Brainscape's Knowledge GenomeTM

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


See full index

Michaelmas 5th year > Nephrology and urology 2 > Flashcards

Nephrology and urology 2 Flashcards

1
Q

Which species has no renal pelvis

A

Cattle

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

What are pale streaks seen in the inner cortex of dogs

A

Fat in the collecting ducts

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

Which species excrete excess calcium as calcium carbonate in urine

A

Horses
Rabbits

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

Why is equine urine foamy

A

Due to mucus content; has mucus glands in renal pelvis

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

In the vascular supply to the kidney which arteries are possible functional end arteries and which are always functional end arteries

A

Possible ones: interlobar arteries
Definitie = interlobular arteries
TOtal supply = renal artery –> interlobar – arcuate –> interlobular –> afferent artery of glomerulus –> efferent

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

What is the functional reserve capacity of the kidney

A

60-75%
At ~60% start seeing PU/PD
At 75% start seeing azotaemia

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

What GFR would be considered renal insufficiency vs renal failure

A

Renal insufficiency = 25-50% of GFR left; here can have azotaemia
Renal failure = just 20-25% left; get uraemia

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

What is the difference between azotaemia and uraemia

A

Azotaemia = elevated urea and creatinine concentrations vs uraemia = clinical signs and pathology assocaited with azotaemia

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

What happens in acute renal failure

A

Sudden loss of 70-100% of nephrons
related to ischaemia, nephrotoxin exposure, complete obstruction

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

What is the key difference in body pathology with chronic renal failure vsacute

A

With chronic there is time for non-renal lesions of uraemia to develop

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

Non-renal lesions of chronic renal failure (basic)

A
  • Gastric haemorrhagic ulceration; due to ammonia
  • Calcium deposits on gastric mucosa and pleura
  • Uraemic pneumonitis
  • Oral cavity ulcerative gingivitis due to conversion of urea to ammonia in saliva

+ can see retinal separation due to hypertension
+ can see osteodytrophia ue to renal secondary hyperparathyroidism
+ can get anaemia

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

Why can we see anaemia with chronic kdieny disease

A

Impairment of erythropoietin secretion from kidney
Uraemia assocaited with increased RBC fragilits

= normocytic, normochromic non-regnerative anaemia

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

What is the difference between dystrophic and metastatic mineralisation

A

Dystrophic = mineralisation in areas of necrosis because dying cells unable to regulate calcium influx

Metastatic = in normal tissues secondary to hypercalcaemia

See both in renal disease because there is vascular necrosis due to ammonia presence AND raised calcium

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

Pathology with uraemic pneumonitis

A

Lungs have firm glassy cut surface
Pulmonary oedema
Mineralisation of alveolar walls
Blood vessel degeneration

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

Why do we get ulcerative gingiivitis, stomatitis etc in chronic renal failure

A

Due to conversion of urea to ammonia in saliva causing vascular necrosis

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

Why can we get retinal separation in chronic renal failure

A

Renal iscaemia activates juxtaglomerular complex and RAAS system to secrete renin to increase blood pressure to restore perfusion
BUT in chronic renal failure, prolonged hypertension damages small arteries/arterioes, exacerbating renal hypoperfusion more so get progressive hypertension

End stage is nephrosclerosis; non-functional glomerulus exacerbates RAAS activation and hypertension even more

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

What cardiac effect can we get with chronic renal failure

A

Left ventricular hypertrophy; due to chronic RAAS activation and hypertension

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

What is osteodystrophia fibrosa in relation to renal disease

A

REnal disease reduced phosphorus excretion
- This causes reciprocal ionised Ca2+ fall which stimulates PTH release (+ PTH release stimulates directly by raised phosphorus)

PTH can’t cause increased phosphorus secretion in chronic renal failure because kidney not functional; still have hyperphosphataemia and more PTH release

PTH causes resorption of calcuim from bone and replacement with fibrous tissue
+ reduction in vit D related Ca2+ uptake because vitD is activated in kidney

–> Get osteodystrophia fibrosa = extensive bone resorption and proliferation of fibrous tissue

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

What do animals with chronic renal failure die from

A

Heart failure related to metabolic acidosis, hyperkalaemia, pulmonary oedema

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

What is more common between glomerulitis and glomerulonephritis and what is the difference

A

Glomerulitis = focal nephritis affecting just the glomerulus; tends to be part of systemic disease where bacteria from bacteraemia lodge in glomeruli

Glomerulonephritis = inglammation of glomeruli and nephrons; more common
- Tends to be related to immune complex deposition in dogs/cats

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

Where do immune complexes in glomerulonephritis come from

A
  • Low pathogenicity infection that causes persistend antigenaemia –> complexes then deposit in the glomerulus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What does a kidney with glomerulonephritis look like in acute vs chronic stages

A

Acute = swollen, pinpoint red dots in cortex
Chronic = shrunken cortex, fine granularity, white dots on cortex

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

What is glomerulosclerosis

A

End stage of chronic glomerulitis; glomeruli and thickened and non-functinoal

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

In amyloidosis, where is the amyloid deposited

A

Mostly in mesangium and glomerular BM

Can get medullary deposition in cats and SHar-pei dogs

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

What are the 3 types of amyloidosis

A

1) Primary = monoclonal gammopathy; immunoglobulin light chain related
2) Secondary; amyloid AA from serum amyloid A i.e with chronic inflammatino
3) Familial amyloidosis

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

Gross pathology of amyloidosis kidney

A

Pale, waxy kidneys with pale swollen cortex
Pin point white foci = glomeruli
Odema

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

What other effects aside from kdieny may be seen in amyloidosis

A

Effects of amyloid deposition on other tissues e.g causing diarrhoea

Can get liver elaboration in response to hypoproteinaemia (nephrotic syndrome) from glomerular damage –> hyper cholesterolaemia seen

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

Histopath of amyloidosis in kidney

A

Protein casts in renal tubules
Amyloid stained with congo red expanding glomerulus
Eosinophilic deposits in glomeruli expant the flomerulus

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

How does amyloidosis lead to uraemia

A

Amyloid deposition and glomerular damage –> leaky basement membrane –> proteinura, hypoproteinaemia (= nephrotic syndrome) –> oedema

as disease workens, capillaries in glomerulus occluded and get failure of filtration, uraemia etc

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

Wht is nephrotic syndrome

A

Where thereare leaky glomerular BMs (from amyloidosis or glomerulonephritis) which causes loss of plasma proteins into urine –> hypoproteinaemia, oedema/ascites etc

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

Why do we get hypercholesterolaemia in nephrotic syndrome

A

Response to hypoproteinaemia –> liver elaboration
This also gives hypercholesterolaemia

32
Q

Difference in infarct appearance in interlobar/arcuate artery occlusion vs interlobular artery occlusion

A

Interlobar gives infarcted triangle of cortex AND medulla
Interlobular arteries jsut affects section of cortex

33
Q

Macroscopic appearance of kidney infarct and how does it change over time

A

WEdge shape and red in acute phase
Then becomes bale
Then get fibrosed and sunken

34
Q

What is hydronephrosis

A

Where there is dilation of renal pelvis and pressure atrophy of rest of kidney due to obstruction of renal flow in face of continued filtration

35
Q

What is renal dysplasia and when might it be seen

A

disorganised development of renal parenchyma
- In utero or early post-natal life before nephrogenesis is complete

Get a small, mishsapen, cystic and fibrsed kidney

36
Q

Histopathology of kidney with renal dysplasia

A

Structures are inappropriate to development stage; e.g retained fetal glomeruli

37
Q

Key difference between renal cysts and hydronephrosis

A

In cysts, the fluid expands from cyst in medulla/cortex vs from renal pelvis in hydronephrosis

38
Q

Which breeds is polycystic kidney disease seen in

A

Bull terriers, Persian cats
Westies, cairn terriers

39
Q

Which breed has hereditary nephropathy related to X linked COL4A5 gene

A

Samoyeds

40
Q

What is E cuniculi

A

Obligate intracellular microsporidian parasite
Affects rabbits

41
Q

What signs can E cuniculi cause in rabbits

A

Neurological disease; head tilt, paresis
Renal disaese; PU/PD, weight loss, haematuria non-regnerative anaemia

42
Q

What do the kidneys look like in rabbit with E cuniculi

A

Irregularly pitted
Have granulomatous interstitial nephritis and fibrosis

43
Q

What do we tend to fnd on histopathology in chronic kidney disease

A

diffuse tubulointerstitial nephritis and fibrosis with secondary glomerulonephritis and mineralisation

44
Q

What must we ensure before IRIS staging CKD

A

That the animal is stable and hydrated to avoid contributions to azotaemia from pre-renal azotaemia

45
Q

What are the IRIS stages of CKD

A

1 = normal creatinine/normal to increase SDMA but there are indicators of renal disease present
2 = mild renal azotaemia; only mild clinical signs
3 = moderate renal azotaemia with clincial signs present
4 = severe renal azotaemia; high risk of getting into crisis

46
Q

What is the main cause of renal proteinuria in CKD

A

Tubular dysfunction causing inability to rebasorb protein

There is also contribution from increased glomerular protein flux with flomerular hypertension secondary to nephron loss

47
Q

Factors associated with the progression of CKD

A

Mineral and bone disorders
Proteinuria
Hypertension
Hypoxia, hypoperfusion, ischaemia

48
Q

How does CKD cause metabolic bone disease and what factor mediates this

A

Net increase in serum phosphate in early stages triggers FGF-23 increase which inhibits PTH and active vit D (calcitriol)

FGF-23 is renaly cleared; as GFR falls it is excreted less + less phosphate removal so more FGF-23

End organ resistance to FGF-23 decreases ability to inhibit PTH

Get reduction in ionised calcium which stimulated PTH secretion and causes calcium and phosphate resorption
Eventually have high Ca2+ and high phsophate at high time

49
Q

What electrolyte changes lead to mineralisation of tissues in end stage CKD

A

High calcium and phosphate

50
Q

Why do we have normal phosphate in IRIS stage 1 and 2

A

Because there is intial compensation via FGF-23
- Increase in PTH precedes hyperphosphataemia

51
Q

Consequences of CKD-MBD

A

Renal osteodystrophy; rubber jaw
Soft tissue mineralisation

52
Q

How is hypertension a risk factor for CKD progression

A

Exacerbates glomerular hypertension and causes glomerulosclerosis and proteinuria

53
Q

How does hypoperfusion lead to renal medullary hypoxia

A

Efferent arteriole vasoconstricts to preserve GFR but this decreases blood flow to glomerulus, exacerbating hypoxia to the medulla

54
Q

How to increase hydration in CKD

A

Switch to wet food
water fountains
IV fluids
Subcut fluids
Feeding tube

55
Q

Dietary management of CKD

A

Most important = phosphorus restriction; if not at target via diet add in phosphate binders
Highly digestible protein
Add in soluble fibre to reduce colonic pH to act as a nitrogen trap and reduce urea
K+ supplementation; lost in PU
Metabolic acidosis common so may want alkalinising deit

56
Q

At what IRIS stage do we introduce renal diets

A

2

57
Q

What is a risk of starting a renal diet when the serum phosphate is not high i.e already in target

A

Can get hypercalcaemia which drives renal progression
So want to switch to senior or EARLY renal diet

58
Q

What is the goal for blood pressure in CKD treatment and what do we use for this

A

Want between 120-160mmHg
Amlodipine, ACe inhibtiors

59
Q

Why do we not start with amlodipine to treat hypertension in dogs and why can we in cats

A

In dogs it preferentially dilates the afferent arteriole which can increase capillary hydrostatic pressure and GFR and glomerular hypertension

Doesn;t happen in cats

60
Q

How much sodium do we want in renal diets

A

Too low associated with RAAS activation and doesn’t decrease BP
Want mild sodium restriction to enhance anti-hypertensive effects of drugs

61
Q

How much do we want to reduce proteinuria by depending on original UPC

A

If UPC starts at <2 then go to <0.5 in dogs and 0.4 in cats
If UPC >2 want minimum of 50% decrease

62
Q

How does RAAS activation work in CKD

A

Decreased GFR in CKD causes activation of RAAS; get contsriction of efferent arteriole to improve the GFR BUT leads to glomerular hypertension, proteinuria, pro-inflammatory and pro-fibrotic pathways
Get progression of disease

63
Q

What is ACE escape

A

When ACE-independent pathways produce angiotensin II which makes them refractory to treatment part way through

64
Q

Which angiotensin receptor do we want to block

A

the AT1: since this one causes vasoconstriction, symp activation etc
Don’t want to block AT2 since this is renoprotective and causes vasodilation etc

65
Q

What advantage do angiotensin receptor blockers have over ACE-inhibtiros

A

Not affected by ACE escape

66
Q

When should we take caution with reducing blood pressure in CKD

A

In stage 4 CKD, GFR is so low already that cuasing this vasodilation will make it much worse

Avoid if patient is dehydrated because this angiotensin II mediated efferent arteriole constriction may be the only thing maintaining the GFR

67
Q

What electrolyte are renal diets supplemented with

A

K+

68
Q

Treating anaemia in CKD

A

Darbopoietin = human recombinant erythropoietin; use mostly in stage 3/4
+ can add in parenteral iron monthly injections

69
Q

Where do we want to get the PCV to in CKD

A

Lower end of normal

70
Q

When could we do calcitriol treatment in CKD and what are the risk

A

Only if phosphate controlled and ionised calcium/phosphate monitored well
There is a risk of causing hypercalcaemia and leading to renal minterlisation and progression

= to suppress PTH

71
Q

Summary of management of glomerular disaese

A

Treat hypertension
Treat proteinuria
Renal diets
May do immunsuppression only if renal biopsy indicated immune based pathogenesis

72
Q

When might we add in darbopoietin as part of CKD treatment

A

If PCV <20% in cats, <25-30% in dogs `

73
Q

Hallmarks of nephrotic syndrome

A

Proteinuria
Hypoalbuminaemia
Oedema
Hypercholesterolaemia

74
Q

When should we start blood pressure treatment straight away in kidney patients

A

If BP >200mmHg or there is target organ damage

e.g retinal retachment, left ventricular hypertrophy, brain hypertensive encephalopathy

75
Q

How do phosphate binders work

A

Complex with dietary phosphate to prevent GI absorption
- Must be done alongside renal diet with low phosphat

76
Q
A

Michaelmas 5th year (41 decks)

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