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BIOL354: Pathobiology > Lecture 9: Diabetes 1 > Flashcards

Lecture 9: Diabetes 1 Flashcards

1
Q

What is diabetes mellitus?

A

a group of metabolic diseases characterised by hyperglycemia resulting from defects in insulin secretion, insulin action, or both

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2
Q

Which organs are affected by microvascular complications of DM?

A

eyes (retinopathy), kidneys (nephropathy), neurons (neuropathy)

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3
Q

Which organs are affected by macrovascular complications of DM?

A

heart, lower limbs (peripheral vascular disease) strokes

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4
Q

What is the pathophysiology of hyperglycaemia (8 reasons)?

A

beta cells in pancreas impaired insulin secretion
increased glucagon secretion from alpha cells
increased hepatic glucose production (gluconeogenesis)
Neurotransmitter dysfunction
Decreased glucose uptake by musculoskeletal system
Increased glucose reabsorption
Increased lipolysis
Decreased incretin effect (hormones secreted in the gut in response to food that increases insulin secretion)

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5
Q

what is the renal glucose threshold?

A

The kidneys reabsorb all glucose from filtrate until a level of 10mmols (excess leaves in urine)
SGLT1 and 2 (sodium-glucose cotransporters) responsible for glucose reabsorption
-> increased expression of SGLTs results in increased glucose uptake by kidneys

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6
Q

Describe the production and processing of insulin?

A

insulin produced in beta cells in isets of langerhans produced as pre-proinsulin that is cleaved to proinsulin, which is cleaved to mature insulin and C-peptide in equimolar amounts.

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7
Q

What are the overall effect of insulin?

A

Reduce blood sugars by:
- increase cellular uptake of glucose by muscle and liver where it is stored as glycogen
- increase uptake by adipocytes for storage as triglycerides

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8
Q

How does insulin act to reduce blood glucose levels?

A

increase hunger
increase glucose metabolism by liver and muscle
decrease hepatic glucose production
increase glucose storage as glycogen
lipogenesis increased and decrease in lipolysis

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9
Q

Why is insulin called an anabolic hormone?

A

helps to build up: stimulate cell growth
- increase muscle mass
- increase in protein anabolism
- increase in lipogenesis

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10
Q

What is the difference between type 1 and type 2 DM?

A

Type 1 = autoimmune descrution of beta cells so insulin not produced, need to be given insulin for survival (anabolic hormone required for growth, not able to make energy so turn to fat stores and die if untreated), often younger age of onset, develops rapidly

Type 2 = insulin resistance - insulin not binding to receptor, develops slowly, often later age of diagnosis, patients often do not need insulin treatment (at least not in the start)

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11
Q

What are the counter-regulatory hormones of insulin?

A

Glucagon is the main one but also other stress hormones such as adrenaline, noradrenaline, cortisol, growth hormone oppose insulin action

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12
Q

What stimulates insulin secretion?

A

Food (glucose)
amino acids
GIP (an incretin hormone released by K cells of duodenum and jejunum)
parasympathetic stimulation (rest and digest)

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13
Q

What inhibits insulin secretion?

A

glucagon (and noradrenaline, adrenaline, cortisol)
Sympathetic stimulation

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14
Q

What stimulates glucagon secretion?

A

low glucose
amino acids
sympathetic stimulation
adrenaline

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15
Q

What inhibits glucagon secretion?

A

insulin
GIP

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16
Q

What are the symptoms of DM?

A

Fatigue and tiredness
Frequent urination (osmotic pressure of high glucose in filtrate)
weight loss (breakdown of fat and muscle)
Wounds that wont heal (impair immunity and microvasculature)
Always hungry
Sexual dysfunction (vasculature and neuropathy problems)
Blurry vision (change in osmotic pressures in lens)
Numb or tingling of hands or feet (neuropathy)
Always thirsty (due to increased urination)

17
Q

What is the diagnostic criteria for DM?

A

HbA1c (Hb becomes glycated overtime, RBC half life about 3 months) - high level of HbA1c = insight into glucose control over past 3 months –> 6.5% or above = diabetes

Fasting blood glucose (FBG) –> 7.0 mmol/L or above = diabetes

2 hour OGTT (75g of glucose and measure glucose 2 hours later)
–> 11.1 mmol/L or above = diabetes

Random blood glucose –> 11.1 mmol/L or above = diabetes

18
Q

What is gestational diabetes?

A

Develops in 2nd or 3rd trimester of pregnancy
- placenta produces hormones that increase insulin resistance to increase glucose for baby
- goes away after pregnancy (if it remains then was undiagnosed type 2 DM)
- often needs insulin treatment

19
Q

What are the causes of type 1 DM?

A

autoimmune disease
genetic predisposition (HLA/MHC)
Environmental factor (intrauterine, early life, geography)

20
Q

True or false: T1DM is most often sporadic and patients typically do not have an affected 1st degree relative?

A

True (family history is usually taken when querying T2DM)

21
Q

What environmental factors affect incidence of T1DM?

A

Viruses (E.g. cytomegalovirus, Epstein-Barr, Mumps)
Diet (Cow’s milk, caffeine, nitrates)
Lifestyle (stress)

22
Q

Describe the geographical variation and incidence of T1DM

A

risk rises with increasing geographical latitude (distance from equator) and risk increases with relocation from a low to high incidence region (suggests a causative role of environmental factors)

23
Q

Which 4 common auto-antibodies are screened for in diagnosis of T1DM?

A

anti-GAD antibodies
anti-islet cell antibodies
anti-IA-2 antibodies
anti-ZnT8 (zinc transporter 8)

24
Q

What effect does T1DM have on c-peptide levels?

A

eventually not measurable since no insulin being produced

25
Q

True or false: there are strong links with obesity and hypertension and T1DM?

A

False: there are strong links with T2DM and obesity and hypertension (especially central obesity)

26
Q

What is the correlation between BMI and risk of developing T2DM?

A

positive correlation (higher BMI = higher risk of T2DM)

27
Q

How does obesity and inflammation link to T2DM?

A

Adipocytes are a source of pro-inflammatory cytokines: adiponectin, TNF-alpha and Chemokine molecule CXCL5
- have toxic effect on beta cells and can reduce insulin function and increase insulin resistance

28
Q

Describe the core defects leading the development of T2DM

A

Initial insulin resistance seen with hyperinsulinaemia with normal glucose tolerance

Impaired beta cell function results in insulin resistance with declining insulin levels and impaired glucose tolerance (pre-diabetes)

This then develops into T2DM

29
Q

How does beta cell mass on day of diagnosis differ between T1 and T2 diabetes?

A

T1DM = no beta cell mass left when diagnosed

T2DM = 50% of beta cell mass has been lost

30
Q

What are the major metabolic defects in T2DM?

A

Peripheral insulin resistance in muscle and fat - increased lipolysis, decreased breakdown of triglycerides, decreased glucose uptake, decreased glucose utilisation

Hepatic insulin resistance - decreased glucose uptake and utilisation

Relative insulin deficiency = insulin secretion not sufficient to overcome insulin resistance

31
Q

What is ketoacidosis?

A

Occurs when triglycerides are broken down for energy - results in ketone production. Accumulation of ketones in the body results in ketoacidosis - can be fatal

32
Q

Is ketoacidosis rare in T2DM? why/why not?

A

Yes

why?
because there is some insulin still present that stops excessive breakdown of triglycerides
- could occur in stress response (increase in stress hormones renders whatever insulin was left to be non-existent and drive patient into diabetic ketoacidosis)

33
Q

How can we differentiate between T1DM and T2DM?

A

Symptoms, age, BMI
autoantibody test (positive = type 1)
C-peptide (low = type 1 - not making enough insulin, usually normal in type 2)
Urinary C-peptide to creatinine ratio

34
Q

Why is C-peptide measured over insulin?

A

insulin has a very shirt half life and fluctuates a lot

35
Q

What is MODY?

A

Monogenic diabetes -Maturity onset diabetes of the young
- arises from specific genetic mutations ( glucokinase, HNF1alpha, HNF1beta)

36
Q

What is MIDD?

A

Monogenic diabetes - Maternally inherited diabetes and deafness
- arises from mutation of mtDNA

37
Q

Name three endocrine diseases that can cause diabetes

A
  1. Cushing’s disease (excess cortisol)
  2. Acromegaly (excess growth hormone)
  3. Phaeochromocytoma (tumour usually in adrenal glands resulting in excess catecholamine - noradrenaline and adrenaline)
38
Q

what can cause secondary diabetes?

A

pancreatic disease (typically seen in individuals with prolonged alcohol abuse) - pancreas loses endocrine and exocrine function - chronic malnutrition and malabsorption

39
Q

What drugs/toxins can causes diabetes?

A

steroids (steroid induced hyperglycaemia) - high blood sugars that go down after stopping steroids

BIOL354: Pathobiology (10 decks)

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