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Endocrinology > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What is diabetic ketoacidosis?

A 
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
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2
Q

Specific Symptoms of DKA

A

Polydipsia
Polyuria
Kussmaul breathing

Other Symptoms:
Nausea
Vomitting
Abdominal pain
Poor appetite
Tiredness
Weakness
Coma
Cerebral Oedema
Thrombotic Events
Death
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3
Q

Three characteristics of DKA?

A

Hyperglycaemia
Hyperketonemia
Metabolic acidosis

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4
Q

Counter regulatory hormones that increase glucose production?

A

Glucagon
Cortisol
Catecholamines

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5
Q

Most common causes of DKA?

A

Not taking medication
Infection
Alcohol abuse

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6
Q

What does adrenaline do?

A

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

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7
Q

Cortisol and gluoneogenesis?

A

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

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8
Q

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

A

Cortisol

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9
Q

Growth hormone, glucose and lipolysis?

A

GH reduces hepatic uptake of glucose

GH stimulates lipolysis

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10
Q

pH and bicarbonate levels in DKA?

A

pH <15mmol/l

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11
Q

Why would you check blood gases in DKA?

A

To look at H+ and bicarbonate levels

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12
Q

Why would you check urea and electrolytes in DKA?

A

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

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13
Q

What would urine show in diabetic ketoacidosis?

A

Low pH (<7.30)
Glucose
Ketones

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14
Q

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

A

Urinary infection

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15
Q

Three main ketone bodies?

A

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)

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16
Q

Why is alcohol of significance in DKA?

A

It gives the person the fruity breath smell

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17
Q

What will blood gases show in patient with Kussmaul breathing?

A

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

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18
Q

What would hyponatremia suggest in a patient with DKA?

A

That they have been vomitting

lose sodium when they vomit, also lose through urine due to osmotic diuresis caused by hyperglycemia

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19
Q

What causes dehydration in DKA?

A

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

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20
Q

Specific DKA symptoms

A

Polyuria
Polydipsia
Kussmaul breathing

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21
Q

General symptoms of DKA

A 
Vomitting
Nausea
Abdominal Pain
Weakness
Tiredness
Coma
Cerebral oedema
Thrombotic events
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22
Q

Immediate effects of low insulin

A

Hyperglycemia
Increased hepatic gluconeogenesis
Increased levels of chatecholamines

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23
Q

Best way to treat CVD risk in type 2 diabetes?

A

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

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24
Q

What is diabetes mellitus?

A

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

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25
Q

Drugs which can cause diabetes

A

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

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26
Q

Infection that could cause diabetes

A

Cytomegaolvirus

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27
Q

How is T1DM characterised?

A

By the presence of anti-GAD/anti-islet antibodies

T2DM is a diagnosis of exclusion

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28
Q

Useful discriminatory tests used to diagnose between T1DM and T2DM?

A
  • Anti-GAD and anti-islet antibodies
  • Ketones
  • C peptide (plasma)
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29
Q

Syptoms of Cushings

A

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.

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30
Q

Name an alpha glucosidase inhibitor

A

Acarbose

-slows absorption of starchy foods from the intestine

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31
Q

SIGN guidance for cholesterol medication for diabetes?

A

Simvastatin 40mg

Atorvastatin 10mg

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32
Q

Blood pressure target for diabetics

A

130/80

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33
Q

HbA1c target for diabetics

A

<7.5%

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34
Q

Is low dose aspirin recommended for diabetes?

A

No

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35
Q

Commencing insulin therapy

A

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)

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36
Q

Metabolic acidosis

A

Arterial blood pH <22mol/L

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37
Q

Rapid acting insulins

A

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

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38
Q

Short acting insulin (soluble/regular)

A

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

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39
Q

Intermediate acting (isophane)

A

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

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40
Q

Long-acting analogue

A

e.g. Lantus or Levemir

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41
Q

Rapid acting analogue-intermediate analogue

A

e.g. Humalog Mix25 / Mix50 or NovoMix30

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42
Q

Short acting-intermediate mixture

A

e.g. Humulin M3,

Insuman Comb 15, 25, 50

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43
Q

Another name for aspart?

A

NovoRapid

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44
Q

Another name for lispro?

A

Humalog

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45
Q

Another name for Glulisine?

A

Aphidra

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46
Q

What type of insulin is in an insulin pump?

A

Short acting

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47
Q

Pancreatic insulin secretion vs Insulin Pump

A 
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
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48
Q

Issues with inhaled insulin?

A
  • Non-linear dosing
  • Cost
  • Risk of lung cancer
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49
Q

Issues with oral insulin

A

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

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50
Q

Smart Insulin

A

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

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51
Q

Anti-CD3 monoclonal antibody

A

Treatment with the monoclonal antibody against C3 improves insulin production

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52
Q

What is a kidney-pancreas transplantation?

A

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

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53
Q

Rapid acting vs Short Acting Insulin

A 
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
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54
Q

The 2 components of advanced carbohydrate counting?

A

1) insulin to carbohydrate ratio

2) Insulin sensitivity factor/correction factor

55
Q

Islet amyloid is a pathogenic feature of which condition?

A

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
Q

HLA association and T1DM?

A

HLA genes represent ~50% risk of T1DM

57
Q

Highest risk genotype for T1DM

A

DR3-DQ2 / DR4-DQ8

95% of patients diagnosed under 30 have one or both of those genotypes

58
Q

Islet auto-antibodies

A

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

59
Q

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

A

GAD65

IA-2

60
Q

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

A

Raised glucose

Ketones

61
Q

Enuresis

A

Bed wetting

62
Q

Classic T1DM presenting triad?

A

Polyuria (enuresis in children)
Polydipsia
Weight loss

63
Q

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

A
  • DKA
  • Significant ketonemia
  • Severe vomitting
  • Under 2 years old
  • emotional/social needs
  • live a long way from the hospital
64
Q

HbA1c target level for T1DM children?

A

<7.5%

65
Q

Annual review assessment for T1DM esp. children

A 
Weight
Blood pressure
Bloods: HbA1c, lipids, renal function
Retinal Screening
Foot risk assessment
66
Q

Conditions that can lead to secondary diabetes

A 
Cystic fibrosis
Hemochromatosis
Chronic pancreatitis
Polycystic ovary syndrome (PCOS)
Cushing's syndrome
Pancreatic cancer
Glucagonoma
Pancreatectomy
67
Q

Drug induced Diabetes

A 
Corticosteroids
Thiazide diuretics
Beta-blockers
Antipsychotics (e.g. Phenytoin)
Statins
68
Q

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

A

Monogenic :P

69
Q

Antibodies found in LADA?

A

GAD

ICA (islet cell antibodies)

70
Q

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

A

∆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
Q

What type of therapy is preferred for CF diabetic patients?

A

Insulin

72
Q

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

A

OGTT from age ten years recommended

73
Q

Are patients with CF and diabetes prone to complications?

A

Yes

74
Q

DIDMOAD/Wolfram

A 
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
Q

Chronic Fatigue and Wolfram/DIDMOAD

A

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

76
Q

Renal problems in Wolfram/DIDMOAD?

A

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
Q

Neurological problems in DIDMOAD/Wolfram

A 
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
Q

Deafness in Wolfram/DIDMOAD

A

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

79
Q

Antibodies in MODY?

A

Negative

80
Q

Autoimmune conditions associated with diabetes

A 
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
Q

Albumin and calcium levels in coeliac?

A

Low

82
Q

What is diabetic ketoacidosis?

A

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
Q

Diabetic ketoacidosis diagnosis

A

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
Q

WBC and DKA?

A

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

85
Q

Amylase in DKA

A

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

86
Q

Normal ketone levels

A

<0.6mmol/L

87
Q

What does blood ketone testing measure?

A

Beta hydroxybutyrate

88
Q

What does urine ketone testing measure?

A

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
Q

Why does ketonuria persist after clinical improvement?

A

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

90
Q

When should you consider hospital admission for DKA?

A 
Unable to tolerate oral fluids
Persistent vomiting
Persistent hyperglycaemia
Persistent positive/increasing levels of ketones
Abdominal pain / breathlessness
91
Q

Where does lactate come from?

A

Red blood cells
Skeletal muscle
Brain
Renal medulla

92
Q

Lactic acidosis: classification

A 
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
Q

Type A lactic acidosis

A

Associated with tissue hypoxaemia:

  • Infacted tissue
  • Cardiogenic shock
  • Hypovolaemic shock: sepsis, haemorrhage
94
Q

Type B lactic acidosis

A
  • 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
Q

Lactic acidosis in Diabetes

A

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
Q

Clinical signs of lactic acidosis

A

Hyperventilation
Confusion
Stupor/Coma if severe

97
Q

Lab findings of lactic acidosis

A

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
Q

Causes of a high anion gap

A

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

99
Q

Phosphate levels in lactic acidosis

A

Raised

100
Q

How to calculate anion gap?

A

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

101
Q

Is there ketonemia present in lactic acidosis?

A

No it is absent

102
Q

Bicarbonate in lactic acidosis

A

Lowered

103
Q

Treatment of lactic acidosis

A 
Underlying condition:
-Fluids
-Antibiotics
Withdraw offending medication:
-Usually medication
104
Q

Renal function in HHS?

A

Significant renal impairment

105
Q

How to calculate osmolality

A

2x[Na + K) + Urea + Glucose

106
Q

Normal Osmolality

A

285-295

107
Q

Medication that can cause HHS?

A

Diuretics and steroids

108
Q

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

A

‘Older’ type 2

109
Q

LMWH and HHS?

A

LMWH for all unless contraindicated

110
Q

Which type of acidosis is associated with Diabetes?

A

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
Q

Where does lactate come from lol

A

Red blood cells
Skeletal muscle
Brain
Renal medulla

112
Q

Lab findings of lactic acidosis

A

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
Q

Biochemistry of HHS

A

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
Q

Cause of HHS?

A

STEROIDS/DIURETICS
Fizzy drinks
Under diagnosed DM
Carbohydrate

115
Q

Drugs which can cause HHS?

A

Diuretics, steroids

116
Q

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

A

LMWH

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

117
Q

Patients with HHS may develop lactic acidosis, why?

A

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

118
Q

Hypothyroidism and effects of glucose?

A

Prolongs effects of insulin

119
Q

Renal impairment and effects of insulin

A

Prolongs effects of insulin

120
Q

Liver failure and effects of insulin

A

Prolongs effects of insulin

121
Q

Alcohol and gluconeogensis

A

Alcohol suppression of gluconeogenesis

122
Q

Growth hormone and glucose

A

Raises blood glucose level

  • GH reduces hepatic uptake of glucose from blood
  • GH stimulated lipolysis
123
Q

What is the limiting factor of good glycemic control?

A

Hypoglycemia

124
Q

Amyotrophy and possible sypmtom

A

Progressive muscle weakness

-muscle pain is also a symptom

125
Q

Types of neuropathy?

A

Peripheral
Autonomic
Focal
Proximal

126
Q

Autonomic neuropathy?

A

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

127
Q

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

A

Autonomic

128
Q

Give an example of proximal neuropathy?

A

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

129
Q

Focal neuropathy?

A

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
Q

Neuropathy more likely in type 1 or type 2 diabetes?

A

Type 1

131
Q

Complications of peripheral neuropathy?

A

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

132
Q

What are oxycodone and tramadol?

A

Opiods

133
Q

Painful neuropathy treatment algorithm?

A

-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

Endocrinology (30 decks)

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