Deck 1 Flashcards

1
Q

What is the definition of the metabolic syndrome

A

Insulin resistance or T2DM plus 2 of the following:

  • Microalbuminuria
  • Obesity (BMI>30)
  • Hypertension (BP>160/90)
  • Dyslipidemia (TG>1.7, HDL <1.0)
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2
Q

What are common symptoms of Type 2 Diabetes.

A

Polyuria, Polydipsia, Tiredness, Blurred vision, recurrent UTIs,

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3
Q

Stepladder of Type 2 Diabetes Mellitus

A

Lifestyle changes –>
Monotherapy –>
Combo therapy w/o insulin –>
Combo therapy with insulin

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4
Q

First line treatment of T2DM

A

Metformin

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5
Q

First line treatment of T2DM if Metformin is contraindicated

A

Sulfonylureas

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6
Q

What type of patient should not receive Pioglitazone

A

Patients with Heart failure

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7
Q

What is a long term risk in females on Pioglitazone

A

Fractures

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8
Q

What are treatment target for HbA1c

A

<7%

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9
Q

Target for BP in diabetic patients

A

<130/80

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10
Q

Name a Biguanide drug

A

Metformin

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11
Q

Name some sulfonylureas drugs

A

Glicazide
Glibenclamide (Glyburide in the US)
Glimeparide
All start with Gli-

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12
Q

Name a Thiazolidinedione

A

Pioglitazone

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13
Q

Metformins effect on body weight

A

Often reduces weight

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14
Q

Is Metfromin safe in pregnancy

A

Yes

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15
Q

What are the renal function levels where metformin dosage needs to be altered

A

eGFR below 45 but above 30 - Half dose

eGFR <30 ml/min - Stop Metformin

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16
Q

Does Metformin have liver toxicity

A

It is a rare adverse effect

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17
Q

How does Sulfonylureas work

A

Binds to SUR1 of the Potassium channels on the pancreatic beta cells causing them to close. When closed it causes depolarization, opening Ca+ channels which release insulin

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18
Q

Does Sulfonylureas cause weight gain

A

Yes

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19
Q

When should you avoid Sulfonylureas

A

In severe Renal and Hepatic failure

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20
Q

How does Thiazolidinediones act

A

Binds to a nuclear receptor, this allows transcription of multiple proteins involved in fatty acid take up and breakdown plus GLUT4 transporter

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21
Q

Does Thiazolidinediones cause weight gain

A

Yes, due to increased subcutaneous fat and fluid retention

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22
Q

What does Thiazolidinediones double the risk for

A

Heart failure due to fluid retention

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23
Q

How does SGLT2 inhibitors work

A

Block the SGLT2 transporter in the kidney, thereby limiting the reabsorption of glucose so the body excrete glucose in the urine

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24
Q

Name an example of a SGLT2 inhibitor

A

Dapagliflozin

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25
Q

What two molecules are in the incretin pathway

A

Glucagon-like peptide 1 (GLP-1)

Glucose-dependent insulinotropic polypeptide (GIP)

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26
Q

What molecule inactivates GLP-1 and GIP

A

Dipeptidyl peptidase-4 (DPP-4)

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27
Q

What cells secrete GLP-1

A

L cells

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28
Q

What cells secrete GIP

A

K cells

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29
Q

How does GLP-1 and GIP act

A

Bind on beta cells of pancreas causing increased cAMP which release insulin

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30
Q

Examples of GLP-1 receptor agonists

A

Exenatide, Exendin, Liraglutide, Lixisenatide

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31
Q

Does GLP-1 receptor agonists cause weight gain

A

No, causes weight loss

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32
Q

Examples of DPP-4 inhibitors

A

Vildagliptin
Sitagliptin
Saxagliptin
Linagliptin

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33
Q

Does DPP-4 inhibitors cause weight gain

A

No, it is weight neutral

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34
Q

Why is DPP-4 inhibitors less effective

A

Only work if there is natural GLP-1 present

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35
Q

Where is the SGLT2 transporter located

A

Proximal tubules of hte kidney

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36
Q

Does SGLT2 inhibitors cause weight gain

A

No, it causes weight loss

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37
Q

Side effects with SGLT2 inhibitors

A

Sugar in urine may cause increase in trush and UTI’s

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38
Q

What kind of drug is Tolbutamide

A

1st generation Sulfonylurea

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39
Q

How does Meglitinides work

A

Bind to SUR1 to close the K+ ATP-channel on pancreatic beta cells and trigger insulin release

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40
Q

Name examples of Meglitinides

A

Repaglinide and Nateglinide

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41
Q

How does Meglitinides differ from Sulfonylureas

A

Rapid kinetics, therefore less likely to cause hypoglycemia

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42
Q

Where in the intestine are K cells and L cells

A

K cells - Duodenum/jejunum

L cells - Ileum/colon

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43
Q

What is the route of administration of GLP-1 analogues

A

Subcutaneously

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44
Q

How does Acarbose work

A

It is a alpha-glucosidase inhibitor, delay absorption of glucose from gut

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45
Q

Adverse effect of Acarbose

A

Undigested carbs are eaten by colonic bacteria causing flatulence, loose stools, bloating and Abdominal pain

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46
Q

How does Metformin work

A

Reduce hepatic gluconeogenesis
Increase glucose uptake and usage in skeletal muscles
Reduce carb absorption
Increase fatty acid oxidation

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47
Q

What nuclear receptor Thiazolidinediones bind to

A

Peroxyisome proliferator-activated receptor-gamma (PPAR-y)

48
Q

Example of a SGLT2 inhibitor

A

Dapagliflozin

49
Q

What antibodies may you look for in a Type 1 Diabetes Mellitus diagnosis

A

GAD/IA2 Antibody

C-peptide antibody

50
Q

How does T1DM look on histology

A

Lymphocyte infiltration

51
Q

What HLA is higest risk association with T1DM

A

HLA DR3-DQ2

HLA DR4-DQ8

52
Q

What Auto-antibodies are related to T1DM

A

GAD (Glutamine acid decarboxylase)
IA2 (Islet antigen 2)
IAA (Insulin)
ZnT8 (ZnT8 Transporter)

53
Q

What are normal levels of ketones in blood

A

<0.6 mmol/L

54
Q

What are dangerously high levels of ketones in blood

A

> 3.0 mmol/L

55
Q

What is Enuresis

A

Inability to control urine

56
Q

What is Somnolence

A

Drowsiness

57
Q

What are HbA1c targets in mmol in T1DM

A

Ideal range 48-58 mmol/L

58
Q

What is LADA acronym for

A

Latent onset Diabetes of Adulthood

59
Q

Diabetes in children under 6 months is most likely

A

Neonatal Diabetes

60
Q

Features of LADA

A

Male 25-40
Non-obese
Auto-antibody +ve
Associated auto-immune conditions

61
Q

What is the association between Cystic fibrosis and Diabetes

A

> 25% of 20y CF patients develops diabetes

62
Q

What is Wolfram syndrome

A
Also called DIDMOAD, genetic disorder causing:
Diabets Insipidus
Diabetes Mellitus
Optic Athropy
Deafness
63
Q

What is the Bardett-Biedl Syndrome

A
Pleiotropic genetic disorder causing:
Polydactaly
Hypogonadism
Visual and hearing impairment
Mental retardation
Diabetes
64
Q

What type of genetic disease is MODY

A

Autosomal dominant

65
Q

What are the two distinct phenotypes of MODY

A

Transcription factor 1-alpha (HNF-1a)

Glucokinase

66
Q

What is the onset of Glucokinase mutation MODY

A

Adolescence/Young Adult

67
Q

What is the difference in hyperglycemia between different MODY mutations

A

Glucokinase mutation - Stable hyperglycemia

HNF-1a - progressive hyperglycemia

68
Q

Wha’s the treatment for glucokinase mutation MODY

A

Diet

69
Q

Roughly how long does transient neonatal diabetes last

A

12 weeks

70
Q

What is the error in Permanent Neonatal Diabetes

A

Raised ATP in beta cells fail to close the K+ ATP channel –> No insulin secretion

71
Q

What is the treatment in HNF-1a MODY patients

A

Sulfonylureas

72
Q

In T1DM, what are the pre-meal target for blood glucose

A

3.9-7.2 mmol/L

4-7 mmol/L

73
Q

In T1DM, what are the 1-2 h post meal target for blood glucose

A

<10 mmol/L

74
Q

How much insulin should be given to 10g of carbohydrates

A

1 unit

75
Q

What insulin regime tends to best mimic physiological insulin production

A

Basal bolus

76
Q

What is an adverse effect at the insulin injection site is not moved around

A

Lipohypertrophy

Might cause uneven insulin release if site is still used

77
Q

Over what time period does HbA1c reflect blood glucsoe levels

A

6-8 weeks

Unless there is an incresed RBC turnover

78
Q

Treatment for hypoglycemia in awake patient

A

15-20g of glucose which is about 1/2 cup of soda

79
Q

Treatment of severe hypoglycemia

A

Glucagon 1mg, inject into buttock, arm or thigh

80
Q

What is Impaired hypoglycemia Awareness

A

When hypoglycemia occur but patient doesn’t experience symptoms

81
Q

Who is most likely to have Impaired hypoglycemia Awareness

A

Frequent low blood glucose patients.

Intensively treated T1DM with low HbA1c

82
Q

What are the ketone bodies formed in DKA

A

Acetone
Acetoacetate
Beta-hydroxyl butyric acid

83
Q

What ketone bodies are used for energy

A

Acetoacetate

Beta-hydroxyl butyric acid

84
Q

Common precipitants of Diabetic Ketoacidosis

A

Infections
Drug and Alcohol use
Non-compliance of Diabetic treatment
Undiagnosed diabetes

85
Q

Diagnostic blood results of Diabetic Ketoacidosis

A

Ketonemia >3mmol/L
Blood glucose >11.0 mmol/L
pH <7.3

86
Q

What are Creatine and Sodium levels in DKA

A

Creatine is often raised

Sodium is often reduced

87
Q

What ketone body is measured on ketone blood test

A

Beta-hydroxyl butyric acid

Also called Beta hydroxylbuturate

88
Q

What is the ion gap calculation

A

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

89
Q

A high anion gap indicates

A

Acidocis

90
Q

High ion gap but low ketone levels indicate what condition

A

Lactic acidosis

91
Q

What is Type A lactic acidosis associated with

A

Tissue hypoxemia

92
Q

Why is the anion gap raised in lactic acidosis

A

HCO3- is depleted to balance out the lactate production

93
Q

What drugs increase risk of Hyperglycemic Hypersomolar Syndrome

A

Corticosteroids

Thiazid

94
Q

Median glucose level in Hyperlglycemic Hypersomolar Syndrome

A

60 mmol/L

95
Q

Typical patient that gets Hyperglycemic Hypersomolar Syndrome

A

Older type 2 Diabetes

96
Q

Precipitating events to Hyperglycemic Hypersomolar Syndrome

A

Frequent infection, commonly chest

Refined sugars

97
Q

Important to remember about fluid resucitation in Hyperglycemic Hypersomolar Syndrome

A

Slow progress due to risk of cerebral odema

98
Q

What should all patients with Hyperglycemic Hypersomolar Syndrome be given

A

Low Molecular Weight Heparin unless contraindicated to prevent vascular events

99
Q

Osmolality calculation formula and normal value

A

2x[Na+ + K+] + [Urea] + [Glucose]

Normal between 285-295

100
Q

What are some microvascular complications of Diabetes

A

Neuropathy, Retinopathy, Nephropathy, Peripheral vascular disease, ulcerations

101
Q

What types of Neuropathy is seen in Diabetes

A

Peripheral, Autonomic, Proximal, Focal Neuropathy

102
Q

What kind of drug is Amitryptiline

A

Tricyclic Antidepressant (TCA) used also for neuropathic pain as an adjuvant

103
Q

What kind of drugs is Gabapentin

A

Anticonvulsant drug also used for neuropathic pain as an adjuvant

104
Q

What is Gastroparesis

A

Condition where the stomach can’t empty itself properly

105
Q

What is Gustatory sweating

A

Sweating on forehead, face, scalp and neck occuring soon after ingesting food

106
Q

What is Diabetic nephropathy

A

Increased GFR leads to sclerosis and reduced GFR causing microalmuminuria and proteinuria

107
Q

Who should have urinary albumin creatine ratio screening and how often

A

All diabetic over 12.

At diagnosis and anually

108
Q

Normal values for Albumin-Creatine Ratio (ACR)

A

Male <3.5 mg/mmol Creating

109
Q

Treatment of microalbuminuria and proteinuria

A

ACE inhibitor

110
Q

What are some common eye involvements in Diabetes

A

Retinopathy, Cataracts, Glaucoma, Acute hyperglycemia causing reversible blurred vision

111
Q

What does SIGN guidelines say about cholesterol lowering drugs in T2DM

A

Give lipid lowering treatment in all Diabetics over 40y regardless of baseline cholesterol

112
Q

What are some modifiable risk factors in newly diagnosed T2DM

A

Weight, activity level, Alcohol reduction, Smoking, BP, Glycemic control

113
Q

What kind of drug is Gliclazide

A

Sulfonylurea

114
Q

What investigations should be done at a diabetes check-up

A

Urinanalysis
HbA1c
U&Es
Cholesterol/lipid profile

115
Q

Who is the sexiest man alive

A

That would be Mattias