T1DM

Question 1

ambiguity between T1 and T11

Answer 1

there is autoimmune diabetes leading to insulin deficiency called LADA- similar to T1: monogenic diabetes can also present similarly children may get T11DM ketoacidosis is a feature of late T2DM diabetes may be due to endocrine damage eg cushings/phaeochromocytoma/ALCHOL

Question 2

pathogenesis of T1DM

Answer 2

autoantibodies against B cells destroy them, causing C peptide BELOW DETECTION- - may be because effector T cells exceed regulator T cells

Question 3

why immune change in T1DM important

Answer 3

can lead to increased risk of autoimmune disease eg B12 deficiency/addisons, as well as in relatives (family history) antibodies can also be measured for treatment eg islet cell antibodies/insulin antibodies- more prevalent in T1 diabetics

Question 4

genetic susceptibility

Answer 4

HLA markers on Chr6- DR3/4 alleles increase risk significantly

Question 5

environmental factors

Answer 5

increased prevalence in winter, possibly due to virus- also more prevalent in different parts of world

Question 6

symptoms of diabetes

Answer 6

osmotic symptoms (poly/noct/polydipsia) blurry vision thrush (candida infection= rashes) weight loss fatigue

Question 7

signs of diabetes

Answer 7

dehydration hyperventilation (kussmahls) glycos/ketonuria cachexia (weakness of body)

Question 8

important organs involved in T1DM

Answer 8

liver, muscle and adipocytes- glucose produced by liver goes into blood, lack of insulin prevents glucose taken into muscle: muscle releases a.a’s, and adipocyte releases glycerol, both of which produce even more glucose in liver, exacerbating hyperglycaemia fatty acids from LIPOLYSIS (NOT glycerol) become ketone bodies (acetoacetate+ hydroxybutyrate) (in liver

Question 9

aims of treatment of T1DM

Answer 9

prevent early mortality, and long term micro/macrovascular complications (retin/nephro/neuropathy and vascular disease)

Question 10

diet in T1DM

Answer 10

reduce fat calories, less refined/more complex carbs + more soluble fibre

Question 11

insulin treatment DIAGRAM

Answer 11

SHORT ACTING insulin given with meals, as well as BACKGROUND insulin (lasts longer)- depending on when meals eaten, there is FLEXIBILITY in insulin treatment insulin pump also given as injecting insulin time consuming- leads to continuous insulin prodcution

Question 12

islet cell transplants

Answer 12

extract from an individual and given to patient via portal vein- problem is patients are immunosurpressed their whole life

Question 13

how to monitor treatment+ problems where appropriate

Answer 13

capillary glucose levels (not as accurate as venous glucose levels) CGM’s (continuous glucose monitoring)- alerts you when glucose goes out of target range: works as correlates with lower HBA1C’s HBA1C

Question 14

explain HBA1C, target+ problem+ why so good

Answer 14

reflection of glucose over 3 months (should be below 42mmol, above 48 is diabetes) as haemoglobin carries glucose- those with anaemia shouldn’t use this, as RBC’s die quickly, so not reflective HBA1C as shows long term glycaemic control- closely linked with microvascular complications

Question 15

acute effects of T1DM

Answer 15

hyperglycaemia- glucose used by muscle/fat, and liver producing glucose as well metabolic acidosis/ketoacidosis- pH, HCO3- and CO2 low (due to hyperventilation)

Question 16

hypoglycaemia- define and effects at different glucose elvels

Answer 16

glucose less than 3.6mm- neural issues below 3, unconciousness below 2

Question 17

who at risk and when most at risk

Answer 17

patients with low HbA1C- occurs pre-lunch and NOCTURNAL (difficult to treat)

Question 18

why hypoglycaemia occurs

Answer 18

exercise/fasting, alcohol, too much insulin

Question 19

symptoms of hypoglycaemia

Answer 19

increased SNS- tachycardia, tremor, sweating, cold extremities, anxiety CNS effects- confusion, drowisness, different behaviour, eventual coma

Question 20

treating hypoglycaemia

Answer 20

orally- simple carbs initially, then complex carbs to prevent glucose crash paraenterally (if conciousness affected)- IV dextrose, glucagon (glucose released from liver)

Question 21

what causes DKA DIAGRAM

Answer 21

infections mainly, but also not taking insulin, new diagnosis and ischaemic event

Question 22

bicarbonate generation DIAGRAM

Answer 22

CO2 converted into H2CO3 using CARBONIC DEHYDRATASE- HCO3- goes into blood, and H+ goes into tubule using HK transporter, with help of NA- dehydration= less GFR, so less bicarbonate, so less HCO3- buffering

Question 23

DIAGRAM henderson hasselbach equation and arterial blood gases

Answer 23

its a metabolic acidosis- low PH, low HCO3- as compensation CO2 goes down too (hyperventilation) anion gap is difference between +ve and -ve ions- a POSITIVE anion gap may be due to DKA (as bicarbonate goes down)

Question 24

electrolyte issues in DKA

Answer 24

water lost in urine, but also Na and K- acidosis shows high blood K+ but low total body K- this is because K+ mainly intracellular, so acidosis drives out K+

Question 25

overall pathogenesis DIAGRAM

Answer 25

insulin deficiency and stress hormones (due to FASTING) causes high glucose, which causes osmotic DIURESIS- if you vomit/ don’t drink enough, leads to DEHYDRATION the insulin deficiency/fasting also leads to KETOSIS- this causes acidosis, leading hyperventilation and vomiting (effect of acid on stomach), leading to MORE dehydration- leads to less renal perfusion, causing less H+ excretion (as less HCO3-), which makes acidosis even worse fever ie infection worsens the dehydration

Question 26

clinical features of DKA

Answer 26

osmotic symptoms, glycos/ketonuria dehydration, hyperventilation, ab pain/vomiting, and eventual coma- there is a risk of arrhythmia and infection

Question 27

investigate DKA

Answer 27

glucose levels, arterial blood gases, creatinine (high due to less GFR) and K+/Na+ (K+ high in plasma) ECG/Xray for heart/pneumonia, and FBC (for WBC count due to infection) also amylase

Question 28

treating DKA

Answer 28

IV fluids, insulin, potassium and bicarbonate (HCO3- often doesn’t help though)

Question 29

fluids

Answer 29

saline- don’t replace fluids too quickly, as can cause differences in CSF/plasma= CEREBRAL OEDEMA thus given given 500ml every few minutes like a SLIDING SCALE

Question 30

insulin

Answer 30

given intravenously as person with acidosis will have less absorption in gut due to dehydration- given as a sliding scale, adjusting according to capillary glucose

Question 31

potassium

Answer 31

insulin drives K+ into cells- can cause hypokalaemia (ie in blood), so given via sliding scale rather than all at once

Question 32

bicarbonate

Answer 32

acidosis causes heart effects and low BP, as well as brain effects- bicarbonate treatment can cause hypokalaemia/hypernatremia, but benefits outweigh the costs

Question 33

causes of death in DKA

Answer 33

disease too much, social factors, delay seeking help, inadequate treatment- all quite equal