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Year 3 > Urinary > Flashcards

Urinary Flashcards

1
Q

What % of blood plasma becomes glomerular filtrate?

A

16%

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2
Q

How do the kidneys affect vitamin D?

A

Convert vitamin D to active form, facilitating Ca2+ absorption from intestines

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3
Q

Where is renin produced?

A

Juxtaglomerular cells

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4
Q

How big should a kidney be?

A

2.5-3 x length of a lumbar vertebrae

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5
Q

What is an ectopic kidney?

A

Abnormal kidney migration eg in pelvic region
Mainly unilateral
Dogs, pigs

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6
Q

What is the difference between aplasia, hypoplasia, and dysplasia regarding kidneys?

A

Aplasia: kidneys never developed (agenesis)
Hypoplasia: incomplete development (fewer nephrons and lobules)
Dysplasia: small, misshapen, fibrosed, cystic kidneys. Structures are primitive for their age

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7
Q

Polycystic kidney disease affects which cat breed in particular?

A

Persians

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8
Q

Congenital tubular function abnormalities affect which species?

A

Dog

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9
Q

Autoregulation of renal blood flow is under the control of what?

A

Prostaglandins

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10
Q

How would a kidney with infarction appear histologically?

A

Central necrosis, mild inflammation with congested capillaries. Replacement of necrotic tissue by fibrosis -> depressed scar

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11
Q

What is infarction of the kidney?

A

Coagulative necrosis of the parenchyma due to vascular occlusion by emboli

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12
Q

What name is given to the capillaries supplying the medulla of the kidneys?

A

Vasa recta renis

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13
Q

How can treatment with NSAIDs cause papillary necrosis?

A

NSAIDs inhibit prostaglandin synthesis, prostaglandins regulate renal blood flow
Papillary necrosis occurs due to impaired blood flow in the vasa recta capillaries supplying the medulla

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14
Q

Give the 2 types of necrosis that can result from cortical ischaemia of the kidney

A

Renal cortical necrosis (diffuse cortical damage)
Acute tubular necrosis (tubular epithelium of PCT-cells die, slough and occlude the tubular lumen -> oliguric renal failure)

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15
Q

What is meant by oliguria?

A

Production of very small amounts of/almost no urine

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16
Q

What is amyloidosis?

A

The deposition of insoluble, proteolysis-resistant, beta-pleated sheets of protein, derived from modified forms of circulating proteins

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17
Q

What are the 2 kinds of amyloid that cause amyloidosis, and what are they formed from?

A

Amyloid AL: formed from immunoglobulin light chains

Amyloid AA: formed from serum amyloid A (hepatic acute phase protein)

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18
Q

What is the main site of deposition of amyloid plaques in the kidney?

A

Glomeruli

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19
Q

Amyloid depositions in the kidneys can result in what?

A 
Proteinuria
Hypoproteinaemia (nephrotic syndrome)
Increased glomerular permeability 
Pressure atrophy of the glomerular tuft
Nephron atrophy
Chronic renal failure
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20
Q

How does a kidney with amyloidosis appear grossly?

A

Enlarged, pale, ‘waxy’ kidneys, with glomeruli possibly standing out as dots, which stain positive with Lugol’s iodine

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21
Q

Which other organs (besides kidneys) can be affected by amyloid deposition?

A

Pancreas (cat)
Liver (esp Siamese cats)
Spleen and skin (horse)
Coronary artery (dog)

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22
Q

What is hydronephrosis?

A

Dilation of the renal pelvis secondary to any obstruction of urine flow.
Fluid builds up -> pressure -> occlusion of blood vessels -> ischaemia of medulla

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23
Q

Describe hypercalcaemic nephropathy

A

High Ca2+ impairs Na+ transport, leading to natriuresis (excretion of sodium in urine), and interferes with action of ADH on tubules (ADH causes water to be reabsorbed) -> nephrogenic diabetes insipidus
PU/PD, although this is reversible at this stage
More common in dogs

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24
Q

What 3 things does filtration depend on in the glomerulus?

A

Size, charge (anions are repelled by the negative charge of the barrier) and adequate blood pressure in the glomerulus

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25
Q

What make up the filtration barrier of the glomerulus?

A

Fenestrated epithelium
Glomerular basement membrane (inc mesangial cells which are phagocytic and secrete cytokines)
Epithelial cells with podocyte processes forming slit pores (non-regenerative)

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26
Q

Give the 2 main consequences of glomerular damage

A

Increased permeability

Reduced perfusion of downstream parts of the tubule

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27
Q

Which kind of conditions cause glomerulitis?

A

Acute septicaemia

Viral glomerulitis

28
Q

Glomerulonephritis in animals is usually what type?

A

Immune-complex type, ie results from immune complexes deposited directly from circulation or developed in-situ after entrapment of an antigen

29
Q

Describe porcine dermatitis and nephropathy syndrome

A

Growing/finishing pigs
Results in a severe fibrino-necrotising glomerulonephritis and necrotising vasculitits, with haemorrhages in the skin and other organs
(suggesting an immune complex-based pathogenesis)

30
Q

How may a dog acquire canine leptospirosis?

A

Direct transmission: infected urine, venereal/placental transfer, bite wounds, ingestion of infected tissues
Indirect transmission: exposure to contaminated water sources, soil, food, bedding
Rat urine is a common source of infection

31
Q

Which organism is responsible for ‘white spot kidney’ in cattle?

A

E.coli

32
Q

How does suppurative interstitial nephritis occur?

A

Pyogenic organisms localise in the kidney either haematogenously due to bacteraemia, or in infected emboli which lodge in the renal vasculature
Formation of foci of pus/abscesses scattered through the kidney

33
Q

What is pyelonephritis?

A

Inflammation of pelvis and renal parenchyma

34
Q

Why are cells of the PCT particularly susceptible to damage by toxins?

A

High metabolic activity

35
Q

How does antifreeze poisoning result in renal failure?

A 
Ethylene glycol (antifreeze) is oxidised to glycoaldehyde, glycolic acid, glyoxylate and oxalate by the liver
Oxalate combines with calcium -> hypocalcaemia -> calcium oxalate crystals precipitate in renal tubules -> acute renal failure by obstruction
36
Q

What are the clinical signs of ethylene glycol poisoning?

A

Ataxia, convulsions, vomiting, uraemia but no fever

37
Q

What clinical signs would you see with calciferol poisoning?

A

Calciferol=vit D

Hypercalcaemia, hyperphosphataemia, soft tissue mineralisation

38
Q

Describe oak tannin poisoning

A

Oak tannins cause irritation to the GI tract
Tannins and their metabolites are also nephrotoxic and hepatotoxic
Signs: colic, anorexia, constipation followed by scant dark faeces with blood in, icterus, dehydration
PM: pale enlarged kidneys surrounded by gelatinous blood-tinged oedema and haemorrhages in the capsule and peri-renal fat

39
Q

‘Purple kidney disease’ affects which species?
What is it caused by?
What are the clinical signs?

A

Sheep (lambs)
Caused by Clostridium perfringens type D
Acute, infectious, non-contagious disease of lambs; convulsions, hyperglycaemia, sudden death
Epsilon enterotoxin causes damage to vascular endothelium in lungs, brain, kidneys

40
Q

Are males and females more prone to infection or obstruction regarding their lower urinary tract? Why?

A

Females: infection due to close proximity to rectum, and short wide urethra
Males: obstruction due to narrow tortuous urethra and its associated structures

41
Q

In which animals is patent urachus most common?

A

Foals and calves

42
Q

Give 3 causes of bladder haemorrhage

A

Severe haemorrhage: ventral trauma eg being kicked
Treatment with the chemotherapeutic agent cyclophosphamide can cause a sterile haemorrhagic cystitis in dogs
Petechiation or ecchymoses are a feature of septicaemic or toxaemic conditions eg classical swine fever

43
Q

What is hydroureter/hydrourethra?

A

Dilation of the ureter/urethra due to an obstruction of urine outflow by blockage eg calculi, chronic inflammation, neoplasia, strictures

44
Q

What is urolithiasis?

A

Formation of calculi within the urinary tract causes obstruction, pressure necrosis with ulceration at site of impaction, and acute heamorrhagic cystitis, urethritis or nephritis due to bacterial overgrowth in the static urine

45
Q

Give some factors which predispose an animal to urolithiasis

A

pH: acidic= oxalates, alkaline= struvite
Bacterial infection
Dietary factors: high phosphate diets, oxalate-rich plants, dehydration, vit A defiency
Hereditary: urates in dalmations
Sex
Species: calcium carbonate (horses), struvite (dogs)

46
Q

Describe feline urologic syndrome

A

Obstructive urethral urolithiasis
Male neutered cats
Dry diets, alkaline urine
Urethral obstruction -> post-renal azotaemia, dysuria, haematuria
Secondary bacterial infection causes severe haemorrhagic transmural cystitis. Rupture and uroperitoneum may occur
Grossly, the bladder is distended and haemorrhagic

47
Q

Give the 4 types of cystitis

A

Acute: haemorrhage, necrosis, catarrhal exudate
Chronic: polypoid mucosal changes, squamous metaplasia, thickening of bladder wall
Emphysematous: bacterial fermentation of glucose-loaded urine (diabetes mellitus)
Granulomatous: rare, can occasionally occur with tuberculosis or other granulomatous organisms

48
Q

Give 4 factors which protect against cystitis

A

Urethral sphincters
Frequent voiding of urine
Antibacterial properties of urine (urea, high osmolarity, organic acids)
Secretory IgG and mucin (mucosal defences against colonisation)

49
Q

Give some factors that predispose an animal to cystitis

A 
Urine stasis
Incomplete voiding of urine
Bladder trauma (catheterisation)
Glycosuria (diabetes mellitus)
Urine of dilute concentration or high pH
Short wide urethra (female)
50
Q

Give some agents which cause cystitis

A 
E.coli
Proteus
Streptococci 
Staphylococci 
Eubacterium suis (pigs)
51
Q

Enzootic haematuria occurs in cattle due to chronic ingestion of what?

A

Bracken

52
Q

What is the commonest bladder tumour in dogs?

A

Transitional cell carcinoma

53
Q

What is uraemia?

A

The clinical syndrome of toxicosis from renal failure

54
Q

What is azotaemia?

A

Higher than normal blood urea (or other nitrogen-containing compounds)

55
Q

What is isosthenuria?

A

Specific gravity of urine is the same as protein-free plasma. It is fixed at around 1.010, irrespective of fluid intake

56
Q

What is hyposthenuria?

A

Urine of low specific gravity

57
Q

Give some causes of pre-renal renal failure

A 
Hypoperfusion due to:
hypovolaemia by haemorrhage
dehydration
shock
trauma
cardiac failure
58
Q

Give some causes of intrinsic renal failure

A 
Renal infections
Nephrotoxicity eg drugs, ethylene glycol, Hb, heavy metals
Neoplasia
Inflammation
Fibrosis
Congenital disease
59
Q

Give some causes of post-renal renal failure

A

Acute lower urinary tract obstruction
Bladder rupture
Bladder dysfunction

60
Q

Describe acute renal failure

A

Sudden loss of 70-100% of nephron capacity
Caused by: ischaemia, nephrotoxins, complete outflow obstruction
Kidneys are often painful and swollen
Animals are typically anuric or oliguric. Urine tends to be isosthenuric.
Prognosis depends on degree to which regeneration is possible

61
Q

Describe chronic renal failure

A

Gradual and progressive loss of nephrons:
-Interstitial nephritis
-Glomerulonephritis
-Pyelonephritis
-Amyloidosis
Results from persistent disease process. Overloading of residual tubules -> poor concentrating ability -> hyposthenuria, PUPD

62
Q

How can you use urine to differentiate between acute and chronic renal failure?

A

Acute will be isosthenuric

Chronic will be hyposthenuric

63
Q

What are the effects of renal failure?

A

Build up of waste products -> azotaemia (urea, creatinine, phenols etc)
Failure of acid base regulation -> metabolic acidosis
Failure of fluid volume regulation (dehydration, PU with hyposthenuria and secondary PD)
Electrolyte disturbances (phosphate and K+ retention, Ca2+ loss with secondary hyperparathyroidism)
Endocrine disturbances (reduced erythropoietin -> anaemia; activation of RAAS -> high blood pressure; failure of vit D conversion -> hypocalcaemia)

64
Q

Give some clinical signs of uraemia

A

PUPD, pallor, anorexia, lethargy, weakness, muscle wasting, hypothermia, mouth and tongue ulcers, vomiting (+/- blood), melaena (blood in faeces), non-regenerative anaemia, skeletal softening (rubber jaw)
Terminal CNS signs: dullness, drowsiness, tremors, ataxia, coma

65
Q

Give some conditions that can occur as a result of uraemia

state why they occur

A

Cachexia (prolonged catabolic state)
Haemorrhagic gastritis (ammonia secretion)
Soft tissue mineralisation (hyperparathyroidism)
Non-regenerative anaemia (decreased erythropoietin)

66
Q

How does renal failure lead to ‘rubber jaw’?

A

RETENTION OF PHOSPHATE
Reduction in GFR -> retention of phosphate; hyperphosphataemia
Hyperphosphataemia inhibits renal conversion of Vit D to calcitriol -> reduced intestinal calcium absorption
High phosphate precipitates out calcium in tissues
Hypocalcaemia
Increased PTH secretion, parathyroid glands become hyperplastic
Chronic PTH secretion -> resorption of mineralised bone
Softening, enlargement and rarefaction of bones, esp facial and mandibular - ‘rubber jaw’

67
Q

What are the functions of the kidneys?

A

Excretion of waste products, particularly nitrogenous waste, by the formation of urine
Conservation of water (loop of Henle, urea gradient, ADH)
Acid-base regulation (bicarbonate reclamation)
Electrolyte regulation (Na+/K+ -RAAS, phosphate)
Endocrine roles (erythropoietin, vit D conversion)

Year 3 (28 decks)

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