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Endocrinology > epidemiology of diabetes > Flashcards

epidemiology of diabetes Flashcards

1
Q

3 ways of making GLC?

A

oral intake - absorbed in gut
gluconeogensis in liver
glycogen breakdown in liver

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2
Q

how does glycogenolysis/gluconeogenesis occur?

A

alpha cells promote the action of glucagon, promoting glycogenolysis/gluconeogenesis

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3
Q

describe 3 results of insulin secretion?

A

reduced lipolysis (adipose)
reduced GLC production (liver)
increased GLC uptake (muscle)

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4
Q

definition of diabetes mellitus?

A

Group of metabolic diseases characterized by hyperglycaemia together with disturbances of metabolism resulting from defects in insulin secretion +/ action

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5
Q

symptoms of hyperglycaemia? (THINK: type 1 diabetes)

A 
polydipsia
polyuria
blurred vision
weight loss
infections
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6
Q

metabolic decompensation of hyperglycaemia?

A

DKA/HHS

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7
Q

microvascular long term complications of hyperglycaemia?

A

retinopathy
neuropathy
nephropathy

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8
Q

macrovascular long term complications of hyperglycaemia?

A

stroke
MI
PVD

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9
Q

OGTT?

A

oral GLC tolerance test

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10
Q

normal values v.s. diabetes for OGTT?

A

fasting: <6 v >7
random: <11.1 v >11.1
2hr: <7.7 v >11.1

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11
Q

requirements for diagnosis of diabetes?

A

either -
symptoms + 1 abnormal GLCs
OR….
2 abnormal GLCs/HbA1c (if asymptomatic)

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12
Q

diagnostic HbA1c value?

A

> 48 mol/mol

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13
Q

what is intermediate diabetes and what management is provided?

A

people in-between normal and diabetic values - i.e those to watch -
management:
yearly check ups for BP, weight management, regular eye tests

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14
Q

intermediate values for diagnosis?

A

values between that of normal and diabetics:
fasting glucose 6.1-7 mmol/l
glucose tolerance 2h glucose ≥7.8 and <11mmol/l
HbA1c 42-47mmol/mol

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15
Q

why is the Fasting BG level set at 7 for diabetics?

A

this is the level where complications begin to arise

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16
Q

adv & disadv. of GLC as a diagnostic tool?

A

adv:
feasible in developing world
more established
directly measures molecule that causes diabetes

disadv:
fasting state needed
may need OGTT
varies between individuals

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17
Q

adv & disadv. of HbA1c as a diagnostic tool?

A

adv:
don’t fast
marker of glycemic control
low variability between people

disadv:
differs with age and ethnicity
costly
surrogate marker of hyperglycaemia

18
Q

examples of when HbA1c CANNOT be used?

A 
young people and children 
pregnancy
medications acute pancreatic damage/post pancreas related surgery 
renal failure 
HIV patients
19
Q

how many people in Scotland have diabetes?

A

~300,000 - ~5% population

20
Q

which antibodies are found to attack islets in type 1?

A

anti-GAD antibodies

21
Q

what is the greatest risk of developing type 1 diabetes from genes?

A 
identical twin - 30-50% risk
both parents - 30% 
non-identical twin - 10%
sibling - 8%
father - 6%
mother - 1%
22
Q

what are type 1 diabetics more likely to develop?

A

another autoimmune disease?

e.g. coeliac

23
Q

defence mechanisms against hypoglycaemia?

A 
increase in - 
glucagon
cortisol
catecholamines 
GH
24
Q

what can increase in glucagon be due to when not diabetes?

A

stress

25
Q

symptoms of type 1?

A 
Thirst
Tiredness
Polyuria / nocturia
Weight loss
Blurred vision
Abdominal pain – children
26
Q

examination findings in type 1?

A

Ketones on breath (+in blood)
Dehydration
May have increased respiratory rate, tachycardia, hypotension
Low grade infections, thrush / balanitis

27
Q

development of type 2 diabetes?

A

over course of years:
insulin resistance increases
->insulin release increases
->pancreas cannot keep up secretion to overcome resistance

28
Q

genetics of type 2 diabetes?

A 
Identical twin: 90-100%
One parent: 15%
Both parents: 75%
Sibling: 10%
Non-identical twin: 10%
29
Q

describe 3 results of insulin and type 2?

A

altered lipolysis (adipose)
increased GLC production (liver)
reduced GLC uptake (muscle)

30
Q

symptoms type 2?

A

often asymptomatic

Thirst
Tiredness
Polyuria / nocturia
Sometimes weight loss
Blurred vision
31
Q

signs of type 2?

A

NOT ketotic
Usually overweight but not always
Low grade infections, thrush
/ balanitis

32
Q

screening for diabetes in asymptomatic populations?

A 
aged 25-39 people of non-white ethnicities 
NOT pregnant women 
of the following conditions:
CVD
hypertension
obesity
stroke
polycystic ovary syndrome
a history of gestational  diabetes
mental health problems
33
Q

MODY?

A

monogenetic diabetes, an autosomal dominant condition - will appear in FAMILY history
single geen defect impaired beta-cell function

34
Q

MODY - types of mutations?

A

1) glucokinase mutations

2) transcription factor mutations

35
Q

glucokinase mutations - presentation?

A

Onset at birth

Stable hyperglycaemia Diet treatment Complications rare

36
Q

transcription factor mutations - presentation?

A

(HNF-1a HNF-1B HNF-4a
Adolescence/young adult onset
Progressive hyperglycaemia 1/3 diet, 1/3 OHA, 1/3 Insulin Complications frequent

37
Q

gestational diabetes?

A

Increasing insulin resistance in pregnancy

mothers don’t have diabetes @ start of pregnancy, but do so @ the end

38
Q

when is gestational diabetes most common?

A

if mother is inactive and overweight

39
Q

when does gestational diabetes develop?

A

2nd/3rd trimester

40
Q

what neonatal problems arise due to gestational diabetes?

A

macrosomia/ resp. distress/ HYPOglycaemia

41
Q

causes of 2y diabetes?

A

Alcohol and Gallstones are v common causes, also -

1) diseases of exocrine pancreas -
Chronic pancreatitis
Haemochromatosis
Cystic fibrosis

2) endocrine disorders -
Acromegaly
Cushing’s syndrome

3) drug-induced -
steroids

Endocrinology (21 decks)

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