Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Endocrine > Diabetes > Flashcards

Diabetes Flashcards

1
Q

compare diabetes mellitus vs diabetes insipidus?

A

similar symptons (eg large volumes of urine, excessive thirst)

DM- problem with glucose regulation
DI- problem with water regulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is diabetes mellitus?

A

a group of metabolic disease characterised by hyperglycemia resulting from defects in insulin secretion, insulin action or both

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

for the diagnosis of diabetes, what must the HbA1c be?

A

48 m/m +

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is the normal range of HbA1c?

A

41 m/m and below

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

for the diagnosis of diabetes, what must the fasting glucose be?

A

7.0 mmol/L +

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the normal range of fasting glucose?

A

6.0 mmol/L and below

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

for the diagnosis of diabetes, what is the 2-hr glucose in OGTT?

A

11.1 mmol/L +

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the normal range of 2-hr glucose in OGTT?

A

7.7 mmol and below

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

for the diagnosis of diabetes, what is the random glucose?

A

11.1 mmol/L +

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what defines type 1 diabetes?

A

pancreatic beta cell destruction
-anti-GAD/anti-islet cell antibodies usually
insulin is required for survival

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is the initial management of type 2 diabetes?

A

diet control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

compare type 1 and type 2 diabetes in terms of the presence of ketonuria at diagnosis?

A

type 1: present

type 2: minimal or absent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

compare type 1 and type 2 diabetes in terms of the presence of microvascular disease at diagnosis?

A

type 1: no evidence

type 2: evidence in 20% of cases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

compare type 1 and type 2 diabetes in terms of age at onset?

A

type 1: pre-school, peri-puberty

type 2: middle aged/elderly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are the 3 most useful tests to discriminate between type 1 and type 2 diabetes?

A
  • GAD/anti-islet cell antibodies
  • ketones
  • C-peptide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is type 3 diabetes?

A

diabetes secondary to a disease/syndrome/drug/monogenic cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are the 3 main pancreatic causes of type 3 diabetes?

A

chronic/recurrent pancreatitis
haemochromatosis
cystic fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what are the 4 main endocrine causes of type 3 diabetes?

A

cushings syndrome
acromegaly
phaechromocytoma
glucagonoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are the 3 main drug-induced causes of type 3 diabetes?

A

glucocorticoids
diuretics
b-blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what are the 3 main genetic causes of type 3 diabetes?

A

CF
myotonic dystrophy
turner’s syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

will C-peptide be positive or negative in monogenic diabetes?

A

positive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is type 4 diabetes?

A

gestational diabetes:

any degree of glucose intolerance arising or diagnosed during pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

HbA1c provides a measure of glucose control over the past how many months?

A

2-3 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is the classic triad of type 1 diabetes symptoms?

A
  • polyuria (enuresis in children)
  • polydipsia
  • weight loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is the ideal HbA1c range for a type 1 diabetic patient?

A

48-58 mmol/l

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

are children more likely to get type 1 diabetes if their mother or father has diabetes?

A

father

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

the normal release of insulin after a meal is biphasic how long does each phase last?

A

rapid phase of pre-formed insulin: 5-10 minutes

slow phase: 1-2 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

which blood vessel is insulin secreted into?

A

hepatic portal vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

compare type 1, type 2 and MODY diabetes in terms of length of symptoms and severity?

A

type 1: short length with severe symptoms

type 2 and MODY: gradual progression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

are children under 6 months presenting with diabetes more likely to have type 1 or monogenic diabetes?

A

monogenic diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what is LADA?

A

latent onset diabetes of adulthood-
elevated levels of pancreatic auto-antibodies in patients with recently diagnosed diabetes who do not initially require insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what age does LADA tend to occur?

A

(males usually) 25-40

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what is wolfram syndrome?

A

a rare genetic syndrome causing diabetes insipidus ,diabetes mellitus, optic atrophy, deafness and neurological anomalies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what is bardet-biedl syndrome caused by?

A

a genetic disorder

can be caused by consanguineous parents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what are the 6 main symptoms of bardet-biedl syndrome?

A
  • polydactyly
  • hypogonadal
  • visual impairment
  • hearing impairement
  • mental retardation
  • diabetes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what is the primary and secondary dysfunctions in type 2 diabetes?

A

primary: insulin resistance
secondary: beta cell dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what are the main 2 causes of insulin resistance?

A
  1. ectopic fat accumulation and increased circulating free fatty acids
  2. increased inflammatory mediators
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what is insulin resistance a precursor for?

A

type 2 diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what happens to the insulin levels over a period of time in a patient with impaired glucose tolerance?

A

insulin initially rises but then falls due to pancreatic burnout (beta cell dysfunction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what 2 toxicities caused by insulin resistance causes declining beta-cell function?

A

glucotoxicity (hyperglycaemia)

lipotoxicity (elevated free fatty acids and triglycerides)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

is beta-cell dysfunction reversible in type 2 diabetes?

A

yes

reversed by controlling diet in patients diagnosed less than 10 years ago

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

who is more likely to get diabetes- someone with a pear or apple shape?

A

apple shape- greater fat distribution around abdominal organs
[central adiposity]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

are micro or macrovascular complications more likely in type 2 diabetic patients?

A

microvascular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what are the 3 main red flags which will help you distinguish LADA from type 2 diabetes?

A
  • thin patient
  • patient losing weight
  • PMHx of pancreatic disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

why do we treat hyperglycaemia in type 2 diabetes?

A

to reduce the risk of complications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what is the only biguanide used in the treatment of type 2 diabetes?

A

metformin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

how do biguanides work in the treatment of type 2 diabetes?

A

improves sensitivity to insulin

reduced insulin resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

is there a hypogylcaemia risk with metformin?

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what is the effect of metformin on weight?

A

weight neutral usually

can reduce weight

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

does metformin prevent from microvascular complications?

A

yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

does metformin prevent from macrovascular complications?

A

yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

is metformin safe to use in pregnancy?

A

yes

-so can be used in gestational diabetes of pre-existing type 2 diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

lactic acidosis is a rare side effect of metformin, what patients are more likely to get this?

A

patients with severe renal, cardiac or liver failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

what happens to the tissues in lactic acidosis?

A

become hypoxic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

how do you reduce the potential GI side effects of metformin? (nausea, diarrhoea, anorexia, abdo pain, diarrhoea)

A

‘start low and go slow’

start at a very low dose and slowly work your way up

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

how do you reduce the potential lactic acidosis side effect of metformin?

A

use with caution in patients with liver, cardiac or renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

what must the eGFR be to avoid or stop the treatment of type 2 diabetes with metformin?

A

below 30 eGFR stop metformin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

what must the eGFR be to half the treatment dose of metformin in a diabetic patient/

A

30-45 eGFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

what is the first line agent for type 2 diabetes?

A

metformin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

how do sulphonylureas work?

A

close the ATP-dependent potassium channes causing depolarisation of the pancreatic beta cell

this depolarisation causes the opening of voltage gated calcium channels and an influc of calcium which stimulates the release of insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

which has a faster action period- sulphonylureas or insulin sensitisers?

A

sulphonylureas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

is there a risk of hypoglycaemia with sulphonylureas?

A

yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

do sulphonylureas prevent microvascular complications?

A

yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

do sulphonylureas prevent macrovascular complications?

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

how do sulphonylureas accelerate the progression of type 2 diabetes?

A

by causing the accelerated demise of pancreatic beta cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

what is the effect of sulphylureas on weight?

A

weight gain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

when must use avoid using sulphonylureas?

A

in severe renal or heatic failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

what is the only thiazolidinediones (TZD) available in the treatment of type 2 diabetes?

A

pioglitazone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

how do thiazolidinediones (TZDs) work?

A

work on nuclear receptors (PPAR-gamma) to increase gene transcription

this increases glucose and fatty acid uptake
(insulin sensitiser)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

is there a risk of hypoglycaemia with thiazolidinediones? (TZD)

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

do TZDs prevent microvascular complications?

A

no

but improve microalbuminuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

do TZDs prevent macrovascular complications?

A

yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

what are the effects of TZD on heart attack risk and heart failure?

A

reduces risk of heart attacks

but makes heart failure worse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

which diabetes drug increases the risk of hip fractures?

A

pioglitazone (TZD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

why does the oral response to glucose result in a higher insulin release than glucose entering blood vessels directly? (ie IV)

A

incretin effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

what are incretins stimulated by?

A

glucose in the gut

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

what enzyme breaks down incretins quickly?

A

DPP-IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

what are the 5 main effects of incretins?

A
  • stimulate insulin secretion
  • reduce liver gluconeogenesi
  • delay gastric emptying (feeling of satiety)
  • direct effect on appetite center (feeling of satiety)
  • decrease glucagon secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

how do incretins (and incretin agonists) cause an increased insulin release?

A

make the beta cells more sensitive to glucose

80
Q

are patients on incretin agonists (eg GLP-1) at risk of hypoglycaemia?

A

no

81
Q

how do DPP-IV inhibitors work in the treatment of type 2 diabetes?

A

prevent the action of DPP-IV enzymes therefore prolong the actions of incretins

82
Q

which is more potent, GLP-1 mimetics or DPP-IV inhibitors?

A

GLP-1 mimetics

83
Q

what is the main disadvanatage of GLP-1 over DPP-IV?

A

injection to administrate

DDP-IV is oral

84
Q

what is the effect of GLP-1 receptor agonists on weight?

A

weight loss

85
Q

what is the effect of DPP-IV inhibitors on weight?

A

weight neutral

86
Q

How do SGLT-2 inhibitors work?

A

prevent the reabsorption of glucose within the kidney tubules by SGLT-2 transporters

87
Q

is there a risk of hypoglycaemia with DPP-IV inhibitors?

A

no

88
Q

is there a risk of hypoglyaemia with SGLT-2 inhibitors?

A

no

89
Q

what is the effect of SGLT-2 inhibitors on weight?

A

weight loss

90
Q

what are the main disadvantages of SGLT-2 inhibitors? and explain why?

A

thrush
UTIs

due to increased sugar in urine

91
Q

what are the 2 broad classes of drugs for type 2 diabetes mellitus? (ignoring insulin)

A
  • insulin dependent

- insulin independent

92
Q

within the insulin dependent drug group for type 2 diabetes mellitus, what are the 2 sub-groups of drug action?

A
  • drugs which increase insulin secretion

- drugs which increase insulin sensitivity

93
Q

within the insulin independent drug group for type 2 diabetes mellitus, what are the 2 sub-groups of drug action?

A
  • drugs which slow glucose (or lipid) absorption from the GI tract
  • drugs which increase kidney excretion of glucose
94
Q

what is the action of orlistat for type 2 diabetes?

A

orlistat decreases the absorption of fats
(insulin-independent)

this indirectly is a benefit to diabetes because it leads to weight loss

95
Q

compare the polarisation state of a pancreatic beta cell when there is high blood glucose and when there is low blood glucose?

A

high blood glucose- depolarised

low blood glucose- resting potential is maintained

96
Q

what is the structure of a ATP-sensitive K channel?

A

4 inner Kir6.2 subunits

4 outer SUR1 subunits

97
Q

what are the functions of the Kir6.2 and SUR1 subunits within the ATP-sensitive K channel?

A

4 Kir6.2 subunits form the potassium selective ion channel

SUR1 subunits regulare the activity of the potassium ion channel

98
Q

when extracellular glucose is high, ATP binds to what part of the ATP-sensitive K channel and what does this cause?

A

ATP binds to Kir6.2 subunits

causes closing of channels and depolarisation

99
Q

when extracellular glucose is low, ADP-Mg++ binds to what part of the ATP-sensitive K channel and what does this cause?

A

ADP-Mg++ binds to SUR1 subunits

causes opening of channels and maintains the resting potential

100
Q

sulfonylureas bind to what part of the ATP-sensitive K channel and what does this cause?

A

bind to SUR1 subunits and so displace the binding of ADP-Mg++

causes closing of channels and depolarisation

101
Q

compare 1st generation sulfonylureas to 2nd generation sulfonylureas in terms of potency and acting-time?

A

2nd generation are more potent and longer acting than 1st

102
Q

why can sulfonylureas cause hypoglycaemic episode?

A

excessive insulin secretion

103
Q

which generation of sulfonylureas have a higher hypoglycaemia risk?

A

2nd generation

104
Q

why might you give an elderly patient or a patient with reduced hepatic/renal function a 1st generation SU instead of 2nd generation?

A

to reduce risk of hypos

this patient group is at higher risk

105
Q

what is the action of glinides for type 2 diabetes?

A

glinides act similarly to sulfonylureas

bind to SUR1 subunits on ATP-sensitive K channel to close channel and cause depolarisation and hence insulin secretion

(insulin dependent, cause increased insulin secretion)

106
Q

which drug is more likely to cause hypoglycaemia- sulfonylureas or glinides?
and why?

A

sulfonylureas

longer-acting than glinides which have rapid onset/offset kinetics

107
Q

when are glinides taken and why?

A

before/with meals to reduce postprandial rise in blood glucose

108
Q

what is GLP-1?

A

glucagon like peptide-1

109
Q

what is the function of GLP-1?

A

enhances glucose uptake by pancreatic beta cells

decreases glucagon release from pancreatic alpha cells

decreases gluconeogenesis by the liver

all to reduce blood glucose

110
Q

what is GIP?

A

glucose-dependent insulinotrophic peptide/

gastric inhibitory peptide

111
Q

what is the function of GIP?

A

enhances glucose uptake by pancreatic beta cells

slows gastric emptying

both to decrease blood sugar

112
Q

what cells produce GLP-1?

A

L cells from ilium and colon

113
Q

what cells produce GIP?

A

K cells from jejunum/duodenum

114
Q

what blood vessel do GLP-1 and GIP first enter?

A

hepatic portal vein

115
Q

what hormone do incretin analogues mimic?

A

GLP-1

116
Q

what type of drug is extenatide?

A

incretin analogue

117
Q

how is extenatide administered?

A

twice a day subcutaneously

118
Q

what type of drugs are gliptins?

A

DDP-IV inhibitors

119
Q

what is the function of a-glucosidase?

A

breaks down starch/diasaccharides into absorbable glucose

120
Q

what is the action of a-glucosidase inhibitors?

A

inhibit the action of a-glucosidase and so delay absorption of glucose and therefore reduce postprandial increase in blood glucose

121
Q

what are the main side effects of glucosidase inhibitors?

A 
GI Upset:
flatulence
loose stools
diarrhoea
abdo pain
bloating
122
Q

do a-glucosidase inhibitors cause hypos?

A

no

123
Q

what are the 3 main adverse effects of TZDs?

A

weight gain
fluid retention
increased risk of bone fractures

124
Q

what type of T2DM drus ig dapagliflozin?

A

SGLT2 inhibitor

125
Q

what does MODY stand for?

A

Maturity Onset Diabetes of the Young

126
Q

what type of inheritence is Maturity Onset Diabetes of the Young (MODY)?

A

autosomal dominant inheritance

127
Q

what is the age of onset of Maturity Onset Diabetes of the Young (MODY)?

A

usually before the age of 25

128
Q

what are the 2 mutations causing Maturity Onset Diabetes of the Young (MODY) that give 2 distinct phenotypes?

A

mutation in transciption factor HNF

mutation in glucokinase

129
Q

compare MODY glucokinase mutations to transcription factor mutations in terms of onset?

A

glucokinase mutations- onset at birth

transcription factor mutations- young adult onset

130
Q

compare MODY glucokinase mutations to transcription factor mutations in terms of hyperglycaemia progression?

A

glucokinase mutations- stable hyperglycaemia

transcription factor mutation- progressive hyperglycaemia

131
Q

compare MODY glucokinase mutations to transcription factor mutations in terms of treatment?

A

glucokinase mutations- diet treatment

transcription factor mutations- 1/3 diet, 1/3 oral hypoglycaemic agents, 1/3 insulin

132
Q

compare MODY glucokinase mutations to transcription factor mutations in terms of complications?

A

glucokinase mutations- complications rare

transcription factor mutations- complications frequent

133
Q

what are the 2 classes of neonatal diabetes?

A

transient neonatal diabetes

permanent neonatal diabetes

134
Q

when is permanent neonatal diabetes usually diagnosed?

A

0-6 weeks

135
Q

when should insulin treatment for transient neonatal diabetes be stopped?

A

once diabetes has resolved

usually after 3 months

136
Q

when should insulin treatment for permanent neonatal diabetes by stopped?

A

lifelong treatment

137
Q

what is the target blood glucose concentration for a type 1 diabetic pre-meal?

A

4-7 mmol/l

138
Q

what is the target blood glucose concentration for a type 1 diabetic 1-2 hours after a meal?

A

5-9 mmol/l

139
Q

what are the 4 life-threatening complications of diabetic ketoacidosis?

A
  • cardiac arrest due to hyperkalaemia
  • cerebral oedema
  • ARDS
  • aspiration due to gas in stomach
140
Q

what is the typical osmolarity in a normal patient?

A

285 - 295

141
Q

what is the osmolarity of a patient in hyperglycamic hyperosmolar Syndrome typically?

A

around 400

142
Q

how do you calculate osmolarity?

A

2(Na + K) + glucose + urea

143
Q

how do you treat hyperosmolar hyperglycaemic state?

A
  • treating underlying cause
  • replace fluid and electrolyte losses
  • normalising blood glucose
144
Q

what is the normal range of lactate?

A

0.6 to 1.2 mmol/L

145
Q

how do you calculate the ion gap?

A

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

146
Q

what is the normal ion gap range?

A

10 - 18 mmol/L

147
Q

what is usually associated with type A lactic acidosis?

A

tissue hypoxaemia

infarcted tissue, cardiogenic shock, hypovolaemic shock

148
Q

which type of lactic acidosis is associated with diabetes?

A

type B lactic acidosis

149
Q

what are the 3 clinical features of lactic acidosis?

A

hyperventilation
mental confusion
stupor/coma

150
Q

does a raised anion gap suggest metabolic acidosis or alkalosis?

A

metabolic acidosis

151
Q

compare severe DKA to alcohol-induced keto-acidosis in terms of blood glucose levels?

A

DKA- high blood glucose levels

alcohol-induce keto-acidosis- normal blood glucose lebels

152
Q

as Hb1Ac increases, what happens to the risk of microvascular complications?

A

increases

153
Q

what is the basis of neuropathy?

A
  • small blood vessels to nerves become damaged due to high glucose levels
  • reduced oxygen supply causes the nerves to become damaged
154
Q

what are the 4 main types of neuropathy caused as a complication of diabetes?

A
  • peripheral neuropathy
  • autonomic neuropathy
  • proximal neuropathy
  • focal neuropathy
155
Q

what type of neuropathy leads to hypoglycaemic unawareness?

A

autonomic neuropathy

156
Q

what is amyotrophy?

A

progressive wasting of muscle tissues

157
Q

what distribution is peripheral neuropathy usually in?

A

glove + stocking distribution

158
Q

is there an increased risk of neuropathy with type 1 or type 2 diabetes?

A

type 1 diabetes

159
Q

what is allodynia?

A

pain from a non-painful stimulation of the skin

160
Q

what is gastroparesis?

A

slow stomach emptying

161
Q

what symptoms does gastroparesis cause?

A

nausea
vomitting
bloating
loss of appetite

162
Q

why can gastroparesis make blood glucose levels fluctuate widely and make patient susceptible to hypoglycaemia?

A

abnormal food digestion

insulin may be in system before food has been absorbed

163
Q

what is gustatory sweating?

A

sweating after eating

164
Q

why might a patient with autonomic neuropathy have trouble seeing in the dark?

A

autonomic system not working properly so pupil might not dilate enough

165
Q

what is focal neuropathy?

A

sudden weakness in one nerve/group of nerves causing muscle weakness

166
Q

how many times a year should diabetics have a foot exam?

A

at least once a year

167
Q

what does low risk mean in terms of diabetic foot risk stratification?

A

no loss of sensation or pulses

168
Q

what does moderate risk mean in terms of diabetic foot risk statification?

A

loss of sensation OR loss of pulses

169
Q

what does high risk mean in terms of diabetic foot risk stratification

A

loss of sensation AND loss of pulses

170
Q

what is charcot foot?

A

progressive degeneration of weight-bearing joints leading to deformity

171
Q

how does a charcot foot present?

A

hot, red, swollen foot
-often mistaken for cellulitis, DVT
(maybe be deformed)

172
Q

what are the 3 main consequences of diabetic nephropathy?

A
  • development of hypertension
  • decline in renal function
  • accelerated vascular disease
173
Q

what do you use to screen for diabetic kidney disease?

A

urinary albumin creatinine ratio

174
Q

what drug is used to improve mortality in diabetic kidney disease (ie microalbuminuria or proteinuria)?

A

ACE inhibitors

175
Q

can pioglitazone (TZD) be used in chronic kidney disease?

A

yes

176
Q

can gliclazide (SU) be used in chronic kidney disease?

A

in moderate disease yes

not in severe disease

177
Q

can metformin be used in chronic kidney disease?

A

in moderate disease yet

not in severe disease

178
Q

what is glaucoma?

A

increase in fluid pressure in the eye leading to optic nerve damage

179
Q

compare diabetic retinopathy and acute hyperglycaemia visual blurring in terms of reversibility?

A

diabetic retinopathy- irreversible

acute hyperglycaemia- visual blurring- reversible

180
Q

what are the 4 main stages of retinopathy?

A

mild non-proliferative
moderate non-proliferative
severe non-proliferative
proliferative

181
Q

what are cotton wool spots on retinopathy?

A

ischaemic areas

182
Q

what are hard exudates the break down products of?

A

lipids

183
Q

what hormone does the fertilised egg release which is used to detect pregnancy?

A

HCG

184
Q

what are the 3 main hormones that the placenta produces?

A

human placental lactogen
placental progesterone
placental oestrogens

185
Q

what 2 hormones produced by the placenta cause insulin resistance in the mother?

A

placental progesterone

human placental lactogen

186
Q

if the mother is already predisposed to insulin resistance, what happens when the placental hormones cause further insulin resistance?

A

raised blood glucose and gestational diabetes

187
Q

in what trimester does gestational diabetes tend to come on?

A

third trimester

188
Q

why does gestational diabetes tend to come on in the third trimester?

A

because this is the time when the placental grows significantly and so the levels of placental hormones increases

189
Q

what are the 3 main complications of gestational diabetes? (before delivery)

A

macrosomia
polyhydramnios
intrauterine death

190
Q

what are the 3 main complications of maternal diabetes in neonates? (after delivery)

A

respiratory death (due to immature lungs)
hypoglycaemia
hypocalcaemia

191
Q

why can neonates born to diabetic mothers (DM or gestational) have hypoglycaemia after delivery?

A

high sugar load from mother near birth causes excess insulin production.

once born, the baby no longer gets the high blood sugars yet still has high insulin production causing hypoglycaemia

192
Q

why can macrosomia be a complication of babies born to diabetic (DM or gestational) mothers?

A

hyperglycaemia causes excess insulin production

insulin is a major growth factor

193
Q

why should a diabetic pregnant woman have regular eye checks?

A

pregnancy accelerates retinopathy

194
Q

compare folic acid dose for a non-diabetic pregnant patient to a diabetic pregnant patient?

A

diabetic: 5mg

non-diabetic: 400 micrograms

195
Q

what is the one exception to avoiding the use sulfonylureas in pregnancy?

A

glibenclamide in MODY

196
Q

why must you do a post natal glucose tolerance test 6 weeks after delivery in a patient with getational diabetes?

A

to ensure diabetes has gone

if it still remains after 6 weeks- patient now has type 2 diabetes

Endocrine (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions