Chemical Path Flashcards
What are the 2 main roles of calcium in the body?
1) Skeleton
2) Metabolic - e.g. action potentials and IC signalling
What are the normal plasma ranges of calcium?
2.2 - 2.6mmol/l
How is calcium distributed in the blood?
40% bound to albumin (so affected by the level of albumin - must use corrected level)
50% ionised (free - active)
10% complexed - citrate/phosphate
What 2 main hormones are involved in calcium metabolism?
1) PTH
2) 1,25(OH)2D - Calcitrol
Give 4 functions of PTH
1) mobilises Ca from bone
2) increases renal calcium reabsorption
3) increases renal phosphate excretion
4) increases tubular 1alpha hydroxylaton of vit D (25(OH)D)
How do you work out corrected calcium?
- dependent on the amount of albumin
- Serum (Ca2+) + 0.02 X (40-serum albumin in g/L)
What % of calcium is actually in the serum
1% - the 99% left in the bones
What is the corrected calcium if the albumin level is 30 and total calcium is 2.2
(2.2 + (0.02 X (40 - 30)) = 2.4 mM
Why must normal plasma calcium level be maintained?
for nerve and muscle function
What is hypocalcaemia detected by?
the parathyroid gland
What 3 sources does the PTH get Ca2+ from/
1) Bone
2) gut (absorption)
3 Kidneys (resorption AND 1 alpha hydroxylase activation)
how is vitamin D synthesised? Draw the 4 step process
7-dehydrocholesterol –> (SUN/SKIN –> cholecalicferol (D3) —> liver) —> dihydrocholecalciferol –> (PTH) –> 1,25 dihydrocholecalciferol
What is the other namefor vitamin D3 and where is it synthesised?
cholecalciferol - in the skin (SUN)
What enzyme in the kidney activates vitamin D3, and what does it become?
1 alpha hydroxylase
1,25-(OH)2 D3
aka 1,25-dihydrocholecalciferol
Where are 25 hydroxylase enzymes found and what do they do/
in the liver - convert cholecalciferol (D3) to 25-hydroxycholecalciferol (te inactive and stored version of vitamin D3)
Give 4 risk factors for vitamin D deficiency
1) malabsorption
2) Dark skin
3) lack of sunlight exposure
4) diet
What 3 things would you see in the biochem to indicate osteomalacia?
1) Low Ca
2) Low Pi
3) Raised ALP
What are Looser’s zones?
pseudofractures seen in osteomalacia. airline incomplete stress fractures. Most commonly found on pelvic rami, humeral ad femoral necks, and the axillary edge of the scapulae
what is the significance of a patient coming in with bone pain and eats loads of chappatis?
chapatis contain phytic acid –> high dietary intake of phytic acid is known to cause hypocalcaemia as it disrupts absorption and so increases risk of viramin D deficiency and osteomalacia / rickets
What clnical features might you see in rickets in children/
1) bowed legs
2) costochondral swelling
3) widened epiphyses at the wrists
4) myopathy
name a class of drug which is known to have an effect on vitamin D levels?
anticonvulsants e.g. phenytoin –> induce breakdown vitD so risk of bone disease
what is the difference between osteoporosis and osteomalacia/
Osteomalacia –> demineralisation due to low Ca / vitamin D deficiency
Osteoporosis –> redcution in bone density (normal mineralisation) so noral biochemistry
How would you diagnose osteoporosis and what score would you get?
DEXA scan: T-score of < -2.5
What would a T score of -1 and -2.5 indicate?
osteopenia
What would a T-score f < -2.5 indicate?
osteoporosis
Give as many causes of osteoporosis as you can
1) Normal - normal age related decline in bone mass
2) Endocrinologoical - early menopause, hyperprolactinaemia, thyrotoxicosis, cushings
3) Drugs - steroids
4) lifestyle - sedentary, smoking, low BMI
5- others: genetic, prolonged illness / childhood illness
wHAT IS THE tX FOR OSTEOPOROSIS
Lifestyle - weight bearing exercise, stop smoking, reduce EtOH
Drugs- Vit D/C
Bisphosphonates - e.g. alendronate
Strontium
SERMs e.g. raloxifene
How do bisphosphonates work and give an example of one
alendronate
they encourage apoptosis of osteoclasts
What is the most common electrolyte abnormality in inpatients?
hyponatraemia
What is the normal range for serum sodium?
135 - 145mmol / L
Where is ADH released from?
Posterior pituitary
What receptors does ADH act upon, where are they, and wht does this achieve?
V2 receptors in the collecting duct of the nephron, insertion of aquaporins
ADH action on V1 receptors has what effect?
Vasoconstriction of vascular smooth muscle
What are the 2 main stimuli for ADH secretion?
- high serum osmolality
2. low blood volume / pressure
what detects the blood volume/pressure resulting in ADH secretion?
baroreceptors in the carotids, atria, aorta
what is the 1st step in the clinical assessment of a hyponatraemic patient?
fluid status
what are the clinical signs of hypovolaemia?
- tachycardia
- postural hypotension
- dry mucous membranes
reduced tissue turgor - confusion / drowsiness
- reduced urine output
- low urine Na+ (<20)
what are 3 clinical signs of hypervolaemia
raised JVP
bibasal crackles
peripheral oedema
If you suspect a patient is hypovolaemic and hyponatraemic, what 4 differentials must you think of?
vomiting
diarrhoea
diuretics
salt losing nephropathy
what are 3 causes of hyponatraemia in a hypervolaemic patient
cardiac failure
cirrhosis
renal failure
Why do you get hypervolaemia and hyponatraemia in heart failure?
reduced cardiac output, reduced blood pressure due to failing heart, causing increased ADH release due to baroreceptor stimulation, resulting in increased water retention and low sodium
why does liver cirrhosis result in hypervolaemic hyponatraemia?
increased NO, vasodilation, reduced BP, sensed by baroreceptors, ADH secretion, water retention
what are the 3 causes of hyponatraemia in a euvolaemic patient?
- hypothyroidism
- adrenal insufficiency
- SIADH
What investigations would you like to do in a patient with euvolaemic hyponatraemia?
- TFTs (hypothyroidism)
- Short synacthen test (ACTC - see cortisol rise, or NOT if Adrenal insufficiency)
- plasma and urine osmolality (if SIADH - will have low plasma ad high urine osmolality)
How do you diagnose SIADH? (4 steps)
- ensure not hypovolaemic - clinically and ask about vomiting/diarrhoea
- check TFTs (hypothyroidism)
- Rule out adrenal insufficiency
- Check urine and plasma osmolality - in SIADH serum Os = Low and urine = high
would also check for tumours with CT etc and chest
What is the serum and urine osmolality in SIADH?
serum = low urine = high
how would you manage a euvolaemic patient wth hyponatraemia?
- fluid restriction
- treat the underlying cause
what should you think about using to treat a severely hyponatraemic patient who is seizing and low GCS?
Hypertonic saline (3%)
What is the most important thing to remember when correcting hyponatraemia?
- NEVER correct serum Na >8-10mmol/L in the first 24 hours because there is a massive risk of osmotic demyelinaton (central pontine myelionlysis)
What is an iatrogenic cause of central pontine myelinolysis?
Increasing serum sodium too fast: should never be more than 8-10 mmol/L in the 1st 24h
what 2 drugs can you consider to treat SIADH?
- Demeclocycline
2. Tolvaptan
which is consistent wit SIADH:
- reduced plasma osmolality & urine osmolality
- reduced plasma osmolality and increased urine osmolality
2!!
What are the main causes of hypernatraemia
- unreplaced water loss - GI, sweat, renal (diuretics, reduced ADH release, diabetes insipidus)
- patient cannot control intake e.g. children, elderly
What investigations would you order in a patient with suspected diabetes insipidus?
- serum glucose (DM)
- serum potassium (hypokalaemia)
- serum calcium (hypercalcaemia)
- plasma and urine osmolality
- water deprivation test
What would the plasma and urine osmolality look like in diabetes insipidus?
less water reabsorbed due to inadequate ADH
urine = low plasma = high
Why can low potassium and high calcium cause diabeted insipidus?
causes resistance to ADH - nephrogenic DI
what happens in a water deprivation est to a DI patient
don’t drink - urine normally becomes more concentrated but in DI urine will remain dilute due to non secreton of ADH so urine osmolality will remain low
what is the correct treatment of hypernatraemia?
water replacement with 5% dextrose, and correct ECF volume depletion with 0.9% saline
What are the 4 routes of entry of CNS infection
- haematogenous
- direct implantation
- local extension - secondary to esstablished infection
- PNS into CNS - viruses
what is the most common route of CNS infection?
local extension - secondary to established infection …. nasopharyngeal spread
what are the major causative agents of meningitis?
- neisseria meningitides
- strep pneumoniae
- H. influenzae
- TB
- viruses
- cryptococcus neoformans
Is meningococcal meningitis classified as acute, chronic or aseptic?
Acute
What is the number 1 cause of meningitis?
Neisseria meningitides
What are the 2 most commonly identified organisms in aseptic meningitis?
Coxsackievirus group B & echoviruses
What’s the difference between meningitis and meningoencephalitis?
meningitis = inflammation of meninges & CSF
Menigoencephalitis = inflammation of meninges & brain parenchyma
what are the 2 most common viral causes of encephalitis?
HSV (1 & 2)
enteroviruses (coxsackie A & B, echovirus, polio)
What virus is becoming a leading and deadly ause of encephalitis internationally?
West Nile Virus
what species have a hign salt tolerance and can reside on contact lensess, potentially leading to abcesses & meninigits?
Acanthamoeba
what are the 2 main routes of brain abscesses occurring?
- ear infections/otitis media spreading medially e.g. streptococci
- staph. aureus flicking off heart valves (endocarditis) and spreading haematogenously
what investigations should you consider for CNS infections?
MRI CT LP (NOT if septic) brain biopsy Blood culture Throat Swab Blood PCR
CSF report shows 2500 neutrophils, and is turbid - what is the likely diagnosis?
pyogenic (bacterial) meningitis - ? neisseria meningitides, pneumococcus, listeria
CSF sample is clear, has a high protein level of 5g/L and contains 300 lymphocytes, negative gram stain
TB
Gram positive diplococci causing neck stiffness and headache in 21 year old student?
Strep pneumoniae
18 year old with headache and neck stiffness, CSF shows gram negitive diplococci>
Neisseria meningitides
treatment for meningitis (generic)
Ceftriaxone IV 2 bd
if >50 yrs / immunocompromised + amoxicillin Iv g 4hourly
Tx for generic meningoencephalitis?
Aciclovir 10mg/kg IV tds
Ceftriaxone IV 2g bd
if >50 / immunocompromised + amoxicillin IV 2g 4 hourly
What is a major clinicl way of differentiating between meningitis and meningo-encepalitis?
both have neck stiffness etc but meningo-encephalitis also presents with confusion
what should be the main things you want to do quickly in clinical assessment and initial Ix and Tx of patent presenting with headache fever and neck stiffness
- full history
- are they immunocompromised??
- get LP
- give Abx
how to you calculate the anion gap?
na + K - Cl - bicarb
what is the normal anion gap?
18mM
What 2 substances are thee most common causes of a high anion gap?
ketones and lactate
what causes a respiratory alkalosis?
primary hyperventilation - e.g anxiety
Whymight a hyperventilating patient get carpal spasm?
pH gets higher and higher due to low CO2, respiratory alkalosis, which increases the binding of calcium to albumin, reducing free ionised calcium, resulting in paralysis
how do you calculate osmolality?
2(Na + K) + Glucose + Urea mosm/kg
why do patients become unconscious if they are in a hypermolar hyperosmotic state?
Draws water out of the brain - becomes very dehydrated
low CO2 and low pH means…..
metabolic acidosis
What can an overdose of metformin cause?
Lacic acidosis (because i inhibits conversion of lactate back to glucose, resulting in it bulding up in the blood- akalosis)
What is the basic test to diagnose diabetes
fasting glucose >7 mM
If glucose is <7mM but you are still suspicious that a patient has diabetes, what test would you consider?
glucose tolerance test
- give 75g glucose at time 0 and check plasma glucose after 2 hours - if >11.1mM then iabetes
Which LFT is markedly elevated in bile duct obstruction / obstructive jaundice?
ALP
what are 3 major reasons for a low albumin?
- low production - chronic liver disease, malutrition
- loss - e.g. gut / kidneys (nephrotic syndrome)
- sepsis - 3rd space loss
What does AFP test for?
hepatocellular carcinoma - but also raised in pregnancy, and testicular cancer
When looking at LFTs, what does a normal albumin level suggest?
preserved synthetic function
what drug is a commo cause of cholestatic jaundice?
augmentin
what is Courvoisier’s sign ad what does it indicate?
painless palpable gall bladder in the presence of jaundice - unlikely to be gall stones
which hepatitis is the commmonest cause of acute hepatitis and jaundice and diarrhoea
Hep A
What do you treat a paracetamol overdose with
N-acetyl cystine an potentially liver transplant
Which hormone causes the hypotension in Addison’s disease
Aldosterone
what 2 hormones does TRH stimulate?
TSH AND prolactin
what 6 hormones are released by the anterior pituitary?
- prolactin
- GH
- LH
- FSH
- TSH
- ACTH
If you suspect a macroadenoma, what clinical sign should you look for?
bitemoporal hemianopia
What is the diagnosis if prolactin is >6000
always a prolactinoma - so huigh that cells must be making prolactin
What should be your next main investigation if we suspect a prolactinoma and already know that prolactin levels are >6000
Pituitary function test
What does a pituitary function test involve
administer “stress” with insulin to induce hypoglycaemia, + GnRH + TSH
What are the 2 major contraindication for the combined pituitary function test’?
- cardiac risk factors are present e.g. IHD, angina and abnormal ECG –> highly likely to have a MI
- No history of epilepsy
What is the term for a patient who’s glucose is <1.5nM and unconscus
neuroglycopenia
When is it legal to publically restrain someone
If they are diabetic, having a hypo, confused and aggressive, and you tackle and force them to eat something - legally fine!
how do you treat a patient who becomes severely hypoglycaemic during a combined pituitary function test?
50ml of 20% dextrose
What level of glucose should you aim to achieve during a combined pituitary function test?
<2.2mM - if it does not get this low then should administer more insulin
Why might you get high prolactin in a non functioning adenoma>
adenoma presses on the pituitary stalk, causing pit failure and also preventing dopamine reaching pituitary resulting in increased prolactin
what tests should you consider if suspecting Acromegaly
- bloods - GH
- Glucose tolerance test - will not suppress GH in acromegaly
- IGF-1
what is the best treatment for acromegaly?
pituitary surgery - best outcomes OR - cabergoline - octerotide - pit radiotherapy
Which part of the adrenal makes cortisol?
Zona reticularis
Which part of the adrenals make adrenaline?
Medulla
which part of the adrenals makes aldosterone
zona glomerulosa
In patients with primary hypothyroidism, what are thy also likely to have
aDDISONS DISEASE
what test should you do to confirm addisons?
Synacthen test - synthetic ACTH administered IM and measure cortisol - if it remains low then shows adrenal insufficiency
WHAT ARE THE 3 DIFFERENTIALS YOU SHOULD THINK ABOUT when a patient presents with HTN and an adrenal mass?
- phaeochromocytoma
- Conns
- Cushings
What is the treatment of phaeochromocytoma?
- alpha blockade URGENTLY (to prevent arrythmias/cardiac arrest) - phenoxybenzamine
- add beta blocker
- surgery
what is the likely diagnosis: 33 year old with HTN and hypokalaemia. Plasma aldosterone raised and plasma renin suppressed
Conn’s syndrome
What is the most common cause, apart from oral steroids, of Cushing’s?
85% due to pituitary dependent cushing’s disease
What are 2 less common causes of cushings? (10% and 5%)
10% caused by adrenal adenoma
5% caused by ectopic production of ACTH from lung cancer
What should be the next investigation if you have already done a dexamethasone suppression test (0.5mg 6 hoourly) which indicates cortisol suppression and s Cushing’s?
High dose dexamethasone suppression test (2mg every 6 hours for 48 hours) to help you determine the cause of cushing’s –> if suppressed to 50% of baseline then you can be sure the diagnosis is pituitary dependent cushings
What would be your next investigation if you have performed a high dose dexamethasone suppression test which has shown 50% suppression of cortisol?
Pituitary MRI –> suspect pituitary dependent cushings disease and so look for a microadenoma which you would then consider removing with surgery
What are the clinical lab criteria for SIADH?
- euvolaemic hyponatraemia
- inappropriately high urine osmolarity (should be keeping the Na)
- increase Na excretion >20mmol/l
- normal renal, crida, thyroid and adrenal function
- Diagnosis of exclusion
What is the most common malignant cause of SIADH
small cell lung cancer (secreting ADH ectopically)
What lab findings are there with Diabetes insipidus
Euvolaemic Hypernatraemia
very dilute urine (low osmolality)
May have
What investigations would you want to do for diabetes insipidus?
Serum glucose (DM)
blood potassium (hypo) and Calcium (hyper) - as these can cause nephrogenic DI
blood and urine osmolarity
water deprivation test (8h)
How can you tell between cranial and nephrogenic Diabetes insipidus?
In a water deprivation test, neither will concentrate urine naturally.
If you give DESMOPRESSIN - cranial DI will be treated and urine can be concentrated, but nephrogenic DI lacks the receptors so urine still remains dilute
How would you treat hypernatraemia?
treat underlying cause
fluid replacement
What is the normal potassium range
3.5-5.5 mmol/L
What is the normal Sodium range>
135-145mmol/L
Does acidosis cause potassium to increase or decrease and why
acidosis or dropping pH causes potassium to rise - due to the tight link between H+ and K+ where if pH drops by 0.1 then K+ rises by 0.7 as it moves out of the cells
is potassium mainly intra or extracellular?
K+ is predominantly INTRACELLULAR
Which liver enzyme is most raised in alcohol cirrhosis
AST
what are the main causes of elevated ALP?
- cholestasis (intra or extra hepatic, obstructive jaundice)
- bone disease (metastatic)
- Pregnancy ++
what causes a raised GGT?
- chronic alcohol use
- bile duct disease
- hepatic metastasis
What causes a low albumin
- reduced production - e.g. in chronic liver disease, malnutrition
- increased loss - e.g. gut/kidney
- sepsis - 3rd space loss
which tumour marker helps the diagnosis of hepatocellular cancer?
AFP - alpha-feto protein
which liver enzyme is very raised in pregnancy?
ALP
Which enzyme is faulty in Gilbert’s syndrome
glucuronyltransferase
Gilbert’s syndrome causes a build up of which type of bilirubin
/
unconjugated
Which gene is responsible for Gilbert’s syndrome
UGT1A1 gene on Ch2
If a jaundiced patient has very high ALP, but on USS there is no dilatation, what is the likely cause of the raised bilirubin?
drug induced cholestasis e.g. by augmentin following an infection
What is courvoisier’s sign?
in the presence of a painless palpable gallbladder, jaundice is unlikely to be caused by gallstones
What are the 3 components of the combined pituitary function test?
- Metabolic stress test: Administer insulin (0.15units/kg) to induce hypoglycaemia must be <2.2mM - to stimulate cortisol
- TRH test to stimulate TSH –> should be higher at 30 mins >60 mins
- gonadotrophin releasing hormone test –> LHRH to stimulate LH and FSH, if reduced will be an early sign of hypopituitarism
Where is ALP present?
Bone, liver, placenta, Liver
What are the 3 creatinine kinase forms?
CK-MM (skeletal muscle)
CK- MB (cardiac muscle)
CK-BB (brain)
what are some pathological causes of raised CK?
MI Myopathy e.g. Duchenne's muscular dystrophe muscle damage statin related myopathy severe exercise
A 64 year old man who smokes and has a family history of cardiovascular disease has recently been started on atorvastatin. Three weeks after commencing the tablet, he complains of generalised muscle pain. What is the working clinical diagnosis?
statin related myopathy
A 64 year old man who smokes and has a family history of cardiovascular disease has recently been started on atorvastatin. Three weeks after commencing the tablet, he complains of generalised muscle pain. What enzyme will help with the diagnosis?
CK
which type of creatinine kinase is most useful for MI?
CK-MB
when should you measure troponin after chest pain?
6H AND 12H
sensitivity rises from 17% to 92%
What is the unit of measurement for plasma enzyme activity ?
U/L
Which type of vitamin D do we commonly measure?
25-hydroxy vitamin D (deactivated) - gives an indication of storage
What does vitamin B3 or Niacin deficiency cause?
Remember the 3 D’s
dementia, diarrhoea, dermatitis
What can an excess of vitamin C cause?
renal stones
What can a deficiency of vitamin cause?
colour blindness
What is the average GFR?
120 ml/min 0r 7.2 L per hour
What is the equation for calculating the kidney clearance?
C= (Urine conc x vol)/plasma conc
What is the gold standard measure of GFR
Inulin clearance - but only really used for research
What 3 characteristics must markers of GFR have?
- not bount to proteins
- freely filtered by the glomerulus
- not modified by tubules
Which factor(s) limit(s) the use of serum creatinine as a marker of GFR?
It is influenced by intake of fat It is lower in the black population It is related to muscle mass It is reabsorbed by the renal tubules All of the above
Related to muscle mass
How much age related decline is there in renal GFR?
1ml/hr/year
what is an alternative endogenous marker to creatinine?
Cystatin C
what is a more paractical way of measuring proteinura than a 24h urine collection
Protein:creatinine ration
A 50 year old, known alcoholic, presents generally unwell, seemingly intoxicated, with acute kidney injury. Urine microscopy reveals calcium oxalate crystals, what diagnosis do you suspect?
ethylene glycol poisoning
You admit a 28 year old man who you suspect has a renal stone, what is your first choice of imaging?
a) Plain KUB
b) CT
c) Ultrasound KUB
d) IVU
e) MRI
nowadays CT KUB is the investigation of choice - mush more accessible
what is the hallmark of pre-renal AKI?
reduced renaal perfusion
What is the most common cause of pre-renal AKI
True volume depletion
Causes of pre-renal AKI
- true volume depletion
- renal ischaemia ie renal artery stenosis
- Hypotension
- oedema
- Drugs (decreasing renal blood flow)
Which class of drugs may predispose patients to developing pre-renal AKI?
a) NSAIDs - decrease afferent arteriolar dilatation
b) Calcineurin inhibitors - decrease afferent arteriolar dilatation
c) ACEi or ARBs - decrease efferent arteriolar constriction
d) Diuretics
what is the hallmark of post-renal aki?
phsical obstruction to the urine flow
Causes of post-renal AKI?
blocked catheter
prostate/urethral blockage
ureter blockage (causing bilateral)
Give 3 exampkles of long term injuries the kidneys can get due to prolonged obstruction?
- tubular damage
- Glomerular ischaemia
- long term interstitial scarring
what are exogenous and endogenous causes of tubular injury causing intrinsic AKI?
endogenous: myoglobin + immuoglobulins
Exogenous: Contrasts, acyclovir, aminoglycosides
What two measures do we use to define severity of acute kidney injury?
urine output
Creatinine
What are the 3 most common causes of CKD?
1) diabetes
2) atheroslerotis
3) HTN
How can you treat a patient with anaemia due to chronic kidney disease/
ESA (erythropoietin stimulating agent) e.g. EPO alpha/beta or Darbopoietin (Aranesp)
What types of ESA are there
EPO alpha
EPO beta
Darbopoietin (aranesp) `
What is the condition where you have osteoclat resorption of calcified bone leading to replacement with fibrous tissue?
Osteitis fibrosa
What is the most important consequence of chronic kidney disease?
Cardiovascular disease - GFR directly predicts risk of CVS event (reduced below 60 is where it starts!)
What is the active from of vit D
1,25-(OH_2 dihydroxycholecalciferol
What should ou always check if there is hypercalcaemia/
PTH - is it suppressed?
If PTH is suppressed in hypercalacaemia what should you suspect?
MALIGNANCY
What should you suspect if PTH is not suppressed in hypercalcaemia?
primary hyperparathyroidism - the high calcium should normally suppress the parathyroid gland production of PTH so this is an abnormal response showing something wrong with the regulatory system.
What is a rare cause of hypercalcaemia without PTH suppression?
Familial hypocalciuric hypercalcaemia
in which receptor is there a mutation in Familial hypocalciuric hypercalcaemia
the calcium sensing receptor on parathyroid gland - CaSR
What is the order of the layers of the adrenal gland from outside to in?
Outside = zona glomerularis
Zona fasciculata
Zona reticularis
Medulla
What do the medulla, zona fasciculata and Zona glomerulosa of the adrenal produce
medulla = adrenaline fasciculata = cortisol glomerulosa = aldosterone
What are the 3 classic lab findings for addisons?
Low Na+
Low Glucose
High K+
++ ADDisons
What is the name of the combination of primary hypotthyroidism and addisons?
Schmidt’s syndrome (old)
now polyglandular autoimmune syndrome
what test should you do to confirm addisons disease
Synacthen test
what are the 3 important differentials for adrenal mass with hypertension
Cushings
Conns
Phaeochromocytoma
what is a phaeochromocytoma
tumour in the adrenal medulla causing increased production of catecholamines like adrenaline
what is the urgent treatment of a phaeo?
ALPHA BLOCKADE with phenoxybenzamine to stop arrythmias from pulses of adrenaline and death
conn’s syndrome signs and symtpms
Hypertension
low potassium
High aldosterone, low renin
treatment of conn’s
aldosterone antagonist
K+ SPARING diuretics e.g. spironolactone
cushings DISEASE means
there is a PITUITARY tumour making too much ACTH
causes of cushing’s syndrome
- iatrogenic steroids
- pituitary adenoma
- adrenal tumour
- Tumour secreting ectopic ACTH
What are you looking for with a high dose dexamethasone suppression test?
Want to see a pituitaary response from the 2mg every 6h for 2 days –> get a drop in the ACTH of 50% then it must be pituitary, if not then the ACTH must be from somewhere else
What are the 3 most common causes of Hypothyroidism?
- Hashimoto’s (autoimmune)
- Atrophy of the thyroid
- Post Grave’s (surgery etc)
how do you manage hypothyroidism?
investigate the cause - look for anti thyroid peroxidase antibodies
- check for other autoimmune conditions e.g Addisons (early morning cortisol) and Coeliac screen
- Do an ECG - CVS risk
- Give T4 (levothyroxine)
Do you give T3 or T4 to treat hypothyroidism?
T4 - no evidence of more benefit of T3
what are the top 3 causes of hyperthyroidism
- graves disease
2, toxic multinodular goitre - single toxic adenoma
also subacute thyroiditis and postpartum thyroiditis
Which causes of hyperthyroidism have a high uptake on a technetium scan?
Grave’s, toxic multinodular goitre ad single toxic adenoma
What should you avoid when treating patients with Grave’s eye disease
Dont treat with radioactive iodine…. the autoantibodies to thyroid receptor also in the eyes and Tx can damage them
How do you screen for medullary thyroid carcinoma
Calcitonin or CEA
What is thyroglobulin a marker for
Thyroid cancer - used to screen for recurrance of a cancer post-surgery and Thyroxine
