BIOCHEMISTRY (principles and transition) Flashcards

1
Q

what does OIL RIG stand for

A

oxidation is loss (of electrons)

reduction is gain (of electrons)

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2
Q

what is catabolism

A

breakdown of something

Catabolism = Cut

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3
Q

what is anabolism

A

build up of molecules (Anabolism = Add)

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4
Q

what is a zwitterion

A

amino acid with no charged side groups

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5
Q

what is a primary protein

A

amino acid chain

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6
Q

what is a secondary protein (2)

A

alpha helix

beta sheets

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7
Q

what is a tertiary protein

A

3D globular/fibrous protein

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8
Q

what is a 4th generation (i cant remember the name lol) protein

A

several tertiary proteins eg haem

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9
Q

where are steroid receptors

A

inside the cell

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10
Q

what does splicing do

A

remove introns, leaves exons

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11
Q

where does splicing start (base code)

A

AUG

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12
Q

what is an isozyme

A

an enzymes ‘cousin’

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13
Q

which enzymes do not follow the michaelis menton kinetic model

A

allosteric enzymes

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14
Q

what happens to K in competitive antagonists in the michaelis menton kinetic model

A

it changes

C ompetitive = K C hanges

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15
Q

in DKA do you want to give K+ even if K+ is normal

A

yes

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16
Q

is hyperkalaemia caused by K+ salt in IV drugs common

A

no its rare

17
Q

at what CK is renal failure likely in rhabdomyolysis

A

CK >10000 U/L

18
Q

cause of hyperkalaemia and hypocalcaemia on blood results

A

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!

19
Q

what happens to K+ in blood samples stored in fridge overnight eg in GP practice

A

hyperkalaemia

20
Q

hyperkalaemia differentials

A

haemolysis
renal failure
antihypertensive drugs eg spironolactone, ACEi
pseudohyperkalaemia

21
Q

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

A

benchtop centrifuge in the practice

though in the formative this isn’t the most right answer!

22
Q

hypercalcaemia initial management

A

rehydration

23
Q

if low vit D what should you do

A

probs nothing

only prescribe vit D supplements if symptomatic

24
Q

in malignancy is PTH high or undetectable

A

undetectable

25
Q

why is primary hyperparathyroidism diagnosed much earlier

clinical significance of this (what do we no longer see)

A

hypercalcaemia is detectable

no longer see radiological changes eg osteitis fibrosa cystica

26
Q

what does ADH act on

A
kidneys 
blood vessels 
heart
pituitary 
liver 
lots of things...

basically more than just the kidneys!

27
Q

what is used to distinguish between central and nephrogenic diabetes insipidus

A

DDAVP (synthetic analogue of AVP (ADH))

28
Q

when might you do synacthen tests in ITU

A

to monitor prognosis

poor adrenal function = poor prognosis

29
Q

does ACTH distinguish between primary and secondary adrenal insufficiency

A

yes

30
Q

if cortisol is being measured, what drugs do you need to withhold

A

steroids!

31
Q

if HPA axis is suppressed (by drugs etc) how much replacement steroids does someone need

A

7.5mg daily

32
Q

what happens to patients with adrenal insufficiency when given saline (sodium) in comparison to ‘normal’ people

A

they cant retain it

33
Q

mineralocorticoid activity definition

A

exchange of Na+ with K+ or H+

34
Q

what happens to circulating blood volume in oedema

A

it decreases

35
Q

is pseudohyponatraemia common

A

no, rare cause of abnormally low Na+ conc

36
Q

which ion do kidneys excrete to regulate volume

A

Na+

37
Q

ECG for hyperkalaemia

A

tall T waves

38
Q

what causes pseudohyperkalaemia

A

increased time between blood being taken and being tested on
eg high K+ in GP but fine when admitted to hospital