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Y2 Revision > Diabetes > Flashcards

Diabetes Flashcards

1
Q

what are the three main microvascular complications of diabetes?

A

neuropathy
nephropathy
retinopathy

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2
Q

how does microvascular compromise generally occur in diabetes?

A

reduced blood flow to small vessels, causing hypoperfusion of nerves in that area

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3
Q

which part of the body is most susceptible to diabetic neuropathy?

A

feet

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4
Q

what will peripheral neuropathy predominantly cause?

A

pain/loss of sensation in the feet/hands

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5
Q

true or false: neuropathy is more common in type 2 diabetes than type 1 diabetes

A

false

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6
Q

what are the major complications of peripheral neuropathy?

A

infections
ulcers
deformities
amputations

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7
Q

what is gustatory sweating?

A

abnormal function of sweat glands, causing profuse sweating at night or during meals

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8
Q

true or false: diabetes is the most common cause of kidney failure

A

true

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9
Q

what is a reliable sign of diabetic kidney failure that should be screened for?

A

raised albumin

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10
Q

list causes of false positives for microalbuminuria

A 
menstruation 
pregnancy 
UTI 
vaginal discharge 
non diabetic renal disease
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11
Q

which class of drugs is useful for diabetics with kidney failure?

A

ACE inhibitors

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12
Q

what eye pathologies do people with diabetes get?

A

retinopathy
cataracts
glaucoma
visual blurring

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13
Q

what is the main sign of background retinopathy?

A

leaky blood vessels (dots)

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14
Q

what are the main signs of proliferative retinopathy?

A

angiogenesis due to ischaemia
haemorrhage
leaky blood

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15
Q

what are the main signs of diabetic maculopathy?

A

build up of fluid in macula, causing exudates

blurred vision or complete loss of vision

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16
Q

true or false: erectile failure occurs in about 50% of diabetic men

A

true

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17
Q

true or false: in scotland, incidence of diabetes has overtaken CVD and cancer

A

true

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18
Q

define diabetes mellitus

A

a group of metabolic diseases characterised by hyperglycemia, due to inadequate insulin production, availability or action

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19
Q

why is type 1 diabetes an example of absolute insulin deficiency?

A

insulin is not produced because the beta cells in the pancreas are destroyed

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20
Q

what is the normal range of glycated hemoglobin (HbA1c)?

A

41 m/m and below

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21
Q

what is the normal range for fasting glucose?

A

6mmol/l and below

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22
Q

what value of HbA1c is diabetes diagnosed at?

A

48mmol/mol and above

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23
Q

what value of fasting glucose is diabetes diagnosed at?

A

7mmol/l and above

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24
Q

what value of random blood glucose is diabetes diagnosed at?

A

11.1mmol/l

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25
Q

which antibodies are associated with type 1 diabetes?

A

anti-GAD

anti islet cell

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26
Q

true or false: autoantibodies in type 1 diabetes actually appear years before the onset of diabetes

A

true

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27
Q

list clinical features of type 1 diabetes

A 
polyuria
polydipsia
weight loss 
fatigue 
ketonuria
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28
Q

what is the typical age of onset for type 1 diabetes?

A

pre school/pre puberty

another peak in late 30’s

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29
Q

which type of diabetes is more associated with obesity?

A

type 2

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30
Q

list clinical features of type 2 diabetes

A 
thirst 
polyuria 
weakness 
thrush 
blurred vision 
neuropathy
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31
Q

what is LADA?

A

late onset autoimmune diabetes of adulthood

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32
Q

which type of diabetes is more associated with ketosis?

A

type 1

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33
Q

what does HbA1c provide a measure of?

A

glycated Hb

provides a measure of blood glucose over 2-3 months

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34
Q

list macro-vascular complications of diabetes

A

MI

stroke

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35
Q

list micro-vascular complications of diabetes

A

retinopathy
nephropathy
neuropathy

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36
Q

HLA genes represent how much of familial risk of type 1 diabetes?

A

30-50%

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37
Q

what is the highest risk genotype for type 1 diabetes?

A

DR3-DQ2

DR4-DQ8

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38
Q

true or false: people with pear shaped weight distribution have higher risk of CVD than those with apple shaped weight distribution

A

false

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39
Q

what are the main aims behind diabetes therapy?

A

alleviate hyperglycemic symptoms
weight loss
reduce risk of complications

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40
Q

what is the first line pharmacological therapy for type 2 diabetes?

A

biguanides (metformin)

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41
Q

give examples of sulphonylureas

A

gliclazide
glibenclamide
glimepiride

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42
Q

give an example of a thiazolidinedione (TZD)

A

pioglitazone

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43
Q

what are the main effects of metformin?

A

reduces insulin resistance
prevents vascular complications
reduces triglycerides and LDL

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44
Q

list some possible adverse effects of metformin

A

GI upset
lactic acidosis
liver failure
rash

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45
Q

true or false: sulphonylureas have more rapid reduction of hyperglycemia compared to metformin

A

true

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46
Q

true or false: sulphonylureas prevent micro and macro vascular complications

A

false

they do not prevent macrovascular complications

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47
Q

true or false: TZDs can cause weight gain

A

true

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48
Q

true or false: TZDs increase the risk of hip fractures

A

true

not recommended in those over 65

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49
Q

what are incretins?

A

hormones that cause intestinal secretion of insulin

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50
Q

name the two main incretin hormones

A

GLP-1 from L cells

GIP from K cells

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51
Q

list the effects of incretins

A

delay gastric emptying
decrease appetite
stimulate insulin secretion
reduce glucose production by liver

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52
Q

name a GLP-1 agonist that can be used for diabetes

A

exenatide

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53
Q

name a DPP-1 inhibitor that can be used for diabetes

A

sitagliptin

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54
Q

how are SGLT2 inhibitors useful in diabetes?

A

reduce reabsorption of glucose, causing glycosuria

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55
Q

what is a downside of SGLT2 inhibitors?

A

increase risk of UTIs

56
Q

list ways to evaluate metabolic control of diabetes

A

HbA1c
blood glucose
ketone monitoring
urinalysis

57
Q

what is the main treatment for type 1 diabetes?

A

insulin

58
Q

list the devices available for administering insulin

A

syringe
disposable pen
cartridge pen
continuous subcutaneous pump

59
Q

what is basal insulin?

A

background production of insulin to keep blood glucose normal outwith meal times

60
Q

what is prandial insulin?

A

insulin produced in relation to increased glucose following a meal

61
Q

when is the onset and peak action of rapid acting insulin analogues?

A 
onset = 15 mins 
peak = 1-2 hours
62
Q

give examples of rapid acting insulin analogues

A

novorapid

humalog

63
Q

when is the onset and peak action of short acting insulin analogues?

A 
onset = 30-60 mins 
peak = 2-4 hours
64
Q

give examples of short acting insulin analogues

A

actrapid

humulin S

65
Q

what is the onset of action of basal insulin analogues?

A

1-3 hours

66
Q

give examples of basal insulin analogues

A

insulatard

humulin I

67
Q

what is humalog Mix25 composed of?

A

25% short acting

75% intermediate acting

68
Q

what is the aim behind a basal-bolus insulin regime?

A

mimic endogenous production

take short acting before a meal, long acting before sleeping

69
Q

what is involved in a once daily insulin regime?

A

long/intermediate acting given before bed

not suitable for type 1

70
Q

what is involved in a twice daily insulin regime?

A

injection before breakfast and dinner

high risk of hypoglycemia, only works if the patient eats three meals a day

71
Q

what is the target for blood glucose pre-meal?

A

3.9-7.2 mmol/L

72
Q

what is the target for blood glucose 1-2 hours after starting a meal?

A

less than 10 mmol/L

73
Q

do insulin pumps deliver short, intermediate or long acting insulin?

A

short acting

74
Q

what are the three main limitations of insulin injections vs pancreatic insulin?

A

injected into subcutaneous tissue instead of blood
slower peak
slow clearance

75
Q

name a long acting human insulin injection

A

ultratard

76
Q

name a long acting insulin analogue

A

lantus

levemir

77
Q

list drug classes that increase secretion of insulin through insulin independent action

A

sulphonylureas
incretin analogues
DPP 4 inhibitors

78
Q

list drug classes that decrease insulin resistance and reduced hepatic glucose output through insulin dependent action

A

biguanides

thiazolidinediones (TZD’s)

79
Q

list a drug class that slows glucose absorption from the GI tract through insulin independent action

A

alpha glucosidase inhibitors

80
Q

list a drug class that blocks reabsorption of glucose in the kidneys through insulin independent action

A

SGLT2 inhibitors

81
Q

through which transporter does glucose enter the beta cell in the pancreas?

A

GLUT 2

82
Q

what effect does ATP in the beta cell of the pancreas have on K channels?

A

closes them, causing depolarisation of the membrane

83
Q

how is insulin released following depolarisation of the membrane of the beta cell?

A

depolarisation causes opening of the calcium channels, causing insulin containing vesicles to exocytose

84
Q

list the components of the Katp channel

A

4 Kir6.2 units

4 SUR1 units

85
Q

which part of the Katp channel does ATP bind to?

A

Kir6.2 unit

86
Q

what binds to the SUR1 part of the Katp channel and what does this cause?

A

ADP-Mg

repolarisation to inhibit insulin secretion

87
Q

how do sulphonylurea drugs work?

A

displace ADP-Mg from SUR1 on Katp channel to cause depolarisation to promote insulin release

88
Q

true or false: the effect of sulfonylurea drugs is independent of glucose concentration

A

true

89
Q

give examples of sulphonylureas

A

tolbutamide
glibenclamide
glipizide

90
Q

what is the main difference between tolbutamide and glibenclamide?

A

glibenclamide is more potent and longer acting, so you only need to take it once a day

91
Q

can sulfonylureas cause hypoglycemia?

A

yes

greater risk with long acting agents

92
Q

how do glinides differ from sulphonylureas?

A

bind to specific part of SUR1

rapid action - less likely to cause hypoglycemia

93
Q

what are the two main endogenous incretin hormones?

A

GLP-1

GIP

94
Q

what effect does GLP-1 have on glucagon?

A

decreases glucagon release from alpha cells

95
Q

give an example of an incretin analogue

A

exenatide

96
Q

which enzyme rapidly inhibits the action of incretin hormones?

A

DPP-4

97
Q

how do DPP-4 antagonists work?

A

inhibit DPP-4 to prolong actions of GLP-1 and GIP

98
Q

give an example of a DPP-4 inhibitor

A

sitagliptin

99
Q

what is the function of alpha-glucosidase in the intestine?

A

breaks down carbohydrates into absorbable glucose

100
Q

how do alpha glucosidase inhibitors work?

A

inhibit alpha glucosidase to delay absorption of glucose, thus reducing postprandial increase in blood glucose

101
Q

give an example of an alpha glucosidase inhibitor

A

acarbose

102
Q

true or false: acarbose has a great risk of hypoglycemia

A

false

no risk at all

103
Q

what is the first line therapy for type two diabetes?

A

biguanides

104
Q

what is the proposed action of metformin?

A

reduces hepatic gluconeogenesis by stimulating AMPK

enhances glucose uptake by muscle

105
Q

does metformin cause hypoglycemia?

A

no

106
Q

true or false: metformin causes weight gain

A

false

causes weight loss

107
Q

list a significant adverse effect of metformin

A

lactic acidosis

108
Q

how do TZDs work?

A

agonist of PPAR alpha which is associated with RXR to enhance the transcription of genes that encode insulin signalling

109
Q

which transported moves glucose into skeletal muscle?

A

GLUT4

110
Q

true or false: TZDs can cause weight gain

A

true

111
Q

how do SGLT2 inhibitors work?

A

block reabsorption of glucose in convoluted tube of nephron to cause glycosuria

112
Q

name a SGLT2 inhibitor

A

dapagliflozin

113
Q

what is the main adverse effect of SGLT2 inhibitors?

A

increased risk of UTI

thrush

114
Q

give an example of TZD

A

pioglitazone

115
Q

list the main diabetic emergencies

A 
diabetic ketoacidosis
HHS
lactic acidosis 
alcoholic ketoacidosis 
hyperglycemia
116
Q

what is diabetic ketoacidosis?

A

metabolic state that occurs in the context of insulin deficiency, resulting in increase of counter regulatory hormones

117
Q

how do excess ketones form as a result of insulin deficiency?

A

increased lipolysis causes increased free fatty acid in the liver, producing more ketones

118
Q

how does hyperglycemia result from insulin deficiency?

A

less glucose utilisation by muscle tissues
increased proteolysis
increased glycogenolysis

119
Q

is DKA more common in type 1 or type 2 diabetes?

A

type 1

120
Q

outline the biomechanical diagnosis of DKA

A

ketonemia greater than 3
glucose greater than 11
bicarbonate less than 15/pH less than 7.3

121
Q

what is the most common precipitant of DKA?

A

non compliance with insulin therapy

122
Q

list symptoms of DKA

A 
thirst 
polyuria 
vomiting 
abdominal pain 
breathlessness 
acetone breath
123
Q

what is the blood measurement of ketones?

A

beta-hydroxybutarate

124
Q

what is the urine measurement of ketones?

A

acetoacetate

125
Q

list some electrolytes that can be lost in DKA

A

sodium
potassium
phosphate

126
Q

list the main complications of DKA

A

hypokalaemia
ARDS
cerebral oedema
aspiration

127
Q

outline main initial treatment of DKA

A

fluids
potassium
insulin

128
Q

why might ketonuria persist even after clinical improvement of DKA?

A

mobilisation of ketone stores from fat

129
Q

list the typical features of hyperglycemia hyperosmolar syndrome (HHS)

A

high glucose
renal impairment
raised osmolality
less ketonaemic

130
Q

how do you calculate osmolality?

A

(2 x [Na + K]) + urea + glucose

131
Q

what is the normal range for osmolality?

A

285-295

132
Q

true or false: DKA and HHS tend to occur in younger diabetics

A

false

DKA in younger, HHS in older

133
Q

is HSS more commonly associated with type 1 or 2 diabetes?

A

type 2

134
Q

how does treatment in HHS differ from DKA?

A

more slow and cautious, often just diet related
may not require insulin
vascular events are more likely

135
Q

what is the normal range of lactate?

A

0.6-1.2

136
Q

what is the normal anion gap?

A

10-18

Y2 Revision (95 decks)

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