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Liv Path > Chempath - LFTs, Cardaic Enzymes and Renal Function > Flashcards

Chempath - LFTs, Cardaic Enzymes and Renal Function Flashcards

1
Q

Marks of liver synthetic function

A

Clotting (INR)
Albumin
Glucose

However bare in mind that all of these things can go off by issues not directly cased by the liver.

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2
Q

Markers of liver cell damage

A

Hepatocyte cell damage - ALT, AST
Biliary stasis - ALP, GGT
Bilirubin

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3
Q

Aspartate aminotransferase (AST)

A

Found in the Liver, cardiac and skeletal muscle, and the kidney and brain.

AST:ALT = 2 is supportive of alcoholic hepatitis - alcohol makes an ASS out of you

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4
Q

Alanine aminotransferase

A

Found primarily in the
liver, more sensitive than AST for hepatocyte damage.

Raised when hepatocytes die. AST:ALT =1 supportive of viral hepatitis.

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5
Q

Alkaline Phosphatase (ALP)

A

Found in the liver, bones, placenta.

Raised with cholestasis (either intrahepatic or extrahepatic) and bone disease, ↑++ in pregnancy

CAUSES of raised ALP:
Physiological: Pregnancy (3rd trimester), Childhood (during growth spurt)

Pathological:

  • > 5x ULN = Bone (Pagets, osteomalacia), Liver (Cholestasis, Cirrhosis)
  • <5x ULN = Bone (tumours, fractures, osteomyelitis), Liver (infiltrative disease, hepatitis)
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6
Q

Gamma GT

A

Found in hepatocytes and biliary cells, also found in the kidney and pancreas.

Elevated in chronic alcohol use

Also bile duct disease and metastases. Used to confirm hepatic source of ↑ALP

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7
Q

Alpha fetoprotein

A

Tumour marker. Also raised in hepatic damage/regeneration, pregnancy & testicular ca.

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8
Q

Albumin

A

Average adult synthesises 200mg/kg of albumin per day

Important serum protein which binds many hormones, calcium and other metabolites.

Hypoalbuminaemia is common in hospital patients as acute illness/systemic inflammation and malnutrition can contribute to a reduced albumin. Causes:

  • Low production - chronic liver disease, malnutrition
  • Loss - gut, kidney(nephrotic syndrome)
  • Sepsis - “3rd spacing”

Hypoalbuminaemia in critically ill patients is a poor prognostic factor

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9
Q

Clotting Factors

A

The liver synthesises Factor V, VII, IX, X, XII, XIII and fibrinogen and prothrombin

In practical terms INR (International normalised ratio) is measured, this is the prothrombin time standardised for age and population expressed as a ratio of ‘normal’.

Deranged clotting is not diagnostic of hepatocellular dysfunction on its own as it could be due to multiple other aetiologies – for example iatrogenic (therapeutic warfarinisation), hereditary thrombophillia, acquired consumption (DIC).

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10
Q

3 things get transaminases >1000

A

Ischaemia, viruses and toxins (OD)

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11
Q

Pre-hepatic jaundice - causes

A

Haemolysis

Congestive heart failure

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12
Q

Pre-hepatic jaundice - lab findings

A

Elevated unconjugated bilirubin
Reduced haemoglobin Reduced haptoglobin
Raised LDH

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13
Q

Hepatic jaundice - Causes

A

Acute or chronic liver failure Gilbert syndrome
Crigler-Najjar syndrome Viral Hepatitis
Alcoholic Hepatitis
PBC

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14
Q

Hepatic jaundice - Lab Findings

A

Elevated Unconjugated bilirubin
Raised Aminotransferases Synthetic dysfunction may be present

Gilbert’s: deficiency in UDP-glucoronyl transferase. Crigler-Najjar is a severe form of this.

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15
Q

Post-Hepatic Jaundice - Causes

A

Obstruction of the biliary tree from any cause (Think intraluminal – Stones, strictures, Luminal – Mass/Neoplasm, Inflammation e.g. PSC/PBC,
Extra-luminal – Pancreatic Ca, cholangio Ca

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16
Q

Post-Hepatic Jaundice - Lab Findings

A

Elevated conjugated bilirubin Elevated bilirubin in the urine [Dark urine pale stools]

17
Q

Cirrhosis LFTs

A

Reasonably normal unless they are decompensating.

18
Q

Acute Liver Failure LFTs

A

Wildly elevated liver enzymes and deranged clotting.
Albumin may be normal as it doesn’t immediately fall.
Pts will have rising bilirubin as they progress.

19
Q

Cholestasis LFTs

A

Predominantly raised ALP. Others may be mildly raised.

20
Q

Acute Alcohol Abuse LFTs

A

Raised gamma GT, mild rise in other enzymes

21
Q

Amylase

A

high serum levels in acute pancreatitis (usually >10x upper limit of normal)

22
Q

Creatine kinase

A

Most widely used as a marker of muscle damage (CK-MM = skeletal muscle, CK-MB (1&2) = cardiac muscles.)

Raised levels due to:

  • Physiological: Afro-Caribbean (<5x upper limit of normal)
  • Pathological: Duchenne Muscular Dystrophy (>10xULN), MI (>10xULN), Statin related myopathy, Rhabdomyolysis
23
Q

Brain Natriuretic Peptide (BNP)

A

A natriuretic hormone that is primarily released from the ventricles in the heart

Released in response to ventricular stretch, has roles in reducing systemic vasoconstriction, sodium retention and renal sympathetic activity.

Levels of <100 are highly specific for excluding heart failure, >400 is highly sensitive for heart failure

Confounding factors to interpretation include CKD

NT-proBNP is more sensitive than BNP and has greater prognostic value

24
Q

Troponin

A

Troponin I/T = myocardial injury biomarker

Measure at 6 hours and then at 12 hours post onset of chest pain (100% Se and 98% Sp at 12-24 hours). Rise at 4-6 hours post MI. Peak at 12-24 hours post MI.

Remains elevated for 3 – 10 days.

None of the current cardiac biomarker levels rise quickly enough to aid in decisions regarding thrombolysis.

25
Q

Normal GFR & age related decline

A

120ml/hr.

Age-related decline of approx 1ml/hr/yr.

26
Q

Renal Clearance

A

Clearance = the volume of plasma that can be completed cleared of a marker substance in a unit of time.
If marker is not bound to serum proteins, freely filtered by the glomerulus, and not secreted/reabsorbed by tubular cells, then clearance = GFR.

Gold standard measure of GFR = inulin. But requires steady state infusion and difficult to assay so it is reserved for research purposes only.

Creatinine is endogenous marker. This is used in clinical practice to measure renal function. Very variable between individuals and therefore it is best to monitor the trend and use it to look for change over time. Creatinine is a byproduct of muscle turnover, so muscular individuals will have a higher creatinine than others. Age, sex and ethnicity also affect levels.

Different equations use the serum creatinine with variable combinations of age, weight, sex and ethnicity to estimate GFR e.g. Cockcroft-Gault and MDRD (modification of diet in renal disease study). Currently we use CDK-EPI equation.

27
Q

Urine Examination - Single Sample

A

Dipstick testing - sensitive to albumin but not bench jones proteins, -ve for blood reliably excludes haematuria

Microscopic examination

Proteinuria quantification (protein:creatinine ratio (PCR))

28
Q

Urine Examination - 24 hour collection

A

Proteinuria quantification (superceded by PCR above)

Creatinine clearance estimation

Electrolyte estimation

Stone forming elements

29
Q

Urine microscopy

A

Crystals (stones)

Red blood cells (stones, UTI)

White blood cells (UTI, glomerulonephritis)

Casts (glomerulonephritis)

Bacteria (UTI)

30
Q

AKI definition

A

Rise in serum creatinine over 26.5 in 48h or to 1.5x baseline in 48h (3x is severe). It can also be defined as a urine output of less than 0.5mls/kg/hr

31
Q

AKI - causes

A

Pre-renal – reduced renal perfusion with no structural abnormality pof the kidney, it can become renal if the ischaemia leads to necrosis. Responds to volume replacement

Renal – vascular, glomerular, tubular or interstitial

Post-renal – characterised by obstruction to urinary flow, glomerular filtration requires a pressure gradient, reversal can lead to scarring and permanent renal impairment

32
Q

Indications for emergency dialysis

A

1) Pulmonary oedema
2) Refractory hyperkalaemia
3) Metabolic acidosis
4) Uraemic encephalopathy
5) Also some drug toxicity (lithium for example)

33
Q

CKD - Causes

A 
Diabetes
Atherosclerotic renal disease
Hypertension
Chronic Glomerulonephritis
Infective or obstructive uropathy
Polycystic kidney disease
34
Q

Consequences of CKD

A

Progressive failure of homeostatic function

  • Acidosis
  • Hyperkalaemia

Progressive failure of hormonal function

  • Anaemia (loss of EPO synthesis)
  • Renal Bone Disease (secondary hyperparathyroidism due to low Vit D)

Cardiovascular disease:

  • Vascular calcification and subsequent atherosclerosis (biggest mortality in CKD)
  • Uraemic cardiomyopathy

Uraemia and Death

35
Q

Renal Replacement Therapy in CKD

A

Dialysis: haemodialysis, peritoneal

Transplant

Liv Path (24 decks)

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