endocrine Flashcards
what does the anterior pituitary release
TSH
adenocorticotropic hormone (ACTH)
FSH and LH
GH
prolactin
what does the posterior pituitary release
oxytocin and ADH
thyroid hormone feedback
hypothalamus
thyrotropin releasing hormone (TRH)
anterior pituitary
TSH
thyroid gland
triiodothyronine (T3) and thyroxine (T4)
negative feedbacl
adrenal feedback lloop
hypothalamus
corticotropin releasing hormone (CRH)
ant pituitary
ACTH
adrenal gland
cortisol
negatibe feedback
what id cortisol and functiond
stress hormone
inhibits immune system, inhibits bone formation, increases blood glucose, increases metabolism, increases alertness
how do cortisol levels vary
diurnal variation - peaks in early morning, lowest late evening
GH feedback loop
hypothalamus
GHRH
ant pituitaty
GH
liver
IGF1
roles of GH
stimulates muscle growth
increases bone density and strength
stimulates cell regeration and reproduction
stimulates growth internal organs
when is PTH released
low serum Ca/Mg or high phosphate
roles of PTH
increase activity and number of osteoclasts
increase Ca reabsorption in kindeys
stimulates kidneys to convert vit D3 into calcitriol (active)
drescribe renin angiotensin system
low bp
renin released from juxtaglomerular cells in afferent and efferent arterioles kindey
renin converts angiotensinogen from liver to angiotensin I
angiotensin I converted to angiotensin II in lungs by ACE enzyme
angiotensin II causes vasoconstriction and aldosterone release from adrenal gland
where is renin released from
juxtaglomerular cells in afferent and efferent arterioles kidney
roles angiotensin II
causes vasoconstriction and aldosterone release from adrenal gland
what is aldosterone
mineralocorticoid steroid hormone
role aldosterone
acts on nephrons in kidneys to:
increase sodium reabsorption in distal tubule
increase K secretion from distal tubule
increase H secretion from collecting ducts
sx cushings
round middle
thin and weak limbs
HTN
cardiac hypertrophy
hyperglycaemia
depression
insmonia
osteoporosis
easy brusing
poor skin healing
cause of cushings
prolonged elevated cortisol
causes of cushings syndrome
exogenous steroids, cushings disease, adrenal adenoma, paraneoplastic (releases ACTH)
cause of cushings disease
pituitary adenoma
diagnosing cushings
dexamethasone suppression test: do at 10pm, measure 9am. low dose (1g) if normal (suppressed)=rules out cushings.
then give high dose (8g)
24hr urinary cortisol
results of high dose dexamethasone suppression test
if cortisol not suppressed and ACTH low =pituitary,
if cortsol low and ACTH high=adrenal
cortisol not suppressed and ACTH high=ectopic
cause of adrenal insufficiency
not enough steroid hormones
types adrenal insufficiency
primary=addisons, often AI
secondary=damaged pituitary
tertiary=inadequate CRH from hypothalamus-usually due to oral steroid
sx adrenal insufficiency
fatigue
nausea
abdo pain
bronze skin
decreased blood pressure
decreased na
increased k
ix adrenal insufficiency
if AI: adrenal cortex Ab and 21-hydroxylase Ab
short synacthen test: in morning give synacthen (ACTH) and measure cortisol at base, 30m, 60m. if cortisol rises less than 2xbaseline = primary insufficiency
mx adrenal insufficeincy
hydrocortisone (for cortisol), fludrocortisone (for aldosterone)
double dose in acute illness
sx addisonian/adrenal crisis
decreased consciousness, increased bp, decreased glucose, decreased na, increased k
mx addisonina/adrenal crisis
IV hydrocortisone 100mg stat, then 100mg 6hrly
IV fluids
hormone levels hyperthyroif
low TSH, increased T3 and 4
hormone levels primary hypothyroid
increased TSH, low T3 and 4
hormone levels secondary hypothyroid
low TSH, T3 and T4
thyroid problems with anti-TPO Ab
graves, hashimotos
thyroid problems with antithyroglobulin Ab
graves, hashimotos, cancer,
thyroid problems with TSH receptor Ab
graves
graves thyroid radioisotope scan
diffuse high uptake
what thyroid prpblems have focal high uptake on radiisotope scan
toxic multinodular goitre
adenoma
thyroid cancer radioisotope scan
‘cold ‘ area = low uptake
thyrotoxicosis
abnormal and excessive thyroid hormone in body
sx graves
diffuse goitre, eye disease, exopthalmos, pretibial myxoedema
cause de quervains thyroiditis
viral infection
sx de quervains thyroiditis
fever, neck pain, dysphagia, features hyperthyroid
mx de quervains thyroiditis
self limiting
BB, NSAIDs
sx thyroid storm/thyrotoxic crisis
hyperthyroid and pyrexia
increase HR
delirium
mx thyroid storm/thyrotoxic crisis
tx hyperthyroid
fluids
BB
anti-arrhythmic
mx hyperthyroidism
- carbimazole: if block all will need levothyroxine
- propylthiouracil: risk severe hepatic rxn
- radioactive iodine
- propanolol (tx sx not cause)
- surgery
causes hypothyroidd
hashimotos
too little iodine
se hyperthyroid tx
lithium
amiodarone
tumour
infection
sheehans syndrome
mx hypothyroidism
levothyroxine (synthetic T4, metabolises to T3)
ideal blood glucose
4.4-6.1
insulin
produced by B cells in islets of langerhans in pancreas
decreases blood glucose
glucagon
produced by alpha cells in islets of langerhans in pancrease
increases blood glucose by glycogenolysis and gluconeogenesis
ketogenesis
no glucose so FA->ketons - can cross BBB
what is T1DM
no insulin produced
causes T1DM
genetic
coxsackie B virus
enterovirus
mx T1DM
background long acting and short acting insulin
need to monitor HbA1c and capillary glucose
Hba1c
glucose levels avg over 3m
what is DKA
ketoacidosis from ketogenesis and dehydration (due to hyperglycaemia causing polyuria) and potassium imbalance (insulin normal drives K into cells)
sx DKA
polyuria
polydipsia
N+V
acetone breath
LOC
diagnosis DKA
blood glucose >11 and ketosis (ketones >3) and acidosis (ph<7.3)
mx DKA
fluids: IV saline - 1L stat then 4L +K over 12h
insulin infusion at 0.1unit/kg/hr
monitor glucose, add desxtrose when <14
monitor K
tx trigger .g. infrction
chart fluid balance
monitor ketones
restart normal insulin regime before stop infusion
short term complications DM
hypoglycaemia
hyperglycaemia
long term complications DM
hyperglycaemia ->leaky endothelial cells
macrovascular: coronary arter disease, ischaemic feet, HTN, stroke
microvascualr: peripheral neuropathy, retinopathy, glomerulosclerosis
infection: UTI, pneumonia, fungal (oral/vagina, feet)
T2DM
body resistant to insulin
pre diabetes
HbA1c 42-47
impaired fasting glucose: 6.1-6.9
impaired glucose tolerance (@2h): 7.8-11.1 OGTT
diagnosing DM
HbA1c>48
random glucose >11
fasting glucose >7
OGTT>11
aim for T2DM tx
HbA1c <48
if on more than just metformin <53
mx T2DM
- diet and exercise
- metformin
- sulfonylurea, pioglitazone, DPP4i, SGLT2i
- metformin +2 or metformin and insulin
patients with CVD: use SGLT2i or GLP1 mimetics
drug class metformin and actions
biguanide
increases insulin sensitivity, decreases liver glucose production
SE metformin
diarrhoea
abdo pain
lactic acidosis
give an e.g. sulfoylurea and actions
gliclazide
increases insulin release
SE sulfonylureas
increased wt
hypoglycamiea
CVD
MI
class drug pioglitazone and actions
thiazolidinedione
increased insuline sensitivity, decreased liver glucose
SE pioglitazone
increased wt
increased fluid
anaemia
HF
give e.g. DPP4i and action
sitogliptin
increased GLP1 activity
SE DPP4 i
GI upset
sx urti
pancreatitis
e.g. SGLT2i and action
empagliflozin
block glucose reapsorption from urine
SE SGLT2i
glucosuria,
uti
decreased wt
DKA
e.g. GLP1 mimetics
Liraglutide
SE GLP1 mimetics
GI upset
decreased wt
dizzy
cause acromegaly
increased GH
pituitary adenoma
sx acromegaly
bitemporal hemianopia
large
HTN
T2DM
mx acromegaly
surgery
pegvisomant(GH antagonist)
somatostatin analogue (block GH release)
octreotide
bromocriptine (dopamine agonists-block GH release)
what produces PTH
chief cells
primary hyperparathyroid
caused by tumour
increased PTH and Ca
mx hyperparathyroid
primary=surgery for tumour
secondary=correct vit d or renal transplant
tertiary=surgery
secondary hyperparathyroid
caused by low vit D or CKD
increased PTH, normal or decreased Ca
tertiary hyperparathyroid
caused by hyperplasia
high PTH and Ca
primary hyperaldosteronism
conns syndrome
adrenal glands produce too much aldosterone so low serum renin
cause=adrenal adenoma, hyperplasia, familial, adrenal carcinoma
secondary hyperaldosteronism
excessive renin
cause: renal artery stenosis/obstruction, HF
ix hyperaldosteronism
renin:aldosterone ratio
HTN
decreased K
alkalosis
CT/MRI
mx hyperaldosteronism
aldosterone antagonists: eplerenone, spironolactone
tx cause-surgery
SIADH causes
caused by too much ADH - post op, infection (atypical pneumonia), HI, medication (thiazide diuretics, carbazepine, cyclophosphamide, antipsychotics, SSRIs, NSAIDs), malignancy (SCLC), meningitis
sx SIADH
headache
fatigue
cramps
low sodium->seizure, LOC
mx SIADH
slow correction na to avoid central pontine myelinolysis
fluid restriction: <500ml-1l
tolvaptan: ADH receptor blocker
what is diabetes insipidus
low/lack of response to ADH
sx DI
polyuria
polydipsia
dehydration
decreased BP
increased Na
types/causes DI
nephrogenic: kidneys dont respond-lithium, genes, kidney disease, low K, increased Ca
cranial: hypothalamus doesnt produce ADH-brain tumour, HI, brain infection, brain surgery
ix DI
low urine osmolality, increased serum osmolality
water deprivation/desmopressin stimulation: no fluid for 8h, give desmopressin, measure urine osmolality 8h later
results water deprivation/desmopressin stimulation in DI
cranial DI: urine osmolality low after deprivation but high after ADH
nephrogenic DI: urine osmolality low after deprivation and after ADH
primary polydipsia: urine osmolality high after deprivation and ADH
mx DI
tx cause
desmopressin
what is phaeochromocytoma
tumour of chromaffin cells (produce adrenaline in adrenal gland) so secrete unregulated and excessive adrenaline
associated with multiple endocrine neoplasia type 2
sx phaeochromocytoma
fluctuate:
sweating, headache, HTN, tremor, palpitations, Increased HR, paroxysmal AF
ix phaeochromocytoma
24hr urine catecholamines, plasma free metanephrines
mx phaeochromocytoma
alpha blocker: phenoxybenzamine
BB
adrenalectomy
What to do with diabetic meds on VRIII
Only continue long acting and basal insulin
Stop all others: oral, short acting, pre mixed
When to stop VRIII
NORMAL VBG
eating and drinking
How to stop VRIII
give meal related long acting insulin
Remove VRIII one hr later
Review and restart other diabetics meds
VRIII set up
Constant rate glucose and K in one cannula
Variable insulin in other based on hourly CBG
When to give insulin in T2DM
HBa1c over 58 after 3m dual oral therapy
Starting total daily dose for T1DM
Total number units over 24h on VRIII - however often overestimating
0.5 units per kg wt
Insulin regimes T2DM
LONG ACTING only= if still produce some insulin
Mixed BD = if struggle with hyperglycaemia after meals
How is basal bolus regime split T1DM
Usually half units long acting - morn and evening
Half units short acting which correlate with meals (so usually split into 3)
When are pre mixed insulin given
Always with meals as risk of hypos
Never before bed
hyperosmolar hyperglycaemic state
hypovolaemia
gluc>30
osmolality >320
no ketonaemia/acidosis
mx hyperosmolar hyperglycaemic state
- IV access, U+E, LFTs, clotting, CRP, CXR, urine C&S, BC, lab glu and osm, VBG
- IV NaCl
IV insuline (0.05 units/kg) when BG stopped falling with IV saline - aim to fall less than 5 /hr - aim for fluid balance 3-6 L by 12 h
- eat and drink asap
what can adrenal haemorrhage cause
primary adrenal insufficiency
emergency mx preimary adrenal insufficeincy
hydrocortisone 100mg IV STAT then 50mg 6hrly
IV fluids 0.9% NaCL
tx hypoglycaemia
refer endo
mx sev hyponatraemia
170ml 2.7% hypertonic saline over 20m
repeat if seizures/low GCS/cardiaresp arrest otherwise only repeat if VBG rise Na<5
stop infusion when sx improve or Na increases >10 or total >130 (whichever first)
monitor Na until stabe (6h, 12h, daily)
what should Na rise be limited to in low Na tx
less than 10 in first 24h
then less than 8 in next 24h
risk myelinolysis
what can cause pituitary apoplexy
prolactinoma
what is pituitary apoplexy
bleeding into pituitary
imapired blood supply pituitary
sx pituitary apoplexy
sudden headache and visual field defects/double vision
mx pituitary apoplexy
steroids: 100mg IM hydrocortisone then 50-100 mg QDS IM
surgery if severe reduced visual acuity, persistent visual field defects, deteriorating GCS
HDU/ITU
hypercalcaemia mx
IV fluid: 4-6L NaCl 24h
bisphosponate: zolendronic acid 4mg over 15m
calcium nadir from 2-4d
tx cause
what diabetes meds can cause euglycaemia ketoacidosis
SGLT2i
HDU referral DKA
potassium <3.5
pH <7.1, HCO3 <5, ketones>6
18-25y or elderly
pregnant
GCS<12
HR>100/<60, SBP<90, oxygen <92%
what to be aware of in DKA mx
hypoglycaemia - is why you need dextrose cover when give insulin
