Clinical chemistry Flashcards
Name 4 things causing hyponatraemia
• Hypovolaemic (decreased extracellular volume)
–– Renal losses (diuretics, salt-losing nephropathy)
–– Non-renal losses (vomiting, diarrhoea)
–– Adrenal insufficiency (Addison’s disease)
• Euvolaemic
–– Excess fluid replacement (5 per cent dextrose for example)
–– Syndrome of inappropriate ADH secretion
–– Hypothyroidism
–– Psychogenic polydipsia (excess water consumption)
• Hypervolaemic (increased extracellular volume)
–– Congestive cardiac failure
–– Nephrotic syndrome
–– Cirrhosis with ascites
Typical findings in SIADH biochem
Hyponatraemia with a low plasma osmolality and inappropriately high
urine osmolality and urine sodium levels is typical of SIADH
Name 3 causes of raised prolactin
physiological factors, such as emotional stress,
pregnancy and breast feeding;
drugs especially dopaminergic antagonists such as
chlorpromazine, risperidone, domperidone and metaclopramide;
pituitary tumours;
polycystic ovary syndrome;
and severe thyroid failure
3 causes of raised bNP
2 causes of lowered
Heart failure
left ventricular hypertrophy, myocardial
ischemia, tachycardia, right ventricular overload, hypoxaemia (including pulmo
nary
embolism), renal dysfunction, sepsis, chronic obstructive pulmonary disease (COPD), diabetes, age
>70 years, cirrhosis of the liver, obesity
Lowered in…
Treatment with diuretics, ACE (angiotension
converting enzyme) inhibitors, beta-blockers, angiotensin II receptor antagonists
(ARBs) and aldosterone antagonists
3 conditions causing hyperK
Acute renal failure, Addison’s disease, metabolic acidosis of any aetiology, tumour
lysis syndrome
3 key biochem in conns (Primary hyperaldosteronsism)
How would 2ndary be different?
hypoK
HyperNa -> HTN
+ metabolic Alkalosis
Low renin (due to -ve feedback from aldosterone)
(Due to tumor -> excess aldosterone on K/Na channel + H+ channel )
2nd - High renin
Mx of hyperaldosteronism
spironolactone
surgery if tumour eg conns
Name 3 causes of HypoK
Conns / 2nd hyperaldosteronism / familial (AD)
Saline infusion
loop diuretics
D+V
Mx of familial hyperaldosteronism
dexamethasone
3 causes of hypoCa
Malabsorption vit D deficiency / hypoPTH chronic renal failure Pancreatitis Cell breakdown - rhabdomyolysis / Tumour lysis
How does lithium relate to hypothroidism
increases intrathyroid iodine
inhibits production of t3/4
name 3 drugs that affect TFTs
lithium
SSRI
phenytoin / carbamazepine
amiodarone
Cerebral causes of diabetes insipidus
cerebral trauma, infection, tumours
Nephrogenic causes of DI
chronic renal failure,
interstitial nephritis, hypercalcaemia, hypokalaemia and drugs, such as lithium
How would you differentiate cranial / nephro DI and psychogenic polydipsia
water deprivation test
Check urine osmolality following:
[Deprive of water] - {give synthetic ADH}
Normal (psychogenic) [High] - N/A
Cranial DI [Low] - {High}
Nephrogenic DI [Low] - {Low}
3 causes of hyperCa
Bony mets HyperPTH / vit d High bone turnover addisons acromegaly thiazides
Name 4 causes of a high anion gap
‘Dr Maples’
D, DKA R, renal failure M, methanol A, alcoholic ketosis P, paracetamol poisoning L, lactic acidosis E, ethylene glycol S, salicylate poisoning
Name 4 things on examination to indicate fluid loss
pulse (tachy) and blood pressure postural drop, loss of skin elasticity, dry mucus membranes,
increased respiratory rate, thirst, low urine volume and high urine concentration
Is fluid loss from upper GI hyper/iso/hypo tonic
isotonic -> losses provoke severe dehydration quickly compared to water loss
[Think of body compartments …. in a 70kg
-Isotonic fluid loss is taken just from the 18 litres of extracellular fluid
-water loss is taken from the 42 litres
of total body water.
Hence the symptoms of shock are present only following a much greater fluid loss if this is hypotonic.]
Urea / creatinine in dehydration
Urea is raised more (both raised tho)
2 reasons Why would someone have hypoK in prolonged vomiting
Vomit some out
Main is due to Poor kidney perfusion
- > secretion of renin
- > aldosterone
- > loss of K from tubules (and retention of Na)
What clinical conditions are associated with a respiratory alkalosis?
Hyperventilation, e.g. anxiety state
• Drugs , e.g. Aspirin (salicylate), theophylline,
catecholamines
• Hypoxia in early pulmonary disease, e.g. asthma, pulmonary embolus
• Increased cerebral respiratory drive, e.g. head injury, stroke, meningitis
• Non-cerebral increase in respiratory drive, e.g. heat exposure, hepatic failure
How do you calculate an anion gap
Nomal range?
(sodium concentration + potassium concentration)
− (chloride concentration + bicarbonate concentration)
10–20 mmol/L
Why does blood glucose get raised in sepsis
Metabolic response to injury
- glucose mobilization via glycogenolysis and gluconeogenesis - due to high glucagon / catechloamines
- Inhibition of insulin
2 reasons you might have low t4 and low TSH and how to differentiate
Sepsis / pit failure
Cortisol secretion - high in sepsis, low in pit failure
Bar low GFR, nbame 3 other markers of CKD
high
creatinine and urea, anaemia, hypocalcaemia, hyperphosphataemia, raised alkaline
phosphatase, raised PTH and raised triglyceride
low bicarbonate and CKD… what acid base balance would you suspect and why
chronic metabolic acidosis.
The acidosis is due to the accumulation of organic acids together with anions,
such as phosphate and sulphate
Why do you get secondary hyperPTH in CKD
HyperPO4 - stimulates
HypoCa - Ca usually inbitis
Lack of calcitrol by kidney - calcitrol usually inhibits
- [calcitrol also usually helps intestinal absorbsion of Ca]
Why might an ALP be high in a teenager
due to bones growing
Conditions predisposing to calcium phosphate stones
hyperparathyroidism and renal tubular acidosis.
Is raised FSH/LH in an older woman diagnostic of the menopause ?
No, they are consistent with menopause, they cannot
be considered diagnostic.
Menopause is: absence of menstrual activity for 2 years
3 causes of riased t3/4
Graves
thyroiditis (viral infection) - will be tender
Hashimoto’s (early stage) - then low
Adenoma - thyroid / pituitary TSH
amiodarone - could be raised / low levels
thyroxine
What conditions have a raised TPO?
hashimotos 95%
primary myxodema 90%
graves 18%
Why might you get variation in TSH levels when on thyroxine
missed doses
time of day taking dose
name 3 medical conditions or treatments may be associated with elevated troponin T
concentrations
congestive heart failure cisplatin treatment end-stage renal failure myocarditis, NSTEMI (non-ST elevation myocardial infarction) polymyositis pulmonary embolus severe infections
they are really markers of any process that damages cardiac muscle whether that be from ischaemia, trauma, infection, ‘strain’ on the heart or toxic effects.
[Eg 30% of marathon runners have raised troponin levels after a race]
why are troponin assays good for a marker of MI
they rise within 4 hours
high sensitivity
[its good to take them again later Eg at 6hrs and see if they have raised more]
SOB and raised bilirubin levels.
Dx?
What type of bilirubin?
Other findings?
PE
unconjugated raised (AST) and LDH
[to the breakdown of red cells in the blood clot that is causing the embolus]
[ALT/ALP would be normal unless there is right heart failure -> liver damage]
3 causes of raised d dimer
DVT/PE disseminated intravascular coagulation; following surgery trauma; aortic dissection; in inflammatory conditions, including rheumatoid arthritis, malignancy, liver disease and in pregnancy
Why might you get hyperglycaemia in hypothermia
increased release of glucagon and catecholamines (stress response) causing increased glycogenolysis and gluconeogenesis
Why do you get elevated lactate following reperfusion in hypothermia
vascular shut down associated with hypothermia, increased lactate production [lack of oxygen].
On reperfusion, lactate which has accumulated in muscle is washed out and plasma lactate levels rise
2 causes of raised CK in someone found on floor
hypothermia
pressure
[both cause muscle damage]
Half life of PSA
2-3 days
How does free PSA reflect cancer risk
if free PSA is BELOW 15% (of total PSA)
This reflects increased Ca risk
Why does reference range of PSA increase with age
The volume of the prostate increases with age and therefore the amount of PSA it produces
Give 3 uses of cancer markers
Aid diagnosis Determine prognosis Guidance for potential reposnse to treatment Eg HER2/Oestrogen Monitoring response to therapy Marker of reccurence
3 issues with using cancer markers
Lack of specificity [bar PSA]
Often inefficient at detecting early disease
lack of sensitivity
Causes of raised metanephrines
Phaeochromocytoma acute psychological stress, hypoglycaemia, obstructive sleep apnoea, vigorous exercise, conditions linked to clinical shock, such as myocardial infarction, severe injury, pulmonary embolus, and use of recreational drugs, such as cocaine.
In suspected phaeochromocytoma why would you repeat 24hr urinary metanephrines if values were 3x normal?
When is best to start collection
values 1-4x are not diagnositic and could be due to other reasons
Should start collection at onset of Sx
Bar metanephrines, what other test would you do in suspected phaeo ? Why?
Chromogranin A
Adrenal medullary tissue is derived from chromaffin cells which secrete chromogranin A
[high levels found in tumours]
Why do you get increased glucose during an attack of phaeo?
increased catechloamines
-> increased mobilisation of glucose
[gluconeogeneis, inhibit insulin]
If phaeo and rasied Calcium what are you thinking?
hyperparathyroidism and that the phaeochromocytoma is part of MEN2
[thyroid, phaeochromocytoma
and parathyroid adenoma]
Relevance of ST segment depression with digoxin therapy
This is a marker of therapy - NOT toxicity
name 2 metabolic conditions enhance digoxin toxicity
hypokalaemia, hypercalcaemia, diuretics (e.g.
furosemide), hypomagnesaemia and hypothyroidism
Route of elimiation of dixogin
Kidney
-> injury will increase levels
After Mx with Digibin (digoxin antidote) why would levels still be high?
captures digoxin in the circulation making it unavailable
for uptake by tissues
-still detectable though
Bar liver what other tissues have ALP?
How could you differentiate the cause between these?
bone, liver and placenta (+Smalll amount in intestines)
separated by electrophoresis
In primary biliary cirrhosis and gall stone obstruction
ALP+?
GGT
[ALP + GGT = biliary obstruction]
Alcoholic cirrhosis LFTs?
AST is usually elevated more than the ALT and in addition
the GGT would usually be elevated.
What Is a better marker of iron overload
ferritin or %saturation of transferrin
Causes of increased saturations ? Name 2
%sat of transferrin
[ferritin could be raised in any liver damage + is an acute phase protein]
A high saturation may be found in
haemochromatosis, haemosiderosis, haemolytic anaemia,
sideroblastic anaemia and iron poisoning
Name 2 non haem/iron conditions may be associated with an elevated serum ferritin?
What could you do to see if the rise was due to ferritins properties as an acute phase protein
Obesity, NAFLD, thyrotoxicosis
measure CRP when ferritin is requested
Which organs may be affected by haemachromatosis and with what effect
liver, testicles, skin, thyroid, pancreas, joints, heart and pituitary.
[Love The Skin That Protects Hamish’s Joints]
Liver - cirrhosis and Ca [usually first organ affected]
Testie / Pit - ED
Skin - Bronze
Pancreas - deposit in beta cells leading to glucose intolerance and eventually overt diabetes
Joint - Pain
Heart - heart failure / arrythmia
Thyroid - Hypo
AST:ALT in Alcoholic vs NAFLD ?
In obesity / diabetes?
AST:ALT ratios > 2 indicate alcoholic disease.
In obesity and diabetes, the AST:ALT ratio is usually less than 1
