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Life Maintenance > Week 13 - Pancreas > Flashcards

Week 13 - Pancreas Flashcards

1
Q

The ideal experimental study will be… (5)

A 
Controlled (placebo)
Randomized
Double blind
Large
Analysed by 'intention to treat' method
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2
Q

Considerations when testing medical interventions. So what are the implications for your trial?

A

Patients will tend to get better naturally
Placebo effect
Effect of treatment itself

Can’t conduct study in sick patients

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3
Q

Why is random allocation good? (4)

A

Best way to ensure intervention / control groups have similar characteristics
Avoids allocation bias
Simplifies interpretation of different between intervention / control
Facilitates blinding

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4
Q

Significance of blinding

A

Need to keep key people (patient, outcome assessor, statistician) blind to randomization code

Single blind - patient OR assessor
Double blind - Patient AND assessor
Triple blind - Patient + outcome assessor + statistician

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5
Q

Which trial outcomes should be used?

A

Symptom, clinical sign, biochemical test, development of clinical disease, death

Ideally objective
Should be important for both patient and doctors
Can have several

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6
Q

3 basic designs of randomised control trial

A

Parallel group - single intervention
Crossover trial - single intervention switched part way through (for rapidly achieved, reversible outcomes)
Factorial design - 2 or more interventions

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7
Q

What is the importance of trial size?

A

If too small, statistical power is limited
May fail to detect an important intervention effect (TYPE 2 ERROR)
Estimate of trial effect will be imprecise

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8
Q

What is a type 2 error?

A

May fail to detect an important intervention effect because trial too small

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9
Q

What are the advantages of a large sample size?

A

Higher statistical power
More precise estimate of effect size
Ability to think about impact of intervention in different sub-groups
BUT this does not automatically make the trial more representative - still need to do good sampling

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10
Q

Discuss the ethics of randomized control trials

A

Intervention must be LIKELY to benefit rathre than harm
Control group to get usual care - not no care
Informed consent crucial
Monitoring / reporting safety and adverse effects

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11
Q

What is the null hypothesis?

A

Assumption that there will be no difference between intervention and control groups - important first step of analysis

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12
Q

Steps of trial analysis (3)

A
  1. Compare characteristics of intervention and control groups at entry
  2. Establish whether intervention has been applied, how did it meet endpoints
  3. Does outcome differ? (Measurement depends on what the outcome is)
    & what does this mean in terms of risk, relative risk, absolute risk, etc.
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13
Q

ISSUE with trial anaylsis

A

No all patients will comply with study
Some will choose to stop, have to stop, etc.
Can be correct with ‘Intention to treat analysis’
LOOK AT THIS xxxx

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14
Q

Cost-benefit vs cost-effectiveness

A

Benefit - how much does it cost to ‘save a life’ using this treatment?
Effectiveness - Cost of benefit compared with other clinical interventions

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15
Q

What are the acute metabolic complications of diabetes?

A

DKA and HHS

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16
Q

Outline Type 1 diabetes pathophysiology

A

Complete lack of insulin
Compensatory hormones are secreted
Ketone bodies produced

Insulin deficiency leads to ketosis (which leads to acidosis) and hyperglycaemia (which leads to osmotic diuresis and dehydration)

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17
Q

What are the compensatory hormones secreted in type 1 diabetes?

A

Glucagon
Catecholamines
Cortisol
Growth hormones

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18
Q

What do Type 1 diabetes lose through osmotic diuresis?

A

Water, sodium, total body potassium, chloride, calcium, phsophate, magnesium

Electrolyte imbalance particularly bad for electrical tissues in heart

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19
Q

Diagnosing DKA - 2 signs

A

Ketones +++

Glucose high

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20
Q

What do you give to someone in DKA?

A

Insulin
Fluids
Metabolic correction

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21
Q

Investigations for DKA

A 
pH less than 7.3
Capillary and seum glucose - can be normal
Ketones
ABG
ECG - heart attacks can put you in a DKA (and vice versa)
CE - cardiac enzymes (troponin)
FBC - infection
Amylase
CXR
Blood cultures
MSU - infection
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22
Q

How do you diagnose type 1 diabetes?

A

Random blood sugar of over 11.1 (if they have symptoms)

If no symptoms, need two random readings above 11.1

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23
Q

Ongoing management of diabetic patient with DKA

A

Hours early warning scores & blood gas
Hourly fluid balance
Electrolytes every 2-4 hours
XXX

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24
Q

Definition of hyperglycaemic hyperosmolar state

A

Hyperglycaemia (>30mmol/l) without significant ketosis or acidosis
Dehydration with some depression consciousness

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25
Q

Management of hyperglycaemic hyperosmolar state

A

Fix hypokalaemia
Insulin
Fluids

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26
Q

Chronic complications of diabetes

A

Microvascular - nephrology, rentinopathy, neuropathy

Macrovascular - CHD, stroke, PVD, blood pressure

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27
Q

What is the pathophysiology of the chronic complications?

A

Leakage of PAS positive glycated plasma proteins, which increase extracellular matrix, hypertrophy and hyperplasia of endothelium

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28
Q

What is HbA1c?

A

Average of amount of glucose over the past 90 days
Also called amadori product
This process happens will all proteins

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29
Q

Controllable risk factors for microvascular complications in patients with diabetes

A

xxx

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30
Q

Risk factors for retinopathy (4)

A

Poor glycaemic control
Genetic factors
High BP
smoking

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31
Q

Classification of diabetic retinopathy

A

Proliferative and non-proliferative (with or without maculopathy)

IT will be the first microvascular complication

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32
Q

Markers of nonproliferative DR

A

xxx

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33
Q

Markers of proliferative diabetic retinopathy

A

xxx

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34
Q

Treatment for proliferative retinopathy

A

burn about 1000 holes in retina to decrease the oxygen demand for the retina.
Lose some peripheral vision, but helps to maintain central vision

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35
Q

Nephropathy - risk factors and incidence

A

xxx

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36
Q

How do we screen for nephropathy?

A

Microalbuminuria
Albumin : creatinine random sport collection
24h urine collection with creatinine
Timed collection

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37
Q

Treatment and prevention of diabetic nephropathy (4)

A

Tight BM control
Tight BP control
ACE inhibitor
Low protein diet, lipid control

BP is key

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38
Q

Types of diabetic neuropathy

A

xxx

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39
Q

Describe autonomic neuropathy

A 
Damage to nerves supplying major organs
Rare complication (occurs after 12-20 ts poor control)
Feeling dizzy, delayed stomach emptying, diabetic diarrhoea, sweating when eating, bladder and erectile dysfunction)
40
Q

Describe neuropathic vs ischaemic foot

A

Neuropathic - Sensory defect, but you still have pulses, foot starts to claw and you are no longer walking on fat pads, ulceration and callus formation where you are walking

Ischaemic foot - not necessarily going to have sensory defect but will lose pulse, foot structure is maintained and ulceration will not necessarily be at pressure points

41
Q

Cardiovascular disease risk in diabetes

A

Risk in type 2 diabetes patients same as people who have already had a heart attack

SO need to use secondary prevention methods in diabetes patients xxx ADD EXAMPLES

42
Q

HbA1c targets XXX

A

XXX

43
Q

Outline of general diabetic management

A 
Advice
Blood pressure
Cholesterol
Diabetic control
Eye care
Foot care
Guardian drugs (ACE inhibitors)
44
Q

What causes obesity? (5)

A 
Metabolism
Appetite regulation
Energy expenditure
Genetics
Behavioural and cultural factors
45
Q

Common findings in obese patients (2)

A

Lack of feeling of fullness

Night eating habits

46
Q

Factors that contribute to weight gain (6)

A 
Socio-economic status
Smoking cessation
Hormonal
Inactivity
Psychosocial / emotions
Medications
47
Q

Medical complications of obesity

A 
Pulmonary disease
Stroke
Cataracts
CHD
Diabetes
Cancer (various)
ETC
48
Q

What is insulin resistance syndrome?

A

Physiologic response inadequate for amount of insulin secreted

49
Q

What are the clinical manifestations of insulin resistance syndrome?

A 
Central obesity
Glucose intolerance
Atherosclerosis
Hypertension
Polycystic ovary syndrome
50
Q

What is metabolic syndrome?

A

xxx

51
Q

What causes NAFLD?

A

Excessive intake of fat
Reduced hepatic oxidation of FFA
Increased De Novo lipogenesis
Increased delivery of FFA

52
Q

In what patients would you consider drug therapy?

A

xxx

53
Q

Potential pharmacological interventions for obesity?

A

Orlistat - inhibits pancreatic lipase causing fat malabsorption

GI adverse effects

54
Q

What are incretins?

A

GI hormones that are released after meals, stimular insulin secretion
GLP1 signalling system

55
Q

What is the gold standard treatment in obesity?

A

Bariatric surgery

56
Q

Outline insulin analogues - quick overview of types and benefits

A

xx

Faster

57
Q

Commonest drug with errors - why?

A

Insulin - wrong dose, wrong time,

58
Q

Sick day rules for patients with diabetes

A

NEver stop insulin
If BM less than 11
If BM 11-17
If BM

xx

59
Q

Common causes of hypoglycaemia

A 
Missed/delayed meals
Overdose / estimation of insulin
Weight loss
Increased physical activities
xxx
60
Q

Outline the stepwise management of type 2 diabetes

A

Diete and exercise
oral monotherapy
oral combination
insulin + oral agents

61
Q

What is metformin?

A

Insulin sensitiser

xxx

62
Q

What are sulphoylureas?

A

Stimulate insulin secretion
Act on beta cells
Risks of hypo

63
Q

Discuss action of incretin hormones / GLP-1 analogues?

A 
B-cell
A-cell
Liver
Stomach 
Brain

INJECTION
Work on pancreas
xxxx

64
Q

Discuss actions of DPP-4 inhibitors

A

Works on same pathway as GLP-1 analogues, but less effective

ORAL
Work on pancreas
xxxx

65
Q

Discuss actions of SGLT-2 inhibitors

A

xxx
Inhibits SGLT2 receptors in PCT, patient will pee out glucose
Can cause UTIs

66
Q

How would you classify diabetes?

A

Vascular disease

& this is the biggest risk for mortality (especially macrovascular)

67
Q

What is the sequence of hormones that come in in response to hypoglycaemia?

A

xxx

68
Q

What is the plasma glucose concentration (when constant)?

A

5 mmol/L

Range is 4-7 mmol/L in healthy people

69
Q

What is the critical glucose level for the brain?

A

Less than 2.5 mmol/L

70
Q

What prevents plasma glucose surging / plummeting?

A

Hormone control of metabolism to maintain constant levels

71
Q

Roles of insulin

A

Stimulates nutrient storage - uptake of glucose, glycogen synthesis, uptake of FA and AA
Inhibits nutrient release - Inhibits release of glucose from liver, inhibits fat and protein breakdown

72
Q

What are the counter-regulatory hormones and their role?

A

Stimulate pathways leading to energy release
Glucagon: principal effects in liver
Stimulates hepatic glucose production
Adrenaline (and sympathetic NS)
Stimulates hepatic glucose production
Stimulates lipolysis: release of FA from adipose tissue stores
Cortisol
Stimulates hepatic glucose production
Stimulates proteolysis: release of amino acids from body proteins (skeletal muscle)

73
Q

Metabolic pathways that prioritise energy STORAGE (3)

A

Glycogenesis - Synthesis of glycogen from glucose
Lipogenesis - Synthesis of FA from acetyl CoA
Triglyceride synthesis - Esterification of FA for storage as TG

74
Q

Metabolic pathways that prioritise energy RELEASE (4)

A

Glycogenolysis - Release of glucose from glycogen stores
Gluconeogenesis - De novo synthesis of glucose from non-carbohydrate substrates
Lipolysis - Release of FA from TG breakdown
Ketogenesis - Production of ketone bodies from Acetyl CoA via beta-oxidation (FA to Acetyl Co A)

75
Q

Outline the metabolic response to hypoglycemia

A

Imediate response is glucagon from pancreas, fall in plasma glucose is detected by pancreas (which starts secreting more glucagon) xxxx

76
Q

Short, medium and long term defences against hypoglycemia

A

Short - glucagon, epinephrine, sympathetic NS
Medium - Ketogenesis (this protects muscle tissues from proteolysis)
Long - Cortisol stimulate proteolysis to supply AA substrates for gluconeogenesis

77
Q

Defences against hyperglycemia

A

Insulin - stimulates glucose uptake by tissues, inhibits liver glucose production
Lack of insulin action leads to hyperglycemia, DM (type 1 and type 2)

78
Q

What does insulin stimulate in Liver, adipose tissue and muscle?

A 
Insulin stimulates
Liver 
glycogenesis
glycolysis
lipogenesis  	
Adipose tissue 
glucose uptake
free fatty acid uptake
lipogenesis
Muscle 
glucose uptake
amino acid uptake
glycogenesis
79
Q

What does insulin inhibit in liver and adipose tissue?

A

Insulin inhibits
Liver
glycogenolysis
gluconeogenesis

Adipose tissue
Lipolysis

80
Q

2 vehicles for fat transport

A 
Chylomicrons
VLDL particles (carry from liver
81
Q

How is fat stored?

A

As triglycerides (transported as free fatty acids)

82
Q

How do you turn free fatty acid into triglyceride

A

Esterification

83
Q

What transporter does adipose tissue do to take up glucose?

A

GLUT4, insulin dependent

84
Q

Describe metabolic pathway in adipose tissue

A

xxx

85
Q

Describe metabolic pathway in muscle

A

Muscle has a private store of glycogen (it an’t be shared with the rest of the body) - will only leave cell as lactate, fatty acid, AA
Skeletal muscle is MOST IMPORTANT IN GLUCOSE UPTAKE

86
Q

What transporter does muscle tissue do to take up glucose?

A

GLUT4, insulin dependent

87
Q

What is most important in glucose uptake? Good buffer to prevent spikes

A

Skeletal muscle

88
Q

Describe glucose and amino acid metabolism in the liver

A

xxx

89
Q

Describe fatty acid metabolism in the liver

A

FA can be turned into acetyl CoA via B-oxidation (stimulated by glucagon) BUT this process leads to development of keto acids if overloaded
FA can be turned into triglycerides for transport by VLDLs

90
Q

What is ketogenesis?

A

synthesis of acetoacetate and hydroxybutyrate (ketone bodies) from Acetyl Co A

91
Q

Overview of diabetic ketoacidosis

A

xx

92
Q

Overview of the metabolic disturbances in DM

A

xxx

93
Q

What is a SGLT transporter? Types and characteristics

A

xxx

94
Q

Role of somatostatin? Where is it made?

A

xxx

95
Q

What can measuring C protein show us?

A

Whether insulin is being secreted

96
Q

Factors regulating insulin secretion

A

xxx

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