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Year 3 - Met3b > Diabetes - Aetiology, Diagnosis and Presentation > Flashcards

Diabetes - Aetiology, Diagnosis and Presentation Flashcards

1
Q

How many people have diabetes

A

3 million people have diabetes

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2
Q

at the current rate how many people will have diabetes by 2025

A
  • higher than 5 million by 2025
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3
Q

what counts for 85-95% of all cases of diabetes

A

type 2 diabetes

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4
Q

what percentage of the population have diabetes

A

4-9%

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5
Q

How many people at the London have diabetes

A

1 in 5

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6
Q

which type of diabetes is more acute

A
  • Type 1 diabetes is more acute

- Type 2 diabetes is subacute/ more non specific symptoms such as tiredness

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7
Q

What are the classic symptoms of diabetes

A
  • polyuria - osmotic diuresis by hyperglycaemia
  • polydipsia
  • nocturia - osmotic diuresis by hyperglycaemia
  • weight loss - glucose coming out of urine
  • fatigue - lack of glucose
  • blurred vision - osmotic effect on the lens
  • pruritic
  • recurrent urinary or genitourinary infections
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8
Q

Name a word you would use to describe the classic symptoms of diabetes

A
  • Osmotic - due to the osmotic effect of hyperglycaemia creating an osmotic diuresis
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9
Q

Name two acute emergency presentations of diabetes

A

Hyperosmolar hyperglycaemic syndrome (HHS)

diabetes ketoacidosis (DKA)

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10
Q

How can diabetes present with complications

A

 skin infections – staphylococcal skin abcesses, oral or genital candidiasis

 foot problems – ulcers or neuropathic pain

 retinopathy – perhaps found on routine eye test

 acute myocardial infarct / stroke – diagnosed whilst in hospital

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11
Q

What are the ways to diagnose diabetes

A
  1. Fasting plasma glucose (FPG) - not a capillary glucose test (fingerpick test)
  2. Random plasma glucose (RPG)
  3. 75 gram oral glucose tolerance test (OGTT) - this is when they fast for a minimum of 9 hours, you then check the fasting plasma glucose (FPG) and then give 75g of glucose (lucozade) and check 2 Horus later the plasma glucose
  4. Haemoglobin A1c( HbA1c) - this is a test that measures for average glucose control over a 3 month period
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12
Q

How does a 75 gram oral glucose tolerance test (OGTT) work

A

this is when they fast for a minimum of 9 hours, you then check the fasting plasma glucose (FPG) and then give 75g of glucose (lucozade) and check 2 Horus later the plasma glucose

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13
Q

What does haemoglobin A1c( HbA1c) measure

A
  • this is a test that measures for average glucose control over a 3 month period
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14
Q

What are the normal ranges for Haemoglobin A1c( HbA1c)

A

Normal range <42 mmol/mol

Good control varies from individual to individual (depending on age, co-morbidities etc.)

Generally HbA1c < 53 mmol/mol indicates well controlled diabetes

if HbA1c is greater than 48 mol/mol for two times then you have diabetes

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15
Q

For an individual who has no diabetes symptoms how many tests do you have to do

A

two diagnostic tests are required (eg 2x FPG, or HbA1c, but only one abnormal OGTT is required)

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16
Q

For an individual with symptoms of diabetes how many tests do you have to do

A

One diagnostic test is enough to diagnose diabetes for someone with symptoms

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17
Q

What is the gold standard for diagnosing diabetes

A

75 gram oral glucose tolerance test (OGTT)

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18
Q

list the numbers needed for diagnosis of diabetes for each test

  • Fasting plasma glucose
  • 2 hour plasma glucose
  • random plasma glucose
  • HbA1c
A
  • Fasting plasma glucose = greater than 7 mmol/L
  • 2 hour plasma glucose = greater than 11.1mmol/L
  • random plasma glucose = greater than 11.1mmol/L
  • HbA1c = greater than 48mmol/mol(6.5%)
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19
Q

what do you use to measure impaired glucose tolerance and what does it mean

A

can only be diagnosed using an oral glucose tolerance test

  • so the 2 hour plasma glucose
  • this is between 7.8-11 mol/L - the is not a diagnosis of diabetes but it is abnormal
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20
Q

What is used to measure impaired fasting glucose and what does it mean

A
  • Slightly higher than normal which is less than 6 but it is not quite in the diabetes range yet
  • measured by using fasting plasma glucose
  • between 6.1-6.9 mol/L
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21
Q

What does impaired glucose tolerance and impaired fasting glucose indicate

A
  • they indicate a higher risk for developing diabetes

- need to monitor patient carefully

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22
Q

List the differences between type 1 and type 2 diabetes

A 
Type 1 diabetes 
- ketone prone - due to lack of insulin and will develop ketoacidosis 
- insulin deficiency 
- autoimmune (GAD and ICA antibodies 
- acute onset 
- non obese 
- juvenile onset (usually less than 35 years of age) 
- HLA DR3 and HLA DR4 present 
- 50% concordance in MZ twins 
FH positive in 10%

type 2 diabetes

  • non ketosis prone
  • insulin resistant or/and deficiency
  • Non- autoimmune - associated with metabolic syndrome
  • insidious onset
  • often obesity associated
  • usually greater than 35 years of age but common below this age as well
  • No HLA relation
  • 100% concordance in MZ twins
  • FH positive in 30%
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23
Q

what HLA present in type 1 diabetes

A
  • HLA DR3 and HLA DR4 present
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24
Q

what autoimmune antibodies are present in type 1 diabetes

A

GAD and ICA antibodies

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25
Q

List the secondary causes of diabetes

A 
- Pancreatic disease 
 Endocrine disease
 Drug induced
 Genetic defects of b-cell function
 Genetic defects of insulin action
 Infections
 Genetic syndromes
 Gestational diabetes
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26
Q

How does pancreatic disease lead to the onset of diabetes

A
  • due to damage of the beta cells therefore reducing there production of insulin
27
Q

What can cause pancreatic disease that can lead to type 1 diabetes

A
  • trauma - leading to a pancreatectomy
  • pancreatitis
  • pancreatic cancer,
  • cystic fibrosis causing pancreatic damage to the exocrine gland leading damage to the endocrine gland,
  • haemochromatosis/thalassaemia due to iron overload
  • Fibrocalculous pancreatopathy (Pancreatic damage associated with malnutrition)
28
Q

Name the endocrine diseases that may cause secondary diabetes

A
  • Acromegaly - excess growth hormone
  • Cushing syndrome - excess cortisol
  • Glucagonoma - excess glucagon
  • phaechromocytoma - excess catecholamines
  • Hyperthyroidism - excess thyroid hormone
  • Conn’s syndrome - excess aldosterone
29
Q

What drugs increase the risk of diabetes

A

 Glucocorticoids - similar to Cushing syndrome
 b-blockers - increase risk by about 30%
 Thiazide diuretics - increase risk by about 30%
 Tacrolimus (used in transplantation – may cause “New Onset Diabetes after Transplantation” [NODAT])
 Atypical anti-psychotics – eg. olanzapine, risperidone, clozapine - increase appetite and induce metabolic problems

30
Q

what drug causes NODAT

A

Tacrolimus (used in transplantation – may cause “New Onset Diabetes after Transplantation” [NODAT])

31
Q

What infections increase the risk of diabetes

A

 Congenital rubella

 Cytomegalovirus

32
Q

Type 2 diabetes is a ..

A

 Type 2 diabetes is a heterogenous syndrome

33
Q

what two interactions does the pathogenesis of type 2 diabetes involve

A

 Environmental factors – obesity, poor physical activity

 Diabetogenic genes – genes contributing to insulin resistance

(genetic and environmental causes)

34
Q

How does the genetic and environment lead to type 2 diabetes

A
  • causes various combinations of insulin resistance and B cell failure
35
Q

what is insulin resistance and B cell failure exacerbated by

A

Hyperglycaemia

36
Q

What is glucose toxicity

A
  • High levels of glucose lead to poorer B cell function
  • this leads to reduce insulin secretion as they switch off
  • therefore if you lower glucose this can help B cell function
37
Q

what is the genetic influence of type 2 diabetes

A

possibly 40-80% of susceptibility

38
Q

B cell failure gets..

A

worse over time

- even at diagnosis there is already a lot of beta cell function

39
Q

Name a gene associated with type two diabetes

A

Thrifty genes

40
Q

What are thrifty genes

A
  • These are genes that favour fat storage and or/insulin resistance to help us in times of famine (ancestors survived famines in families)
  • these don’t help us in times of decrease physical activity and increased energy intake
41
Q

why type of adiposity is not good in type two diabetes

A
  • Abdominal. visceral adiposity is not good

- pro-inflammatory cytokines from adipocytes contribute to insulin resistance

42
Q

in terms of alpha and beta cells in the pancreas what happens to the percentage of them in type 2 diabetes

A
  • Beta cell mass is preserved (50% at autopsies)

- alpha cell population is increased - leads to excess glucagon relative to insulin

43
Q

where is the insulin resistance in type 2 diabetes

A

post receptor insulin resistance

44
Q

when are amyloid peptide deposition happening in type 2 diabetes

A

Amyloid peptide deposition in the pancreatic islets occurs late in the disease (hence a possible link between diabetes and dementia)

45
Q

What are the factors in metabolic syndrome

A
  • central obesity (waist circumference increase)
  • blood pressure abnormalities
  • low HDL concentration (lipid abnormalities)
  • increase in triglyceride (glucose abnormalities)
46
Q

Who should be screened for diabetes

A

 Overweight / Obese - BMI > 30 kg/m2

 Strong family history of diabetes

 History of gestational diabetes

 Ethnic minorities
▪ South Asian – 6x increased risk
▪ Afro-Caribbean – 2x increased risk

 Individuals with known vascular disease
▪ Coronary Heart Disease, Peripheral Vascular Disease, Cerebrovascular disease

 Patients on steroids / atypical anti-psychotic therapy / transplants

 Unexplained foot ulcers / recurrent candida / skin abscesses

47
Q

What is type 1 diabetes caused by

A
  • Pancreatic B cell destruction leading to absolute insulin deficiency
  • autoimmune destruction of pancreatic islets in predisposed individuals (usually islet cell (ICA) AND glutamic acid decarboxylase (GAD antibodies positive)
48
Q

What autoimmune antibodies are present in type 1 diabetes

A
  • islet cell antibodies (ICA)
  • glutamic acid decarboxylase (GAD) antibodies positive
  • can be idiopathic and antibody negative
49
Q

What is latent autoimmune diabetes in adults

A

 Diagnosed in adulthood
 Usually non-acute, hence may be diagnosed at Type 2 diabetes
 ICA or GAD+ve
 Usually require insulin fairly soon after diagnosis

50
Q

what is the concordance in monozygotic twins for type 1 diabetes v type 2

A
  • Type 1 30-50%

- Type 2 >90% - stronger

51
Q

what is the evidence of environmental factors for type 1 diabetes

A

 Peak age of onset 5-7 years
 Puberty
 Seasonal variations
 Predominantly Europid populations

52
Q

What is the pathogenic sequence seen in type 1 diabetes

A

You have a genetic susceptibility:
 HLA genes on Chromosomes 6q (MHC) – HLA DR3/4 appears high risk  Also genes on chromosomes 2q, 15q, 11q

You get an environmental insult:
 Eg Virus such as cocksackie or parvovirus
 Possibly exposure to Cows Milk Protein? - breast milk lower risk

You develop an insulitis:
 Infiltration of activated T-lymphocytes

You have activation of autoimmunity:
 non-self to self transition

You develop an immune attack on b-cells:
 isletcell/GADantibodies
 cell mediated immunity

You develop diabetes mellitus:
 when >90% of b-cells are destroyed

53
Q

what infections can cause diabetes

A
  • Congenital rubella

- CMV

54
Q

Name some genetic syndromes that are associated with diabetess

A
  • Down syndrome
  • Friedreich’s ataxia
  • Huntington’s chorea
  • Klinefelter syndrome
  • Laurence-Moon-Biedl syndrome
  • Myotonic dystrophy
  • Porphyria
  • Prader-Willi syndrome
  • Turner syndrome
  • Wolfram syndrome
55
Q

name some uncommon forms of immune mediated diabetes

A
  • Stiff person syndrome

- anti-insulin receptor antibodies

56
Q

What is impaired glucose tolerance (IGT)

A
  • 2hr OGTT - is greater than 7.8 and less than 11.1
57
Q

What is impaired fasting glucose

A

fasting glucose is greater than 6.1mmol/L and less than 7mmol/l

58
Q

What is prediabetic

A
  • this is when HbA1c is between 42-47mmol/mol or 6-6.4%
59
Q

What factors in obesity contribute to insulin resistance

A
  • Adipokines – due to higher body fat content, especially abdominal/visceral
  • Inflammation – chronic low-grade inflammation
  • Lipids – accumulation of lipids and their metabolites (eg DAG and FFAs)
60
Q

Define insulin resistance

A

= diminution in the response of the body’s tissues to insulin, so that higher concentrations of serum insulin are required to maintain normal circulating glucose levels; eventually the islet cells can no longer produce adequate amounts of insulin for effective glucose lowering, resulting in hyperglycaemia

61
Q

Define glucose tolerance

A
  • the boys ability to absorb and use glucose
62
Q

What 4 conditions make up metabolic syndrome

A
  1. central obesity
  2. dyslipidemia
  3. hypertension
  4. imparted fasting glucose
63
Q

What is central obesity

A

BMI greater than 30 or was it circumference

  • Caucasian men = >94cm
  • Caucasian women = >80cm
  • south asian men = >90cm
  • south asian women = > 80cm
64
Q

What is hypertension

A
  • Systolic ≥130mmHg
  • Diastolic ≥85mmHg
  • or on treatment

Year 3 - Met3b (26 decks)

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