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Endocrine > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What is the threshold for diabetes diagnosis on a fasting plasma glucose?

A

> /= 7mmol/L

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2
Q

What is the threshold for diabetes diagnosis, 2 hours following a glucose load?

A

> /= 11.1mmol/L

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3
Q

What is the HbA1c threshold which suggests a patient is diabetic?

A

> /= 48mmol/mol

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4
Q

How is the fasting glucose threshold needed to diagnose changed for gestational diabetes (i.e. in pregnant mothers)?

A

It is a lower threshold of >/= 5.6mmol/L.

This is due to the associated risk to the neonate being the point of reference (outwith pregnancy this is aimed at preventing the onset of retinopathy).

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5
Q

Which type of cells secrete insulin?

A

Pancreatic beta cells

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6
Q

What type of cells secrete glucagon?

A

Pancreatic alpha cells

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7
Q

What can C-peptide level measure, and why?

A

Endogenous insulin production

It is a component of an insulin precursor which is cleaved when insulin becomes active. Crucially, synthetic insulin does not leave the molecule when injected.

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8
Q

What are the two mechanisms by which insulin can become ineffective?

A

Issues with production
Development of resistance

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9
Q

What occurs in T1DM?

A

Autoimmune destruction of pancreatic beta cells, leading to an insufficiency (cannot produce insulin).

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10
Q

What age group is affected by T1DM?

A

Any age - often thought of as a disease of the young, but not always. It has an unknown trigger in those with a genetic predisposition.

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11
Q

What occurs in T2DM?

A

Predominately insulin resistance - can have a secretory issue too.

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12
Q

Is diabetes symptomatic?

A

No - symptoms appear in episodes of hypoglycaemia/hyperglycaemia.

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13
Q

What are the two types of emergency in diabetes

A

Diabetic ketoacidosis (DKA)
Hyperosmolar hyperglycaemic state (HHS)

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14
Q

What is HbA1c?

A

A blood test used to measure the amount of glycated haemoglobin within the circulation.

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15
Q

What are the three microvascular complications that may result in T1DM?

A

Retinopathy
Nephropathy
Neuropathy

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16
Q

In which individuals may HbA1c be less effective as a diagnostic tool?

A

Those with a high RBC turnover (e.g. haemolytic anaemia).

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17
Q

In those with T2DM, what should be the aim for HbA1c?

A

Keep below 53mmol/mol.

This reduces the risk of complications.

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18
Q

Is T2DM reversible?

A

Yes, if weight loss and diet alterations are made at the point of diagnosis, the patient may enter remission.

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19
Q

Are beta cells completely dysfunctional in T2DM?

A

No, they are just reduced in function - this may result in end-stage T2DM. At this point, insulin therapy may be required.

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20
Q

What sugar level is defined is hypoglycaemia?

A

A capillary glucose level of < 4mmol/L.

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21
Q

What is a normal blood ketone level?

A

0.0 - 0.6 mmol/L.

If any level above this suggests potential DKA.

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22
Q

What glucose and ketone levels would raise suspicion of DKA?

A

Ketones >/= 3.0mmol/L
Blood glucose >/= 14.ommol/L

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23
Q

What type of cells can be found in the Islets of Langerhans?

A

Alpha cells
Beta cells
Delta cells
PP cells

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24
Q

What is secreted by delta cells in the pancreas?

A

Somatostatin

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25
Q

What is secreted by PP cells in the pancreas?

A

Pancreatic polypeptide

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26
Q

What are the roles of somatostatin and pancreatic polypeptide?

A

To control the function of alpha and beta cells.

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27
Q

How does glucose enter the pancreatic beta cells?

A

GLUT2 transporters (come from areas of higher concentration to lower concentration).

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28
Q

Which enzymes phosphorylate glucose into G6P?

A

Glucokinase

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29
Q

Which form of T2DM medication stimulates insulin secretion, through mimicking ATP (preventing K+ channels opening in the beta cell membrane)?

A

Sulphonylureas

Examples include gliclazide, glipizide and glimepiride.

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30
Q

Are suplonylureas glucose-dependent?

A

No, as a result there is a risk of hypoglycaemia.

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31
Q

Are incretins glucose-dependent?

A

Yes

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32
Q

How is T1DM treated?

A

Exogenous insulin (as their body can no longer produce this themselves).

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33
Q

Alongside T1DM and T2DM, what other forms of diabetes exist?

A

Gestational diabetes
Maturity-onset diabetes of the young (MODY)
Neonatal diabetes
Latent autoimmune diabetes in adults (LADA)

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34
Q

Why do women develop gestational diabetes?

A

They already have declining beta cell function - hence they are likely to develop T2DM in the future.

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35
Q

How is gestational diabetes treated?

A

Largely lifestyle alterations will address the issue - some may need metformin treatment.

If sugars above 7mmol/mol on fasting then give insulin.

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36
Q

What is MODY?

A

A monogenic disease producing beta cell dysfunction. Will develop at an early age, with family history common.

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37
Q

What is neonatal diabetes?

A

A rare monogenic form of diabetes caused by issues in the glucose-sensing mechanism.

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38
Q

How does MODY differ from T1DM?

A

MODY patients still have a degree of beta cell function, thus can be treated with sulphonylureas.

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39
Q

What are the symptoms of DKA?

A

Vomiting
Dehydration
Raised HR
Acetone-smelling breathing

40
Q

Is DKA more likely in T1DM or T2DM?

A

T1DM

41
Q

Why do ketones accumulate in the absence of insulin?

A

In the absence of insulin, the body cannot utilise glucose as an energy source, so switches to lipolysis as an alternative energy source - a by-product of this process is ketone production.

42
Q

T2DM patients over 40yo should be prescribed which drug?

A

A statin

43
Q

Why is insulin needed in those with long-standing T2DM?

A

Beta cells have began to fail after years of compensatory overactivity.

44
Q

Should insulin be stopped if a T1DM patient is unwell?

A

No, as risk of DKA remains. This may be circumvented by titrating the dosage given appropriately.

Never stop insulin in T1DM patients.

45
Q

Where is glucose level monitored by a flash glucose sensor?

A

Interstitial fluid

46
Q

How does fat storage threshold help explain the relationship between obesity and insulin resistance?

A

When healthy body fat storage becomes full (i.e. subcutaneous tissue), it is then stored within the viscera.

The capacity of the subcutaneous tissue differs from individual to individual, thus obesity does not always produce T2DM.

47
Q

What should be measured in any patient with a blood glucose of >15mmol/L?

A

Blood ketones

48
Q

Are autoantibodies found in MODY?

A

No

49
Q

What are the 3 procedures that can be used to reduce weight?

A

Gastric bypass
Gastric band
Sleeve gastrectomy

50
Q

Which individuals are eligible for a weight reduction surgery?

A

BMI >40
BMI >35, plus an obesity-related comorbidity (e.g. T2DM)

51
Q

How should hypoglycaemia be treated?

A

15-20g of rapidly absorbable carbohydrates.

52
Q

What is the most common form of monogenic diabetes?

A

MODY

53
Q

When are infants diagnosed with T1DM?

A

Usually after 6 months of life.

If before this, it is called neonatal diabetes.

54
Q

What causes acanthosis nigricans?

A

Errors in insulin signalling - it is a direct result of insulin driven overgrowth of the epithelium.

55
Q

What pattern of inheritance is seen in MODY?

A

Autosomal dominant

56
Q

What is a characteristic description of MODY?

A

Non-insulin dependent diabetes in those under 25 years of age.

57
Q

What are the 2 most common MODY sub-types?

A

Those affecting glucokinase activity.

Those impacting on the action of transcription factors.

58
Q

How can MODY be identified?

A

Poor diabetic control despite taking exogenous insulin.

59
Q

What are the 3 microvascular complications of diabetes?

A

Retinopathy
Nephropathy
Neuropathy

60
Q

How often should diabetes patients be screened?

A

Yearly

Involves digital retinal screening, foot risk assessment, and urine albumin levels.

61
Q

What produces microvascular complications in diabetes?

A

Hyperglycaemia

Overworked mitochondria within cells means glycolysis goes into overdrive. A consequence is the build-up of waste products (e.g. ROS).

62
Q

What forms of eye disease are associated with diabetes?

A

Diabetic retinopathy
Diabetic macular oedema
Cataracts
Glaucoma

Also, be aware that acute hyperglycaemia may cause reversible visual blurring.

63
Q

What is optical coherence tomography (OCT) used to assess?

A

The amount of oedema on the retina.

64
Q

What are the characteristic signs of diabetic nephropathy?

A

Proteinuria, with scarring of the glomeruli.

65
Q

What is the most common cause of kidney failure?

A

Diabetes

66
Q

What tests should be performed to check for nephropathy in diabetic patients?

A

Urinary albumin
Serum creatinine

These should be checked at the point of diagnosis and then yearly thereafter.

67
Q

How should microalbuminuria/proteinuria be treated?

A

Give an ACE inhibitor - these are nephroprotective.

68
Q

What is the most common form of neuropathy?

A

Peripheral neuropathy

Results in the loss of pain/feeling in the hands/feet. Begins distally, spreading more proximally - numbness is an end-stage feature.

69
Q

What is a common focal neuropathy which can develop as a consequence of diabetes?

A

Carpal tunnel syndrome

70
Q

What is Charcot’s foot?

A

A destructive, inflammatory process that results in severe damage to the structure of the foot. Produces deformity.

71
Q

What are 2 potential consequences of autonomic neuropathy?

A

Gastroparesis
Postural hypotension

72
Q

What are the 4 types of neuropathy that can develop in diabetic patients?

A

Peripheral neuropathy
Proximal neuropathy
Focal neuropathy
Autonomic neuropathy

73
Q

What three autoantibodies, if present together, make the likelihood of developing T1DM >95%?

A

anti-GAD
IA-2
ZnT8

74
Q

Which form of diabetes is linked to amyloidosis of the pancreas?

A

T2DM

75
Q

Is HBA1c helpful in diagnosing T1DM?

A

No, as this will appear normal - it does not account for rapid onset. It may be used for management.

Remember that HBA1c is a measure over 3 months.

76
Q

What medication may cause euglycaemic ketonaemia?

A

SGLT2 Inhibitors

77
Q

What are the causes of death that can follow DKA?

A

Hypokalaemia
ARDS
Aspiration pneumonia (due to the unconscious state)
Cerebral oedema (usually in children)

78
Q

How does DKA present metabolically?

Think changes to - BM, Bicarb, Ketones, K+, Creatinine, Na+, Lactate, Am

A

Hyperglycaemia
Low bicarbonate (<15mmol/L - indicates acidosis)
High ketones
Raised serum K+ levels (will rapidly fall with insulin treatment - beware hypokalaemia)
Creatinine raised
Low Na+ levels
High lactate levels
High amylase levels (check patients for pancreatitis)
High WC count (a result of inflammation)

79
Q

Is hyperglycaemic hyperosmolar state (HHS) linked to ketosis?

A

No - it is a stress response to failing insulin production levels.

80
Q

How does HHS present metabolically?

A

Hyperglycaemia (will be very severe e.g. 30-50mmol/L)
No/Mild ketosis
Hypovolaemia
No acidosis
High osmolarity (>320mosmol/kg)

81
Q

How do you calculate osmolarity?

A

[2xNa+] + Urea + Glucose

82
Q

Is mortality rate greater in HHS or DKA?

A

HHS

83
Q

How is HHS treated?

A

Give LOTS of fluids - there is a deficit of 10-12L.

Beware this in the elderly and those with heart failure.

84
Q

How should high sodium be corrected?

A

Give saline.

85
Q

Why should HHS patients be given LMWH?

A

It is a hypercoagulable state.

86
Q

How does alcohol-induced ketoacidosis present?

A

DKA symptoms, but NO hypoglycaemia
History of alcohol abuse

87
Q

How is alcohol-induced ketoacidosis treated?

A

IV pabrinex
IV fluids
IV dextrose
IV anti-emetics

Some may also need insulin.

88
Q

Can normal diabetes treatment regimens be continued during pregnancy?

A

No, many (e.g. gliclazides) are contraindicated. Thus, insulin is often given during this time.

89
Q

What should diabetic mothers aim to do prior to conception?

A

Achieve good glycaemic control
Take 5mg of folic acid daily for 3 months prior to pregnancy

90
Q

What are common issues attached with GDM?

A

Macrosomia (birth weight>4kg)
Polyhydramnios (increase fluid, decreased baby size)
Intrauterine death

91
Q

What is the benefit of insulin resistance in obese patients?

A

Stops them adding more glucose to their already large stockpiles.

92
Q

What is the sole function of cytokines?

A

To bring about inflammation.

93
Q

What molecule is released from fat to inform body it is no longer hungry?

A

Leptin

Thus, orlistat can be given to prevent lipase action - this breaks down leptin.

If stopped, the patient will not feel hungry as leptin levels persist.

94
Q

What is the function of a gastric band?

A

A band at the top of the stomach that restricts the volume of food an individual can consume.

Will produce lots of weight loss, however, risks include slipping of the band. It could completely obstruct the passage of food.

95
Q

What is a vertical sleeve gastrectomy?

A

Removal of part of the stomach, restricting uptake.

It is preferred to a gastric band as it cannot slip.

96
Q

What is a gastric bypass?

A

When a small part of the stomach is connected to the jejunum, preventing a proportion of food intake being properly digested.

97
Q
A

Endocrine (11 decks)

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