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Renal Flashcards

1
Q

Embryology of Kidney

  • Pronephros -> when does it go away
  • Mesonephros -> what does it give rise to
  • Metanephros -> what does it give rise to
A
  • till week 4 then degenerates
  • Mesonephros will grow into ureteric bud and come into contact with metanephros causing its differentiation; mesonephros will be ureter, pelix, caylx, and collecting ducts
  • will form glomerulus to DCT
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2
Q

Potters

  • what is it
  • sxs
  • causes
A
  • oligohydraminos -> baby isnt producing urine and so decrease in amniotic fluid
  • pulm hypoplasia (AF fills lungs to help develop), oligohydraminos, twisted face and skin, extremity defects, renail failure
  • posterior uretheral valve, bilateral renal agenesis, and others
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3
Q

Horshoe kidney

  • what is it
  • associated with
A
  • inferior poles of the kidney fuse and are unable to rose to proper position because thy hook under inferior mesenteric a
  • trisomy 13, 18, 21
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4
Q

Unilateral renal agenesis

  • what is it
  • why
A
  • only one kidney forms

- ueteric bud is unable to form for one kidney s-> no kidney or ureter

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5
Q

Multicystic dysplastic kidney

  • pathogenesis
  • what is it
  • characteristics and sequlae
A
  • ureteric bud does not induce differentiation of metnephric mesenchyme and so glomeruli to DCT not formed
  • non functional kidney consisting of cysts and CT- unilateral and will cause Potters syndrome
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6
Q

Duplex collecting system

  • what is it
  • why
  • sequlae
A
  • Y shaped ureter
  • The ureteric bud bifurcates before encountering the metanephric mesenchyme
  • vesicuourteral reflux and ureteral obsrtruction, increase risk for UTI
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7
Q

posterior urethral valve

  • what is it
  • sequlae
A
  • membrane remnant in posterior urethra of males

- lead to urethral obsturction -> hydronephrosis

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8
Q

kidney anatomy and structure

  • left renal vein characteristics, length and connections
  • which part of nephron is deficient in blood
A
  • longer renal vein (used in donor transplantation), connects to suprarenal and left gonadal veins (obstruction will cause left vericocele),
  • medulla, at highest risk for infarct
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9
Q

Ureter Anatomy

  • path with arteries
  • blood supply
  • points of obstruction
A
  • from renal pelvis under gonadal arteries -> over common iliac -> under uterine/vas defrens arteries
  • prox:,renal arteries middle: gonadal and common/internal illiac, distal:internal iliac and superior vesical
  • wreteropelvic junstion, pelvic inlet, ureterovesical junction (entering bladder)
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10
Q

Fluid compartments

- body vs ICF vs ECF

A
  • 60% H20, 40% ICF, 20% ECF
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11
Q

Glomerular filtration barrier

  • made up of
  • types of barriers
A
  • fenestrated capillaries, basement membrane, podocytes

- charge and size

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12
Q

Clearance Ratio

  • equation
  • more than inulin
  • equal to inulin
  • less than inulin
A
  • renal clearance of substance/ renal clearance of inulin
  • secreted and filtered
  • only filtered
  • secreted and reabsorbed
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13
Q

Renal clearance

- equation

A
  • [sub]u x amnt urine excreted/time /// [sub]p
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14
Q

Renal Plasma Flow

  • equation
  • renal blood flow correlation
A
  • [ Paraamino Hippouric acid ]u x amnt urine excreted/time /// [PAH] renal artery
  • RPF/ 1-HCT
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15
Q

Filtration factor

- equation

A
  • GFR/RPF
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16
Q

GFR

  • what is it
  • equation
A
  • renal clearance of inulin -> bs inulin can only be filtered
  • [inulin]u x amnt urine excreted/time /// [inulin] p
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17
Q

Glucose Clearance of Kidney

  • normal plasma level
  • 200
  • 375
  • effect of pregnancy
A
  • 100% reabsorbed
  • some glucose begins to be excreted
  • all transporter are full saturated and glucose excretion is very high
  • increase in fluid -> increase in filtration -> more glucose filtered -> glucosuria at normal glucose levels
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18
Q

Nephron Transport

  • PCT
  • Thin LOH
  • Thick LOH
  • early DCT
  • late DCT
  • CT
A
  • Na (PTH and ANP), K, Ca, glucose, bicarb, PO4 (PTH)
  • only H2O out -> concentrates urine
  • Cl, Na, K transporters out, also Mg, Ca out -> dilute urine
  • Na/Cl transporters and Ca transporters (PTH)
  • ENAC, Na/H2O in and K out, responds to aldosterone
  • alpha (H+ out, HCO3 into blood), beta (HCO3 out, H+ into blood)
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19
Q

Renal tubular defects

  • Fanconi: what is it, caused by, presentation
  • Bartter: what is it, caused by, presentation
  • Gitelman: what is it, caused by, presentation
  • Liddle: what is it, caused by, presentation, tx
A
  • defect in reabsorption at PCT -> only one that results in met acidosis (loss of lots of bases); Wilsons dx
  • defect in reabsorption at thick LOH; AR; similar to loop diurteic
  • defect in reabsorption at DCT, decrease of Na and Cl reabsorption; AR; similar to thiazide diuretic
  • increase in reabsorption at CT, increase in Na reabsorption, AD, presents similar to hyperaldosteronism, amilioride
20
Q

Renin- angiotenin- aldosterone pathway

  • starts because
  • pathway
  • effects of AGII
  • ANP/BNP
A
  • decreased renal perfusion, baroreceptors in afferent arteriole, increase in sympathetic tone, or decrease in Cl and Na delivered to macula densa cells in DCT
  • renin+angiotensinogen -> angiotensin I + ACE -> angiotensin II
  • aldosterone release, ADH release (Thirst and increase aquaporins CT), constrict efferent arteriole, vasoconstrict
  • release when heart is over stretched, inhibit renin release
21
Q

Kidney endocrine fxns

  • EPO
  • Vit D
  • Prostaglandins
  • Dopamine
A
  • Secreted in response to low O2 levels -> increase RBC proliferation
  • In PCT vit D 25 OH is converted to Vit D 1-25 OH (calciferol) the active form
  • vasodilate afferent arteriole, paracrine signaling, inhibited by NSAIDs
  • low doses will dilate afferent arteriole while higher doses vasoconstrict
22
Q

Acid base physiology: what is it, why and compensation

  • met acidosis
  • met alkalosis
  • resp acidosis
  • resp alkalosis
A
  • not enough bicarb; hyperventilate
  • too much bicarb, hypoventilate
  • not breathing enough -> too much CO2; increase Bicarb reabsorption
  • breathing too much -> not enough CO2; decrease bicard reabsorption
23
Q

Met acidosis causes

  • w/ increased anion gap
  • w/ normal anion gap
A
  • MUDPILES: methanol, uremia, DKA, propylene glycol, iron, lactic acidosis, ethylene glycol, salicylates
  • HARDASS: Hyper Cl, addisons, renal tubular acidosis, diarrhea, acetazolamide, spironolactone, saline infusion
24
Q

Renal tubular acidosis

  • Distal: what is it, causes
  • Proximal
  • Hyperkalemic
A
  • alpha intercalated cells cant get rid of H+ -> Bicarb can’t continue to be made -> met acidosis; ampho B/AI dx/ analgesic nephropathy;
  • PCT unable to reabsorb bicarb -> increase in excretion of HCO3; fancon’i/ mult myeloma
  • hypoaldosteronism -> hyperkalemia
25
Q

Nephrotic syndrome

  • Minimal change dx: epi, micro, cause
  • Focal segmental sclerosis: EM, LM
  • Membranous: EM, LM, IF
  • Amyloidosis: LM
  • Diabetic: LM
A
  • children, effacement of podocytes, infection
  • electric micro: effacement of podocytes and sclerosis of specific segments on light micro
  • EM: spike and dome, LM: glomerular thickening, IF: + Ig
  • LM: amyloid deposition in mesangium that turns green with congo red staining
  • most common cause of ESRD in UC; glycosylation of tissue proteins -> mesangial expansion and GBM thickening
26
Q

Nephritic syndrome

  • IgA nephropathy: IF
  • post strep: sxs, IF
  • diffuse proliferative: cause; LM, EM
  • membrano proliferative: stain
  • alport: pathogen, other sxs, EM
A
  • IF: IgA based immunocomplexes in mesangium
  • cola urine, antibodies deposit into kidney (IgM, IgG, C3)
  • SLE, LM: wire capillaries, w/ IgG depostion on EM
  • mesagnial growth -> GBM splitting, tram track appearance
  • mutation in type IV collagen -> thinning and splitting of GBM ; also has vision and hearing problems; basket weave
27
Q

Kidney stones

  • Ca: types - cause, shape, tx
  • Ammonium magnesium phosphate: cause, shape, other name, tx
  • Uric acid: cause, x-ray, shape, associations
  • Cysteine: cause, shape, associations, tx
A
  • oxalate: low citrate, shaped in envelope, most common; phosphate: high pH wedge shaped; low Na diet, thiazide, citrate
  • high pH- infections that are urease + will hydrolyze urea to ammonia, coffin lid; struvite/staghorn; eradication of infection
  • decreased pH, radiolucent, rhomboid/rosette; hyperurecemia (gout) -> dx with high cel turnover (leukemia)
  • low pH- genetic, hexagonal, cysteine reabsorbtion in PCT does not work and cysteine precipitates in urine, starts as child, low Na diet, alkalating urine
28
Q

Hydronephrosis

  • what is it
  • effect
A
  • distention/dilation of renal pelvis and calyces

- compression and atrophy of renal cortex and medulla

29
Q

Renal Cell Carcinoma

  • location of origin
  • sxs
  • tx
  • mets
  • gross/histo
  • subtype
A
  • PCT
  • hematuriapalpable mass, flank pain, fever, weight loss
  • surgery
  • lung and bone
  • polygonal clear cells with lots of lipds, yellow
  • clear cell, deletion of chrom 3 - inherited is called Von Hippel
30
Q

Renal Oncocytoma

  • cell of origin
  • histo
A
  • DCT

- eosinophilic with lots of mitochondria

31
Q

Nephroblastoma

  • other name
  • epi
  • sxs
  • cause
  • syndromes
A
  • Wilms tumor
  • children
  • large, palpable, unilateral flank mass
  • loss of function of WT1 or 2 on chrom 11
  • WAGR (wilms, aniridia, GU malformations, retardation) , Denys Drash (wilms tumor + diffue mesangial sclerosis and Dysgenesis of gonads), Beckwith-Wiedemann (wilms tumor, big tongue and other organs)
32
Q

Transitional Cell carcinoma

  • what is it
  • location
  • sxs
  • histo
A
  • most common tumor of the urinary tract system
  • renal calyces, pelvis, ureters, bladder
  • painless bleeding
  • fibrovasc core with dysplastic urothelium
33
Q

Sqamous cell carcinoma of the bladder

  • pathogen
  • sxs
A
  • irritation of bladder -> squamous metaplasia -> dysplasia

- painless hematuria

34
Q

Incontinence: what is it and tx

  • stress
  • urgency
  • mixed
  • overflow
A
  • something has damaged muscles in control of bladder and with increased pressure will pee themselves -> kegel exercises and weight loss
  • urge to go is immediate and unable to make it to bathroom on time -> timing breaks
  • both stress and urgency
  • unable to fully empty bladder and leak when bladder is over filled -> cath or relieve obstruction
35
Q

Pyelonephritis

  • acute: pathogenesis, dx, tx
  • chronic: pathogenesis, effects
  • xanthogranulomatous: what is it, causes
A
  • PMNs infiltrate renal interstitum, caused by infection (ascending or hemat spread), WBC in urine and striated parenchyma of kidney on CT, antibiotics
  • recurrent or inadequately treated acute episodes, usually need predisposition to infections -> causes scarring of cortex and medulla
  • cause by proteus infection -> will have foamymacrophages that have formed granulomas in kidney interstitium
36
Q

AKI

  • prerenal azotemia
  • intrinsic
  • post renal
A
  • decrease in RBF will decrease GFR, and Na, H2O, and urea retained to conserve vol -> high BUN/creatinine
  • necrosis of tubular cells -> debris obstructs tubule -> fluid backs up -> decrease GFR; urea reabsorption impaired, low BUN/creatinine
  • outflow obstruction
37
Q

Consequences of Renal failure

- MAD HUNGER

A
  • Metabolic Acidosis, Dyslpipidemia, High K, Uremia, Na and water retention, Growth retardation, EPO fail, Renal osteodystrophy
38
Q

Acute interstital nephritis

  • what is it
  • causes, 5P’s
A
  • inflammation in the renal insterstitum but due to esoinophila bc of drugs that are haptens
  • pee (diuretics), pain free (NSAID), penicillen, PPI, rifamPin
39
Q

Acute tubular necrosis

  • what is it
  • cause
  • tx
  • sequale
A
  • death of tubular cells
  • ischemic or nephrotoxic
  • spontaneously resolves
  • intrinsic acute kidney injury
40
Q

Renal cyst dx

  • Auto dom polycyst: location, effects, genetics, association, tx
  • Auto recessive polycyst: location, in utero complication
  • Auto dom tubulointerstitial: location, effects, sequlae
  • simplex vs complex
A
  • cysts in cortex and medulla, bilateral, destroy parenchyma, mutation in PKD1/2, causes chronic kidney dx, berry aneurysms, ACEi / ARB with HTN
  • cysts on collecting ducts, can lead to potters
  • medullary cysts, causes fibrosis of interstitium, unable to concentrate urine
  • s: anechoic, only fluid/ c: has solid components
41
Q

Mannitol

  • MOA
  • indications
  • side effects
  • contraindications
A
  • increase tubular fluid osmolality -> not as much water can leave
  • drug overdose, intracranial/ocular pressure
  • pulm edema, dehydration
  • HF
42
Q

Acetazolamide

  • MOA
  • side effects
A
  • carbonic anhydrase inhibitor -> decrease Na and bicarb reabsorption -> decrease H2O reabsorption
  • proximal renal tubular acidosis
43
Q

Loop

  • examples/ suffix
  • MOA
  • indications
  • side effects
A
  • ide; furosemide
  • sulfonamide, inhibits Na/K/Cl transporter
  • edematous states (HF, pulm edema, nephrotic syndrom), HTN, hyperCa
  • ototox, hypo kalemia and mg, dehydration, allergy, gout
44
Q

Ethacrynic Acid

  • MOA
  • side effect
A
  • non sulfa druge that inhibits Na/K/Cl in LOH

- more ototoxic

45
Q

Thiazide

  • examples
  • MOA
  • indication
  • adverse effects
A
  • HCTZ, cholorthalidone
  • inhibit Na/Cl transporter in DCT
  • HTN, HF, idiopathic hypercalciuria
  • hypokalemia and natremia, hyper glycemia, lipidemia, uricemia, calcemia
46
Q

K sparing

  • examples
  • MOA
  • indication
  • side effects
A
  • spironolactone and amiloride
  • spironolactone competitive aldosterone receptor antagonists -> less aldosterone is made; amilioride blacks ENAC channels
  • hyperaldosterolism, hypokalemia
  • hyperkalemia

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