Endocrinology Flashcards
acromegaly Cx
HTN, LVH, IHD, diabetes, sleep apnoea, arthritis, bitemporal hemianopia from pituitary tumour
adrenal insufficiency overview
primary AI - impairment of adrenal cortex - low cortisol/aldosterone
secondary AI - low cortisol from low ACTH
AI presentation
tanned, tired, toned, tearful
signs
- vitiligo
- tanned skin
- pigmentation (face, neck, palmar creases) - primary AI
- hypotension - loss of aldosterone
- dehydrated
- lean
symptoms
- lethargy, depression
- dizzy
- weight loss
- nausea/vomiting
- diarrhoea, constipation, abdo pain
- impotence/amenorrhea
Conn’s DDx
secondary hyperaldosteronism - excess renin and AgII release (renal artery stenosis can cause this)
Cushing’s syndrome overview
excess cortisol
Cushing’s disease overview
excess cortisol from inappropriate ACTH secretion - pituitary adenoma
Cushing’s Ix
Dexamethasone suppression test - usually suppresses cortisol level - failure to suppress is diagnostic
CT/MRI of adrenals/pituitary
DM Ix
random plasma glucose >11.1mmol/L
fasting plasma glucose >7mmol/L
OGTT >7mmol/L (>6 for impaired glucose tolerance)
HbA1c >6.5% normal (48mmol/mol)
Which T2DM drugs cause weight loss/gain?
Biguianide (metformin) - reduce glycogenolysis, gluconeogenesis, increase muscle uptake of glucose - weight loss
Sulfonylurea (gliclazide) - stimulate insulin release - weight gain, hypo risk
DPP4 inhibitors (sitagliptin) - no weight change
Glitazone (pioglitazone) - weight gain
DM complications
Macrovascular - atherosclerosis, stroke, IHD, PAD
Microvascular - diabetic retinopathy, nephropathy, neuropathy, infections
DKA, HHS, hypoglycaemia
DKA causes
Lack of insulin, glucose cannot be taken up by cells
FFAs -> acetyl-coA -> ketone bodies
excessive ketonegenesis
HHS/DKA differentials
HHS - hypovolaemia, marked hyperglycaemia without acidosis, higher osmolality
Hypoglycaemia
plasma glucose <3mmol/L
insufficient glucose to brain
Thyroid carcinoma Mx
Radioactive iodine
Levothyroxine (T4) - keep TSH reduced
Chemo
Partial/full thyroidectomy
Hypercalcaemia presentation
symptoms
bones - excess bone resorption - pain, fractures, osteoporosis
stones - biliary stones
groans - abdo pain, malaise, polydipsia, nausea
psychiatric moans - depression, anxiety
signs
QT shortening
Hypoparathyroidism
Low PTH
Primary - low due to parathyroid gland failure
Secondary - after parathyroidectomy/thyroidectomy
Pseudo - failure of target cell response to PTH
Pseudopseudo - same as pseudo but no Ca abnormalities
Hypoparathyroidism Ix
Bloods - calcium low, PTH low (high in pseudo)
ECG - long QT
Parathyroid ABs
SIADH Ix
FBC, U+E
Hyponatraemia, low plasma osmolality, high urine osmolality
acromegaly overview
excess growth hormone -> overgrowth of all organ systems
gigantism in children
acromegaly causes
pituitary adenoma secreting too much GH
acromegaly presentation
signs
- big hands, feet, jaw
- acral and soft tissue overgrowth
- big tongue, widely spaced teeth
- coarse facial features
- prognathism
symptoms
- arthralgia
- acroparaesthesia
- headache
- decreased libido
- acral enlargement
- wonky bite (malocclusion)
acromegaly DDx
pseudo-acromegaly - same physical appearance without elevated GH/IGF-1
acromegaly Ix
check IGF-1 levels (not GH, is pulsatile secretion)
oral glucose tolerance test - normally, rise in blood glucose suppresses GH levels
MRI pituitary fossa for adenomas
acromegaly Tx
transsphenoidal surgery
somatostatin analogues (IM octreotide) dopamine agonist (oral cabergoline) GH antagonist (pegvisomant)
radiotherapy
AI causes
primary
- worldwide, TB
- in UK - autoimmune adrenalitis (Addison’s disease)
- adrenal metastases, long term steroid use, opportunistic infections
secondary
- long term steroid therapy
- hypothalamic-pituitary disease - tumours, trauma, surgery
AI Ix
Bloods - hyponatraemia, hyperkalaemia (low aldosterone), hypoglycaemia (low cortisol)
Synacthen test
measure plasma cortisol before/30min after IM tetracosactide (ACTH analogue), cortisol remains low in primary AI, increases in secondary
Adrenal ABs - 21 hydroxylase AB in Addisons
AXR/CXR
AI Tx
primary
acute - IV hydrocortisone, saline, glucose infusion
oral hydrocortisone/prednisolone (glucocorticoids) oral fludrocortisone (mineralocorticoid)
secondary
oral hydrocortisone
AI Cx
Adrenal crisis - acute lack of cortisol (tx hydrocortisone)
Reduced QoL
Osteoporosis (from regular steroids)
Conn’s syndrome overview
primary hyperaldosteronism
excess aldosterone production -> increased sodium, water retention
Conn’s causes
2/3 - adrenal adenoma
1/3 - bilateral adrenocortical hyperplasia
Conn’s presentation
Often asymptomatic
Hypertension
Metabolic alkalosis
Hypokalaemia - weakness/cramps, paraesthesia, polyuria/polydipsia
Conn’s Ix
U/E
Spot renin/aldosterone levels - aldosterone raised, renin low
ECG - hypokalaemia
CT/MRI adrenals
Conn’s Mx
Aldosterone antagonist - oral spironolactone
Laproscopic adrenalectomy
Conn’s Cx
Cx from HTN - stroke, MI, kidney failure
Cushing’s syndrome causes
ACTH-dependent (high ACTH)
Cushing’s disease - ACTH-secreting pituitary tumour
ACTH-producing tumour elsewhere
ACTH-independent (low ACTH due to -ve feedback from raised cortisol)
adrenal tumour releasing cortisol
oral steroids
Cushing’s presentation
CUSHING Cataracts Ulcers Skin - striae Hypertension, hyperglycaemia Infections increase Necrosis Glucosuria
Central obesity, wasted limbs Moon face Buffalo hump Acne, hirsuitism, weight gain Mood change, gonadal dysfunction, protein wasting
Cushing’s DDx
Pseudo-Cushing’s - same presentation, not from pituitary-adrenal axis problems - eg prolonged excess alcohol consumption
Cushing’s Tx
Cushing’s disease - transphenoidal removal of pituitary adenoma
Adrenal adenoma - adrenalectomy
Adrenal carcinoma - radiotherapy, adrenolytic drugs (mitotane)
Ectopic ACTH - surgery if tumour located, drugs that inhibit cortisol synthesis (metyrapone, fluconazole)
Cushing’s Cx
HTN, metabolic syndrome, diabetes, obesity, coagulopathy, osteoporosis, Nelson’s syndrome
Nelson’s syndrome
increase skin pigmentation from ACTH increase from enlarging pituitary tumour after adrenalectomy (remove negative feedback against ACTH)
Diabetes mellitus
deficiency/diminished effectiveness of insulin, hyperglycaemia
T1DM
body fails to produce sufficient insulin
prone to DKA
T2DM
resistance to insulin
Gestational diabetes
high blood glucose levels in pregnancy
Maturity-onset diabetes of the young (MODY)
autosomal dominant form of T2DM - single gene defect altering beta cell function
secondary diabetes
inc pancreatic disease, endocrine…
T1DM causes
autoimmune
idiopathic
genetic component
T2DM causes
decreased insulin secretion/increased resistance
obesity, lack of exercise, calorie excess
polygenic
T1DM risk factors
Northern European, family history, other autoimmune disorders
T2DM risk factors
FHx, increasing age, obesity, poor exercise, ethnicity, overweight around abdomen
DM presentation
signs
ketonuria (ketoacidosis) - pear drop breath (T1)
complications (eg retinopathy)
symptoms
polyuria/nocturia
polydipsia
weight loss
T1 - leaner than T2
T1DM Mx
synthetic human insulin
short acting insulins - eg for before meals
sort-acting insulin analogues - fast onset, eg with evening meal
longer-acting insulins - 12-24hrs
complications - hypoglycaemia, weight gain
T2DM Mx
1st line - lifestyle - diet, exercise, weight loss, ramipril/statins/orlistat
2nd - oral metformin
Add sulfonylurea (oral gliclazide)
later - insulin/glitazone (oral pioglitazone) - increase tissue sensitivity to insulin
DKA overview
Ketonaemia (/ketonuria)
Hyperglycaemia
Acidosis
DKA presentation
signs
Pear drop breath
Kussmaul’s respiration (deep, rapid)
Disturbance of consciousness
symptoms Vomiting Drowsiness Abdo pain Dehydration - eyes sunken, slow cap refill, tachycardia, weak pulse, hypotension
DKA DDx
alcoholic ketoacidosis, hyperosmolar hyperglycaemic state, lactic acidosis
DKA Ix
Bloods show: hyperglycaemia, raised plasma ketones, acidaemia, metabolic acidosis with bicarb reduced
Urine stick testing - glycosuria and ketonuria
Check plasma osmolality and anion gap (both elevated, plasma osmolality more elevated in HSS)