Week 13 - Diabetes Mellitus Flashcards

1
Q

carbohydrate digestion

A

polysaccharides > (pancreatic and salivary amylase) > hydrolysis > disaccharides > (brush-border enzymes - sucrase, lactase, maltase) > hydrolysis > monosaccharides

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2
Q

negative feedback loop of glucose digestion

A

intestines absorb glucose
increasing blood glucose level
pancreas responds - secretes insulin
insulin stimulates glucose uptake by liver, skeletal muscles and other tissues
homeostasis restored

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3
Q

what process turns glucose to pyruvate

A

glycolysis

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4
Q

what process turns glucose to glycogen

A

glycogenesis

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5
Q

what process turns glycogen to glucose

A

glycogenolysis

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6
Q

what is produced by pyruvate through an anaerobic pathway

A

lactate

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7
Q

what does lactate produce

A

pyruvate or glucose

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8
Q

what does pyruvate produce though an aerobic pathway

A

acetyl-CoA and co2

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9
Q

risk factors for type 2 diabetes mellitus

A

overweight/obesity
age
abdominal/central obesity
low socioeconomic status
sedentary lifestyle
unhealthy diet choices
cigarette smoking
genetic ancestry
family history
psychosocial stress and depression

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10
Q

diabetes mellitus presentation

A

asymptomatic and symptomatic hyperglycaemia

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11
Q

symptoms of hyperglycaemia

A

polyuria, polydipsia. thirst
fatigue
recurrent infection
weight loss (type 1)

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12
Q

diabetes diagnosis

A

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

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13
Q

pre-diabetes impaired glucose tolerance diagnosis

A

fasting plasma glucose < 7mmol/L and 2hr glucose after 75g glucose load 7.8-11.1mmol/L

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14
Q

pre-diabetes impaired fasting glucose

A

fasting glucose > 6.1 and < 7mmol/L

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15
Q

process of creation of haemoglobin A1c

A

glucose enters blood stream and RBC
glucose naturally binds to Hb
binding creates glycated haemoglobin (HbA1c)

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16
Q

what is HbA1c often used for

A

monitoring response to treatment
reference range 20-42mmol/mol

17
Q

treatment of type 1 DM

A

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

18
Q

pathogenesis of type 2 DM

A

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

19
Q

what factors lead to hyperglycaemia

A

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

20
Q

treatment of type 2 DM - lifestyle advice

A

nutritional
weight loss
exercise
stop smoking
reduce alcohol

21
Q

treatment of type 2 DM - clinical

A

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

22
Q

type 2 DM drug treatments

A

sulphonylureas
thiazolidinedione (TZD)
DPP4 inhibitor (gliptins)
SGLT2 inhibitor (flozins) - most likely second line drug)
GLP1 receptor agonist
insulin

23
Q

complications of DM

A

hypertension
kidney disease
retinopathy
CVD
neuropathy - autonomic or peripheral
infections