Kidney Pathophy

Front 1

inulin

Back 1

not reasborbed or secreted, so their clereance =GFR

Front 2

PAH

Back 2

highest clearence
both filtered and secreted.

Front 3

esinophils

Back 3

seen in acute analgestic nephtopathy and chronic pyelonephritis

Front 4

neutrophils

Back 4

seen in aCUTE pyelonephritis and post step glomerulonephtitis.

Front 5

conn's syndrome:

Back 5

primary hyper aldosteroniam
hypertension, hypokalemia
metablic alkalosis
low plama renin

Front 6

angiotensin II

Back 6

CONSTRICTS EFFERENT ARTERIOLES:increases GFR
decreases RBF
FF increases.
it also increases Na as welll as bicarbonate absorption, so it causes contraction alkalosis that occurs secob=ndarty to volume contraction.

Front 7

prostaglandins

Back 7

dilate afferent arterioles
increaes RBF,GFR, and FF remains constant.

Front 8

only afferent is affectes

Back 8

benign hypertension

Front 9

diabetes

Back 9

both afferebnt and efferent arterioles are affected but more efferent is affceted than the other.

Front 10

onion skin proliferation of intimal cell

Back 10

malignant hypertension:flea bitten apperaence of the kidney. pinpoint petechial hemmorages on the cortical surfaces.
Also the endothelial injury leads to escape of fibrin, PDGF fron activated platelets induced SM proliferation=onion skinning>>leading to further narrowing of the lumen. Now kidneys become markedely ischemic..

Front 11

aldosterone secreated

Back 11

in response to increased plasma K and decreased bllod volume.
Itr causes K, H secretion and Na absorbption.

Front 12

creatinine clearance

Back 12

approx meaure of GFR, as it ia partially secrested by PT

Front 13

urea

Back 13

is reabsorbed iin the PT and medullarty collecting duct via the influence of ADH. It is excreted from our body when ADH is low and urien flow rate is high.

Front 14

macula densa

Back 14

Na sensor part of th e DCT. Part of the JGA

Front 15

JG cells

Back 15

modified smooth muscle cells of the affrent arterioles, secrete renin in respose to decreased BP.

Front 16

JGA appratus: secrestes renin, in response to decreased BP and low Na delivery to DCT.

Back 16

mecula densa: senses Na
JG cells: midified SM cells of afferent arterioles

Front 17

endothelial cells of the pertubular cappilaries

Back 17

secrete erythropoietin. in respose to hypoxia.

Front 18

ADH /vassopresin

Back 18

secreted more in response to increased plasma osmolarity than decreased Blood volume.

Front 19

ethanol: decreased ADH

whereas, pain and stress

Back 19

AS WELL AS NECOTINE INCREASED ADH

Front 20

lithium

Back 20

damages ADH mediated water absorptionq

Front 21

respiratory acidosis: pco2>45mmhg

respiratoy alkalosis: pco2 < 35 mmhg
metabolic acidosis: HCO3 < 22 mmhg + base deficit of <-2

metabolic alkalosis : HCO3> 28 mmhg + base defoicit of >+2

Back 21

none,.

Front 22

papillary necrosis

Back 22

seen in:
diabetic nephropatthy analgestic abuse
sickel cell patients
as well as in hydronephros (sometimes)
acute pyelonephritis

Front 23

subepithelial electron dense deposits like humps

Back 23

acute post strep glomerulonephritis.

Front 24

massive protenuria selective for albumin.
No hypertension,
no azotemia(no renal failure)
broadining and degenaration and fusion of foot proceesss.
no e dense deposits noticed.

Back 24

minimum change diease: affects children 1-7 yrs

Front 25

minimum change disease:

LM, as well as IF normal

Back 25

defective t CELLS >>>>cytolines>>>damage epithelial cells and increases glomerular. permeablity.
responsive to steriods.
Broadning and degenerationand fusion of foot prosesses.

Front 26

effacement of podocytes
subepithelial e dense deposits
spikes on silver stain
thick basement membrane

Back 26

membranous glomerulonephritis

Front 27

membranous glomerulonephritis
does not respond to steroids
ESRF in 10-20 yrs in 20% of cases.

Back 27

85% idopathic
hep B,C, SLE, , syphilus, drugs, diabetes mellitus

Front 28

split apperence on PAS ans silver stain-tram track .

Back 28

membrano proleferative glomerulonephritis

Front 29

membrano proleferative glomerulonephritis

Back 29

sub endothelial deposits

Front 30

only place to see hypocomplementamia

Back 30

membrano proleferative glomerulonephritis Type II: irregelar ribbion like e dense deposits within the lamina densa.

Front 31

c3 nephrotic factor antibodies

Back 31

membrano proleferative glomerulonephritis

Front 32

Ig M +c3

Back 32

focal segmental glomerulonephritis

Front 33

HiV, heroien, sickel cell disease, Iv drugs abusers, obesity

Back 33

focal segmental glomerulonephritis

Front 34

IgA contains deposits in teh mesangium

Back 34

IgA nephropathy.

Front 35

IgA nephropathy seen mostly in

Back 35

celiac diseases, liver probllems resulting in excess IgA

Front 36

recurrent hematuria (within 2-3 days of infection):
GI or respiratory tract infcetioins can induce the reoccurance as there will be increased production of IgA

Back 36

IgA nephropathy.

In comparision: on post strep glomerulonephritis, the 3-4 weeks after the post strep attack.

Front 37

kimmelstiel wilson nodulalr lesion

Back 37

diabetic nephropathy

Front 38

wireloop lesion(irreregulat thickening of BM like twisted wire due to irregeular dense immune complex deposits) with subepithelial lesion(.
hematoxyphil bodies(small dense bluish bodies representing denatured nuclear material).

Back 38

SLE

Front 39

only place to see subendothelial deposits:
and rest almost everywhere we saw subepithelial deposits.

Back 39

membrano proliferative glomerulonephritis. Also a little bit in SLE(we see every thing there)..

Front 40

alkaline urine(high PH)

Back 40

calcium, as well as ammonium magmesium phosphate stones are seen. They both are opaque.

Front 41

acidic urine, Low PH

Back 41

uric acid stones(radiolucent): often seen with high cell oturmovers like leukemias and myloprolifertive disorders

Front 42

aNTIFREEZE, VIT c ABUSE, hypercalemia, PTH increase, vit D increase, cancer

Back 42

CALCIUM OXYLATE stones: enveloped shaped crystals

Front 43

struvite/staghorn calculi

Back 43

Ammoinum mag phosphate (massive stone)stones(coffin lid). seen with urease positive like proteus vulgaris, strep, (recurrent UTI) klebseila etc

Front 44

cystine stones: autosoma recessive disorder of transport problems with ornithine, cystienne etc.

Back 44

treated with alkalization of urine

Front 45

smoking

Back 45

increase chances of renal cell carcinoma as well as pancreatic cancer, as well as bladder cancer.

Front 46

paraneoplastic syndroems with renal cell carcinioma

Back 46

increase:
EPO
ACTH
PTHrP
prolactin,
renin,
ADH

Front 47

renal cell carcinoma: pain less hematuria.

Back 47

50-70 yrs:
if younger then VHL gene deletion (on chromoseome 3) association.

Front 48

painless hematuria

Back 48

seen in renal cell carcinoMA as well as bladder cancers.

Front 49

granular muddy brown casts

Back 49

acute tubular necrosis

Front 50

epithelial casts

Back 50

acute renal failure

Front 51

waxy casts

Back 51

CRF/adnvanced renal disease.

Front 52

uremia

Back 52

increased creatine, as well as BUN with associated symptoms

Front 53

adult polycystic disease associatins

Back 53

berry anurysms 10%
polycystic liver disease 40%
mitral valve prolapase 25%
cysts in lungs, spleen and pancreas (rare).

Front 54

infantile polycyctic kidney disease

Back 54

hepatic cysts
and fibrosis

Front 55

thyrodization(dilated atropic tubules, eosinophilic casts, chronic inflammation).
broad coarse scars(poles)
distorted medulla and calyses

Back 55

seen with chronic pyelonephritis.

Front 56

Acute pyelonephritis

Back 56

papillary necrosis
perinephretic abssess/microabssess
under lying hydronephrosis

Front 57

cephalosporins
thaizides
NSAIDS
cimetidin

Back 57

cuasues drug induced inter stitial nephriris

Front 58

fever
hematuria
mild portenuria
wbc casts
esinophils
rash,
macrophages, lymphocytes,granulomas (may be.)

Back 58

esp after a drug therapy indicates drug induced interstitial mephriris. seen in interstitum

Front 59

analgetic nephropathy:

Back 59

asprin, acetamenophen
caffine
Complication: transition cell carcinoma of renal or bladder.
renal papillary necrosis seen.

Front 60

rupture of tubular membrane
tubular casts
skip areas of tubular necrosis
interstitial edema
decreased urine output
weak pulse
serum Cr and BUN increased

Back 60

all indicate acute tubular necrosis due to ARF.
3 stages: intiating,maintanenec,recovery.

Front 61

in toxic acute tubular necrosis:
in case of ethylene glycol(antifreeze) posoining

Back 61

tubular vacuolization,
diffuse necrosis in PT
non oliguric acute tubular nectosis.

Front 62

ischemic necrosis

Back 62

skip type necrosis;
wherease in toxic necrosis there is a diffuse necrosis esp in PT and less in DCT etc.

Front 63

hyaline arteriosclerosis

Back 63

benign hypertension: kidney surface has a even fine granularity and the cortex is thinnned.

Front 64

in hemolytic uremic syndrome

Back 64

no autoantibodies or immune complex formation occurs.
actual cause is endothelial injury due to bacterial endotoxins, cytoxins, virus or antiEC anibodies.

Front 65

HUS: main cause of acute renal failure in chioldren.

Back 65

Ecoli(O157:H7): produces shiga like toxin

viruses.

Results: oliguria
hematuria
MAHA
fever, renal failure, thrombocytopenia

Front 66

adult polycystic disease

Back 66

Symptoms:
FLANK PAIN
heavy dragging sensation
hematuria
mass
hypertension
infections
mat progress to chronic renal failure.
rare;ly present at the age of (30-40).

Front 67

childhood polycystic disease

Back 67

Autosomal recessive
death in infancy
Associations: polycystic liver and heaptic fibrosis.
Mutations: PKD1 coding for fibrocystin (chromosome 6p)
small cysts right anngle to cortical surface completely replace medulla and cortex: sponge like appearence.
oligohydromas present in mother: potter;s face, low set ears, parrort beak nose, and hypoplastic lungs.

Front 68

medullary sponge kidney

Back 68

5mm cysts in renal papillae connect with collecting ducts, not life threatning, associated with
UTIs, hematuroa, calculi(medullary nephrocalcinosis)

Front 69

dialysis acquired cysts

Back 69

in patients with ESRD and prologed dialysis
often asymptomatic
hematuria
renal cell carcinoma in 7%
multiple 1-2 cm cortical and medullary bilateral cysats.

Front 70

simpel renal cysts

Back 70

single -multiple cortical cysts
incidental findings on autopsy
rarely present with hematuria ddue to rupture

Front 71

renal cysts

Back 71

often confused with rena;l cancer
CRF

Front 72

rena;l cell carcinoma: located mostly in cortex
cells are clear filled with glycogen/lipid

Back 72

age approx 50-70
painless hematuria
costovertebral pain
fever
weight loss
palpable mass
anemia, poolycythemisa due to erythropoitein
other neoplastic symptoms
yellow with areas of hemmorahe\\
tendency to invade renal vein
associated:
smoking, cadmium exposure
chronic dialysis(3-6X)
genetioc 5%
metastasis: lungs (50%) and bone (33%)

Front 73

inherited renal cell carcinomas

Back 73

Will be BILATERAL
multifocal
younger age
Genetic: Von Hippel Lindau syndrome

Front 74

Von Hippel Lindau syndrome

Back 74

autosomal dominant
unbalanced translocatioin(3:6, 3:8, 3:11)
VHL gene: 3p25-26.
multiple renal cell carcinomas
hemangioblastoms CNS and eye
pheochromocytomas

Front 75

hydronephrosis

Back 75

dilated renal peivis/calyces
tubular atrophy, interstitial fibrosis, chronic inflammation.
obstruction could be bilateral(at or below the level of bladder) or unilateral(at or above ureters).
if complete obstruction to the out flow of urine(papillary necrosis): permanent renal damage in 3 weeks as wel;l as anuria.
obstruction: spinal cord damage, forign body, calculi, BPH, pregnancy etc.
early symptoms: impaired ability to conc urine: polyuria
later renal failure.
kidney may be massively enlarged.
often unilateral obstruction can remail silent for lonf time.

Front 76

creatinine doubles

Back 76

50% of GFR is lost.(big changes in GFR with little changes in creatinine).

Front 77

AS WE AGE DOES GFR INCREASES OR DECREASES

Back 77

DECREASES: SO DRUG DOSING IS IMP IN ADULTS VERSUS ELDERLY.

Front 78

BUN/Cr ratio

Back 78

normal 10:1
prerenal oliguria>10:1

Front 79

primary hypertension: essential hypertension
secondary hypertension:

Back 79

primary aldosteronism
oral contraceptives
cushing;s disease
pheochromocytoma.

Front 80

osmolality: number of particles of solute per unit of solvent.

Back 80

=2(Na)+BUN/2.8 +glucose/18
large part controlled by Na, little bu others.
=(2*140)+(10/2.8)+(100/8)
=288 mOsm/kg

Front 81

primary GN: NONPROLIFERATIVE

Back 81

Minimum change disease
focal segmental glomersclerosis
membranous nephropathy

Front 82

decreased osmolality of blood

Back 82

decreased Na

Front 83

increased osmolality of urine

Back 83

decreased Na in urine.

Front 84

chronic renal failure

Back 84

lithium
cyclosporine(chronic interstitial nephritis)
heavy metals(intense interstitial fibrosis)
cystic diseases like polycyctic kidney diasese etc
chronic interstitial nephritis: sickel cell. diabetes, analgestics all cause papillary necrosis.

Front 85

fanconi syndrome

Back 85

renal tubular acidosis
aminoaciduria
phosphaturia
renal glycosuria

Front 86

UTI of pregnannt women: asymptomatic

Back 86

treat for 2-6 weeks

Front 87

persistent bacteriuria:
US normal and less than 75 yrs

Back 87

TREAT FOR 2 WEEKS

Front 88

persistent bacteriuria:
US abnormal and less than 75 yrs

Back 88

treat for 6 weeks

Front 89

recurrent infections:
relapse: same org, upper tract,<2 weeks

Back 89

recurrent infection:
reinfection: different org, lower tract, >2 weeks