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random endocrine Flashcards

1
Q

what are the symptoms of cushings syndrome

A

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

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2
Q

what is the test for cushings

A

overnight 1mg dexamethasone suppression test <50 the next morning is normal if >100=abnormal

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3
Q

how can you work out where the causative thing for cushings is

A

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

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4
Q

what are the risk factors in acromegaly

A

hypertension, cardiac failure through myopathies eg left ventricular hypertrophy, cardiomyopathy, arrhythmias also increased risk in IHD and stroke
COLON CANCER RISK INCREASED

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5
Q

what are the treatment options for acromegaly

A

surgery to remove the adenoma
drugs-somatostatin analogues-octreotide/lanreotide
or GH antagonists eg pegvisomat if intolerant to SSA

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6
Q

what is the aetiology of Cushings

A

Cushings disease=pituitary

cushings syndrome=adenoma of adrenal, ectopic, pseudo=alcohol and depression, steroid medication

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7
Q

differentiating pituitary cushings and ectopic cushings

A

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

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8
Q

what is a high dose dexamethasone test

A

6 hours after: 2 days of 2mg dexamethasone 6 hourly (ie 8mg/day)

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9
Q

what is a hypophysectomy

A

removal of the pituitary gland

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10
Q

what are the drug treatment options if surgery doesn’t work for cushings

A

metyrapone (while waiting for radio to work)
ketoconazole (nb hepatotoxic)
Pasireotide-new SSA, receptor 2 and 5 blocked

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11
Q

what does GH do

A 
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
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12
Q

what are the risks of testosterone replacement

A

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)

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13
Q

what is addisons disease

A

primary adrenocortical insufficiency, destruction of the adrenal cortex

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14
Q

what symptoms does addisons disease cause

A

lethargy, weight loss, dizzy, flu like myalgias/arthralgias, nausea, vomiting abdo pain, increased pigmentation in buccal mucosa

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15
Q

why do you get dizzy with addisons

A

reflection of hypotension from decreased ECF

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16
Q

why do you get pigmentation with addisons

A

increase in ACTH( because nothing is converting it to cortisol) and it contains MSH which is melanocyte stimulating hormone

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17
Q

what is secondary adrenal insufficiency

A

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

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18
Q

what is the most important thing to tell patients with Addisons disease about

A

DO NOT STOP TAKING STEROIDS, wear bracelets and inform GPs of their diagnosis, make sure that they increase their steroids when they are ill

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19
Q

what is a trophic hormone

A

a hormone that regulates the release of other hormones

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20
Q

what is the goitre like in subacute thyroiditis

A

PAINFUL

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21
Q

what are the symptoms of congenital hypothyroidism and why is it important to diagnose

A 
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
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22
Q

what is a dermoid cyst

A

rare congenital cyst
usually presents in teenage years
soft non fluctuant

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23
Q

what is a brachial cyst

A

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

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24
Q

what type of swelling is a cystic hygroma

A

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

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25
Q

how can you check if a neck lump is a lymph node

A

lymph nodes don’t move on swallowing

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26
Q

what is impaired fasting glucose

A

fasting glucose <7 but >6.1mmol/l

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27
Q

what would you do if you had a patient with impaired fasting glucose

A

do an OGTT to rule out DM, if OGTT shows glucose of <11.1 but >7.8 mmol/l

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28
Q

what is impaired glucose tolerance

A

fasting glucose <7mmol/l and OGTT 2 hr glucose >7.8mmol/l but <11.1mmol/l

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29
Q

how is diabetes diagnosed

A

fasting blood glucose >7mmol/l
random blood glucose >11.1mmol/l
HbA1c>48mmol/l 6.5%

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30
Q

what genes are involved in type 1 diabetes

A

HLA DR3 and HLA DR4

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31
Q

what is Potts disease

A

TB in the intervertebral discs

32
Q

how does infliximab work

A

TNFa inhibitor

33
Q

how does ritixumab work

A

CD 20 monoclonal antibody

34
Q

how does etanercept work

A

TNFa inhibitor

35
Q

how does abatacept work

A

T cell function disruptor

36
Q

what does Tocilizumab do

A

IL1 and IL6 inhibition

37
Q

what is pancytopenia

A

a reduction in number of red cells, white cells and platelets

38
Q

what is pancytopenia a potential complication from

A

immunosuppression

39
Q

where do SGLT2 inhibitors act

A

in the proximal tubule

40
Q

what can pioglitazone prevent against

A

macrovascualar complications, no prevention of microvascular but improvement in microalbuminaemia

41
Q

what can SUs prevent against

A

microvascular disease

no prevention of macrovascualr disease

42
Q

how do a glucosidase inhibitors work

A

they delay the absorption of glucose so there is a decrease in post prandial increase in blood glucose

43
Q

what is charcot foot

A

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.

44
Q

what are the symptoms of charcots foot

A

swelling or redness of the foot or ankle, skin warmer at the point of injury
flattening of the arch

45
Q

what is the pathological appearance of psoriatic conditions

A

elongation of the rete ridges

46
Q

what is the classification of lichenoid damage

A

basal layer damage
irregular saw tooth acanthosis
hypergranulosis and orthohyperkeratosis
bandlike upper dermal infiltrate of lymphocytes
basal damage with formation of cytoid bodies

47
Q

which layer does lichenoid pathologies affect

A

the basal layer

48
Q

what cells are involved in lichenoid disorders

A

infiltrate of lymphocytes and formation of cytoid bodies

49
Q

describe the autoimmune reactin in pemphigus vulgaris

A

igG autoantibodies made against desmoglein 3
desmoglein 3 maintains desosomal attachements
complement activation and protease release
disruption of desmosomes

50
Q

is there evidence of acantholysis in bullous pemphigoid

A

no

51
Q

where does bullous pemphigoid act

A

on the hemidesmosomes

52
Q

where does pemphigus vulgaris act

A

on the desmosomes

53
Q

give examples of vesiculobullous diseases

A

bullous pemohigoid, pemphigus vulgaris and dermatitis herpetiformis

54
Q

what is the hallmark of dermatitis herpetiformis

A

intensely itchy lesions that are symmetrical
elbows, knees and buttocks-often excoriated
but hallmark is PAPILLARY DERMAL MICROABSCESSES

55
Q

deposits of what are found in dermatitis herpetiformis in the dermal papillae

A

deposition of IgA in dermal papillae

56
Q

what are some of the major glucocorticoid actions

A

increase in cardiac output and hence increase in BP

increase in renal blood flow and GFR

57
Q

how does glucocorticoids affect the CNS

A

mood lability
euphoria/psychosis
decrease in libido

58
Q

how do glucocorticoids affect the bone and connective tissue

A

accelerates osteoporosis by decreasing serum calcium decrease collagen formation
and decreases wound healing

59
Q

how does cortisol affect metabolic rate

A

increase in blood sugar
increase in lipolysis and central redistribution of fats
increase in proteolysis

60
Q

immunological affects of cortisol

A

decrease in capillary dilatation/permeability
decrease in leucocyte migration
decrease in macrophage activity
decrease in inflammatory cytokine production

61
Q

what are the 6 classes of steroid receptors

A 
glucocorticoid
mineralcorticoid 
progestin 
oestrogen 
androgen 
vitamin D
62
Q

what does aldosterone do to the sodium/potassium balance

A

potassium (and h+) excretion

na reabsorption

63
Q

how do you diagnose adrenal insufficiency

A

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

64
Q

adrenal autoantibodies in Addisons

A

21 hydroxylase

65
Q

adrenal autoantibodies in congenital adrenal hyperplasia

A

17 hydroxyprogesterone (these levels are v high and hence 21 hydroxylase levels very low)

66
Q

what is the difference in primary and secondary adrenal insufficiency

A

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

67
Q

what is the commonest cause of cortisol excess

A

Iatrogenic cushings syndrome

68
Q

what is iatrogenic cushings syndrome most often caused by

A

prolonged high dose steroid therapy eg asthma, RA, IBD, transplants

69
Q

what does iatrogenic cushings syndrome cause

A

chronic suppression of pituitary ACTH production and adrenal atrophy

70
Q

what is cushing’s disease

A

increased secretion of ACTH from anterior pituitary often caused as a result of pituitary adenoma

71
Q

what is the most common presentation in MEN 1

A

hypercalcaemia

72
Q

what are the main causes of hypercalcaemia

A

primary hyperparathyroidism

myeloma

73
Q

what is the clinical picture in MEN1

A

parathyroid hyperplasia
pituitary adenoma
pancreatic tumours

74
Q

what is the gene in MEN1

A

MEN1 gene

75
Q

what is the clinical picture in MEN IIA

A

parathyroid hyperplasia
phaeochromocytoma
medullary thyroid cancer

76
Q

what is the clinical picture in MEN 11B

A

phaeochromocytoma
medullary thyroid cancer
mucosal neuromas/marfanoid body

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