BIOCHEMISTRY (principles and transition) Flashcards
what does OIL RIG stand for
oxidation is loss (of electrons)
reduction is gain (of electrons)
what is catabolism
breakdown of something
Catabolism = Cut
what is anabolism
build up of molecules (Anabolism = Add)
what is a zwitterion
amino acid with no charged side groups
what is a primary protein
amino acid chain
what is a secondary protein (2)
alpha helix
beta sheets
what is a tertiary protein
3D globular/fibrous protein
what is a 4th generation (i cant remember the name lol) protein
several tertiary proteins eg haem
where are steroid receptors
inside the cell
what does splicing do
remove introns, leaves exons
where does splicing start (base code)
AUG
what is an isozyme
an enzymes ‘cousin’
which enzymes do not follow the michaelis menton kinetic model
allosteric enzymes
what happens to K in competitive antagonists in the michaelis menton kinetic model
it changes
C ompetitive = K C hanges
in DKA do you want to give K+ even if K+ is normal
yes
is hyperkalaemia caused by K+ salt in IV drugs common
no its rare
at what CK is renal failure likely in rhabdomyolysis
CK >10000 U/L
cause of hyperkalaemia and hypocalcaemia on blood results
contaminant from purple top to yellow top
purple top contains K+ EDTA
happens if you don’t get enough blood, so take some out of another tube = DONT DO IT!
what happens to K+ in blood samples stored in fridge overnight eg in GP practice
hyperkalaemia
hyperkalaemia differentials
haemolysis
renal failure
antihypertensive drugs eg spironolactone, ACEi
pseudohyperkalaemia
in rural GP practices, what can be used to minimize the effects of hyperkalaemia caused by long time between collecting blood sample and processing blood sample
benchtop centrifuge in the practice
though in the formative this isn’t the most right answer!
hypercalcaemia initial management
rehydration
if low vit D what should you do
probs nothing
only prescribe vit D supplements if symptomatic
in malignancy is PTH high or undetectable
undetectable
why is primary hyperparathyroidism diagnosed much earlier
clinical significance of this (what do we no longer see)
hypercalcaemia is detectable
no longer see radiological changes eg osteitis fibrosa cystica
what does ADH act on
kidneys blood vessels heart pituitary liver lots of things...
basically more than just the kidneys!
what is used to distinguish between central and nephrogenic diabetes insipidus
DDAVP (synthetic analogue of AVP (ADH))
when might you do synacthen tests in ITU
to monitor prognosis
poor adrenal function = poor prognosis
does ACTH distinguish between primary and secondary adrenal insufficiency
yes
if cortisol is being measured, what drugs do you need to withhold
steroids!
if HPA axis is suppressed (by drugs etc) how much replacement steroids does someone need
7.5mg daily
what happens to patients with adrenal insufficiency when given saline (sodium) in comparison to ‘normal’ people
they cant retain it
mineralocorticoid activity definition
exchange of Na+ with K+ or H+
what happens to circulating blood volume in oedema
it decreases
is pseudohyponatraemia common
no, rare cause of abnormally low Na+ conc
which ion do kidneys excrete to regulate volume
Na+
ECG for hyperkalaemia
tall T waves
what causes pseudohyperkalaemia
increased time between blood being taken and being tested on
eg high K+ in GP but fine when admitted to hospital
