MedEd Chem 2 Flashcards
what is osmolality vs osmolarity
osmollity = mass of solvent
osmolarity = volume of solvent
how do you calculate osmolality
2 (Na + K) + glucose + urea
what is a normal osmolality
275 - 295
causes of a raised osmolality
(ions that aren’t in the equation)
alcohol
sugars
lipid
proteins
what is the main contributor to osmolality
sodium
rank the following in order of highest to osmolality to lowest
DI
DKA
HHS
pneumonia
SIADH
HHS
DKA
DI
pneumonia
SIADH
what is HHS
hyperosmolar hperglycaemia state (T2DM DKA)
why does HHS / DKA have higher osmolality
high glucose
why does pneumonia have a lower osmolality
can lead to SIADH
why does SIADH have a very low osmolality
lots of water resorption so decreases ion conc (osmolality)
describe the mechanism of sodium regulation when the blood volume increases inc receptors, what they are detecting and hormones released
increased blood volume –> atrial stretch –> baroreceptors –> ANP release –> decreased aldosterone / ADH / renin release –> decreased Na conc
where is renin released from
kidney
high osmolality –> ___ (body’s physiological response) + ADH _____ –> _____ Na conc
thirst
released
decreased
low osmolality –> ADH ______ –> _____ Na conc
suppression
increased
which is more important for ADH, the control of blood volume or osmolality
blood volume –> ADH increases the blood volume which decreases the osmolality
what is the commonest electrolyte imbalance
hyponatraemia
what is the first thing to check if someones blood show low Na & why
plasma osmolality
- to exclude pseudohyponatraemia (low Na with normal / high osmolality)
what are causes of pseudohyponatraemia and how can you distinguish them
high lipids / proteins - normal osmolality
high sugars / alcohol - high osmolality
(in hyponatraemia, the osmolality should be LOW tho, so even normal is abnormal !)
after excluding pseudohyponatraemia, what is the next thing to check in someone with hyponatraemia
check fluid status - hypo/eu/hypervolaemic
what is the ADH level in hypovolaemic hyponatraemia
appropriately high
what Ix is useful in someone with hypovolaemic hyponatraemia
urinary sodium osmolality
what cause for hypovolaemic hyponatraemia is suggested by a urinary Na conc of <20
extra renal losses (kidneys working) eg D&V, burns
what cause for hypovolaemic hyponatraemia is suggested by a urinary Na conc of >20
renal losses (kidneys not working) eg renal disease, diuretics, cerebral salt wasting
mx of hypovolaemic hyponatraemia
treat underlying cause eg loperamide
IV 0.9% NaCl
or slow IV hypertonic 3% NaCl (ITU for Sx pts)
if someone is hypervolaemic hyponatraemia, where/what is the problem
low effective arterial blood volume ie the blood volume is not sufficient to supply cells
what can cause hypervolaemic hyponatraemia
reduced cardiac output - CCF
increased peripheral arterial vasodilation - cirrhosis
what does a urinary sodium of <20 suggest in hypervolaemic hyponatraemia
CCF, cirrhois, nephrotic syndrome
what does a urinary sodium of >20 suggest in hypervolaemic hyponatraemia
CKD
tx of hypervolaemic hyponatraemia
treat underlying cause
fluid restriction
what is the umbrella cause of euvolaemic hyponatraemia
endocrinological
what does a urinary sodium of <20 suggest in euvolaemic hyponatraemia
psychogenic polydipsia, tea and toast diet
what does a urinary sodium >20 suggest in euvolaemic hyponatraemia
hypothyroidism
adrenal insufficiency
SIADH
mx of euvolaemic hyponatraemia
- inc resistant SIADH
treat underlying cause
fluid restrict
demeclocycline / tolvaptan for resistant SIADH
causes of SIADH
brain - craniopharyngoma / tumours
lung - pneumonia, small cell lung ca
drugs - SSRIs, PPIs, DA antagonists
how do you diagnose SIADH
diagnosis of exclusion !!
check TFTs and cortisol first
urinary / plasma Na
diagnostic criteria of SIADH
low plasma sodium (<135) / osmolality (<270)
high urinary sodium (>20) / osmolality (>100)
no adrenal / thyroid / renal dysfunction
causes of hypovolaemic hypernatraemia
osmotic diuresis
diarrhoea
burns
causes of hypervolaemic hypernatraemia
hypertonic 3% NaCl use
hyperaldosteronism
causes of euvolaemic hypernatraemia
DI
Mx of hypernatraemia
oral intake of water
slow IV 5% dextrose (1L/6hr) - guided by urine utput / plasma sodium
2 types of DI and what the defect is in each
central = lack of production of ADH
nephrogenic = ADH resistance in kidneys
causes of central DI
pituitary surgery
irradiation
tumour
trauma
mx of central DI
desmopressin
causes of nephrogenic DI
electrolyte disturbances (low K, high Ca)
drugs - lithium, demeclocycline
mx of nephrogenic DI
thiazides
primary Ix for ?DI
excluding other causes
- serum glucose (DM)
- serum K (hypoK)
- serum Ca (hyperCa)
diagnostic tests for DI
plasma / urine osmolality
** water deprivation test **
post water deprivation test…
urine concentrates after fluid restriction
Dx?
normal or primary polydipsia
post water deprivation test…
urine concentrates after desmopressin
Dx?
central DI
post water deprivation test…
urine remains dilute after desmopressin
Dx?
nephrogenic DI
diagnostic criteria for DI
despite raised plasma osmolality, urine is dilute with urine:plasma osmolality of <2:1
best Ix for SIADH
paired urinary:plasma osmolality
PC of low K
muscle weaknes
cramps
hypotonia
ECG of low K
flattened / inverted T wave
prominent U waves
prolonged PR
ST depresion
3 groups of causes of low K
increased K loss
increased cellular influx
decreased intake
causes of increased loss causing low K
GI losses - D&V, high output stoma
renal losses - Conn’s, diuretics, congenital defects eg Bartter / Gitelman syndrome
causes of increased cellular influx leading to low K
insulin
beta agonits
refeeding syndrome
metabolic alkalosis
what acid base picture does hypokalaemia cause
metabolic alkalosis
what causes a metabolic acidosis in low K
renal tubular acidosis
partially treated DKA
key Ix for hypokalaemia
serum Mg
aldosterone:renin ratio (if HTN)
if low K and low Mg what needs to be done
correct them together - correcting low k alone won’t work
mx of mild to mod low K (2.5-3.5)
oral sando K (replacement)
mx of severe low K (<2.5)
10mmol/hour IV KCl with continuous ECG monitoring
what Ix needs to be done with any mx of low K
daily U&Es
ecg features of hyperK
tall tented T waves
small p wave
widened QRS
prolonged PR interval
sine wave
groups of causes of hyperK
artefact
iatrogenic
reduced excretion
increased cellular release
what does artefact causing hyperK mean
haemolysis - release of intracellular K causing high K
what iatrogenic causes can lead to high K
massive blood transfuion
xs K+ mx
causes of high K due to reduced excretion
renal disease
aldosterone deficiecny
drugs - K-sparing diuretics, ACEi, ARBs
causes of low K due to increased cellular release
metabolic acidosis
tissue breakdown eg rhabo
ixs for hyperK
U&Es
eGFR
CK - rhabdo
cortisol / short synthACTHen test
mx of hyper K
IV calcium gluconate
IV insulin with dextrose
consider: nebulised salbutamol, K binders, dialysis
when would you tx hyperK
ECH changes or K >6.5
where is ca found in the body
99% in bone
1% serum
how is calcium found in the serum (%s)
50% free, ionised (biologically active)
bound to albumin 40%
complexed with citrate / phosphate 10%
what are the 2 main functions of PTH
increase serum Ca
decrease serum PO43
which hormone decreases serum Ca and increases serum PO43
calcitonin
3 actions of PTH
bone resorption by osteoclasts
increased Ca resorption at DCT / increased PO43 excretion at PCT
increased ca reabsorption in gut
3 actions of calcitonin
less bone resorption by osteoclasts
decreased ca reabsoprtion at DCT
decreased ca reabsoprtion in gut
which hormone aids the actions of PTH
calcitriol
sx of hypocalcaemia
paraesthesia (peri oral)
arrythmia
convulsions
tetany / spasms
2 signs associated with hypocalcaemia & what each is
trousseau’s sign - tetany
Chvostek’s sign - spasms
causes of hypocalcaemia
hypoparathyroidism - digeorge (primary) or post-thyroidectomy (secondary), low Mg
vitamin D deficiency
fatal result of hypocalcaemia with sx
laryngospasm - hoarse voice, inability to swallow
who gets laryngospasm
post thyroidectomy surgery
ix of low ca
ECG
bloods - Mg, PO43, PTH level, LP
imaging - DEXA
mx of mild hypoCa (>1.9, no sx)
oral calcium
vit D
mx of severe hypoCa (<1.9, sx)
IV calcium gluconate
sx of hypercalcaemia
stones, bones, moans, groans
when you see high ca, what else do you need to look at to start thinking of cause
PTH
causes of high ca with low PTH
malignancy - PTHrP, bony mets, MM
hyperthyroidism
hypodrenalism
sarcoidosis
thiazides
vitamin d excess
causes of high ca with high PTH
primary / tertiary hyperparathyroidism
ix for hyperca
myeloma screen
TFTs
cortisol
mx of hypercalcaemia
IV 0.9% NaCl +/- diuretics
biphosphonates if cancer
parathyroidectomy is PTH adenoma
biochem of pagets
isolated high ALP
biochem of osteoporosis
normal ca, PTH, PO43
–> just density of bone is abnormal
what is the defect in primary hyperPTH
increase in PTH eg parathyroid adenoma
what is the defect in secondary hyperPTH
renal osteodystrophy
what is the defect in tertiary hyperPTH
autonomous PTH secretion post renal transplant
rank the plasma Ca conc highest to lowest
primary hyperPTH
secondary hyperPTH
osteoporosis
osteomalacia
parathyroid carcinoma
parathyroid carcinoma
primary hyperPTH
osteoporosis
secondary hyperPTH
osteomalacia
which enzyme is raised in pagets and osteomalacia and is caused by osteoblast activation
ALP (alkaline phosphatase)
commonest cause of high Ca in community
parathyroid adenoma
commonest cancers that met to bone
prostate
breast
lung
4 steps of interpreting a blood gas acid base status
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
when can anion gap be useful when interpreting blood gases
when you’re not sure what type of acid base status it is
how do you calculate anion gap
(Na + K) - (HCO3 + Cl)
what is a normal anion gap
14 to 18
what can cause a raised anion gap
alcohol
uraemia
DKA
iron
lactic acid
salicylates / isoniazid
which LFTs are markers of liver function
clotting - PT / INR
albumin
BR
which LFTs are markers of liver damage
BR
ALT, AST
GGT
ALP
when are the following LFTs raised in liver damage
- ALT
- AST
- GGT
- ALP
- viral hep
- viral hep
- alcoholic hep
- obstructive
prehepatic causes of jaundice
HA
ineffective erythropoesis
hepatic concepts causing jaundice
hepatocellular dysfunction
impaired conjugation
impaired BR uptake
post hepatic causes of jaundice
obstruction - stones / pancreatic cancer
2 key features of prehepatic jaundice **buzzwords
absent conjugated BR
absent urinobilinogen
2 key features of post hepatic jaundice **buzzwords
dark urine - raised urobilinogen
pale stools - low stercobilinogen
raised ALT > AST dx?
viral hep
raised AST > ALT dx?
alcoholic hep
causes of ALT/AST in 1000s
ischemia
viral hep
toxins
causes of raised unconjugated BR
increased haemolysis
drugs that impair hepatic uptake eg rifampacin
impaired conjugation - Gilberts, crigler-najjar
what is crigler-najjar
severe gilberts (gilberts is deficiency of an enzyme but CN is complete lack of it)
causes of raised conjugated BR
hepatocellular dysfunction
decreased hepatic excretion
what other organs make ALP
bone, placenta, GIT, kidney, prostate
causes of isolated raised ALP
pregnancy
childhood growth spurts
pathological - mets
causes of raised ALP and GGT
obstructive cholestasis - gallstones, drugs (OCP, co-amox)
alcoholic hepatitis
best marker of liver func in acute liver injury
PTT
