Chem path Flashcards
Causes of hypokalaemia
-GI loss: vomiting, diarrhoea
- renal loss: hyperaldosteronism, thiazide and loop diuretics, renal tubular acidosis type 1 and 2
- redistribution into cells: insulin, b-blockers, refeeding syndrome
consequences of hypokalaemia
muscle weakness
nephrogenic DI (polyuria and polydipsia)
ECG changes: T wave flattening, U waves, arrhythmias
normal range of potassium
3.5-5.5mmo/L
investigations and management of hypokalaemia
U&Es
monitor ECG changes
aldosterone:renin ratio (if high suggests conn’s as high aldosterone will negatively feedback on renin)
K replacement:
3-3.5mmol/L –> Oral KCl (2 sandoK tablets, TDS for 48hrs)
<3mmol/L –> IV KCl (10mmol/hr) risk of cardicac arrest
Causes of hyperkalaemia
Artefact- haemolysis when taking blood
intracellular –> extracellular mvmt of K: DKA(insulin shortage), rhabdomyolysis, haemolysis
decreased excretion:
mineralocorticodeficiency (Addisons), K sparing diuretics, ACEi, ARBs, NASAIDs, renal tubular acidosis type 4
Describe the ECG changes in hyperkalaemia
Tall tented T waves
loss of P wave
widened QRS
arrhythmia
management of hyperkalaemia
- repeat bloods incase artefact
- 10mls 10% calcium gluconate (stabilise myocardium)
- 100mls 20% dextrose + 10units short acting insulin eg. actrapid (draws K into cells and dex to prevent hypo)
- nebulised salbutamol
- treat cause
acid- base balance: pCO2 and pH in each met/resp acidosis/ alkalosis
metabolic acidosis- pCO2 low, pH low
metabolic alkalosis - pCO2 high, pH high
respiratory acidosis - pCO2 high, low pH
respiratory alkalosis- pCO2 low, pH high
causes of each met/resp acidosis/ alkalosis
met acidosis:
DKA, renal tubular acidosis, addisons, lactate(shock, sepsis), aspirin, ETOH
met alkalosis
bicarbonate ingesion, Conns, vomiting, burns
resp acidosis
hypoventilation: COPD, opioids, sedatives
resp alkalosis
hyperventilation: panic disorder/ anxiety, asthma,
causes of metabolic acidosis with a high anion gap
KULT
Ketoacidosis
uraemia (renal failure)
lactate
toxins (alcohol, salicylate, mannitol)
equation to calculate the anion gap
normal range
anions- cations
(Na+K)- (Cl+HCO3)
normal range: 14-18mol/L
what is the best marker of liver function?
prothrombin time
causes of isolated raised ALP
physiological: pregnancy (ALPregnancy), growth spurths
pathological: osteoblast activation; Pagets disease, osteromalacia, cholestasis, cirrhosis
why is ALP normal in myeloma?
plasma cells suppress osteoblasts
osteoblast activation secretes ALP
Causes of low albumin
nephrotic syndrome
chronic liver disease
protein losing enteropathy
sepsis
raised GGT and ALP
cholestatic/ obstructive picture
raised GGT in alcoholic liver disease
raised AST:ALT 2:1
supportive alcoholic liver disease
remember ALT- Last in the ratio
raised AST:ALT 1:1
supportive of viral liver disease
ALT>AST
chronic liver disease
what is the INR
it is the prothrombin time (time for the production of thrombin) which has been standardised to age and population and expressed as a ratio of ‘normal’
which clotting factors does the liver synthesise
V, VII, IX, X, XII, XIII
causes of pre, hepatic and post hepatic jaundice
pre hepatic- haemolysis, congestive cardiac failure, thalassaemia
hepatic- viral/ alcoholic hepatitis, cirrhosis, gilberts syndrome, crigler Najjar syndrome
post hepatic- primary biliary cholangitis, sclerosing cholestasis, gall stones, cancer of head of pancreas, cholangio carcinoma
features of acute porphryia
the P’s:
Painful abdomen
peripheral neuropathy
Psychosis
acute abdominal pain and neuropsychiatric Sx (eg. confusion, halluconations)
–> AIP until proven otherwise
HMB (hydroxymethylbilane) synthase deficiency leading to build up of porphobilinogen
what are porphryias
rare metabolic conditions where there is enzyme deficiencies in the haem biosynthesis leading to build up of toxic haem precursors
features of porphyria cutanea tarda
commonest
uroporphyrinogen decarboxylase deficiency
leading to uroporphyrin build up
photosensitivity
facial hyperpigmantation
blistering
milia
scarring
exacerbated by ETOH
describe the combined pituitary function test
administration of GnRH, TRH and insulin then measure levels of pituitary hormones at 0,30,60.90 and 120 mins
thyroxine, glucose, cortisol, LH/FSH, prolactin, TSH, GH
insulin: should raise ACTH and GH
TRH: should raise TSH and prolactin
GnRH: should raise LH/FSH
fasting overnight
pituitary macroadenoma
tumor >1cm
can compress pituitary stalk leading to less dopamine reaching the lactotrophs –> hyperprolactinaemia
can compress optic chiasm - bitemporal hemianopia with superior quadrantinopia
(NB craniopharyngoma causes inferior quadrantinopa)
causes of pseudohyponatraemia
hyperlipidaemia
hyperproteinaemia
Na actually normal but the lipids/proteins take up a large proportion of the serum and dilute the sodium because the conc of Na is calculated by Na/serum vol not Na/H20
how to calculate osmolarity
2(Na+K) + glucose + urea
Enzyme deficiency in acute porphryia
hydroxymethylbilane synthase deficiency
Enzyme deficiency in acute intermittent porphryia
hydroxymethylbilane synthase (same as acute porphryia)
Management of high K on blood test
- repeat blood test as may be artefact
- 10ml 10% calcium gluconate
- 100mls 20% dextrose and 10units short acting insulin
- nebulised salbutamol
Enzyme deficiency in porphyria cutanea tarda and resultant raised intermediate
uroporphyrinogen decarboxylase
raised urinary uroporphyrins and coproporphyrins (pink red flourescence with wood lamp)
Precipitating factors for acute intermittent porphyrias
ALA synthase inducers- steroids, barbituates, ethanol
stress- infection, surgery
reduced caloric intake
features of porphyria cutanea tarda and precipitating factors
photosensitivity
facial hyperpigmentation
blistering
milia
scarring
exacerbated by ETOH
Causes of excess ADH
Lung- SCLC, pneumonia
Brain- traumatic brain ingery, meningitis, tumours
Iatrogenic- SSRIs, amitryptilin, carbamazapine, PPIs
Most common type of thyroid neoplasia
Papillary (75-85%)
Risk for MALT lymphoma
chronic H pylori infection
chronic hashimotos
Histology of medullary cancer of thyroid
sheets of dark cells, amyloid deposition within tumour
Histology of papillary cancer of thyroid
Psammoma bodies (foci of calcification), orphan annie eyes (empty appearing nuclei with central clearing)
Histology of anaplastic thyroid cancer
undifferentiated follicular, large pleomorphic giant cells, spindle cells with sarcomatious appearance
tumour markers for different thyroid cancers
papillary and follicular - thyroglobulin
medullary- CEA and calcitonin
Which neoplasias are involved in MEN1
(3Ps)
Pituitary
Pancreas (insulinoma)
Parathyroid
Which neoplasias are involved in MEN2a
(2P 1M)
Parathyroid
Phaeochromocytoma
Medullary thyroid
Which neoplasias are involved in MEN2b
(1P 2M)
Phaeochromocytoma
Medullary thyroid
Mucocutaneous neuroma
(Marfanoid)
Drug toxicity signs:
Ataxia and nystagmus
Phenytoin
Drug toxicity signs:
Arrhythmias, heart block, confusion, seeing yellow-green
Digoxin
Drug toxicity signs:
tremor, lethargy, fits, arrhythmias, renal failure
Lithium
Drug toxicity signs:
Tinnitus, deafness, nystagmus, renal failure
aminoglycosides
ie. gentamycin, vancomycin
Drug toxicity signs:
Arrhythmias, convulsions, anxiety, tremor
Theophylline
Most common cause of hypercalcaemia
hypercalcaemia of malignancy
X ray appearance of uric acid
radiolucent
X ray appearance of calcium oxalate
radio-opaque
fat soluble vitamins
A, D, E and K
Signs of B3 deficiency
Niacin
Pellagra - B3=3Ds
Dementia
dermatitis
diarrhoea
signs of B6 deficiency
Dermatitis
anameia (sideroblasti)
Signs of B2 deficiency
Riboflavin
Glossitis
features of Bartter syndrome
automomal recessive
defect in thick ascending limb of loop of henle
NKCC2 or ROMK gene mutations
hypokalaemia, alkalosis and hypotension
hypercalcuria
effect of ACE inhibitors on potassium
Causes hyperkalaemia due to reduced potassium excretion
reduced angiotensin II and hence reduced aldosterone therefore reduced excretion
what is an AST and ALT of >2000IU/L indicative of?
paracetamol poisoning
what is Crigler-Najjar syndrome
reduction in UDP glucuronosly transferase needed in the conjugation of bilirubin
more severe version of Gilberts
What is Dublin-Johnson syndrome?
reduced secretion of conjugated bilirubin into bile
raised conjugated bilirubin levels
tumour marker in hepatocellular carcinoma
alpha-fetoprotein
level of plasma cortisol indicative of adrenal insufficiency after short and long synACTHen test
short synACTHen <550nmol/L
long synACTHen <900nmol/L (indicative of primary adrenal insufficiency)
what is Schmidst syndrome
also known as autoimmune polyendocrine syndrome type 2
associated with:
addisons
hypothyroidism and T1DM
vitamin deficiency signs:
ataxia and areflexia
vitamin E deficiency
cause of vitamin B6 deficiency
TB treatment esp isoniazid
features of phenylketonuria
fair haired
developmental delay between 6-12 months
low IQ