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Week 13 - Pancreas Flashcards

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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
Management of hyperglycaemic hyperosmolar state
Fix hypokalaemia Insulin Fluids
26
Chronic complications of diabetes
Microvascular - nephrology, rentinopathy, neuropathy | Macrovascular - CHD, stroke, PVD, blood pressure
27
What is the pathophysiology of the chronic complications?
Leakage of PAS positive glycated plasma proteins, which increase extracellular matrix, hypertrophy and hyperplasia of endothelium
28
What is HbA1c?
Average of amount of glucose over the past 90 days Also called amadori product This process happens will all proteins
29
Controllable risk factors for microvascular complications in patients with diabetes
xxx
30
Risk factors for retinopathy (4)
Poor glycaemic control Genetic factors High BP smoking
31
Classification of diabetic retinopathy
Proliferative and non-proliferative (with or without maculopathy) IT will be the first microvascular complication
32
Markers of nonproliferative DR
xxx
33
Markers of proliferative diabetic retinopathy
xxx
34
Treatment for proliferative retinopathy
burn about 1000 holes in retina to decrease the oxygen demand for the retina. Lose some peripheral vision, but helps to maintain central vision
35
Nephropathy - risk factors and incidence
xxx
36
How do we screen for nephropathy?
Microalbuminuria Albumin : creatinine random sport collection 24h urine collection with creatinine Timed collection
37
Treatment and prevention of diabetic nephropathy (4)
Tight BM control Tight BP control ACE inhibitor Low protein diet, lipid control BP is key
38
Types of diabetic neuropathy
xxx
39
Describe autonomic neuropathy
``` 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
Describe neuropathic vs ischaemic foot
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
Cardiovascular disease risk in diabetes
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
HbA1c targets XXX
XXX
43
Outline of general diabetic management
``` Advice Blood pressure Cholesterol Diabetic control Eye care Foot care Guardian drugs (ACE inhibitors) ```
44
What causes obesity? (5)
``` Metabolism Appetite regulation Energy expenditure Genetics Behavioural and cultural factors ```
45
Common findings in obese patients (2)
Lack of feeling of fullness | Night eating habits
46
Factors that contribute to weight gain (6)
``` Socio-economic status Smoking cessation Hormonal Inactivity Psychosocial / emotions Medications ```
47
Medical complications of obesity
``` Pulmonary disease Stroke Cataracts CHD Diabetes Cancer (various) ETC ```
48
What is insulin resistance syndrome?
Physiologic response inadequate for amount of insulin secreted
49
What are the clinical manifestations of insulin resistance syndrome?
``` Central obesity Glucose intolerance Atherosclerosis Hypertension Polycystic ovary syndrome ```
50
What is metabolic syndrome?
xxx
51
What causes NAFLD?
Excessive intake of fat Reduced hepatic oxidation of FFA Increased De Novo lipogenesis Increased delivery of FFA
52
In what patients would you consider drug therapy?
xxx
53
Potential pharmacological interventions for obesity?
Orlistat - inhibits pancreatic lipase causing fat malabsorption GI adverse effects
54
What are incretins?
GI hormones that are released after meals, stimular insulin secretion GLP1 signalling system
55
What is the gold standard treatment in obesity?
Bariatric surgery
56
Outline insulin analogues - quick overview of types and benefits
xx | Faster
57
Commonest drug with errors - why?
Insulin - wrong dose, wrong time,
58
Sick day rules for patients with diabetes
NEver stop insulin If BM less than 11 If BM 11-17 If BM xx
59
Common causes of hypoglycaemia
``` Missed/delayed meals Overdose / estimation of insulin Weight loss Increased physical activities xxx ```
60
Outline the stepwise management of type 2 diabetes
Diete and exercise oral monotherapy oral combination insulin + oral agents
61
What is metformin?
Insulin sensitiser | xxx
62
What are sulphoylureas?
Stimulate insulin secretion Act on beta cells Risks of hypo
63
Discuss action of incretin hormones / GLP-1 analogues?
``` B-cell A-cell Liver Stomach Brain ``` INJECTION Work on pancreas xxxx
64
Discuss actions of DPP-4 inhibitors
Works on same pathway as GLP-1 analogues, but less effective ORAL Work on pancreas xxxx
65
Discuss actions of SGLT-2 inhibitors
xxx Inhibits SGLT2 receptors in PCT, patient will pee out glucose Can cause UTIs
66
How would you classify diabetes?
Vascular disease | & this is the biggest risk for mortality (especially macrovascular)
67
What is the sequence of hormones that come in in response to hypoglycaemia?
xxx
68
What is the plasma glucose concentration (when constant)?
5 mmol/L | Range is 4-7 mmol/L in healthy people
69
What is the critical glucose level for the brain?
Less than 2.5 mmol/L
70
What prevents plasma glucose surging / plummeting?
Hormone control of metabolism to maintain constant levels
71
Roles of insulin
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
What are the counter-regulatory hormones and their role?
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
Metabolic pathways that prioritise energy STORAGE (3)
Glycogenesis - Synthesis of glycogen from glucose Lipogenesis - Synthesis of FA from acetyl CoA Triglyceride synthesis - Esterification of FA for storage as TG
74
Metabolic pathways that prioritise energy RELEASE (4)
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
Outline the metabolic response to hypoglycemia
Imediate response is glucagon from pancreas, fall in plasma glucose is detected by pancreas (which starts secreting more glucagon) xxxx
76
Short, medium and long term defences against hypoglycemia
Short - glucagon, epinephrine, sympathetic NS Medium - Ketogenesis (this protects muscle tissues from proteolysis) Long - Cortisol stimulate proteolysis to supply AA substrates for gluconeogenesis
77
Defences against hyperglycemia
Insulin - stimulates glucose uptake by tissues, inhibits liver glucose production Lack of insulin action leads to hyperglycemia, DM (type 1 and type 2)
78
What does insulin stimulate in Liver, adipose tissue and muscle?
``` Insulin stimulates Liver glycogenesis glycolysis lipogenesis Adipose tissue glucose uptake free fatty acid uptake lipogenesis Muscle glucose uptake amino acid uptake glycogenesis ```
79
What does insulin inhibit in liver and adipose tissue?
Insulin inhibits Liver glycogenolysis gluconeogenesis Adipose tissue Lipolysis
80
2 vehicles for fat transport
``` Chylomicrons VLDL particles (carry from liver ```
81
How is fat stored?
As triglycerides (transported as free fatty acids)
82
How do you turn free fatty acid into triglyceride
Esterification
83
What transporter does adipose tissue do to take up glucose?
GLUT4, insulin dependent
84
Describe metabolic pathway in adipose tissue
xxx
85
Describe metabolic pathway in muscle
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
What transporter does muscle tissue do to take up glucose?
GLUT4, insulin dependent
87
What is most important in glucose uptake? Good buffer to prevent spikes
Skeletal muscle
88
Describe glucose and amino acid metabolism in the liver
xxx
89
Describe fatty acid metabolism in the liver
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
What is ketogenesis?
synthesis of acetoacetate and hydroxybutyrate (ketone bodies) from Acetyl Co A
91
Overview of diabetic ketoacidosis
xx
92
Overview of the metabolic disturbances in DM
xxx
93
What is a SGLT transporter? Types and characteristics
xxx
94
Role of somatostatin? Where is it made?
xxx
95
What can measuring C protein show us?
Whether insulin is being secreted
96
Factors regulating insulin secretion
xxx

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