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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
renal clearance of X=
C(x)= ( [X in Urine] * rate of urine flow )/ ([X in plasma])
26
GFR=
( [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
27
whats another way to measure GFR?
= ( Pg- Pb) - (Poncg - PoncB)
28
whats a normal GFR?
100 mL/min
29
RPF=
( [PAH in Urine] * rate of urine flow) / ([ PAH in plasma]) = (RBF) (1-HCT)
30
how do you calculate Filtration Fraction (FF)=
GFR/RPF | remember its rPf NOT RBF!!!
31
whats a normal filtration fraction
20%
32
how do you calculate filtered load??
Filtered Load of X= GFR * [X in plasma]
33
what do prostaglandins do at glomerulus? | what does angII do at glomerulus?
PDA, ACE prostaglandins dilate Afferent arteriole ang II constricts efferent arteriole
34
what does dehydration do to GFR, RPF, and FF
decrease GFR reallllyyy decrease RPF and b/c FF= GFR/RPF... FF will show an increase
35
how do you calculate the reabsorption rate of X | how do you calculate the secretion rate of X?
Filtered Load- Excretion rate | Excretion rate- Filtered load
36
how do you calculate what FRACTION of X was excreted?
Fe(x)= ( [X in urine]*[P cr]) / ([urine Cr]*[X in plasma])
37
at what plasma glucose concentration does glucosuria begin?
200 mg/dL
38
Fanconi Syndrome
- gen reabsorptive defect of PCT - metabolic acidosis - loss of Na+, HCO3-, AA, glucose, PO43-
39
Bartter Syndrome
- 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
Gitelman Syndrome
- 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
Liddle Syndrome
AD GOF mut of ENAC. presents like hyperaldosteronism (but aldosterone levels are low) - increase Na+ reabsorption-- htt - hypokalemia - metabolic alkalosis
42
Syndrome of Apparent Mineralocorticoid Excess
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
whats in the juxtoglomerular apparatus
``` 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
what is Dopamine's role in the glomeruli?
secreted by PCT promotes natueresis low dose- vasodilator high dose- vasoconstrictor
45
hypo-osomolality and alkalosis cause what K shift | hyperosmolality and acidosis cause what K shift
- K shift into cells (hypokalemia) with alkalosis and hypo-osmolality - k shift out of cells (hyperkalemia) with hyperosmolality and acidosis
46
flat t wave | Uwave
hypokalemia
47
peaked T wave | wide QRD
hyperkalemia
48
causes of anion gap metabolic acidosis
``` Methanol Uremia DKA Propylene Glycol Iron (INH) Lactic acidosis Ethylene glycol Salicylates (late) ```
49
causes of non-gap metabolic acidosis
``` Hyperalimentation Addison's RTA Diarrhea Acetazolamide Spironolactone Saline ```
50
what is responsible for the increases acid secretion into urine seen in metabolic acidosis?
- PCT makes glutamine into ammonium
51
In ATN due to hypovolemia which parts of the kidney are most affected?
medulla: PT and TAL
52
when are crescents seen on IF? | what are they made of?
RPGN | renal parietal cells, macrophages, monocytes, fibrin
53
what value is needed to work up Metabolic alkalosis
need to know: urine Chloride levels if low: then vomiting if high: then thaizides, loops, or mineralocorticoid excess
54
RCC arises from?
epithelial cells of PCT
55
what undergoes hyperplasia in chronic renal A stenosis
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
nsaid use can do what to the kidney?
chronic interstitial nephritis
57
how can you tell TTP-HUS apart from DIC?
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
maintenance phase vs recovery phase whats the [K+] anomaly
hyperkalemia - maintenance | hypokalemia- recovery
59
what can differentiate pyelonephritis from acute UTI/cystitis
WBC casts
60
what indicates poor prognosis to PSGN
being an adult
61
edema + "frothy" urine in kiddo?
Minimal change disease | EM: podocyte foot effacement
62
where else is type IV collagen found, apart from renal and pulmonary BM?
lens of the eye
63
what is the blood supply of the renal medulla? what disease can increase the risk of ischemia to here?
Vasa recta | SCD
64
abdominal mass in child (1) if crosses the midline it is (2) if lateral,doesnt cross the midline
(1) neuroblastoma | (2) Wilm's
65
increased circulating PLA2 antibodies is assn w/?
Membranous Glomerulonephritis
66
in Membranous Glomerulonephritis, what is often seen elevated in the blood?
LDL, chol, TGs
67
Renal Tubular Acidosis Type I
at the CD, alpha intercalated cells can't secrete H+ so no new HCO3- made only RTA with urine pH>5.5
68
Renal Tubular Acidosis Type II
at the PCT, defect in HCO3- reabsorption | urine pH <5.5
69
Renal Tubular Acidosis Type IV
at the CD, hypoaldosteronism only RTA with hyperkalemia urine pH <5.5
70
whats the "cutoff" between nephritic and nephrotic syndrome?
nephritic is when the urine protein <3.5 g/day | nephrotic is when the urine protein> 3.5 g/day
71
LM: hypercellular IF: starry sky , granular ,lumps and bumps EM: humps whats it called? whats the deposit?
Post Strep Glomerulonephritis | Type III HS- immune complex deposition sub-epithelial of IgG, IgM, and C3
72
LM: crescenteric shape IF: linear deposits along GBM (if Goodpasture's) whats it called? what the deposit?
Rapidly Progressive Glomerulonephritis: which includes Goodpasture's, Wegener's (c-ANCA), Microscopic Polyangiitis (p-ANCA) crescent= macrophages, monocytes, c3b and FIBRIN
73
what type of HS is Goodpastures's?
Type II HS | antibodies against GBM (type IV collagen)
74
LM: "wire looping" EM: subendothelial immunecomplexes of IgG (also C3) IF: granular
Diffuse Proliferative Glomerulonephritis - SLE - membranoproliferative GN
75
LM: mesangial proliferation | EM/IF : mesangial IgA immune complex deposits
``` IgA nephropathy (Berger's) often caused by HSP (= abdominal pain + arthralgia+palpable purpura on legs and butt) ```
76
LM: thin and splitting GBM EM: basket weave
Alport Syndrome- XD mut in type IV Collagen | " can't see, can't pee, can't hear a bee"
77
LM: "tram track" on PAS/H&E stain due to GBM splitting by subendothelial immune complex growth
Membranoproliferative Glomerulonephritis | causes: idiopathic, hep B/C; antibodies against C3 which decrease C3 levels
78
LM; normal EM: podocyte foot effacement in a child
Minimal Change disease , kiddo w frothy urine + edema | usually idiopathic, can be following infection, can be due to lymphoma
79
LM: thickening of GBM segmentally and hyalinosis EM: podocyte effacement
Focal Segmental Glomerulosclerosis | in AA/hispanics
80
LM: DIFFUSE capillary and GBM thickening EM: "spike and dome" IF; granular
Membranous Glomerulonephritis (nephropathy) most common in caucasians (also seen in SLE) can be due to PLA2 antibodies, drugs, infections solid tumors
81
LM: congo red stain shows apple green bifringence in mesangium
Amyloidosis
82
LM: Kimmelsteil-Wilson lesions (big ovoid eosinophilic), mesangial and GBM thickening
Diabetic Glomerulonephropathy | caused by non-enzymatic glycosylation
83
most common type of kidney stone? cause looks like treat with
``` 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
what is the less common type of calcium stone? cause looks like treat with
calcium phospate cause: increase pH wedge-shaped prism tx: low sodium and thiazides
85
your kidney stone looks like a coffin? whats it made of whats the cause what do you treat with
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
your kidney stone is clear and rhomboid shaped? whats it made of whats the cause what you treat with
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
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
- 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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