diabetes quiz

Question 1

summarise normal glucose homeostasis *

Answer 1

depends on insulin secretion from teh pancreas

insulin secreted in response to meal

insulin signasl to cells around body that they should start using glucose - especially muscle and liver

insulin turns on the glut 4 pump - glut4 is sat inside membrane and comes to surface and therefore glucose enters cells

small amount of insulin is very potent because a lot of fat and lipid cells

k and phosphate

Question 2

describe insulin *

Answer 2

signal that you have been fed

switches on all pathways that use up glucose adn store glycogen as fat

glycogen synthase is turned on

glycolysis in liver and muscle is turned on

stimulates fat generation

suppress ketone production

gluconeogenesis is switched off - this is where new glucose is made by insulin- alanine amino transferase (ALT) is the enzyme that does this

Question 3

what happens to insulin during starvation *

Answer 3

levels fall

Question 4

what substrates are available during starvation *

Answer 4

glucose

glycogen

TG - not converted to glucose, fa used as fuel - good source of energy

protein - only for survival, become weak

Question 5

what is switched on during satrvation *

Answer 5

insulin levels are low but not zero

glyccogenolysis - liver glycogen stores last <24hours

liver switches on ketogenesis becasue fa cant cross the bbb - so need ketones for survival - this ketone production is turned on by insulin - there will be ketones in the urine

if have 0 insulin make way more ketones than you need

Question 6

what type of insulin deficiency is type 1 and 2 dm *

Answer 6

type 1 - absolute

type 2- relative

Question 7

describe the pathology of t1dm *

Answer 7

immune system destroys the islets of langerhans in the pancreas - immune system meant to kkill the virus taht expresses b cell marker but also kills the b cell

resultant total def of insulin

all cells fail to take up glucose glut4 not switched on

plasma glucose rises

glucose leaks into urine

therefore have polyuria and polydipsia

complete insulin def causes acidosis

Question 8

what happens when insulin levels are 0 *

Answer 8

liver behaves as if no fuel for brain to work so makes huge levels of ketones

blood turns acidic with all the ketones

the brain cannot function in an acid ph - become unconscious

Question 9

describe diabetic ketoacidosis *

Answer 9

blood glucose high becasue cant get into cells

blood full of ketones - acids

severe dehydration

air hunger - slow deep respiration - kussmaul’s breathing is the way to get rid of co2 body is causing resp alkalosis to counteract the metabolic acidosis

Question 10

How do you manage dka *

Answer 10

rehydrate with saline

iv insulin - problem is becasue there is no insulin so use insulin to treat it - try to stop the production of ketones

Question 11

what is teh treatment of t1dm *

Answer 11

insulin

diet and reduce the risk factors for retinopathy, nephropathy, and neuropathy

Question 12

describe the pathology of t2dm *

Answer 12

insulin doenst work effectively - only some glucose enters the cell

insulin turns of ketogenesis - no ketones present

pancreas increase insulin secretion because not getting a response

eventually panc exhausted so get t2dm

dont become very sick because have dont have ketones - dont present with dka

Question 13

phenotype of t2 diabetics *

Answer 13

usually older - mature onset

usually obese

non insulin dependant

not prone to ketoacidosis

no hla associations ]no islet ab

100 % concordance between monozygouys twins

manage with diet/oral hypoglycaemic agents

very high glucose

glucose slowly rises causing polyuria and polydipsia thirsty pts drink sweet drinks

develop hyper osmolar non ketotoc coma (HONCK) - didnt know had dm and are suddenly uncoscious and dehhydrated, more likely to die than with dka because older - have been dehydrated for 3 months for eg, so if rehydrate quickly they get brain oedema

Question 14

how would you manage HONKC *

Answer 14

rehydrate with normal saline slowly

if you go to fast cause a shift in the electrolytes = cerebal oedema = death

Question 15

how do you manage t2dm *

Answer 15

lose weight

avoid sugar

high fibre diet to cause slow absorption of carbohydrate

make yourself more sensitive to insulin - metformin which is a biguanide

insulin/drugs that stimulate the pancreas more ie sulphonylureas like gliclazide

use secretagogues - substance that causes something else to be excreted

Question 16

if a pt has a fasting glucose of >7 what is the daignosis *

Answer 16

t2dm - t1 would present with dka

Question 17

if a pt has other autoimmune conditions what type of dm are they likely to have *

Answer 17

t1

Question 18

if pt has a strong fh what type of dm are they likely to have *

Answer 18

t2 - concordance in familiues is string

Question 19

what are the classes fo dm drugs *

Answer 19

thiazolidinediones (pioglitazone)

biguanide (metformin)

sulfonylurea (glicazide, glibenclamide)

incretins (glp1 analogues, exanatide)

dipeptidyl peptidase IV inhibitors (gliptins)

glifozines (sglt2 inhibitors): dapaglifloxzin

insulin

Question 20

what medication prevents dm *

Answer 20

metformin

Question 21

what was more effective as a dm treatment than metformin *

Answer 21

lifestyle

Question 22

summarise t1dm *

Answer 22

immune destruction of panc

insulin dependant

young 12-16

dka

quite high glucose

prone to ketoacidosis

acute onset

non-obese

hla dr3 and dr4

islet cell ab

30-40% concordance

always need insulin