Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Renal > Pathology of the urinary tract > Flashcards

Pathology of the urinary tract Flashcards

1
Q

Erythropoietin - funtion

A

Produced in response to ↓ oxygen tension → stimulate maturation of erythrocytes in the bone marrow.

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

Calcitriol (activated vitamin D) - function

A

Facilitates Ca absorption in the small intestine.

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

pre-renal failure - causes

A

Secondary to circulatory collapse (shock, hypovolaemia) or local obstruction of vascular supply (thrombus or lodgement of embolus)

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

renal failure - causes

A

Tubular necrosis - infectious agents, toxins and toxic metabolites, nephrotoxic drugs and chemicals.
Embolic disease or ascending pyelonephritis

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

post-renal failure - causes

A

Ascending infection, urolithiasis or neoplasms

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

acute renal failure

A

Occurs when >75% of renal functional capacity is abruptly impaired.
Failure to excrete waste products and to maintain fluid and electrolyte homeostasis

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

acute renal failure effects

A

Abrupt decr in serum concentrations of urea + creatinine (azotaemia)
nitrogenous waste products of protein catabolism - indices of diminished renal function.
Retention of K+ - cardiac dysrrhythmia (& arrest).
Retention of phosphates - binds ionised calcium (hypocalcaemia) - muscular tremors & coma.
Disturbances of electrolytes and ↓ pH - metabolic acidosis.
Hypertension.
Oliguria/anuria

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

chronic renal failure

A

insufficient glomerular filtration - progressive
retention of nitrogenous metabolites
failure of tubular function

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

chronic renal failure - effects

A

progressive salt and water retention, metabolic acidosis, other electrolyte imbalances (esp hyperkalaemia)
decr phosphates - secretion - hyperphosphataemia & Ca2+ precipitation, decr active Vit D3 (calcitriol)
hypertension

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

Chronic renal disease - clinical signs

A

Polyuria, isosthenuria, polydipsia, etc
Halitosis, dribbling, lank coat, loss of weight
older cats & dogs

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

CRF - histological appearance

A

incr of interstitial connective tissue.
Renal tubules absent, atrophic or compressed.
Hyperplastic + hypertrophic tubules.
Intraluminal protein.
Thickened hyalinised basement membranes.
Calcification of vessels and basement membranes.
Multiple acquired cysts.
Glomerulosclerosis.
Foci of interstitial lymphocytes and plasma cells

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

end stage renal failure - kidney appearance

A

replacement of renal parenchyma with mature fibrous tissue
Kidneys are firm and distorted.
Distortion due to contraction of mature fibrous tissue (scarring)

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

uraemia - define

A

urea in the blood

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

4 stages of developing uraemia

A
  1. decr renal reserve, GFR 50% asymptomatic
  2. Renal insufficiency, GFR is 20-50% azotaemia + polyuria
  3. Renal failure, GFR 20-25% , kidneys can not maintain
    homeostasis, uraemia (GI, cv, respiratory and skeletal
    complications).
  4. End-stage renal disease, GFR <5% terminal uremia.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Systemic Effects of Uraemia

A

retention of nitrogenous metabolites.
NaCl and water retention, metabolic acidosis, other electrolyte imbalances (esp hyperkalaemia).
Plasma protein loss (oedema).
Hyperphosphataemia and secondary renal hyperparathyroidism.
↓ Production of erythropoietin → ↓ stimulation of erythropoietic maturation → non-regenerative anaemia.
Hypertension.

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

Secondary Renal Hyperparathyroidism due to uraemia - chain of events

A

GFR <25% phosphate is no longer adequately secreted by the kidneys.
Hyperphosphataemia precipitates ionised calcium conc in serum.
decr calcitriol - decr intestinal absorption of calcium.
decr ionised serum Ca stimulates PTH secretion - Ca
release via osteoclastic bone resorption.
try to incr renal excretion of phosphate + reabsorption of Ca.
Parathyroid chief cell hyperplasia - renal secondary
hyperparathyroidism.

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

Secondary Renal Hyperparathyroidism - effects - kidneys

A

Fibrous osteodystrophy and mineralisation of soft tissues.
Renal disease made worse by nephrocalcinosis - calcification of tubular BMs, Bowman’s capsules and necrotic tubular epithelium

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

Secondary Renal Hyperparathyroidism - effects - non-renal

A

Endothelial degeneration and necrosis - vasculitis with
secondary thrombosis and infarction
mineralisation
ulcers

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

examples of non-renal lesions due to Secondary Renal Hyperparathyroidism

A 
Caustic injury to epithelium of the oral cavity and stomach (ulceration) 
Ulcerative glossitis and stomatitis
Ulcerative and haemorrhagic colitis
Ulcerative and haemorrhagic gastritis
Uraemic encephalopathy
Uraemic pneumonitis + Pulmonary calcification 
Intercostal mineralisation
Fibrinous pericarditis
Arteritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

portals of entry to the kidney

A

haematogenous
glomerular infiltrate
ascending from the ureter
direct penetration

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

main Diseases of the Glomeruli

A

Immune mediated glomeruolonephritis.
Glomerular Amyloidosis
Acute suppurative glomerulitis
Glomerulosclerosis

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

Causes of glomerular damage

A 
Damage tofiltration barrier - deposition of immune complexes. 
thromboemboli and bacterial emboli. 
Direct viral or bacterial infection 
Damage to other parts of the nephron. 
Reduced blood flow. 
Chronic loss of tubular function. 
Amyloid deposition.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Functions of the glomerulus affected

A 
Plasma ultrafiltration. 
Blood pressure regulation. 
Peritubular blood flow regulation. 
Tubular metabolism regulation. 
Circulating macromolecule removal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Protein losing nephropathy

A

albumin leaks into filtrate - too much protein to be absorbed in PCT
high protein filtrate in dilated tubular lumina - proteinuria and hypoproteinaemia
renal protein loss - decr plasma colloid osmotic pressure + loss of antithrombin III - nephrotic syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

nephrotic syndrome

A

generalised oedema, ascites, pleural effusion, hypercoagulability and hypercholesterolaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Responses of glomeruli to injury

A 
Necrosis. 
Proliferation of cells and membranes. 
Infiltration of leukocytes. 
decr vascular perfusion. 
Incr vascular permeability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

response of glomeruli to continued/severe injury

A

atrophy and fibrosis of the glomerular tuft (sclerosis) and secondarily atrophy of renal tubules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Immune mediated glomerulonephritis - how it happens

A

Circulating immune complexes in subepithelial,
subendothelial or mesangial locations.
antibodies against entrapped nonspecific antigens or
antigens within the GBM.
release of proteineases and oxygen derived free
radicals - damage the basement membrane.
Activation of both glomerular epithelial cells and mesangial cells to produce damaging mediators such as oxidants and proteases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Immune mediated glomerulonephritis - causative diseases

A

persistent infections
Specific viral infections → FeLV and FIP.
Chronic bacterial infection → pyometra or pyoderma.
Chronic parasitism.
Autoimmune diseases such as SLE.
Neoplasia
Transient infection
Continual exposure of glomeruli to soluble IC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Immune mediated glomerulonephritis - diagnosis

A

IF or IHC of immunoglobulin + complement components in the glomerular tufts.
specific causative antigen often hard to identify
electron dense deposits in mesangial, subepithelial
or subendothelial locations by EM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Immune mediated glomerulonephritis - gross appearance on kidneys

A

Glomeruli visible as pinpoint red/pale dots on the cut surface of the cortex.
Fine granularity to the cortical surface.
Capsule may be adherent.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Immune mediated glomerulonephritis - histopathology

A

↑ cellularity + proliferation of glomerular cells.
Dilated renal tubules filled with homogenous proteinaceous fluid.
Interstitial and periglomerular fibrosis.
Foci of interstitial lymphocytes & plasma cells.
Glomerulosclerosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Glomerular Amyloidosis

A

associated with chronic inflammatory disorders, systemic infectious disease or neoplasia.
deposits - fragments of a serum acute phase reactant protein.
Glomeruli are the most common renal sites for deposition
of amyloid.
Idiopathic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Glomerular Amyloidosis - consequences

A

PLN and the nephrotic syndrome
decr RBF through the glomeruli and the vasa recta
tubular atrophy, degeneration and fibrosis. In severe cases
renal papillary necrosis.
Medullary amyloidosis is usually asymptomatic unless papillary necrosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Glomerular Amyloidosis - gross appearance on kidneys

A

Enlarged, pale, smooth to finely granular capsular surface
Amyloid laden glomeruli may be visible as fine glistening dots on the cut surface of the cortex.
Brown staining of glomeruli after treatment with iodine.
Medullary amyloidosis not grossly visible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Glomerular Amyloidosis - histopathology

A

Glomerular amyloid in mesangium and subendothelium.
Acellular eosinophilic homogenous to fibrillar material.
tubules - dilated and contain proteinaceous and cellular casts
stains with Congo red - amyloid deposits have
apple green birefringence under polarised light

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Acute suppurative glomerulitis - cause

A

bacterial or embolic nephritis.
Bacteraemia - bacteria in glomerular and interstitial capillaries
formation of microabscesses in cortex.
glomeruli are targeted but manifestation of renal vascular disease
Produce toxic by products → damage endothelium →
localised vasculitis and colonisation → embolic nephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Acute suppurative glomerulitis - bacterial causes

A

Actinobacillus equuli in foals.
Erysipelothrix rhusiopathiae in pigs.
Corynebacterium pseudotuberculosis in sheep and goats.
Arcanobacterium pyogenes in cattle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Acute suppurative glomerulitis - gross appearance on kidneys

A

Multifocal random raised tan pinpoint foci - subcapsular and cut surface of renal cortex.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Acute suppurative glomerulitis - histopathology

A

Glomerular capillaries - bacterial colonies admixed with necrotic debris and neutrophils.

 Glomerular or interstitial haemorrhage.

 Can persist as focal residual abscesses
or progressively replaced by chronic
inflammation and coalescing scars.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Glomerulosclerosis

A

↓ in the no. of functional glomeruli.
Loss of glomerular capillaries + replacement of mesangial matrix and Bowman’s space by FCT.
↓ blood flow through the vasa recta from glomerular efferent arteriole.
hypoxia → tubular epithelial degeneration and loss.
Chronic proteinuria.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Diseases of the Tubules

A

Inherited Abnormalities, Acute Tubular Necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Causes of tubular disease

A 
Blood borne infections 
Ascending infections (intratubular pathogens). 
Direct damage from toxins (intratubular effects). 
Ischemia. 
Infarction. 
Tubular obstruction. 
Interstitial fibrosis. 
External compression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Responses of the tubules to injury

A

Degeneration, necrosis, apoptosis and/or atrophy → PCT most vulnerable.
Cells slough into the lumen to form cellular casts.
compensatory hypertrophy → attempt to maintain overall renal function
no regeneration of nephrons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Responses of the tubular basement membrane to injury

A

retained more consistently after toxic rather than ischemic results.
if it remains intact → repair by proliferation of the remaining viable epithelial cells.
Severe damage to or loss of tubular basement membranes → necrosis, failure of functional repair and replacement by fibrosis.

46
Q

Primary renal glycosuria

A

Inherited disorder
decr reabsorbtion of glucose by tubular epithelial cells
no gross or histological findings.
Predisposes to bacterial infections of LUT

47
Q

Fanconi syndrome

A

hereditary defect in tubular reabsorption of protein, glucose, phosphate, amino acids.
Can develop progressive renal insufficiency & associated renal fibrosis.

48
Q

cystinuria

A

Sex linked inherited tubular defect in male dogs

predisposes to calculus formation and obstruction of the LUT.

49
Q

acute tubular necrosis - effect

A

decr renal perfusion → ↓ GRF & activation of arteriolar vasoconstriction → prolonged ischemia

50
Q

Nephrotoxic pigments - Haemoglobinuric nephrosis - causes

A

chronic copper toxicity in sheep, babesiosis in

cattle, red maple toxicity in horses and AIHA in dogs.

51
Q

Nephrotoxic pigments - Myoglobinuric nephrosis

A

extensive muscle necrosis
azoturia of horses, capture myopathy of exotic or wild
animals and severe trauma.

52
Q

Acute Tubular Necrosis - Heavy metals

A

Lead → membrane/mitochondrial damage in the PCT cells
Acid fast IN inclusions present in the PCT epithelium
specific metal can’t be identified by renal lesions alone

53
Q

Acute Tubular Necrosis - oak poisoning in cattle

A

toxic substances are metabolites of tannins.
Target endothelial cells → vascular leakage.
Perirenal oedema.

54
Q

Acute Tubular Necrosis - oxalate containing plants - cattle + sheep

A

Calcium oxalates precipitate in BVs or within
renal tubules.
obstruction and epithelial cell necrosis.
Neuromuscular dysfunction → hypocalcaemia

55
Q

Acute Tubular Necrosis - Ethylene glycol (antifreeze)

A

Dogs, cats and occasionally pigs.
Readily absorbed from GIT.
Oxidised by hepatic alcohol dehydrogenase to toxic metabolites - glycolic acid and oxalate.
Filtered by the glomeruli.
Direct toxic effect on tubules.
Calcium oxalate crystals precipitate in renal tubular lumens → intrarenal obstruction.

56
Q

Acute Tubular Necrosis - bacterial toxins

A

Clostridium perfringens type D → epsilon toxin

Pulpy kidney → acute tubular degeneration and/or necrosis, interstitial oedema + haemorrhage

57
Q

Diseases of the Interstitium

A

Interstitial nephritis

58
Q

renal interstitium - define

A

fibrovascular stroma that surrounds the nephron

59
Q

Diseases of the Interstitium - Caused by

A

Ascending infection → pyelonephritis.
Haematogenous infection of tubules and interstitium → E-coli and Leptospira spp, Canine adenovirus.
Secondary to injury of the vasculature or tubules or glomeruli.

60
Q

Responses of the interstitium to injury

A

Oedema.
Haemorrhage.
Inflammation.
Fibrosis.

61
Q

Diseases of the Interstitium - gross appearance

A

grey foci on the capsular and cut surface.

62
Q

Diseases of the Interstitium - Histopathology

A 
Initially oedema, haemorrhage and neutrophilic infiltration. 
Later lymphocytes and plasma cells. 
Tubular epithelial degeneration. 
Vascular compromise. 
Fibrosis
63
Q

Diseases of the Interstitium - E-coli septicaemia

A

E-coli septicaemia:
‘White spotted kidney’
Embolic nephritis or nonsuppurative interstitial nephritis.
Microabscess replaced by lymphocytes, plasma cells and
macrophages.

64
Q

Diseases of the Interstitium - Equine arteritis virus or PRRS

A

Multifocal lymphohistiocytic tubulointerstitial nephritis with
interstitial oedema.
Vasculitis - fibrinoid necrosis and lymphohistiocytic infiltrates.
Virus can be found in the endothelium and macrophages

65
Q

Diseases of the Interstitium - Canine adenovirus infection

A

viral glomerulitis
Transient immune complex GN.
virus leaves glomeruli - reappears in tubular epithelial cells
Basophilic intranuclear viral inclusions.
Persistence of virus in tubular epithelium for weeks to months.
Viral induced cytolysis → tubular epithelial necrosis → production of chronic lymphoplasmacytic and less commonly histiocytic interstitial nephritis.

66
Q

Diseases of the Interstitium - Leptospirosis - pathophysiology

A

Bacterial tubulointerstitial nephritis.
organisms localise in renal interstitial capillaries.
Migrate through vascular endothelium → persist in the interstitial spaces.
Migrate into renal tubular lumina.
Degeneration and necrosis of tubular epithelial cells.
Infiltrate of macrophages, lymphocytes and plasma cells in the interstitium and neutrophils can be present in tubular lumina

67
Q

Diseases of the Interstitium - Feline infectious peritonitis

A

Granulomatous necrotising vasculitis.
Interstitial pyogranulomas.
other causes of granulomatous interstitial nephritis - Mycobacteria, Fungi, Parasites.

68
Q

Responses of the vasculature to injury

A 
Hyperaemia and congestion. 
Haemorrhage and thrombosis. 
Infarction. 
Papillary (medullary crest) necrosis. 
Embolic nephritis.
69
Q

causes of haemorrhage in the kidney

A

Direct trauma.
Coagulopathies.
Septicaemia - erysipelas, streptoccocal infections.
Embolic bacterial diseases → Actinobacillus equuli.
Vasculitis - FIP.
Vascular necrosis → Canine herpesvirus.
DIC.

70
Q

Disseminated intravascular coagulation

A

abnormal coagulation → generation of excess thrombin
Diffuse vascular damage → endotoxin induced → exposure of tissue factor → induced activation of extrinsic coagulation to produce thrombin.
Formation of widespread fibrin thrombi in the renal
microcirculation → platelet and coagulation factor consumption → widespread haemorrhages.
Not primary disease but a potential complication of any
condition associated with widespread activation of thrombin.
Results in cortical infarction and ischemic (coagulative) necrosis

71
Q

Sources of renal emboli

A

Cardiac mural or valvular thrombi.
Endarteritis in parasitic diseases such equine strongylosis.
Neoplastic cell emboli.
Bacterial or septic emboli → Arcanobacterium pyogenes
in cattle, Erysipelas rhusiopathie in pigs and Staphylococcus aureus in dogs.

72
Q

Neoplasia of the kidney

A

<1% of total neoplasms reported.
Usually unilateral.
Primary renal tumours - highly malignant and metastatic disease is common

73
Q

Epithelial tumours -

A

Renal adenomas - usually incidental at necropsy.

74
Q

Epithelial tumours - Renal carcinomas

A

Large with foci of haemorrhage, necrosis and cystic degeneration, occupy and obliterate one pole of the kidney.
Paraneoplastic condition -polycythaemia - overexpression of erythropoietin

75
Q

Epithelial tumours - Transitional cell papillomas and

carcinomas

A

Arise in the renal pelvis and LUT.
Can obstruct urinary outflow.
Can invade into the kidney

76
Q

Metastatic tumours

A

Carcinomas and sarcomas arising in other organs can metastasise to the kidneys.
Randomly scattered multiple nodules.
Usually involving both kidneys.
Renal lymphoma - cats and cattle

77
Q

Diseases of the renal pelvis - Hydronephrosis

A

Dilation of the renal pelvis d/t obstruction of urine outflow → incr pelvic pressure - atrophy of renal parenchyma.
interstitial vessels collapse + renal blood flow decr - hypoxia and ischemic necrosis - tubular atrophy and interstitial fibrosis.
if bacteria enter hydronephrosis kidney → becomes filled with pus → pyonephrosis

78
Q

Diseases of the renal pelvis - Hydronephrosis - causes

A 
Congenital malformation. 
Ureteral/urethral blockage due to urinary calculi. 
chronic inflammation. 
Ureteral/urethral neoplasia. 
Neurogenic functional disorders.
79
Q

Diseases of the renal pelvis - Hydronephrosis - unilateral

A

hydronephrosis can be become notable
continual urine production and pooling of urine into the
expanding pelvis.

80
Q

Diseases of the renal pelvis - Hydronephrosis - Bilateral

A

uraemia occurs before pelvic enlargement becomes extensive.

81
Q

Pyelonephritis

A

Bacterial infection of the pelvis with extension into the renal tubules and concomitant interstitial inflammation.
form of suppurative tubulointerstitial disease.
frequently bilateral and recurrent infections common.
Associated with parturition, service and catheter use

82
Q

Pyelonephritis - Bacteria involved

A

Corynebacterium spp, E coli, Staphylococcus
spp, Streptococcus spp, Pseudomonas aeruginosa and
Arcanobacterium pyogenes.

83
Q

pyelonephritis - Competency of vesicoureteral valve is

compromised

A

causes incr reflux
when pressure is incr in the urinary bladder - urethral obstruction.
Infl of the bladder wall - cystitis.
Endotoxin from G-ve bacteria - inhibit ureteral peristalsis.

84
Q

Pyelonephritis - gross

A

Ureters distended with suppurative exudate.
Exudate in the pelvis and medulla.
May extend into cortex
olar scars.
Infl can extend through the surface of the kidneys - peritonitis.

85
Q

Pyelonephritis - Histopathology

A

Transitional epithelium is necrotic and sloughed.
Necrotic debris, fibrin, neutrophils + bacterial adhere to denuded surface and accumulate in tubular lumina.
Interstitial infl, haemorrhage + oedema.
If vasa recta are obstructed - papillary necrosis.
Extend radially into the cortical tubules.
Lymphocytes, plasma cells macrophages and fibrosis.

86
Q

Primary papillary necrosis

A

Prolonged treatment or overdose with NSAIDs - damage to medullary interstitial cells.
decr PG synthesis (vasodilator) - decr blood flow - ischemic necrosis of the inner medulla

87
Q

Secondary papillary necrosis - causes

A

decr vasa recta blood flow - glomerular amyloidosis or
glomerulosclerosis.
Compression of the vasa recta within the medulla -
interstitial oedema or fibrosis.
Compression of the renal papilla - pelvic calculi, LUT obstruction, pyelonephritis and vesiculoureteral reflux

88
Q

papilary necrosis - effects on kidney

A

Sharply delineated coagulative necrosis of the inner medulla.
Eventually sloughs - detached fragment in the pelvis.
Large fragments could obstruct the ureter - hydronephrosis.
formation of calculi
Rarely lead to progressive renal damage + failure.

89
Q

disease of the LUT - causes

A 
Infection: 
Neoplasia. 
Toxins/poisons. 
Congenital defects. 
Physical trauma → urolith. 
Obstruction
90
Q

defense mechanisms of the LUT

A

Flushing action of urine minimises risk of ascension of bacteria.
Peristalsis acts to eliminate bacteria with adhesion capabilities.
Inhospitable environment for bacterial growth controlled by urine pH.
Protective urothelial mucus coating.
Innate, humoral and cellular immune responses.

91
Q

LUT response to injury

A

Dilation and pressure necrosis caused by obstruction.
Inflammation.
Neoplastic transformation

92
Q

ectopic ureters

A

Empty into the urethra, vagina or bladder neck.
Predisposed to obstruction or infection.
Present clinically with urinary continence.

93
Q

patent urachus

A

Foals.
Foetal urachus fails to close → direct channel between the bladder and the umbilicus.
Underlying omphalitis or congenital urethral obstruction.
↑ Bladder pressure → due to obstruction → forces urine out into the urachus.
Dribble urine from umbilicus.

94
Q

acquired causes of obstruction of the LUT

A 
Calculi. 
Neoplasia. 
Trauma and inflammation. 
Circumferential fibrosis. 
Bladder paralysis. 
Vaginal and/or uterine prolapse. 
Feline urologic syndrome - fine struvite crystals in a mucoid protein matrix fill the urethra
95
Q

Consequences of obstruction of LUT

A 
Distended/ruptured bladder. 
Transmural ecchymotic haemorrhages. 
Mucosal ulceration and haemorrhages. 
peritonitis. 
Infl
96
Q

acute cystitis - clinical signs

A

Dysuria, stranguria and haematuria

97
Q

acute cystitis - causes

A

Bacterial infection  most common cause.
Uropathogenic E coli in many spp, Corynebacterium renale in cattle and Eubacterium suis in pigs.
Hydrolysis of urea by urease producing bacteria  C renale and E suis in pigs - release excessive ammonia  damage mucosa &  urine pH

98
Q

acute cystitis - affect of LUT

A

Denuded oedematous mucosa, adherent neutrophils, bacterial colonies, hyperaemia and haemorrhage

99
Q

acute cystitis - predisposing factors

A 
Urinary stasis. 
Infrequent urination 
Calculi. 
Catheterisation. 
Prolonged antibiotic use
100
Q

Chronic Cystitis - difuse

A

Thickened mucosa infiltrated with mononuclear infl cells
Submucosal fibrosis.
Hypertrophy of the muscularis.

101
Q

Chronic Cystitis - follicular

A

Multiple small red nodules on the mucosal surface.
Hyperplastic lymphoid cells surrounded by hyperaemia and haemorrhage.
Associated with uroliths

102
Q

Chronic Cystitis - polypoid

A

Multiple masses of proliferative nodules of connective tissue (polyps).
Lymphocytes and neutrophils

103
Q

Emphysematous cystitis

A

Glycosuria enhances bacterial growth.
Glucose split by bacteria - E coli, Clostridium perfringens
release of CO2 into the bladder lumen.
Absorption of gas into the bladder lymphatics - emphysema

104
Q

Toxic cystitis

A

Chronic ingestion of bracken fern - enzootic haematuria -
haemorrhage, chronic cystitis or bladder neoplasia.
Active metabolites of cyclophosphamide used to treat neoplasia and IMD

105
Q

epithelial tumours

A

Transitional cell papillomas or carcinomas
SCC & adenocarcinomas can arise from transitional epithelium
Metastasis regional lymph nodes, lungs and kidney

106
Q

Mesenchymal tumours:

A

Leiomyomas
Fibromas from the lamina propria.
Lymphoma.
Rhabdomyosarcomas

107
Q

Developmental Disorders - Renal aplasia

A

failure of one or both kidneys to develop.

108
Q

Developmental Disorders - Hypoplasia

A

incomplete development of one or both kidneys

fewer than normal nephrons.

109
Q

Developmental Disorders - Ectopic kidneys

A

pelvic canal or inguinal position
histological structure and function usually normal but malposition of the ureters predisposes then to
obstruction - secondary hydronephrosis.

110
Q

Developmental Disorders - Fused kidneys

A

fusion of cranial or caudal poles
horseshoe shape
structurally and functionally normal.

111
Q

Developmental Disorders - Dysplasia

A

abnormal differentiation in one or both kidneys

112
Q

Developmental Disorders - Progressive juvenile

nephropathy

A

Severe bilateral renal fibrosis.
Shrunken pale kidneys with a pitted surface.
Foetal glomeruli, interstitial infl, fibrosis and tubular dilation

Renal (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions