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Data Interpretation > Biochemistry > Flashcards

Biochemistry Flashcards

1
Q

What do U&E measure:

A 
Electrolytes (Potassium and Sodium) 
Renal function (Urea and Creatinine)
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2
Q

Hyponatraemia Sodium level

A

Less than 135mmol/L

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3
Q

What is important to look at for hyponatraemia

A

Osmalality: this is lower in true hyponatraemia

Volume status

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4
Q

Causes of hypovolaemia hyponatraemia

A

Vomiting, Diarrhoea

Renal: Diuretics (K sparing), Nephropathy (PKD, NAIDs, pyelonephritis), Adrenal insufficiency/Addison’s

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5
Q

Causes of isovolaemic hyponatraemia

A

SIADH (high urine osmolality assoc)
Drugs
Renal failure / AKI
Hyperthyroidism

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6
Q

Causes of hypervolaemic hyponatraemia

A

Liver failure
Congestive heart failure (fluid overload)
Renal failure / AKI
Nephrotic syndrome

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7
Q

Causes of hypernatraemia

A

Diabetes insipidus (Polydispsia and polyuria causes fluid and salt loss)

Poor water intake (e.g. elderly, bed bound)

Too much IV sodium

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8
Q

Hypokalaemia level

A

Potassium less than 3.5

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9
Q

Causes of hypokalaemia

A

Drugs: Diuretic (e.g Thiazides - Indapamide), Tx DKA

GI: D&V, high stoma output

Renal: renal tubular acidosis or drug induced renal damage

Endocrine: Metabolic acidosis

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10
Q

Causes of hyperkalaemia

K over 6.5 - this is a medical emergency needing an ECG monitoring and Tx

if less than 6.5 then Tx needed if ECG is abnormal

A

Renal failure / AKI (And also missing dialysis appt)

Drugs: K sparing (Spironolactone), Potassium supps

Rhabdomyolysis, DKA

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11
Q

ECG changes in hypokalaemia

A

Flat broad T-waves
ST-depression
Long QT
Ventricular dysrhythmia

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12
Q

ECG changes in hyperkalaemia

A

Tall-tented T-waves (moving to Sine-wave - this is very severe stage)
Loss of P
QRS broadening
Cardiac arrest rhythms

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13
Q

What needs to be looked at for creatinine

What takes this into account

A

Age, sex and muscle bulk.

An old thin lady with normal range creatinine may be in renal failures this is high for her.

eGFR

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14
Q

Ways of predicting GFR

A

eGFR

Creatinine clearance

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15
Q

What does osmolarity take into account

A

U&Es

Blood Glucose

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16
Q

What factors determine nutritional profile

A

Magnesium
Calcium
Phosphate
Albumin

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17
Q

Refeeding syndrome

A

Insulin release causes increased glycogen, fat and protein synthesis.

This requires magnesium, phosphate and potassium which are already depleted

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18
Q

Urine in Pre-renal AKI (hypoperfusion) Vs Renal AKI from ATN

A

In pre-renal the urinary sodium is low as Juxtaglomerular apparatus is function and can activate RAAS

In Renal AKI from ATN urinary sodium is high due to breakdown in physiological mechanisms

Similarly in pre-renal uraemia, Urine will be more concentrated than in ATN

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19
Q

Ways of predicting GFR

A

eGFR

Creatinine clearance

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20
Q

What does osmolarity take into account

A

U&Es

Blood Glucose

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21
Q

What factors determine nutritional profile

A

Magnesium
Calcium
Phosphate
Albumin

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22
Q

Refeeding syndrome

A

Insulin release causes increased glycogen, fat and protein synthesis.

This requires magnesium, phosphate and potassium which are already depleted

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23
Q

Urine in Pre-renal AKI (hypoperfusion) Vs Renal AKI from ATN

A

In pre-renal the urinary sodium is low as Juxtaglomerular apparatus is function and can activate RAAS

In Renal AKI from ATN urinary sodium is high due to breakdown in physiological mechanisms

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24
Q

What needs to be looked at for creatinine

What takes this into account

A

Age, sex and muscle bulk.

An old thin lady with normal range creatinine may be in renal failures this is high for her.

eGFR

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25
Q

Ways of predicting GFR

A

eGFR

Creatinine clearance

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26
Q

What does osmolarity take into account

A

U&Es

Blood Glucose

27
Q

What factors determine nutritional profile

A

Magnesium
Calcium
Phosphate
Albumin

28
Q

Refeeding syndrome

A

Insulin release causes increased glycogen, fat and protein synthesis.

This requires magnesium, phosphate and potassium which are already depleted

29
Q

Urine in Pre-renal AKI (hypoperfusion) Vs Renal AKI from ATN

A

In pre-renal the urinary sodium is low as Juxtaglomerular apparatus is function and can activate RAAS

In Renal AKI from ATN urinary sodium is high due to breakdown in physiological mechanisms

30
Q

Components of Bone Profile

A

Calcium
Phosphate
Alk Phosphatase
Albumin

(Other factors: PTH, Vit D)

31
Q

PTH actions

A

(released due to low calcium)

Increased Calcium reabsorption from bone
Increased renal calcium reabsorption
Increased renal excretion of phosphate
Inc absorption of Ca from gut (Vit D mediated)

32
Q

Osteoporosis
Calcium
Phosphate
ALP

A

Calcium Normal
Phosphate Normal
ALP Normal

33
Q

Osteomalacia
Calcium
Phosphate
ALP

A

Calcium Reduced
Phosphate Reduced
ALP Increased

34
Q

Pagets
Calcium
Phosphate
ALP

A

Calcium Normal
Phosphate Normal
ALP Increased

35
Q

Mets
Calcium
Phosphate
ALP

A

Calcium Increased
Phosphate Increased
ALP Increased

36
Q

Primary hyperPTH (from PTH overactivity)
Calcium
Phosphate
ALP

A

Calcium Increased
Phosphate Decreased
ALP Increased

37
Q

Secondary hyperPTH (due to vitamin D def)
Calcium
Phosphate
ALP

A

Calcium Low
Phosphate Increased
ALP Increased

38
Q

Tertiary hyperPTH (due to renal failure)
Calcium
Phosphate
ALP

A

Calcium Increased
Phosphate Decreased
ALP increased

Differentiated from Primary with Hx of renal impairment

39
Q

Causes of hypercalcaemia

A

Bone mets
Multiple Myeloma
Hyperparathyroidism
Excessive Vit D

40
Q

Seven Factors to test in LFTs

A 
Bilirubin
AST (not liver specific - muscle damage)
ALT
ALP (not liver specific - bone turnover)
GGT
Albumin
PT
41
Q

Autoimmune hepatitis test and result

A

Autoanitbody screen

ANA
Anti-smooth muscle
Anti-microsomal

42
Q

PBC test

A

Anti-mitochondrial antibody

43
Q

Coeliac test

A

Anti-Tissue Transglutaminase

44
Q

Haaemochromatosis biochem

A

High Iron, ferritin and transferrin saturation

Low TIBC

45
Q

Wilson’s disease biochem

A

Low Caeruloplasmin and elevated 24 hour urine copper conc

46
Q

HCC biomarker

A

Alpha-Fetoprotein

47
Q

Hepatocellular pattern of LFT dysfunction

A

Transaminitis (AST and ALT raised)

48
Q

Obstructive pattern of LFT dysfunction

A

Elevated ALP and GGT
Bilirubin also high

(in severe cases AST and ALT may also rise due to back pressure in liver although not as much as ALP and GGT)

49
Q

Causes og hepatocellular damage

A 
Viral hepatitis
Autoimmune hepatitis
Drugs and toxins
Alcohol
Metabolic (Haemochromatosis, Wilson)
NAFLD
Malignancy (primary and mets)
Congestive cardiac failure
50
Q

Tumour markers: Colorectal

A

Carcinoembryonic antigen

51
Q

Albumin and inflammation

A

Albumin is negative acute phase protein as it goes down in inflammation

52
Q

What is CRP

A

Produced in Liver

Acute phase protein: high in infection and inflammation

53
Q

When is ESR high and CRP normal

A

SLE

Multiple Myeloma

54
Q

Uric acid metabolism

A

Produced during metabolism of purines and excreted by kidneys

55
Q

Causes of high urate

A

Increased consumption of purines
Impaired uric acid excretion

(this is what causes gout - acute mono arthritis)

56
Q

Tumour markers: HCC

A

Alpha-Fetoprotein

57
Q

Tumour markers: Testicular teratoma, seminoma, choriocarcinoma

A

Human chorionic gonadotropin

58
Q

Tumour markers: Prostate ca

A

PSA

59
Q

Tumour markers: Ovarian

A

Ca-125

60
Q

Tumour markers: Pancreatic Ca

A

Ca-19-9

61
Q

Tumour markers: Colorectal

A

Carcinoembryonic antigen

62
Q

Cause, Symptoms & Test for Cystic Fibrosis

A

Mutation in the gene for Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) responsible for Chloride transport across epithelial cells

Causes viscous secretions in lungs and pancreas and also infertility

Sweat test (Over 60mmol/L Chloride)

63
Q

Fluid balance: E.g. of fluid entering the body

A

Food and drink
IV
Enteral or parenteral nutrition
Blood products

64
Q

Fluid balance: E.g. of fluid leaving the body

A 
Urine
Bowel motions
Blood loss
Fluid from drains e.g. chest drain
Insensible losses (expired and sweat) - 500ml/day (higher in burns, fever etc)

Data Interpretation (13 decks)

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