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
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
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
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
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
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
7
Q
posterior urethral valve
- what is it
- sequlae
A
- membrane remnant in posterior urethra of males
- lead to urethral obsturction -> hydronephrosis
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
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)
10
Q
Fluid compartments
- body vs ICF vs ECF
A
- 60% H20, 40% ICF, 20% ECF
11
Q
Glomerular filtration barrier
- made up of
- types of barriers
A
- fenestrated capillaries, basement membrane, podocytes
- charge and size
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
13
Q
Renal clearance
- equation
A
- [sub]u x amnt urine excreted/time /// [sub]p
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
15
Q
Filtration factor
- equation
A
- GFR/RPF
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
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
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)
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
Nephrotic syndrome
- Minimal change dx: epi, micro, cause
- Focal segmental sclerosis: EM, LM
- Membranous: EM, LM, IF
- Amyloidosis: LM
- Diabetic: LM
- 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
Nephritic syndrome
- IgA nephropathy: IF
- post strep: sxs, IF
- diffuse proliferative: cause; LM, EM
- membrano proliferative: stain
- alport: pathogen, other sxs, EM
- 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
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
- 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
Hydronephrosis
- what is it
- effect
- distention/dilation of renal pelvis and calyces
| - compression and atrophy of renal cortex and medulla
29
Renal Cell Carcinoma
- location of origin
- sxs
- tx
- mets
- gross/histo
- subtype
- 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
Renal Oncocytoma
- cell of origin
- histo
- DCT
| - eosinophilic with lots of mitochondria
31
Nephroblastoma
- other name
- epi
- sxs
- cause
- syndromes
- 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
Transitional Cell carcinoma
- what is it
- location
- sxs
- histo
- most common tumor of the urinary tract system
- renal calyces, pelvis, ureters, bladder
- painless bleeding
- fibrovasc core with dysplastic urothelium
33
Sqamous cell carcinoma of the bladder
- pathogen
- sxs
- irritation of bladder -> squamous metaplasia -> dysplasia
| - painless hematuria
34
Incontinence: what is it and tx
- stress
- urgency
- mixed
- overflow
- 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
Pyelonephritis
- acute: pathogenesis, dx, tx
- chronic: pathogenesis, effects
- xanthogranulomatous: what is it, causes
- 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
AKI
- prerenal azotemia
- intrinsic
- post renal
- 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
Consequences of Renal failure
| - MAD HUNGER
- Metabolic Acidosis, Dyslpipidemia, High K, Uremia, Na and water retention, Growth retardation, EPO fail, Renal osteodystrophy
38
Acute interstital nephritis
- what is it
- causes, 5P's
- inflammation in the renal insterstitum but due to esoinophila bc of drugs that are haptens
- pee (diuretics), pain free (NSAID), penicillen, PPI, rifamPin
39
Acute tubular necrosis
- what is it
- cause
- tx
- sequale
- death of tubular cells
- ischemic or nephrotoxic
- spontaneously resolves
- intrinsic acute kidney injury
40
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
- 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
Mannitol
- MOA
- indications
- side effects
- contraindications
- increase tubular fluid osmolality -> not as much water can leave
- drug overdose, intracranial/ocular pressure
- pulm edema, dehydration
- HF
42
Acetazolamide
- MOA
- side effects
- carbonic anhydrase inhibitor -> decrease Na and bicarb reabsorption -> decrease H2O reabsorption
- proximal renal tubular acidosis
43
Loop
- examples/ suffix
- MOA
- indications
- side effects
- 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
Ethacrynic Acid
- MOA
- side effect
- non sulfa druge that inhibits Na/K/Cl in LOH
| - more ototoxic
45
Thiazide
- examples
- MOA
- indication
- adverse effects
- HCTZ, cholorthalidone
- inhibit Na/Cl transporter in DCT
- HTN, HF, idiopathic hypercalciuria
- hypokalemia and natremia, hyper glycemia, lipidemia, uricemia, calcemia
46
K sparing
- examples
- MOA
- indication
- side effects
- spironolactone and amiloride
- spironolactone competitive aldosterone receptor antagonists -> less aldosterone is made; amilioride blacks ENAC channels
- hyperaldosterolism, hypokalemia
- hyperkalemia
