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Endocrine > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What can cause insulin resistance

A

Obesity
T2DM
MASLD

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2
Q

What endocrinopathies can cause high blood glucose

A

Cushing’s syndrome
Acromegaly
Phaeochromocytoma
Glucagonoma

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3
Q

What can cause reduced insulin secretion

A

T1DM
MODY
Neonatal diabetes
Pancreatic disease
- pancreatitis, malignancy, CF, haemochromatosis

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4
Q

Summarise diabetes/ high blood glucose aetiology

A

Insulin resistance
- T2DM
- MASLD
- Obesity
- MODY

Endocrinopathies
- Cushing’s syndrome
- Acromegaly
- Pheochromocytoma
- Glucagonoma

Reduced insulin secretion
- T1DM
- Neonatal diabetes
- MODY

Pancreatic disease
- pancreatitis
- CF
- Haemochromatosis
- malignancy

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5
Q

How is the blood glucose threshold for diabetes defined

A

Risk of retinopathy
Except in gestational - risk to foetus

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6
Q

What can be used to measure endogenous insulin secretion

A

C peptide

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7
Q

What is HbA1c

A
  • Haemoglobin exposed to glucose becomes glycated
  • The amount of glycation is proportional to the glucose
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8
Q

Why is HbA1c useful

A

As a RBC survives for ~90 days the HbA1 gives a measure of glucose exposure over the last 90 days - used in diagnosis and monitoring

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9
Q

In what conditions might HbA1c not be as useful

A

HbA1c should be used with caution in conditions of increased or reduced RBC turnover e.g. haemolytic anaemia

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10
Q

Diabetes diagnosis investigations

A

If symptomatic => At least one test on one occasion must be positive

If asymptomatic => At least one test on two occasions must be positive

Either:
- Fasting glucose >/= 7mmol/L OR
- Random glucose >/= 11.1 OR
- 2 hr glucose in OGTT >/= 11.1 OR
- HbA1c >/= 48 mmol/mol

NOTE: HbA1c can’t be used in T1DM or gestational diabetes

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11
Q

Diabetes clinical features

A

Polydipsia, polyuria & polyphagia (3 P’s classic triad) +/-

Tiny (weight loss), Tired, Terrible (blurred) vision, (genital) Thursh (4T’s)

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12
Q

What is T1DM

A

Absolute insulin deficiency due to T cell mediated autoimmune destruction of pancreatic beta cells

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13
Q

What HLA genotype is associated with T1DM

A

DR3-DQ2 or DR4-DQ8

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14
Q

If you were to biopsy the pancreatic beta cells of a patient with T1DM what would you find

A

Insulitis visable on β-cell biopsy with lymphocytic infiltrate

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15
Q

T1DM diagnosis

A
  • General diabetes diagnostic criteria
  • Can measure GAD/IA2 antibodies if in doubt
  • C peptide will be low after ~3 months AFTER initial diagnosis (not on diagnosis)
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16
Q

T1DM treatment

A

Basal-bolus insulin regime (MDI or CSII)
Carb counting
Pre exercising glucose measuring
Sick day rules
If severe episodic hypoglycaemia => islet transplantation

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17
Q

T1DM sick day rules

A

S - sugar checks around every 4 hrs
I - (continue normal) insulin
C - carbs in small portions, keep hydrated
K - ketone check & escalate

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18
Q

What causes insulin resistance in skeletal muscle cells in obesity

A

Impairment of insulin signalling!

  • FFAs decreases insulin receptor tyrosine kinase
  • This decreases the activation of downstream proteins
  • This eventually results in GLUT4 not being translocated to the skeletal muscle membrane
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19
Q

What causes insulin resistance in adipose tissue in obesity

A

Obesity-induced inflammation as adipose tissue secretes pro-inflammatory cytokines e.g. TNF-⍺

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20
Q

What causes insulin resistance in hepatic tissue in obesity

A

In the liver pathway selective insulin resistance occurs where insulin binding still causes lipogenesis but not glucose uptake & metabolism

This is because of the increased FFAs in patients with obesity that need to be removed from the bloodstream & converted to VLDL in the liver by lipogenesis

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21
Q

What are two genetic conditions that cause insulin resistance (by acting on insulin receptors

A

Leprechaunism (Donohue syndrome)
Rabson Medenhall syndrome

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22
Q

What is the gold standard technique to investigate insulin sensitivity/resistance

A

hyperinsulinemic-euglycemic clamp

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23
Q

What is T2DM

A

Relative insulin deficiency
Combination of insulin resistance & less severe deficiency

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24
Q

T2DM risk factors

A
  • Afro-carribean/African/south Asian ethnicity
  • Obesity
  • Age
  • High fat diet, fried foods, saturated foods, sugary drinks
  • Physical inactivity
25
Q

Why does not everyone with obesity develop diabetes

A

Insulin resistance occurs when fat can no longer be stored in subcutanous adipose tissue causing spill over of FFA to the viscera

People with ‘healthy’ obesity are able to safely store lots of fat, whereas others have a low fat storage threshold & go on to develop T2DM

26
Q

Briefly summarise insulin resistance

A

Central obesity→ increasedplasma levels of FFAa→ impaired insulin-dependentglucose uptake into hepatocytes, myocytes and adipocytes

Increasedtyrosine kinaseactivity in liver, fat andskeletal musclecells→ decreased activation of downstream proteins → decreasedexpression of GLUTchannels→ decreasedcellular glucose uptake

27
Q

Describe how insulin secretion typically changes in T2DM

A
  • 1st - compensatory insulin hypersecretion
  • 2nd - loss of 1st phase in normal biphase insulin secretion
  • Hyperglycaemia & high FFAs in blood stream persist
  • 3rd - damage to beta cells due to lipotoxicity & glucotoxicity causes reduced insulin secretion
28
Q

What is the first sign of reduced insulin secretion in T1DM

A

loss of the first phase of the normal biphasic insulin secretion

29
Q

What happens to glucagon secretion in T2DM

A

Increased

30
Q

What happens to incretin effect in T2DM

A

Decreased

31
Q

T2DM clinical presentation

A
  • Gradual onset
  • May be asymptomatic
  • Diabetic complications may be the first sign
  • Acanthosis nigricans (severe insulin resistance)
32
Q

What clinical feature of severe insulin resistance can be seen on a patients skin

A

Acanthosis nigricans

33
Q

Why can hyperglycaemia cause recurrent infections

A

Hyperglycaemia weakens the immune system

34
Q

T2DM investigations

A

Usual diabetic investigations

35
Q

T2DM management

A

Weight loss (if BMI 30)! If lose >10% can cause remission

First line - Metformin & lifestyle
First line if have atherosclerotic CVD - Metformin & GLP-1RA
First line if have HF or CKD - Metformin & SGLT2i

Other drugs - DPP4i, SUs, TZDs,

36
Q

What is MODY & what genetic inheritance pattern is it

A

Mature-onset diabetes of the young
Autosomal dominant

37
Q

What would make you think of MODY

A

Early onset diabetes (<25yrs)
& glucose sensitivity defect
+/- insulin secretion defect

38
Q

What two mutations are most commonly associated with MODY

A

Glucokinase mutation
Transcription factor mutation

39
Q

MODY Pathophysiology

A

Glucokinase mutation - increased insulin release threshold
Transcription factor mutation - abnormal beta cell function

40
Q

MODY time of onset

A

Glucokinase mutation - At birth, stable hyperglycaemia
Transcription factor mutation - In adolescence, progressive hyperglycaemia

41
Q

MODY investigation findings

A

Glucokinase mutation
- Abnormal fasting glucose
- Normal OGTT

Transcription factor mutation
- Normal fasting glucose
- Abnormal OGTT

42
Q

MODY treatment

A

Glucokinase mutation - diet alone
Transcription factor mutation - Diet & SU or insulin

43
Q

MODY risk of microvascular complications

A

Glucokinase mutation - no microvascular complications
Transcription factor mutation - yes

44
Q

What is neonatal diabetes

A

Rare monogenic form of diabetes
Defect in glucose sensing mechanisms e.g. Katp channels

45
Q

Neonatal diabetes clinical features

A

Diagnosis @ <6 months age
Polydipsia, polyuria, dehydration
DKA

46
Q

Neonatal diabetes investigations

A

Blood glucose

47
Q

Neonatal diabetes treatment

A

SUs

48
Q

Gestational diabetes pathophysiology

A

Placental progesterones and hPL produce insulin resistance in the mother. This allows more nutrients to be diverted to the foetus

If the mother is insulin resistant before pregnancy, developing further insulin resistance will raise blood glucose too high and result in gestational diabetes

49
Q

Gestational diabetes risks to foetus

A

Macrosomia
Polyhydramnios
Interuterine death
Neonatal hypoglycaemia

50
Q

Why does gestational diabetes cause macrosomia

A

Maternal hyperglycaemia => foetal hyperglycaemia =>
Foetal hyperinsulinaemia =>
Excessive growth (insulin is a major growth factor)

51
Q

Why does gestational diabetes risk neonatal hypoglycaemia

A
  • Foetal hyperglycaemia => foetal hyperinsulinaemia
  • Hyperinsulinaemia takes a while to down regulate & so risks hypoglycaemia in the newborn
52
Q

Gestational diabetes investigations

A
  • fasting blood glucose > 5.6mmol/l
  • 2hr OGTT > 7.8 mol/l
53
Q

Gestational diabetes treatment

A

Lifestyle & Metformin
(& possibly insulin)

54
Q

Gestational diabetes after birth management

A
  • 6 wk post natal fasting blood glucose or OGTT
  • If the diabetes persists, patient has T2DM
55
Q

General risk to foetus & neonates with diabetes

A
  • Congenital malformation
  • Prematurity
  • Intra-uterine growth retardation (IUGR)
  • Respiratory distress due to immature lungs
  • Hypoglyaemia/hypocalcaemia → fits
  • CNS defects - anencephaly, spina bifida
  • Skeletal abnormalities - caudal regression syndrome
  • Genital and GI abnormalities - ureteric duplications
56
Q

T1DM & T2DM treatment during pregnancy

A
  • Folic acid 5mg 3 months prior to conception
  • Monitor HbA1c, BP, glucose, eyes

BP meds
- Avoid ACEi & statins
- Use labetolol, nifedipine or methyldopa for BP
- Start aspirin at 12 wks (to reduce risk hypertension)

Glucose meds
- T1DM - insulin (may have to increase dose)
- T2DM - Metformin & insulin later on

57
Q

Diabetic treatment during labour

A

IV insulin and IV dextrose

58
Q

What 2 diabetic drugs are safe in pregnancy

A

Insulin & Metformin

Endocrine (22 decks)

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