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YEAR 5: Chemical Pathology AS > ChemPath: Assessment of Renal Function 2 > Flashcards

ChemPath: Assessment of Renal Function 2 Flashcards

(44 cards)

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1
Q

Compare AKI and CKD

A

abrupt decline vs longstanding decline

potentially reversible vs irreversible

treatment targeted to precise diagnosis + reversal vs prevention of complications + limiting progression

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2
Q

Define AKI.

A

Rapid reduction in kidney function, leading to inability to maintain electrolyte, acid-base and fluid homeostasis.

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3
Q

What are the three stages of AKI?

A

Stage 1: increase in serum creatinine by 1.5-1.9 times baseline/ >/ 26umol/L

Stage 2: increase in serum creatinine by 2-2.9 times baseline

Stage 3: increase in serum creatinine by >3 times baseline or >/354umol/L

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4
Q

What is pre-renal AKI?

A

AKI caused by reduced renal perfusion

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5
Q

Describe the normal response to reduced circulating volume.

A
  • Activation of central baroreceptors and renin-angiotensin system
  • Release of vasopressin
  • Activation of sympathetic system
  • Results in vasoconstriction, increased cardiac output and renal sodium retention
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6
Q

Name and describe the two mechanisms that maintain renal blood flow despite changes in systemic blood pressure.

A
  • Myogenic stretch - if the afferent arteriole gets stretched due to high pressure, it will constrict to reduce the transmission of that pressure to the glomerulus
  • Tubuloglomerular Feedback - high chloride concentration in the early distal tubule (suggestive of high GFR) stimulates constriction of the afferent arteriole which lowers GFR and, hence, chloride concentration
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7
Q

List some causes of pre-renal AKI.

A
  • True volume depletion: diabetes insipidus/ dehydration
  • Hypotension
  • Oedematous state
  • Selective renal ischaemia (e.g. renal artery stenosis)
  • Drugs affecting renal blood flow
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8
Q

List some drugs that affect renal blood flow.

A
  • ACE inhibitors - reduce efferent arteriolar constriction
  • NSAIDs - decreased afferent arteriolar dilatation
  • Calcineurin inhibitors - decrease afferent arteriolar dilatation
  • Diuretics - affect tubular funciton and decrease preload
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9
Q

Pre-renal AKI vs ATN

A

AKI not asssociated with structural renal damage

prolonged insult= ATN

ATN does not respond to restoration of circulating volume

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10
Q

What is a consequence of prolonged pre-renal insult?

A

Acute tubular necrosis (ATN)

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11
Q

Examples of causes of intrinsic/renal AKI

A

vascular disease: vasculitis

glomerular disease: glomerulonephritis

tubular disease: ATN

intersititial disease: analgesic nephropathy

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12
Q

What might be seen on urine microscopy in a patient with ATN?

A

Epithelial cell casts

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13
Q

What causes post-renal AKI?

A

Physical obstruction of urine flow

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14
Q

List some sites of urine obstruction.

A
  • Intra-renal
  • Ureteric (bilateral)
  • Prostatic/urethral
  • Blocked urinary catheter
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15
Q

Outline the pathophysiology of post-renal AKI.

A
  • GFR is dependent on a hydraulic pressure gradient
  • Obstruction results in increased tubular pressure
  • This results in an immediated decline in GFR
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16
Q

What are some consequences of prolonged renal obstruction?

A
  • Glomerular ischaemia
  • Tubular damage
  • Long-term interstitial scarring
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17
Q

List the possible sites of disease in intrinsic AKI.

A
  • Vascular (e.g. vasculitis)
  • Glomerular (e.g. glomerulonephritis)
  • Tubular (e.g. ATN)
  • Interstitial (e.g. AIN)
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18
Q

What examples of immune dysfunction can cause intrinsic AKI?

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A

glomerulonephritis

vasculitis

19
Q

What can cause direct tubular injury?

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A
  • Ischaemia (MOST COMMON)
  • Endoengous toxins (e.g. myoglobin, immunoglobulin)
  • Exogenous toxins (e.g. contrast, aminoglycosides, amphotericin, aciclovir)
20
Q

Which diseases can cause AKI due to infiltration/abnormal protein deposition?

Study These Flashcards
A
  • Amyloidosis (associated with nephrotic syndrome)
  • Lymphoma
  • Myeloma
21
Q

List the possible outcomes of AKI.

Study These Flashcards
A
  • Complete recovery
  • Partial recovery of renal function
  • Discharged with increased serum creatinine
  • Discharged requiring chronic dialysis
  • Death
22
Q

What are the biochemical definitions of AKI?

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A
  • Increase in serum creatinine > 26.5µmol/L within 48 hours
  • Increase in serum creatinine > 1.5 times baseline within the previous 7 days
  • Urine volume < 0.5 ml/kg/hr for 6 hours
23
Q

What are the four processes of acute wound healing?

Study These Flashcards
A
  • Haemostasis
  • Inflammation
  • Proliferation
  • Remodelling

imbalance between scarring and remodelling= kidney injury

24
Q

What are the stages of CKD?

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A
  • Stage 1: >90 kidney damage with normal GFR
  • Stage 2: 60-89
  • Stage 3: 30-59
  • Stage 4: 15-29
  • Stage 5: <15
25
How can risk of CKD be predicted?
eGFR and albumin:creatinine ratio
26
List some causes of CKD.
* Diabetes mellitus * Hypertension * Chronic glomerulnephritis * Atherosclerotic renal disease * Infective or obstructive uropathy * Polycystic kidney disease
27
What are the normal roles of the kidney?
* Excretion of water-soluble waste * Water balance * Electrolyte balance * Acid-base homeostasis * Endocrine (EPO, RAS, vitamin D)
28
Outline the consequences of CKD.
* Progressive failure of homeostatic function (acidosis, hyperkalaemia) * Progressive failure of hormonal function (anaemia, renal bone disease) * Cardiovascular disease (vascular calcifiction, uraemic cardiomyopathy) * Uraemia and death
29
What are the consequences of renal acidosis?
* Metabolic acidosis * Muscle and protein degradation * Osteopaenia due to mobilisation of bone calcium * Cardiac dysfunction
30
How is renal acidosis treated?
Oral sodium bicarbonate
31
What are the consequences of hyperkalaemia?
* Cardiac dysfunction (arrhythmia VT then vFIB) * Muscle dysfunction NOTE: hyperkalaemia causes membrane depolarisation
32
Which medications can cause hyperkalaemia?
* ACE inhibitors * Spironolactone * Potassium-sparing diuretics
33
What type of anaemia does chronic renal disease cause?
Normochromic, normocytic anaemia
34
How is anaemia of chronic renal disease treated?
* Erythropoietin alfa (Eprex) * Erythropoietin beta (NeoRecormon) * Darbopoietin (Aranesp) NOTE: if CKD is not responding to erythropoiesis stimulating agents, consider iron deficiency, malignancy, B12 deficiency etc.
35
List some types of renal bone disease.
* Osteititis fibrosa cystica * Osteomalacia * Adynamic bone disease * Mixed osteodystrophy
36
Outline the pathophysiology of renal bone disease.
* Damaged kidneys are unable to excrete phosphate and activate vitamin D * Phosphate retention stimulates the production of FGF23 and Klotho * This lowers the levels of activated vitamin D * To try and get rid of the excess phosphate, the body will produce more PTH * Furthermore, to try and increase levels of vitamin D, the body will produce more PTH (i.e. there are two stimuli for PTH release) * High levels of PTH will result in the bone becoming resistant to PTH
37
What is osteitis fibrosa cystica?
Caused by osteoclastic resoprtion of calcified bone and replacement by fibrous tissue (feature of hyperparathyroidism) Brown tumours
38
What is adynamic bone disease?
Overtreatment leading to excessive suppression of PTH results in low bone turnover and reduced osteoid as less osteoblast activity
39
Outline the treatment of renal bone disease.
* Phosphate control - dietary, phosphate binders * Vitamin D activators - 1-alpha calcidol, paricalcitol * Direct PTH suppression - cinacalcet (works by increasing the sensitivity of the calcium sensing receptor)
40
What is the most important consequence of CKD?
Cardiovascular disease - this is most likely to kill them
41
How can CKD affect the cardiovascular system?
vascular calcification: heavy calcium plaques (not lipid rich atheroma) uraemic cardiomyopathy
42
What are the three phases of uraemic cardiomyopathy?
* LV hypertrophy * LV dilatation * LV dysfunction
43
What are the treatment options for patients with CKD?
* Transplantation * Haemodialysis * Peritoneal dialysis
44
How can risk of CKD be predicted?
eGFR and albumin:creatinine ratio

YEAR 5: Chemical Pathology AS (27 decks)

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