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Scientific Basis of Clinical Practice > Clinical Biochemistry > Flashcards

Clinical Biochemistry Flashcards

1
Q

define accuracy

A

closeness to the true value

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2
Q

define precision

A

reproducibility of agreement with each other for multiple trials

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3
Q

define true value

A

standard or reference of a known or theoretical value

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4
Q

what results show in a blood sample that has been haemolysed?

A

collected too vigorously
red cells have been broken down
artificially high level of potassium

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5
Q

describe how a false negative occurs

A

there is a proportion of the diseased population, where for the result of the test, fall into the reference range

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6
Q

define sensitivity

A

true positive / true positive + false negative

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7
Q

define specificity

A

true negative / true negative + false positive

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8
Q

what factors affect reference ranges and results?

A 
age
gender
diet
pregnancy
sample handling
sample type
time of day/month/year
weight
fasting
posture
sample collection procedure
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9
Q

where is calcium distributed in the body?

A

99% in bone
1% in plasma
of that, 50-60% is bound to plasma proteins
remainder is ionised (active, required for nerve conduction and muscle contraction)

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10
Q

what affects plasma calcium concentration?

A

alteration in protein levels
vitamin D
parathyroid hormone
renal function
prolonged tourniquet application (increases protein levels)
reduced/increased by 0.02mmol for each g albumin falls below/above 40

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11
Q

what is the role of parathyroid hormone?

A

released when Ca levels fall
increases renal reabsorption of Ca and excretion of PO4
stimulates osteoclasts, increases bone reabsorption and increases Ca released from bone
increases vitamin D synthesis

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12
Q

describe vitamin D metabolism

A

UV light converts cholesterol to vitamin D3
hydroxylated at 25 site in the liver
converted from vitamin D to 1,25 vitamin D (active form) in the kidneys

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13
Q

what are the causes of hypercalcaemia?

A 
PTH excess
vitamin D excess (ingestion, sarcoid)
increased Ca intake (milk-alkali syndrome in PUD)
thiazide diuretics
bony metastases in malignancy
PTH-secreting tumours
haematological malignancy
thyrotoxicosis
addison's disease
familial hypocalcuric hypercalcaemia
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14
Q

what are the signs and symptoms of hypercalcaemia?

A 
malaise
depression
polydipsia
polyuria
abdominal pain (renal stones)
features of underlying disease (malignancy, sarcoid)
low PO4 and high Ca (excess PTH)
high PO4 and Ca (excess vitamin D)
high ALP (bone disease, haematological malignancy)
renal function
CXR (sarcoid)
plasma protein electrophoresis (myeloma)
urinary calcium
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15
Q

what is the management of hypercalcaemia?

A

rehydration (orally, normal saline 4-6L over 24hrs)
monitor urine output
loop diuretic (furosemide)
monitor K levels if lots of excretion
bisphosphonates (bind Ca to prevent if being released from bone)
hydrocortisone (in myeloma or sarcoid)

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16
Q

what are the causes of hypocalcaemia?

A 
not corrected for albumin
renal failure (increased PO4 and vitamin D may not be converted to the active form)
hypoparathyroidism
vitamin D deficiency
hypomagnesaemia
bisphosphonates
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17
Q

what are the symptoms and signs of hypocalcaemia?

A

neuromuscular irritability
tetany
positive Chvostek’s sign (tap on facial nerve and spasm of facial muscle)
positive Trousseau’s sign (inflation of BP cuff causes wrist flexion and finger extension)
QT prolongation

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18
Q

what is the management of hypocalcaemia?

A

oral calcium
milk
vitamin D
IV calcium gluconate (severe cases)

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19
Q

describe the storage and uses of PO4

A

85% stored in bone within cells
required for ATP
important constituent of cell membranes and nucleic acid

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20
Q

what are the causes of hypophosphataemia?

A 
poor diet, reduced intake
reduced absorption (malnutrition, vitamin D deficiency)
increased shift into cells (respiratory alkalosis, insulin, glucose, amino acids)
increased urinary excretion (excessive PTH, renal tubular defects)
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21
Q

what are the clinical features of hypophosphataemia?

A 
refeeding syndrome, post IV, enteral or normal feeding
alcohol abuse
asymptomatic
rhabdomyolysis
cardiomyopathy
renal failure
impaired RBC function
impaired white cell function (susceptible to infection)
reduced phagocytosis
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22
Q

what is the treatment of hypophosphataemia?

A

milk
oral supplements
IV dipotassium hydrogen phosphate over 12hr and once in 24hr (too much causes calcium deposits in tissues)

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23
Q

what are the causes of hyperphosphataemia?

A

renal failure
cellular phosphate leak
cell breakdown (rhabdomyolysis or tumour lysis)

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24
Q

describe the storage of magnesium

A

67% in bone

31% intracellular

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25
Q

what are the causes of hypomagnesaemia?

A

poor intake
malabsorption
increased losses (renal or GI)
diarrhoea or fistula (losses of gut fluid)
refeeding syndrome
alcohol abuse/withdrawal
increase in amount of fluid lost in the loop of henle

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26
Q

what are the symptoms and signs of hypomagnesaemia?

A

similar to hypocalcaemia
tetany
Chovstek’s sign
neuromuscular problems

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27
Q

what is the treatment of hypomagnesaemia?

A

oral or IV magnesium

30mmol in first 24hrs then 20mmol in each 24hr period after that (IV)

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28
Q

where is ALP found?

A

liver
bone
intestines
placenta

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29
Q

what are the causes of high ALP?

A

bone growth
pregnancy (placenta)
bone fracture healing
bony metastases
Paget’s disease (excessive bone growth and abnormal bone remodelling)
hyperparathyroidism (osteoclasts stimulated to release Ca)
obstructive jaundice

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30
Q

describe osteoporosis

A

Ca, PO4 and ALP normal
asymptomatic
usually found in a DEXA scan if there are no fractures

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31
Q

describe osteomalacia

A

defective bone mineralisation (similar to rickets)
low Ca and PO4 and high ALP
usually due to low vitamin D

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32
Q

describe Paget’s disease

A

abnormal bone remodelling due to increased ALP
normal Ca and PO4
usually elderly

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33
Q

describe bony metastases

A

high Ca and ALP, normal or high PO4

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34
Q

describe myeloma

A

Ca alone high

ALP usually normal

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35
Q

describe primary hyperparathyroidism

A 
adenoma on parathyroid gland causing excess PTH
high Ca (hypercalcaemia), ALP and low/normal PO4
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36
Q

define tumour markers

A

molecules which indicate the presence of a cancer or provide information of the likely future behaviour of a cancer

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37
Q

what are the use of tumour markers?

A

detect cancer in asymptomatic patients
differentiate between malignant and benign tumours
post-surgery to detect the amount that was removed
detect recurrence
predict how a tumour responds/has responded to treatment

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38
Q

what are the categories for the ideal tumour marker?

A 
high PPV and NPV
highly sensitive and specific
inexpensive
simple
circulating level correlates with amount of tumour
acceptable to subjects
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39
Q

describe some non-specific markers involved in detecting malignancy

A

hyponatraemia - indicates SIADH secondary to NSCLC
LDH - haematological malignancy
ALP - bony metastases, bone malignancy
total protein - multiple myeloma, Waldenstrom’s macroglobulinaemia
ferritin - renal cell carcinoma, leukaemia, hepatocellular carcinoma

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40
Q

define oncofetal antigens

A

present in cells in early development

reactivated in more undifferentiated cancer cells

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41
Q

describe 2 types of oncofetal antigens and what they look for

A

AFP - hepatocellular carcinoma, ovarian and testicular tumours
carcinoembryonic antigen - colorectal carcinoma

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42
Q

describe some hormones that are used as tumour markers

A

HCG - choriocarcinoma, testicular tumours, trophoblastic tumours
metanephrines - pheochromocytoma
calcitonin - medullary carcinoma of thyroid
IGF1 - pituitary malignancy

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43
Q

describe some glycoproteins that are used as tumour markers

A

CA19-9 - pancreatic tumours
CA125 - ovarian, breast, pancreatic and lung tumours
can be increased in benign conditions

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44
Q

describe some enzymes that are used as tumour markers

A

PSA - prostate cancer, other prostatic conditions

neurone-specific enolase - SCLC, neuroendocrine tumours

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45
Q

describe some cell components/antigens used as tumour markers

A

SCC antigen - gynae, head and neck and lung tumours
immunoglobulins - multiple myeloma
CEA - breast, pancreatic, ovarian, lung, stomach, colon and prostate cancer

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46
Q

what markers are produced by a multiple myeloma?

A

heavy and light immunoglobulin chains (detected as a paraprotein band)
Bence Jones protein (urine)
free light chains
beta-2 microglobulin (measures mass of tumour present)

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47
Q

what markers are produced by ovarian cancer?

A 
CA125
inhibin
HCG
AFP
carcinoembryonic antigen
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48
Q

what markers are produced by carcinoid tumours?

A

serotonin
S-hydroxytryptamine
catecholamines
chromogranin A

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49
Q

what are the causes of PSA increase?

A 
prostate tumour
BPH
needle biopsy
prostatitis
urinary retention

rises occur rapidly and can take several days to return to normal

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50
Q

with what symptoms should CA125 be measured for ovarian cancer?

A 
abdominal distension
loss of appetite
abdominal pain
new onset irritable bowel syndrome
>50

measured along with a pelvic US

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51
Q

what are the causes of CA125 increase?

A

ovarian, pancreatic, lung, breast, uterus, cervix and GI tract tumours
pancreatitis
peritonitis
hyperthyroidism
PID
ascites, HF, pleural effusion (fluid accumulation)

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52
Q

what patients should have an AFP test?

A

those known to have hep B and C-related cirrhosis

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53
Q

what are HCG and AFP used to detect?

A

non-seminoma type testicular germ cell tumours

follow-up to detect recurrence

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54
Q

what are HCG and LDH used to detect?

A

pure seminoma tumours

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55
Q

what are the causes of an AFP increase?

A 
hepatocellular carcinoma
ovarian tumour
testicular tumour
cirrhosis
hepatitis
ataxia telangiectasis
pregnancy
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56
Q

what are the causes of a HCG increase?

A 
pregnancy
marijuana use
choriocarcinoma
trophoblastic tumour
testicular tumour
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57
Q

what affects the reference range of CEA?

A 
smoking
other tumours
IBD
pancreatitis
liver disease
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58
Q

what are the causes of CA19-9 increase?

A

pancreatic, colorectal, lung, liver and ovarian cancers
pneumonia
hepatobiliary disease
renal failure

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59
Q

name some examples of lipids

A 
fats
steroids
fatty acids
fat soluble vitamins (K, E and A)
phospholipids
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60
Q

what are the functions of lipids?

A

maintain the structure of cell membranes
store energy
hormone synthesis
signalling

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61
Q

what are the functions of cholesterol?

A

hormone production (cortisol and sex hormone synthesis)
main component of cell membranes
vitamin D synthesis
bile acid synthesis (role in digestion)

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62
Q

what is the function of triglycerides?

A

efficiency way of storing and transferring energy

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63
Q

describe lipoproteins

A

required for lipid transportation in the circulation

contain apolipoproteins - made in the liver, bind to receptors, allow transportation

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64
Q

what is the function of chylomicrons?

A

transport triglycerides (mainly dietary)

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65
Q

what is the function of VLDL?

A

transport triglycerides from the liver to other tissues

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66
Q

what are the functions of apolipoproteins?

A

allow the transfer of different cholesterol fractions between different lipoprotein particles
co-factors for some of the enzymes used in cholesterol metabolism
bind to receptors in the cells
allow lipids to be taken up into cells

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67
Q

what are the pathways of lipid transport?

A

dietary
hepatic
tissue to liver (reverse cholesterol)

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68
Q

describe dietary lipid transport

A

mainly via chylomicrons
can go directly to cells if required (muscle, fat)
can go to liver to be processed and stored

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69
Q

describe hepatic lipid transport

A

the liver exports some of these stored triglycerides and moves them to the various tissues as required
the fraction that remain are transported back to the liver for further processing

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70
Q

describe reverse cholesterol transport

A

via HDL
cholesterol can go back to the liver and be removed from the circulation
doesn’t contribute to atheroma

71
Q

what do apo A levels show?

A

the extent of reverse cholesterol transport

low - increased risk of atherosclerosis

72
Q

what do apo B levels show?

A

an idea of the total number of atherogenic particles

high - increased risk of cardiovascular disease

73
Q

what do lp a levels show?

A

genetic links

FHx of premature cardiovascular disease

74
Q

describe Tangier’s disease

A

very low/absent alpha lipoprotein or apolipoprotein A
no mechanism for clearing cholesterol from the circulation
cholesterol deposited in tissues
enlarged orange tonsils (cholesterol deposits)

75
Q

how is LDL cholesterol calculated?

A

friedewald-levy-fredrickson formula
= TC - HDL C - (TG/2.2) mol/L
not valid for very high triglycerides

76
Q

describe atherogenic lipoprotein particles

A

LDL, IDL, VLDL, Lp a

= total cholesterol - HDL

77
Q

what are the causes of increased LDL cholesterol?

A 
hypothyroidism
nephrotic syndrome
ciclosporin
cholestasis
anorexia nervosa
78
Q

what are the causes of decreased LDL cholesterol?

A

malabsorption
liver disease
malnutrition

79
Q

what are the causes of increased HDL C?

A

exercise
moderate amounts of alcohol
oestrogen

80
Q

what are the causes of decreased HDL C?

A 
smoking
metabolic syndrome
T2DM
malnutrition
anabolic steroids
systemically unwell
81
Q

what are the causes of increased VDL C?

A 
obesity
diabetes
hepatitis
alcohol
renal disease
protease inhibitors
retinoid acid-based treatments
82
Q

describe familial hypercholesterolaemia

A 
autosomal dominant
associated with high coronary mortality
50% of men will have an MI <50 and 30% of women will have an MI <60
high lipid levels in children
tendon xanthoma
premature corneal arcus
xanthelasma

problem with Apo B on the LDL particle or the LDL receptor on the cell

83
Q

describe familial dysbetalipoproteinaemia

A

abnormality in the apo E receptors
apo E2 binds poorly to receptors and results in cholesterol not being removed as effectively from the circulation
1/170 are homozygous E2/E2

84
Q

describe classical dyslipidaemia

A

cholesterol and triglycerides are numerically similar
increased cardiovascular risk
responds well to fibrates

85
Q

which factors increase cardiovascular risk?

A 
reduced eGFR
known cardiovascular risk
T1DM
>40
FH
mental health disorders
inflammatory conditions (RA)
86
Q

what is involved in the lifestyle management of dyslipidaemia?

A

fat should be <30% of calorie intake, saturated fat <7%
5x fruit and vegetable portions
high amount of whole green foods
2x fish/week, 1x oily
4-5x non-salted nuts or seeds/week
150mins moderate or 75mins vigorous intensity exercise

87
Q

what is involved in the pharmacological management of dyslipidaemia?

A

primary prevention - atorvastatin 20mg
secondary prevention - atorvastatin 80mg
aim for >40% reduction in non-HDL cholesterol

fat soluble - simvastatin, atorvastatin
water soluble - pravastatin, fluvastatin, rosuvastatin

88
Q

what are the causes of hypertriglyceridaemia?

A 
obesity
DM
alcohol excess
metabolic syndrome
renal failure
protease inhibitors
isotretoin
second generation antipsychotics (phenothiazines)
primary dyslipidaemia
89
Q

what are the consequences of hypertriglyceridaemia?

A

cardiovascular risk
raised cholesterol
pancreatitis

90
Q

what is the management of hypertriglyceridaemia?

A 
low fat diet (10% fat)
diabetes control
avoid alcohol
fibrates
statins
fish oils
91
Q

what is the treatment of combined dyslipidaemia?

A

statins 1st line
if triglycerides remain >5.6mmol/L then use fibrates
fish oils (omacor 4g/day)

92
Q

describe BNP

A

produced by myocardial cells
released into the circulation in high concentration whenever myocardial cells are under stress or excess stretch
pro-BNP -> pre-pro-BNP

93
Q

what are the consequences of increased BNP production?

A

promotes vasodilation
increased urinary Na retention, reducing the circulating blood volume
promotes myocyte growth
worse prognosis

94
Q

how can heart failure be excluded?

A

if ECG and BNP are both normal

95
Q

what can BNP be used for?

A

heart failure
LV failure following MI
assess prognosis in elderly, PE, general population
monitor treatment

96
Q

what are the functions of the liver?

A

synthesis of proteins
detoxification (metabolism and elimination of waste)
metabolises proteins to ammonia
storage of glycogen and can replenish glucose when needed

97
Q

describe bilirubin production

A

red blood cells are broken down into haem and globin
haem metabolised by haem oxygenase to produce iron and biliverdin
biliverdin is reduced by biliverdin reductase to produce bilirubin

98
Q

describe bilirubin transport

A

initially binds to albumin (unconjugated) because it is insoluble and can’t pass into urine alone

99
Q

describe hepatic uptake and conjugation of bilirubin

A

transported to hepatocytes
binds to ligandin
this allows it to be transferred to the endoplasmic reticulum and undergoes conjugation
via UPD glucuronosyltransferase
it becomes bilirubin diglucoronide (soluble)

100
Q

describe excretion and enterohepatic recirculation of bilirubin

A

conjugated bilirubin goes into the bile via the gallbladder and bile duct
passes into the intestine
degraded by intestinal bacteria to urobilinogen (colourless)
passes through the intestine and is converted to stercobilin (brown)
exerted into faeces
some is bilirubin and urobilinogen is reabsorbed by the portal vein
passes back into the liver and goes into the systemic circulation
some urobilinogen passes through the kidneys (some becomes oxidised to urobilin (yellow)) and is excreted

101
Q

what are the causes of unconjugated hyperbilirubinaemia?

A

haemolysis (along with raised AST, LDH and reticulocyte count and decreased haptoglobin)
problem with liver uptake of bilirubin from the circulation)
physiological neonatal jaundice (babies have an increased erythrocyte load and reduced ligandin)
gilbert syndrome (AD, reduced glucuronosyltransferase)
crigler-najaar syndrome (AR, two forms, more severe form of Gilbert syndrome)

102
Q

describe the exocrine glands of the pancreas

A 
allow digestive enzymes pass through a duct to the intestine
trypsin
chymotrypsin
elastase
lipase
amylase
103
Q

what happens when acidic fluid containing amino acids arise in the duodenum?

A

the small intestine produces cholecystokinin and secretin

104
Q

what are the functions of cholecystokinin and secretin

A

causes gallbladder contraction
empties bile into the duodenum
allows digestion of fats
stimulate the production of alkaline fluid and pancreatic enzymes

105
Q

describe some disorders of the exocrine pancreas

A

acute pancreatitis
pancreatic insufficiency (chronic pancreatitis, cystic fibrosis - chronic ongoing inflammation)
pancreatic cancer

106
Q

what are the features of acute pancreatitis?

A

acute abdominal pain, relieved by leaning forward
shock, 3rd space fluid loss
acutely unwell
mortality 5-10%
amylase (pancreas and salivary glands)
lipase (more specific for pancreas)
CT - oedema and inflammation surrounding pancreas

107
Q

what are the causes of acute pancreatitis?

A 
gallstones
ERCP
hypertriglyceridaemia (fat obstruct pancreatic blood flow, >10mmol/L)
alcohol excess
viral
drugs
108
Q

what are the causes of raised amylase?

A 
mumps
calculi of salivary ducts
CKD (reduced amylase excretion)
duodenal ulcer perforation
ruptured AAA
DKA
acute pancreatitis
109
Q

what are associated with poor prognosis in acute pancreatitis?

A

increased age
increased LDH (cell breakdown)
increased urea (kidney dysfunction, multiple organ failure)
increased WCC
increased blood glucose
reduced albumin (negative acute phase reactant)
reduced Ca (auto-digestion of mesenteric fat)

110
Q

what are the causes and features of pancreatic insufficiency?

A

removal of some necrotic areas of pancreas
chronic pancreatitis
cystic fibrosis

malabsorption (anaemia, weight loss, diarrhoea, steatorrhoea)
abdominal discomfort
osteomalacia
low Ca
low vitamin D
hyperglycaemic (check plasma glucose and HbA1c)
low faecal elastase (pancreatic dysfunction)

111
Q

what tumour markers are associated with pancreatic cancer?

A

CEA

CA19-9

112
Q

describe neuroendocrine pancreatic tumours

A

produce other hormones; insulin or glucagon

better prognosis

113
Q

what are the purposes of therapeutic drug monitoring?

A

ensure that there are constant levels of the drug in plasma
avoid toxicity
identify non-compliance

114
Q

name some drugs which require monitoring

A

lithium
vancomycin, aminoglycosides
cyclosporin, tacromilus, mycophenolate

digoxin
theophylline, caffeine (given in COPD and asthma)
anti-epileptics (phenytoin, phenobarbitone, carbamazepine, sodium valproate)

115
Q

what tests are used to measure drugs?

A 
clinical response (BP)
INR/PT - warfarin
renal function - ACEi, diuretics, NSAIDs
potassium - spironolactone
liver function - statins
urinary protein - pencillamine, gold (for RA, can cause nephrotic syndrome)
116
Q

what are the uses and complications of lithium?

A

treatment of bipolar disorder

diabetes insipidus
renal function
thyroid function

117
Q

what are the complications of ahminoglycosides and vancomycin?

A

ototoxicity (auditory nerve)

nephrotoxicity

118
Q

what are the complications of immunosuppressants?

A

nephrotoxicity

careful when used in immunosuppression of kidneys

119
Q

how does paracetamol overdose occur?

A

converted to a toxic metabolite
usually inactivated by conjugation with glutathione
glutathione becomes depleted when an excess of paracetamol is taken
NABQI binds to sulphhydryl-containing groups on liver cell membranes, causing liver necrosis

120
Q

what is the treatment of paracetamol overdose?

A

acetylcysteine
replaces glutathione and mops up toxic metabolite
most effective within the first 8hrs
measure INR and creatinine

121
Q

what factors affect the metabolisation of paracetamol?

A

history of alcohol abuse

taking drugs that may induce liver enzymes (phenytoin)

122
Q

what are the signs and symptoms of aspirin overdose?

A 
vomiting
sweating
tinnitus
blurred vision
respiratory alkalosis (adults)
metabolic acidosis
renal failure
123
Q

what is the management of aspirin overdose?

A

mild - oral fluids
vomiting - IV fluids
potassium monitoring, require supplements
oral activated charcoal (50g 4hrly)
alkalinisation (1L 1.26% NaCl over 2hrs, maintain urinary pH>7.5, allows salicylate to be excreted in the urine)
severe - haemodialysis (persistent acidosis, falling consciousness, levels >1000mg/L)

124
Q

what are the features and management of ethanol excess?

A

depressed consciousness
hypoglycaemia (children)

fluids
monitoring
ensure airway is open in vomiting
glucose if required

125
Q

what is the management of benzodiazepine and tricyclic antidepressant overdose?

A

benzodiazepines - flumazenil in respiratory depression
detection tests
do not provide the levels of drug (not useful in someone who’s already taking them)
monitoring
treat symptomatically

126
Q

what are the symptoms and signs of lead poisoning?

A

abdominal pain
anaemia
bone marrow suppression
peripheral neuropathy (mononeuropathy)

127
Q

what is the treatment of lead poisoning?

A

remove from source (occupational exposure)
chelation therapy (Ca EDTA or penicillamine)
monitoring of lead levels

128
Q

what are the signs and symptoms of iron poisoning?

A

abdominal pain (gastric erosion)
nausea
hypotension
hepatic injury

129
Q

what is the treatment of iron poisoning?

A

chelation therapy (desferrioxamine)
increases excretion
prevents toxic effects
monitoring

130
Q

what is the pathology of methanol and ethylene glycol?

A

methanol produces formate and ethylene glycol produces glycolate
cause severe metabolic acidosis
liver and kidney toxicity
blindness

131
Q

what is the treatment of methanol and ethylene glycol overdose?

A

ethanol
prevents metabolisation and formation of toxic metabolites
severe cases - haemodialysis

132
Q

describe myoglobin

A

contains iron
provides an oxygen store
released into the blood during muscle damage
filtered by the glomerulus

133
Q

what are the features of myoglobin excess?

A

damage and blockage of the renal tubules
AKI
brown/tea coloured urine (blockage of tubules)
CK increase

134
Q

what are the muscle enzymes that are measured?

A

creatinine kinase
aspartate aminotransferase
lactate dehydrogenase

135
Q

describe creatinine kinase

A

used in ATP regeneration
composed of 2 subunits (M or B)
main type in skeletal - CK-MM
main type in cardiac - CK-MB

136
Q

what is the cause of high levels of CK-MB?

A

cardiac muscle damage

137
Q

what are the causes of high levels of AST?

A

liver dysfunction
skeletal or cardiac muscle dysfunction
haemolysed sample

138
Q

what are the causes of high levels of LDH?

A

increased cell breakdown or an increased number of cells

tumour growth - leukaemia and lymphoma

139
Q

how is CK-MB affected by ischaemia?

A

rises after 4-9 hours
more cardiac-specific (can be affected by other muscle)
should return to baseline after 48-72 hours
second rise in CK-MB = second event

140
Q

describe myalgia

A

muscle pain
no rise in CK
no severe muscle tenderness

141
Q

describe myositis

A

mild increase in CK

increased muscle breakdown

142
Q

describe rhabdomyolysis

A 
rapid muscle breakdown
CK increase (5-10x upper limit of normal)
143
Q

what are the consequences of rhabdomyolysis?

A

increase in CK and myoglobin
monitor urea, creatinine, GFR (AKI)
increase in potassium phosphate (electrolyte release)
cardiac arrhythmias (K)
metabolic acidosis (AKI, organic acids released from muscle, ischaemia of muscle causing lactic acidosis
hypocalcaemia (falls initially then rises as muscles recover)

144
Q

what are the causes of skeletal muscle disease (rhabdomyolysis)?

A 
crush syndrome (excess alcohol)
ischaemia
seizure (rapid tonic-clonic muscle contraction)
inflammation
autoimmune disorders (polymyositis or dermatomyositis)
hypothyroidism (mild increase in CK)
hypo/hyperadrenalism
hypo/hyperkalaemia, hypocalcaemia, hypohosphataemia, hypomagnesaemia
statins (myalgia, not rhabdomyolysis)
ecstasy, cocaine
muscular dystrophies (CK increase)
malignant hyperpyrexia
fatty oxidation defects
mitochondrial disorders
paraneoplastic syndrome
145
Q

describe the troponin complex

A

troponin C - binds to Ca, allows muscle contraction
troponin I - inhibitory
troponin T - anchors the tropomyosin complex

146
Q

how are cardiac troponins affected by ischaemia?

A

large increase
put o 7 days to return to baseline
may be difficult to detect re-infarction

147
Q

what are the causes of increased troponin levels?

A 
ischaemia
myocarditis (viral or autoimmune)
post-cardiac surgery
aortic dissection
cardiomyopathy
acutely unwell, cardiac strain (ICU)
PE
SAH
stroke (other cerebral cause)
CKD
sepsis
severe exertion (marathon
148
Q

describe BNP

A

secreted by atrial and ventricular myocytes when the heart is under strain
cause natriuresis (loss of Na and water) and relaxation of smooth muscle
increase in acute/chronic heart failure, age, female

149
Q

what are the uses of BNP?

A

diagnosing heart failure (rule out test)
screening for left ventricular function in those with IHD
risk stratification/prognosis

150
Q

what action should be taken if a patient with a Hx of IHD presents with shortness of breath?

A

proceed to echocardiography (most likely due to HF)

151
Q

what action should be taken if a patient presents with shortness of breath and no cardiac Hx?

A

measure BNP

if high, refer to echocardiography

152
Q

what are the causes of an increase in BNP?

A 
PE
septic shock
liver cirrhosis
kidney injury
COPD with cor pulmonale
acutely ill from SAH or stroke
AF
IHD
hyperthyroidism
153
Q

how is water distributed in the body?

A

60% of the body weight is water
2/3s is intracellular fluid and 1/3 is extracellular fluid
of the extracellular fluid - 1/4 is in the vasculature, 3/4 is interstitial fluid

154
Q

what is the main electrolyte present in intracellular fluid?

A

potassium

155
Q

how is plasma Na regulated?

A

by the regulation of salt and water
volume receptors respond to changes in the intravascular volume via the kidneys
osmoreceptors respond to changes in the composition of plasma via thirst and water reabsorption

156
Q

describe ANP

A

volume receptor in the left atrium
causes Na to be lost in the urine via natriuresis
reduces the amount of angiotensin and aldosterone, reducing the amount of Na reabsorbed

157
Q

what is the impact of stretch receptors stimulating sympathetic activity when circulating volume falls?

A

increased renin secretion

angiotensin, aldosterone and sodium reabsorption

158
Q

how do osmoreceptors regulate water?

A

thirst stimulation when osmolarity is increased

when osmolarity is increased, dehydration occurs and ADH is released from the posterior pituitary, preventing diuresis

159
Q

what re the causes of a pseudo hyponatraemia?

A

hypertriglyceridaemia

hyperproteinaemia

160
Q

what are the causes of Na movement into cells?

A

non-ketotic hyperosmolar coma

diabetic ketoacidosis

161
Q

how does hyponatraemia cause symptoms?

A

water moves into cells
cerebral oedema
this results in nausea, headache, malaise, seizures, coma

162
Q

what are the causes and features of hypervolaemic hyponatraemia?

A

congestive cardiac failure
cirrhosis
nephrotic syndrome

urinary Na <20 (without diuretics)
reduced albumin (cirrhosis and nephrotic syndrome)
increased urinary protein (nephrotic syndrome)

163
Q

what are the causes and features of hypovolaemic hyponatraemia?

A

GI loss; diarrhoea, vomiting, fistula (low urinary Na)
renal loss; obstruction, (thiazide) diuretics, hyperglycaemia (high urinary Na)

skin turgor reduction, dry tongue, postural hypotension, tachycardia

164
Q

what are the causes of euvolaemic hyponatraemia?

A

addison’s (synacthen test)
hypothyroidism
SIADH

165
Q

describe SIADH

A

water retention when it is not necessary
plasma becomes diluted, plasma osmolarity falls and a concentrated urine is produced
high urinary Na

166
Q

what re the causes of SIADH?

A 
pain
nausea
carbamazpeine
SSRI (sertraline, lustral)
paraneoplastic syndrome (most commonly small cell carcinoma of the lung)
167
Q

what is the management of hyponatraemia?

A

slowly corrected Na by 1-2 mmol/hr
not more than 12 mmol in 24hrs
faster - brain shrinkage and cerebral haemorrhage
treat underlying cause
Na depletion - oral or IV Na
SIADH - fluid restriction (1L/24hrs)
not responding/require Na correction rapidly - demeclocycline (causes nephrogenic diabetes insipidus, blocks ADH action)
aquaporin receptor antagonists - block Na reabsorption

168
Q

what are the causes of hypovolaemic hypernatraemia?

A

dermal loss; burns, sweating, fever
GI loss; vomiting, diarrhoea, fistula
renal loss; diuresis (loop diuretics), AKI, CKD, PKD, hyperosmolar non-ketotic coma

169
Q

what are the causes of hypervolaemic hypernatraemia?

A

iatrogenic
excess hypertonic saline administered
antibiotic infusions of a very high Na content

170
Q

what are the causes of euvolaemic hypernatraemia?

A 
diabetes insipidus (polyuria, polydipsia)
fever (water loss in excess of salt)
mechanical ventilation (insensible fluid loss in excess of Na)
171
Q

describe diabetes insipidus

A

ADH deficiency; not enough being produced or posterior pituitary damage

172
Q

what are the causes of diabetes insipidus?

A

tumour of pituitary
sarcoid (can infiltrate the pituitary)
ADH resistance (action blocked by the kidneys)

confirmation by water deprivation test (check urine, plasma osmolarity and fluid output)

173
Q

what is the treatment of hypernatraemia?

A

treat the underlying cause
fluid replacement (hypovolaemic or euvolaemic)
correct Na 1-2 mmol/hr, 10-12 mmol/24hrs

Scientific Basis of Clinical Practice (10 decks)

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