Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Renal Path MC > Renal 5 > Flashcards

Renal 5 Flashcards

(80 cards)

Start Studying
1
Q

examples of interstitial disease

A

ischemic papillary necrosis, toxic and HS (drugs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

most common cause of intrinsic renal disease and ARF

A

ATN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

two most common causes of ATN

A

acute toxic or ischemic damage (loss blood flow)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

this combination depicts spectrum of symptoms present in ATN

A

loss tubular function and GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what occurs due to toxic or ischemic damage of tubules

A

acute necrosis of tubular epithelium with acute suppression renal function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what occurs intracellularly due to tubular ischemic injury

A

depletion ATP, accumulation Ca, activation proteases and phospholipases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

morphology of ATN (regardless of etiology)

A

focal tubular epithelial necrosis/apoptosis, rupture BM, occlusion tubular lumens by casts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

part of tubule most commonly injured by toxins

A

proximal segment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

toxicity of carbon tetrachloride is characterized by this

A

neutral lipid accumulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

characterizes ethylene glycol poisoning of kidney

A

ballooning and hydropic or vacuolar degeneration w/ formation calcium oxalate crystals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what occurs in initiating phase of ATN

A

declining urine output, increasing BUN (36 hours)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what occurs in recovery phase of ATN

A

increase urine output (3 L/day), hypokalemia, gradual improvement concentrating ability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what occurs in maintenance phase of ATN (several days)

A

diminished renal output, salt and water overload, increased BUN, hyperkalemia, metabolic acidosis (ALL FROM DECREASED GFR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

possible causes of acute interstitial nephritis

A

HS to drugs or metabolic dysfunction, ARF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

gentimycin potentially causes this kind of kidney damage

A

ATN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

synthetic penicillins (methicillin, ampicillin) potentially cause this kind of kidney damage

A

acute interstitial nephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

drugs that are known to cause acute interstitial nephritis

A

sulfonamides, synthetic penicillins, diuretics (thiazides), NSAIDS (phenylbutazone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

chronic analgesic abuse is associated with development of this

A

transitional papillary carcinoma of renal pelvis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

this is associated with development of transitional papillary carcinoma of renal pelvis

A

chronic analgesic abuse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

causes of papillary necrosis

A

analgesic nephropathy, diabetes, urinary tract obstruction, sickle cell (anemia or trait), renal TB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

benign renal tumor with eosinophilic cells and LOTS of mitochondria

A

oncocytoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

clinical presentation of Wilm’s tumor (nephroblastoma)

A

large abdominal mass, hematuria/pain after trauma, intestinal obstruction, HTN (damage to blood flow)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what renal cell carcinoma tumors arise from

A

tubular epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

nephrotoxic agents that can cause ATN

A

gentamicin, radiographic contrast agents, heavy metals, carbon tetrachloride

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
common scenarios that lead to ATN
transfusion reaction, ethylene glycol or methanol poisoning, hemoglobinuria or myoglobinuria (crush injury, alcohol binges), shock
26
ischemic changes seen in tubular cell injury
cell swelling, blebbing, loss of polarity, necrosis/apoptosis
27
this signals feedback mechanism to constrict afferent arteriole (decreasing delivery of filtrate) in ATN pathogenesis
increased Na in distal tubules
28
this complicates tubular ischemia (other than change in glomerular flow rate)
reflex vasoconstriction and decreased GFR
29
this determines re-epithelializatoin and return of tubule function
integrity tubular BM
30
this makes up casts in ATN -> huge glycoprotein secreted in loop of Henle and distal tubules
Tamm-Horsfall protein
31
these all contribute to cast formation in ATN (eosinophilic hyaline or pigmented granular casts)
Tamm-Horsfall protein, hemoglobin, myoglobin, plasma proteins
32
where Tamm-Horsfall proteins are secreted
loop of Henle and distal tubules
33
morphology of regenerating epithelial cells
flattened, hyperchromatic nuclei, mitotic figures
34
form of ATN that is usually related to non-oliguric presentation (50%)
toxic
35
primary cause of interstitial disease; secondary?
infection, toxin, obstruction; vascular, cystic, glomerular disease progression
36
this distinguishes interstitial nephritis from other renal disease
absence nephritic/nephrotic syndrome
37
signs of secondary tubular function defect related to interstitial disease
impaired concentrating ability, salt wasting, metabolic acidosis, isolated defect tubular reabsorption/secretion
38
possible cause of chronic interstitial nephritis; what is morphology?
slowly progressing toxic dysfunction (analgesic abuse); infiltration mononuclear cells, interstitial fibrosis, tubular atrophy
39
symptoms of HS reaction in acute drug-induced interstitial nephritis -> 2-6 weeks after exposure
fever, eosinophilia, rash (25%), renal abnormalities (ARF, increasing serum Cr)
40
associated condition with chronic analgesic abuse
chronic tubulointerstitial nephritis with renal papillary necrosis
41
this analgesic has metabolites with direct toxic effects to the kidney; how does it cause damage?
phenacetin; oxidative damage
42
this potentiates phenacetin oxidative injury on kidney
prostaglandin inhibitors (causes ischemia)
43
what occurs first in chronic analgesic abuse: papillary necrosis or tubulointerstitial nephritis?
papillary necrosis
44
morphology of acute HS interstitial nephritis
edema, interstitial monocyte/lymphocyte infiltrate (some PMN and eosinophil also)
45
these drugs cause interstitial granuloma formation
methicillin, thiazides
46
chronic morphological changes in interstitial nephritis
tubular atrophy, interstitial fibrosis, inflammation, surface depression, papillary necrosis/calcification/fragmentation, coagulative necrosis
47
signs/symptoms of analgesic nephropathy
inability concentrate urine, metabolic acidosis, stone formation, HA, anemia, GI symptoms, HTN
48
consequences of papillary necrosis
urinary obstruction, infection, stone formation
49
various mechanisms of NSAID nephropathy
lack vasodilation causing ARF, acute HS reaction, acute interstitial nephritis and lipoid nephrosis, membranous GN w/ nephrotic syndrome
50
consequence of hypercalcemia and nephrocalcinosis -> deposition of calcium leading to chronic tubulointerstitial disease
tubular atrophy, interstitial fibrosis and inflammation
51
mechanisms of interstitial fibrosis
CRF, transplant, angiotensin II (chronic activation RAS), TGF-b induction thru NFK-b
52
direct complications of MM tumor leading to renal disease
hypercalcemia, hyperuricemia, obstruction ureters
53
forms of MM related kidney disease
light-chain GN, tubular obstruction and cast nephropathy (deposition, combine with Tamm-Horsfall to make casts)
54
morphology of MM kidney disease
Bence Jones tubular casts, adjacent interstitial inflammation, amyloid deposits, granulomatous inflammatory rxn
55
MM related ARF may be precipitated by these factors
dehydration, hypercalcemia, infection, nephrotoxic antibiotics
56
characteristic of amyloidosis
Congo red positive fibrillary deposits in mesangium and sub endothelium, obliteration glomerulus, blood vessel walls, kidney interstitium
57
where are benign renal papillary adenomas found? what are they derived from?
cortex; tubular epithelium
58
renal papillary adenoma does not differ from this malignant cancer -> only distinguishing feature is size
low-grade papillary renal cell carcinoma
59
benign renal tumor in children
cystic nephroma
60
most common primary renal tumor of childhood (ages 2-5)
Wilm's tumor (nephroblastoma)
61
inheritable syndromes of wilm's tumor associated with this
specific aberrations multiple loci chromosome 11 (WT1 -> tumor supressor gene)
62
premalignant condition associated with wilm's tumor -> multi centric or diffuse foci immature nephrogenic elements
nephroblastomatosis
63
found in nephroblastomatosis (premalignant) -> second genetic insult results in malignant tumor formation
immature nephrogenic elements
64
diagnostic morphology of Wilm's tumor
recapitulation different stages nephrogenesis, metanephric blastemic and immature stromal/epithelial elements
65
this may represent precursor lesions to Wilm's tumor
neprogenic tests
66
associated clinical syndrome of Wilms tumor -> WAGR
wilms tumor, aniridia, GU anomalies, mental retardation
67
associated clinical syndrome of Wilms tumor -> Denys-Drash syndrome (DDS)
wilms tumor, intersexual disorders, glomeruopathy
68
associated clinical syndrome of Wilms tumor -> Beckwith-Wiedemann syndrome (BWS)
wilms tumor, overgrowth (gigantism), visceromegaly, macroglossia
69
renal cell carcinoma cells resemble these
clear cells of adrenal cortex
70
risk factors for renal cell carcinoma
tobacco, obesity, HTN, unopposed estrogen tx, asbestos/petroleum exposure, CRF, dialysis (acquired cystic disease)
71
genetic abnormality associated with clear cell carcinoma (most common renal cell carcinoma)
unbalanced translocation chromosome 3 -> loss of VHL gene
72
what gives rise to chromophobe renal carcinoma (excellent prognosis)
intercalated cells collecting ducts
73
autosomal dominant cause of renal cell carcinoma -> characterized by renal cysts and bilateral renal cancer, hemangioblastomas of cerebellum and retina
Von Hippel-Lindau syndrome
74
genetic abnormalities in hereditary papillary carcinomas
trisomies 7, 16, 17, loss of y in male, mutation c-met protooncogen
75
morphology of renal cell carcinoma
upper pole (more commonly), solitary or unilateral lesion, bright yellow/gray-white, large necrotic area
76
where does renal cell carcinoma tend to fungate?
ureter and renal vein (thru IVC to right side of heart)
77
morphology of papillary tumors
multifocal or bilateral, hemorrhagic and cystic
78
can stain for these components in clear cell carcinoma
glycogen and lipids
79
morphology of clear cell carcinoma
rounded or polygonal, delicate branching vasculature, cystic or solid, glycogen and lipids
80
morphology of papillary carcinoma
papillary formations, cuboidal or low columnar cells, psamomma bodies

Renal Path MC (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions