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year 2 > diabetes > Flashcards

diabetes Flashcards

1
Q

what is involved in type 1 diabetes

A

absolute insulin deficiency - autoimmune beta cell destruction

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2
Q

what is the inflammation seen in beta cells in diabetes called

A

insulitis

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3
Q

T1DM has a strong link to what HLA genes

A

HLA DQA
HLA DQB
HLA DR3 +/- DR4

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4
Q

what antibodies are seen in T1DM

A

anti-GAD (GAD65)
anti-islet cell
tyrosine phosphatases (IA-2, IA2B, ZnT8)

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5
Q

what age does T1DM usually present

A

pre-school and puberty

small peak in late 30s

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6
Q

is the onset of T1DM acute or gradual

A

acute

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7
Q

what are the s/s of T1DM

A 
polyuria
polydipsia
fatigue
weight loss
ketonuria
blurred vision
genital thrush
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8
Q

is there normally evidence of microvascular disease at diagnosis in T1DM

A

no

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9
Q

what infections are people with diabetes more prone to

A

candida infections

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10
Q

what is the treatment for T1DM

A

insulin

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11
Q

what is target blood glucose pre meal

A

4-7 mmol/L

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12
Q

what is the target glucose 1-2 hours after a meal

A

5-9 mmol/L

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13
Q

what is LADA

A

late onset diabetes of adulthood - elevated levels of pancreatic autoantibodies in a patient with previously diagnosed diabetes who did not initially require insulin

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14
Q

who tends to get LADA

A

non-obese males, 25-40

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15
Q

how is LADA differentiated from T2DM

A

patient is thin/losing weight or has a history of pancreatic disease

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16
Q

is LADA autoantibody positive or negative

A

positive

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17
Q

what is idiopathic T1DM

A

patients have permanent insulinopenia and prone to DKA but no evidence of Beta cell autoimmunity

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18
Q

what race are people with idiopathic T1DM

A

african/asian

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19
Q

is idiopathic T1DM familial/HLA assocaited

A

strongly inherited

not HLA associated

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20
Q

what is T2DM

A

non insulin dependent diabetes mellitus

relative insulin deficiency

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21
Q

what is the first line management in T2DM

A

diet control

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22
Q

who tends to get T2DM

A

elderly/middle aged

usually obese

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23
Q

are there usually complications at the point of diagnosis of T2DM

A

yes (prediagnosis time of 6-10 years) e.g. blurred vision

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24
Q

what are 2 causes of insulin resistance

A

ectopic fat accumulation and increased circulating fatty acids
increased inflammatory mediators

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25
Q

is there usually ketonuria at diagnosis of T2DM

A

no

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26
Q

what is the WHO criteria for T1DM

A 
raised venous glucose on 2 occasions
or 
OGTT 2 hr value > 11.1
or
HbA1c > or = 48 mmol/L
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27
Q

according to WHO, what must a person have in addition to symptoms of hyperglycaemia to have T1DM

A

raised venous glucose detected once (fasting > 7 or random > 11.1)

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28
Q

according to WHO what must a persons venous glucose be on 2 occasions to have T1DM

A

raised venous glucose on 2 occasions (fasting > 7 or random > 11.1)

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29
Q

according to WHO what must a persons results be from a OGTT to have T1DM

A

OGTT 2hr value > 11.1

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30
Q

according to WHO what must a persons HbA1c be to have T1DM

A

> or = 48mmol/L

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31
Q

what is more accurate to measure glucose levels - urine or blood

A

blood

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32
Q

what ethnicity is more prone to diabetes

A

asian/african/afro-carribean

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33
Q

what is the pathophysiology of T2DM

A

hyperglycaemia –> hyperinsulinaemia –> insulin resistance
compensatory Beta cell hyperplasia causing normoglycaemia
beta cell early failure causing impaired glucose tolerance
beta cell late failure causing diabetes

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34
Q

increased what causes the hyperglycaemia in diabetes

A

lipolysis
glucose reabsorption
glucagon secretion
hepatic glucose production

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35
Q

decreased what causes the hyperglycaemia in diabetes

A

insulin secretion
incretin effect
glucose uptake
neurotransmitter dysfunction

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36
Q

what does HbA1c measure

A

glucose control over past 2-3 months

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37
Q

what is a normal HbA1c

A

< or = 41

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38
Q

what is a diabetic HbA1c

A

> or = 48

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39
Q

what is a normal fasting glucose

A

< or = 6

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40
Q

what is a diabetic fasting glucose

A

> or = 7

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41
Q

what is a normal 2 hr glucose in OGTT

A

< or = 7.7

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42
Q

what is a diabetic 2 hr glucose in OGTT

A

> or = 11.1

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43
Q

what would a diabetic random glucose test be

A

> 11.1 mmol/L

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44
Q

what are the levels of C peptide like in T1 and T2 diabetes

A

T1 diabetes - no C peptide

T2 diabetes - some C peptide

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45
Q

what type of diabetes is gestational diabetes

A

type 3

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46
Q

what is gestational diabetes

A

any degree of glucose intolerance arising or diagnosed during pregnancy

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47
Q

how is gestational diabetes caused

A

placental hormones that cause insulin resistance in mother - human placental lactogen and placental progesterone

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48
Q

when is gestational diabetes most likely to occur and why

A

3rd trimester

- placenta grows most so levels of placental hormones increase

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49
Q

what are the 3 main complications of gestational diabetes in utero

A

macrosomia
polyhydramnios
intrauterine death

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50
Q

what are the 3 main complications of gestational diabetes in the baby after delivery

A

respiratory death due to immature lungs
hypoglycaemia
hypocalcaemia

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51
Q

why would you get macrosomia in a baby whose mother has gestational diabetes

A

hyperglycaemia causes excess insulin production which is a growth factor

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52
Q

why would a neonate whose mother has gestational diabetes become hypoglycaemic

A

high sugar load from mother near birth causes excess insulin production - once the baby is born no longer getting the high blood sugars yet still has high insulin producing hypoglycaemia

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53
Q

what should be done 6 weeks after delivery to decide if the gestational diabetes is now actually T2DM

A

glucose tolerance test

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54
Q

what is gestational diabetes screened for with

A

OGTT

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55
Q

Monogenic diabetes is…
young/old onset
GAD positive/negative
C peptide negative/positive

A

young onset
GAD negative
C peptide positive

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56
Q

monogenic diabetes has a strong family history

true/false

A

true

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57
Q

what are some assocaited features of monogenic diabetes

A

renal cysts

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58
Q

what is MODY

A

mature onset diabetes of young

monogenic diabetes with genetic defect in beta cell function - primary defect in insulin secretion

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59
Q

what is the inheritance of MODY

A

autosomal dominant

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60
Q

how is MODY differentiated from T1DM

A

genetic screening

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61
Q

what is the treatment of MODY

A

diet treatment and sulfonylurea

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62
Q

do MODY patients usually have no Beta function or some

A

some beta function

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63
Q

where can mutations occur to cause MODY

A

glucokinase (GCK/MODY2)

several transcription factors

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64
Q

how does a defect in glucokinase cause MODY

A

alters the point where glucokinase can sense present of glucose, meaning body can only sense glucose above 7 leading to stable hyperglycaemia

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65
Q

when is the onset of MODY2

A

birth

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66
Q

what is the treatment of MODY2 with a genetic defect in glucokinase

A

diet treatment

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67
Q

what is the onset of MODY if the defect is in one of the transcription factors

A

young adult onset

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68
Q

what is the most common form of MODY

A

genetic defect in transcription factors

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69
Q

what is MODY1

A

defect in HNF-4alpha

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70
Q

what is MODY3

A

defect in HNF-1alpha

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71
Q

what is MODY4

A

defect in IPF1

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72
Q

what is MODY6

A

NDF1/neuroD1/B2

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73
Q

what do HNF-transcription factors play a key role in

A

pancreas foetal development and neogenesis

also regulate B cell differentiation and function

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74
Q

what is the hyperglycaemia like that is seen in MODY with defects in transcription factors

A

progressive

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75
Q

what is the treatment for MODY with defects in transcription factors

A

diet treatent
sulfonylureas
insulin

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76
Q

are complications frequent with MODY with defects in transcription factors

A

yes

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77
Q

what are the 4 categories of type 4 diabetes

A

pancreatic disease
endocrine disease
drug induced
problems with insulin and its receptor

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78
Q

what pancreatic diseases cause type 4 diabetes

A

chronic or recurrent pancreatitis
haemochromatosis
cystic fibrosis

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79
Q

what endocrine diseases can cause type 4 diabetes

A

cushings
acromegaly
phaeochromocytoma
glucagonoma

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80
Q

what drugs can cause diabetes

A

glucocorticoids
diuretics
BBs

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81
Q

give 3 genetic diseases that can cause diabetes

A

cystic fibrosis
myotonic dystrophy
turners syndrome

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82
Q

what is the incretin effect

A

insulin response to oral glucose is greater than the response to IV glucose

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83
Q

what happens to the incretin effect in T2DM

A

it is reduced

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84
Q

ingestion of food stimulates the release of what (2)

A

GLP-1

GIP

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85
Q

where is GLP-1 released from

A

L cells of the ileum

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86
Q

where is GIP released from

A

K cells in the duodenum

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87
Q

where do GLP-1 and GIP go when they are released

A

into the hepatic portal vein

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88
Q

what do GLP-1 and GIP do

A

enhance insulin release from pancreatic B cells and delay gastric emptying causing enhanced glucose uptake and utilisation

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89
Q

what effect do GLP-1 and GIP have on the diet

A

cause feeling of satiety

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90
Q

what does GLP-1 do to liver gluconeogenesis

A

reduces

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91
Q

what effect does GLP-1 have on glucagon release from pancreatic alpha cells

A

decreases glucagon production –> decreased glucose production

92
Q

how are the actions of GLP-1 and GIP terminated and by what

A

DPP4 within minutes

dipeptidyl peptidase 4

93
Q

where is insulin released into

A

hepatic portal vein

94
Q

what does insulin do to gluconeogenesis

A

inhibits

95
Q

what does insulin do to glycogenolysis

A

inhibits

96
Q

what does insulin do to glucogenesis

A

stimulates

97
Q

how does insulin inhibit lipolysis

A

encourages entry of fatty acids into adipose tissues of body

98
Q

how does insulin promote protein synthesis

A

promotes uptake of amino acids into muscles and other tissues

99
Q

how would you describe the normal release of insulin

A

biphasic - rapid phase of preformed insulin (5-10 mins) and slow phase (1-2 hours)

100
Q

what are 2 macrovascular complications of diabetes

A

heart disease

stroke

101
Q

what does AGE-RAGE stand for

A

Advanced Glycation End products

Receptor for AGE

102
Q

what is glycation

A

non-enzymatic covalent bonding of a protein or lipid molecule with carbohydrates such as glucose

103
Q

what are the 3 main microvascular complications of diabetes

A

retinopathy
nephropathy
neuropathy

104
Q

how do these microvascular complications happen

A

Hyperglycaemia + hyperlipidaemia –> AGE-RAGE, hypoxia, oxidative stress, inflammation, mitochondrial dysfunction

105
Q

how does neuropathy occur

A

small blood vessels to vessels become damaged due to high glucose levels - reduced oxygen supply causes nerves to become damaged

106
Q

how do you describe the distribution of peripheral neuropathy in diabetes

A

glove and stocking distribution

distal symmetric or sensorimotor neuropathy

107
Q

what are some s/s that indicate peripheral neuropathy

A 
numbness//insensitivity
tingling/bussing
sharp pains/cramps
sensitivity to touch
allodynia
loss of balance coordination
108
Q

what are some treatments for painful neuropathy

A 
amitriptyline
duloxetine
gabapentin
pregabalin
(Combinations not recommended)
109
Q

what is diabetic focal neuropathy

A

appears suddenly and affects specific nerve/group of nerves

110
Q

what nerves/groups of nerves are most commonly affected in focal neuropathy

A

head
torso
leg

111
Q

what are some s/s of focal neuropathy

A

unable to focus eye/double vision/aching behind eyes
bell’s palsy
pain in thigh/chest/lower back/pelvis
pain on outside of foot

112
Q

proximal neuropathy is more common in who

A

elderly T2DM

113
Q

what is proximal neuropathy assoc. with

A

proximal muscle weakness and marked weight loss

114
Q

what are some other names for proximal neuropathy

A

lumbosacral plexus neuropathy, femoral neuropathy or diabetic amyotrophy

115
Q

what does proximal neuropathy start with

A

pain in the thighs, hips, buttocks or legs

116
Q

does proximal neuropathy usually start on one or both sides of the body

A

one

117
Q

what is the name for the neuropathy that affects nerves regulating heart rate and blood pressure as well as control of internal organs e.g. those involved in gastric motility, respiratory function, urination, sexual function and vision

A

autonomic neuropathy

118
Q

why might someone with autonomic neuropathy not be able to see well in the dark

A

autonomic system not working so not able to dilate pupil properly

119
Q

what are 4 manifestations of autonomic neuropathy affecting the digestive system

A

constipation (gastric slowing)
diarrhoea (gastric frequency)
gastroparesis
oesophagus nerve damage

120
Q

what is gastroparesis

A

slow stomach emptying

121
Q

what are some s/s of gastroparesis

A

persistent nausea and vomiting, bloating and loss of appetite

122
Q

how can gastroparesis make someone at risk of hypo

A

can make blood glucose fluctuate widely and insulin may be in system before food is digested due to abnormal digestion

123
Q

what is some dietary advice you could give to someone with gastroparesis

A

smaller, more frequent food portions
low fat, low fibre
may need liquid meals

124
Q

what drugs can help with gastroparesis

A

promotility drugs
anti-nausea medications
serotonin antagonists

125
Q

what are 3 examples of promotility drugs

A

metoclopramide
domperidone
erythromycin

126
Q

what is an example of an anti-nausea drug

A

prochlorperazine

127
Q

what is an example of a serotonin antagonist

A

ondansetron

128
Q

how could you treat the abdominal pain in gastroparesis

A 
NSAIDs
low dose tricyclic antidepressents
gabapentin
tramadol
fentanyl
129
Q

what are 2 other treatments for gatroparesis

A

botulinum toxin

gastric pacemaker

130
Q

what would be a symptom of oesophageal nerve damage

A

difficulty swallowing

131
Q

how can diabetic autonomic neuropathy affect the sweat glands

A

stops them working so cant regulate temperature or causes perfuse sweating at night or while eating (gustatory)

132
Q

what are some treatments for diabetic autonomic neuropathy affecting the sweat glands

A

topical glycopymolate
clonidine
botulinum toxin

133
Q

how does diabetic autonomic neuropathy affect the heart and blood vessels

A

interferes with ability to adjust BP and HR

134
Q

in diabetic foot screening for diabetic neuropathy what is considered low risk

A

no loss of sensation or pulses

135
Q

in diabetic foot screening for diabetic neuropathy what is considered moderate risk

A

loss of sensation or pulses

136
Q

in diabetic foot screening for diabetic neuropathy what is considered high risk

A

loss of sensation and pulses

137
Q

what are 4 other diagnostic tools for diabetic neuropathy

A

nerve conduction studies/electromyography
HR variability
US of bladder/urinary tract
gastric emptying study

138
Q

what is diabetic nephropathy

A

progressive kidney disease caused by damage to capillaries in kidney glomeruli

139
Q

what is diabetic nephropathy characterised by

A

nephrotic syndrome and diffuse scarring of glomeruli

140
Q

what are 2 other names for diabetic nephropathy

A

kimmelsteil wilson syndrome

nodular glomerulosclerosis

141
Q

what are the consequences of diabetic nephropathy

A

hypertension
decline in renal function
accelerated vascular disease

142
Q

who is screened for diabetic nephropathy

A

all patients 12 or older at diagnosis and annually

143
Q

what is used to screen for diabetic nephropathy

A

urinary ACR
dipstick test
U+Es (eGFR)
may use random rather than first pass sample as initial check

144
Q

what are some risk factors for nephropathy progression

A 
hypertension
cholesterol
smoking
poor glycaemic control
albuminuria
145
Q

what is the target BP in all diabetic patients

A

< 130/80

146
Q

what is the target HbA1c in diabetic patients

A

around 53 (48-58)

147
Q

what should diabetic patients with microalbuminuria or proteinuria be started on

A

ACEI/ARB

148
Q

what eye changes occur in acute hyperglycaemia

A

visual blurring (reversible)

149
Q

what 4 other diabetic eye diseases are there

A

diabetic retinopathy
cataracts
glaucoma
retinal detachment

150
Q

what are the 4 stages of diabetic retinopathy

A

mild non-proliferative (background)
moderate non-proliferative
severe non-proliferative
proliferative

151
Q

how is retinopathy graded

A

R0-R4

M1 and M2

152
Q

how often should diabetic patients be screened for retinopathy

A

annually

153
Q

what are cotton wool spots

A

ischaemic areas

154
Q

what are hard exudates

A

lipid breakdown products

155
Q

what is IRMA

A

intra-retinal microvascular abnormalities - abnormalities of blood vessels/precursor to neovascularisation but blood vessels aren’t leaking

156
Q

what are some treatments for diabetic retinopathy

A

laser
vitrectomy
anti-VEGF injections

157
Q

what % of diabetic men have erectile dysfunction

A

50%

158
Q

what are the 2 causes of erectile dysfunction in diabetes

A

vascular

neuropathy

159
Q

what causes diabetic ketoacidosis

A

uncontrolled lipolysis

160
Q

what are some precipitants of DKA

A

insulin omission
infection
MI

161
Q

who is more prone to DKA type 1 or 2

A

type 1

162
Q

in DKA what would ketonaemia be

A

> 3 mmol

163
Q

in DKA what would ketonuria be

A

> ++

164
Q

in DKA what would blood glucose be

A

> 11

165
Q

in DKA what would bicarbonate be

A

< 15

< 10 in severe

166
Q

in DKA what would venous pH be

A

< 7.3

167
Q

in DKA what would K be

A

> 5.5

168
Q

in DKA what would creatinine be

A

raised

169
Q

in DKA what would Na be

A

low

170
Q

in DKA what would lactate be

A

raised

171
Q

in DKA what would amylase be

A

raised

172
Q

in DKA would the anion gap be raised or decreased

A

raised

173
Q

what are some s/s of DKA

A 
thirs/dehydration
polyuria
flushed
vomiting
abdo pain
kussmaul breathing
smell of ketones on breath (pear drops)
increased HR
174
Q

what is the treatment for DKA

A

fluids - 0.9% saline
insulin: IV infusion, 0.1 unit/kg/hour
once glucose is below 15 start infusion of 5% dextrose

175
Q

what does blood ketone testing measure

A

beta-hydroxybutyrate

176
Q

what is normal blood ketone level

A

< 0.6

177
Q

what does urine ketone testing measure

A

acetoacetate - measures levels 2-4 hours previously

178
Q

what are some life threatening complications of DKA

A 
cardiac arrest due to hyperkalaemia - arrhythmias
cerebral oedema following fluid resus
ARDS
aspiration due to gas in stomach
gastric stasis
thromboembolism
AKI
179
Q

who is more prone to hyperglycaemic hyperosmolar syndrome

A

T2DM

180
Q

what is the mortality rate of DKA

A

<2 %

181
Q

what is the mortality rate of HHS

A

10-50%

182
Q

who tends to get HHS

A

older patients or younger afro-carribean

183
Q

what has often occurred pre presentation of HHS

A

high refined CHO intake

184
Q

what drugs is HHS associated with

A

glucocorticoids/steroids

thiazide diuretics

185
Q

is diabetes always known on presentation of HHS

A

not always

186
Q

what are some precipitants of HHS

A

infection

187
Q

is hyperglycaemia higher in DKA or HHS

A

HHS, usually > 50

188
Q

is there any ketonuria in HHS

A

none/mild

189
Q

what is bicarbonate level in HHS

A

> 15

190
Q

what is the venous pH in HHS

A

> 7.3 - not acidotic

191
Q

what is osmolality in HHS

A

> 320, usually around 400

192
Q

what is Na like in HHS

A

raised

193
Q

what is the treatment of HHS

A

fluids
insulin
sodium (o.5 mmol/L/hr)
LMWH

194
Q

why should fluids be given more cautiously in HHS

A

higher risk of fluid overload

195
Q

is insulin always required in HHS

A

no

also given more slowly as more sensitive (3 units/hour)

196
Q

why is LMWH given in HHS

A

comorbidities common - screen for vascular events e.g. MI, sepsis

197
Q

what is going on…
elderly female
heavy alcohol intake for years
admitted with recurrent vomiting
on 16 different medications including acamprosate
she is hypotensive, tachypnoeic and difficult to rouse

A

alcohol induced ketoacidosis

198
Q

what is the treatment for alcohol induced keto-acidosis

A

IV pabrinex
IV fluids
IV antiemetics
insulin (maybe)

199
Q

is there ketonuria/ketonaemia in AIKA

A

ketonaemia > 3

ketonuria significant

200
Q

what is bicarb usually in AIKA

A

< 15

201
Q

what is venous pH in AIKA

A

< 7.3

202
Q

what is glucose levels in AIKA

A

normal/low

203
Q

what is lactate

A

end product of anaerobic metabolism of glucose

204
Q

clearance of lactate involves ____ uptake and ____ conversion into _____ then _____

A

hepatic uptake
aerobic conversion
pyruvate
glucose

205
Q

what is normal lactate

A

0.6 - 1.2

206
Q

when is lactate lowest

A

fasting state

207
Q

what can increase lactate to 10

A

severe exercise

208
Q

what happens to the ion gap in lactic acidosis

A

raised

209
Q

what is the ion gap

A

[K+ + Na+] - [HCO3- + Cl-]

210
Q

what is a normal ion gap range

A

10-18

211
Q

what is lactic acidosis type A

A

assoc. tissue hypoxaemia

e. g. infarcted tissue (ischaemic bowel), cardiogenic shock, hypovolaemic shock, sepsis, haemorrhage

212
Q

what is lactic acidosis type B associated with

A

liver disease
leukaemic states
diabetes
rare inherited conditions

213
Q

what are the clinical features of lactic acidosis

A

hyperventilation
mental confusion
stupar/coma

214
Q

what happens to bicarbonate in lactic acidosis

A

reduced

215
Q

is there ketonaemia in lactic acidosis

A

no

216
Q

what happens to phosphate in lactic acidosis

A

raised

217
Q

what is the tx of lactic acidosis

A

fluids, antibiotics

218
Q

what is wolfram syndrome

A

rare genetic condition causing DI, DM, optic atrophy, deafness and neuro abnormalities (DIMOAD)

219
Q

what is the equation for osmolarity

A

2(Na + K) + glucose + urea

220
Q

what is charcot foot

A

progressive degeneration of weight bearing joints leading to deformity

221
Q

how does charcot foot present

A

hot red swollen foot

222
Q

what can charcot foot often be mistaken for

A

DVT or cellulitis

223
Q

what causes Bardet Biedl syndrome

A

insest parents

224
Q

what are some s/s of bardet biedl syndrome

A 
polydactyly
hypogonadal
visual/hearing impairment
mental retardation
diabetes
obese
225
Q

what is the folic acid dose for non-diabetic pregnant patient

A

400mcg

226
Q

what is the folic acid dose for diabetic pregnant patient

A

5mg

year 2 (19 decks)

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