Week 13 - Diabetes Mellitus Flashcards
carbohydrate digestion
polysaccharides > (pancreatic and salivary amylase) > hydrolysis > disaccharides > (brush-border enzymes - sucrase, lactase, maltase) > hydrolysis > monosaccharides
negative feedback loop of glucose digestion
intestines absorb glucose
increasing blood glucose level
pancreas responds - secretes insulin
insulin stimulates glucose uptake by liver, skeletal muscles and other tissues
homeostasis restored
what process turns glucose to pyruvate
glycolysis
what process turns glucose to glycogen
glycogenesis
what process turns glycogen to glucose
glycogenolysis
what is produced by pyruvate through an anaerobic pathway
lactate
what does lactate produce
pyruvate or glucose
what does pyruvate produce though an aerobic pathway
acetyl-CoA and co2
risk factors for type 2 diabetes mellitus
overweight/obesity
age
abdominal/central obesity
low socioeconomic status
sedentary lifestyle
unhealthy diet choices
cigarette smoking
genetic ancestry
family history
psychosocial stress and depression
diabetes mellitus presentation
asymptomatic and symptomatic hyperglycaemia
symptoms of hyperglycaemia
polyuria, polydipsia. thirst
fatigue
recurrent infection
weight loss (type 1)
diabetes diagnosis
random plasma glucose or 2hrs after 75g glucose load - > 11.1mmol/L
fasting plasma glucose - > 7mmol/L
haemoglobin A1c - > 48mmol/mol
asymptomatic patients - need 2 investigations separated in time
pre-diabetes impaired glucose tolerance diagnosis
fasting plasma glucose < 7mmol/L and 2hr glucose after 75g glucose load 7.8-11.1mmol/L
pre-diabetes impaired fasting glucose
fasting glucose > 6.1 and < 7mmol/L
process of creation of haemoglobin A1c
glucose enters blood stream and RBC
glucose naturally binds to Hb
binding creates glycated haemoglobin (HbA1c)
what is HbA1c often used for
monitoring response to treatment
reference range 20-42mmol/mol
treatment of type 1 DM
destruction of pancreatic beta cells - insulin deficient
requires insulin therapy - common to have a basal long acting insulin combined with meal insulin boluses of short acting insulin
continuous subcutaneous insulin pumps
pathogenesis of type 2 DM
pancreas - altered/reduced insulin secretion
adipose tissue - increased lipolysis, increased FFA release, decreased glucose uptake, inappropriate release of adipokines
muscle - decreased glucose uptake
liver - increased glucose production
what factors lead to hyperglycaemia
decreased incretin effect
increased lipolysis - adipose
increased glucose resorption - kidneys
decreased glucose uptake - tissues
inflammation
neurotransmitter dysfunction
vascular insulin resistance
increased hepatic glucose production
decreased insulin secretion - pancreatic β-cells
increased glucagon secretion - pancreatic ⍺-cells
treatment of type 2 DM - lifestyle advice
nutritional
weight loss
exercise
stop smoking
reduce alcohol
treatment of type 2 DM - clinical
initially with metformin - sensitises insulin action, opposes action of glucagon, reduces hepatic gluconeogenesis, increases muscular glucose uptake, causes weight loss
most common side effect - GI upset
monitor HbA1c - aim for 48mmol/mol - ref range 20-42
type 2 DM drug treatments
sulphonylureas
thiazolidinedione (TZD)
DPP4 inhibitor (gliptins)
SGLT2 inhibitor (flozins) - most likely second line drug)
GLP1 receptor agonist
insulin
complications of DM
hypertension
kidney disease
retinopathy
CVD
neuropathy - autonomic or peripheral
infections
