Brainscape's Knowledge GenomeTM

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


See full index

Renal > Acute Renal Failure/Kidney Injury > Flashcards

Acute Renal Failure/Kidney Injury Flashcards

1
Q

Define ARF

A
  • clinical syndrome of sudden onset of haemodynamic, filtration and excretory failure of kidneys
  • subsequent accumulation of metabolic (uraemia) toxins and dysregulation of fluid, electrolyte and acidness balance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Define ARF

A
  • clinical syndrome of sudden onset of haemodynamic, filtration and excretory failure of kidneys
  • subsequent accumulation of metabolic (uraemia) toxins and dysregulation of fluid, electrolyte and acidness balance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Define AKI

A
  • acute kidney injury
  • abrupt decline in kidney function
  • acute ^ in creatinine concentration and/or acute decline in urine output (even if patient has not become azotaemic)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Is ARF reversible?

A

Potentially if dx early and animal supported while renal injury repaired
- irreversible renal damage may occur -> death

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

Define oliguria. How does its cause affect tx?

A

typically

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

How does ARF present? How can it be diagnosed?

A
  • many cases no hx or CS
  • potentially known toxin ingestion
  • anuric/polyuric
  • more often, lethargy, unwell, V+ or azotemia detected on bloods
  • ureic signs (smell, ulcers etc.)
  • dehydration
  • brady/tachycardia
  • painful kidneys
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Define AKI

A
  • acute kidney injury
  • abrupt decline in kidney function
  • acute ^ in creatinine concentration and/or acute decline in urine output (even if patient has not become azotaemic)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Is ARF reversible?

A

Potentially if dx early and animal supported while renal injury repaired
- irreversible renal damage may occur -> death

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

Clinical signs of ARF?

A
  • anuria and oliguria characterise severe forms
  • does NOT occur in all cases
  • some will be PU
  • NB: GFR does NOT = urine output
    > GFR can v as urine output ^ if reabsorption is becoming less effective
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How can pre-renal and renal azotemia be differentaited?

A
  • need urine and bloods obtained simultaneously (before starting IVFT)
    > USG >1.035 [cat] or >1.030 [dog] for pre-renal, 1.007-1.025 typically for a 1* renal
    > urine sediment inflam/casts with 1* renal sometimes
    > dipstick may show glycosuria in 1* renal sometimes
  • no biochem results can be used to make a distinction BUT hyperkalaemia more common in ARF or post-renal causes (though can occur in terminal phases of CKD
  • respnse to fluid tx dramatic with pre-renal, minimal if renal cases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does ARF present? How can it be diagnosed?

A
  • many cases no
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Can pre-renal azotemia ever be present when USG

A

Yes : diuretics or drugs affecting concentrating ability (functional impediment to urine concentration)
- fluids, diuretics, glucocorticoids, Addiosons, hypercalcaemia
> can be better prognosis if functional renal failure present rather than structural intrinsic renal disease (where nephrons have physically been lost)

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

Causes of post-renal azotemia?

A
  • urethral obstruction

- bladder rupture

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

Causes of pre-renal azotemia?

A
  • severe dehydration
  • shock
  • any condition -> poor renal perfusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How can pre-renal and renal azotemia be differentaited?

A
  • need urine and bloods obtained simultaneously (before starting IVFT)
    > USG >1.035 [cat] or >1.030 [dog] for pre-renal, 1.007-1.025 typically for a 1* renal
    > urine sediment inflam/casts with 1* renal sometimes
    > dipstick may show glycosuria in 1* renal sometimes
  • no biochem results can be used to make a distinction BUT hyperkalaemia more common in ARF or post-renal causes (though can occur in terminal phases of CKD
  • respnse to fluid tx dramatic with pre-renal, minimal if renal cases §
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

DO failing kidneys produce dilute urine?

A

NO! Canot dilute so hyposthenuria does NOT occur in kidney failure

17
Q

Can pre-renal azotemia ever be present when USG

A

Yes : diuretics or drugs affecting concentrating ability (functional impediment to urine concentration)
- fluids, diuretics, glucocorticoids, Addiosons, hypercalcaemia
> can be better prognosis if functional renal failure present rather than structural intrinsic renal disease (where nephrons have physically been lost)

18
Q

How can ARF and CKD be differentiated?

A
  • NO LAB TESTS! Hyperphosphatemia seen with both acute and chronic
    > Except renal BIOPSY (but this is invasive and results take a long time)
  • PE: poor BCS, poor quality haircoat
  • Hx: wt loss, v apetite, PUPD v hx of access to nephrotoxic drugs or toxins
  • non-regenerative anaemia typically with CKD but can occour with ARF (eg. d/t haemorrhagic shock) or overhydration
  • renal size (generally v with CKD, ^ with ARF but some chronic dz -> normal/^ kidney size)
  • presence of CKD mineral bone disorder (renal 2* hyperparathyroidism) : resorption of bone esp. around the teeth
    > NB: rubber jaw may be a presenting sign but very rare and only seen in young growing animals
19
Q

3 main causes of acute renal failure?

A

> pre-renal
intrinsic renal
- tubular necrosis (v. common) d/t ichaemia or toxins or both
- interstitial nephritis (common)
- acute glomerulonephritis (uncommon, next lect)
post-renal

20
Q

What is hospital acquired ARF/AKI?

A
  • ischaemia and toxin effects on kidney working synergistically -> tubular necrosis
  • eg. CV dz pre-existing, age, fever, dehydration, drugs
21
Q

Cause and clinical signs of pyelonephritis? How is it diagnosed?

A

> ascending UTI -> renal pelvis and medulla causing an INTERSTITIAL NEPHRITIS
CS
- systemic illness (fever, renal pain, nephromegaly)
- BUT signs may be absent
- PUPD esp with E. Coli
- can cause acute/chronic renal azotemia
Dx presumptive based on cultures obtained from LUT, imaging and hx findings
- if pelvis dilated can aspirate for culture under u/s guidance

22
Q

Tx pyelonephritis?

A

As for complicated UTIs (selection of ABx based on culture, 4-6w tx, cultures a week after starting and finishing tx)

23
Q

What infectious organism also causes an interstitial nephritis?

A

> Leptiospriosis

  • ZOONOTIC
  • spirochete bacteria (each serovar typuically has 1+ host species that carry the organism asymptomatically and shed in the urine)
24
Q

Clinical signs of leptospirosis in a non-host organism>

A
  • ARF

- hepatocellular necoris

25
Q

Most common route of infection of leptospirosis?

A
  • contaminated water

> most commonly now non-vaccinal serovars that affect dogs (ie. not canicola or icterohaemorrhagica)

26
Q

Do cats get lepto?

A

No resistant

27
Q

How can lepto be dx?

A
  • high Ab titre to non-vaccinal serovars
  • rising titre over a few weeks
  • PCR (not very sensitive, maybe d/t Ab use before testing?)
28
Q

Tx leptospirosis?

A
  • tx ARF
  • penicillins (usually amoxicillin)
  • if dx confirmed then 2w course doxycycline prescribed to eliminate infection and prevent dog become a chronic carrier
29
Q

What must be remembered about lepto?

A

ZOONOTIC

- carefully manage patients, don’t come into contact with urine

30
Q

2 causes of tubular necrosis?

A

> ischaemia
- outer medulla exists in a constant state of oxygen deprivation
- cells of PCT high metabolic rate
- mitochondrial injury, cell swelling, tubular obstruction
- d/t yhpovolaemia, v effective circulating volume (heart failure/cirrhosis), thrombosis, excessive renal vasoconstriction
- pre-renal azotemia can -> renal d/t ischameia if hypoperfusion not rectified
toxins
- may occour concurrently and synergistically with ishaemia
- often leaves some BM intact so if given the supportive tx kidneys can recover

31
Q

Egs of nephrotoxic drugs and substances?

A 
> drugs
- Abx (aminoglycosides, tetracyclines, amphotericin B [fungal]) 
- chemotx (doxorubicin [cats], cis and carboplatin, methotrexate) 
- NSAIDs
- ACEI
- IV contrast agents 
> other
- hypercalcaemua
- rasins/grapes (dogs) 
- ethylene glycol (cats) 
- plants [lillies] (cats) 
-myoglobin/haemoglobin 
- heavy metals
- pesticides/herbicides
- snake venom
32
Q

3 miscellaneous causes of ARF/AKI?

A 
> lyme disease
- borrelia burgdorferi 
- acute glomerular disease
> Renal lymphoma 
> cutaneous/renal vascular glomerulopathy (New FOrest Syndomre/Alabama Rot) 
- thrombotic microangiopathy
33
Q

How can ARF be prevented?

A

> some unavoidable (toxins etc.)
in the hospital ID patients at high risk
- pre-existing CKD
- dehydrationhypovolaemia/hypotension
- sepsis/fever/hyperthermia
- systemic dz/multiple organ failure
- prolonged anaesthesia
- drug tx (NSAIDs, aminoglycosides, cisplatin, amphotericin, ACEI)
more effectively prevented by correcting fluid deficits and mild ECF volume expansion

34
Q

Tx ARF/AKI?

A

aim to maintain the animal while kidneys repair themselves
> prevent continued toxin exposure or give antidotes
- induce vomiting, NB: maintain euvolaemia
- 4-methylpyrazole for ethyleme glycol $$$
> Tx 1* underlying disease if possible
> correct fluid deficits
- monitor in and outs to prevent overhydration
- aim for mild 3-5% ECVF fluid expansion
> Recitfy potassium and acid/base balance
> attempt to ^ urine output if required
- NB: urine output does NOT = GFR
> other pharmacological tx
- controversial and infrequently used
> control V+
- address nutritional requirements
> renal replacement tx
- haemodialysis or peritoneal dialysis

35
Q

Give examples of drugs that can be used to attempt to ^ urine output if necessary?

A

> mannitol
- slow IV bolus
- ^ renal blood flow, v cellular swelling, dispense tubular debris and scavenge free radiacal (Appaz)
- indicated early in course of ARF but animal MUST BE EUVOLAEMIC, not in hert failure or overhydrated
- only useful if already producing some urine
- rarely used
furosemide
- boluses or CRI
- +- other drugs
- promotes formation of urine, facilitates management of overhyration and hyperkalaemia
- may deplete circulating volume -> pre-renal insult

36
Q

Which other pharmacological tx may be used 9controversially) with ARF?

A

> dopamine
- suggested to cuase renal vasodilation and ^ blood flow at low dodses
- not recommended unless ^ BP needed- high doses -> tachycardia, arrhythmias, vasoconstriction
- do not use in cats
Fenoldopam
- selective DA1 ag sometimes used in preference
Diltiazem
- pre-glomerular arteriolar dilation and improve renal blood flow
- v calcium influx into damaged tubular cells may also be beneficial

37
Q

Can extensive tubular injury be repaired?

A
  • even if potentially reversible usually not possible to keep patients alive for weeks/months like humans on dialysis to allow regeneration
38
Q

What can be used as an earlier indicator of acute renal failure?

A

Enzymeuria (occurs before azotaemia begins)

Renal (23 decks)

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