1
Q
where are renal cysts usually located
A
cortex
2
Q
what are the 3 mechanisms for urinary cysts
A
1) obstructive
2) altered tubular basement membrane
3) disordered growth of tubular epithelial cells -> focal hyperplastic lesions
3
Q
what are the types of polycystic kidney disease
A
- Autosomal dominant PKD
- Autosomal recessive PKD
- Congenital PKD
4
Q
what are the characteristics of ADPKD (Autosomal dominant PKD)
A
- bilaterally the convoluted tubules expand -> renal failure
- may or may not have hepatic or pancreatic cysts as well
5
Q
what mutation is responsible for ADPKD and in what breed
A
PKD1 (polycystin proteins) - Persians
6
Q
ARPKD may or may not be associated with
A
biliary cysts
7
Q
what is CPKD associated with
A
- stillbirth
- renal failure (fatal) in first weeks of life
8
Q
what are signs that PKD started at the same time in a kidney
A
all the cysts are uniform in size
9
Q
what is the flow of blood and relative demand in the cortex? what is the cortex sensitive to?
A
cortex: high flow, high demand and sensitive to hypoxia
10
Q
blood from most glomeruli supplies what area of the kidney
A
cortex (with veins exiting directly)
11
Q
what glomeruli supply most of the blood to the medulla to allow maintenance of blood flow
A
juxtamedullary glomeruli
12
Q
what allows maintenance of oxygenation and blood flow in the medulla to protect against hypoxia (3)
A
- autoregulation of blood flow
- prostaglandins
- nitric oxide
13
Q
why do NSAIDs cause medullary necrosis? what is a consequence?
A
they inhibit the protective effects of autoregulated blood flow and prostaglandins in the medulla -> medullary hypoxia -> medullary necrosis
consequence: necrotic debris can emboli -> obstruction
14
Q
what are signs of acute papillary (medullary) necrosis
A
- hematuria
- proteinuria
- casts
- oliguria -> polyuria
15
Q
over time, with renal papillary necrosis we see what effect on renal concentrating ability
A
poor concentration function (since the main role of the medulla = concentrating)
16
Q
T/F infarcts are commonly seen in the kidney and are much less frequently clinically significant
A
T
17
Q
the lesions observed due to infarction are directly influenced by (2)
A
- the cause
- the vessel affected
18
Q
if you see an infarct in the cortex, what vessels are likely affected
A
interlobular and arcuate
19
Q
if you see an infarct extending from the cortex into the medulla what vessels are likely affected
A
interlobar (can anyone confirm)
20
Q
what is a sign that an infarct is chronic
A
sinking down (contracting)
21
Q
where do infarcts tend to form in cats? what does it resemble?
A
at the poles; pyelonephritis
22
Q
renal neoplasia is (common/rare) ; the 3 main types are:
A
rare; adenoma, carcinoma, nephroblastomas
23
Q
of the types of neoplasia, which is most rare? when it is seen, it is most common in (2)
A
adenoma; horse, cow
24
Q
what species are most likely to get renal carcinomas
A
cows > dogs, horses
25
what species are most likely to get renal nephroblastomas
chickens, pigs
26
in general, renal neoplasms are well/poorly demarcated
well
27
T/F you can distinguish between renal adenoma and carcinoma on post-mortem
F
28
what are 3 characteristics of renal carcinomas (1 is on histo and 2 are gross)
- protrude
- often > size of kidney
- clear cells
29
are male or female dogs more likely to get renal carcinoma
male
30
what is the appearance of most renal carcinomas on gross section
mixed red and tan ; tan = necrosis; red = hemorrhage
31
what type of neoplasia is most common in young animals
nephroblastoma
32
what do we often see in animals with nephroblastoma
cartilage and stroma in the tumor (since it is a tumor of pluripotent cells)
33
what is the term for nephroblastoma when it occurs in the spinal column of dogs; hint: "____________ ______________ tumor of young dogs"
why does this happen?
"thoracolumbar spinal tumor of young dogs"
due to improper migration of cells during development
34
what is the most common type of renal neoplasm in cats
lymphoma (remember it can go wherever it wants)
35
what 2 forms can renal lymphoma have
diffuse and nodular
36
one of the most important roles of the kidney is to maintain (3)
- salt
- H2O
- K
37
what molecules does the kidney produce
- renin
- EPO
- prostaglandins
- active Vitamin D
38
what are the 3 basic needs of the kidney
1) adequate inflow (renal perfusion)
2) adequate functional mass (GFR)
3) adequate outflow (aka no obstruction)
39
what are the components of the glomerular filter
- endothelium
- fenestrated basement membrane
- epithelium
40
all 3 components of the endothelium are (anionic/cationic)
anionic
41
what are the 2 types of selection the glomerular filter uses
- sized based (small molecules get through)
- charge based (anions get through, cations do not)
42
what are the 4 types of glomerulonephritis
- membranous
- proliferative (mesangioproliterative)
- membranoproliferative
- glomerulosclerotic
43
what type of glomerulonephritis is end-stage
glomerulosclerotic (fibrosis)
44
___________ occuring in the absence of _____________ is suggestive of glomerular damage
proteinuria in the absence of urinary tract inflammation
45
TF membranous glomerulonephritis is counterintuitive because it involves thickening of the glomerular wall but more leakiness
T
46
at what point does glomeruloephritis go from leakier to less leaky
when it becomes glomerulosclerotic
47
what are the 3 pathogeneses of glomerulonephritis and which is the #1 cause in vetmed
- alternative complement activation
- **immune complex deposition**
- anti glomerular basement membrane disease
48
what is the pathogenesis of immune complex glomerulonephritis
deposition of circulating Ab-Ag complexes in the:
- subendothelium
- subepithelium
- intramembranous
leading to complement activation
49
we believe immune complex glomerulonephritis occurs when
antigen is in slight excess of antibody (or even)
50
T/F any infection of high pathogenicity that is able to produce persistent antigenemia has the potential to cause immune-complex disease
F; low pathogenicity
51
T/F renal biopsies are only useful for acute diseases as the histological features are the same for acute vs chronic
T; can tell apart acute from chronic grossly
52
what is the pathogenesis by which immune complex deposition and subsequent complement activation leads to chronic glomerulonephritis
injury to glomerulus -> decreased filtration of protein -> proteinuria damages/activates tubules -> pro-inflammatory cytokines, growth factors produced -> interstitial fibrosis -> altered blood flow -> hypoxia
fibrosis further affects renal function
53
what happens if antigen exposure is resonably short and can be cleared in patients with immune complex glomerulonephritis
resolution and some repair/clearance of complexes
54
what makes progression to end-stage renal failure irreversible in patients with immune complex glomerulonephritis
when GFR decreases to 30-50% of normal (due to fibrosis)
55
what are the types of amyloidosis
- reactive (secondary)
- immunoglobulin derived (primary)
- familial (can be reactive or immunoglobulin derived)
- apolipoprotein
- islet amyloid polypeptide
56
what are characteristics of amyloidosis and why
massive proteinuria without fibrosis; due to damage induced by pressure atrophy from amyloid deposition
thrombosis; hypercoagulable state
57
amyloidosis is most common in (age and species)
older dogs
58
in cats and cows amyloidosis tends to be medullary which has what consequence
impaired concentrating ability
59
T/F histo will tell you that amyloidosis has occured
F; need special staining
60
what are the outcomes of massive proteinuria
- thrombosis (loss of antithrombin III and TPA)
- nephrotic syndrome (leads to hypoalbuminemia, edema, and hyperlipidemia)
61
why is embolic nephritis common
the kidney has lots of bloodflow and is therefore susceptible to hematogenous pathogens
62
what are the characteristics of embolic nephritis if the emboli lodges in:
- smaller vessel
- larger vessel
- small emboli forming single to multiple abscesses (microscopic potentially)
- large emboli forming infarcts and abscesses
63
what agents are especially good at causing embolic nephritis in:
- foals
- pigs
- cattle
- calves
- sheep/goats
foals: Actinobacillus equuli
pigs: Erysipelas
cattle: Truepurella pyogenes
calves: E. coli
sheep/goats: Corynebacterium pseudotuberculosis
64
the blood volume is filtered _____x per day with _____% reabsorbed by the tubules
100; 99
65
____% of tubular function must be lost before you see acute renal failure
75
66
what are the 3 types of acute renal failure
1) acute tubular necrosis
2) obstructive nephropathy (uroliths, neoplasia)
3) renal ischemia
67
what are causes of acute tubular necrosis (3)
- bacteria/viruses
- toxins
- nephrotoxic drugs
68
what are causes of renal ischemia and necrosis
- vasculitis
- vascular obstruction from bacteria
- vascular obstruction from tumor emboli
69
what are the main consequences of acute renal failure
elevated K -> cardiotoxic
metabolic acidosis
pulmonary edema
70
T/F when acute tubular necrosis occurs macroscopic lesions are minimal so we must look at histo
T
71
what are causes of acute tubular necrosis
- anoxia
- hypoxemia
- anemia
- low renal blood flow
- toxicity
72
what does the term tubulorrhectic imply
patchy focal tubular necrosis and disruption of basement membranes secondary to ischemia
73
how can we tell apart ischemic vs toxic causes of acute tubular necrosis
ischemic: basement membrane disrupted (tubulorrhectic)
toxic: basement membrane preserved
both: necrosis (can be extensive)
74
are you more likely to see tubular regeneration following a toxic or ischemic insult
toxic (basement membrane intact)
75
what is a very important cause of toxic acute tubular necrosis
ethylene glycol
76
what makes ethylene glycol toxic
the metabolites:
- glycoadlehyde
- glycoxylate
77
how do signs of ethylene glycol toxicity change over time? what is the associated timeline?
peracute: neurologic
12h: respiratory and cardiovascular
1-3 days: renal failure
78
what are causes of hemoglobinuric nephrosis (caused by hemoglobin and myoglobin in urine)
- copper toxicity in sheep
- IMHA in dogs
- red maple toxicity in horses
- myoglobinuric disease in horses
79
T/F Hb is directly toxic to the kidneys
F (we think); the damage is by exacerbating hypoxia and anoxia
80
what is a very important cause of interstitial nephritis and in what species
leptospira; dogs, calves and pigs
81
T/F most leptospira is subclinical but we can see disease when there is species adaptation of the bacteria to maintenece and incidental hosts
T
82
how can we make a definitive diagnosis of leptospirosis
- histo and special staining
83
what is the name of the disease that causes white lesions on the kidney in cows and what age is affected? is it commonly incidental or not and why
white spotted kidney disease; calves; incidental (<50% of kidney affected)
84
what is the main cause of white spotted kidney disease
E. coli
85
how does white spotted kidney disease change in predominant cell type over time
suppurative (mainly neutrophils) to non-suppurative (lymphocytes and plasma cells) with chronicity
86
T/F you cannot differentiate lymphoma from chronic white spotted kidney disease
T
87
granulomatous nephritis in cats is classically caused by _______; the lesions are unique grossly in that they
FIP; follow blood vessels
88
why is the medulla highly susceptible to bacterial infection
- poor blood supply
- the increased osmolality in the interstitium (due to salt) inhibits neutrophil function
- the high NH3 inhibits complement activation
89
do we more commonly see pyelonephritis in male or female dogs
female
90
what are the main bacterial causes of pyelonephritis
- uropathogenic E. coli
- Proteus vulgaris
- Strep
- Staph
- C. renale in cows (contagious bovine pyelonephritis)
- actinobaculum suis in pigs (porcine contagious pylelonephritis)
91
T/F gram positive bacteria produce exotoxins that can inhibit normal ureteral peristalsis
F; gram-negative LPS does this
92
describe the location and appearance of lesions associated with pyelonephritis
coming up from medulla; segmental
can look like infarcts
93
how does the kidney look after chronic uremia
- fibrosed
- mineralized
- sclerotic glomeruli
- sometimes areas of hyperplastic and hypertrophic tubules
94
what is metastatic mineralization and why does it happen
mineralization due to calcium-phosporus mismatch in patients with kidney disease -> precipitate forms in alkaline tissues
dogs tend to get it subpleural
95
where is the mineralization in uremic gastropathy
midzone
96
what are consequences of uremic gastropathy
- mineralization
- ischemia
- vasculopathy -> mucosal infarction
Sys Path
flashcards
Decks in class (38)
# Cards
-
Hemolymphatic 187
-
Hemolymphatic 213
-
Hemolymphatic 336
-
Hemolymphatic 431
-
WB Biochemistry - Quality Control10
-
WB Biochemistry - Enzymology Intro36
-
WB Biochemistry - Acid Base40
-
WB Biochemistry - Electrolyte Biochem and Body Water Balance49
-
WB Biochemistry - Minerals36
-
WB Biochemistry - Lipids and Proteins37
-
GI Biochemistry - Liver and Exocrine Pancreas50
-
Hepatobiliary Pathology 1116
-
Hepatobiliary Pathology 2136
-
GI Pathology 1131
-
GI Pathology 2120
-
GI Pathology 3130
-
GI Pathology 4119
-
GI Pathology 594
-
GI Pathology 698
-
Endocrine 1 - Hyperadrenocorticism43
-
Endocrine 2 - Hypoadrenocorticism, Thyroid, ADH47
-
Endocrine 3 - Pancreas, Hyperparathyroidism39
-
Endocrine Anatomic Pathology83
-
Derm Path 1 - Review and Lumps53
-
Derm Path 2 - Biopsy42
-
Derm Path 3 - Pruritis49
-
Derm Path 4/5 - Scales and Crusts86
-
Derm Path 6 - Nodular Disease48
-
Derm Path 7 - Erosive and Depigmentation Disorders36
-
Derm Path 8 - Non-inflammatory Skin Lesions42
-
Derm Path 9 - Cytopathology of Skin and SQ Tumors53
-
Urinary Anatomic Path 165
-
Urinary Anatomic Path 296
-
Laboratory Evaluation of the Renal System71
-
Urinalysis71
-
Special Senses - Ear50
-
Special Senses - Eye42
-
Neuropath139
