6- CKD and AKI Flashcards

(40 cards)

1
Q

What is an AKI

A

Renal function deterioration over hours/days

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2
Q

What rises in AKI (Blood)

A

Urea and creatinine

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3
Q

Is AKi reversible

A

Can be

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4
Q

Consequences of AKI

A

Volume overload, metabolic acidosis, hyperkalemia

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5
Q

What causes the most AKIs

A

Pre renal cause

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6
Q

Pre-renal causes

A

Hypovolemic
Shock
Renal artery stenosis
NSAIDs and ACEI

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7
Q

How do NSAIDs and ACEI cause AKI

A

Impair mechanism of renal autoregulation

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8
Q

Intrinsic causes of AKI

A

Acute tubular necrosis- ischemia, rhabdomyolysis, drug toxicity, toxins

Acute interstitial nephritis- drugs, hypercalcemia, myeloma

Glomerular disease- acute glomerulonephritis, rapidly progressive glomerulonephritis.

Vascular disease- vasculitis, malignant hypertension, thrombotic microangiopathies

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9
Q

What is a sign of Rhabdomyolysis

A

Dark urine. Muscle breakdown–> myoglobin –> filtered but toxic.

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10
Q

Post renal causes of AKI

A

Bladder outflow obstruction
Tumour
Stone- bilateral to cause AKI
Retroperitoneal fibrosis causing ureteral obstruction

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11
Q

Basic investigations

A

Urine test- microscopy, dipstick, cytology
Bloods
Imaging

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12
Q

What biochemical changes occur

A

Increased plasma urea, creatinine, urate, phosphate, potassium
Decreased plasma sodium, calcium
Metabolic acidosis
Increased anion gap

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13
Q

How to manage AKI

A

Fluid replacement to optimise flow and correct hypovolemia
Correct electrolyte imbalances
Catheter if obstruction

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14
Q

What are the life threatening complications of AKI

A

Hyperkalemia
Pulmonary oedema
Bleeding

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15
Q

What is CKD

A

Progressive loss of function over months and years

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16
Q

Is CKD reversible

A

No, renal tissue replaced by extracellular matrix in response to damage.

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17
Q

Whats a good GFR

18
Q

Stage 2

19
Q

Stage 3

20
Q

Stage 4

21
Q

Stage 5

A

<15 -dialysis or transplant

22
Q

Increased incidences in what people

A

Ethnic, elderly, multi-morbid, social deprivation, diabetes, hypertension

23
Q

Pathology of CKD- what happens to kidney

A

Medulla maintains but cortex (where nephrons are) thin.

24
Q

Who gets CKD screening

A

Diabetes
Hypertension
CVD
Those on nephrotoxic drugs

25
What blood tests to use
``` U&Es eGFR Bone biochemistry FBC CRP Iron PTH ```
26
Other investigations for CKD
USS- kidney size Biopsy CT MRI
27
Management
``` Lifestyle modification Uncontrolled diabetes control Hypertension control Proteinuria - ACEI Lipid control ```
28
What are the functions of the kidneys
BP, volume, pH, electrolytes, osmolality, excretion of waste, metabolism of drugs
29
What is the endocrine function of the kidneys
Inactive Vit D, renin, EPO
30
Water handling in kidney during CKD
Reduced GFR means lost ability to maximally dilute and concentrate urine.
31
Nocturia in CKD
Small filtrate but same solute loads causes osmotic diuresis- reduces maximum concentrating ability and response to ADH
32
Effect on low GFR on K+ (and ACEI)
Hyperkalaemia | Need to stop ACEI as aldosterone helps to excrete K+ by increasing ROMK expression
33
CKD and bone mineral disease
Decreased activation of Vit D = less Ca = PTH stimulated = bone breakdown. As kidneys aren't functioning well then PO4 isn't excreted = precipitates = vessels, joints, skin. Manage: give Vit D supplements
34
Drug sensitivity in CKD
Increased as elimination is impaired.
35
Accumulation of waste products- symptoms
Uraemic symptoms- reduced appetite, nausea and vomiting, pruritus
36
End stage renal failure
GFR < 15mls/min | Requires RRT
37
Symptoms of dialysis
Tiredness, sleep issues, concentration issues, volume overload, nausea, restless legs, sexual dysfunction, increased infection
38
Hemodialysis times and pills
4 hrs x 3 times a week + 19 tablets, EPO and iron
39
Peritoneal dialysis
4-5 bags and day or overnight
40
Transplant
Reduced morbidity and mortality QOL Infection risk Immunosuppressants- diabetes, hypertension risk