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Endocrinology > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Define diabetes mellitus?

A
  • An elevation of blood glucose above a diagnostic threshold
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2
Q

What is the threshold for diabetes diagnosis based upon?

A
  • The risk of developing retinopathy
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3
Q

For the diagnostic criteria of diabetes mellitus what is the critical value for fasting plasma glucose that defines diabetes?

A
  • Fasting plasma glucose >7mmol/L
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4
Q

For the diagnostic criteria of diabetes mellitus what is the critical value for 2hr plasma glucose that defines diabetes?

A
  • 2 hour plasma glucose >11.1 mmol/L
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5
Q

For the diagnostic criteria of diabetes mellitus what is the critical value for HbA1c that defines diabetes?

A
  • HbA1c > 48mmol/L
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6
Q

What is gestational diabetes referring to?

A
  • Diabetes during pregnancy

- Risk to fetus

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7
Q

The diagnostic criteria for gestational diabetes is __lower/higher___ than that for diabetes mellitus?

A
  • Lower
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8
Q

Insulin is secreted from___

A
  • beta cells in the pancreatic islet in response to blood glucose levels
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9
Q

Insulins main function is to___

A
  • lower blood glucose levels
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10
Q

Glucagon is secreted from____

A
  • alpha cells in the pancreatic islet in response to blood glucose levels
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11
Q

Glucagon ____ blood glucose levels?

A
  • Increases blood glucose level
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12
Q

Explain c-peptide

A
  • Useful way to measure endogenous insulin
  • c-peptide + insulin = pro-insulin, which is then cleaved to produce insulin
  • c-peptide is not found in injectable insulin therefore is a marker of insulin production
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13
Q

What are the 2 scales of diabetes?

A
  • Failure of production of insulin

- Insulin resistance

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14
Q

Name some disorders of insulin secretion?

A
  • type 1 diabetes
  • MODY
  • Pancreatitis caused by alcohol, CF, haemochromatosis
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15
Q

Name some disorders of insulin action

A
  • Donohue-syndrome
  • obesity
  • type 2 diabetes
  • NAFLD
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16
Q

Type 2 diabetes is __homogenous/heterogenous___

A
  • highly heterogenous
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17
Q

Type 1 diabetes is characterised by what?

A
  • pancreatic autoantibodies
  • autoimmune condition of beta-cells
  • anti GAD
  • 1A2
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18
Q

What are some symptoms of diabetes?

A
  • polyuria
  • thirst
  • blurred vision
  • fatigue
  • weight loss
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19
Q

What microvascular complications are associated with diabetes?

A
  • neuropathy
  • retinopathy
  • nephropathy
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20
Q

What macrovascular complications are associated with diabetes?

A
  • MI
  • stroke
  • PVD
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21
Q

A HbA1c level of ___ in a diabetic indicates good control?

A
  • 48mmol/mol
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22
Q

What is the HbA1c blood test assessing?

A
  • control of diabetes over 3 months (90 days)

- glycated haemoglobin which is proportional to sugar levels

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23
Q

What will the affect of haemolytic anaemia have on the HbA1c test?

A
  • reduced life-span of RBC

- not a true level of control

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24
Q

What percentage weight loss can put diabetes type 2 into remission?

A
  • 10-15%
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25
Q

Explain what is meant by a relative insulin deficiency in T2DM?

A
  • Insulin resistance and beta cell dysfunction
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26
Q

What are some environmental risk factors for T2DM?

A
  • Obesity
  • age
  • pregnancy
  • calorie dense diet
  • sedentary lifestyle
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27
Q

How will the islet of langerhans appear in the microscope?

A
  • highly vascularised

- dense collection of cells

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28
Q

What do delta cells of the pancreas secrete?

A
  • somatostatin
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29
Q

What is the role of somatostatin from the pancreas?

A
  • inhibits both insulin and glucagon release
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30
Q

How does obesity affect insulin production?

A
  • fat reduces insulin action
  • beta cells produce more insulin as compensation
  • long term compensation may lead to T2DM
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31
Q

What stabilises insulin vesicles within the beta cell before they are exocytosed?

A
  • zinc
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32
Q

What would a long term diabetes pancreas appear like down the microscope?

A
  • marked reduction in the quantity of beta cells

- known as degranulation

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33
Q

1st phase of the biphasic release of insulin releases what type of insulin?

A
  • readily releasable
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34
Q

Explain the cascade of low glucose in an alpha cell?

A
  • low glucose
  • K/ATP channels open
  • Na+ gates open
  • Ca2+ channels open
  • glucagon exocytosis
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35
Q

What happens in the alpha cell when glucose is increased?

A
  • Closure of K/ATP channel
  • SGLT2
  • Ca2+ gates closed
  • no glucagon released
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36
Q

What is the role of glucagon?

A
  • Acts on the liver to promote hepatic glucose production

- raises blood glucose levels

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37
Q

Paracrine signalling requires___?

A
  • the 2 cells to be close together
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38
Q

Explain the incretin effect?

A
  • insulin secretion is greater from oral glucose relative to an isoglycaemic IV infusion
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39
Q

Name 2 incretin hormones?

A
  • GLP-1

- GIP

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40
Q

GLP-1 is released from what cells?

A
  • L cells of the gut
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41
Q

Name a GLP-1 receptor agonist drug?

A
  • liragluitde
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42
Q

How does GLP-1 RA drugs work?

A
  • bind to GLP-1 GPCR
  • Increases insulin secretion
  • promotes beta cell proliferation
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43
Q

What other positive effects of GLP-1 RA are there other than insulin increase?

A
  • reduced appetite
  • delayed gastric emptying
  • inhibition of glucagon secretion
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44
Q

What breaks down GLP-1?

A
  • DPP 4
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45
Q

Name a DPP4 inhibitor drug?

A
  • sitagliptin
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46
Q

Natural form of GLP-1 has a __long/short__ half life?

A
  • short

- for drugs analogues are given

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47
Q

Insulin resistance can be linked to what other conditions?

A
  • diabetes
  • neurodegenerative diseases
  • chronic kidney disease
  • gout
  • heart failure
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48
Q

What is the gold standard for measurement of insulin sensitivity?

A
  • Hyperinsulinemic-euglycemic clamp
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49
Q

Explain how the hyperinsulinemic-euglycemic clamp works?

A
  • keeps glucose levels static
  • fixed increased insulin dose
  • measure how much glucose is required to maintain levels
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50
Q

More glucose required to maintain levels on the hyperinsulinemic-euglycemic clamp suggests what?

A
  • good insulin sensitivity
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51
Q

What are the 3 insulin resistance mechanisms?

A
  • impairment in insulin signalling
  • inflammation
  • hepatic insulin resistance
52
Q

Monogenic diabetes is caused by what?

A
  • a single gene mutation
53
Q

Most common monogenic diabetes?

A
  • MODY

- mature onset of diabetes in the young

54
Q

How many genes have been linked to neonatal diabetes?

A
  • 35
55
Q

What is the most common neonatal diabetes gene?

A
  • KCNJ11

- Mutations in K/ATP channel

56
Q

Treatment of neonatal diabetes?

A
  • off insulin

- high dosage sulphonylureas

57
Q

Acanthosis nigricans is found where and is a sign of what?

A
  • found in flexural creases

- sign go hyperinsulinaemic state

58
Q

How many genes have been linked to MODY?

A
  • 11 genes
59
Q

MODY is autosomal ____

A
  • dominant
60
Q

MODY is characterised by what?

A
  • beta cell deficiency

- non-insulin dependant

61
Q

Non-insulin dependant diabetes under the age of 25?

A
  • MODY
62
Q

Most common gene mutation in transcriptional factor MODY?

A
  • HNF-1 alpha
63
Q

Two types of MODY?

A
  • Transcriptional factor

- glucokinase mutation

64
Q

Normal blood glucose in early childhood MODY? Normal fasting glucose

A
  • transcriptional factor MODY
65
Q

MODY that won’t respond well to a glucose tolerance test?

A
  • Transcriptional factor
66
Q

Treatment of transcription factor MODY?

A
  • Off insulin

- low dose sulphonylureas

67
Q

KCNJ11 mutation associated with what?

A
  • neonatal diabetes

- permanently open K/ATP channels

68
Q

HNF-1alpha patients are 4 times more sensitive to ____ that patients with T2DM?

A
  • Sulphonylureas
69
Q

Glucokinase in the beta cell is the ___

A
  • Rate determining step
70
Q

In glucokinase MODY homeostatic level of glucose is ___higher/lower___ than the normal population?

A
  • higher

- graph shifted to the right

71
Q

Glucokinase MODY responds well to glucose challenge testing?

TRUE OR FALSE?

A
  • TRUE

- they can produce enough insulin if challenge enough

72
Q

Distinct high fasting glucose in a new born who responds well to a glucose challenge/tolerance test, suggests what?

A
  • Glucokinase mutation MODY

- Stable hyperglycaemia

73
Q

Treatment of glucokinase MODY?

A
  • Off insulin

- no treatment

74
Q

Why is no treatment given to glucokinase MODY?

A
  • Glucokinase receptors in brain still work and programmed to hyperglycaemia, will counteract any drug given
  • no complications associated with glucokinase MODY so no need for treatment
75
Q

In glucokinase MODY the beta cell is functionally not working?
TRUE OR FALSE?

A
  • FALSE
  • homeostatic hyperglycaemic
  • can produce enough insulin in challenge
  • beta cell is normal otherwise
76
Q

What occurs during the annual screening appointment of diabetics?

A
  • digital retinal screening
  • foot risk assessment
  • albumin:creatinine ratio
77
Q

What is the complications of hyperglycaemia?

A
  • excess glucose with mitochondrial dysfunction leads to build up of reactive oxygen species
78
Q

What eye diseases are associated with diabetes?

A
  • diabetic retinopathy
  • diabetic macular oedema
  • cataracts
  • glaucoma
  • acute hyperglycaemia
79
Q

Haemorrages on fundoscopy appear as what?

A
  • dot
  • blobs
  • flames
80
Q

Cotton wool spots on fundoscopy indicates what?

A
  • ischaemic areas
81
Q

Hard exudates on fundoscopy indicates what?

A
  • lipid breakdown products
82
Q

What is the 1st line treatment for retinopathy?

A
  • laser

- pan retinal photocoagulation

83
Q

Explain laser pan retinal photocoagulation?

A
  • reduces oxygen requirements of retina

- reduces ischaemia

84
Q

If laser pan retinal photocoagulation doesn’t work in the treatment of retinopathy what may be done?

A
  • vitrectomy
85
Q

What is the first line treatment for diabetic macular oedema?

A
  • intravitreal anti-VEGF

- 2nd line - grid laser to macula

86
Q

Explain nephropathy?

A
  • progressive kidney disease cause by damage to the capillaries in the kidney’s glomeruli
87
Q

What are some consequences of nephropathy?

A
  • development of hypertension
  • decline in renal function
  • accelerated vascular disease
88
Q

Microalbuminuria is a ACR of what?

A

<30

89
Q

Proteinuria is an ACR of what?

A

> 30

90
Q

How is microalbuminuria measured?

A
  • not on normal urine dipsticks
  • radioimmunoassay
  • special dipsticks
91
Q

How many positive results do you need to confirm diabetic microalbuminuria?

A
  • 2/3 positive
92
Q

What is the treatment of microalbuminuria?

A
  • ACE inhibitors
  • ARB
  • SGLT2 inhibitors
93
Q

Risk factors for neuropathy?

A
  • increased length of diabetes
  • poor glycaemic control
  • high cholesterol
  • smoking
94
Q

Peripheral neuropathy has what distribution?

A
  • glove and stocking
95
Q

Symptoms of peripheral neuropathy?

A
  • numbness
  • tingling/burning
  • sensitivity to touch
96
Q

Consequences of peripheral neuropathy?

A
  • painless trauma
  • charcot foot
  • foot ulcer
97
Q

What are the 4 different types of neuropathy?

A
  • peripheral
  • proximal
  • autonomic
  • focal
98
Q

Explain charchot arthropathy?

A
  • destructive inflammatory process

- deformity of the foot

99
Q

Treatment of charcot arthropathy?

A
  • total cast or air cast
100
Q

Presentation of charcot arthropathy?

A
  • swollen hot foot
101
Q

Treatment for painful neuropathy?

A
  • amitripyline

- gabapentin

102
Q

Autonomic neuropathy examples?

A
  • gastroparesis

- gustatory sweating

103
Q

HbA1c gives an indication of glucose levels over how many weeks?

A
  • 6-8 weeks
104
Q

What is the target HbA1c for a diabetic?

A
  • <53mmol/mol

- <48mmol/mol in a younger pt

105
Q

T1DM BG target in children and adults?

A
  • before meal 4-7mmol/l

- after meal 5-9mmol/l

106
Q

T2DM BG target?

A
  • before meal 4-7mmol/l

- after meal <8.5mmol/l

107
Q

Why is the insulin to carb ratio needed?

A
  • to calculate the amount of rapid acting insulin needed to cover a specific amount of carbohydrate
108
Q

What is the insulin sensitivity factor aka. correction factor?

A
  • Used to calculate the drop in glucose for each unit of insulin
109
Q

What are the benefits of self-monitoring glucose?

A
  • glucose control
  • lifestyle exercise
  • carb counting
110
Q

Benefits of continuous glucose monitoring?

A
  • 24hr profile given

- traces silent hypos

111
Q

What are the 2 types of continuous glucose monitoring?

A
  • Continuous

- Flash

112
Q

Why is it important to improve glucose control?

A
  • Increased glucose control corresponds to a reduced risk of microvascular and macrovasular complications
113
Q

What is diabetic ketoacidois?

A
  • metabolic state that usually occurs in absolute or relative insulin deficiency –> lipolysis –> ketogenesis –> ketone bodies
114
Q

What is the diagnostic criteria for diabetic ketoacidosis?

A
  • ketonaemia >3mmol/L
  • Blood glucose >11.0mmol/L
  • Bicarbonate <15mmol/L
115
Q

What are potential causes of diabetic ketoacidosis?

A
  • infections
  • inflammation
  • intoxication
  • infarction
116
Q

Symptoms of DKA?

A
  • Drowsiness
  • polyuria
  • polydipsia
  • Kussmaul’s respiration
117
Q

Treatment of DKA?

A
  • Fluids
  • Insulin infusion
  • potassium
118
Q

Potential consequences of DKA?

A
  • Arrythmia
  • cerebral oedema
  • ARDS
  • Gastic ileus
119
Q

What is normal blood ketone levels?

A
  • <0.6mmol/L

- ketosis = >3mmol/l

120
Q

What causes hyperglycaemia hyperosmolar syndrome?

A
  • unwell T2DM patient

- electrolyte loss

121
Q

Diagnosis of HHS?

A
  • Hyperglycaemia >30mmol/l
  • no ketonaemia <3mmol/l
  • bicarbonate >15mmol/l
  • osmolality >320
122
Q

How is osmolality calculated?

A

2xNa + urea + glucose

  • normal 275-295
123
Q

Treatment of HHS?

A
  • Fluids
  • insulin (if ketones high)
  • LMWH
124
Q

Diagnosis of alcohol induced keto-acidosi?

A
  • history of alcohol
  • dehydration
  • ketonaemia >3mmol/l
  • bicarbonate <15mmol/l
  • glucose normal or lo
125
Q

Treatment of alcohol induced keto-acidosis?

A
  • IV pabrinex
  • IV fluids
  • IV anti-emetics
126
Q

Lactic acidosis is a blood lactate of?

A
  • > 5mmol/l

Endocrinology (16 decks)

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