Kidneyss Flashcards

(41 cards)

1
Q

Pronephros

A

week 4 then degenerates

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2
Q

Mesonephros

A

functions as interim kidney for 1st trimester; later contributes to male genital system

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3
Q

metanephros

A

permanent, first appears in 5th week of gestation; nephrogenesis continues though 32-36 weeks of gestation

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4
Q

ureteric bud

A

derived from the caudal end of the mesonephric duct; gives rise to the ureter, pelvices, calyces and collecting ducts, fully canalized by the 10th week

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5
Q

The kidneys are derivitives of?

A

mesoderm

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6
Q

the urethra is a derivitive of?

A

endoderm

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7
Q

Metanephric mesenchyme and utereric bud interact

A

the interaction induces differentiation and formation of glomerulus through to distal convoluted tubule, if the interaction goes wrong –> congenital malformations

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8
Q

Ureteropelvic junction

A

last to canalize –> most common site of obstruction (hydronephrosis) in fetus

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9
Q

Potter sequence

A

oligohydramnios –> compression of developing fetus –> limb deformities, facial anomalies (low sets ears and retrognathia), compression of chest (pulmonary hyperplasia leads to death)

causes include: ARPKD, posterior urethral valves and bilateral renal angenesis

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10
Q

Potter mnemonic

A
Pulmonary hypoplasia
oligohydramnios
twisted face
twisted skin
extremity defects
renal failure in utero
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11
Q

horse shoe kidney

A
  • inferior poles of both kidneys fuse
  • as the ascend from pelvis during fetal development they get trapped under the IMA and remain low in the abdomen.
  • kidney function is normal
  • increased risk for ureteropelvic junction obstruction, hydronephrosis, renal stones and rarely renal cancer (wilms tumor)

assoc with TURNERS

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12
Q

multicystic dysplastic kidney

A

-due to abnormal interaction of the ureteruc bud and the metanephric mesenchyme —> cysts and connective tissue issues and non functioning kindey, can be seen on US

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13
Q

What do we use to estimate the GFR? why?

A

Creatinine
GFR = clearance of creatinine = UV/P
it is freely filtered, not reasorbed and not secreted, well just a tiny bit of secretion

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14
Q

What do we use to measure RPF?

A

PAH, to measure the ERPF = UV/P = clearance of PAH
RBF= RPF (1-hct)
PAH is both filtered and actively secreted in the proximal tubule, nearly all PAH entering the kidney is excreted

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15
Q

Hartnup disease

A

autosomal recessive disorder

  • deficiency of neutral amino acid transporters in the PT.
  • lose tryptophan, need tryptophan to make niacin with the help of B6
  • pellagra (diarrhea, dementia and dermatitis)
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16
Q

Fanconi syndrome

A
  • reabsorption defect in PT
  • assoc with increase excretion of nearly all amino acids, glucose, HCO3 and PO4
  • may result in metabolic acidosis
  • type II renal acidosis (cant reabsorm HCO3/make)
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17
Q

Bartter sydrome

A
  • reabsorption defect in thick ascending loop
  • Na/K/2Cl transporter, autosomal recessive
  • lead to hypokalemia and metabolic alkalosis with hypercalciura (Mg and Ca will not be reabsorbed)
18
Q

Gitelman syndrome

A
  • autosomal recessive
  • DCT
  • Na/Cl channel defect
  • like a thiazide so more calcium resorbed
  • hypokalemia and metabolic alkalosis
19
Q

Liddle syndrome

A

Autosomal dominant

  • increased Na reabsorption in distal and collecting tubules (increased activity of the Na channel)
  • result in HTN
  • hypokalemia
  • metabolic alkalosis
  • decrease aldosterone
    treat: amiloride
20
Q

Where is EPO made?

A

interstitial cells in the peritubular capillary bends

21
Q

Where does vitamin D get activated?

A

Proximal tubule

22
Q

What affect does prostaglandins have on the kidney?

A

paracrene sections vasodilate the AFFERENT arterioles leading to increase RBF.
-so if we have NSAIDS this will block the renal protective prostaglandin and lead to decreased GFR which may result in renal failure

23
Q

Anion gap metabolic acidosis

MUDPILES

A
methanol
uremia
diabetic ketoacidosis
propylene glycol
iron tablets or INH
lactic acidosis
ethylene gylcol
salicylate toxicity late
24
Q

normal anion gap metabolic acidosis

HARD-ASS

A
Hyperalimentation
addison disease
renal tubular acidosis
diarrhea
acetazolamide
spirinolactone
saline infusion
25
Type 1 distal renal tubular acidosis urine ph>5.5 (but the serum is metabolic acidosis)
defect in a-intercalated cells to secrete H+ via the H+ATPase, thus no new HCO is generated. Since the lumen remains "-ve" more K is secreted --> hypokalemia -increase urine pH has increase risk for calcium phosphate kindey stones causes? amphoteriblecinB, analgesics, MM and obstructions
26
Type 2 proximal renal tubular acidosis urine pH<5.5
defect in PT HCO3 reabsorption results in increase secretion of HCO3 in urine and subsequent metabolic acidosis, hypokalemia. - the urine is acidified by a intercalated cells in the CT - increased risk for hypophosphatemic rickets - causes fanconi syndome, chemical toxins (lead, aminogylcosides), CA inhibitors
27
Type IV renal tubular acidosis "hyperkalemic"
- hypoaldosteronism, aldosterone resistance, or K+ sparring diuretics, ENAC issue - result in hyperkalemia
28
Calcium kidney stones
- decrease pH calcium phosphate - increase pH calcium oxalate - radioopaque crystal: envelope of dumbbell shaped - promoted by hypercalciuria - oxalate cyrsals can be from ethelene glycol, vitamin C or crohns disease treat: citrate, thiazides
29
Ammonium magnesium phosphate (stuuvite) stone
- increased pH precipitation - radioopaque - coffin lid shaped cystals - caused by infection with urease + bugs (proteus, staph, kleb) --> alkalization - can form staghorn caliculi treat: erradication of infection and surgical removal of stone
30
Uric acid stones
- decreased pH precipitates - RADIOLUCENT but can be seen on ultrasound, CT assoc. with hyperuricemia, leukemia treatments treat: alkaline the urine
31
Cystine stones (cystine is cysteine -S-cysteine)
- cystinuria, Autosomal recessive, defect in PT amino acid transporter (cysteine, ornithine, arginine) - sodium nitroprusside test treat: alkalinize the urine and hydration
32
Wilms tumor (nephroblastoma)
-age 2-4 common child renal malignancy -loss of function mutations -WT1, WT2 on chromosome 11 -may be a part of Beckwith-Wiedemann syndome: wilms tumor, aniridia, genitourinary malformations and mental retardation
33
common associations with transitional cell carcinoma
phenacetin (acetominophen is one) smoking aniline dyes cyclophasohamide (hemmoragic cystitis)
34
Acute pyelonephritis histo
- affect cortex with relative sparing of glomeruili/vessels | - neutrophillic infiltration of renal interstitium
35
Chronic pyelonephritis histo
-course, asymmetric corticomedullary scarring, blunted calyx | tubules can contain eosinophilic casts resembling thyroid tissue (thyroidization of kidney)
36
What drugs are associated with drug-induced interstitial nephritis (tubulointerstitial nephritis)
nephritis 1-2 weeks after drug diuretics, penicillin derivatives, sulfonamides, rifampic -NSAIDS can occur months later!
37
What are the three stages of Acute tubular necrosis
1. inciting event 2. maintenance phase- oliguric; lasts 1-3 weeks; risk of hyperkalemia, metabolic acidosis 3. recovery phase-polyuric; BUN and serum creatinine fall; risk of hypokalemia
38
What can cause ATN?
Ischemia secondary to -decrease RBF Nephrotoxicity secondary -aminoglycosides, radio contrast, lead, cisplatin, crush injury/myglobinuria, hemoglobinuria PT is especially susceptible
39
Renal papillary necrosis
``` sloughing of renal papillae -gross hematuria and proteinura -may be triggered by a recent infection of immune stimulus assoc with: DM Acute pylonephritis chronic phenacetin use sickle cell and trait ```
40
What is the mutation in ADPKD?
autosomal dominant - mutation in PKD1 chromosome 16 85% - mutation on PKD2 chromosome 4 15% assoc with berry aneurisms, mitral valve prolapse, benign hepatic cysts
41
complex cysts
complex cysts including those that are septated, enhanced, or have solid components as seen on CT, require follow up or removal due to risk of renal cell carcinoma