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endocrine (mine) > Diabetes > Flashcards

Diabetes Flashcards

1
Q

what is type 1 DM

A

autoimmune disorder resulting in absolute insulin deficiency due to beta cell failure

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2
Q

when/how do symptoms occur in type 1 DM

A

acute onset pre-school and during puberty

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3
Q

what are the symptoms of type 1 DM

A 
severe weight loss
ketonuria +/- metabolic acidosis 
thirst 
polyuria
thrush 
weakness/fatigue 
diabetic ketoacidosis
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4
Q

what are the investigations of type 1 DM

A

autoimmune markers
raised ketones in urine
low c-peptide levels

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5
Q

what are the autoimmune markers of type 1 DM

A 
GAD
tyrosine phosphates: 
- IA-2
- IA-2 beta
- ZnT8 
HLA association 
- DQ8 
- DQ4
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6
Q

what is the treatment of type 1 DM

A

insulin dependent

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7
Q

what is Autoimmune Diabetes of Adults (LADA)

A

this is late onset of type 1 DM

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8
Q

what are the typical symptoms of Autoimmune Diabetes of Adults (LADA)

A

same as type 2 DM symptoms
non-obese
associated autoimmune conditions

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9
Q

what is the common age affected by Autoimmune Diabetes of Adults (LADA)

A

25-40

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10
Q

what are the investigations of Autoimmune Diabetes of Adults (LADA)

A

autoantibody positive

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11
Q

what HbA1c suggest diabetes, what is normal

A 
diabetes = 48 and above
normal = 41 and lower
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12
Q

what fasting glucose suggests diabetes, what is normal

A 
diabetes = 7 and above 
normal = 6 and below
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13
Q

what results in a OGTT suggests diabetes, what is normal

A 
diabetes = 11.1 and above
normal = 7.7 and below
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14
Q

what random glucose suggests diabetes

A

11.1

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15
Q

what does HbA1c provide a measure of

A

average glucose control over the past 2-3 months

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16
Q

who should be tested for diabetes, how often

A

women with GDM = tested every 3 years

pre-diabetes = tested yearly

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17
Q

when should repeat testing be carried out for diabetes diagnosis

A

In the absence of unequivocal hyperglycaemia results

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18
Q

what is type 2 DM

A

relative insulin deficiency involving hyperinsulinemia and insulin resistance

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19
Q

when/how do the symptoms of type 2 DM start

A

middle aged/elderly over a few months - years

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20
Q

what are the symptoms of type 2 DM

A 
thirst
polyuria
thrush
weakness/fatigue 
blurred vision
weight loss
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21
Q

what type of diabetes presents with microvascular disease

A

type 2 DM

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22
Q

what tests are done to diagnose diabetes

A 
Fasting plasma glucose
2hr plasma glucose during oral glucose tolerance test (OGTT)
HbA1C
C-peptide (plasma)
Random plasma glucose
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23
Q

what are the macrovascular complications of type 2 DM

A

heart disease/atheroma

stroke

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24
Q

what are the microvascular symptoms of type 2 DM

A

neuropathy
retinopathy
nephropathy

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25
Q

how is type 2 DM treated

A

in order:

lifestyle changes (lower BMI)
treat other CVD risk factors
lower blood glucose via drugs

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26
Q

what blood glucose should be aimed for in type 2 DM if >70

A

53

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27
Q

what blood glucose should be aimed for in type 2 DM if <70

A

48

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28
Q

what is the first line drug in type 2 DM if treatment

A

metformin

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29
Q

what is the 2nd line drug treatment of type 2 DM

A

add a second drug to metformin. usually a sulphonylurea

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30
Q

what is the 3rd line drug in treatment of type 2 DM

A

add a glitazone

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31
Q

what is

Maturity-onset diabetes of the young (MODY)

A

this is a type of monogenic diabetes with a genetic defect in beta function. familia former early-onset type 2 DM

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32
Q

what are the causes of

Maturity-onset diabetes of the young (MODY), which is more common

A

autosomal dominant mutation in:

  • glucokinases
  • transcription factors (MODY) = 75%
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33
Q

what would make you suspect Maturity-onset diabetes of the young (MODY)

A

onset before 25
strong family history
GAD negative
c-peptide positive

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34
Q

what is the symptoms of Maturity-onset diabetes of the young (MODY) caused by impaired glucokinase activity

A

onset at birth

stable hyperglycaemia

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35
Q

what is the treatment of MODY caused by impaired glucokinase activity

A

diet

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36
Q

what is the link between glucokinase and insulin production

A

Glucokinase acts as the pancreatic glucose sensor

If glucokinase activity is impaired the blood glucose threshold for insulin secretion is increased

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37
Q

what is the symptoms of MODY caused by mutation in transcription factors

A

onset = adolescence/young adult
progressive hyperglycaemia
frequent complications

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38
Q

what is the treatment of MODY caused by mutation in transcription factors

A

diet, medication, insulin

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39
Q

when can sulphonylureas be used to treat MODY

A

if mutation is in HNFA1

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40
Q

what are the two types of neonatal diabetes

A

transient

permanent

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41
Q

when is transient neonatal diabetes diagnosed, when does it resolve

A

diagnosed <1wk

resolved at 12 wks

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42
Q

how is transient neonatal diabetes treated

A

insulin until it resolves

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43
Q

when is permanent neonatal diabetes diagnosed

A

0-6wks

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44
Q

what is the treatment of permanent neonatal diabetes

A

lifelong insulin or sulphonylureas

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45
Q

what is the cause of permanent neonatal diabetes

A

potassium channel gene mutations

46
Q

what symptom must be asked about in a child with suspected diabetes

A

new bed wetting

47
Q

what symptoms must be asked about in a child with suspected DKA

A

abdominal pain
vomiting
heavy breathing

48
Q

what is type 3 diabetes

A

gestational diabetes

49
Q

what is gestational diabetes

A

any degree of glucose intolerance arising or diagnosed during pregnancy

50
Q

when does gestational diabetes usually occur

A

2nd or 3rd trimester

51
Q

what is the treatment of gestational diabetes during labour

A

maintain blood glucose via IV insulin and dextrose

52
Q

what is the treatment of gestational diabetes

A

lifestyle
metformin
insulin

53
Q

what investigation should be done after giving birth? when?

A

fasting glucose or OGTT 6wks postnatal to ensure resolution

54
Q

what is type 4 DM

A

diabetes secondary to another conditions

55
Q

what conditions can cause type 4 DM

A 
CF
haemochromatosis 
cushing's
acromegaly
Pheochromocytoma
56
Q

what drugs can cause type 4 DM

A

Glucocorticoids
Diuretics
B-blockers

57
Q

what is diabetic ketoacidosis (DKA)

A

a disordered metabolic state that usually occurs in the context of an absolute or relative insulin deficiency accompanied by an increased in counter-regulatory hormones

58
Q

what conditions can cause DKA, which is more common

A

Type 1 DM = more common

type 2 DM

59
Q

what are the symptoms of DKA

A 
flushed
vomting
abdominal pain/tenderness
breathless
coma
60
Q

what are the biochemical markers that should be checked in a diagnosis of DKA

A 
ketoaemia
significant ketonuria (++)
blood glucose
Bicarb
Venous pH 
CK
Sodium 
K
Blood ketones
61
Q

what Bicarb would you suspect in DKA

A

<15

severe <10

62
Q

what venous pH would you suspect in DKA

A

<7.3

63
Q

what ketoaemia would you suspect in DKA, what else could you measure

A

> 3

OR significant ketonuria (++)

64
Q

what Blood Glucose would you suspect in DKA, when would you not need this

A

> 11

BG is not needed if the patent is already known diabetic

65
Q

what CK would you suspect in DKA

A

raised

66
Q

what Na and K would you suspect in DKA

A

Na = low

K >5.5

67
Q

what blood ketones would you suspect in DKA

A

> 5

68
Q

what amylase and lactate levels would you suspect in DKA

A

raised

69
Q

what is the treatment of DKA

A 
replace losses: 
- fluid (0.9% NaCl, switch to dextrose once glucose <15)
-insulin
-K
prophylactic LMWH
monitor ketones
70
Q

how are ketones monitored in DKA

A

measure beta-hydroxybutyrate (optimum meter) in blood

measure acetoactate in urine

71
Q

what is hyperglycaemic hyperosmolar syndrome

A

a complication of diabetes in which high blood sugar results in high osmolarity without significant ketoacidosis

72
Q

what are the risk factors to getting hyperglycaemic hyperosmolar syndrome

A

elderly
type 2 DM
steroids

73
Q

what are the biochemical markers of hyperglycaemic hyperosmolar syndrome

A 
Hypovolaemia (usually marked)
Hyperglycaemia >30 
No/mild ketonaemia 
Bicarb >15 
Venous pH >7.3
74
Q

what causes alcoholic ketoacidosis

A

excessive consumption of alcohol

75
Q

what biochemical markers would you expect to find in alcoholic ketoacidosis

A 
dehydrated
ketonaemia >3
significant ketonuria (++)
Bicarb <15
venous pH <7.3 
glucose normal but may be low
76
Q

what causes lactic acidosis

A

build up of lactate resulting in a low pH

77
Q

treatment of alcoholic ketoacidosis

A 
IV pabrinex = high dose vitamins
IV fluids = particularly dextrose
IV anti-emetics
Insulin may be required on occasion
Address alcohol dependency
78
Q

what are the symptoms of alcoholic ketoacidosis

A

Abdominal pain
Vomiting
Hypotensive
tachypnoeic

79
Q

what are the types of lactic acidosis

A

A and B

80
Q

what is type A lactic acidosis associated with

A

tissue hypoxaemia (infarct, sepsis, haemorrhage)

81
Q

when might type B lactic acidosis occur

A

liver disease
diabetes/ DKA
leukaemic states

82
Q

what is the treatment of lactic acidosis

A

Treat underlying condition
Fluids
Antibiotics
Withdraw offending medication

83
Q

what are the symptoms of lactic acidosis

A

Hyperventilation
Confused
Coma if severe

84
Q

what biochemical markers would you expect in lactic acidosis

A

Reduced bicarb
Glucose variable (often raised)
Absence of ketonaemia
Raised phosphate

85
Q

when should diabetes tested for in asymptomatic patients

A

if they are >45 with a BMI >25 (or >23 if asian) and have 1 risk factor

86
Q

what risk factors would make you consider screening for diabetes

A 
First degree relative with diabetes 
High-risk ethnicity (non-white)
History of CVD
Hypertension
high HDL cholesterol  
Polycystic ovary syndrome
87
Q

how often should diabetes testing be carried out in those with risk factors

A

minimum of every 3 years

88
Q

how often should a woman who had gestational diabetes be tested

A

minimum of every 3 years

89
Q

what class of drugs metformin

A

biguanides

90
Q

what is the mechanism of action of metformin

A

stimulates AMP-activated protein kinase (AMPK) to reduce hepatic gluconeogenesis.

this decreases insulin resistance and reduces hepatic glucose output

91
Q

what are the contraindications to metformin

A

Significant hepatic disease
Significant renal disease (CKD)
Excessive alcohol consumption = risk of lactic acidosis

92
Q

give examples of Sulfonylureas

A

gliclazide, glipizide

93
Q

what is the mechanism of action of Sulfonylureas

A

cause pancreatic beta cells to secrete insulin by displacing the binding of ADP from the SUR1 subunit which blocks the KATP channel

increases secretion of insulin

94
Q

what are the side effects of Sulfonylureas

A

weight gain
hypoglycaemia
abnormal LFTs

95
Q

what are the contraindications of Sulfonylureas

A

pregnancy

CDK

96
Q

give examples of glinides

A

repaglinide

97
Q

what are the contraindications to glinides

A

hepatic impairment
pregnancy
breast feeding

98
Q

when would glinides be used

A

if the patient has CKD

99
Q

give examples of SGLT2 inhibitors

A

dapagliflozin, canagliflozin, empagliflozin

100
Q

what is the mechanism of SGLT2 inhibitors

A

selectively blocks the reabsorption of glucose by SGLT2 un the proximal tubule of the kidneys

101
Q

what is the side effect of SGLT2 inhibitors

A

aids weight loss
UTI
thrush

102
Q

give an example of a glitazone

A

pioglitazone

103
Q

when is gliazones used the treatment of type 2 DM

A

3rd line

104
Q

what are the side effects of gliazones

A

weight gain
fluid retention
increased incidence of bone fracture

105
Q

what is the mechanism of action of gliazones

A

enhance the action of insulin at target tissues but do not directly affect insulin secretion i.e. they reduce insulin resistance

106
Q

give examples of incretin analogues

A

extenatide, liraglutide

107
Q

what is the mechanism of action of incretin analogues

A

mimic the action of GLP-1, bind to receptors to increase intracellular cAMP concentrations which stimulates insulin expression and release.

108
Q

how is incretin analogues administered

A

SC

109
Q

what are the side effects of incretin analogues

A

nausea
pancreatitis
NO hypoglycaemia

110
Q

what is the mechanism of action of gliptins

A

competitively inhibits GLP-1 and GIP by the enzyme DPP-4 causing the plasma tireless insulin

111
Q

give examples of gliptins

A

sitagliptin (most common), saxagliptin, vildagliptin, linagliptin, alogliptin

112
Q

what are the side effects of gliptins

A

nausea

endocrine (mine) (12 decks)

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