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MedEd Path > MedEd Chem 2 > Flashcards

MedEd Chem 2 Flashcards

1
Q

what is osmolality vs osmolarity

A

osmollity = mass of solvent
osmolarity = volume of solvent

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2
Q

how do you calculate osmolality

A

2 (Na + K) + glucose + urea

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3
Q

what is a normal osmolality

A

275 - 295

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4
Q

causes of a raised osmolality

A

(ions that aren’t in the equation)
alcohol
sugars
lipid
proteins

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5
Q

what is the main contributor to osmolality

A

sodium

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6
Q

rank the following in order of highest to osmolality to lowest
DI
DKA
HHS
pneumonia
SIADH

A

HHS
DKA
DI
pneumonia
SIADH

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7
Q

what is HHS

A

hyperosmolar hperglycaemia state (T2DM DKA)

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8
Q

why does HHS / DKA have higher osmolality

A

high glucose

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9
Q

why does pneumonia have a lower osmolality

A

can lead to SIADH

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10
Q

why does SIADH have a very low osmolality

A

lots of water resorption so decreases ion conc (osmolality)

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11
Q

describe the mechanism of sodium regulation when the blood volume increases inc receptors, what they are detecting and hormones released

A

increased blood volume –> atrial stretch –> baroreceptors –> ANP release –> decreased aldosterone / ADH / renin release –> decreased Na conc

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12
Q

where is renin released from

A

kidney

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13
Q

high osmolality –> ___ (body’s physiological response) + ADH _____ –> _____ Na conc

A

thirst
released
decreased

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14
Q

low osmolality –> ADH ______ –> _____ Na conc

A

suppression
increased

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15
Q

which is more important for ADH, the control of blood volume or osmolality

A

blood volume –> ADH increases the blood volume which decreases the osmolality

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16
Q

what is the commonest electrolyte imbalance

A

hyponatraemia

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17
Q

what is the first thing to check if someones blood show low Na & why

A

plasma osmolality
- to exclude pseudohyponatraemia (low Na with normal / high osmolality)

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18
Q

what are causes of pseudohyponatraemia and how can you distinguish them

A

high lipids / proteins - normal osmolality
high sugars / alcohol - high osmolality
(in hyponatraemia, the osmolality should be LOW tho, so even normal is abnormal !)

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19
Q

after excluding pseudohyponatraemia, what is the next thing to check in someone with hyponatraemia

A

check fluid status - hypo/eu/hypervolaemic

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20
Q

what is the ADH level in hypovolaemic hyponatraemia

A

appropriately high

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21
Q

what Ix is useful in someone with hypovolaemic hyponatraemia

A

urinary sodium osmolality

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22
Q

what cause for hypovolaemic hyponatraemia is suggested by a urinary Na conc of <20

A

extra renal losses (kidneys working) eg D&V, burns

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23
Q

what cause for hypovolaemic hyponatraemia is suggested by a urinary Na conc of >20

A

renal losses (kidneys not working) eg renal disease, diuretics, cerebral salt wasting

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24
Q

mx of hypovolaemic hyponatraemia

A

treat underlying cause eg loperamide
IV 0.9% NaCl
or slow IV hypertonic 3% NaCl (ITU for Sx pts)

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25
Q

if someone is hypervolaemic hyponatraemia, where/what is the problem

A

low effective arterial blood volume ie the blood volume is not sufficient to supply cells

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26
Q

what can cause hypervolaemic hyponatraemia

A

reduced cardiac output - CCF
increased peripheral arterial vasodilation - cirrhosis

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27
Q

what does a urinary sodium of <20 suggest in hypervolaemic hyponatraemia

A

CCF, cirrhois, nephrotic syndrome

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28
Q

what does a urinary sodium of >20 suggest in hypervolaemic hyponatraemia

A

CKD

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29
Q

tx of hypervolaemic hyponatraemia

A

treat underlying cause
fluid restriction

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30
Q

what is the umbrella cause of euvolaemic hyponatraemia

A

endocrinological

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31
Q

what does a urinary sodium of <20 suggest in euvolaemic hyponatraemia

A

psychogenic polydipsia, tea and toast diet

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32
Q

what does a urinary sodium >20 suggest in euvolaemic hyponatraemia

A

hypothyroidism
adrenal insufficiency
SIADH

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33
Q

mx of euvolaemic hyponatraemia
- inc resistant SIADH

A

treat underlying cause
fluid restrict
demeclocycline / tolvaptan for resistant SIADH

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34
Q

causes of SIADH

A

brain - craniopharyngoma / tumours
lung - pneumonia, small cell lung ca
drugs - SSRIs, PPIs, DA antagonists

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35
Q

how do you diagnose SIADH

A

diagnosis of exclusion !!
check TFTs and cortisol first
urinary / plasma Na

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36
Q

diagnostic criteria of SIADH

A

low plasma sodium (<135) / osmolality (<270)
high urinary sodium (>20) / osmolality (>100)
no adrenal / thyroid / renal dysfunction

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37
Q

causes of hypovolaemic hypernatraemia

A

osmotic diuresis
diarrhoea
burns

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38
Q

causes of hypervolaemic hypernatraemia

A

hypertonic 3% NaCl use
hyperaldosteronism

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39
Q

causes of euvolaemic hypernatraemia

A

DI

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40
Q

Mx of hypernatraemia

A

oral intake of water
slow IV 5% dextrose (1L/6hr) - guided by urine utput / plasma sodium

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41
Q

2 types of DI and what the defect is in each

A

central = lack of production of ADH
nephrogenic = ADH resistance in kidneys

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42
Q

causes of central DI

A

pituitary surgery
irradiation
tumour
trauma

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43
Q

mx of central DI

A

desmopressin

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44
Q

causes of nephrogenic DI

A

electrolyte disturbances (low K, high Ca)
drugs - lithium, demeclocycline

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45
Q

mx of nephrogenic DI

A

thiazides

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46
Q

primary Ix for ?DI

A

excluding other causes
- serum glucose (DM)
- serum K (hypoK)
- serum Ca (hyperCa)

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47
Q

diagnostic tests for DI

A

plasma / urine osmolality
** water deprivation test **

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48
Q

post water deprivation test…
urine concentrates after fluid restriction
Dx?

A

normal or primary polydipsia

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49
Q

post water deprivation test…
urine concentrates after desmopressin
Dx?

A

central DI

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50
Q

post water deprivation test…
urine remains dilute after desmopressin
Dx?

A

nephrogenic DI

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51
Q

diagnostic criteria for DI

A

despite raised plasma osmolality, urine is dilute with urine:plasma osmolality of <2:1

52
Q

best Ix for SIADH

A

paired urinary:plasma osmolality

53
Q

PC of low K

A

muscle weaknes
cramps
hypotonia

54
Q

ECG of low K

A

flattened / inverted T wave
prominent U waves
prolonged PR
ST depresion

55
Q

3 groups of causes of low K

A

increased K loss
increased cellular influx
decreased intake

56
Q

causes of increased loss causing low K

A

GI losses - D&V, high output stoma
renal losses - Conn’s, diuretics, congenital defects eg Bartter / Gitelman syndrome

57
Q

causes of increased cellular influx leading to low K

A

insulin
beta agonits
refeeding syndrome
metabolic alkalosis

58
Q

what acid base picture does hypokalaemia cause

A

metabolic alkalosis

59
Q

what causes a metabolic acidosis in low K

A

renal tubular acidosis
partially treated DKA

60
Q

key Ix for hypokalaemia

A

serum Mg
aldosterone:renin ratio (if HTN)

61
Q

if low K and low Mg what needs to be done

A

correct them together - correcting low k alone won’t work

62
Q

mx of mild to mod low K (2.5-3.5)

A

oral sando K (replacement)

63
Q

mx of severe low K (<2.5)

A

10mmol/hour IV KCl with continuous ECG monitoring

64
Q

what Ix needs to be done with any mx of low K

A

daily U&Es

65
Q

ecg features of hyperK

A

tall tented T waves
small p wave
widened QRS
prolonged PR interval
sine wave

66
Q

groups of causes of hyperK

A

artefact
iatrogenic
reduced excretion
increased cellular release

67
Q

what does artefact causing hyperK mean

A

haemolysis - release of intracellular K causing high K

68
Q

what iatrogenic causes can lead to high K

A

massive blood transfuion
xs K+ mx

69
Q

causes of high K due to reduced excretion

A

renal disease
aldosterone deficiecny
drugs - K-sparing diuretics, ACEi, ARBs

70
Q

causes of low K due to increased cellular release

A

metabolic acidosis
tissue breakdown eg rhabo

71
Q

ixs for hyperK

A

U&Es
eGFR
CK - rhabdo
cortisol / short synthACTHen test

72
Q

mx of hyper K

A

IV calcium gluconate
IV insulin with dextrose
consider: nebulised salbutamol, K binders, dialysis

73
Q

when would you tx hyperK

A

ECH changes or K >6.5

74
Q

where is ca found in the body

A

99% in bone
1% serum

75
Q

how is calcium found in the serum (%s)

A

50% free, ionised (biologically active)
bound to albumin 40%
complexed with citrate / phosphate 10%

76
Q

what are the 2 main functions of PTH

A

increase serum Ca
decrease serum PO43

77
Q

which hormone decreases serum Ca and increases serum PO43

A

calcitonin

78
Q

3 actions of PTH

A

bone resorption by osteoclasts
increased Ca resorption at DCT / increased PO43 excretion at PCT
increased ca reabsorption in gut

79
Q

3 actions of calcitonin

A

less bone resorption by osteoclasts
decreased ca reabsoprtion at DCT
decreased ca reabsoprtion in gut

80
Q

which hormone aids the actions of PTH

A

calcitriol

81
Q

sx of hypocalcaemia

A

paraesthesia (peri oral)
arrythmia
convulsions
tetany / spasms

82
Q

2 signs associated with hypocalcaemia & what each is

A

trousseau’s sign - tetany
Chvostek’s sign - spasms

83
Q

causes of hypocalcaemia

A

hypoparathyroidism - digeorge (primary) or post-thyroidectomy (secondary), low Mg
vitamin D deficiency

84
Q

fatal result of hypocalcaemia with sx

A

laryngospasm - hoarse voice, inability to swallow

85
Q

who gets laryngospasm

A

post thyroidectomy surgery

86
Q

ix of low ca

A

ECG
bloods - Mg, PO43, PTH level, LP
imaging - DEXA

87
Q

mx of mild hypoCa (>1.9, no sx)

A

oral calcium
vit D

88
Q

mx of severe hypoCa (<1.9, sx)

A

IV calcium gluconate

89
Q

sx of hypercalcaemia

A

stones, bones, moans, groans

90
Q

when you see high ca, what else do you need to look at to start thinking of cause

A

PTH

91
Q

causes of high ca with low PTH

A

malignancy - PTHrP, bony mets, MM
hyperthyroidism
hypodrenalism
sarcoidosis
thiazides
vitamin d excess

92
Q

causes of high ca with high PTH

A

primary / tertiary hyperparathyroidism

93
Q

ix for hyperca

A

myeloma screen
TFTs
cortisol

94
Q

mx of hypercalcaemia

A

IV 0.9% NaCl +/- diuretics
biphosphonates if cancer
parathyroidectomy is PTH adenoma

95
Q

biochem of pagets

A

isolated high ALP

96
Q

biochem of osteoporosis

A

normal ca, PTH, PO43
–> just density of bone is abnormal

97
Q

what is the defect in primary hyperPTH

A

increase in PTH eg parathyroid adenoma

98
Q

what is the defect in secondary hyperPTH

A

renal osteodystrophy

99
Q

what is the defect in tertiary hyperPTH

A

autonomous PTH secretion post renal transplant

100
Q

rank the plasma Ca conc highest to lowest
primary hyperPTH
secondary hyperPTH
osteoporosis
osteomalacia
parathyroid carcinoma

A

parathyroid carcinoma
primary hyperPTH
osteoporosis
secondary hyperPTH
osteomalacia

101
Q

which enzyme is raised in pagets and osteomalacia and is caused by osteoblast activation

A

ALP (alkaline phosphatase)

102
Q

commonest cause of high Ca in community

A

parathyroid adenoma

103
Q

commonest cancers that met to bone

A

prostate
breast
lung

104
Q

4 steps of interpreting a blood gas acid base status

A

what is the pH
is CO2 high / low ? is this causing the change?
is bicarb driving the change?
is there compensation? - pH in normal range or not

105
Q

when can anion gap be useful when interpreting blood gases

A

when you’re not sure what type of acid base status it is

106
Q

how do you calculate anion gap

A

(Na + K) - (HCO3 + Cl)

107
Q

what is a normal anion gap

A

14 to 18

108
Q

what can cause a raised anion gap

A

alcohol
uraemia
DKA
iron
lactic acid
salicylates / isoniazid

109
Q

which LFTs are markers of liver function

A

clotting - PT / INR
albumin
BR

110
Q

which LFTs are markers of liver damage

A

BR
ALT, AST
GGT
ALP

111
Q

when are the following LFTs raised in liver damage
- ALT
- AST
- GGT
- ALP

A
  • viral hep
  • viral hep
  • alcoholic hep
  • obstructive
112
Q

prehepatic causes of jaundice

A

HA
ineffective erythropoesis

113
Q

hepatic concepts causing jaundice

A

hepatocellular dysfunction
impaired conjugation
impaired BR uptake

114
Q

post hepatic causes of jaundice

A

obstruction - stones / pancreatic cancer

115
Q

2 key features of prehepatic jaundice **buzzwords

A

absent conjugated BR
absent urinobilinogen

116
Q

2 key features of post hepatic jaundice **buzzwords

A

dark urine - raised urobilinogen
pale stools - low stercobilinogen

117
Q

raised ALT > AST dx?

A

viral hep

118
Q

raised AST > ALT dx?

A

alcoholic hep

119
Q

causes of ALT/AST in 1000s

A

ischemia
viral hep
toxins

120
Q

causes of raised unconjugated BR

A

increased haemolysis
drugs that impair hepatic uptake eg rifampacin
impaired conjugation - Gilberts, crigler-najjar

121
Q

what is crigler-najjar

A

severe gilberts (gilberts is deficiency of an enzyme but CN is complete lack of it)

122
Q

causes of raised conjugated BR

A

hepatocellular dysfunction
decreased hepatic excretion

123
Q

what other organs make ALP

A

bone, placenta, GIT, kidney, prostate

124
Q

causes of isolated raised ALP

A

pregnancy
childhood growth spurts
pathological - mets

125
Q

causes of raised ALP and GGT

A

obstructive cholestasis - gallstones, drugs (OCP, co-amox)
alcoholic hepatitis

126
Q

best marker of liver func in acute liver injury

A

PTT

MedEd Path (10 decks)

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