ENDOCRINE

Question 1

define a hormone..

Answer 1

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.

Question 2

what is the difference between paracrine and autocrine?

Answer 2

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

Question 3

what groups of hormones do you know, give examples..

Answer 3

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

Question 4

Outline the mechanism feedback pathway and hence the control of hormone release

Answer 4

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

Question 5

do you know any hormones under positive feedback?

Answer 5

oxytocin at labour
LH surge from higher levels of Oestrogen

Question 6

where is the hypothalamus and what does it do?

Answer 6

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

Question 7

how do the hypothalamus and pituitary relate?

Answer 7

Hypothalamus has 2 connections to pituitary
to anterior pituitary via a hypophyseal circulation
to anterior pituitary by a stalk containing neurons

Question 8

what is meant by a trophic hormone?

Answer 8

one that stimulates growth and development e.g. GH

Question 9

what is a portal circulation?

Answer 9

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

Question 10

tell me about the pituitary gland..

Answer 10

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

Question 11

tell me about ADH..

Answer 11

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.

Question 12

do you know any drugs interferring with ADH release?

Answer 12

increase release - morphine and nicotine
inhibit release - alcohol

Question 13

tell me about oxytocin..

Answer 13

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.

Question 14

Tell me about growth hormone

Answer 14

one of the major hormones released by anterior pituitary
involved in growth and metabolism via ILGFs

Question 15

what is the action of ACTH

Answer 15

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

Question 16

what is TSH?

Answer 16

A thyrotrophic hormone released from anterior pituitary, regulating relase of T3/T4
Induced by TRH from hypothalamus

Question 17

Describe the anatomy of the tyroid gland..

Answer 17

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.

Question 18

describe the anatomy of thyroid hormones..

Answer 18

1. thyroglobulin made by ribosome- rich in amino acid tyrosine.
2. packed into vesicles and exocytosed into follicle
3. iodine is actively transported from blood across the epithelial cells into the follicles
4. thyroid peroxidase oxidises iodine to iodide
5. iodide can now iodinate tyrosine residues of thyroglobulin (iodinase enzyme)
6. this produces T3 and T4 bound as thyroglobin ready for release
7. 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.

Question 19

how do thyroid hormones exert there effects

Answer 19

intranuclear receptors regulating gene expression
the thyroid hormones are lipophillic in nature so cross lipid bilayer readily

Question 20

explain the blood supply to thyroid ..

Answer 20

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

Question 21

what are the effects of thyroxine..

Answer 21

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

Question 22

draw the hypothalamic pituitary axis…

Answer 22

TSH causes growth of thyroid gland
plus increase in iodine uptake
plus increase in secretion of T3/4

somatostatin inhibits TSH release

Question 23

what are the symptoms of hypo/hyperthyroidism?

Answer 23

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

Question 24

causes of hyper and hypothyroid

Answer 24

hyper - Graves (Antibodies to TSH receptor and thyroid peroxidase, pituitary adenoma, thyroiditis

hypo - hashimotos (antibodies against TSH), iodine deficiency, subacute thyroiditis, thyroid surgery, congenital

Question 25

what is thyroid storm and how is it managed?

Answer 25

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)

Question 26

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)

Answer 26

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

Question 27

what anaesthetic concerns are there in someone with thyroid disease..

Answer 27

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

Question 28

what investigations would you want pre op in someone with thryoid disease and a goitre?

Answer 28

neck USS and CXR - assess size of goitre and tracheal compression, maybe even CT TSH, T3/4 pulmonary function tests, ECG/ ECHO

Question 29

how to anaesthetise someone with thyroid disease..

Answer 29

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.

Question 30

what is a myxoedmea coma?

Answer 30

severe life threatening form of hypothyroid resp depression, bradycardia, shock, hypoglycaemia, hypothermia IV levothryoxine and steroids needed.

Question 31

What is the treatment for hyperthyroidism?

Answer 31

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,

Question 32

what is the main ADR of carbimazole?

Answer 32

agranulocytosis - warn patients of sore throat.

Question 33

what is the treatment of hypothyroid?

Answer 33

levothyroxine - works of thyroid receptors. need TSH checking regularly

Question 34

what is sick euthryoid?

Answer 34

low T3/4 normal TSH associated with critical illness dont treat

Question 35

how would you interpret these results... TSH - low T3 and T4 normal

Answer 35

subclinical hyperthyroid

Question 36

describe the structure of the adrenal glands..

Answer 36

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.

Question 37

describe the synthesis of the catecholamines..

Answer 37

PNMT tyrosine comes from phenylalanine (essentail aa) - phenylalanine hydroxylase.

Question 38

describe the adrenal blood supply..

Answer 38

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.

Question 39

describe the breakdown of catecholamine..

Answer 39

in synapse - reuptake into nerve terminals. broken down by MAO peripherally - COMT enzyme main breakdown product is VMA

Question 40

describe the pathway for steroid hormone synthesis..

Answer 40

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.

Question 41

tell me about cortisol..

Answer 41

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.

Question 42

tell me about aldosterone..

Answer 42

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.

Question 43

draw the HPA axis...

Answer 43

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

Question 44

what controls aldosterone release

Answer 44

mainly controlled by RAAS ATII stimulates aldosterone release some control by ACTH

Question 45

what are the components of the juxtamedullary apparatus?

Answer 45

macula densa - in DCT located close to glomerule juxtaglomerular cells - specialised cells in afferent arterioles that contain and secrete renin.

Question 46

what are the stimuli to renin release..

Answer 46

hypovolaemia - reduced GFR - less NaCl to macula densa, less ATP and adenosine made (these normally inhibit renin release) B1 adrenoceptors

Question 47

what are the causes and outcomes of hypo/hyperadrenalism?

Answer 47

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

Question 48

how is cushings and addisons tested for?

Answer 48

cushings - dexamethasone supression test. should cause drop in cortisol by inhibiting pituitary ACTH release addisons - short synacthen test - should stimulate cortisol and aldosterone release

Question 49

how is addisons managed?

Answer 49

replace cortisol and aldosterone hydrocortisone, fludrocortisone need to double steroid dose in times of stress

Question 50

what is a pheochromocytoma?

Answer 50

tumour of adrenal medulla chromaffin cells resulting in exagerated response to sympathetic stimulation intermittetn HTN, tachycardia, flushing, headaches.

Question 51

what are the clinical effects of steroids..

Answer 51

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.

Question 52

how would you manage a patient on steroids for surgery..

Answer 52

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

Question 53

how do the steroids differ in their glucocorticoid activity?

Answer 53

dex - strongest glucocorticoid activity prednisolone next hydrocortisone is weakest fludrocortisone - mineralocorticoid

Question 54

tell me about calcium homeostasis..

Answer 54

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

Question 55

role of vitamin D in calcium homeostasis

Answer 55

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.

Question 56

how is Ca found in the body?

Answer 56

mostly found in ECM of bone in ECF travels in free form 2.5mM and bound to albumin very low intracellular

Question 57

what are the causes of hypo and hypercalcaemia?

Answer 57

hypo - parathyroidectomy, poor intake , congenital (DiGeorge) hyper - PTHrH from tumour, hyperparathyroid, sarcoid

Question 58

symptoms of hypo and hypercalcaemia?

Answer 58

hypo - tetany, spasms, seizures, trousseaus sign. long QT - torsades hyper - stones, abdo pain and constipation, depression, short QT, thirst

Question 59

why do you get tetany with hyperventilation? (this has come up before)

Answer 59

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

Question 60

what is the effect of PTH on phosphate at the kidney?

Answer 60

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.

Question 61

what is the stress response?

Answer 61

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.

Question 62

is the stress response useful?

Answer 62

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

Question 63

how can we modify the stress response?

Answer 63

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.

Question 64

how long for humeral responses of stress response to have an efect?

Answer 64

within first 30-60mins not as immediate as sympathetic NS but cortisol and adrenaline will start having effects intra op and last post op.

Question 65

why may regional anaesthesia improve the stress response?

Answer 65

blocking sensory pain afferents - less activation of hypothalamic / medullary stress response less anxiety than having a GA

Question 66

what is the role of nitrogen balance in the stress response? (Something about nitrogen balance has come up before)

Answer 66

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.

Question 67

tell me about the pancreas

Answer 67

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)

Question 68

how is glucose homeostasis achieved?

Answer 68

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.

Question 69

how is insulin release regulated?

Answer 69

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

Question 70

what is C peptide?

Answer 70

A marker of endogenous insulin proinsulin is made by B cells and when cleaved to insulin, releases C peptide.

Question 71

what are the regulators of insulin release?

Answer 71

hyperglycaemia sympathetic NS - inhibits insulin release via a2 receptors

Question 72

why is insulin used to treat hyperkalaemia?

Answer 72

promotes uptake of K+ by cells

Question 73

what is the difference between cushings disease and cushings syndrome?

Answer 73

cushings disease - pitutary adenoma - ACTH and causes high cortisol cushings syndrome - the signs and symptoms seen with excess cortisol. may be exogenous, adrenal tumour,

Question 74

what are the indications for insulin therapy?

Answer 74

diabetes - type 1 and type 2 hyperkalaemia B blocker OD

Question 75

how is exogenous insulin made and presented?

Answer 75

made from genetically engineered cells 100units/ ml colourless solution

Question 76

what different types of exogenous insulins are there? how can their onset be manipulated?

Answer 76

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.

Question 77

what insulin regimes do you know?

Answer 77

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

Question 78

what are the side effects of insulin?

Answer 78

hypoglycaemia weight gain lipodystrophy from injection site - can alter subsequent absorptieon

Question 79

categorise the hypoglycaemic agents other than insulin you know

Answer 79

oral hypoglycaemics - increase secretion - sulphonylurea - increases sensitivity - biguanides, TZDs (glitazones) - delay glucose absorption - alpha glycosidase inhibitors, DDP4 inhibtors, gliflozins paraenteral hypoglycaemic agents - GLP1 anaglogues

Question 80

MoA of sulphonylureas and main side effects?

Answer 80

inhibit ATP sensitive K+ channels insulin exocytosis side effects - hypoglycaemia, weight gain e.g. gliclazide and glibenclamide first line if metformin contraindicated.

Question 81

MoA of metformin and main side effects?

Answer 81

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

Question 82

MoA of TZDs (glitazones) and main side effects?

Answer 82

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

Question 83

MoA of alpha glycosidase and main side effects?

Answer 83

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

Question 84

what are DDP4 inhibitors? side effects?

Answer 84

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.

Question 85

what are gliflozins?

Answer 85

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.

Question 86

what do you know about GLP 1 analogues?

Answer 86

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

Question 87

what are the guidelines for management of T2D?

Answer 87

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

Question 88

what are the main anaesthetic concerns of diabetic patients perioperatively.

Answer 88

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.

Question 89

how is endocrine function assessed?

Answer 89

history , examination, investigations e.g. bloods - TSH, T3, T4 urinary catecholamines 9am cortisol dexamethaone supression and synacthen test glucose levels , C peptide