W06: CHRONIC & ACUTE KIDNEY DISEASE (2) Flashcards

1
Q

State the symptoms and signs of uraemia

A
Elevated levels of urea in the blood
Cognitive dysfunction (problems with thinking and remembering).
Fatigue.
Shortness of breath from fluid accumulation.
Loss of appetite.
Muscle cramps.
Nausea and vomiting.
Itching.
Unexplained weight loss.

Worse kidney function and more proteinuria is associated with worse outcomes

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2
Q

Describe biochemical investigations of renal disorders.

A

eGFR for excreting function

URINE DIPSTICK to detect proteins and traces of blood
or 24hrURINECOLLECTION

PROTEIN QUANTIFICATION for protein:creatinine

ANATOMY: histology (biopsy), imaging (chronic indicated in USS)

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3
Q

Describe the concept of eGFR and the classification of Chronic Kidney Disease based on this derived formula.

A

Kidney Damage / Normal or high GFR
>90 (1)

Kidney Damage / Mild reduction in GFR
60-89 (2)

-CHRONIC KIDNEY DISEASE UNDER 60-

Moderately Impaired
45-59 (3a)
30-44 (3b)

(4) Severely Impaired
15-29

(5) Advanced or on Dialysis
< 15

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4
Q

Describe the clinical features, biochemical and physiological abnormalities, investigations and principles of management of chronic renal failure.

A

DETECTION

  • pallor (anemia), HT, cog. decline, SOB,
  • kidneys (img)

SLOWING RENAL DECLINE via GENERIC TX
*BP control

*Control proteinuria (particularly ACE inhibitors / ARBs)

ASSESS COMPLICATIONS OF REDUCED eGFR

  • HT; anaemia; Vit D deficiency; acidosis
  • hyperphosphateaemia; hypoalbuminaemia
  • hyperparthydroidism

PREPARATION FOR RENAL REPLACEMENT THERAPY

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5
Q

Explain the significance of the relationship between plasma creatinine and GFR.

A

Creatinine is a product of muscle breakdown, and its clearance to estimate
GFR = C(in) = C(cr)

GFR = 1/P(cr) (proportional to classic GFR eq.)
NON-LINEAR

  • muscle mass varies
  • Creatinine will not be raised above the normal range until 60% of total kidney function is lost
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6
Q

Current CKD definition

A

Chronic kidney disease (CKD) is defined by either the presence of kidney damage (abnormal blood, urine or x-ray findings) or GFR<60 ml/min/1.73m2 that is present for ≥3 months

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7
Q

CKD aetiology

A
DM
Glomerulonephritis
HT
Renovasc.
Polycystic kidney disease: inherited, non-malignant, fluid filled cysts. decline in funct.
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8
Q

Significance of kidney imaging findings

A
THIN CORTICES (bilat.)
suggestive of intrinsic disease e.g. GLOMERULONEPHRITIS

UNILATERAL SMALL KIDNEY
suggestive of RENAL ARTERIAL DISEASE

CLUBBED CALYCES and CORTICAL SCARRING
suggestive of reflux + chronic infection/ischaemia

ENLARGED CYSTIC KIDNEY DISEASE
suggestive of CYSTIC KIDNEY DISEASE

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9
Q

HD vs PD

A

hemodialysis, blood is pumped out of your body to an artificial kidney machine, and returned to your body by tubes that connect you to the machine.

In peritoneal dialysis, the inside lining of your own belly acts as a natural filter. Wastes are taken out by means of a cleansing fluid called dialysate, which is washed in and out of your belly in cycles.

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10
Q

Definition of AKD

A

Increase in SCreatinine

  • ≥ 26.5 μmol/l (0.3 mg/dl ) (48 hours)
  • or to ≥ 1.5 times baseline (within 7d)

+Urine volume <0.5 ml/kg/h for 6 hours

AKI 1
creatinine: 1.5–1.9 times baseline
OR ≥ 26.5 μmol/l increase

output: <0.5 ml/kg/h for 6–12 hours

AKI 2
creatinine: 2.0–2.9 times baseline

output: <0.5 ml/kg/h for ≥12 hours

AKI 3
creatinine: 3.0 times baseline
OR Increase to ≥354 μmol/l (and above)
OR Initiation of renal replacement therapy

output: <0.3 ml/kg/h for ≥ 24 hours OR Anuria for ≥12 hours

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11
Q

Immediate consequences of AKI

A

AEIOU

A cidosis

E lectrolyte imbalance

I ntoxication

O verload

U raemic complications

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12
Q

Aetiological Factors of AKI

A

PRE-RENAL

  • cardiac failure
  • haemorrage
  • sepsis
  • n/v

INTRINSIC

  • Glomerulonephritis
  • Vasculitis
  • Radiocontrast
  • Myeloma
  • Rhabdomyolosis
  • Drugs

POST-RENAL

  • Tumours
  • Prostate disease
  • Stones
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13
Q

Describe biochemical investigations of renal disorders.

A

a

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14
Q

Discuss the presentation, natural history and principles of management of patients with acute renal failure.

A

PRINCIPAL MGMT:

  1. Volume status management
2. SHOUT
S epsis
H ypovol.
O bstruction
U rinanalysis
T oxins: cessation of tx acting on vasculature, avoid gentamicin, co-trimix., contrast media, stop metformin
3. REVIEW - BUMP
B loods - daily; bicarbs; ?hyperkalaemia
U ltrasound
M edicines - apt doses? 
P lan for fluid maintenance - fluid volume status
  1. FOLLOW-UP - RRT; d/t AEIOU ?
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15
Q

AKI sick day rules

A

v/diarrhoea; systemic

cessation of:
ACE inhibitors
ARBs
NSAIDS
Diuretics
Metformin
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16
Q

Investigating Hyperkalaemia

A

ECG:
peaked tented T-waves (first sign)

+ P = widens, flattens, eventually disappers
+ PR = lengthens
+ prolonged QRS

  • high-grade AV block, ventricular escape
  • conduction block
  • sinus brady. or slow AF
  • sine-wave apperance

•CARDIAC ARREST

17
Q

HYPERKALAEMIA Tx

A

Stabilise (myocardium)
*Calcium Gluconate

Shift (K+ intracellularly)

  • Salbutamol
  • Insulin-Dextrose

Remove

  • Diuresis
  • Dialysis
  • Anion exchange resins
18
Q

Urine dip interpretation

A

Urine specific gravity and osmolality values will be higher in pre-renal causes, whilst urine Na excretion will be lower, due to the kidney actively conserving Na and water in pre-renal cases, compared to intrinsic causes.

Any glomerulonephritis will show high levels of blood and protein.