ENDOCRINE Flashcards
define a hormone..
A chemical produced by a tissue, usually peptides, amino acid derivatives or steroid based, which is secreted by an endocrine gland into the blood and acts on receptors of distant target cells to produce a response.
what is the difference between paracrine and autocrine?
paracrine messangers are released from cells into ECF and act locally at differnet cells e.g. somatostatin from D cells of stomach and small intestines acts at stomach to reduce gastrin release.
autocrine is a molecule released from a cell which acts on the same cell. e.g. thromboxane from platelets
what groups of hormones do you know, give examples..
peptides e.g. ADH and oxytocin
amines e.g. catecholamines, thyroid hormones - these are derived from tyrosine
steroids e.g. cortisol, sex steroids - derived from cholesterol
Eicosanoids - fatty acid derivatives - e.g. prostaglandins etc derived from archidonic acids
Outline the mechanism feedback pathway and hence the control of hormone release
most of the hormones are under negative feedback control
e.g. thyroid..
allows its release to be controlled.
Other things also feed into hypothalamus e.g. stress
do you know any hormones under positive feedback?
oxytocin at labour
LH surge from higher levels of Oestrogen
where is the hypothalamus and what does it do?
The hypothalamus is a small but crucial region of the brain located below the thalamus and just above the brainstem. floor of third ventricle closely related to pituitary.
vital role in homeostatic functions. also in regulating autonomic NS, thirst / osmolarity, appetitie, thermoregulation
Releases - CRH, TRH, GnRH, GHRH, PRLH (prolactin releasing horomone), somatostatin and dopamine.
it also makes ADH which is transported and released from posterior pituitary
how do the hypothalamus and pituitary relate?
Hypothalamus has 2 connections to pituitary
to anterior pituitary via a hypophyseal circulation
to anterior pituitary by a stalk containing neurons
what is meant by a trophic hormone?
one that stimulates growth and development e.g. GH
what is a portal circulation?
a circulation that passes between two sets of capillary beds before returning to the heart e.g. pituitary, portal vein from GIT to liver and also glomerulus to loop of henle (same organ so not official)
allows direct transfer between 2 tissues without dilution in systemic circulation - good for toxins from GIT, hormones from hypothalamus to pituitary
tell me about the pituitary gland..
small gland sitting in sella turcica of the sphenoid bone made of 2 parts - anterior and posterior
anterior produces 6 hormones - GH, LH, FSH, TSH, ACTH (adrenocorticotrophic) and prolactin
posterior pituitary - connected to hypothalamus by stalk of neurons - released ADH and oxytocin
tell me about ADH..
9 aa peptide hormone
synthesised by supraoptic and paraventricular nucleus of hypothalamus and released from posterior pituitary
in response to high osmolarity, hypovolaemia and stress
has 3 receptor targets
VR1 causes vasoconstriction
VR2 causes fluid retention by inserting aquaporins in the kidneys for water reabsorption.
VR3 - involved in ACTH secretion
also involved in factor 8 synthesis.
do you know any drugs interferring with ADH release?
increase release - morphine and nicotine
inhibit release - alcohol
tell me about oxytocin..
9aa peptide hormone, similar in structure to ADH synthesised by hypothalamus and released from posterior pituitary.
involved in lactation, uterine contractions in labour and sexual arousal.
GPCR receptors of myometrium of uterus causes muscle contraction.
Tell me about growth hormone
one of the major hormones released by anterior pituitary
involved in growth and metabolism via ILGFs
what is the action of ACTH
acts on GPCRs of adrenal cortex
increasing production and release of aldosterone and cortisol (mainly cortisol)
also has a trophic response on the gland
its release is controlled by CRH from hypothalamus
what is TSH?
A thyrotrophic hormone released from anterior pituitary, regulating relase of T3/T4
Induced by TRH from hypothalamus
Describe the anatomy of the tyroid gland..
highly vascular structure consisting of 2 flat lobes connected by an isthmus
found from level C5 to T1 (2nd and 4th tracheal ring)
made up of many follicles surrounded by thyroid epithelial cells. These follicles contain thyroid bound thyroglobulin ready for release.
There are also C cells responsible for calcitonin release - this is involved in calcium homeostasis.
describe the anatomy of thyroid hormones..
- thyroglobulin made by ribosome- rich in amino acid tyrosine.
- packed into vesicles and exocytosed into follicle
- iodine is actively transported from blood across the epithelial cells into the follicles
- thyroid peroxidase oxidises iodine to iodide
- iodide can now iodinate tyrosine residues of thyroglobulin (iodinase enzyme)
- this produces T3 and T4 bound as thyroglobin ready for release
- TSH bind GPCR Gs triggering secretion of thyroglobin back into epithelial cells where it is cleaved to T3 and T4 which are secreted into blood
T4 is made x13 more than T3
but T3 a lot more active. T4 can be converted to T3 peripherally
half life of T4 is longer and therefore is slowly converted to T3.
how do thyroid hormones exert there effects
intranuclear receptors regulating gene expression
the thyroid hormones are lipophillic in nature so cross lipid bilayer readily
explain the blood supply to thyroid ..
supplied by inferior and superior thyroid arteries.
superior thyroid artery is a branch of external carotid
whereas inferior thyroid artery from subclavian via thyrocervical trunk
sometimes thyroid ima artery directly from subclavian and lies more centrally
venous drainage via superior and inferior thyroid veins
inferior into left brachiocephalic
superior into IJV
what are the effects of thyroxine..
Acts on nuclear receptors to alter gene expression
overall upregulation of enzymes to increase BMR and core temp. overall increased metabolism
Resp - rise in minute volume due to increased CO2 production.
CVS - sensitises the myocardium to catecholamines but has direct chronotrophic and ionotrophic effects e.g. tachycardia
GIT - increased appeptite and GI motility
also has a role in growth and development e.g. congenital lack of thyroid results in poor growth and mental disability
draw the hypothalamic pituitary axis…
TSH causes growth of thyroid gland
plus increase in iodine uptake
plus increase in secretion of T3/4
somatostatin inhibits TSH release
what are the symptoms of hypo/hyperthyroidism?
hyperthyroid
* tachycardia , HTN
* diarrhoea
* increased RR
* increased body temp + sweating
* increased BMR, weight loss
* Anxiety and irritability
* lid retraction (graves exopthalmos)
hypothyroid
* bradycardia
* constipation
* low BMR, weight gain
* cold
* lethargy/ depression
causes of hyper and hypothyroid
hyper - Graves (Antibodies to TSH receptor and thyroid peroxidase, pituitary adenoma, thyroiditis
hypo - hashimotos (antibodies against TSH), iodine deficiency, subacute thyroiditis, thyroid surgery, congenital
what is thyroid storm and how is it managed?
excess T3/T4
leading to hypermetabolic state
emergency
tachycardia, tremor, fever, high RR
treated with B blockers, fluids, cooling, carbimazole or propothiouracil and cortisol (blocks T4 to T3)
patient with a goitre has a GA, start getting symptoms of tachycardia and high CO2, how do you differentiate between thyroid storm and MH?
(previous question)
thyroid storm is usually more gradual in onset over days whereas MH will be immediate upon trigger (anaesthetic agents) so clues will be before anaesthetic e.g. if already tachycardic, sweating etc should do a TSH pre op
In MH you get muscle rigidity e.g. masseter spasm whereas not seen in thyroid storm. otherwise both cause rise in CO2, temp and tachycardia. however MH will have more significant CO2 rise
If unsure intraoperatively, i would call for help and treat for MH - stop all volatiles, switch to TIVA, dantrolene and cooling.
some of the supportive measures are the same for each - 100% O2, cooling, fluids.
take bloods to distinguish between the two - T3/T4 vs CK
what anaesthetic concerns are there in someone with thyroid disease..
Airway - goitre - may make cricoid pressure and front of neck difficult, if large enough may also compress the trachea. distortion of neck/ airway may make intubation difficult
breathing - tracheal narrowing and airway obstruction, dyspnoea may be worsened under GA. may need high MV / have high O2 consumption if hyperthyroid - risk of hypoxia
Circulation - risk of thyroid storm with poorly treated hyperthyroid and stress of surgery. important to get TSH before. risk of tachycardias and MIs
hypothyroid - also goitres, but risk of low metabolism - effects drug metabolism. and hypothermia intraop
what investigations would you want pre op in someone with thryoid disease and a goitre?
neck USS and CXR - assess size of goitre and tracheal compression, maybe even CT
TSH, T3/4
pulmonary function tests, ECG/ ECHO
how to anaesthetise someone with thyroid disease..
pre op - symtoms, thyroid meds, previous thyroid storm. Investigation TSH/T3/T4. check for goitre - may need CXR or neck USS.
intraop - normothermia, avoid triggers e.g. tachycardia at laryngoscopy - use fentanyl etc. good analgesia, stress response can trigger thryoid storm.
in hyper - avoid drugs like ketamine and ephedrine that trigger sympathetic activity. can give B blockers for tachycardia
MAC is increased in hyper and reduced in hypo.
hypo may clear drugs more slowly due to reduced metabolism.
post op - good analgesia to reduce stress, monitor for thyroid storm.
what is a myxoedmea coma?
severe life threatening form of hypothyroid
resp depression, bradycardia, shock, hypoglycaemia, hypothermia
IV levothryoxine and steroids needed.
What is the treatment for hyperthyroidism?
Anti-thyroid drugs
Carbimazole - inhibits thyroid peroxidase (preventing T3/4 synthesis).
Propylthiouracil - also inhibits thryoid peroxidase
symptomatic - B blockers.
radioactive iodine treatment - initially worsening of symptoms.
thyroidectomy - recurrent laryngeal nerve damage, haematoma and airway risk, hypoparathyroidism,
what is the main ADR of carbimazole?
agranulocytosis - warn patients of sore throat.
what is the treatment of hypothyroid?
levothyroxine - works of thyroid receptors.
need TSH checking regularly
what is sick euthryoid?
low T3/4
normal TSH
associated with critical illness
dont treat
how would you interpret these results…
TSH - low
T3 and T4 normal
subclinical hyperthyroid
describe the structure of the adrenal glands..
2 small glands located on superior pole of kidneys within retroperitoneum at level of T12
consists of outer cortex (90%) and inner medulla (10%)
medulla specilaised ganglia consisting of chromaffin cells responsible for release of catecholamines (80% adrenaline, 20% NA, some dopamine and others).
cortex is divided into 3 layers…
zona glomerulosa - mineralocorticoids
zona fasciculata - glucococorticoids
zona reticularis - sex steroid hormones.
describe the synthesis of the catecholamines..
PNMT
tyrosine comes from phenylalanine (essentail aa) - phenylalanine hydroxylase.
describe the adrenal blood supply..
suprarenal arteries (superior suprarenal from phrenic artery, middle suprarenal are direct branches of aorta and inferior suprarenal arise from renal artery)
Venous drainage is through the right adrenal vein into the IVC and the left adrenal vein into the left renal vein.
describe the breakdown of catecholamine..
in synapse - reuptake into nerve terminals. broken down by MAO
peripherally - COMT enzyme
main breakdown product is VMA
describe the pathway for steroid hormone synthesis..
synthesised by cholesterol
progesterone is an intermediate
17a hydroxylase and 21a hydroxylase are key enzymes in converting progesterone to intermediates for further aldosterone, cortisol and androgen production.
tell me about cortisol..
steroid hormone produced by zona fasciculata of adrenal cortex
classed as a stress hormone
follows a circadian rhythm for release - peaks in early morning and falls at night.
acts on intracellular receptors to alter gene expression
overall alters metabolism
* increased gluconeogenesis and glycogenolysis
* hyperglycaemia
* decreases protein synthesis
* proteolysis of periperal muscles and lipolysis
Renal
* increased Na reabsorption and fluid retention and K+ excretion.
CVS
* sensitises to catecholamines , without cortisol hypotension occurs
in long term can cause immunosupression, osteoporosis, mood changes and central obesity.
tell me about aldosterone..
mineralocorticoid released from zona glomerulosa from adrenal cortex in response to activation of RAAS.
plays a role in water and salt reuptake by renal collecting ducts.
draw the HPA axis…
corticotrophin releasing hormone
adrenocorticotrophic releasing hormone
ACTH release has diurnal pattern - in early hours and dips in evening.
ACTH is inhibited by cortisol, somatostatin, opioids
ACTH stimulated by stress (surgery and sepsis) and hypoglycaemia
what controls aldosterone release
mainly controlled by RAAS
ATII stimulates aldosterone release
some control by ACTH
what are the components of the juxtamedullary apparatus?
macula densa - in DCT located close to glomerule
juxtaglomerular cells - specialised cells in afferent arterioles that contain and secrete renin.
what are the stimuli to renin release..
hypovolaemia - reduced GFR - less NaCl to macula densa, less ATP and adenosine made (these normally inhibit renin release)
B1 adrenoceptors
what are the causes and outcomes of hypo/hyperadrenalism?
hypoaldrenalisms
* addisons disease - main cause - autoimmune destruction and lack of cortisol and aldosterone
* may also be caused by infection, tumours, etomidate
* tiredness, weight loss
* addisonian crisis:
* hyponatraemia, hyperkalaemia, metabolic acidosis
* hypotension, hypoglycaemia , vomitting
hyperadrenalism
* excesss aldosterone/ cortisol
* e.g. cons - aldosterone secreting tumour - hypernatraemia, hypokalaemia, metabolic alkalosis
* e.g. cushings - too much steroids - central obesity, fat deposits on back, gynacemastia, straie, osteoporosis , wasting of legs. hypernatramia, fluid retension, hypoK, hyperglycaemia
how is cushings and addisons tested for?
cushings - dexamethasone supression test. should cause drop in cortisol by inhibiting pituitary ACTH release
addisons - short synacthen test - should stimulate cortisol and aldosterone release
how is addisons managed?
replace cortisol and aldosterone
hydrocortisone, fludrocortisone
need to double steroid dose in times of stress
what is a pheochromocytoma?
tumour of adrenal medulla chromaffin cells resulting in exagerated response to sympathetic stimulation
intermittetn HTN, tachycardia, flushing, headaches.
what are the clinical effects of steroids..
anti-inflammatory - inhibit phospholipase A2 - less prostaglandins. used in asthma and covid for this effect
immunosupression - long term - used in IBD and Rheumatoid arthritis for this reason
Anti-emetic - pre op
reduces swelling - good for reducing pain of sore throat post laryngoscopy, also good for raised ICP from brain tumours or malignant spinal cord compression.
how would you manage a patient on steroids for surgery..
Pre op - Hx
* full hx on type and dose of steroids, how long for and what for. Or if stopped steroids within 3 months
* if >5mg a day for more than 3 weeks - considered at risk of HPA supression
intraop
- hydrocortisone 100mg IV at induction
- followed by hydrocortisone 200mg / 24 hrs
- take double by mouth and then taper to normal dose over 48hrs
- minor op may just double normal oral dose
- confirm with AABGI guidelines
post op
* monitor for signs of adrenal insufficiency - blood tests, blood pressure, vomitting, hypoglycaemia
how do the steroids differ in their glucocorticoid activity?
dex - strongest glucocorticoid activity
prednisolone next
hydrocortisone is weakest
fludrocortisone - mineralocorticoid
tell me about calcium homeostasis..
Calcium extracellular levels are under tight regulation - should be around 2.25 to 2.5 mM
important ion in neuronal function, exocytosis and muscle contraction and clotting.
3 main hormones involved
* PTH
* Vitamin D
* calcitonin
when calcium is low..
* triggers PTH to be released
* acts on kidneys to promote production of vit D to active form
* promotes osteoclasts to break down bone
* reduces Ca excretion
* vit D causes Ca absorption from the gut
when calcium is high
* calcitonin released
* peptide hormones released from parafollicular C cells of thyroid
* inhibits osteoclasts and GI absorption
role of vitamin D in calcium homeostasis
cholecalciferol is produced in skin by UV
in liver it is hydroxylated
and then again in kidneys to activated form.
this final step is under PTH control
acts on intranuclear recepros to increase gut Ca absorption and also kidney reabsorption.
how is Ca found in the body?
mostly found in ECM of bone
in ECF travels in free form 2.5mM and bound to albumin
very low intracellular
what are the causes of hypo and hypercalcaemia?
hypo - parathyroidectomy, poor intake , congenital (DiGeorge)
hyper - PTHrH from tumour, hyperparathyroid, sarcoid
symptoms of hypo and hypercalcaemia?
hypo - tetany, spasms, seizures, trousseaus sign. long QT - torsades
hyper - stones, abdo pain and constipation, depression, short QT, thirst
why do you get tetany with hyperventilation? (this has come up before)
hyperventilation causes an alkalosis
calcium balance is tightly linked to acid- base balance
because H+ and Ca+ compete with same binding sites on albumin
hence less H+, means more Ca+ binds to albumin, less free Ca
causes tingling and tetany
what is the effect of PTH on phosphate at the kidney?
increases phosphate excretion
important phosphate is excreted as it helps promote calcium free levels in blood.
High levels of phosphate can lead to a decrease in serum calcium levels because phosphate can bind to calcium, forming insoluble complexes and reducing the amount of free (ionized) calcium in the bloodstream.
what is the stress response?
multisystem physiological response to body stress e.g. surgery, trauma, critical illness.
aims to produce a metabolic state to support stress
invovles a number of hormones
- cortisol - gluconeogeneissi, glycogenolysis, proteolysis, lipolysis
- increased glucagon, reduced insulin - hyperglycamia
- ADH - fluid retention and vasoconstriction
also Sympathetic NS
- catecholamines - hyperglycaemia, tachycardia improves O2 delivery but also increases myocardial O2 use.
also immune system..
* cytokine release
* acute phase response - CRP , fibrinogen
haematological
* procoagulant state - ready to repair injuries.
is the stress response useful?
important to an extent - there to help repair, maintain fluid balance, and blood pressure. we know this because loss of adrenal response e.g. hypoadrenalism is bad
however excess stress response is associated with
- hyperglycaemia - poor wound healing
- vasoconstriction - poor blood supply and wound healing
- caogulopathy - post surgical DVT etc
- water retention - can worsen HF
- increased myocardial work - precipitate MIs
how can we modify the stress response?
anaesthetic technique
* regional
* TIVA has been found to show reduced stress response
* normothermia
surgical
* minimally invasive e.g. laparoscopic
pharmacology
* opioids - reduce pain and stress, also inhibit ACTH release
* NSAIDs - reduces inflammation
* carb loading pre ortho surgery - reduces starvation and stress response.
how long for humeral responses of stress response to have an efect?
within first 30-60mins
not as immediate as sympathetic NS
but cortisol and adrenaline will start having effects intra op and last post op.
why may regional anaesthesia improve the stress response?
blocking sensory pain afferents - less activation of hypothalamic / medullary stress response
less anxiety than having a GA
what is the role of nitrogen balance in the stress response? (Something about nitrogen balance has come up before)
ncreased Catabolism: Stress triggers the breakdown of proteins and muscle tissue, leading to a negative nitrogen balance as the body uses amino acids for energy and repair.
Tissue Repair: A positive nitrogen balance is vital for repairing tissues damaged during stress. Adequate protein intake supports recovery and healing. hence in recovering surgical patient protein daily recommendation is higher.
Adequate dietary protein is crucial during stress to maintain a positive nitrogen balance. High-quality proteins containing essential amino acids are particularly beneficial.
tell me about the pancreas
vital gland sitting behind the stomach, in close proximation to spleen and liver.
has both exocrine and endocrine functions
exocrine functions include enzymes for digestions - amylase, lipase, typtase and bicarb all secreted into duodenum to protect from stomach acids and aid breakdown of macromolecules
endocrine functions include production of insulin and glucagon from B cells and a cells of islets of langerhan respectively. (also somatostatin from D cells)
how is glucose homeostasis achieved?
under tight control 3.5 to 5mM
by balance of glucagon and insulin
when glucose levels rise after a meal - insulin is released
insulin causes GLUT4 channels to be inserted into adipose and skeletal muscles. uptake of glucose and increase in glucogenesis and inhibition of glycogenolysis and gluconeogenesis. I.e. helps to reduce glucose and store it away. also promotes lipogenesis
glucagon secreted when glucose is low or in response to stress. it causes glycogenolysis, gluconeogenesis and inhibits glucogenesis. all via GPCR on liver. mostly acts on liver, some muscle. kidneys for gluconeogenesis and fat cells for lipolysis.
how is insulin release regulated?
peptide hormone made and stored in vesicles of B cells of islets of langerhan
when glucose is high - enters these cells
glycolysis and ATP production
ATP sensitive K+ channels close –> depolarisation
opens VG Ca channels - exocytosis
what is C peptide?
A marker of endogenous insulin
proinsulin is made by B cells and when cleaved to insulin, releases C peptide.
what are the regulators of insulin release?
hyperglycaemia
sympathetic NS - inhibits insulin release via a2 receptors
why is insulin used to treat hyperkalaemia?
promotes uptake of K+ by cells
what is the difference between cushings disease and cushings syndrome?
cushings disease - pitutary adenoma - ACTH and causes high cortisol
cushings syndrome - the signs and symptoms seen with excess cortisol. may be exogenous, adrenal tumour,
what are the indications for insulin therapy?
diabetes - type 1 and type 2
hyperkalaemia
B blocker OD
how is exogenous insulin made and presented?
made from genetically engineered cells
100units/ ml colourless solution
what different types of exogenous insulins are there? how can their onset be manipulated?
categorised into fast, intermediate and long acting. depends on if complexed with zinc and protamine.
e.g. rapid acting = aspart (novorapid) or lispro (humalog) - these are not complexes with anything and have modifications to prevent hexamer formation and promote rapid absorption and action
e.g. regular insulin - humalin R - complexes with zinc - promotes hexamer formation and slows absorption compared to above
e.g. intermediate = isophane. usually complexed with protamine - allows slower dissociation and absorptions for sustained released
long acting e.g. levimir and lantus - presented in acidic solution and when injected causes precipitation which results in slow release from this site.
what insulin regimes do you know?
basal bolus = 1 long acting + boluses with meals
twice daily - biphasic insulin - intermediate release
once daily - for T2DM
new - continous infusion / pump teherapy.
VRII
Fixed rate insulin infusion
what are the side effects of insulin?
hypoglycaemia
weight gain
lipodystrophy from injection site - can alter subsequent absorptieon
categorise the hypoglycaemic agents other than insulin you know
oral hypoglycaemics
- increase secretion - sulphonylurea
- increases sensitivity - biguanides, TZDs (glitazones)
- delay glucose absorption - alpha glycosidase inhibitors, DDP4 inhibtors, gliflozins
paraenteral hypoglycaemic agents
- GLP1 anaglogues
MoA of sulphonylureas and main side effects?
inhibit ATP sensitive K+ channels
insulin exocytosis
side effects - hypoglycaemia, weight gain
e.g. gliclazide and glibenclamide
first line if metformin contraindicated.
MoA of metformin and main side effects?
increases insulin sensitvity -i.e. increases GLUT4, decreases gluconeogeneis and glycogenolysis.
side effects - diarrhoea, lactic acidosis esp in renal failure, avoid in critically unwell. aids weight loss and low risk hypoglycaemia.
also associated with reduced myocardial events.
first line
MoA of TZDs (glitazones) and main side effects?
act on PPARg receptor to stimulate gene expression associated with insulin i.e. increases insulin sensitivity.
e.g. pioglitazone, rosiglitazone
ADRs - liver dysfunction, fluid retention - avoid in HF
pioglitazone - bladder Ca.
no hypoglycaemia
MoA of alpha glycosidase and main side effects?
alpha glycosidase is an enzyme within brush border of small intestine involved in glucose breakdown and absorption
blocking this delays absorption
e.g. acarbose
side effects - flatulence, diarrhoea
what are DDP4 inhibitors? side effects?
GLP1 - glucaon like peptide. is a hormone secreted after a meal which stimulates insulin secretion, fullness and slows gastric emptying.
DDP4 is an enzyme that breaks this down
by inhibiting this enzyme can increase endogenous GLP1 to promote insulin release
e.g. sitagliptin
low risk of hypoglycaemia can get other GI absorption abnormalities.
what are gliflozins?
dapagliflozin
inhibit SGLT within renal tubules to prevent glucose reabsorption
however result in UTIs
can trigger euglycaemic DKA - should be stopped in criitical illness
particularly useful for diabetics with HF as promotes fluid loss.
what do you know about GLP 1 analogues?
injection of GLP1 can help promote insulin release
GLP1 - glucaon like peptide. is a hormone secreted after a meal which stimulates insulin secretion, fullness and slows gastric emptying.
e.g. semiglutatide - ozempic - very popular
helps weight loss in obesity and supresses appeptite
can be given S/C or IV
what are the guidelines for management of T2D?
1st line
* metformin
* sulphonylureas if not tolerated
* acarbose if above not tolerated
2nd line
* add sulphonylurea / DDP4 / TZD
3rd line
* insulin
* GLP 1 - esp if BMI >35
what are the main anaesthetic concerns of diabetic patients perioperatively.
pre op - Type 1 or 2, normal meds and timings. e.g. insulin, oral hypoglycaemics or diet controlled. previous DKA , how well controlled - recent BMs?
anaesthetic plan
* if more than 1 meal missed - VRII
* otherwise take BM before
* first on list
* take 80% of long acting morning insulin
* omit short acting morning insulin
* omit all oral hypoglycameic morning of.
intra op
* BMs every hour
post op
* recomence normal insulin with first meal
state you would double check with AABGI guidelines.
how is endocrine function assessed?
history , examination, investigations
e.g. bloods - TSH, T3, T4
urinary catecholamines
9am cortisol
dexamethaone supression and synacthen test
glucose levels , C peptide
