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Flashcards in Diabetes Deck (133):
1

What is diabetic ketoacidosis?

An acute metabolic complication of diabetes characterised by hyperglycaemia, hyperketonemia and metabolic acidosis
Diabetic Ketoacidosis (DKA) is a disordered metabolic state that usually occurs in the context of an absolute or relative insulin deficiency accompanied by an increase in the counter-regulatory hormones i.e. glucagon, adrenaline, cortisol and growth hormone

2

Specific Symptoms of DKA

Polydipsia
Polyuria
Kussmaul breathing

Other Symptoms:
Nausea
Vomitting
Abdominal pain
Poor appetite
Tiredness
Weakness
Coma
Cerebral Oedema
Thrombotic Events
Death

3

Three characteristics of DKA?

Hyperglycaemia
Hyperketonemia
Metabolic acidosis

4

Counter regulatory hormones that increase glucose production?

Glucagon
Cortisol
Catecholamines

5

Most common causes of DKA?

Not taking medication
Infection
Alcohol abuse

6

What does adrenaline do?

Stimulates glucagon release and lipolysis, increasing fatty acids but not ketones

7

Cortisol and gluoneogenesis?

Cortisol stimulates gluconeogenesis in the liver from amino acids, lactate, glycerol and propionate

8

Which hormone stimulates gluconeogenesis from amino acids, lactate, glycerol and propionate?

Cortisol

9

Growth hormone, glucose and lipolysis?

GH reduces hepatic uptake of glucose
GH stimulates lipolysis

10

pH and bicarbonate levels in DKA?

pH <15mmol/l

11

Why would you check blood gases in DKA?

To look at H+ and bicarbonate levels

12

Why would you check urea and electrolytes in DKA?

Indication of dehydration (urea, creatinine)
Individual ion and anion levels
Indication of hyperkalaemia

13

What would urine show in diabetic ketoacidosis?

Low pH (<7.30)
Glucose
Ketones

14

What is a common trigger for illness in a person with diabetes?

Urinary infection

15

Three main ketone bodies?

Acetone
Acetoacetate
Beta hydroxybutyrate
(all of these, especially beta hydroxybutyrate will make the patient feel v. sick. This is important to realise as if the patient is sick then this will make their fluid and electrolyte loss even worse)

16

Why is alcohol of significance in DKA?

It gives the person the fruity breath smell

17

What will blood gases show in patient with Kussmaul breathing?

Low partial pressure of CO2
Low bicarbonate
High oxygen saturation (99-100% unless patient has pathologies that prevents this, e.g. COPD)

18

What would hyponatremia suggest in a patient with DKA?

That they have been vomitting
(lose sodium when they vomit, also lose through urine due to osmotic diuresis caused by hyperglycemia)

19

What causes dehydration in DKA?

Dehydration is caused by volume depletion from 2 main causes:
1) Renal loss due to the osmotic diuresis caused by hyperglycemia
2) Fluid loss from vomitting caused by the ketosis

20

Specific DKA symptoms

Polyuria
Polydipsia
Kussmaul breathing

21

General symptoms of DKA

Vomitting
Nausea
Abdominal Pain
Weakness
Tiredness
Coma
Cerebral oedema
Thrombotic events

22

Immediate effects of low insulin

Hyperglycemia
Increased hepatic gluconeogenesis
Increased levels of chatecholamines

23

Best way to treat CVD risk in type 2 diabetes?

Statins/anti-hypertensives
(insulin resistance -> macrovascular complications -> CVD risk etc -> statins/ anti-hypertensives )
(beta cell dysfunction -> hyperglycemia -> MICROvascular complications -> treat with intensive glucose control)

24

What is diabetes mellitus?

Diabetes mellitus is a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both.

25

Drugs which can cause diabetes

High dose corticosteroids (glucocoritcoids), beta-blockers and diuretics
Medications such as anti-pyscotics can also increase risk

26

Infection that could cause diabetes

Cytomegaolvirus

27

How is T1DM characterised?

By the presence of anti-GAD/anti-islet antibodies
T2DM is a diagnosis of exclusion

28

Useful discriminatory tests used to diagnose between T1DM and T2DM?

-Anti-GAD and anti-islet antibodies
-Ketones
-C peptide (plasma)

29

Syptoms of Cushings

Obesity - with fat around the main body area (trunk) rather than the arms and legs. The arms and legs can become quite thin compared with the obese body.
Facial puffiness, and the face often looks redder than usual.
Diabetes.
Facial hair in women.
High blood pressure.
Muscle weakness. In particular a proximal muscle weakness. The proximal muscles are the ones in your arms and legs nearest to the body. So, the muscles around the thigh, pelvis, shoulders and upper arms are the proximal muscles.
Thin skin which bruises easily.
Purple/pink stretch marks (striae) may appear - similar to those seen on some pregnant women.
Tiredness.
Aches and pains - particularly backache.
Mood swings - such as being more irritable, depressed, or anxious than usual.
Lack of sex drive (libido).
Periods may become irregular, or stop, in women.
Osteoporosis ('brittle bones'). You may fracture a bone more easily than usual.
Oedema ('water retention') around the ankles.
Excess thirst.
Increased susceptibility to infections.
Affected children tend to be obese, but grow slowly so are short for their age.

30

Name an alpha glucosidase inhibitor

Acarbose
-slows absorption of starchy foods from the intestine

31

SIGN guidance for cholesterol medication for diabetes?

Simvastatin 40mg
Atorvastatin 10mg

32

Blood pressure target for diabetics

130/80

33

HbA1c target for diabetics

<7.5%

34

Is low dose aspirin recommended for diabetes?

No

35

Commencing insulin therapy

Once daily bedtime NPH insulin should be used when adding insulin to metformin and/or sulphonylurea therapy. Basal insulin analogues should be considered if there are concerns regarding hypoglycaemia risk. (Grade A)

When commencing insulin therapy, bedtime basal insulin should be initiated and the dose titrated against morning (fasting) glucose. If the HbA1c level does not reach target then addition of prandial insulin should be considered. (Grade A)

Soluble human insulin or rapid-acting insulin analogues can be used when intensifying insulin regimens to improve or maintain glycaemic control. (Grade A)

36

Metabolic acidosis

Arterial blood pH <22mol/L

37

Rapid acting insulins

e.g. Humalog* (insulin lispro), NovoRapid, Apidra

38

Short acting insulin (soluble/regular)

e.g., Humulin S (Human insulin), Actrapid, Insuman Rapid

39

Intermediate acting (isophane)

e.g. Insulatard, Humulin I (Isophane human), Insuman Basal

40

Long-acting analogue

e.g. Lantus or Levemir

41

Rapid acting analogue-intermediate analogue

e.g. Humalog Mix25 / Mix50 or NovoMix30

42

Short acting-intermediate mixture

e.g. Humulin M3,
Insuman Comb 15, 25, 50

43

Another name for aspart?

NovoRapid

44

Another name for lispro?

Humalog

45

Another name for Glulisine?

Aphidra

46

What type of insulin is in an insulin pump?

Short acting

47

Pancreatic insulin secretion vs Insulin Pump

Pancreatic insulin secretion:
-directly into blood stream
-rapidly prevents post-meal hyperglycaemic spike
-rapidly cleared
Insulin injection or pump:
- into subcutaneous tissue
-peak too slow to prevent post-meal hyperglycaemic spike
-slow clearance

48

Issues with inhaled insulin?

-Non-linear dosing
-Cost
-Risk of lung cancer

49

Issues with oral insulin

Cost
Variable absorption
Effects of concurrent diet and illness
Only pre-prandial

50

Smart Insulin

Smart Insulin works via competitive binding:
insulin, attached to a sugar group, binds with a sugar-binding molecule in solution.
When glucose in the body is high, it competes with insulin to bind to the sugar-binding molecules, displacing insulin and releasing it into the bloodstream as needed

51

Anti-CD3 monoclonal antibody

Treatment with the monoclonal antibody against C3 improves insulin production

52

What is a kidney-pancreas transplantation?

A kidney-pancreas transplant is an operation to place both a kidney and a pancreas — at the same time — into someone who has kidney failure related to type 1 diabete

53

Rapid acting vs Short Acting Insulin

Rapid Acting Insulin:
-onset of action 10-15 mins
-Peak action 60-90 mins
-Duration of action 4-5 hours
Short Acting Insulin
-onset of action 30-60 mins
-Peak of action 2-4 hours
-duration of action 5-8 hours

54

The 2 components of advanced carbohydrate counting?

1) insulin to carbohydrate ratio
2) Insulin sensitivity factor/correction factor

55

Islet amyloid is a pathogenic feature of which condition?

Type 2 diabetes
Islet amyloid deposition is a pathogenic feature of type 2 diabetes, and these deposits contain the unique amyloidogenic peptide islet amyloid polypeptide.

56

HLA association and T1DM?

HLA genes represent ~50% risk of T1DM

57

Highest risk genotype for T1DM

DR3-DQ2 / DR4-DQ8
95% of patients diagnosed under 30 have one or both of those genotypes

58

Islet auto-antibodies

IA-2 (tyrosine phosphatase islet antigen)
IAA (islet auto-antibodies)
GAD65 (glutamic acid decarboxylase)
ZnT8 (zinc transporter 8)

59

Islet cell antibodies to really look out for because the lecturer highlighted them

GAD65
IA-2

60

Features of clinical T1DM that were highlighted in red in the lecture?

Raised glucose
Ketones

61

Enuresis

Bed wetting

62

Classic T1DM presenting triad?

Polyuria (enuresis in children)
Polydipsia
Weight loss

63

When might hospital management be needed for initial treatment of T1DM?

-DKA
-Significant ketonemia
-Severe vomitting
-Under 2 years old
-emotional/social needs
-live a long way from the hospital

64

HbA1c target level for T1DM children?

<7.5%

65

Annual review assessment for T1DM esp. children

Weight
Blood pressure
Bloods: HbA1c, lipids, renal function
Retinal Screening
Foot risk assessment

66

Conditions that can lead to secondary diabetes

Cystic fibrosis
Hemochromatosis
Chronic pancreatitis
Polycystic ovary syndrome (PCOS)
Cushing's syndrome
Pancreatic cancer
Glucagonoma
Pancreatectomy

67

Drug induced Diabetes

Corticosteroids
Thiazide diuretics
Beta-blockers
Antipsychotics (e.g. Phenytoin)
Statins

68

If children are diagnosed with diabetes <6 months, are they more likely to have monogenic or T1DM?

Monogenic :P

69

Antibodies found in LADA?

GAD
ICA (islet cell antibodies)

70

Which CF gene mutations are more severe and therefore give a greater chance of developing diabetes?

∆508
Diabetes common
>25% at 20 years
Usually found in ‘severe’ mutations, i.e. ∆508
Prone to complications
Insulin therapy preferred
Screening with OGTT from age 10 years recommended

71

What type of therapy is preferred for CF diabetic patients?

Insulin

72

What type of screening should you give CF children to check for diabetes?

OGTT from age ten years recommended

73

Are patients with CF and diabetes prone to complications?

Yes

74

DIDMOAD/Wolfram

Diabetes Insipidus
Diabetes Mellitus
Optic Atrophy
Deafness
Renal Problems
Neurological Problems
Chronic Fatigue
Other features of Wolfram Syndrome include fertility problems and gastrointestinal problems causing constipation or diarrhoea

75

Chronic Fatigue and Wolfram/DIDMOAD

Patients with wolfram have progressively declining physical stamina
They will need increasing amounts of sleep

76

Renal problems in Wolfram/DIDMOAD?

Bed wetting
Increased frequency of urination
Loss of bladder control
You may be able to treat the symptoms of diabetes in Wolfram/DIDMOAD but these renal problems will still occur because the problem itself is to do with the renal tract

77

Neurological problems in DIDMOAD/Wolfram

Loss of balance
Sudden muscle jerks
Depression (25% will have mental health problems at some point)
LOSS OF TASTE AND SMELL
BREATHING PROBLEMS
DEPRESSION

78

Deafness in Wolfram/DIDMOAD

May have trouble hearing high pitched sounds
May have trouble hearing in a crowd
25% will need a hearing aid

79

Antibodies in MODY?

Negative

80

Autoimmune conditions associated with diabetes

Common:
-Thyroid disease
-Coeliac
-Addisons
-Pernicious Anaemia
-IgA deficiency
Rare and Very Rare:
-Auto-immune polyglandular syndromes [Type 1 and Type 2]
-AIRE mutations
-IPEX syndrome

81

Albumin and calcium levels in coeliac?

Low

82

What is diabetic ketoacidosis?

Diabetic Ketoacidosis (DKA) is a disordered metabolic state that usually occurs in the context of an absolute or relative insulin deficiency accompanied by an increase in the counter-regulatory hormones i.e. glucagon, adrenaline, cortisol and growth hormone

83

Diabetic ketoacidosis diagnosis

Ketonemia > 3mmol/L (or significant ketonuria >2+ on standard urine stick)
Blood glucose >11mmol/L or known diabetes (nb. euglycaemic DKA)
Bicarbonate <7.3

84

WBC and DKA?

WBC median count around 25
Does not always infer infection
Stress effect of acidosis on bone marrow

85

Amylase in DKA

Amylase very frequently raised, does not necessarily indicate pancreatitis
Can be salivary in origin

86

Normal ketone levels

<0.6mmol/L

87

What does blood ketone testing measure?

Beta hydroxybutyrate

88

What does urine ketone testing measure?

Aceto acetate
-Indicates levels of ketones from 2-4 hours earlier
-Ketonuria persists after clinical improvement due to mobilisation of ketones from fat tissue

89

Why does ketonuria persist after clinical improvement?

Ketonuria persists after clinical improvement due to mobilisation of ketones from fat tissues

90

When should you consider hospital admission for DKA?

Unable to tolerate oral fluids
Persistent vomiting
Persistent hyperglycaemia
Persistent positive/increasing levels of ketones
Abdominal pain / breathlessness

91

Where does lactate come from?

Red blood cells
Skeletal muscle
Brain
Renal medulla

92

Lactic acidosis: classification

Type A:
Associated with tissue hypoxaemia:
-Infarcted tissue, eg ischaemic bowel
-Cardiogenic shock
-Hypovolaemic shock (Sepsis [endotoxic shock] , Haemorrhage)

Type B:
May occur in Liver disease
-Associated with drug therapy, eg Metformin
-Associated with Diabetes
-10% of cases of DKA associated with lactate >5 mmol/L.
-With Metformin usually in severe illness states or renal failure
-Also consider rare inherited metabolic conditions if well and non-diabetic

93

Type A lactic acidosis

Associated with tissue hypoxaemia:
-Infacted tissue
-Cardiogenic shock
-Hypovolaemic shock: sepsis, haemorrhage

94

Type B lactic acidosis

-May occur in liver disease
-May be caused by drug therapy e.g. Metformin
-Associated with diabetes
-10% of cases of DKA are associated with lactate >5mmol/L
-With metformin, usually in severe illness states or renal failure
-Also, consider RARE, INHERITED CONDITIONS if well and non-diabetic

95

Lactic acidosis in Diabetes

High ion gap yet low ketone level
Exclude other causes of high ion gap
End product of anaerobic metabolism of glucose
Lactate comes from red cells, skeletal muscle, brain and renal medulla
Clearance requires hepatic uptake and aerobic conversion to pyruvate then glucose.

96

Clinical signs of lactic acidosis

Hyperventilation
Confusion
Stupor/Coma if severe

97

Lab findings of lactic acidosis

Reduced bicarbonate
Raised anion gap [(Na+ + K+) – (HCO3 + Cl-)]
Other causes: uraemia, alcohol, ethylene glycol, methanol, renal tubular acidosis, salicylate or paraldehyde poisoning.
Glucose variable – often raised
Absence of ketonaemia
Raised phosphate

98

Causes of a high anion gap

Lactic acidosis, uraemia, alcohol, ethylene glycol, methanol, renal tubular acidosis, salicylate or paraldehyde poisoning

99

Phosphate levels in lactic acidosis

Raised

100

How to calculate anion gap?

(Na+ & K+) - (HCO3 & Cl-)

101

Is there ketonemia present in lactic acidosis?

No it is absent

102

Bicarbonate in lactic acidosis

Lowered

103

Treatment of lactic acidosis

Underlying condition:
-Fluids
-Antibiotics
Withdraw offending medication:
-Usually medication

104

Renal function in HHS?

Significant renal impairment

105

How to calculate osmolality

2x[Na + K) + Urea + Glucose

106

Normal Osmolality

285-295

107

Medication that can cause HHS?

Diuretics and steroids

108

Kind of usual age and type of person who would suffer HHS?

'Older' type 2

109

LMWH and HHS?

LMWH for all unless contraindicated

110

Which type of acidosis is associated with Diabetes?

Type B
Diabetes associated with type B lactic acidosis
-10% of DKA cases associated with lactate >5mmol/L
-with metformin usually in severe illness or renal failure

111

Where does lactate come from lol

Red blood cells
Skeletal muscle
Brain
Renal medulla

112

Lab findings of lactic acidosis

Reduced bicarbonate
Raised anion gap [(Na+ + K+) – (HCO3 + Cl-)]
(Other causes: uraemia, alcohol, ethylene glycol, methanol, renal tubular acidosis, salicylate or paraldehyde poisoning.)
Glucose variable – often raised
Absence of ketonaemia
Raised phosphate

113

Biochemistry of HHS

Higher glucose than in DKA
Median around 60
Significant renal impairment
Sodium often raised on admission
Significant elevation of osmolality – around 400
Osmolality=2x[Na+K] + Urea + Glucose
2 [145+5] + 30 + 65 = 395 [Normal 285 to 295]
Less ketonaemic/acidotic as compared to DKA

114

Cause of HHS?

STEROIDS/DIURETICS
Fizzy drinks
Under diagnosed DM
Carbohydrate

115

Drugs which can cause HHS?

Diuretics, steroids

116

Anti-coagulant you should give when treating HHS and why?

LMWH
Complications more likely, screen for vascular event, e.g. silent MI, sepsis

117

Patients with HHS may develop lactic acidosis, why?

They may be on metformin with marked RENAL FAILURE/may be septic

118

Hypothyroidism and effects of glucose?

Prolongs effects of insulin

119

Renal impairment and effects of insulin

Prolongs effects of insulin

120

Liver failure and effects of insulin

Prolongs effects of insulin

121

Alcohol and gluconeogensis

Alcohol suppression of gluconeogenesis

122

Growth hormone and glucose

Raises blood glucose level
-GH reduces hepatic uptake of glucose from blood
-GH stimulated lipolysis

123

What is the limiting factor of good glycemic control?

Hypoglycemia

124

Amyotrophy and possible sypmtom

Progressive muscle weakness
-muscle pain is also a symptom

125

Types of neuropathy?

Peripheral
Autonomic
Focal
Proximal

126

Autonomic neuropathy?

i.e. change in bowel habit, bladder function, sexual response, blood pressure, heart rate, hypoglycaemic unawareness, sweating

127

changes in bowel, bladder function, sexual response, sweating, heart rate, blood pressure, hypoglycaemic unawareness are what type of neuropathy?

Autonomic

128

Give an example of proximal neuropathy?

e.g.pain in the thighs, hips or buttocks leading to weakness in the legs (Amyotrophy)

129

Focal neuropathy?

e.g. sudden weakness in one nerve or a group of nerves causing muscle weakness or pain e.g. carpal tunnel, ulnar mono neuropathy, foot drop, bells palsy, cranial nerve palsy

130

Neuropathy more likely in type 1 or type 2 diabetes?

Type 1

131

Complications of peripheral neuropathy?

Infections/ Ulcers
Deformities (hammertoes/ collapse of mid-foot)
Amputations- 50%of ampuations may be preventable

132

What are oxycodone and tramadol?

Opiods

133

Painful neuropathy treatment algorithm?

-simple analgesia (paracetemol)
-TCAs (amitryptiline -> small dose at night)
-Gabapentin
-Duloxitine 60mg / Pre Gabalin (50mg bd - 200mg)
-Stronger opiods (oxycodon+tramadol)
Topical Capsaicin Cream
Allodynia - may be helped by use of a plastic film