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Pathology IV > Quiz 2 > Flashcards

Quiz 2 Flashcards

1
Q

The upper pole of each kidney is near the level of which vertebra?

A

12th thoracic

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2
Q

The kidneys process how much blood per minute?

Per day?

A

1 Liter (20% of total cardiac output)

1500L

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3
Q

What functions do the kidneys perform?

A
  • Excrete metabolic waste
  • Regulate electrolytes
  • Buffer acid-base in blood
  • Activate vitamin D
  • Secrete renin
  • Secrete erythropoietin
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4
Q

Structural and functional unit of the kidney:

consists of:

A

Nephron

  • glomerular capsule
  • proximal convoluted tubule
  • loop of Henle
  • distal convoluted tubule
  • collecting duct
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5
Q

Capillary tuft surrounded by Bowman’s capsule:

Blood supply in and out:

A

Glomerulus

Blood IN via Afferent arteriole
Blood OUT via Efferent arteriole

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6
Q

What is the GFR?

A

Glomerulur filtration rate

blood filtration rate, utilizing pressure gradient btw afferent and efferent arterioles to drive filtration

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7
Q

Risk of CAKUT:

A

CAKUT - congenital abn of kidneys and urinary tract

1/3 of anomalies noted on prenatal US
predisposed adult HTN & CVD
40% of childhood end-stage renal failure

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8
Q

Failure of kidney(s) to develop to normal size/weight:

A

Renal hypoplasia

unilateral MC than bilateral
smaller kidney prone to infx & scarring

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9
Q

Kidneys fused at the upper or lower pole:

A

Horseshoe kidney

lower pole MC
often asx
infx may occur d/t urinary stasis

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10
Q

Abnormal location of one/both kidney(s):

A

Ectopic kidney

MC locations - lower abdomen, pelvis

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11
Q

Cystic lesions of the kidneys are (common/rare) and most are (asx/severe).

A

common

asx - found incidentally on imaging or post-mortem

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12
Q

T/F: Simple cysts predispose an individual to developing chronic renal failure and/or neoplasia.

A

False

mb multiple, but never as numerous as polycystic kidney dz

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13
Q

Autosomal recessive form of PKD:

ARPKD

A

childhood PKD

autosomal dominant - adult (ADPKD)

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14
Q

Histopathology of childhood PKD:

A

multiple large cysts
lined by flattened cuboidal epithelium
fibrotic intervening parenchyma
islands of bluish cartilage

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15
Q

T/F: The adult form of PKD is more commonly associated with concurrent liver cysts than is childhood PKD.

A

True

cysts not usu present at birth, develop slowly over time
assoc w/oxalate crystals in urine and cysts

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16
Q

Presumed mechanism for adult PKD:

A

Abnormal collagen and elastin that results in diminished integrity

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17
Q

Familial recurrence rate of ADPKD:

A

50%

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18
Q

Patients on ________ commonly form kidney cysts, and are at increased risk for _________________.

A

dialysis

renal cell carcinoma

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19
Q

Most forms of glomerular injury are found to be __________ mediated. Histo findings include:

A

immunologically

WBC infiltration
inflammatory cell infiltration

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20
Q

Proliferation of mesangial, endothelial and epithelial cells is (common/uncommon) in glomerular dz.

A

Common

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21
Q

In glomerular dz, thickening of the ___________ is a common and important finding.

A

basement membrane

usu d/t deposition of immune complexes on epithelial side of the membrane

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22
Q

Immune complexes are often the result of specific antibodies to the glomerular basement membrane aka:

A

anti-GBM antibodies

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23
Q

Glomerular dz’s presenting as nephrotic syndrome:

A

Lipoid nephrosis
Membranous glomerulopathy
Focal-segmental glomerulosclerosis
Nodular and diffuse glomerulosclerosis

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24
Q

Characteristic findings of nephrotic syndrome (4):

A

Proteinuria (>3 gm per 24 hrs.)
Decreased serum proteins
Increased serum lipid levels
Generalized edema

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25
Q

MC cause of nephrotic syndrome in children:

Peak incidence at ____ years.

A

lipoid nephrosis - 90% of cases

2-3 y.o.

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26
Q

Lipoid nephrosis accounts for ___% of adult nephrotic syndrome.

A

20-30%

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27
Q

Lipoid nephrosis exhibits _______________, in that _______ is the only protein commonly in the urine.

A

selective proteinuria

albumin

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28
Q

Minimal change dz (MCD) is characterized by:

A

effacement of the epithelial cell foot process (podocyte) and loss of the normal charge barrier

albumin selectively leaks out
proteinuria ensues

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29
Q

MC cause of adult nephrotic syndrome:

A

Membranous glomerulopathy (aka membranous glomerulosclerosis)

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30
Q

Etiology of most cases of membranous glomerulopathy:

A

unknown (idiopathic)

can develop via response to antigenic stimulation to infectious agent/toxin

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31
Q

Membranous glomerulopathy is known to follow infx, such as:

or drug therapy, such as:

A 
Hep B
Hep C
Syphilis
Malaria
Schistosomiasis

gold therapy
Captopril

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32
Q

Tumors have been known to lead to membranous glomerulopathy, such as:

A

lung cancer
colon cancer
melanoma
lymphoma

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33
Q

In membranous glomerulopathy, the (capillary loops/loops of Henle) are usually (atrophied/thickened) and prominent.

A

capillary loops

thickened

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34
Q

Light microscopy findings in membranous glomerulopathy:

A
  • diffuse thickening of basement membrane

* spiked appearance w/silver or Jones stain

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35
Q

Membranous glomerulopathy is generally a ____________ mediated disease in which deposits of __________ and _________ collect in the basement membrane.

A

immunologically
IgG and/or IgM
complement (usually C3)

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36
Q

_________________ is the MC cause of nephrotic syndrome in African-Americans.

A

Focal segmental glomerulosclerosis (FSGS)

and accts for 15% of nephrotic syndrome cases in adults and children (1/6 of cases)

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37
Q

T/F: Immune complexes are always in FSGS, pointing to the cause of dz.

A

False.

Immune complexes are not always seen and focal sclerosis appears to be idiopathic.

commonly seen in AIDS pts [d/t dz or drug toxicity; drugs like NSAIDs, lithium, interferon implicated]

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38
Q

T/F: In contrast to minimal change disease, patients with focal segmental glomerulosclerosis are far more likely to present with non-selective proteinuria.

A

True

clinical outcome often poor
inevitable renal failure

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39
Q

The hypercellularity of post-infectious glomerulonephritis is due to increased numbers of:

A
  • epithelial, endothelial, and mesangial cells

* presence of neutrophils in/around the glomerular capillary loops

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40
Q

T/F: Rapidly progressive glomerulonephritis (RPGN) is a description, not a specific disease.

A

True

it can be seen d/t a variety of causes
only rarely seen as result streptococcal infx

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41
Q

MC cause of chronic renal failure in the US:

Thus it’s called:

A

DM

Diabetic nephropathy

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42
Q

In many diabetics, renal sx are (sudden/insidious) and findings include:

A

insidious - over 10-20 years

proteinuria
glycosuria
progressive decrease of renal function

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43
Q

Possible renal complications due to diabetes:

A

arteriosclerosis
glomerulosclerosis
pyelonephritis
renal failure

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44
Q

A commonly noted histologic change seen in patients who develop diabetic nephropathy:

A

glomerulosclerosis - generally appears several years after onset of DM

described as: nodular, diffuse, or mixed

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45
Q

Nodular glomerulosclerosis related to diabetes is referred to as:

A

Kimmelstiel-Wilson disease

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46
Q

The first abN lab in diabetic nephropathy is:

A

microalbuminuria

may also show glucose
late findings - elev serum creatinine and BUN

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47
Q

Etiology of primary amyloidosis:

Characterized by:

A

idiopathic

amyloid depositions in one or more organs

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48
Q

Histologically, amyloid appears:

Light microscopy:

A

pink
eosinophilic
acellular

homogenous
highly refractive
affinity for Congo red

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49
Q

With renal involvement, amyloid is first deposited in:

A

mesangium and capillary walls

eventually in glomerular & tubular BM

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50
Q

Pt undergoes a procedure, and starts to develop spontaneous periorbital ecchymosis without trauma to the face. What should be in your ddx?

A

Amyloidosis

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51
Q

UA of pts with amyloid dz shows:

A

protein
fatty casts
fat bodies

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52
Q

Characteristic amyloidosis finding w/electron microscopy:

A

fibrils within the amyloid deposition

non-branching filaments, 8-12nm wide, perpendicular to BM

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53
Q

Acute nephritis is characterized by the presence of:

A
  • hematuria with red blood casts
  • oliguria
  • uremia
  • varying degree of HTN
  • minimal (no) proteinuria
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54
Q

MC cause worldwide of glomerulonephritis:

A

IgA nephropathy (aka Berger’s dz)

d/t marked hyper secretion of IgA in response to an antigenic stimulus)

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55
Q

T/F: Edema is most usually associated with nephritic syndrome.

A

False - not usually, if present it is mild.

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56
Q

Findings of nephritic syndrome:

A

PHAROH

  • proteinuria
  • hematuria
  • azotemia (elev blood N)
  • RBC casts (KEYNOTE)
  • oliguria
  • HTN (KEYNOTE)
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57
Q

IgA nephropathy is more common in pts with ________.

A

celiac dz

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58
Q

IgA nephropathy pts generally present with new onset hematuria within days of:

A

a respiratory, gastrointestinal or genitourinary infx

usu disappears in days, my recur for mos/yrs
50% renal failure @20yrs

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59
Q

Another dz state of IgA over-secretion, a hypersensitivity vasculitis involving blood vessel walls in the skin, kidneys and/or G.I. tract:

A

Henoch-Schonlein purpura

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60
Q

Exam findings in H-S purpura:

A

PE: skin lesions, jt tenderness
UA: hematuria
Skin bx: vasculitis

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61
Q

H-S purpura may occur at any age, but peak incidence is:

A

3-8 yrs

more severe sx/sequelae in adults

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62
Q

Mesangial deposits - if IgA could be:

If IgG:

A

IgA - H-S purpura OR IgA nephropathy

IgG - lupus nephritis

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63
Q

Primary or secondary immune-mediated renal disease characterized by inflammation of the glomeruli:

A

Glomerulonephritis

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64
Q

Glomerulonephritis may present with:

A
  • isolated hematuria and/or proteinuria
  • nephrotic syndrome,
  • nephritic syndrome
  • acute renal failure
  • chronic renal failure
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65
Q

Non-proliferative glomerulonephritis is characterized by:

Frequently present with (nephritic/nephrotic) syndrome.

A

low numbers of cells (lack of hypercellularity) in glomeruli.
nephrOtic

(e.g. MCD, FSGS)

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66
Q

Proliferative glomerulonephritis is characterized by:

Often present with (nephritic/nephrotic) syndrome and can progress to end-stage renal failure in:

A

increased number of cells (hypercellularity) in the glomerulus.
Nephritic
weeks to years

67
Q

MC cause of acute nephritic syndrome:

A

PSGN (post-streptococcal glomerulonephritis)

68
Q

T/F: PSGN can follow strep throat or impetigo.

A

True

nephrogenic strain of group A beta-hemolytic strep
[compare to Rheumatic Heart Dz - pharynx strain only]

69
Q

PSGN ssx:

A 
1-2 wk latency after infx
RBCs on UA
possible casts
fever
chills
HTN usu develops
70
Q

T/F: Early abx intervention appears to significantly alter the course of PSGN.

A

False

this suggests genetic disposition to certain strains

71
Q

Light microscopy of the glomeruli affected by PSGN usually reveal infiltration by:

A

PMNs and mononuclear macrophages

Endothelial and mesangial proliferation

72
Q

Immunofluorescent studies of PSGN demonstrate a granular deposition of:
Electron microscopy characteristically shows:

A

IgG, C3 and mesangial fibrin

“lumpy” appearance w/ dx finding of sub-endothelial “clumps of humps”

73
Q

Broad term for the type of glomerular destruction and renal dz that may be d/t several different etiologic agents:

A

RPGN (rapidly progressing)

must often begin dialysis and/or await renal transplantation in order to survive.

74
Q

Initial symptoms of RPGN:

A

hematuria
oliguria
HTN

75
Q

Conditions known to cause or increase the risk for RPGN:

A 
vasculitis
polyarteritis
SLE
Goodpasture's syndrome
H-S purpura
IgA nephropathy
membranoproliferative GN
internal organ abcess (any)
Hx of malignant tumor
blood/lymph system d/o
hydrocarbon solvent exposure
76
Q

RPGN is also called __________ GN, for the characteristic bands of ________ that form around _________________.

A

Crescentic
fibrin
glomerular capillaries throughout capillary tufts

77
Q

With RPGN, immunofluorescent staining reveals:

A

deposition of IgM, IgG and fibrin:

  • 1/3 granular
  • 1/3 linear
  • 1/3 non-specific
78
Q

Goodpasture’s often presents with RPGN and is characterized by _________________.
It is MC seen in___________ in their 20s and 30s.
___________ is common.
IgG deposition in a _______ pattern.

A

Circulating anti-basement membrane antibodies
Caucasian males
Pulmonary hemorrhage
linear

79
Q

Goodpasture’s is usu treated aggressively with:

Cause of death is usu:

A

steroids, chemo, plasma exchange

pulmonary hemorrhage

80
Q

Form of vasculitis that commonly involves kidneys, with potential for multi-organ involvement:
Presenting sxs may be:

A

Wegener’s granulomatosis

  • mucosal surface inflammation & ulceration
  • purulent otitis media
  • severe sinusitis.
  • hemoptysis
  • pleuritis
81
Q

Wegener’s granulomatosis findings:

A
  • lung nodules/infiltrates
  • conjunctivitis
  • scleritis/episcleritis
  • swelling/hemorrhage/ulceration of the gums
82
Q

The classic renal pathology in Wegener’s is ______________________ accompanied by ___________ of renal vessels.

A

the combination of focal & segmental glomerulonephritis

granulomatous vasculitis

83
Q

T/F: In Wegener’s, serology is often positive for P-ANCA.

A

False - C-ANCA

P-ANCA is seen in polyarteritis nodosum, another vasculitis.

84
Q

Acute tubular necrosis is characterized by _____________ and is usu classified as being either ______ or ________.

A

proximal tubular epithelium necrosis
toxic or ischemic

Necrotic cells fall into the tubule lumen, obliterating it and eventually resulting in acute renal failure.

85
Q

In toxic ATN, the affected tubular cells characteristically reveal an (absence/abundance) of nuclei and a (heterogenous/homogenous) cytoplasm which stains (mildly/intensely) eosinophilic and preserves it’s normal shape.

A

absence
homogenous
intensely

86
Q

T/F: full recovery of renal function is possible if the underlying ATN cause is removed.

A

True

Because tubular cells normally undergo continual replacement

87
Q

Ischemic ATN causes ________ through the tubules due to differences in ________ within the kidney

A

skip lesions

perfusion

88
Q

Acute interstitial nephritis (AIN) is MC a result of:

It may also be linked to ___________ and may result in ___________.

A

an allergic response to a drug

infectious agents (CMV, streptococcus, legionella)
acute rejection of a renal transplant
89
Q

AIN may be in the ddx when acute renal dz begins after ___________ or the start of a ______________.

A 
recent infx
new medication 
* ibuprofen/NSAIDs
* acetaminophen
* penicillin
* cephalosporin
* cimetidine
* thiazide diuretics
* cyclosporin
90
Q

AIN refers to:

A

presence of edema, inflammatory cell infiltration in renal parechyma, and often tubular injury

drug/infx agent acts as hapten, binds to membrane binding site, w/ 2° immune-mediated injury (type I or IV).

91
Q

Dx findings of AIN:

A

Eosinophilia (serum, urine)

definitive - kidney bx

92
Q

Chronic interstitial nephritis (CIN) is caused by disorders that ultimately lead to _________ of the _________.
Causes include:

A

progressive scarring
interstitium

  • persisting AIN
  • hematologic malignancies (lymphoma, mult myeloma)
  • chronic exposure to toxin (lead)
93
Q

T/F: CIN has no cure.

A

True
some pts will require dialysis
mb eventual transplanation

94
Q

Histopathology of CIN:

A
  • interstitium expanded by fibrosis
  • distortion of tubules
  • peri-glomerular fibrosis
  • glomerulus unchanged
95
Q

Dz of the proximal renal tubules in which glucose, amino acids, uric acid, phosphate & bicarbonate are passed into the urine instead of being reabsorbed:

A

Fanconi’s syndrome

hereditary
drugs
heavy metals

96
Q

T/F: The term renal tubular acidosis (RTA) refers to individuals with poor urinary acidification d/t poor-functioning kidneys.

A

False

RTA refers to poor acidification in otherwise healthy kidneys, and several types exist (1, 2, 4)

97
Q

Compare types 1, 2, and 4 of RTA.

Consider location, acidosis, potassium, & pathophys.

A

Type 1 - distal tubules
severe acidosis
hypOkalemia
no H+ secretion by intercalated cells

Type 2 - proximal tubules
mod. acidosis
hypOkalemia
too little HCO3 reabsorption

Type 4 - adrenal
mild acidosis
hypErkalemia
resistance to/low aldosterone

98
Q

Light microscopy of Fanconi’s:

A

atrophic and hyalinized glomeruli

seen in end-stage kidney dz

99
Q

Analgesic nephropathy occurs after ingestion of (small/large) amounts of analgesics over a (short/long) period of time.

A 
large
long
(vs. AIN which mb 1 dose/short course)

leads to papillary necrosis, spares cortex

100
Q

Two of the MC drugs responsible for analgesic nephropathy:

A

acetaminophen [covalent bond to papilla, 2° oxid. dmg]

aspirin [inhibits prostaglandin synthesis]

101
Q

Atherosclerotic changes in the renal blood vessels:

A

benign nephrosclerosis

occurs as a renal complication of HTN (seen on bx in diabetics w/HTN)

102
Q

The surface of the benign nephrosclerotic kidney has a characteristic granular appearance due to:
Microscopically:

A

patchy ischemic atrophy w/in the kidney
focal loss of parenchyma

hyaline thickening of walls of small arteries/arterioles

103
Q

Malignant nephrosclerosis:

A
  • severe changes in renal architecture d/t malignant HTN
  • focal small hemorrhages
  • small arteries/arterioles become hyperplastic, “onion ring” appearance
104
Q

Narrowing or blockage of a renal artery is called __________ and mb d/t

A

renal artery stenosis (RAS)

  • atherosclerosis
  • fibromuscular dysplasia of renal a.
  • atheroembolic renal dz
  • scar formation
105
Q

T/F: Renal artery stenosis often causes mild HTN that responds well to treatment.

A

False

often causes HTN that may be severe and resistant to tx

106
Q

How is RAS typically found?

A

on work up for difficult to control HTN

in some cases bruits mb heard in mid-back
among the MC causes of 2° HTN

107
Q

Systemic dz that results in widespread thrombosis in capillaries & arterioles, and may have a significant effect on the kidneys and renal function.

A

Thrombotic microangiopathy

hallmark: widespread formation of hyaline thrombi in microcirculation (dense platelet accumulations surrounding fibrin)

108
Q

The 2 MC conditions with thrombotic microangiopathy:

A

HUS and TTP

[or mb better HUS/TTP syndrome d/t overlap]

Hemolytic uremic syndrome
thrombotic thrombocytopenic purpura

109
Q

What appears to be the initiating event in thrombotic microangiopathy?

A 
Endothelial injury resulting in thrombus formation
triggers:
* bacterial endotoxins
* cytotoxins
* cytokines
* viruses
* drugs 
* endothelial abs 
* septicemia
and in many cases is unknown
110
Q

Classic triad of HUS:

A
  • acute renal failure
  • microangiopathic hemolytic anemia
  • thrombocytopenia
111
Q

MC causes of acute renal failure in children:

which involved bacteria is MC?

A

HUS

E coli 0157:H7
verocytotoxin releasing bacteria

112
Q

How does HUS work?

A
  • Endothelium shows inc. adhesion of leucocytes.
  • Inc endothelin production.
  • Loss of endothelial nitric acid production.
  • Cytokines (eg TNF) involved in lysis of endothelial cells.
  • Resultant vasoconstriction & thrombosis causing classis microangiopathy.
113
Q

Hx finding in HUS:

A
  • recent gastroenteritis (83%)
  • fever (56%)
  • bloody diarrhea (50%)
  • seizures
  • acute renal failure
  • anuria
114
Q

Histopathology of HUS:

A
  • capillary lumens often occluded by debris/thrombi
  • patchy or diffuse microangiopathy
  • swelling of endothelium
  • cortical necrosis
  • thick capillary walls in glomeruli
115
Q

HUS/TTP syndrome in adults follows/correlates with:

A
  • viral infx
  • septicemia
  • typhoid, shigella, E coli
  • SLE, scleroderma
  • antiphospholipid ab
  • malignant HTN
  • chemo/immunosuppressive drugs
  • pregnancy/post-partum
116
Q

Source of most renal artery emboli?

A

a cardiac source (i.e. enlarged left atrium)

MC non-cardiac source - ruptured aortic atheromatous plaque (spontaneous or post-sx/angioplasty)

incidence increases with age

117
Q

Biopsy of renal tissue affected by embolic disease often reveals

A

cholesterol laden emboli w/in involved arteries

cholesterol usu dissolves leaving cleft-like spaces on slides

118
Q

T/F: Renal ischemia of any kind will show poor uptake of “vital” stain, which are taken up by metabolically active cells.

A

True

A gross specimen of ischemic renal tissue may appear normal but anoxic tissue to the degree of infarction will have a classic wedge-shape to the infarcted tissue

119
Q

Kidney stones (renal calculi) are:

A

crystalline accumulations that precipitate out of urine they would normally be dissolved in.

120
Q

Does dehydration contribute to stone formation?

A

Yes, because the resulting supersaturation by one or more substances will precipitate out of solution.

121
Q

Kidney stones most often develop in the ________ of the kidney and are usu composed of ___________________.

A

pelvis

  • oxalates
  • phosphates
  • uric acid
  • carbonates
122
Q

Approx 75% of kidney stones are:

A

calcium oxalate stones

123
Q

Remaining 25% of kidney stones are:

A

15% - triple phosphate (struvite) stones
6% - uric acid
1% - cystine

124
Q

T/F: Most calcium oxalate stones are assoc w/ hypercalcemia & hypercalciuria.

A

False! only 5%

abN renal absorption of Ca+ is found in 55%
risk factor: inc serum oxalate
many pts w/stones have NO risk factors

125
Q

Triple phosphate stones (magnesium ammonium phosphate) are seen most commonly in association with:

A

UTIs by bacteria which are urea-splitting:

  • proteus spp.
  • staphylococcus (some)

these convert ammonia to urea => increase pH

126
Q

Staghorn crystals are:

A

triple phosphate stones

some of the largest!

127
Q

Uric acid crystals are seen in:

A
  • normal pts (esp w/acidic urine
128
Q

Cystine stones are caused by:

A

genetic defects in the renal reabsorption of amino acids, including cystine, leading to cystinuria.

Precipitate more readily out of acidic urine.

129
Q

Benign tumors of the kidneys are generally (severe/moderate/asx) and are usually noted ______________.

A

asx

incidentally on autopsy

malignant tumors of the kidney cause considerable morbidity and mortality.

130
Q

Benign renal tumors:

A
  • Renal papillary adenoma (fronds)
  • Renal fibroma or hamartoma
  • Angiomyolipoma
  • Oncocytoma
131
Q

Renal adenomas are often called ______________ because they are MC found in the __________. Most are __mm or (less/more)

A

papillary adenomas

papilla

5mm or less

132
Q

Epithelial tumor composed of oncocytes, large eosinophilic cells that are round to polygonal shaped cells with benign-appearing nuclei with large nucleoli:

A

oncocytoma

133
Q

Characteristic histopathology of oncocytoma:

Electron microscopy:

A
  • large polygonal cells
  • round nuclei
  • uniform appearance
  • numerous prominent mitochondria, “stacked”
134
Q

Primary renal malignancies include:

A
  • renal cell carcinoma
  • transitional cell carcinoma
  • papillary & non
  • Wilm’s tumor (nephroblastoma)
  • renal sarcoma
  • lymphoma
135
Q

MC kidney malignancy:

A

Renal cell carcinoma (85%)

2nd - mets
2nd primary renal malignancy - TCC

136
Q

RCCA is (asx/painful) in early stage, sx are (specific/nonspecific) and mb:

A

asx - until advanced stage (25% have distant mets on dx)

fever
malaise
weakness
wt loss

137
Q

Class triad of RCCA that suggests advanced dz:

A

flank pain
hematuria
palpable abd mass

138
Q

Major risk factors for RCCA:

A 
TOBACCO
cadmium/asbestos exposure
FHx
obesity
HTN
unopposed estrogen therapy
radiation therapy to kidney area
139
Q

RCCA tumors range from _______ cm.

A

2-25cm!

140
Q

What are the 5 types of RCCA? Which is most prevalent?

A 
Clear cell carcinoma (75-85%)
chromophilic carcinoma
chromophobic carcinoma
oncocytic carcinoma
collecting duct carcinoma
141
Q

Histologic appearance of RCCA:

A

neoplastic cells
clear cytoplasm
nest of tumor cells w/intervening vessels

142
Q

Common sites of mets for RCCA:

A 
lungs
lymph nodes
bone
liver
brain
ipsilateral adrenal gland
contralateral kidney
renal vein -> vena cava
143
Q

Risk factors for urothelial (transitional cell) carcinoma:

A 
Cigarette smoking (lower risk w/pipes, etc)
chemical exposure
- petroleum
- paint
- pigments
 * aniline dyes
- agrochemicals
144
Q

MC primary renal tumor in children:
Age of dx:
Related to defects in:

A

Wilm’s tumor
2-5 y.o.
chromosome 11

145
Q

Pt’s with Wilm’s tumor have a noted propensity for:

A

developing other kinds of primary tumors

  • genito-urinary tumors
  • bone tumors
  • soft tissue sarcoma
  • leukemia
146
Q

MC cause of hydronephrosis in infants/children:

A

ureteropelvic junction obstruction

147
Q

Abnormal movement of urine from the bladder into the ureters and potentially to the kidneys:

A

vesicoureteral reflux

148
Q

Obstructive lesions of the ureter:

A
  • calculi - usu
149
Q

Bilateral ureteral obstruction generally occurs as a result of __________, where unilateral obstruction is typically ________.

A

ascending pathology from (near) the bladder - BPH, tumor

descending pathology from the kidney

150
Q

MC ureteral malignancies:

A

Transitional cell carcinoma (TCC)

151
Q

Failure of normal development of the anterior wall of the abdomen and bladder:

A

exstropy - repairable with surgery

inc risk of bladder adenocarcinoma later in life

152
Q

Embryological canal connecting the urinary bladder with the allantoids, which is normally obliterated during development, but leads to risk of cysts when persisting:

A

urachus

bladder adenocarcinoma can arise in cysts

153
Q

Inflammation or infection of the urinary bladder:

A

cystitis

154
Q

Microscopically, the urothelial mucosa of the bladder in chronic cystitis show inflammatory cells in the _____________.

A

lamina propria - mostly lymphocytes

155
Q

Pattern of bladder change as a result of chronic inflammation:

A

malakoplakia

156
Q

Malakoplakia, microscopic findings:

A

foamy histiocytes
round basophilic inclusions
* Michaelis-Gutmann bodies (pathognomonic)

157
Q

Urinary bladder dz of unknown origin characterized by dysuria, frequency, urgency, and pressure:

A

interstitial cystitis

158
Q

Definitive dx of IC requires:

A

cystoscopy

159
Q

The pathognomonic lesion of IC:

A

Hunner’s ulcer

160
Q

Non-infectious causes of IC:

A

cytotoxic anti tumor drugs
* methotrexate
* cyclophosphamide
radiation to the bladder

161
Q

MC bladder cancer:

A

TCC

M:F 3:1

162
Q

Bladder cancer risk factors:

A 
cigarette smoking
long term use of analgesics
radiation to the bladder
aryl amine exposure (industrial)
schistosomiasis infx
163
Q

What are the 2 distinctive precursor bladder cancer lesions:

A
  • noninvasive papillary tumors - MC

* urothelial carcinoma in situ (CIS) - worse prognosis

Pathology IV (6 decks)

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