Endocrinology Flashcards
what is type 1 diabetes ? briefly
insulin deficiency form autoimmune destruction of insulin-secreting pancreatic beta cells
diabetes definition. what are the 3 values ?
- Random plasma glucose > 11.1mol/L
- Fasting plasma glucose > 7.0mmol/L
- HbA1C > 48 mmol/mol
describe the C-peptide levels in T1DM patient ?
C-peptide levels are typically low in T1DM patients
(low for the low one)
what are the 4 ts of DM ?
toilet, thin, tired, thirsty
describe the features of T1DM and briefly what pathophys causes these symptoms ?
thirst, polyuria, weight loss, fatigue, blurred vision
- pee glucose out (glucose pulls water with it whoever it goes) => more dehydration
- hyperglycaemia => neuropathy, blurred vision, damaged blood vessels
what does complete lack of insulin in body cause ? long answer
body is in perceived starved state
- fat breakdown and formation of glycerol + FFA => oxidised to ketone bodes in liver => hyperglycaemia and rising ketone bodies
- glucose + ketones escape in urine => osmotic diarises => reduces circulating blood vol
- rising ketones cause vomiting
general mx of DKA ?
- rehydration, insulin, replacement of electrolytes (K+)
- then treat underlying cause
general Mx of T1DM ongoing ?
insulin deficiency so treatment aims to keep blood glucose as normal as possible
- calculate carb content of meal to calculate insulin dose
- insulin therapy tries to mimic normal physiology
describe basal bolus insulin therapy ?
normally low level insulin secreted by beta cells to balance effects of glucagon/cortisol (patient should take background dose)
describe insulin therapy in T2DM ?
basal insulin: inject once at night - adjust insulin dose themselves based on fasting glucose (but this does not cover exercise or meals)
- before sleep reduces chance of hypoglycaemia
when does ketogenesis normally occur ? why useful
when there is insufficient glucose supply + glycogen stores exhausted (prolonged fasting)
- ketones can cross BBB => brain can use as fuel
where does ketogenesis occur ?
liver takes fatty acids and converts them to ketones (water soluble fatty acids)
what blood gas is DKA ?
life-threatening metabolic acidosis (diabeteic ketoacidosis)
what is initial counter regulatory mechanism to the acidosis in DKA ?
initially kidney makes enough bicarb to contract ketones but eventually => ketoacidosis
what does the excessive hyperglycaemia in DKA cause ? effect on kidneys
hyperglycaemia overwhelms the kidney => glucose filtered into urine => draws water with it (osmotic diuresis) => polyuria => severe dehydration => excessive thirst (polydipsia)
describe insulins affect on K ? what happens with insulin started ?
insulin normally drives K into cells
- when insulin treatment started => increase K in cells => severe hypokalaemia => fatal arrhythmias
what are the different pathophysiological process going on in DKA ? (5)
- hyperglycaemia
- dehydration
- ketosis
- metabolic acidosis
- K imbalance
DKA RF ? (2) (in a diagnosed diabetic)
- inappropriate/inadequate insulin therapy
- infection
DKA Ix ? (4)
- VBG
- Blood ketones
- capillary blood glucose
- FBC
DKA Mx ?
FIGPICK
- Fluids
- Insulin
- glucose (fluids with dextrose infusion)
- Potassium replacement
- infections (treatment underlying trigger)
- Chart (fluid balance)
- Ketones
what values indicate impaired glucose tolerance ? (2)
- fasting plasma < 7
- OGTT 2 hr value 7.8<x<11.1
type 2 diabetes pathophysiology ?
repeated exposure to glucose + insulin => cells become resistant to insulin => more insulin required => pancreas becomes fatigued + damaged => produce less insulin => chronic hyperglycaemia => micro/macrovascular complications + infections
(insulin deficiency + resistance)
what is pre-diabetes ?
heading towards diabetes, is reversible
- high HbA1c, impaired fasting glucose, impaired glucose tolerance
what investigations would you do for diabetes presentaiton ? results ?
- oral glucose tolerance tests: fasting plasma glucose, give 75g glucose drink, measure plasma glucose 2 hrs later
- HbA1c: >48
- random glucose >11
- fasting glucose >7
- OGTT 2 hr resut >11
T2DM Mx ?
dietary modification, exercise, weight loss, monitor complications (retinopathy, kidney disease, diabetic foot)
- drug therapy
describe overall T2DM drug therapy ?
- first line: metformin
- then add: sulphonlyurea, DPP4 inhibitor, SGLT2 inhibitor
- third line: triple therapy with metformin + 2 secondary drugs
- add insulin therapy
what HbA1c is dual therapy commenced for T2DM ?
> 58 mmol/mol
what are incretins ? what do they act on (2)
hormones secreted by intestiatnl endocrine cells that act on stomach to delay gastric emptying
- act on beta cells to increase insulin production
- act on liver to reduce glucagon release
what is HHS ? describe a bit. how different form DKA ?
hyperosmolar hyperglycaemia state
- serious complication of (mainly) T2DM involving hyperglycaemia, hyperosmolaltiy (high solute), vol depletion in the absence of significant ketoacidosis
what prevents HHS from becoming DKA ?
low level insulin suppresses lipolysis + ketogenesis => prevents DKA
what causes HHS ?
results from insulin deficiency and high conc of counter regulatory hormones (glucagon, cortisol, GH)
- blood sugar too high for too long => severe dehydration + confusion
HHS RF ?
- infection
- inadequate insulin
- MI in diabetic patients
- restricted water
(occurs mostly in older people with T2DM, often initial presentaiton)
HHS Px ?
about 1 week Hx
- polyuria, polydyspisa, weakness, weight loss, tachycardia, hypotension, acute cognitive impairment
HHS Ix ? and results (6)
- Blood glucose (high)
- blood ketones (low)
- VBG (mild acidosis)
- serum osmolatliy (high)
- FBC (leukocytosis)
- electrolytes (low K)
HHS Mx ? (4)
- IV fluids + K replacement
- IV insulin
- treat acute illness (infection)
- thromboprophylaxis (LMWH)
when do you give the low dose IV insulin in HHS Mx ? why ?
must be adequately hydrated before insulin administration because insulin drives glucose into cell => water follows
- what little water remained IV => intracellular => circulatory failure => cardiac arrest
HHS treatment complications ? (2)
- insulin related hypoglycaemia
- treatment related hypokalaemia
name some compactions of established diabetes ?
- vascular disease: chief cause of death
- nephropathy
- diabetic retinopathy
- cataracts
- diabetic foot
- diabetic neuropathy
describe a bit about diabetic neuropathy ?
loss of pain sensation => increase mechanical stress => repeated joint injury
- symmetric sensory polyneuropathy (glove + stocking numbers, tingling + pain - worse at night)
what counts as hypoglycaemia ?
plasm glucose < 3mmol/L
but also 4s the floor
which drugs are usually responsible for hypos in a known diabetic ?
insulin or sulphonylurea
(increased activity, missed meal, accidental/non-accidental overdose)
causes of hypos in a non-diabetic ?
- pituitary insufficiency
- Addisons disease (adrenal insufficiency)
- insulinoma (islet cell tumour)
what is hyperthyroidism ?
increased production of thyroid hormone by thyroid gland
main causes of hyperthyroidism ? (3) most common
- graves disease (most common)
- toxic multi nodular goitre
- iodine excess
complications of hyperthyroidism ? (5)
- HF (cardiomyopathy)
- angina
- AF
- bone mineral loss
- thyroid storm
what is primary hyperthyroidism ? due to pathology where ? describe TSH, T3 and T4 levels
due to thyroid pathology, thyroid producing excessive quantities
- low TSH
- high T3/T4
what is secondary hyperthyroidism ? due to pathology where ? describe TSH, T3 and T4 levels
due to hypothalamic or pituitary pathology, thyroid makes excessive thyroid hormone as a result of over stimulation of TSH
- High TSH
- High T3/T4
features/presentation of hyperthyroidism ? (8)
- anxiety, irritabilty
- sweating, heat intolerance
- weight loss
- fatigue
- frequent loose stolls
- tachycardia
- sexual dysfunction
- oligomenorrhoea
what is the general Mx for hyperthyroidism ? (4) think complication
- BB for initial sx mx (lower HR => reduce AF risk)
- carbimazole
- radioactive iodine
- surgery
What is graves disease ?
primary hyperthyroidism
- autoimmune condition where RSH antibodies cause primary hyperthyroidism
what are TSh antibodies ? with what condition are they associated ? what do they cause ?
graves disease
- They are abnormal antibodies produced by immune system that mimic TSH => stimulate thyroid receptors => hyperthyroidism (+thyroid hypertrophy + hyperplasia)
what % of ppl with graves disease present with eye disease ? what is the biggest RF for this ?
thyroid eye disease seen in 25-50% of ppl with graves disease
- smoking is biggest RF
Mx of graves related eye disease ?
Stop smoking !
- if severe disease: high dose steroids (IV Methylpred)
Graves disease oe (4)
- exophthalmos
- pretibial myxoedema
- diffuse goitre
- acropathy
describe these ? associated with what condition ?
- exophthalmos
- pretibial myxoedema
- acropathy
graves disease
- exophthalmos: budging of eyes due to inflam, swelling and hypertrophy)
- pretibial myxoedema: skin reaction to TSH receptor Ab => mucin deposits => discolouration)
- acropathy: swelling of hands, clubbing of fingers
what Ix for graves disease ? what would they show ?
primary hyperthyroidism
- TFT: low TSH, high T3/4
- TSH receptor Ab (+ve)
patient present with thyroid nodules. what is first line Ix ?
US
(and check TSH)
graves disease Mx ?
- prolonged antithyroid drug therapy (carbimazole - normal thyroid function after 4-8 weeks, then titrate down)
- BB initially
- OR radioactive iodine + Pred OR thyroid surgery + levothyroxine
causes of diffuse goitre ? (3)
- iodine deficiency
- de quervains
- autoimmune (graves, hashimotos)
causes of nodular goitre ? (1)
- multi nodular goitre (patients are usually euthyroid)
what is De Quervains thyroiditis ? another name ? describe it ?
subacute granulomatous thyroiditis
- temporary inflame of third gland characterised by triphasic course
- presume to be viral
which thyroid disease has triphasic course ? describe the phases
De Quervains thyroiditis
- transient thyrotoxicosis (due to thyroid follicular damage)
- hypo phase (as TSH levels fall due to -ve feedback)
- euthyroidism
De Quervains thyroiditis presentation ?
- initial thyrotoxic phase: thyroid pain, high T3/4, systemic illness like flu
De Quervains thyroiditis Ix and results ?
- thyroid US
- low TSH
- high T3/4
De Quervains thyroiditis mx ?
sorts itself out so just supportive care with NSAIDS (thyroid pain), BB (for tachycardia) + levothyroxine (for sx of hypothyroidism)
what is thyroid storm ? another name ?
thyrotoxicosis/thyroid storm
- life threatening condition associated with un or underrated hyperthyroidism
thyrotoxicosis/thyroid storm px ?
- tachycardia cardia
- High BP
- high body temp
- High RR
- agitation
- confusion
- goitrethyrotoxicosis/thyroid storm
thyrotoxicosis/thyroid storm Mx ?
do not wait for Ix results if urgent tx needed, confirm with technetium uptake if possible
- high dose antithyroid drugs (carbimazole)
- corticosteroids (prednisolone)
- BB blockers
- supportive care
if left untreated => high mortality rate
what is most common thyroid cancer aetiology ?
papillary most common (60%)
how does thyroid cancer most commonly present ?
asymptomatic thyroid nodule detected by palpation or US in a woman in her 30s or 40s
- uncommon: hoarseness, dysnpoea, dysphagia
how is thyroid cancer diagnosis made ?
fine needle aspiration
thyroid cancer treatment ?
- total thyroidectomy + radioactive iodine ablation + TSH suppression (levothyroxine)
what is hypothyroidism ?
inadequate output of thyroid hormones by thyroid gland
name causes of primary hypothyroidism ? (4) main cause
- autoimmune (primary atrophic hypo, hashimotos - most common)
- post thyroidectomy
- drug induced (treatment of hyper can cause hypo - carbimazole, radioactive iodine, surgery)
- iodine deficiency
name cause of secondary hypothyroidism
hypopituitarism (v rare)
hypothyroidism presentaiton ? (9)
- weight gain
- fatigue
- dry skin
- coarse hair, hair loss
- fluid retention (oedema, ascites)
- heavy or irregular periods
- constipation
- goitre
- eyelid oedema
hypothyroidism RF ? (6)
- female
- meddle age
- iodine deficiency
- treatment for thyroid disease
- FHx of autoimmune thyroiditis
- amiodarone use
hypothyroidism Ix and results ? primary and secondary ?
thyroid hormones abnormally low:
- primary (absence/dysfucntion of thyroid): High TSH, low T3/4
- secondary (pituitary/hypothalammic dysfunction): Los TSH, Low T3/4
hypothyroidism Mx ?
replace thyroid hormone with oral levothyroxine (synthetic T4 which is metabolised to T3 in body)
- titrate until normal TSH levels
hypothyroidism pregnancy associated complications
- eclampsia
- anaemia
- prematurity
- low birth weight
what is hashimotos thyroiditis ?
primary autoimmune hypothyroidism
- caused by autoimmune inflam of thyroid gland
- initially causes goitre => thyroid gland atrophy
hashimotos thyroiditis associated with what antibody ? (2)
anti-TPO and antithyoglobulin Ab
hashimotos thyroiditis pathophys ?
immune system makes Ab that attack thyroid gland => large WBC build up in thyroid => thyroid damage => can’t amen sufficient thyroid hormones
hashimotos thyroiditis Ix ? and results (3)
autoimmune primary hypothyroidism
- high TSH
- low T3/4
- thyroid peroxidase Ab (+ve)
hashimotos thyroiditis Mx ?
levothyroxine
what produces parathyroid hormone ? in response to what ?
chief cells in the parathyroid glands produce parathyroid hormone in response to hypocalcamiea
what does PTH affect ?
acts to raise blood calcium
- increase osteoclast activity
- increase calcium absorption form gut (increase activity of Vit D)
- increase calcium reabsorption form kidneys
hyperparathyroidism presentation ?
- renal stones
- painful bones (+fractures)
- abdominal moans (constipation, N+V)
- psychiatric groans (depression)
primary hyperparathyroidism. caused by what ? describe the PTH and Ca levels
(usually solitary adenoma) caused by uncontrolled PTH produced by tumour of parathyroid gland
- PTH high
- Calcium high
solitary adenoma mx ? what type of hyperparathyroidism is it ?
primary hyperparathyroidism
- treatment: surgical removal of tumour
secondary hyperparathyroidism. caused by what ? describe the PTH and Ca levels ?
(low vit D of CKD) => reduced Ca absorption from intestine, kidneys and bones => hypocalcaemia => high PTH => parathyroid hyperplasia
- PTH high
- Ca low or normal
tertiary hyperparathyroidism. caused by what ? describe the PTH and Ca levels ?
when secondary continues for long rime => parathyroid gland hyperplasia => increase baseline PTH => when corrected, parathyroid gland overactive => hypercalcaemia
- PTH high
- Ca High
what is hypoparathyroidism ? aetiology ? describe Ca and Pi levels
relative or absolute deficiency of PTH => low serum Ca + high serum phosphate
- mostly post surgical
what ECG change may be seen in hypoparathyroidism
prolonged QT interval (low serum Ca)
hypoparathyroidism Mx ?
IV Ca + magnesium sulphate (if low Mg)
hypercalacaemia signs and symptoms ? (4)
bones, shoes, grounds, psychic moans
hypercalacaemia causes ?
most commonly malignancy (bone mets, myeloma or primary hyperparathyroidism (parathyroid demos most common)
- vit D intoxication
- tertiary hyperparathyroidism
what is malignancy associated hypercalcaemia ?
most common metabolic abnormality in cancer patients (+ poor prognostic factor)
- causes: PTH-related protein produced by the tumour, local osteolysis
malignancy associated hypercalcaemia mx ?
- aggressive rehydration
- bisphosphonates
- continue mx of underlying cause: chemo for cancer
hypocalcaemia may be an artefact of what ?
may be artefact of hypoalbuminaemia
hypocalcaemia px ?
campus, perioral numbness
- if severe: seizures - spasms
hypocalcaemia causes ?
- CKD
- hypoparathyroidism
- hypomagnesaemia
- vit d deficiency
hypocalcaemia mx ?
calcium supplement, with daily plasma Ca2+ checks
what is cushings syndrome ?
manifestation of pathological hypercortisolism from any cause
- glucocorticoid excess + loss of normal HPA axis + loss of circadian rhythm of cortisol release
what is cushings disease ?
pituitary adenoma secretes excessive ACTH => cushings syndrome
- bilateral adrenal hyperplasia
causes of cushings syndrome ? (4)
CAPE
- cushings disease
- adrenal adenoma
- paraneoplastic
- exogenous
(can be ACTH dependant or independent)
features of cushings syndrome ? (5)
- round in middle/central obesity
- thin limbs, proximal limb muscle wasting
- moon face
- abdominal straie
- menstrual abnormailites
some other signs of cushings syndrome ?
high stress hormone causes:
- hypertension
- cardiac hypertrophy
- hyperglycaemia (+DM)
- depression + insomnia
- osteoporosis
Dexamethasone suppression test (DST): what result would indicate cushings syndrome ?
low dose: when cortisol level not suppressed => cushings syndrome
Dexamethasone suppression test (DST): what would these results indicate on high dose (after already abnormal low dose test)
- Cortisol suppressed ?
- High cortisol + low ACTH ?
- high cortisol + high ACTH ?
high dose (after already abnormal low dose test): cortisol suppressed => cushings disease
- cortisol high + ACTH low => adrenal adenoma
- high cortisol + high ACTH => ectopic ACTH
if cause of cushings syndrome is adrenal adenoma, what electrolytes might be impacted ?
low potassium if aldosterone also secreted by adrenal adenoma
what is Addisons disease ?
primary adrenal insufficiency
- lean, tanned, tired, tearful
what is adrenal insufficiency ?
where adrenals don’t produce enough steroid hormones (particularly cortisol and aldosterone)
describe primary adrenal insufficiency ? cause ?
Addisons disease
- adrenal glands damaged and adrenal cortex destruction => low aldosterone + low cortisol secretion
(usually autoimmune)
how does aldosterone affect Na + K ? so how they be affected in adrenal insufficiency ?
increased aldosterone => Na absorption + K excretion
- so Addisons: hyponatraemia, hyperkalaemia
describe the train findings in addisonian crisis ?
- hyponatraemia
- hyperkalaemia
- hypoglycaemia
( low mineralocorticoid => low Na + high K)
(low glucose due to low cortisol)
describe secondary adrenal insufficiency ? causes ? (4)
inadequate ACTH => low cortisol
- due to surgical removal of pituitary tumour, infection, loss of blood flow to pituitary, radiotherapy)
describe tertiary adrenal insufficiency ? causes
inadequate CRH
(due to long term oral steroids => hypothalamic suppression)
signs and symptoms of adrenal insufficiency ?
(lean, tanned, tired, tearful)
- fatigue, nausea, cramps, abdo pain, reduced libido
what causes the “tanned” symptom of Addisons
bronze hyperpigmentation
- ACTH => increased melanin from melanocytes
what investigations for adrenal insufficiency ?
- U+E (hyponatraemia, hyperkalaemia)
- early morning cortisol
- ACTH (high in primary, low in secondary)
- short synacthen test (diagnostic)
describe the short synacthen test ? to diagnose what ?
help diagnosis Addisons
- given synacthen (artificial ACTH) => if cortisol level fails to rise => primary insufficiency (Addisons)
Addisons Mx ? (2)
replacement with steroids titrated to signs, symptoms + electrolytes
- hydrocortisone (glucocorticoid to replace cortisol)
- Fludrocortisone (mineralocorticoid to replace aldosterone)
what is addisonian crisis ?
acute presentaiton of severe Addisons, life threatening
addisonian crisis presentation ? (6)
- reduced consciousness
- hypotension
- hypoglycaemia
- hyponaetraemia
- hyperkalaemia
- very unwell
addisonian crisis Mx ? (4)
don’t wait for investigations as is life threatening
- parenteral steroids (IV hydrocortisone)
- IV fluid resuscitation
- correct hypoglycaemia
- monitor fluid + electrolyte balance
how does excess aldosterone affect sodium, water and renin ?
increase sodium
water retention
reduce renin release
how does aldosterone affect electrolyte levels in the kidneys ? state where each is affected
- increase Na reabsorption in distal tubule
- increase K secretion in distal tubule
- increase H+ secretion in collecting ducts
what is primary hyperaldosteroneism ? name the causes ? main cause ?
adrenal gland produce too much aldosterone (=> reduce renin)
- adrenal adenoma (conns syndrome -2/3)
- bilateral adrenal hyperplasia (1/3)
what is secondary hyperaldosteronism ? name the causes/aetiology
excessive renin => stimulate adrenals to secrete increased aldosterone
- aetiology: when BP in is disproportionately lower (renal artery stenosis, renal artery obstruction, HF)
how does conns disease present ?
(hyperaldosteronism)
- hypertension
- lethargy
- mood disturbance
describe the aldosterone and renin levels in primary and secondary hyperaldosteronism ?
1: High A, Low R
2: high A, High R
(also low K for both)
hyperaldosteronism disease Mx ?
hyperaldonsteronism
- aldosterone antagonist (spironolactone)
- treat underlying causes: conns (laparoscopic adrenalectomy), renal artery stenosis (percutaneous renal artery angioplasty)
patient presents with hypertension with hypokalaemia - what should you consider ?
conns disease
in which circumstance should you consider conns as a reason for HTN ? (3)
- hypertension with hypokalaemia
- refractory HTN (despite > 3 antihypertensives)
- HTN occurring before 40 yrs of age (especially in women)
what is phaechromocytoma ?
catecholamine producing tumour
- a tumour of the chromatin cells that secrets unregulated + excessive Ad
where is adrenaline produced ?
adrenaline is produced by chromatin cells (in the adrenal medulla)
(retroperitoneal organ)
what does Ad stimulate ?
hormone and NT that stimulates SNS
- fight or flight
- increase arousal
- increase muscle tone
- increase HR
- increase BP
describe the hormone secretion pattern in pheochromocytoma ?
Ad secreted in bursts => periods of worse symptoms and then settled
pheochromocytoma important Hx point ?
25% are familial so important to ask about FHx
pheochromocytoma px ? classic triad ? what precipitates sx ?
(fluctuate with rise + fall of Ad)
- anxiety
- sweating
- panic attacks
- headaches
- hypertension (can be v high)
- arrhythmias
classic triad: episodic headaches, sweating and tachycardia (patient feel as if about to die)
- precipitated by straining, stress, abdo pressure
pheochromocytoma dx ?
- 24 hr urine catecholamines
- plasma free metanephrine (high) - gold standard
pheochromocytoma mx ? (3)
- alpha blockers (phenoxybenzamine)
- BB (propanolol)
- adrenalectomy
(if malignant: chemo or radiotherapy)
pheochromocytoma complicaiton ?
can progress to stroke, cardiogenic shock
causes of hirsutism ? (4)
- familial
- idiopathic
- increase androgen secretion by ovary (PCOS, ovarian cancer)
- adrenal gland (late onset CAH, adrenal cancer, steroids)
what is the physiology that causes an erection
neuronal release of NO => hyperpolarizes + relaxes vascular + smooth muscle => engorgment
causes of erectile dysfunction (impotence) ? (3)
- smoking
- alcohol
- diabetes (reduce NO + autonomic neuropathy)
erectile dysfunction mx ?
- treat cause
- counselling
- oral phosphodiesterase inhibitors (sildenafil) (relax smooth muscle => improve arterial flow)
in hypopituitarism, in what order are the hormones affected ?
reduced secretion of AP hormones
- GH, FSH/LH, TSH, ACTH, Prolactin
what are the 3 causes of hypopituitarism ?
- hypothalamus (Kallman - isolated GnRH deficiency)
- pituitary stalk: trauma, surgery, craniopharyngioma
- pituitary: tumour, irradiation, ischaemia (Sheehans, pituitary apoplexy)
what is the aetiology of most pituitary tumours ?
almost always benign adenomas
what are the 3 ways the pituitary tumours causes symptoms
- tumour cause pressure on local structure (optic nerve => visual field defect - bilateral temporal hemianopia), headache)
- pressure on normal pituitary
- functioning tumour (producing hormones)
pituitary Ix ?
MRI
- screening tests: IGF-1, ACTH, cortisol, TFTs, LH/FSH, short synacthen test
pituitary tumour tx ?
hormone replacement (steroids before levothyroxine as thyroxin may precipitate adrenal crisis)
- surgery trans-sphenoidal
What is galactorrhea ?
breast milk production no associated with pregnancy or breastfeeding
what does increased prolactin cause ?
high prolactin => reduced GnRH => reduced LH/FSH => hypogonadism (menstrual irregularities, reduced libido ED), infertility, osteoporosis
during pregnancy what stops milk production ?
oestrogen and progesterone inhibit prolactin secretion
causes of hyperprolactinaemia ?
- idiopathic
- prolactinoma (adenoma)
- hypothyroidism
- meds (dopamine antagonists) - most common
what are prolactinomas ?
tumours of pituitary gland that secrete excessive prolactin
- can be micro or macro (present with headaches and bitemporal hemianopia)
prolacitnoma Mx ? depend on what ?
depends on size (pituitary MRI)
- dopamine agonists (cabergoline) to treat symptoms
- transphenoidal surgical removal of pituitary tumour
what is acromegaly ? most common cause ?
clinical manifestation of excessive GH (produced from AP)
- usually caused by unregulated GH production form pituitary adenoma (99%)
- can be secondary to cancer (lung) that secretes ectopic GHRH or GH
acromegaly px ?
- space occupying (headache, visual field defect)
- overgrowth of tissues secondary to GH (prominent brow, large nose + tongue and hands and feet, protruding jaw, arthritis)
- organ dysfunction (hypertrophic heart, HTN, T2DM)
acromegaly Ix ? (3)
random GH level is not useful as fluctuates alot
- IGF-1
- oral glucose tolerance test (increased glucose should suppress GH)
- MRI of brain
acromegaly Mx ?
- trans-sphenoidal surgical removal of pituitary tumour
- if ectopic cause: pegnisomant (GH antagonist), octreotide (somatostatin analogue), cabergoline (dopamine agonists)
acromegaly complications ?
associated with increased morbidity + premature mortality
- impaired glucose tolerance (may present with ketoacidosis)
What is Diabetes insipidus (DI) ? what hormone involved and where ?
lack of ADH of lack of response to ADH
- ADH acts on collecting ducts in kidneys => reabsorb more water form urin
- DI prevents kidney s from being able to concentrate urine => polyuria, polydipsia and formation of inappropriately hypotonic (dilute) urine
describe nephrogenic DI ? caused by ?
collecting ducts don’t respond to ADH (caused by lithium, genetic predisposition, intrinsic kidney disease, electrolyte imbalances)
describe cranial DI ? causes ?
when hypothalamus does not produce ADH for pituitary to secrete
(idiopathic (50%), brain tumour, head injury, infection (meningitis/encephalitis/TB) brain surgery)
DI Ix ?
- U+E (high Na), low urine osmolality, high serum osmolality
- water deprivation test
describe the water deprivation test ? to test for what ?
cranial vs nephrogenic DI
- avoid fluid for 8 hrs, urine osmolality measured, synthetic ADH (desmopressin), 8 hrs later urine osmolatly checked again
- CDI (low urine osmo first, then high after desmo)
- NDI (low uric osmo first, remain low after desmo)
DI Mx ?
treat underlying cause, oral IV fluids
- CDI (desmopressin)
DI complication ?
both can present with hypernatraemia (med emergency)
what is SIADH ? explain a bit/pathophys
syndrome of inappropriate anti diuretic hormone
- inappropriately large amounts of ADH as result of posterior pituitary secreting too much ADH (or small cell lung cancer)
- excessive ADH => excessive water reabsorption in collecting ducts => dilute Na in blood => hyponatraemia (+ not usually fluid overload) =
what type of sodium imbalance does SIADH cause ?
- excessive ADH => excessive water reabsorption in collecting ducts => dilute Na in blood => hyponatraemia (+ not usually fluid overload) => euvolaemic hyponatraemia
- patients have high urine osmolality and high urine sodium
SIADH sx ?
relate to hyponatraemia: fatigue, headache, muscle aches, cramps, confusion
- severe hyponat: seizures + reduced consciousness
SIADH aetiology ?
- post op
- infection (lung pneumonia)
- head injury
- medication (amiodarone)
- malignancy (small cell lung cancer)
how is SIADH Dx ?
diagnosis of exclusion: low serum Na, low serum osmolality, low serum urea, high urine osmolality, high urine sodium
- negative shorty synacthen test
- CXR to look for pneumonia, lung abscess, lung cancer
- if no clear cause then suspect malignancy
SIADH Mx ?
treat underlying cause, stop causative medication, correct Na slowly to prevent central pontine myelinolysis
- IV hypertonic saline + fluid restriction, tolcaptan (ADH receptor blockers) b
what level counts as hyperkalaemia ? main complications ?
it is high serum potassium: plasma K+> 6.5 mmol/L (potential emergency)
- main complications: cardiac arrhythmias (VF) which can be fatal (cardiac arrest)
cause of hyperkalaemia ?
- AKI
- CKD (stages 4-5)
- rhabdomyolysis
- adrenal insufficiency (Addisons)
- medication (aldosterone antagonists (spiro), ACEI, ARB, NSAID
ECG signs of hyperkalaemia ?
- tall peaked T waves
- flattened of absent P waves
- broad GRS
hyperkalaemia Mx ?
stop the medication, change diet
- insulin + dextrose infection (drives carbs into cell - takes K with it)
- and calcium gluconate (stabilises cardiac cells, reduce risk of arrhythmia)
- nebulised salbutamol: temporarily drives K into cells
what counts as hypokalaemia
plasma K+< 2.5 mmol/L
hypokalaemia causes ?
cause by increased K excretion or increased K moving into cells (=> less in blood)
- insuline: can be caused by insulin overdose in T1DM
hypokalaemia presentation ?
- severe muscle weakness or paralysis
- cardiac arrhythmias (palpitations)
- cramps
hypokalaemia ECG changes ?
bradycardia
ST depression
hypokalaemia Mx ?
oral potassium (oral K+ supplment)
- if severe: consider IV K+ continuously
NEVER five K+ as a fast stat bolus dose !!
what counts as hypothermia ? typical patient ?
core (rectal temp) < 35 degrees
- most patients are elderly and do not complain of or feel cold so have to tried to warm up
- in the young: usually from cold exposure (near drowning) or secondary to impaired consciousness (following excessive alcohol or drugs)
hypothermia px ?
if shivering then hypothermia is mild, if not shivering despite <35 then is severe
- sx: confusion, agitation, reduced GCS, coma, bradycardia, hypotension
hypothermia Mx ?
(if heat too quickly => peripheral vasodilation + shock)
ABCDE approach
- slowly reward: aim for 1/2 degree per hr
- remove wet clothing, warm IV, cardiac monitoring
do not declare anyone dead until warm + dead.
what investigation is most appropriate to support diagnosis of carcinoid syndrome ?
urinary 5-HIAA
