random endocrine Flashcards by Erin Prentice

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

How well did you know this?

Not at all

Perfectly

what is the test for cushings

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

what is the aetiology of Cushings

Cushings disease=pituitary

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

what is a high dose dexamethasone test

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

How well did you know this?

Not at all

Perfectly

what is a hypophysectomy

removal of the pituitary gland

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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)

How well did you know this?

Not at all

Perfectly

what is addisons disease

primary adrenocortical insufficiency, destruction of the adrenal cortex

How well did you know this?

Not at all

Perfectly

what symptoms does addisons disease cause

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

How well did you know this?

Not at all

Perfectly

why do you get dizzy with addisons

reflection of hypotension from decreased ECF

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

what is a trophic hormone

a hormone that regulates the release of other hormones

How well did you know this?

Not at all

Perfectly

what is the goitre like in subacute thyroiditis

PAINFUL

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

what is a dermoid cyst

rare congenital cyst
usually presents in teenage years
soft non fluctuant

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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 well did you know this?

Not at all

Perfectly

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

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

random endocrine Flashcards

(76 cards)