Brainscape's Knowledge GenomeTM

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


See full index

Clinical Reproduction & Urology > Pathology of the Urinary Tract 1 > Flashcards

Pathology of the Urinary Tract 1 Flashcards

1
Q

Multipyramidal (Multilobar) kidneys are present in which species?

A

pigs, cattle

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

What animal species has external lobulations of the kidney?

A

Cattle

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

What species have unipyramidal (unilobar) kidneys?

A

Cats, dogs, small ruminants, horses

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

What is unique about equine kidneys?

A
  • mucous glands in the medulla
  • mucus & crystals normally present in renal pelvis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is unique about mature cat kidneys?

A

cortex is often yellow due to large lipid content of tubular epithelial cells

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

kidneys autolyze quickly after…

A

death

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

Autolysed tissues make it so it is not possible to detect…

A

ACUTE tubular necrosis

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

sampling of ocular fluid from the anterior chamber for urea lvls w/i 24 hr of death indicates…

A

acute renal failure

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

The interlobular artery extends into the cortex forming glomerular arterioles where…

A

high pressure favors filtration

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

Efferent glomerular arterioles close to subcapsular region create peritubular capillary network where…

A

low pressure favours reabsorption

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

Why is the medulla especially sensitive to ischaemia?

A

Due to relative avascularity & low HCT in the medullary capillaries

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

How much cardiac output is received in the kidneys?

A

up to 25%

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

How much oxygen content do the kidneys receive?

A

about 10% of the whole body

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

Why do kidneys receive so much oxygen?

A

Needed for resorption of essential solutes predominantly cortical function

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

Kidneys self-regulate the balance of…, ensuring stable…

A

BP
GFR

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

Renal artery & its branches are…

A

end-arteries so goes into cortex then to glomeruli for urinary filtration –> interstitium –> venous flow

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

Medulla receives…

A

very little blood flow (primarily for reabsorption)

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

Glomerular arterioles have high pressure that favours…

A

filtration

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

Efferent arterioles favor low pressure which favours

A

reabsorption

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

Each nephron functions on an…

A

all or none basis

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

Components of a nephron

A
  • Glomerulus
  • Bowman’s Capsule
  • Proximal Convoluting Tubule
  • Loop of Henle
  • Distal Convoluting Tubule
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

if the glomerulus is gone, then the blood supply is gone, meaning there is…

A

a decrease in urine production

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

In progressive renal disease, remaining nephrons respond by…

A

hyperplasia & hypertrophy causing an increase in glomerular filtration & tubular function

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

Damage to tubule but basement membrane is intact means…

A

regeneration can occur

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

What happens when a nephron is defective?

A

Function is impaired causing essential substances wasted in urine

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

uriniferous tubule consists of…

A

nephron & collecting duct

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

Macula densa is used for…

A

sodium concentration & BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

why does the glomerulus need high BP?

A

for filtration purposes

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

Renal corpuscle consists of…

A

glomerulus & Bowman’s capsule

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

Glomerulus produces ultrafiltrate as a result of…

A

difference btw higher systemic hydrostatic BP & lower hydrostatic pressure in tubules

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

What plasma proteins are excluded from filtration in the glomerulus?

A

Albumin & higher molecular weight plasma proteins

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

What are the 3 main features of the proximal convoluted tubules?

A
  1. microvilli w/ brush border
  2. tight jxns
  3. lots of mitochondria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are key features of the distal convoluted tubule & collecting ducts?

A
  1. Principal cells - receptors for ADH & aldosterone
  2. Intercalated cells - role in blood pH homeostasis
  3. Absorption
  4. Tight Jxns
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

The interstitium consists of…

A

blood vessels, CT

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

The interstitium expands in disease such as

A

oedema in acute dz or fibrosis in chronic dz

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

Selective reabsorption occurs in

A

specialised tubular epithelial cells

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

The cells of proximal convoluted tubule are prone to…

A

ischaemia

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

Loop of Henle leads to…

A
  • hypotonic filtrate produced via countercurrent exchange
  • close association w/ peritubular capillary network
  • Na & K ATPase pumps absorb Na & Cl ions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

When does the interstitium become abnormal?

A

Oedema
Cellular infiltration
Amyloid depositions
Fibrosis

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

What are the basic functions of the kidneys?

A
  • Excretion of waste products
  • control of blood volume
  • blood pressure
  • body fluid pH
  • body fluid isotonicity
  • Regulation of acid-base balance
  • endocrine functions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What triggers the renin-angiotensin system?

A

Reduced blood supply at juxtaglomerular apparatus

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

Angiotensin II

A
  • causes vasoconstriction
  • induces aldosterone release in adrenal gland –> reduces excretion of NaCl
  • Activates ADH in the hypothalamus –> fluid retention
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the outcome of Renin-Angiotensin System?

A

Increased BP, salt & water retention

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

The Renin-Angiotensin system…

A

maintains BP
Regulates Na Balance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are the main renal hormones?

A

EPO
Vit D Metabolism
Hypothalamus & ADH

45
Q

Fxnl characteristics of kidney

A
  • large amts of primary urine produced, most reabsorbed
  • enormous reserve capacity (70% lost before clin signs)
  • Regeneration of renal tissue
  • glomerular malfunction (causes tubular & interstitial malfunction)
  • tubular & interstitial malfunction (causes glomerular malfunction)
46
Q

What are the portals of entry of injurious stimul & agents?

A
  • Ascension from lower UT
  • Haematogenous (infarction, embolic, glomerular tufts, interstitial vessels)
  • metabolic (toxic or metabolic substances secreted into filtrate)
47
Q

What are the kidney defence mechanisms?

A
  • barrier system: glomerular & tubular basement membranes
  • monocyte-macrophage system: glomerular mesangium & interstitium
  • immune system: innate, humoral, cellular
48
Q

How does the glomeruli response to injury?

A
  • cellular proliferation
  • leukocytic infiltration
  • thickening of basement membrane
  • hyalinization
  • sclerosis
49
Q

How do the renal tubules respond to injury?

A
  • necrosis, esp of lining of prox tubules
  • basement membrane thickening
  • cell regeneration if basement membrane intact
  • compensatory hypertrophy
50
Q

How does the renal interstitium respond to injury?

A
  • oedema, haemorrhage, inflammation
  • fibrosis
51
Q

How do the blood vessels of the kidney respond to injury?

A
  • arteritis
  • arteriosclerosis
  • thrombosis
52
Q

How does the renal medulla respond to injury?

A
  • accumulation of protein casts
  • papilla (inflammation pyelonephritis, amyloid, necrosis)
53
Q

What are the essential requirements for normal renal fxn that can go wrong and lead to renal failure?

A
  • Adeq perfusion w/ blood (incl BP)
  • Adeq fxnl renal rissue
  • Normal elim of urine thru UT
54
Q

What is the index of failure for renal fxn?

A
  • amt of urea retained
55
Q

Azotaemia is a biochemical abnormality that consists of what parameters?

A
  • increased urea
  • increased creatinine
  • w/ no clin manifestation of renal dz
56
Q

Uraemia is a clinical syndrome of renal failure due to…

A

biochemical disturbances, often due to extra-renal multisystemic lesions

57
Q

What are the 4 steps of renal insufficiency to renal failure?

A
  1. Diminished renal reserve (GFR >50%) -> asymptomatic
  2. Renal insufficiency (GFR 20-50% of normal) -> azotaemia & polyuria
  3. Renal failure (GFR 20-25% of normal) -> uraemia w// GI, CV, resp, skeletal complications
  4. End-stage renal dz (<5% normal) -> terminal stages of uraemia
58
Q

What is unable to be regulated in kidney failure?

A
  • fluid volume (leads to dehydration)
  • Electrolytes (PO4, Ca, Na, K)
  • Acid-base balance (metabolic acidosis)
  • Metabolic waste excretion
  • Endocrine fxns (secondary hyperparathyroidism, non-regn anaemia)
  • hypertension
  • non-specific effects of uraemic toxins
59
Q

Failure of Ca to regulate renal failure looks like…

A
  • increased hypercalcaemic nephropathy
  • decreased tetany
  • osteodystrophy
60
Q

Failure of Na regulation due to renal failure looks like…

A
  • increased oedema
  • decreased dehydration
61
Q

Failure to regulate K in renal failure looks like…

A
  • increased cardiotoxicity
  • decreased muscle weakness
62
Q

Metabolic acidosis due to renal failure looks like…

A
  • decreased production of ammonia in distal & collecting tubules
  • increased retention of H+
  • impaired resorption of HCO3-
63
Q

What are the causes of acute prerenal renal failure?

A
  • sudden & severe BP drop (shock/ischaemia) -OR- interruption of blood flow to kidneys from severe injury or illness

Due to:
* Decreased CO: CHF, arrhythmia, cardiac tamponade
* Shock: systemic vasodilation, anaphylaxis, sepsis
* Hypovolaemia: dehydration, V/D, burns, blood loss
* Vascular ischaemia/obstruction: toxins, thrombi, vasculitis, bacterial emboli

64
Q

What are the causes of acute intrarenal failure?

A
  • Sudden compromised kidney fxn, direct damage to kidneys by inflammation, toxins, drugs, infection, or reduced blood supply

Due to:
* nephrotoxins & drugs
* infectious agents
* vascular obstruction/ischaemia
* immune-mediated
* tumours

65
Q

What are the causes of post-renal renal failure?

A
  • sudden obstruction of urine flow (obstruction of ureter by urolithiasis, congenital, injury, bladder tumour, nephrolithiasis)
66
Q

Acute renal failure can be…

A

reversible

67
Q

Clinical signs of renal failure

A
  • rapid onset of oliguria or anuria
  • azotaemia
  • disturbance in electrolyte balance
  • accumulation of metabolic waste
  • extra-renal lesions (rare) due to severity of uraemic lesions (stomatitis, gastritis, enteritis, vasculitis –> fibrinoid necrosis of vasc wall (often lung) –> increased permeability –> severe pulm oedema)
68
Q

Animals die of acute renal failure b/c:

A
  • metabolic acidosis
  • hyperkalaemia –> cardiotoxicity
  • +/- severe pulm oedema
69
Q

Chronic renal failure is the end-result of …

A

Chronic renal dz’s

70
Q

Chronic renal failure is usually

A

irreversible

71
Q

What characterises chronic renal failure?

A
  • prolonged duration & signs of uraemia which are progressive
  • death imminent
72
Q

What are the clinical effects of chronic renal failure?

A
  • D/V/anorexia
  • altered Ca/P metabolism
  • potential secondary renal PTH
  • non-regen anaemia of EPO
  • heart (angiotensin-induced hypertension leading to L ventricular hypertrophy; mineralisation of atria; myocardial degeneration; vasculitis; fibrinous pericarditis)
  • NS: lethargy, drowsiness, NM twitches, convulsions
  • Lung: alveolar wall mineralisation, pulm oedema
  • Metabolic acidosis: cachexia, oedema
73
Q

Non-renal lesions of uraemia

A
  • dehydration
  • oedema
  • pulmonary oedema
  • ulcerative stomatitis, glossitis
  • ulcerative, haemorrhagic gastritis
  • ulcerative, haemorrhagic enteritis
  • fibrinous pericarditis, hydropericardium
  • atrial/aortic lesions, ulcerations
  • myocardial degeneration
  • congestive heart failure, L ventricle hypertrophy
  • Vascular lesions
  • anaemia, nonregenerative
  • mineralisation of soft tissue/stomach
  • fibrous osteodystrophy
  • secondary hyperparathyroidism
  • uraemic encephalopathies
  • cachexia
74
Q

What is the pathomechanism of dehydration causing uraemia?

A
  • PU, V, D
75
Q

What is the pathomechanism of oedema causing uraemia?

A
  • proteinuria
  • Hypoalbuminaemia
  • leads to increased glomerular permeability nephrotic syndrome
76
Q

What is the pathomechanism of pulmonary oedema leading to uraemia?

A
  • vascular damage, increased permeability
77
Q

What is the pathomechanism of ulcerative stomatitis, glossitis leading to uraemia?

A
  • vascular damage
  • ammonia
  • ammonia production by bacteria from urea in saliva
78
Q

What is the pathomechanism of ulcerative, haemorrhagic gastritis leading to uraemia?

A
  • ammonia
  • vascular damage
  • initially non-inflammatory
  • may get infected
79
Q

What is the pathomechanism of ulcerative, haemorrhagic enteritis leading to uraemia?

A
  • ammonia
  • vascular damage
  • colitis, oedema in stomach & prox SI
80
Q

What is the pathomechanism of fibrinous pericarditis, hydropericardium leading to uraemia?

A
  • vascular damage
81
Q

What is the pathomechanism of atrial/aortic lesions, ulcerations leading to uraemia?

A
  • endothelial/subendothelial damage
82
Q

What is the pathomechanism of myocardial degeneration leading to uraemia?

A
  • vascular damage
  • high K lvls
83
Q

What is the pathomechanism of CHF, L Ventricle hypertrophy leading to uraemia?

A
  • hypertension, RAAS
84
Q

What are the pathomechanisms of vascular lesions that lead to uraemia?

A
  • endothelial damage
  • secondary thrombosis
  • infarction in variety of tissues
85
Q

What are the pathomechanisms of nonregenerative anaemia leading to uraemia?

A
  • EPO deficiency
86
Q

What is the pathomechanism of mineralisation of soft tissue/stomach leading to uraemia?

A
  • altered Ca-P metabolism
87
Q

What is the pathomechanism of fibrous osteodystrophy leading to uraemia?

A
  • altered Ca-P metabolism
  • increased syntehsis of PTH
88
Q

What is the pathomechanism of secondary hyperparathyroidism leading to uraemia?

A
  • altered Ca-P metablism
89
Q

What is the pathomechanism of uremic encephalopathies leading to uraemia?

A
  • metablic acidosis
  • toxic waste products
90
Q

What pathomechanism of cachexia causes uraemia?

A
  • anorexia
  • v/d
91
Q

What is nephrotic syndrome?

A

Protein-losing nephropathy

92
Q

Nephrotic syndrome has damaged…

A

glomeruli in the presence of normally fxning tubules

93
Q

What are signs of nephrotic syndrome?

A
  • proteinuria +++
  • hypoproteinaemia
  • generalised oedema
  • hypercholesteraemia/hyperlipidaemia
94
Q

Clinical syndrome of nephrotic syndrome is characterised by…

A
  • hypoalbuminaemia
  • generalised oedema
  • hypercholesterolaemia
95
Q

Proteinuria in absence of UT inflammation is indicative of

A

glomerular damage

96
Q

Oedema is the result of…

A

decreased plasma colloid osmotic pressure, stimulation of RAAS, and release of ADH in response to hypovolaemia

97
Q

What is the hepatic response to hypoproteinaemia?

A
  • generalised increase in production of proteins incl lipoproteins
  • leads to hyperlipoproteinaemia & hypercholesterolaemia
98
Q

Dependent oedema

A

Hypoalbuminaemia –> plasma colloid osmotic pressure decreases –> interstitial fluid increases –> circulating vol decreases –> angiotensin activated (ADH release), Na retention increases –> dependent oedema increases

99
Q

dependent oedema is often seen in…

A

vental abd & legs due to gravity

100
Q

Renal aplasia

What is it? Predisposed breeds, assoc’d w/ ?

A
  • absence of kidney/renal tissue (bilateral = incompatible w/ life, unilateral = remaining kidney compensatory hyperplasia and increased vulnerability)
  • Predisposed: beagle, doberman, shetland sheepdog
  • Assoc’d w/: ureter aplasia, absent vas deferens/epididymis/uterine horns
101
Q

Renal Hypoplasia

What is it? species affected

A
  • kidney abnormally small but morphologically normal
  • species: cats
  • fxnl capacity lower to start w/ b/c one is smaller
102
Q

Renal Ectopia

What is it? Species affected, Predisposed to:

A
  • kidneys misplaced in pelvic cavity or inguinal region
  • unilateral in pigs/cats/dogs
  • Predisposed to: ureteral obstruction, hydronephrosis, pyelonephritis
103
Q

Renal Fusion

Significance, appearance

A
  • Appearance: horseshoe kidney
  • Significance: no clinical pathological significance
104
Q

Renal cysts

What is it? species affected? acquired how? Mechanism?

A
  • Cysts variable sized fluid-filled spaces lined by flattened epithelium anywhere in nephron
  • Species: All
  • Acquired by: chronic interstitial lesion, steroid txt, dialysis, assoc’d w/ renal dysplasia, chronic renal dz
  • Mechanism: obstruction of nephron, saccular dilation of tubules due to defective basement membrane, focal tubular epithelial hyperplasia
105
Q

Polycystic kidney dz

Species/breeds; associations, commonly leads to

A
  • species/breeds: cats (persians), dogs (Cairn terriers, WHWT), lambs, pigs, calves, foals
  • Associations: cystic bile ducts, pancreatic cysts, bile duct proliferation
  • Commonly leads to: stillbirth, neonatal death, chronic renal failure in 1st few wks of life
106
Q

Familial Renal Dz’s in dogs includes Progressive Juvenile Nephropathy. What is it?

A
  • aka Renal dysplasia
  • non-inflammatory, degenerative, or dvlpmtl chronic renal dz, nephron impacted of obscure pathogenesis in young animals
  • inbred lines of animals (mostly dogs)
  • young dogs: 4 mos to 5 yrs
  • progressive renal failure
107
Q

Renal dysplasia

What is it? Causes? Consequences?

A
  • Altered structural organisation that results from abnromal renal dvlpmt/differentiation
  • causes: familial renal dz in dogs or inherited renal dz in Suffolk shep, Japanese black cattle; foetal infection by teratogenic virus; in utero ureteral obstruction; hypovitaminosis A in piglets; anything that disrupts organogenesis
  • Consequences: diffuse & bilateral –> fxnl overloading of renal excretory capacity w/ time causes uraemia in 1st yr or 2 in life; any superimposed inflammation will hasten onset & dvlpmt of clin syndrome; ureteral anomalies concomitant, dysplastic kidneys abnormally susc to pyelonephritis
108
Q

What are specific tubular dysfxns of multiple transport defects?

A
  • Fanconi syndrome: Basenjis
  • Poor reabsorption of glucose/PO4/Na/K/Uric Acid/ AA’s from prox tubules –> PU, progressive renal failure
109
Q

What are specific tubular dysfxn due to single transport defects?

A
  • glucose –> Norwegian Elkhounds
  • Cystine –> some male dogs
  • No morphological changes
110
Q

Nephrogenic Diabetes insipidus

A
  • dogs, foals
  • Lack of responsiveness of cells of distal tubules & collecting ducts to ADH
  • congenital or acq’d tubulointerstitial dz

Clinical Reproduction & Urology (29 decks)

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