random endocrine Flashcards
what are the symptoms of cushings syndrome
EXCESS STEROID effectively so think so side effects of steroids, thin skin, proximal myopathy, bruising, striae, weight gain, osteoporosis, moon face, buffalo hump, diabetes mellitus,depression, anxiety, psychosis, may can also cause high blood pressure, poor wound healing, increased susceptibility to infection
if excess mineralcorticoids then may have oedema and hypertension
if excess androgens
then virilisation, hirsuitism,acne, oligo/amenorrhoea
what is the test for cushings
overnight 1mg dexamethasone suppression test <50 the next morning is normal if >100=abnormal
how can you work out where the causative thing for cushings is
plasma ACTH levels, if they are low then it is within the adrenals and if high it is ectopic or pituitary causing
can also do MRI to identify the lesion
what are the risk factors in acromegaly
hypertension, cardiac failure through myopathies eg left ventricular hypertrophy, cardiomyopathy, arrhythmias also increased risk in IHD and stroke
COLON CANCER RISK INCREASED
what are the treatment options for acromegaly
surgery to remove the adenoma
drugs-somatostatin analogues-octreotide/lanreotide
or GH antagonists eg pegvisomat if intolerant to SSA
what is the aetiology of Cushings
Cushings disease=pituitary
cushings syndrome=adenoma of adrenal, ectopic, pseudo=alcohol and depression, steroid medication
differentiating pituitary cushings and ectopic cushings
ACTH levels, they will be <300 in pituitary causes but higher than 300 in ectopic causes (adrenal will be less than 1)
and with a high dose dexamethasone suppression pituitary will decrease but ectopic wont decreases
what is a high dose dexamethasone test
6 hours after: 2 days of 2mg dexamethasone 6 hourly (ie 8mg/day)
what is a hypophysectomy
removal of the pituitary gland
what are the drug treatment options if surgery doesn’t work for cushings
metyrapone (while waiting for radio to work)
ketoconazole (nb hepatotoxic)
Pasireotide-new SSA, receptor 2 and 5 blocked
what does GH do
decreases abdominal fat increases muscle mass, strength, exercise capacity and stamina improves cardiac function decreases cholesterol and increases LDL increases bone density given daily by SC injection
what are the risks of testosterone replacement
prostate enlargement-doesn’t cause prostate cancer but may make it grow so monitor with PR exam and PSA at the start
Polycythaemia-monitor RBC
Hepatitis (with oral tablets)
what is addisons disease
primary adrenocortical insufficiency, destruction of the adrenal cortex
what symptoms does addisons disease cause
lethargy, weight loss, dizzy, flu like myalgias/arthralgias, nausea, vomiting abdo pain, increased pigmentation in buccal mucosa
why do you get dizzy with addisons
reflection of hypotension from decreased ECF
why do you get pigmentation with addisons
increase in ACTH( because nothing is converting it to cortisol) and it contains MSH which is melanocyte stimulating hormone
what is secondary adrenal insufficiency
commonest cause is iatrogenic due to long term steroid use leading to suppression of the pituitary adrenal axis
mineralocorticoid production remains intact and there is no hyperpigmentation as decrease ACTH
what is the most important thing to tell patients with Addisons disease about
DO NOT STOP TAKING STEROIDS, wear bracelets and inform GPs of their diagnosis, make sure that they increase their steroids when they are ill
what is a trophic hormone
a hormone that regulates the release of other hormones
what is the goitre like in subacute thyroiditis
PAINFUL
what are the symptoms of congenital hypothyroidism and why is it important to diagnose
prolonged neonatal jaundice delayed mental and physical milestones short stature puffy face and macroglossia hypotonia need to diagnose before 4 weeks or rsik or irreversible cognitive impairment
what is a dermoid cyst
rare congenital cyst
usually presents in teenage years
soft non fluctuant
what is a brachial cyst
an oval mobile cystic mass that develops between the SCM and the pharynx-upper part of anterior triangle
due to failure of obliteration of the 2nd brachial cleft in embryonic development usually present in early adulthood
‘‘half filled hot water bottle’’
FNA-cholesterol crystals
can fistulate
what type of swelling is a cystic hygroma
a congenital lesion-lymphangioma typically found in the neck, classically on the left side POSTERIOR TRIANGLE SWELLING
most are evident at birth, around 90% detected before the age of 2
lymph filled and transilluminate
how can you check if a neck lump is a lymph node
lymph nodes don’t move on swallowing
what is impaired fasting glucose
fasting glucose <7 but >6.1mmol/l
what would you do if you had a patient with impaired fasting glucose
do an OGTT to rule out DM, if OGTT shows glucose of <11.1 but >7.8 mmol/l
what is impaired glucose tolerance
fasting glucose <7mmol/l and OGTT 2 hr glucose >7.8mmol/l but <11.1mmol/l
how is diabetes diagnosed
fasting blood glucose >7mmol/l
random blood glucose >11.1mmol/l
HbA1c>48mmol/l 6.5%
what genes are involved in type 1 diabetes
HLA DR3 and HLA DR4
what is Potts disease
TB in the intervertebral discs
how does infliximab work
TNFa inhibitor
how does ritixumab work
CD 20 monoclonal antibody
how does etanercept work
TNFa inhibitor
how does abatacept work
T cell function disruptor
what does Tocilizumab do
IL1 and IL6 inhibition
what is pancytopenia
a reduction in number of red cells, white cells and platelets
what is pancytopenia a potential complication from
immunosuppression
where do SGLT2 inhibitors act
in the proximal tubule
what can pioglitazone prevent against
macrovascualar complications, no prevention of microvascular but improvement in microalbuminaemia
what can SUs prevent against
microvascular disease
no prevention of macrovascualr disease
how do a glucosidase inhibitors work
they delay the absorption of glucose so there is a decrease in post prandial increase in blood glucose
what is charcot foot
a type of bone deformity
a neuropathic joint caused by loss of pain sensation, leading to mechanical stress (unimpeded by pain) and repeated joint injury.
what are the symptoms of charcots foot
swelling or redness of the foot or ankle, skin warmer at the point of injury
flattening of the arch
what is the pathological appearance of psoriatic conditions
elongation of the rete ridges
what is the classification of lichenoid damage
basal layer damage
irregular saw tooth acanthosis
hypergranulosis and orthohyperkeratosis
bandlike upper dermal infiltrate of lymphocytes
basal damage with formation of cytoid bodies
which layer does lichenoid pathologies affect
the basal layer
what cells are involved in lichenoid disorders
infiltrate of lymphocytes and formation of cytoid bodies
describe the autoimmune reactin in pemphigus vulgaris
igG autoantibodies made against desmoglein 3
desmoglein 3 maintains desosomal attachements
complement activation and protease release
disruption of desmosomes
is there evidence of acantholysis in bullous pemphigoid
no
where does bullous pemphigoid act
on the hemidesmosomes
where does pemphigus vulgaris act
on the desmosomes
give examples of vesiculobullous diseases
bullous pemohigoid, pemphigus vulgaris and dermatitis herpetiformis
what is the hallmark of dermatitis herpetiformis
intensely itchy lesions that are symmetrical
elbows, knees and buttocks-often excoriated
but hallmark is PAPILLARY DERMAL MICROABSCESSES
deposits of what are found in dermatitis herpetiformis in the dermal papillae
deposition of IgA in dermal papillae
what are some of the major glucocorticoid actions
increase in cardiac output and hence increase in BP
increase in renal blood flow and GFR
how does glucocorticoids affect the CNS
mood lability
euphoria/psychosis
decrease in libido
how do glucocorticoids affect the bone and connective tissue
accelerates osteoporosis by decreasing serum calcium decrease collagen formation
and decreases wound healing
how does cortisol affect metabolic rate
increase in blood sugar
increase in lipolysis and central redistribution of fats
increase in proteolysis
immunological affects of cortisol
decrease in capillary dilatation/permeability
decrease in leucocyte migration
decrease in macrophage activity
decrease in inflammatory cytokine production
what are the 6 classes of steroid receptors
glucocorticoid mineralcorticoid progestin oestrogen androgen vitamin D
what does aldosterone do to the sodium/potassium balance
potassium (and h+) excretion
na reabsorption
how do you diagnose adrenal insufficiency
on thoughts of a suspicious biochemistry decreased na and increased potassium
short SYNACTHEN test
measure plasma cortisol before and after 30 mins IV/IM ACTH
normal baseline >250, post ACTH >550
adrenal autoantibodies in Addisons
21 hydroxylase
adrenal autoantibodies in congenital adrenal hyperplasia
17 hydroxyprogesterone (these levels are v high and hence 21 hydroxylase levels very low)
what is the difference in primary and secondary adrenal insufficiency
exogenous steroid is the most common cause for secondary adrenal insuffiency
clinical features are the same except skin pale as no increase in ACTH
aldosterone production intact
what is the commonest cause of cortisol excess
Iatrogenic cushings syndrome
what is iatrogenic cushings syndrome most often caused by
prolonged high dose steroid therapy eg asthma, RA, IBD, transplants
what does iatrogenic cushings syndrome cause
chronic suppression of pituitary ACTH production and adrenal atrophy
what is cushing’s disease
increased secretion of ACTH from anterior pituitary often caused as a result of pituitary adenoma
what is the most common presentation in MEN 1
hypercalcaemia
what are the main causes of hypercalcaemia
primary hyperparathyroidism
myeloma
what is the clinical picture in MEN1
parathyroid hyperplasia
pituitary adenoma
pancreatic tumours
what is the gene in MEN1
MEN1 gene
what is the clinical picture in MEN IIA
parathyroid hyperplasia
phaeochromocytoma
medullary thyroid cancer
what is the clinical picture in MEN 11B
phaeochromocytoma
medullary thyroid cancer
mucosal neuromas/marfanoid body
