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(2020-21 BY2EN2) Endocrinology > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What is Diabetes Mellitus?

A

•Collection of diseases of glucose homeostasis

  • Type 1 Diabetes (T1DM)
  • Type 2 Diabetes (T2DM)
  • Type 3c
  • MODY
  • Gestational Diabetes
  • T2DMY
  • Others
  • Accounts for 10% of NHS budget
  • Associated with serious complications
  • Shortens lifespan/accelerates ageing
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2
Q

Diabetes Diagnosis – FBG/OGTT

A
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3
Q

Diabetes Diagnosis – HbA1c

A

Glucose binds irreversibly to Hb in

erythrocytes, forming HbA1c

  • The higher the glucose, the higher the HbA1c
  • HbA1c reflects the prevailing blood glucose

over the preceding 2-3 months

  • Diagnosis:
  • HbA1c mmol/mol
  • Normal <42 mmol/mol
  • ‘Prediabetes’ 42 to 47 mmol/mol
  • Diabetes 48 mmol/mol or >
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4
Q

History of Diabetes

A

•First described in Ebers Papyrus

  • One of only a few diseases mentioned
  • Notes 3 types of healers (physicians, surgeons and Sorcerers)!
  • No mention of glucose

Treatment was: a measuring glass filled with water from the bird

pond, elderberry, fibres from the asit plant,

fresh milk, beer swill, flower of the cucumber and

green dates’

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5
Q

Describe normal glucose homeostasis post prandially

A

Insulin is key hormone (glucagon and somatostatin also)

Post-prandially (fed)

  • Glucose comes from GI tract via SGLT1
  • Glucose stimulates insulin release from pancreatic-β cells (islets)
  • Insulin promotes glucose uptake in hepatocytes (minor), skeletal muscle (major) and adipocytes and inhibits release of glucose from stores
  • Glucose is stored as metabolites – anabolism occurs )
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6
Q

Describe normal glucose homeostasis in the fasting state

A
  • Glucose drops – lowering insulin
  • Insulin repression of glucose release lessens - catabolism occurs
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7
Q

Describe insulin production

A

•Insulin is produced by pancreatic beta-cells

  • 51aa peptide comprising 2 chains (A and B)
  • Synthesised on RER as pre-proinsulin
  • Signal peptide removed before transfer to Golgi
  • Cleaved by PC1/3 to form mature insulin
  • Stored in secretory granules
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8
Q

Describe insulin release

A
  • Nutrient response (glucose primarily) – biphasic pattern
  • Large role for incretins???
  • Basal secretion does occur (<1.5U/h)
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9
Q

What is insulin secretion increased by?

A
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10
Q
A
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11
Q

Draw a graph of insulin secretion

A
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12
Q

What are inretins?

A
  • Gut hormones that regulate insulin secretion
  • GLP-1 thought to be responsible for >60% of insulin response to glucose
  • Short half life (2-3 minutes) due to DPP-IV
  • New classes of drugs

GLP-1 analogues

DPP-IV inhibitors

•Recent research

Combined GLP-1 and GIP (LY3298176) may be best ever treatment

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13
Q

Effects of intecrins

A
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14
Q

T1DM

A
  • <10% of cases
  • Primarily children and adolescents
  • Cause not understood
  • Almost absolute insulin deficiency – T-cell

mediated autoimmune destruction of pancreatic β-cells

  • Incidence varies dramatically
  • Genetic factors – HLA class II DR-3/-4

(95% of European T1DM)

•GWAS studies – INS promoter, PTPN2, IL2Ra

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15
Q

Presentation of T1DM:

A
  • Short illness (1-4 weeks)
  • Classical diabetes symptoms (polyurea, polydipsia, fatigue weight loss)
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16
Q

What is the risk of developing type 1 diabetes for relatives of people with type 1 diabetes

A
17
Q

Describe type 2 diabetes (T2DM)

A

•The commonest form of diabetes

  • 300 million people worldwide (3 million in UK)
  • Heterogeneous
  • Interaction between genetic predisposition and environment
  • Combination of insulin resistance and pancreatic β-cell dysfunction
  • Traditionally found in older adults
  • Lifetime risk of 1/10
  • In some parts of USA, T2DM as common
  • as T1DM in teenagers
18
Q

TRUE or FALSE: T2DM has greater heritability than T1DM

A
  • Approx. 40-80% of susceptibility
  • More maternal than paternal
  • Several gene polymorphisms identified as increasing risk (see box)
19
Q

What are the key environmental factors of T2DM?

A
  • Obesity – 80% of new cases
  • Physical inactivity
  • Foetal development
  • Ageing
  • These factors drive insulin resistance
20
Q

What is the key cause of T2DM?

A

Insulin resistance

Defined as the inability of insulin to produce its usual biological effects

↓ inhibition of hepatic glucose output

↓ ability to stimulate glucose uptake in muscle and adipose tissue

↓ suppression of lipolysis →

•Potential mechanisms

  • ↓ number of insulin receptors
  • Abnormal insulin receptors
  • Abnormal post-receptor signalling
  • Abnormal GLUT-4 translocation

Lipotoxicity is the key mechanism

21
Q

Define Β-cell Dysfunction

A
  • Loss of β-cell function is the KEY DIAGNOSTIC EVENT
  • Insulin resistance cannot explain the whole story!

Most T2DM are no more insulin resistant that most insulin resistant quartile of general population

Only 20% of insulin resistant people get T2DM

•Causes

Glucolipotoxicty

Genetics

Hormonal – incretins

Obesity

22
Q

Describe the natural history of Diabetes

A
23
Q

What is the main treatment for T1DM?

A

Insulin

24
Q

What is the lifestyle changes help with T2DM?

A
  • Diet
  • VLCD
  • Exercise
25
Q

T2DM treatments: Oral antidiabetics

A
  • Secretagogues
  • Sensitisers
  • Inhibitors of glucose absorption
  • Incretin therapies
26
Q

T2DM treatment: Insulin analogues

A

Long/short acting insulins

27
Q

T2DM treatments: Novel drugs

A
  • SGLT2 inhibitors
  • GLP-1 analogues
  • DPP4 inhibitors
  • GLP-1-GIP combined therapies
28
Q
A
29
Q

Dsecribe microvascular complications

A
  • Affect 80% of people with diabetes
  • Already present in 20-50% of newly diagnosed T2DM
  • Causes – hyperglycaemia (AGEs, sorbitol pathway etc)
  • Retinopathy, nephropathy, neuropathy, diabetic foot
30
Q

Describe macrovascular complications

A
  • Large blood vessels (coronary arteries, aorta, larger arteries in brain/limbs)
  • Commonly – heart disease, cerebrovascular disease, peripheral vascular disease
  • Normally atherosclerosis
  • Diabetes = 4-fold ↑ risk of MI in men, 10-fold in women
  • Causes 65% of all deaths in diabetes.
31
Q

Symptoms of T2DM

A

Retinopathy

  • Most common cause of blindnes in people of working age

Nephropathy

  • 20-44% of all new patients needing renal replacement therapy have diabetes

Erectile dysfunction

  • May affect up to 50% of men ith long-standng diabetes

Macrovascular disease

  • 2-3 fold increase risk of coronary heart disease and stroke

Foot problems

  • 15% of people with diabetes develop foot ulcers; 5-15% of people with diabetic foot ulcers need amputations
32
Q

TRUE or FALSE: T1DM can be prevented

A

FALSE

33
Q

How can T2DM be prevented?

A
  • Screening and aggressive treatment of IGT
  • Increase physical activity
  • Reduce carb/fat load
  • Fasting?
  • Drugs
34
Q
A
35
Q

Lifestyle changes that help with T2DM

A
36
Q

Pharmacological T2DM prevention

A

(2020-21 BY2EN2) Endocrinology (22 decks)

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