
Q

at what plasma glucose concentration does glucosuria begin?

A

200 mg/dL

38
Q

Fanconi Syndrome

A
  • gen reabsorptive defect of PCT
  • metabolic acidosis
  • loss of Na+, HCO3-, AA, glucose, PO43-
39
Q

Bartter Syndrome

A
  • gen reabsorptive defect of TAL (looks like chronic loop dieuretic use)
    -metabolic alkalosis
  • loss of Na/K/Cl and Ca2+
    therefore hypokalemia and hypercalciuria
40
Q

Gitelman Syndrome

A
  • gen reabsorptive defect in DCT (looks like chronic thaizide use_
    -metabolic alkalosis
  • loss of Na/Cl/K/ Mg2+
    -hypokalemia, hypomagnesemia
    less severe than Bartter
41
Q

Liddle Syndrome

A

AD GOF mut of ENAC. presents like hyperaldosteronism (but aldosterone levels are low)

  • increase Na+ reabsorption– htt
  • hypokalemia
  • metabolic alkalosis
42
Q

Syndrome of Apparent Mineralocorticoid Excess

A

deficiency of 11Bhydroxysteroid dehydrogenase (often by eating licorice!)
usually this is responsible for inactivating cortisol in cells with Mineralocorticoid receptors. In this deficiency the cortisol binds to the MR and acts like aldosterone

t(x)- corticosteroids to decrease endogenous cortisol production

43
Q

whats in the juxtoglomerular apparatus

A 
JG cells are modified sm m cells of afferent arteriole 
macula densa (NaCl sensor, part of DCT)

JG cells secrete renin if MD senses low NaCl at DCT
JGA has B1 receptors, and increase renin release in sympathetic activity

44
Q

what is Dopamine’s role in the glomeruli?

A

secreted by PCT
promotes natueresis
low dose- vasodilator
high dose- vasoconstrictor

45
Q

hypo-osomolality and alkalosis cause what K shift

hyperosmolality and acidosis cause what K shift

A
  • K shift into cells (hypokalemia) with alkalosis and hypo-osmolality
  • k shift out of cells (hyperkalemia) with hyperosmolality and acidosis
46
Q

flat t wave

Uwave

A

hypokalemia

47
Q

peaked T wave

wide QRD

A

hyperkalemia

48
Q

causes of anion gap metabolic acidosis

A 
Methanol 
Uremia 
DKA 
Propylene Glycol 
Iron (INH) 
Lactic acidosis 
Ethylene glycol 
Salicylates (late)
49
Q

causes of non-gap metabolic acidosis

A 
Hyperalimentation
Addison's 
RTA
Diarrhea
Acetazolamide
Spironolactone
Saline
50
Q

what is responsible for the increases acid secretion into urine seen in metabolic acidosis?

A
  • PCT makes glutamine into ammonium
51
Q

In ATN due to hypovolemia which parts of the kidney are most affected?

A

medulla: PT and TAL

52
Q

when are crescents seen on IF?

what are they made of?

A

RPGN

renal parietal cells, macrophages, monocytes, fibrin

53
Q

what value is needed to work up Metabolic alkalosis

A

need to know: urine Chloride levels
if low: then vomiting
if high: then thaizides, loops, or mineralocorticoid excess

54
Q

RCC arises from?

A

epithelial cells of PCT

55
Q

what undergoes hyperplasia in chronic renal A stenosis

A

Afferent arteriole
- chronic Renal A stenosis= decreased GFR= decreased NaCl to macula densa= stimulation of renin release from JG cells= JG cells undergo hyperplasia

56
Q

nsaid use can do what to the kidney?

A

chronic interstitial nephritis

57
Q

how can you tell TTP-HUS apart from DIC?

A

DIC involved ovreactive coagulation, causing depletion of coagulation factors and hence increased PT and PTT
however in TTP HUS, only the BT will be increased, not PT or PTT

58
Q

maintenance phase vs recovery phase whats the [K+] anomaly

A

hyperkalemia - maintenance

hypokalemia- recovery

59
Q

what can differentiate pyelonephritis from acute UTI/cystitis

A

WBC casts

60
Q

what indicates poor prognosis to PSGN

A

being an adult

61
Q

edema + “frothy” urine in kiddo?

A

Minimal change disease

EM: podocyte foot effacement

62
Q

where else is type IV collagen found, apart from renal and pulmonary BM?

A

lens of the eye

63
Q

what is the blood supply of the renal medulla? what disease can increase the risk of ischemia to here?

A

Vasa recta

SCD

64
Q

abdominal mass in child

(1) if crosses the midline it is
(2) if lateral,doesnt cross the midline

A

(1) neuroblastoma

(2) Wilm’s

65
Q

increased circulating PLA2 antibodies is assn w/?

A

Membranous Glomerulonephritis

66
Q

in Membranous Glomerulonephritis, what is often seen elevated in the blood?

A

LDL, chol, TGs

67
Q

Renal Tubular Acidosis Type I

A

at the CD, alpha intercalated cells can’t secrete H+ so no new HCO3- made
only RTA with urine pH>5.5

68
Q

Renal Tubular Acidosis Type II

A

at the PCT, defect in HCO3- reabsorption

urine pH <5.5

69
Q

Renal Tubular Acidosis Type IV

A

at the CD, hypoaldosteronism
only RTA with hyperkalemia
urine pH <5.5

70
Q

whats the “cutoff” between nephritic and nephrotic syndrome?

A

nephritic is when the urine protein <3.5 g/day

nephrotic is when the urine protein> 3.5 g/day

71
Q

LM: hypercellular
IF: starry sky , granular ,lumps and bumps
EM: humps

whats it called?
whats the deposit?

A

Post Strep Glomerulonephritis

Type III HS- immune complex deposition sub-epithelial of IgG, IgM, and C3

72
Q

LM: crescenteric shape
IF: linear deposits along GBM (if Goodpasture’s)

whats it called?
what the deposit?

A

Rapidly Progressive Glomerulonephritis: which includes Goodpasture’s, Wegener’s (c-ANCA), Microscopic Polyangiitis (p-ANCA)

crescent= macrophages, monocytes, c3b and FIBRIN

73
Q

what type of HS is Goodpastures’s?

A

Type II HS

antibodies against GBM (type IV collagen)

74
Q

LM: “wire looping”
EM: subendothelial immunecomplexes of IgG (also C3)
IF: granular

A

Diffuse Proliferative Glomerulonephritis

  • SLE
  • membranoproliferative GN
75
Q

LM: mesangial proliferation

EM/IF : mesangial IgA immune complex deposits

A 
IgA nephropathy (Berger's) 
often caused by HSP (= abdominal pain + arthralgia+palpable purpura on legs and butt)
76
Q

LM: thin and splitting GBM
EM: basket weave

A

Alport Syndrome- XD mut in type IV Collagen

“ can’t see, can’t pee, can’t hear a bee”

77
Q

LM: “tram track” on PAS/H&E stain due to GBM splitting by subendothelial immune complex growth

A

Membranoproliferative Glomerulonephritis

causes: idiopathic, hep B/C; antibodies against C3 which decrease C3 levels

78
Q

LM; normal
EM: podocyte foot effacement
in a child

A

Minimal Change disease , kiddo w frothy urine + edema

usually idiopathic, can be following infection, can be due to lymphoma

79
Q

LM: thickening of GBM segmentally and hyalinosis
EM: podocyte effacement

A

Focal Segmental Glomerulosclerosis

in AA/hispanics

80
Q

LM: DIFFUSE capillary and GBM thickening
EM: “spike and dome”
IF; granular

A

Membranous Glomerulonephritis (nephropathy)
most common in caucasians (also seen in SLE)
can be due to PLA2 antibodies, drugs, infections solid tumors

81
Q

LM: congo red stain shows apple green bifringence in mesangium

A

Amyloidosis

82
Q

LM: Kimmelsteil-Wilson lesions (big ovoid eosinophilic), mesangial and GBM thickening

A

Diabetic Glomerulonephropathy

caused by non-enzymatic glycosylation

83
Q

most common type of kidney stone?
cause
looks like
treat with

A 
Calcium Oxalate
- normocalcemic, hypercalcuria 
- hypocitraturia, decreased urine pH 
- other causes: ehtylene glycol, Vit C overdose, malabsorption
looks like: envelope or dumbbell 
treat: thiazides,citrate, low Na diet
84
Q

what is the less common type of calcium stone?
cause
looks like
treat with

A

calcium phospate
cause: increase pH
wedge-shaped prism
tx: low sodium and thiazides

85
Q

your kidney stone looks like a coffin?
whats it made of
whats the cause
what do you treat with

A

Ammonium Magnesium Phosphate aka struvite making staghorn caliculi
cause: P mirabilis, S. saprophyticus, Klebsiella which are urease (+) so make ammonia causing high pH
t(x): get rid of infection! remove staghorn caliculi

86
Q

your kidney stone is clear and rhomboid shaped?
whats it made of
whats the cause
what you treat with

A

Uric A stone
caused by excess uric acid (TLS or Lesch Nyhan) or more commonly decreased urine PH
treat: alkalinize urine (acetazolamide) or allopurinol

87
Q

what if your kidney stone looks like a hexagon and your Na nitroprusside test is +
whats it made of
whats the cause
what you treat with

A
  • Cystine
    cause is a AR mut in the Cystine PCT transporter (note this transporter also reabsorbs COLA: cysteine, ornithine, lysine, arginine)
    presents in childhood
    treatment: low Na, alk urine

need to knows (31 decks)

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