Diabetes mellitus clinical Flashcards

1
Q

Common symptoms of type 1/type 2 DM (7)

A
Polydipsia (excessive thirst)
Polyuria (excessive urinating)
Blurred vision
Weight loss (unexplained)
Fatigue
Thrush/genital itching
Increased vulnerability/recurrent infection
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2
Q

Diagnostic investigations of diabetes mellitus (4)

A

Fasting plasma glucose ≥ 7.0 mmol/l

Random plasma glucose ≥ 11.1 mmol/l

Oral glucose tolerance test 2hr after 75g oral glucose load ≥11.1 mmol/l

HbA1c ≥ 48 mmol/mol (type 2 only)

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3
Q

People with intermediate hyperglycaemia are at risk of what

A

future diabetes

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4
Q

If have the classic diabetes symptoms, how many diagnostic investigations needed

A

ONE LAB GLUCOSE

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5
Q

If no classic diabetes symptoms, how many/ what diagnostic investigations needed

A

TWO LAB GLUCOSE (e.g. random and fasting)

or

just HbA1c

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6
Q

What is HbA1c

A

Glycated haemoglobin

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7
Q

HbA1C gives an indication of BG levels over what time period

A

last 3 months

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8
Q

Does glucose reversibly or irreversibly bind to Hb

A

Irreversibly

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9
Q

When HbA1c can’t be used for diagnosis (6)

A

All children
If pregnant
Acutely ill
If have been on mediation that can cause rapid glucose rise <2 months
Acute pancreatic damage/ if had pancreatic surgery
Post-blood transfusion

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10
Q

Only hormone that lowers BG

A

Insulin

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11
Q

Summarise the factors which may contribute to beta cell damage and the eventual clinical presentation of type 1 DM (2)

A

Genetic factors
+
Environmental factors
-e.g. viral infection

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12
Q

What are ketones produced from + where

A

Free fatty acids

produced in liver

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13
Q

Symptoms (3)/signs (5) of DKA

A

Symptoms

  • Nausea
  • Vomiting
  • Abdo pain/tenderness

Signs:
Ketones in breath (acetone breath)
Tachypnoea/kussmaul breathing (rapid deep breathing)
Tachycardia
Hypotension
Dehydration (fluid depletion) –> dry mucous membranes, sunken eyes

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14
Q

In type 2 DM, what is wrong with the beta cells

A

Due to insulin resistance, glucose persists in blood so beta cells compensate for this by increasing insulin secretion

However beta cells become damaged by lipotoxicity and glucotoxicity and eventually can no longer compensate –> hyperglycaemia

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15
Q

Summarise what type 2 DM is a result of (2)

A

insulin resistance and subsequent B cell dysfunction

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16
Q

Which type of DM may present with no symptoms

A

2

17
Q

What sign of DM is present in type 1 but not type 2

A

Ketones in breath or urine

18
Q

Risk factors of type 2 DM (5)

A
Overweight
Family history of DM
>40yrs old
Gestational diabetes
Sedentary lifestyle/lack of exercise
19
Q

Other types of diabetes mellitus that are not type 1/2 (3)

A

Genetic syndrome
-maturity onset diabetes in the young (MODY)

Gestational diabetes

Secondary diabetes

20
Q

What is maturity onset diabetes in the young (MODY)

A

Single gene defect resulting in reduced insulin production

Most are due to mutations of transcription factor genes

21
Q

Maturity onset diabetes in the young (MODY) is a single gene defect of either … or … (2)

A

Transcription factor genes

  • HNF-1a
  • HNF-1b,
  • HNF-4a

Glucokinase gene

22
Q

Most common form of maturity onset diabetes in the young (MODY) is due to a single gene defect in what gene

A

HNF-1a (a transcription factor gene)

23
Q

How does maturity onset diabetes in the young (MODY) due to a glucokinase mutation present

  • normal function of glucokinase
  • how it presents
  • any treatment
A

Glucokinase helps the body to recognise how high the blood glucose level is so when it isn’t working properly, the body allows the level of blood glucose to be higher than it should be

typically only slightly higher than normal so don’t generally have symptoms

No medical treatment needed

24
Q

How does maturity onset diabetes in the young (MODY) due to a HNF-1a (transcription factor) present

  • age onset
  • pathology
  • any treatment
A

Usually in adolescence/ early 20s

Reduces insulin production by pancreas

Generally don’t need insulin therapy, but may take sulphonylureas

25
Q

Causes of secondary DM (4)

A

Drug induced, e.g. corticosteroids

Pancreatic destruction
-e.g. CF, chronic pancreatitis, pancreatectomy

Genetic syndromes
-e.g. Wolfram syndrome

Endocrine disorders
-e.g. Cushing’s syndrome, acromegaly, pheochromocytoma

26
Q

What is gestational diabetes

A

In females who are not diabetic

-hyperglycaemia during pregnancy due to insulin resistance to some extent

27
Q

What type DM is gestational diabetes more associated with

A

2

28
Q

When taking the family history of someone with possible DM, what should be asked (2)

A

If anyone has DM

If anyone has other autoimmune conditions, e.g. thyroid problems, IBD, rheumatoid arthritis

29
Q

Biochemical triad of DKA

A

Hyperglycaemia
Ketonaemia
Acidaemia

30
Q

Investigations of DKA (4)

A

Plasma glucose - high
ABG - test arterial pH
Urinalysis - for glucose and ketones
U and Es - low serum sodium, high serum potassium, high serum creatinine

31
Q

DKA is characterised by:

  • BG >
  • HCO3- <
  • pH
A

> 14mmol/l

<18mmol/l

<7.3

32
Q

Complications of DKA (5)

A

Hyper/hypokalaemia - due to excessive insulin

Hypoglycaemia - due to excessive insulin

Cerebral oedema - more in children

Arterial or venous thromboembolism

Acute respiratory distress syndrome (ARDS)
-treatment induced reduction in colloid osmotic pressure –> accumulation of water in lungs –> decreased lung compliance –> hypoxaemia

33
Q

The characteristic skin finding associated with type 2 is

A

acanthosis nigricans - due to increased insulin levels