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CSI > CSI Case 5 and 6 > Flashcards

CSI Case 5 and 6 Flashcards

1
Q

What is prediabetes?

A

Pre-diabetes means that your blood sugars are higher than usual, but not high enough for you to be diagnosed with type 2 diabetes. Prediabetes doesn’t have any symptoms.

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2
Q

Key risk factors for type 2 diabetes?

A

Ethnicity, genetics, high blood pressure, overweight, diet. Use of antipsychotic medication and glucocorticoids.

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3
Q

What are the core defects in type 2 diabetes mellitus (T2DM)?

A

Insulin resistance in muscle and the liver, and impaired insulin secretion by the pancreatic β-cells.

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4
Q

What happens to the secretion of hormones from the pancreas in type 2 diabetes?

A

Decreased insulin secretion from beta cells and increase glucagon secretion from alpha cells.

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5
Q

What are incretins and what do they do?

A

Incretins are gut hormones. One of their many physiological roles is to regulate the amount of insulin that is secreted after eating.

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6
Q

What organs/tissues are involved in type 2 diabetes and how are they involved?

A

Liver - Increased hepatic glucose production due to increased glucagon and increased sensitivity to glucagon.

Adipocytes - Accelerated lipolysis and increased plasma free fatty acid (FFA) levels.

Kidneys - . Increased renal glucose reabsorption by the sodium/glucose co-transporter 2 (SGLT2) and the increased threshold for glucose to be excreted in the urine contribute to the maintenance of hyperglycaemia.

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7
Q

What contributes to weight gain in type 2 diabetes?

A

Low brain dopamine and increased brain serotonin levels contribute to weight gain.

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8
Q

Symptoms of type 2 diabetes?

A

Polydipsia, nocturia, polyuria
Feeling very tired
Weight loss
Cuts or wounds take longer to heal
Blurred vision

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9
Q

Microvascular complications of type 2 diabetes? What causes microvascular complications?

A

Retinopathy, nephropathy and
neuropathy. Hyperglycemia (severity and duration).

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10
Q

Macrovascular complications of type 2 diabetes? What causes macrovascular complications?

A

Myocardial infarction, peripheral vascular disease
and stroke. Dyslipidaemia, hypertension,
hyperglycaemia and inflammation.

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11
Q

What causes insulin resistance?

A

Causes of the
insulin resistance include genetic abnormalities,
ectopic lipid accumulation, mitochondrial
dysfunction, inflammation and endoplasmic
reticulum stress.

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12
Q

What is insulin resistance simply put?

A

Impaired insulin receptor signalling.

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13
Q

What to drugs for type 2 diabetes target?

A

Hepatic glucose production, promote insulin secretion, increase sensitivity to insulin, act on the incretin axis or target intestinal and renal glucose absorption.

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14
Q

Single most important risk factor for type 2 diabetes?

A

BMI > 25.

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15
Q

What reaction converts glucose to pyruvate?

A

Glycolysis.

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16
Q

What reaction converts pyruvate to acetyl CoA?

A

Pyruvate oxidation.

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17
Q

What is the insulin dependent glucose transporter?

A

GLUT4.

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18
Q

Low affinity for glucose transporter?

A

GLUT2.

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19
Q

Where is GLUT4 located?

A

Adipocytes and myocytes.

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20
Q

Where is GLUT3 located?

A

Neurones and placenta.

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21
Q

Where is GLUT2 located?

A

Kidney, small intestine, liver and pancreatic beta cells.

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22
Q

Where is GLUT1 located?

A

Endothelium, erythrocytes, blood brain barrier.

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23
Q

High affinity glucose transporters?

A

GLUT3 and GLUT4.

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24
Q

How does insulin resistance work in a muscle cell? How does this cause pancreatic beta cell dysfunction?

A

GLUT4 isn’t translocated to cell membrane when insulin binds to insulin receptor. Results in excess glucose in the blood. Glucose in blood enters pancreatic beta cells as GLUT2 isn’t insulin dependent and causes beta cell dysfunction.

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25
Q

What are other names for prediabetes?

A

Borderline diabetes, impaired fasting glucose, impaired glucose tolerance, impaired glucose regulation and non diabetic hyperglycaemia.

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26
Q

Normal fasting glucose?

A

Less than 6 mmol/l.

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27
Q

Fasting glucose for type 2 diabetes?

A

Greater than 7 mmol/l

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28
Q

What would someone who has impaired glucose tolerance have for glucose tests?

A

High post prandial glucose. 7.8 -11 mmol/l.

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29
Q

What would someone who has impaired fasting glucose have for glucose tests?

A

6.1-6.9 mmol/l fasting glucose and normal post prandial glucose (<7.8 mmol/l).

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30
Q

What are the two types of impaired glucose regulation?

A

Impaired fasting glucose and impaired glucose tolerance.

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31
Q

What predominantly causes impaired fasting glucose?

A

Hepatic insulin resistance. Liver isn’t responding to insulin and so hepatic glucose output isn’t inhibited.

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32
Q

What predominantly causes impaired glucose tolerance?

A

Muscle insulin resistance and impaired post prandial insulin release. Muscle doesn’t take up glucose after a meal.

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33
Q

Examples of ectopic fat deposits? What does ectopic fat deposits lead to?

A

Intra muscular fat and fatty liver. Insulin resistance.

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34
Q

What is hba1c?

A

Glycated haemoglobin.

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35
Q

Advantages of HbA1c test?

A

No fasting necessary. Reflects long-term blood glucose concentration of 3 months. Quick results. Positive correlation of HbA1c with lipid profiles.

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36
Q

Disadvantages of HbA1c?

A

Test can only diagnose patient with diabetes if they have symptoms. HbA1c is normal for people who have recently developed diabetes. Conditions such as acute and chronic blood loss, haemolytic anaemia, splenomegaly and renal failure can all cause falsely lowered A1c results.

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37
Q

HbA1c level for diabetes?

A

> 48mmol/mol (6.5%).

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38
Q

What individuals can you not use HbA1c test to help diagnose diabetes?

A

Pregnant women, children, acutely ill patients.

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39
Q

What is metabolic syndrome?

A

Medical term for a combination of diabetes, high blood pressure (hypertension) and obesity.

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40
Q

What is the EAST framework for behavioural change?

A

Make it easy - offer a taster session, sessions at convenient times
Make it attractive - Offer incentives, highlight the benefits.
Make it social - Use commitment apps, deliver in group sessions.
Make it timely - Provide a deadline for signing up, text reminders to attend sessions and time orientated goals.

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41
Q

First line medication for type 2 diabetes?

A

Metformin.

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42
Q

Metformin advantage?

A

Broad targets, low side effects, cheap, doesn’t cause hypoglycaemia, causes weight loss.

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43
Q

How does metformin target the liver?

A

Decreases gluconeogenesis. Decrease in hepatic glucose output.

44
Q

What enzymes does metformin inhibit?

A

mGPDH (Glycerol-3-phosphate dehydrogenase) and complex I.

45
Q

What does inhibition of complex I do?

A

Inhibition of pumping H+ ions into inter-membrane space. Increase AMP/ATP ratio as less ATP produced. More AMP means inhibition of adenylate cyclase which result in inhibition of glucagon action. More AMP also results in greater AMPK activity. Greater AMPK activity and inhibition of glucagon results in down-regulation of gluconeogenic genes.

46
Q

What does inhibition of mGPDH do?

A

Decrease in glycerophosphate shuttle so less NAD+ produced. Suppression of enzymatic reactions of gluconeogenesis.

47
Q

What is dyspnea?

A

Shortness of breath.

48
Q

What is dyspnea grade 0?

A

Dyspnea only with strenuous exercise.

49
Q

What is dyspnea grade 1?

A

Dyspnea when walking up a slight hill.

50
Q

What is dyspnea grade 2?

A

Walkers slower than people of same age. Has to stop for breath when walking at own pace.

51
Q

What is dyspnea grade 3?

A

Stops for breath after walking 100 yards or after a few minutes.

52
Q

What is dyspnea grade 4?

A

Too dyspneic to leave house or breathlessness when dressing.

53
Q

Smoking cessation withdrawal symptoms?

A

Nicotine cravings, irritability, poor concentration, increased appetite.

54
Q

What is the ‘stop in one go’ approach to smoking cessation?

A

When an individual makes a commitment to stop smoking on or before a particular date (the quit date), rather than by gradually reducing their smoking.

55
Q

What can help with smoking cessation?

A

Combination of drug treatment and behavioural support.

56
Q

What is a ‘harm reduction approach’ to smoking cessation?

A

Cutting down before stopping smoking, reducing smoking (without intending to stop), or temporarily not smoking.

57
Q

What to use when there is an urge to smoke or cravings kick in?

A

Short-acting nicotine preparations.

58
Q

Why does smoking result in increase in drug doses?

A

Polycyclic aromatic hydrocarbons found in tobacco smoke increase the metabolism of some drugs by inducing hepatic enzymes.

59
Q

How long does nicotine replacement therapy last?

A

8-12 weeks.

60
Q

How does Varenicline help with smoking cessation?

A

It reduces cravings for nicotine like NRT, but it also blocks the rewarding and reinforcing effects of smoking.

61
Q

Who can’t take Bupropion?

A

People with epilepsy, bipolar disorder or eating disorders

62
Q

Before giving inhaled therapies for COPD what needs to be done before?

A
  • Offer treatment and support to stop smoking
  • Offer pneumococcal and influenza vaccinations
  • Offer pulmonary rehabilitation if indicated
63
Q

First inhaler therapy to offer for COPD?

A

SABA or SAMA.

64
Q

If asthmatic features are present what inhaler should be offered?

A

Consider LABA + ICSb.

65
Q

Benefits of using a spacer?

A

Makes it easier to get the right amount of medicine straight to your lungs. Using a spacer can also reduce the risk of side effects from your medicine.

66
Q

What inhaler if patient can do quick and deep inhaling manoeuvre?

A

Dry powder inhaler.

67
Q

What inhaler if patient can do slow and steady inhaling manoeuvre?

A

Pressurized metered-dose inhalers or soft mist inhalers.

68
Q

What inhaler if patient can do slow and steady inhaling and quick and deep inhaling manoeuvre ?

A

Dry powder inhaler, Pressurized metered-dose inhalers or soft mist inhalers.

69
Q

Where are pain receptors in the lungs?

A

Parietal pleura.

70
Q

Myocardial infaction pain profile?

A

Pain radiates in left arm. Heavy pain in chest.

71
Q

Pleuritic pain profile?

A

Sharp pain and pain when breathing in.

72
Q

One pack year

A

20 cigarettes a day for a year.

73
Q

What FEV1, FEV1 / FVC ratio for obstructive pulmonary disease?

A

FEV1 80% of what its meant to be, FEV1/FVC < 0.7.

74
Q

Why is breathing out harder in obstructive pulmonary disease?

A

Additional thoracic pressure when breathing out.

75
Q

What part of of breathing does restrictive affect?

A

Breathing in.

76
Q

What are some restrictive pulmonary diseases?

A

Pulmonary fibrosis, congestive heart failure, sarcoidosis, obesity.

77
Q

What enzyme deficiency causes obstructive pulmonary disease?

A

Alpha one anti-trypsin deficiency.

78
Q

2 conditions that are commonly associated with COPD?

A

Chronic bronchitis and emphysema.

79
Q

What is the key driver of COPD?

A

Chronic inflammation - increase in macrophages, neutrophils, proteases and reactive oxygen species.

80
Q

In chronic bronchitis what happens?

A

Chronic inflammation results in increase in proteases which cleave mucin and result in hyperplasia of goblet cells. Mucous gland hypertrophy. Mucous hyper secretion results in airway narrowing.

81
Q

Key symptom of chronic bronchitis?

A

Persistent coughing with sputum.

82
Q

In emphysema why is gas exchange reduced?

A

Chronic inflammation results in destruction of airway walls. This result in enlargement of airways and reduced surface area for gas exchange.

82
Q

In emphysema why is gas exchange reduced?

A

Chronic inflammation results in destruction of airway walls. This result in enlargement of airways and reduced surface area for gas exchange.

83
Q

What causes hyperinflation of lungs in emphysema?

A

Loss of elastic recoil of lungs due to destruction of airway walls.

84
Q

Hyperinflated lungs characteristics in xray?

A

Pushed down diaphragm, ribs get pushed outwards (more than 7 anterior ribs visible on xray), heart pushed towards centre.

85
Q

What kind of drug is salbutamol?

A

Short acting beta agonist (local adrenaline to the lungs).

86
Q

What do beta agonist and muscarinic antagonists do?

A

Relax airway smooth muscle

87
Q

Why are corticosteroids bad for treating COPD?

A

Immunosuppression and so more likely to get infection.

88
Q

How to change posture to making breathing easier?

A

Lean forward and rest arms on something. Hands in pockets/hip when standing.

89
Q

What part of lung does restrictive affect generally?

A

Lung parenchyma.

90
Q

What part of lung does obstructive affect generally?

A

Bronchi or bronchioles.

91
Q

What needs to be measured before spirometry test?

A

Height and weight.

92
Q

What is peak flow rate?

A

Greatest rate of airflow that can be achieved during forced expiration.

93
Q

What does irritants in smoke do to cillia?

A

Shorten and make cilia less mobile.

94
Q

Chest infection mucus colour?

A

Green.

95
Q

What molecules result in COPD steroid resistance?

A

Reactive oxygen species and nitric oxide.

96
Q

Non medical treatment for COPD?

A

Smoking cessation strategies, eating a diet with more fat than carbohydrates as carbohydrates produce more co2 when metabolised. Avoid lower respiratory tract infections (vaccines, hygiene).

97
Q

What muscarinic receptor in lungs does ach bind to?

A

muscarinic 3

98
Q

Suffix for beta agonist?

A

-ol.

99
Q

Suffix for muscarinic antagonist?

A

-ium.

100
Q

What muscarinic receptor in parasympathetic ganglia?

A

M1.

101
Q

What muscarinic receptor in postganglionic nerve?

A

M2.

102
Q

What coupling in muscarinic receptor?

A

GQ coupling.

103
Q

What coupling in beta receptor?

A

GS coupling.

104
Q

Short acting muscarinic antagonist?

A

Ipratropium bromide.

CSI (3 decks)

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