Brainscape's Knowledge GenomeTM

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


See full index

Renal > Acute renal failure > Flashcards

Acute renal failure Flashcards

1
Q

Define ARF

A
  • sudden onset haemodynamic, filtration and excretory failure of kidneys
  • subsequent accumulation of metabolic/uraemic toxins
  • dysregulation of fluid, electrolyte and acid-base balance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Defome AKI

A

= Acute Kidney Injury

  • may be preferred over ARF term
  • abrupt decline kidney function
  • acute increase in [creatinine] and/or acute decline in urine output even if patient hasn’t become azotaemic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Is ARF reversible?

A
  • yes potentially if diagnosed early after onset and animal is supported
  • delay –> irreversible renal damage and death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

CS - ARF

A
  • oliguria and anuria characterise severe ARF (not always though)
  • polyuric (sometimes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Is urine output the same as GFR?

A

No - 99% fluid filtered by glomerulus is reabsorbed by the tubules. If this process becomes less effective and less reabsorption occurs, urine output may increase, even though GFR is declining

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

Define loiguria

A
  • variable definitions

- typically

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

What is physiologica oliguria?

A
  • when oliguria occurs as result of normal hysiology
  • if patient is hypovolaemic it is apprpriate for kidneys to conserve fluid and v. small urine volume to be produce
  • appropriate tx is volume resuscitation, not diuretics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Dx - ARF

A
  • no hx or PE are specific (dehydration, oral ulcer/uraemic colour, hypothermia, bradycardia/tachycardia, swollen painful kidneys or normal)
  • occasioanlly known toxin ingestion or noted animal is anuric or polyuric
  • usually unwell, lethargic or vomiting, azotaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What 2 quesitons should always be asked with newly documented azotaemia?

A
  • acute/chronic?

- pre-renal, renal or post-renal?

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

How do you differentiate acute and chronic azotaemia?

A
  • hx
  • PE incl. renal size
  • non-regenerative anaemia
  • renal ultrasound
  • CKD-Mineral Bone Disorder (secondary hyperparathyroidism). Care - hyperphosphataemia occurs with acute and chronic disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Causes - azotaemia

A
  1. High production of nitrogenous waste (pre-renal, urea only)
  2. Low GR (pre-renal with reduced renal perfusion, renal with intrinsic or functional renal disease or post-renal with urinary obstructin)
  3. Reabsorption urine escaped from urinary tract (Post-renal)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

When is UA indicated?

A

whenever blood tests are performed, especially when evaluating renal function

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

Differentiate pre-renal and renal azotaemia by USG?

A 
PRE-RENAL:
Dog = >1.030
Cat = >1.035
RENAL:
Dog =
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

UA findings - Renal azotaemia

A
  • glucosuria
  • casts
  • Ca oxalate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the response to IVFT with pre-renal and renal azotaemia?

A
  • Good response with pre-renal. May or may not have a response with renal azotaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe pyelonephritis

A
  • cause: ascending infection most common
  • may be PU/PD
  • not always azotaemic
  • consider breaches of UT defences
  • treat aggressively
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Breaches of UT defences that may –> pyelonephritis

A
  • ANATOMICAL: ectopic ureters, perineal urethrostomy
  • MEDICAL: diabetes, renal dz, nephroliths
  • IATROGENIC: catheters, steroid therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Tx - pyelonephritis

A
  • AGGRESSIVE:
  • culture urine, empiric AB initially
  • re-culture on tx, continue 4-6wks
  • reculture 1-2 wks post-tx
19
Q

Commonest leptospira serovars

A
  • L.grippotyphosa
  • L.pomona
  • L.autumnalis
20
Q

CS - leptospirosis

A
  • hepatic necrosis
  • thrombocytopaenia
  • vasculitis
21
Q

Dx - leptospirosis

A
  • rising titre to non-vaccinal serovar

- PCR available, lack sensitivity - perhaps since many have received ABs by time this test is run.

22
Q

Tx - leptospirosis

A 
ACUTE tx:
- penicillins (usually amoxicillin)
- penicillin G or ampicillin
TO CLEAR INFECTION/ carrier status:
doxycycline, 2 weeks
23
Q

3 main types of intrinsic renal failure

A
  • TUBULAR NECROSIS (v common)
  • INTERSTITAL NEPHRITIS (V common)
  • ACUTE GLOMERULONEPHRITIS (uncommon)
24
Q

What are the 2 types of tubular necrosis?

A
  1. ischaemia (common)

2. toxins (common)

25
Q

List toxins causing renal injury

A
  • EG
  • raisins/ grapes
  • plants (lillies in cats)
  • heavy meatals
  • pesticides/ herbicides
  • snake venom
  • myoglobin/ haemoglobin
  • calciferol rodenticides
26
Q

Which therapeutic agents can cause renal injury?

A
  • ANTIMICROBIALS: aminoglycosides, TCs, amphotericin B
  • CHEMOTHERAPEUTICS: doxorubicin (cats), cisplatin and carboplatin, methotrexate
  • NSAIDs
  • ACEIs
  • IV CONTRAST AGENTS
  • MANY MORE
27
Q

Causes - ischaemic ARF/AKI

A
  • reduced intravascular volume
  • hypotension
  • decreased effective intravascular volume (HF, cirrhosis)
  • sepsis
  • drugs (cyclosporine, NSAIDs, ACEI)
  • vascular dz (thrombosis, vasculitis)
28
Q

Why are PCT cells prone to ischaemic injury?

A

v high metabolic rate making them particularly vulnerable –> mitochondrial injury, cell swelling and tubular obstruction

29
Q

T/F: a patient initially presenting with pre-renal azotaemia may progress to intrinsic renal azotaemia d/t ischaemia if hypoperfusion of kidneys not quickly rectified.

A

True

30
Q

Causes - hospital acquired AKI

A
  • advanced age
  • fever
  • dehydration
  • cardiac dz
  • pre-existing renal dz
  • anaesthesia/sx
  • nephrotoxic drugs
31
Q

Pathogenesis - hospital acquired AKI

A
  • decreased glomerular ultrafiltration coefficient
  • intra-tubular obstruction
  • back-leak fluid across disrupted epithelium
  • intra-renal vasoconstriction
32
Q

Management principles - AKI/ARF

A
  • tx inciting cause
  • improve renal haemodynamics (mild volume expansion)
  • maintain homeostasis (K, acid-base)
  • supportive care (nutrition, control V)
  • allow renal repair time to occur
33
Q

Other causes ARF/AKI

A
  • Lyme disease (B. burgdorferi) –> acute glomerular dz
  • Renal lymphoa
  • cutaneous and renal vascular glomerulopathy (‘New Forest Syndrome in UK, ‘Alabama rot’ in USA): caused by a thrombotic microangiopathy
34
Q

Which animals are at particular risk of ARF?

A
  • pre-exisiting CKD
  • dehydration/ hypovolaemia/ hypotension
  • sepsis/ fever / hyperthermia
  • systemic dz/ multiple organ failure
  • prolonged anaesthesia
  • drugs (NSAIDs, aminoglycosides, cisplatin, amphotericin, ACEI)
35
Q

What is the most consistent renal protective effect?

A

correction of fluid deficits and mild ECF volume expansion

36
Q

Antidote - EG

A

4-methylpyrazole (but prohibitively expensive in UK)

37
Q

How much should you aim to expand ECF volume?

A

mild (3-5%) increase. REquires v vareful monitoring including serial measurements of body weight, urine output, CVP, PCV/TP and repeated PE

38
Q

Name 2 drugs that increase urine output

A
  • MANNITOL: if early in ARF course if not hypovolaemic, already overhydrated or in CHF. Thus rarely used.
  • FUROSEMIDE: to promote urine formation, manage overhydration and hyperkalaemia. Improper monitoring –> pre-renal insult on established renal injury
39
Q

Outline use of Dopamine in ARF

A
  • catecholamine suggested to cause renal vasodilation and improved BF at low dose
  • CONTROVERSIAL: should only be used if required to maintain BP
  • high dose –> vasoconstriction, tachycardia and arrhythmias
  • NOT in cats
  • acts on both DA-1 and DA-2 receptors
  • Fenoldopam is a selective DA-1-R agonist sometimes used preferentially
  • diltiazam suggested as alternative
40
Q

Outline diltiazem as alternative to dopamine in ARF

A
  • causes pre-glomerular arteriolar dilation and improves renal BF
  • reduced Ca influx into damaged tubular cells may also be beneficial
41
Q

Can you tx ARF directly?

A
  • No
  • maintain the animal while the kidneys repair
  • usually not possible to keep patient alive for weeks-months if extensive tubular injury has occurred for their repair
42
Q

Describe enzymuria

A
  • measure enzymes in urine
  • early indicator of AKI (before azotaemia)
  • e.g. NAG, yGT, N-Gal
  • monitor when tx with nephrotoxic drugs
43
Q

Parameters to measure fluid balance with AKI patients

A
  • ‘ins and outs’
  • CVP
  • serial body weight
  • serial PE
  • serial PCV/TP
  • OTHERS (electrolytes, ECG, renal function q48-72h)
44
Q

2 methods of increasing urine output pharmacologically

A
  • DIURETICS: furosemide, mannitol

- VASOACTIVE AGENTS: dopamine, fenoldopam, diltiazem

Renal (30 decks)

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