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Pathology > Renal > Flashcards

Renal Flashcards

1
Q

horseshoe kidney

A

most common ceongenital, abnormally in lower abdomen (gets stuck on IMA), conjoined at lower pole

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2
Q

renal agenesis

A

can be uni or B/L

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3
Q

unilateral renal agenesis

A

hypertrophy of existing kidney, hyperfiltration inc. risk of renal failure in life,

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4
Q

B/L renal agenesis

A

oligohydraminos leading to lung hypoplasia, flat face with low set ears, dev. defects of extremities (Potter Sequence); incompatible with life

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5
Q

dysplastic kidney

A

non-inheritaed, congenital malformation of renal parenchyma chatacterized by cysts and abnormal tissue especially cartilage; usually unilaterial

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6
Q

if dysplastic kidney is kidney then what needs to be done

A

must distinguish it from PKD

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7
Q

Polycystic Kidney Disease (PKD) characterisitcs

A

inherited, B/L enlarged kidneys with cysts in renal cortex and medulla,

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8
Q

Autosomal recessive PKD (Juvenile form) characteristics

A

presents in infants, worsening renal failure, HTN, potter sequence may be seen, assoc. with congenital hepatic fibrosis (which will show as portal HTN) and hepatic cysts

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9
Q

Autosomal dominant PKD (Adult, ADult)

A

presents in young adults, HTN, hematuria, worsening renal failure, due to mutations in APKD1 or APKD2, assoc with berry aneurysm (cause of deaths), hepatic cysts, mitral valve prolapse, pt will have inc. renin causing the HTN

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10
Q

family Hx of deaths from intracrainial bleeds from aneuryms and renal disease?

A

think possibly of autosomal dominant PKD

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11
Q

Medullary systic kidney disease

A

inherited (autosomal dominant) defect, cysts in medullary collecting ducts, parenchymal fibrosis causing a shrunken kidneys, worsening renal failure

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12
Q

Acute renal failure is characterized as

A

azotemia often with oliguria

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13
Q

types of acute renal failure

A

prerenal, postrenal, intrarenal azotemia

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14
Q

pre-renal acute renal failure

A

dec. blood flow to the kidney; LABS: dec. GFR, azotemia, oliguria, BUN/Cr > 15 (why? low BF causues renin-aldos sequence leading to inc. Na thus inc. H20 thus inc. BUN reabsorption with Cr excretion not chaning), tubulues activity intact

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15
Q

post-renal acute renal failure

A

dec. outflow, back P in kidney that lowers GFR; decreased GFR, azotemia, oliguria,

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16
Q

intral renal acute renal failure

A

within kidney is a blockage

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17
Q

early stage of post renal azotemia

A

inc. back pressure leads to inc. BUN resorpt to increaces BUN: Cr ration, tubular fxn will be intact

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18
Q

long standing obstruction of post renal azotemia

A

now decreased resorpt of BUN causing BUN:Cr to decrease, decreased reabsorption of sodium, inability to concentrate urine….long standing blockage starts to damage tubules

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19
Q

Intrarenal acute renal failure subtypes

A

ATN, Acute interstitial nephritis, renal papillary necrosis

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20
Q

Acute tubular necrosis

A

injury and necrosis of tubular epi. cells, necrotic cells plug tubules causing obstruction and lowering GFR, brown granular casts seen in urine; decrased reabsort of BUN (BUN:Cr <15), decreased reabsort of Na, cant concentrate urine

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21
Q

most common cause of ARF

A

ATN

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22
Q

etiologies of ATN

A

ischemia and nephrotoxic

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23
Q

Ischemic ATN

A

decreased blood supply causing necrosis of tubules, often preceded by prerenal azotemia, prox tubule and medullary segment of thick ascending limb particularly susceptible

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24
Q

Nephrotoxic ATN

A

toxic agent causes it, prox tubule is susceptible

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25
Q

Nephrotoxic ATN causes

A

aminoglycosides, heavy metals, myoglobinuria, ethylene glycol (cause oxalate crystals in urine), radiocontrast dye, urate

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26
Q

Clinical features of ATN

A

oliguria with brown granular casts, elevated BUN and creatinine, hyperkalemia with metabolic acidosis

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27
Q

oliguria from ATN can last how long

A

2-3 weeks

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28
Q

Acute interstitial nephritis

A

drug induced hypersensitivity rxn, causes include NSAIDs, PCN, diuretics

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29
Q

presentation of acute interstitial nephritis

A

oliguria, fever, rash days to weeks after starting drug, Eosinophils seen in urine, resolves with drug cessation, can progress to renal papillary necrosis

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30
Q

renal papillary necrosis

A

necrosis of the renal papillae

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31
Q

presentation of renal papillary necrosis

A

gross hematuria, flank pain

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32
Q

renal papillary necrosis causes

A

chronic analgesic use, diabetes mellitus, sickle cell traint or disease, severe acute pyelonephritis

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33
Q

Nephrotic syndrome def

A

proteinuria (>3.5 g/day); hypoalbuminemia (cause edema), hypogammaglobulinemia (inc risk of infection), hypercoaguable state (lose ATIII), hyperlipidemia and hypercholesterolemia

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34
Q

Nephrotic Syndromes

A

minimal change disease, FSGS, Membranous nephropathy, membranoproliferative glomerulonephritis, diabetes mellitus cause, Systemic amyloidosis

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35
Q

minimal change disease

A

most common nephrotic in children, usually idiopathic, may be assoc with hodgkin lymphoma

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36
Q

Most common nephrotic syndrome in children

A

minimal change disease

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37
Q

minimal change disease pathogenesis

A

effacement of the foot processes, due to cytokines

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38
Q

MCD histology

A

normal glomeruli on HnE stain, effacement of processes on EM, no Ig complex deposits (negative IF)

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39
Q

MCD proteinuria characterisitc

A

selective; loss of albumin but not Ig

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40
Q

MCD Tx

A

steroids

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41
Q

Focal segmental glomerular sclerosis

A

most common cause of nephrotic syndrome in hispanics and african americans, usually idiopathic; may be assoc. with HIV, heroin use, sickle cell disease

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42
Q

most common cause of nephrotic syndrome in Hispanics and African Americans

A

FSGS

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43
Q

FSGS histology

A

focal and segmental sclerosis on HnE, effacement of foot process on EM, negative IF

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44
Q

what does focal refer to

A

only 1 glomeruli or small number of them

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45
Q

what does segmental mean

A

only portion of the affected glomeruli is affected

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46
Q

if MCD does not respond of steroids and progress it becomes what

A

FSGS

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47
Q

FSGS respnce to steroids

A

poor response and progresses to chronic renal failure

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48
Q

membranous nephropathy

A

usually idiopathic; assoc. with Hep B, Hep C, SOlid tumors, SLE, Drugs…most common cause of nephrotic in caucasian adults

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49
Q

most common nephrotic syndrome in caucasian adults

A

membranous nephropathy

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50
Q

membranous nephropathy histology

A

thick glomerular basement membrane on HnE, granular IF, sub-epi deposits with spike and dome appearance on EM

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51
Q

nephrotic syndrome assoc with SLE

A

membranous nephropathy

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52
Q

if the membrane in glomeruli is thickened then…

A

its membranous nepohropahty or membranoproliferative due to the Ig depot

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53
Q

membranous nephropathy pathogenesis

A

the Ig deposits sub-endothelial and then the podocyte lays down more basement membrane leading to the spike and done appearance

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54
Q

membranoproliferative glomerular nephritis (MPGN)

A

thick capillary membraines on HnE, often with tram track appearance, granular IF

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55
Q

MPGN pathogensis

A

Ig deposits, mesangium proliferates thru the deposit to create tram track

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56
Q

MPGN subtypes

A

Type I: subendothelial, Type II: intramembranous

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57
Q

TYpe I MPGN

A

subendothelial, assoc. with HBV, HCV; mor eoften with tram track look

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58
Q

Type II MPGN

A

intramembranous; assoc. with C3 nephritic factor (an auto antibody that stabalized C3 convertase)

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59
Q

MPGN causes nephrotic or nephritic?

A

can cause either or BOTH

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60
Q

membranous and MPGN distribution in glomeruli

A

membranous type = right under podocytes (epithelial), MPGN I = under endothelial, MPGN = intramembrane

61
Q

Nephrotic syndrome caused by DM

A

high glucose cauises non-enzyme glycosylation of vascular basement membrane resulting in hyaline arteriolosclerosis, efferent artiole more affected than afferent leadin to inc. glomerular pressure

62
Q

DM nephrotic syndrome pathogenesis

A

the NEG cuases back pressure leading to sclerosis of the glomerulus,

63
Q

Tx to slow the DM neptjrotic syndrome progression

A

ACE inhibitor due to angiotensin II acts on efferent vessel

64
Q

Kimmelstiel-wilson noldules

A

seen in the DM nephrotic syndrome from the sclerosis and is patho-neumonic

65
Q

Systemic Amyloidosis

A

kidney most common involved, amyloid deposits in mesangium resulting in nephrotic syndrome, apple green birefringence under polarized light

66
Q

Nephritic syndrome

A

limited proteinuria, oliguria, azotemia, salt retention with periorbital edema and HTN, RBC casts and dysmorphic RBC in urine…glomerular inflammation and bleeding

67
Q

Bx of nephritic syndomr glomeruli

A

hypercellular, inflamed glomeruli; immune complex deposition activates complement, C5a is a chemoattractant for neutros

68
Q

nephritic syndrome subtypes

A

Post. Strept. glomerular nephritis, RPGN, IgA nephropathy, Alport syndrome

69
Q

PSGN

A

nephritic syndrome that arises after group A Beta hemolytic strep infection of skin or pharynx

70
Q

more often PSGN strept need what virulence factor?

A

M protein, defines it as a nephritic strain

71
Q

PSGN presentation

A

2-3 weeks after infection, hematuria (coca cola urine), oliguria, HTN, periorbital edema, more often seen in children but adults can be affected

72
Q

PSGN histology

A

hypercellular, inflames glomeruli on HnE, Ig deposition (granular IF), subepithelial humps on EM

73
Q

PSGN Tx

A

supportive due to the deposits go to sub-epi layer and then eventually disappear; children rarely progress to renal failure; adults could dev. RPGN

74
Q

RPGN

A

nephritic syndrome that progresses to renal failure in weeks to months

75
Q

RPGN Bx

A

crescents in bowens space and the cresencts are made of fibrin and macrophages

76
Q

RPGN IF subtypes

A

linear = Goodpasture syndrome; granular = PSGN, diffuse proliferative glomerularnephritis; Negative IF = wegener granulomatosis, polyangiitis, churg strauss syndrome

77
Q

Goodpasture syndrome

A

Ab againts collagen in glomerular and alveolar basement membranse; presents as hematuria hemoptysis, classically young adult males

78
Q

SLE most common type of renal disease

A

diffuse proliferative golerulonephroitis type, SLE usuallly causes this instead of the nephrotic one mentioned, granular immune complex deposition

79
Q

after a negative IF (pauci immune) then

A

ANCA test is performed; c-ANCA = wegeners granulomatosis (kidney disease is RPGN along with lung invokvement and nasopharynx involvement); p-ANCA is microscopic polyangiitis or churg strauss….to distinguish CS has granulomatous inflammation, eosinophils, asthma

80
Q

IgA nephropathy

A

mose common nephropathy world wide, IgA depot in mesangium

81
Q

IgA nephropathy presentation

A

episodic gross or microscope hematuria with RBC casts following usually a mucosal infection; granular IF; may slowly progress to renal failure

82
Q

ALport syndrome

A

inheritated defect in type IV collagen; most commonly X-linked; results in thinning and splitting of glomerular basement membrane

83
Q

ALport syndrome presentation

A

isolated hematuria, sensory hearing loss, ocular disturbances

84
Q

UTI usually caused by

A

ascending infections

85
Q

cystitis

A

bladder inflammation; presents with dysuria, urinary frequency, urinary urgency, supra-pubic pain; systemic signs are usually absent

86
Q

risk factors for UTI

A

sexual intercourse, urinary stasis, catheters

87
Q

Labs for cystitis

A

UA: cloudy urine with >WBC
Dipstick: + leukocyte esterase and nitrites
CUlture >100,000 CFU

88
Q

etiologies of cystits

A

E. COli (80%), staph. saprophyticus (young sexually active women), kleb. pneumoniae, proteus mirabilis (alkaline urine), enterococcus faecalis

89
Q

sterile pyuria

A

pyuria with - urine culture; suggests urethritis from chlamydia, trachomatis, neisseria gonorrhoeae

90
Q

pyelonephritis

A

kidney infection; usually ascending infection

91
Q

pyelonephritis inc. risk factor

A

vesicoureteral reflux

92
Q

pyelonephritis presentation

A

fever, flank pain, WBC casts, leukocytosis along with the Sx of cystitis ( dysuria, urinary frequency, urinary urgency, supra-pubic pain)

93
Q

pyelonephritis etiologies

A

E. COli (90%), klebsiella species, enterococcus faecalis

94
Q

Chronic pyelonephritis

A

interstiail fibrosis and atrophy of tubules due to multiple bouts of acute form; due to vesicoureteral reflux (children) or obstruction

95
Q

chronic pyelonephritis Bx

A

cortical scarring with blunted calyces; if scarring at upper and lower poles then it is characteristic for vesicoureteral reflux

96
Q

chronic pyelonephritis histology

A

thyroidization of kidney (atrophic tubules contain eosinophilic peoteinaceous material reminiscent of thyroid follicles)

97
Q

chronic pyelopnephritis UA

A

waxy casts seen

98
Q

nepholithiasis

A

urinary solute as a stone; risk factors include high conc. of solute in urinary filtrae and low urine volume

99
Q

nephrolitiasis presentation

A

colicky pain with hematuria and unilateral flank tenderness; stone will pass in hours or else sugery may be required

100
Q

calcium oxalate or calcium phosphate stones

A

most common seen in adults

101
Q

causes of Ca-oxalate or Ca-Pi stones

A

idiopathic calciuria; hypercalcemia causes must be ruled out; may be seen in crohns

102
Q

Tx of Ca-oxalate or Ca-Pi stones

A

thiazides (Ca sparring diuretucs)

103
Q

ammonium, Mg, Pi

A

2nd most common type

104
Q

ammonium, Mg, Pi causes

A

infection with urease + organisms (proteus vulgaris, klebsiella); alkaline the urine causing stone; stag horn stones; usually requires surgery

105
Q

ammonium, Mg, Pi stone Tx

A

staghorn stones thus need surgery, Ab for the offending agent

106
Q

Uric acid stones

A

3rd most common; radiolucent

107
Q

Uric stone causes

A

risks: hot, arid climate, low urine volume, acidic pH; stones seen in gout pt, hyperuricemia or myeloproliferative disorders inc. risk

108
Q

uric stone Tx

A

HYDRATION AND ALKALIZATION OF URINE; allopurinaol can help in gout pt

109
Q

cysteine stones

A

rare, more commonly in children

110
Q

cysteine stones causes

A

cysteinuria (due to genetic defect in tubles)

111
Q

cysteine stone Tx

A

may form stag horns, hydration and alkalization of urine

112
Q

end sdtage kidney failure

A

result from glomerular, tubular, inflammatory, vascularf insults to kidney; most common causes HTN, DM, glomerular disease

113
Q

Uremia

A

azotemia; nausea, anorexia, pericarditis, platelet dysfxn, encepalopathy with asterixis, urea deposition in skin

114
Q

clinical features seen in end stage kidney failure

A

Uremia, salt/water retention (with resultant HTN), hyperkalemia with metabolic acidosis, anemia, hypocalcemia, renal osteodystrophy (damage to bone due to failure; components osteitis fibrosa cystica, osteomalacia, osteoporosis)

115
Q

renal peritubular interstitial cells

A

secrete EPO

116
Q

osteitis fibrosa cystica

A

hypocalcemia…PTH rise….resportion of calcium from bone leading to cysts and fibrosis

117
Q

osteomalacia

A

cannout mineralize the osteoid created

118
Q

end stage renal failure Tx

A

kidneys shrink and due to dialysis they create cysts, increased risk for renal cell carcinoma (pt on dialysis)

119
Q

Angiomyolipoma

A

hamartoma comprised of BV, Smooth Muscle, Adipose tissue; increased frequency in tuberous sclerosis

120
Q

Renal cell carcinoma

A

malignant epithelial tumor arising kidney tubules

121
Q

renal cell carcinoma presentation

A

classic triad: hematuria, palpable mass, flank pain; other Sx: fever, lbs loss, paraneoplastic syndrome (EPO, renin, PTHrP, ACTH)

122
Q

renal cell carcinoma extra things

A

rarely may present with left sided varicocele (only occurs on LEFT side including only L-kidney)

123
Q

most common cell variant for renal cell carcinoma

A

cells with clear cytoplasm

124
Q

renal cell carcinoma pathogenesis

A

loss of VHL tumor suppressor; causes increse inculin growth factor-1, inc. HIF transcription factor that increase VEGF, PDGF

125
Q

sporadic pathway of RCC

A

single tumor, upper pole, adult smoker, assoc. with VHL loss

126
Q

hereditary pathway of RCC

A

younger, multiple and B/L, assoc. with VHL loss

127
Q

Von Hippel-Lindau disease

A

autosomal dom disorder assoc. with inactivation of VHL; increases risk for hemangioblastoma of cerebellum and RCC

128
Q

RCC loves to go where..

A

renal vein

129
Q

Wilms tumor

A

most common to arise in children (avg age is 3), malignant renal tumor comprised of blastema (primitive cells for kidney dev.), primitive glomeruli, tubules, stromal cells

130
Q

Wilms tumor presentation

A

large, unilateral flank mass, hematuria, HTN

131
Q

Wilms tumor gene mutation

A

WT1

132
Q

WAGR syndrome

A

WIlms tumor, Aniridia, Genital abnormalities, Retardation

133
Q

Beckwith-Wiedemann syndrome

A

Wilms tumor, neonatal hypoglycemia, muscular hemihypertrophy, organomegaly (including tongue)

134
Q

urothelial carcinoma

A

malignant tumor from urothelial lining of renal pelvis, ureter, bladder, urethra

135
Q

most common type of lower urinary tract cancer

A

urothelial carcinoma; usually arise in bladder

136
Q

number 1 major risk factor for urothelial carcinoma

A

cigarettes because of the polycyclic aromatic hydrocarbons

137
Q

risk factors for urothelial carcinoma

A

smoking, naphthylamine, azo dyes (coloring including hair), long term cyclophosamide or phenacetin use

138
Q

urothelial carcinoma presentation

A

usually older adults with painless hematuria

139
Q

2 pathways for causation of urothelial carcinoma

A

flat and papillary; papillary growth being a vascularized growth with epi cells (progress from LG to HG then INVADES); flat pathyway is a flat lesion that starts has HG and then invades ,assoc. with earl;y p53 mutations

140
Q

urothelial carcinoma are often multifocal and recur due to

A

the entire urothelial field are exposed to the carfinogens so eventually they are all cancerous or become cancerous

141
Q

squamous cell carcinoma

A

malignant proliferation of squamous cells; usually involves bladder; arises in a background of squamous metaplasia

142
Q

squamnous cell carcinoma risk factors

A

chronic cystitis, schistosoma hematobium (middle eastern usually), long standing nephrolithiasis

143
Q

urothelial cells become what during irriation

A

becomes squamous metaplasia and then allows for squamous cell carcinomas

144
Q

adenocarcinoma

A

malignant proliferation of glands, usually involve bladder

145
Q

adenocarcinoma arise frm

A

urachal remnant, cystitis glandularis, exstrophy

146
Q

urachal remnant

A

from a tube that drains bladder to yolk sac and has glands in it, thus allow for production of adenocarfcinoma; the adenocarcinoma will be at dome of bladder

147
Q

cystits glandularis

A

chronic inflammation leading to a columnar metaplasia to allow for creation of adenocarcinoma of bladder

148
Q

exstrophy

A

congenital defect to form caudal portion of bladder wall and anterior abdom wall

Pathology (7 decks)

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