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MD4001 > Week 10 > Flashcards

Week 10 Flashcards

1
Q

What organ monitors blood glucose?

A

Pancreas

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2
Q

What happens if blood glucose in low?

A

Glucagon released from α cells & upper GI to stimulate glycogen breakdown & gluconeogenesis in the liver

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3
Q

What happens if blood glucose is high?

A

Insulin released from β cells to stimulate liver, adipose & muscle to take up glucose

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4
Q

List the symptoms of diabetes?

A
  • Always tired
  • Wounds don’t heal
  • Sudden weight loss
  • Frequent urination
  • Always hungry & thirsty
  • Sexual problems
  • Blurry vision
  • Numb/tingling hands/feet
  • Vaginal infections
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5
Q

Describe the difference in diagnosis of type 1 & type 2 diabetes?

A

TYPE 1- often in childhood

TYPE 2- usually over 30yrs old

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6
Q

Describe the difference in excess body weight association of type 1 & type 1 diabetes?

A

TYPE 1- NOT associated

TYPE 2- OFTEN associated

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7
Q

Describe the different associations of type 1 & type 2 diabetes?

A

TYPE 1- higher ketone levels at diagnosis

TYPE 2- high blood pressure &/or cholesterol levels at diagnosis

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8
Q

Describe the differences in treatment of type 1 & type 2 diabetes?

A

TYPE 1- insulin injections or insulin pump (replacement therapy)
TYPE 2- initially without medication or with tablets

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9
Q

Describe why there is a natural progression from prediabetes to type 2 diabetes?

A
  • Disruption of ability to metabolise glucose
  • May have hyperinsulinemia due to lower insulin sensitivity
  • Full diabetes progresses when β cell failure surpasses critical threshold ~90%
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10
Q

What is the glucose level aim when treating type 1 diabetes with insulin?

A

4-7mM (preprandial/ fasting)

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11
Q

What should glucose levels be, in normal people, 2hrs after a meal?

A

<7.8mM

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12
Q

What glucose level will overload the renal capacity & be detected in urine?

A

> 10mM

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13
Q

How is insulin now made?

A

By recombinant DNA technology, allows an identical pure preparation, limiting allergic reactions

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14
Q

How is insulin administered and why?

A
  • Parentally because it’s a protein that would be destroyed/ digested by gut if oral
  • Routine use subcutaneously
  • IV infusion in emergencies
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15
Q

Insulin formulations can differ in their _____ of action?

A

Duration

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16
Q

What can altering amino acids in the insulin structure do?

A

Usefully alter insulin kinetics (designer insulins)

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17
Q

Describe the formulation of Insulin Lispro or Insulin Aspart

A
  • Rapid-acting soluble

- Designer insulins that prevent dimer formation allowing more active monomers to be bioavailable & used rapidly

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18
Q

Describe the formulation & action of Neutral Protamine Hagedorn (NPH)/Isophane Insulin?

A

Intermediate-acting insulin that precipitates insulin into suspensions which slowly dissolve

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19
Q

Describe the formulation & action of Insulin Glargine?

A

Longer acting designer Insulin which has decreased solubility at neutral pH, forms aggregates that slowly dissolve.

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20
Q

Describe the formulation & action of Insulin Detemir?

A

Long-acting designer insulin with a fatty acid- this confers albumin binding, which slowly dissociates prolonging circulation

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21
Q

For type 1 diabetes describe the formulation of insulin replacement?

A

Intermediate-acting preparation/ long-acting analogue is often combined with short-acting analogue before meals

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22
Q

What 3 types of diabetes is insulin used for?

A
  1. Type 1 diabetes
  2. 1/3rd of Type 2 diabetes
  3. Gestational diabetes
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23
Q

Describe the pros & cons of FIXED dose insulin regiments?

A
  • PROS: Can be on any injection regiments, simplify understanding of blood glucose results
  • CONS: not offer flexibility of how much carbs patient choose to consume each meal
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24
Q

Describe the pros & cons of FLEXIBLE dose insulin regiments?

A
  • PROS: more control of what they eat & how to balance blood glucose, can have different carb quantities in meals
  • CONS: patients need to understand glucose metabolism, take time & commitment to learn to adjust insulin dose
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25
Q

Describe the once daily insulin regimen & who it’s appropriate for?

A
  • 1 injection in morning
  • Suitable for Type 2
  • Long-acting (Glargine) or Intermediate (NPH)
  • Less flexible & required basic patient understanding
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26
Q

Describe the twice daily insulin regimen & who its appropriate for?

A
  • 2 injections in morning & evening
  • Type 1 & Type 2
  • Short-acting mixed with intermediate
  • Less flexible & requires basic patient understanding
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27
Q

Describe the basal-bolus insulin regimen & who its appropriate for?

A
  • Multiple injections throughout day
  • Type 1 & some Type 2
  • Intermediate or long-acting with short-acting
  • Flexible & requires high patient understanding
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28
Q

Describe the insulin pump regimen & who its appropriate for?

A
  • Semi-automated as needed throughout the day
  • Type 1
  • Short-acting insulin
  • Flexible & requires medium/high patient understanding
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29
Q

What are Oral Hypoglycemic tablets used for?

A

To alter glucose metabolism in Type 2 diabetes

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30
Q

What is the principle oral Hypoglycemic drug?

A

Metformin (biguanide drug)

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31
Q

What are the effects of Metformin (hypoglycemic drug)?

A
  • Potentiate residual insulin by increasing insulin sensitivity
  • Reduce gluconeogenesis in liver & opposes action of glucagon
  • Increases glucose uptake & utilisation in skeletal muscle
  • Slightly delays carb absorption in gut
  • Increases fatty acid oxidation
  • Suppress appetite
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32
Q

How can Metformin stimulate insulin release?

A

By combining it with other drugs

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33
Q

What does Metformin’s effect of increased fatty acid oxidation help with?

A

Obesity associated diabetes & atherosclerosis development

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34
Q

Overall, what does Metformin do?

A

Alters energy metabolism

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35
Q

What is the action of Metformin on the mitochondria & what does this result in?

A
  • Increase AMP:ATP ratios activate AMP-activated protein kinase
  • AMPK increases transcription of genes important for glucose transport fatty oxidation
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36
Q

What are the 2 classes of insulin secretagogues?

A
  1. Sulphonylureas (old)

2. Meglitinides (new)

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37
Q

Give 4 examples of Sulphonylurea’s?

A
  1. Tolbutamide
  2. Chlorpropamide
  3. Glibenclamide
  4. Glipizide
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38
Q

Describe the action of Sulphonylurea’s?

A
  • Interfere with β cell ion channels to potentiate insulin secretion
  • Well tolerated, can lead to weight gain by stimulating appetite
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39
Q

When are Sulphonylurea’s used & why?

A

Early stages of type 2 diabetes as they require functional β cells

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40
Q

What 2 drugs can Sulphonylurea’s be combined with?

A
  1. Metformin

2. Glitazones

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41
Q

What can the interaction between Sulphonylurea’s & other drugs produce?

A

Severe hypoglycaemia due to competition for metabolising enzymes, plasma binding proteins & excretory pathways.

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42
Q

What is the action of Meglitinides (next generation insulin secretagogues)?

A

Block K-ATP channels to increase insulin release

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43
Q

What does the short duration of Meglitinides lead to?

A

Lower risk of hypoglycaemia

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44
Q

Where are the high affinity receptors for Sulphonylurea drugs present

A

β cell membranes

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45
Q

What are Glitazones also known as?

A

Thiazolidinediones

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46
Q

Describe the effects of Pioglitazone (Thiazolidinediones/ Glitazone)?

A
  • Increases insulin sensitivity
  • Reduces exogenous insulin needed by ~30%
  • Reduces blood glucose & free fatty acid conc
  • Promote transcription of several genes with products important in insulin signalling
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47
Q

What do Pioglitazone & Rosiglitazone’s (Thiazolidinediones/ Glitazone) act on?

A

Peroxisome proliferator activated receptor (PPAR-γ) agonists in adipose tissue, muscle & liver

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48
Q

What 2 side effects can Pioglitazone cause?

A
  1. Weight gain

2. Fluid retention

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49
Q

What 3 diseases have been linked to Pioglitazone?

A
  1. Bladder cancer
  2. Heart failure
  3. Osteoporotic fractures
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50
Q

What is the function of PPAR-γ ligand?

A

Promote transcription of genes important in insulin signalling (lipoprotein lipase, fatty acid transporters, Glut-4 etc)

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51
Q

What is Pioglitazone used for clinically?

A

Additive to other oral hypoglycaemic drugs ie. Metformin & Sulphonylureas

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52
Q

What is Acarbose?

A

Inhibitor of intestinal α-glucosidase

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53
Q

What is the effect of Acarbose?

A

Delays carbohydrate absorption in small intestine reducing the postprandial spike in glucose

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54
Q

When is Acarbose used?

A

Type 2 diabetes often in combination with other hypoglycemics

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55
Q

What are the 2 side effects of Acarbose?

A
  1. Flatulence

2. Diarrhoea

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56
Q

Give 3 examples of selective sodium glucose cotransporter 2 (SGLT2) inhibitors?

A
  1. Canagliflozin
  2. Dapagliflozin
  3. Empagliflozin
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57
Q

When are selective sodium glucose cotransporter 2 (SGLT2) inhibitors used?

A

Type 2 diabetes as mono therapy when diet & exercise along not adequate for whom metformin is contraindicated or inappropriate

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58
Q

What are the actions of selective sodium glucose cotransporter 2 (SGLT2) inhibitors?

A
  • Block glucose reabsorption by proximal tubule leading to therapeutic glucosuria
  • Controls glycaemia independently of insulin pathways
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59
Q

What do selective sodium glucose cotransporter 2 (SGLT2) inhibitors lead to compared to placebo?

A
  • Reduced HbA1c up to 1.17%

- Well tolerated, reduce weight & systolic BP

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60
Q

What is the side effect of selective sodium glucose cotransporter 2 (SGLT2) inhibitors?

A

Associated with increased risk of urinary tract infections

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61
Q

Where are glucagon-like peptide-1 (GLP-1) secreted?

A

L-cells in the gut

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62
Q

Where are gastric inhibitor peptide (GIP) secreted?

A

K-cells in gut

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63
Q

What are the effects of Incretins?

A
  • Directly stimulate insulin biosynthesis & secretion
  • Inhibit glucagon secretion in pancreas, delay gastric emptying, increase cardiac output & satiety signals in brain
  • Indirectly increase insulin sensitivity in muscle & decrease gluconeogenesis in liver
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64
Q

What are Incretins rapidly degraded by?

A

Enzyme called dipeptidyl peptidase-4 (DPP-4)

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65
Q

Give 3 examples of Incretin mimetics? (analogs of extending-4/GLP-1)

A
  1. Exenatide
  2. Exenatide LAR
  3. Liraglutide
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66
Q

What is the regimen of Exenatide & its side effect?

A
  • Twice daily

- Nausea

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67
Q

What is the regimen of Exenatide LAR & its side effect?

A
  • Long-acting release formulation administered weekly

- Less nausea

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68
Q

What is the action of Liraglutide?

A

Additional fatty side-chain that confers albumin binding & slows renal clearance

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69
Q

What are the actions of Incretin mimetics/analogs?

A

Lowers blood glucose after meal by increasing insulin secretion & suppressing glucagon secretion

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70
Q

When would you use dIncretin mimetics/analogs?

A

Type 2 diabetes in addition to oral agents to improve control & aid weight loss

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71
Q

What is the route of Incretin mimetics/analogs?

A

Subcutaneously as peptide analogs

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72
Q

What are the potential side effects of Incretin mimetics/analogs?

A
  • Hypoglycemia

- Range of GI effects

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73
Q

Give 2 examples of DDP-4 inhibitors/Gliptins?

A
  1. Sitagliptin

2. Vildagliptin

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74
Q

What are the effects of DDP-4 inhibitors/Gliptins?

A
  • Enhance endogenous incretin effects by blocking DPP-4

- Lowers blood glucose by increasing 1st phase of insulin response after meals

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75
Q

Describe Sitagliptin as a drug?

A

Well tolerated & weight neutral

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76
Q

What are the side effects of Vildagliptin?

A
  • Respiratory tract infections
  • Headache
  • Serious pancreatitis
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77
Q

What does the adrenal cortex arise from?

A

Intermediate mesoderm

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78
Q

Describe the location of the adrenal glands?

A

Retroperitoneally on upper pole of the kidneys

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79
Q

List the 5 layers of the adrenal gland from exterior to interior?

A
  1. Capsule (fibrous)
  2. Zona glomerulosa
  3. Zona fasciculata
  4. Zona reticularis
  5. Medulla
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80
Q

What hormone is produced in the Zona glomerulosa (adrenal cortex)?

A

Mineralocorticoid (aldosterone)

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81
Q

What hormone is produced in the Zona fasciculata (adrenal cortex)?

A

Glucocorticoids (cortisol)

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82
Q

What hormone is produced in the Zona reticularis (adrenal cortex)?

A

Androgens (DHEA & androstenedione)

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83
Q

What hormone is produced in the adrenal medulla?

A

Epinephrine/Adrenaline

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84
Q

What is the zona glomerulosa controlled by?

A

Renin-angiotensin

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85
Q

What is the function of the aldosterone release from zona glomerulosa?

A

Electrolyte & fluid homeostasis

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86
Q

What is the zona fasciculata controlled by?

A

ACTH

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87
Q

What is the function of the glucocorticoid release from zona fasciculata?

A

Carbohydrate, lipid & protein metabolism

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88
Q

The adrenal cortex produces _____ hormones?

A

Steroid

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89
Q

What is the blood supply of the adrenal cortex?

A
  • Superior, middle & inferior adrenal arteries which anastomose under the capsule
  • Cortex receives short cortical arteries run in parallel with cords of cells to medulla
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90
Q

What is the blood supply of the adrenal medulla?

A
  • Draining from the cortex

- Fresh arterial blood in long cortical arteries

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91
Q

What does the blood draining from the cortex into the medulla contain?

A

Adreno-corticosteroids which influence the production of adrenaline by medullary cells

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92
Q

What are the 6 short-term stress responses to increased catecholamines from the adrenal medulla?

A
  1. Increased heart rate
  2. Increased BP
  3. Liver converts glycogen to glucose & releases it to blood
  4. Dilation of bronchioles
  5. Changes in blood flow patterns leading to decreased digestive system activity & reduced urine output
  6. Increased metabolic rate
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93
Q

What are the 2 long-term stress responses to increased mineralocorticoids from the adrenal cortex?

A
  1. Retention of sodium & water by kidneys

2. Increased BP & blood volume

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94
Q

What are the 3 long-term stress responses to increased glucocorticoids from the adrenal cortex?

A
  1. Proteins & fats converted to glucose/ broken down for energy
  2. Increased blood glucose
  3. Suppression of immune system
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95
Q

What is the major role of cortisol?

A

Ability to cope with physical (trauma, infection, allergies) or neurological (anxiety, restraint) stresses

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96
Q

What are the 3 pharmacological actions of cortisol?

A
  1. Anti-inflammatory
  2. Anti-allergic
  3. Anti-immune
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97
Q

What are the 4 possible causes of Cushing’s disease/syndrome (glucocorticoid excess)?

A
  1. ACTH-releasing pituitary tumour
  2. Ectopic ACTH-releasing tumour (usually in lungs, pancreas or kidney)
  3. Tumour of the adrenal cortex = hyper-secretion of cortisol
  4. Administration of pharmacological doses of glucocorticoid drugs
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98
Q

What are the 7 clinical features of Cushing’s disease/syndrome?

A
  1. Hyperglycaemia
  2. Muscle wasting
  3. Increase free fatty acid (FFA) in plasma
  4. Increased insulin release
  5. Tissue edema, hypokalemia, hypertension
  6. GI Tract ulceration
  7. Decreases in protein synthesis
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99
Q

Why does Cushing’s disease/syndrome result in hyperglycaemia?

A
  • Gluconeogenesis in liver

- Sometimes called adrenal/steroid diabetes

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100
Q

Why does Cushing’s disease/syndrome result in muscle wasting?

A

Loss of protein synthesis in muscle & bone (& most tissues)

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101
Q

Why does Cushing’s disease/syndrome result in increase FFA in plasma?

A

Reduced lipogenesis & enhanced lipolysis

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102
Q

What does increased insulin release in Cushing’s disease/syndrome result in?

A
  • Redistribution of fat stores to face, neck, upper trunk
    “buffalo hump”
  • β-cell exhaustion
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103
Q

Why does Cushing’s disease/syndrome result in tissue edema, hypokalaemia, hypertension?

A

Increased glomerular filtration (glucocorticoid effect) & water & Na+ retention (mineralocorticoid effects)

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104
Q

Why does Cushing’s disease/syndrome result in GI tract ulceration?

A

Excess H+ secretion & decreased mucous production (alkalosis due to increased H+ loss in GI tract & kidney)

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105
Q

What are the 2 possible treatments for Cushing’s disease/syndrome?

A
  1. Surgical removal of tumour

2. Decreases in drug dosage

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106
Q

What 3 pathways stimulate the glomerulosa cells to synthesise aldosterone?

A
  1. Increase renin-angiotensin cascade
  2. Increase ACTH from anterior pituitary
  3. Increase plasma [K+]
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107
Q

What effects does aldosterone have on the kidney?

A
  • Decrease Na+ & H2O excretion
  • Increase [K+] excretion
  • Increase effective circulating volume, extracellular fluid volume & BP
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108
Q

What is the Juxta-glomerular apparatus?

A
  • Specialized structure formed by distal convoluted tubule & glomerular afferent arteriole
  • Main function is regulate blood pressure & filtration rate of glomerulus
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109
Q

List the structures that form the Juxta-glomerular apparatus?

A
  • Granular cells/ Juxtaglomerular cells on the afferent arteriole (from renal artery)
  • Macula densa on the distal tubule
  • Extraglomerular mesangial cells
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110
Q

What does the Granular cells/ Juxtaglomerular cells allow?

A

Renin to pass into the afferent arteriole

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111
Q

What do the macula dense cells detect?

A

Sodium concentrations in the distal tubule (osmolality)

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112
Q

Describe the suppression of glucocorticoid activity in renal cortical tubular cells?

A
  • 11 beta-HSD metabolises cortisol, making it have little affinity for mineralcortisol receptor (MR)/glucocorticoid receptor (GR). Aldosterone, not metabolised & occupies MR & GR
  • Glycyrrhetinic acid inhibits 11 beta-HSD, cortisol is not metabolised & occupies MR & Gr over aldosterone
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113
Q

What are the 4 primary causes of Addison’s disease (primary adrenal cortical insufficiency)?

A
  1. Tuberculosis/ metastatic tumours
  2. Autoimmune adrenalitis –> adrenal failure
  3. HIV - decreased immunity & increased viral & bacterial infections
  4. Atrophy due to prolonged steroid therapy
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114
Q

What are the 6 clinical features of Addison’s disease?

A
  1. Loss of weight/appetite, muscle weakness, nausea, vomiting
  2. Low plasma glucose esp. after fasting
  3. Hyponatriemia & Hyperkalaemia
  4. Dehydration & hypotension due to 3
  5. Lethargy & dizziness on standing up due to 4
  6. Severe present with skin pigmentation
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115
Q

Why in severe cases of Addison’s disease do patients present with skin pigmentation?

A

Excess ACTH acting as Melanocyte stimulating hormone (MSH)

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116
Q

Describe the 2 possible treatments for Addison’s disease?

A
  1. Glucocorticoid replacement therapy- Hydrocortisone administration morning (25mg)/afternoon (12.5 mg)
  2. IV saline infusion if severely dehydrated & condition life threatening & administration of Fludrocortisone (mineralocorticoid agonist)
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117
Q

What does the adrenal medulla develop from?

A

Neural crest cells

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118
Q

What important cell does the adrenal medulla contain?

A

Chromaffin cells (postganglionic sympathetic neurons) which produce catecholamines

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119
Q

What are chromaffin cells directly controlled by?

A

Preganglionic sympathetic neurons

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120
Q

What 2 catecholamines do the 2 populations of chromaffin cells secrete?

A
  1. Epinephrine (adrenaline) - 90/80%

2. Norepinephrine (noradrenaline)

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121
Q

What 2 hormones have chromaffin cells also been shown to secrete?

A
  1. Dopamine

2. Enkephalins (pain control)

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122
Q

What 2 ways can we compare groups in evidence?

A
  1. Comparing results with gold standard

2. Comparing one sample with another after an intervention

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123
Q

What does the T-test allow for?

A

Statistically compare means between 2 groups (1 dependent continuous variable ie. height, 1 independent binary categorical variable ie. sex)

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124
Q

What does the Chi-square-test allow for?

A

Statistically compare frequencies (1 dependent categorical variable ie. alternative drug types, 1 independent categorical variable ie. deprivation category)

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125
Q

What does the T-test give?

A

Probability (p-value) that such a difference (or greater difference) would be found by chance, if the null hypothesis is TRUE

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126
Q

How do we know when the probability is unlikely?

A

We chose an arbitrary cut-off p<0.05 (reject the null hypothesis)

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127
Q

Describe the 3 slightly different t-tests?

A
  1. Comparison of mean with a single value
  2. Comparison of means of independent samples
  3. Comparison of means of paired data
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128
Q

What 2 things should you report in the t-statistics?

A
  1. Degrees of freedom (df)

2. Associated probability (p-value)

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129
Q

What does a P<0.05 mean?

A

Sample means significantly different

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130
Q

What does a P>0.05 mean?

A

Sample means NOT significantly different

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131
Q

What does a difference in the Chi-square test imply?

A

A “relationship” or “association” ie. values of one variable may influence values of the other

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132
Q

What is the Chi-square test for independence?

A

Association between 2 categorical variables (ie. is cholesterol status associated with gender)

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133
Q

What is the Ch-square test for goodness of fit?

A

Tests the difference between frequencies of a single categorical variable and some hypothesised frequency

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134
Q

What is Correlation?

A

Measures the strength of relationship between 2 numerical variables measured by the correlation coefficient (r)

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135
Q

What does r= -1 mean?

A

A perfect negative correlation (as 1 variable increases the other decreases)

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136
Q

What does r= +1 mean?

A

A perfect positive correlation (as 1 variable increases so does the other)

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137
Q

What do you use for basic correlation?

A

Continuous data

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138
Q

What is linear regression used to Predict?

A

Relationship between independent variables & an outcome (dependent) variable

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139
Q

What must there be between independent & outcome for regression?

A

Linear relationship

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140
Q

What is the regression coefficient?

A

Slope of the best-fitting straight line through a scatter plot of data

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141
Q

What is linear regression closely related to?

A

Correlation

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142
Q

What is the linear regression equation?

A 
y= βx + c (intercept)
(β= slope of the best fitting straight line)
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143
Q

What does the p-value of the regression coefficient (β) indicate?

A
  • Probability that the “true” slope of the line is= 0 (null hypothesis is NO SLOPE)
  • Significant p-value (p<0.05) indicates that there is a significant slope (β NOT equal to 0)
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144
Q

In Scotland, how many people & their families each year will require palliative care?

A

~40,000

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145
Q

What is palliative care according to WHO?

A

Improves quality of life of patients & families facing life-threatening illness
through prevention & relief of suffering by
means of early identification & impeccable assessment & treatment of pain & other problems, physical, psychosocial & spiritual

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146
Q

Whats the GMC definition of “Approaching the end of life”?

A

Likely to die within the next 12 months

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147
Q

End of life, according to GMC guidance, is those facing imminent death & those with what 4 factors?

A
  1. Advanced, progressive, incurable conditions
  2. General frailty (likely to die in 12 months)
  3. At risk of dying from sudden crisis of condition
  4. Life threatening conditions caused by sudden catastrophic events
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148
Q

Give 4 examples of non-cancer disease which require palliation of symptoms?

A
  1. Motor Neurone disease
  2. End-stage Cardiac failure
  3. End- stage COPD
  4. Advanced renal disease
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149
Q

What are the 4 key themes for palliative care development?

A
  1. Early identification of patients who may need palliative care
  2. Advance/ anticipatory care planning (decisions with cardiopulmonary resuscitation (DNACPR))
  3. Care in last days/ hours of life
  4. Delivery of effective & timely care
150
Q

What are the Liverpool Care pathway (LCP) report findings?

A
  • Where used properly, many people died peaceful, dignified deaths
  • But… in many cases it was associated with poor experiences of care
151
Q

What is the response from the Liverpool Care pathway (LCP) report?

A
  • ‘One chance to get it right’: 5 priorities
    for care of dying people
  • ‘Care for people in the last days & hours of life’
152
Q

What are the 3 Palliative care aims?

A
  1. Whole person approach
  2. Focus on quality of life, including good symptom control
  3. Care encompassing the person with the life- threatening illness & those that matter to them
153
Q

List the 6 principles of good end of life care?

A
  1. Open communication
  2. Anticipating care needs & encouraging discussion
  3. Effective input from multidisciplinary team
  4. Symptom control (physical & psycho-spiritual)
  5. Preparing for death- patient & family
  6. Providing support for relatives both before & after death
154
Q

What is Generalist palliative care?

A

Integral part of routine care delivered by all health & social care professionals to those with progressive & incurable disease, whether at home/ care home/ hospital

155
Q

What is Specialist Palliative care?

A

Same principles of palliative care, but can help people with more complex palliative care needs

156
Q

List the physical symptoms of end of life?

A
  • Pain
  • Dyspnoea
  • Nausea/vomiting
  • Anorexia / weight loss
  • Constipation
  • Fatigue
  • Cough
157
Q

What are the 4 different physical causes of pain at end of life?

A
  1. Cancer related (85%)
  2. Treatment related
  3. Associated factors- cancer & debility
  4. Unrelated to cancer
158
Q

Describe bone pain?

A

Worse on pressure or stressing bone / weight

bearing

159
Q

Describe nerve pain (neuropathic)?

A

Burning/ shooting/ tingling/ jagging/ altered sensation

160
Q

Describe liver pain?

A

Hepatomegaly/ right upper quadrant tenderness

161
Q

Describe raised intracranial pressure pain?

A

Headache (&/or nausea) worse with lying down, often present in the morning

162
Q

Describe colic pain?

A

Intermittent cramping pain

163
Q

How effective is the 3-step approach WHO pain ladder?

A

70-90%

164
Q

What is the regimen for painkillers in cancer?

A
  • Oral

- Analgesics should be given at regular intervals, not on demand

165
Q

What are the functions of Adjuvants in the WHO analgesic ladder for cancer pain?

A

To help calm fears & anxiety, adjuvant drugs may be added at any step of the ladder

166
Q

Give 3 examples of non-opioids in the 1st step of the WHO analgesic ladder for cancer pain?

A
  1. Aspirin
  2. Paracetamol
  3. NSAID
167
Q

Give 3 examples of weak opioids in the 2nd step of the WHO analgesic ladder for cancer pain?

A
  1. Codeine
  2. Dihydrocodeine
  3. Tramadol
168
Q

Give 4 examples of strong opioids in the 3rd step of the WHO analgesic ladder for cancer pain?

A
  1. Morphine
  2. Diamorphine
  3. Fentanyl
  4. Oxycodone
169
Q

What are the indications for morphine use (1st line strong opioid)?

A
  • Moderate-severe pain

- Dyspnoea

170
Q

What are the actions of morphine (1st line strong opioid)?

A
  • Opioid receptor agonist (μ-receptors)

- Centrally acting

171
Q

What are the cautions of morphine (1st line strong opioid)?

A
  • Longlist in BNF, including renal impairment & elderly

- Avoid in acute respiratory depression

172
Q

What are the most common side effects of morphine (1st line strong opioid)?

A
  • N&V, constipation, dry mouth, biliary spasm

- Watch for signs of opioid toxicity

173
Q

How do you administer Morphine (1st line strong opioid)?

A
  • Enterally- oral/ rectal
  • Parenterally- IM / SC injections
  • Delivery via syringe driver over 24 hours
174
Q

List the signs & symptoms of opioid toxicity?

A
  • Shadows edge of visual field
  • Increasing drowsiness
  • Vivid dreams / hallucinations
  • Muscle twitching / myoclonus
  • Confusion
  • Pin point pupils
  • Rarely, respiratory depression
175
Q

Describe the prescription of modified release of morphine?

A
  • ‘Background’ pain relief
  • Either twice daily preparation at 12 hourly intervals
  • Or once daily preparation at 24 hourly intervals
176
Q

Describe the prescription of immediate release of morphine?

A
  • ‘Breakthrough’ pain
  • As required (PRN)
  • Oramorph liquid/ Sevredol tabs
177
Q

What can you prescribe for the opioid side effect- Constipation?

A
  • Stimulant & softening laxative
  • Senna / Bisacodyl + Docusate
  • Magrogol e.g. laxido / movicol
  • OR Co-Danthramer alone
178
Q

What can you prescribe for the opioid side effect- Nausea?

A
  • Antiemetic
  • Metoclopramide
  • Haloperidol (consider QT interval)
179
Q

What are the 4 principles to go by when moving on to step 3 opioids?

A
  1. Stop any ‘Step 2’ weak opioids
  2. Titrate immediate release strong opioid
  3. Convert to modified release form
  4. Monitor response & side effects
180
Q

What adjunct medication can you give for liver capsule pain/ raised intracranial pressure?

A
  • Steroids (e.g. Dexamethasone)

- Remember to consider gastroprotection

181
Q

What adjunct medication can you give for neuropathic pain?

A
  • Amitriptyline
  • Gabapentin
  • Carbamazepine
182
Q

What adjunct medication can you give for bowel/bladder spasm?

A

Buscopan (Hyoscine Butylbromide)

183
Q

What adjunct medication can you give for bony pain/ soft-tissue infiltration?

A
  • NSAIDs

- Radiotherapy for bony metastases

184
Q

Describe Diamorphone & its uses (other opioid)?

A
  • Semi-synthetic morphine derivative
  • More soluble than Morphine → smaller volumes needed
  • Used for parenteral administration (injection /syringe driver)
185
Q

Describe Oxycodone & its use (oxynorm/oxycontin)?

A
  • 2nd line opioid

- Less hallucinations, itch, drowsiness, confusion

186
Q

Describe Fentanyl patch & its uses?

A
  • Second line opioid
  • Lasts 72 hours
  • Only use in stable pain
  • Useful if oral & SC routes not available
  • Useful if persistent side-effects with morphine / diamorphine
187
Q

Describe the use of syringe drivers for opioids?

A
  • Delivery over 24 hours- usually sub-cutaneous
  • Useful when oral route inappropriate
  • Often useful for rapid symptom control
  • Multiple medications can be added
188
Q

What does psychospiritual distress exacerbate?

A

Physical symptoms

189
Q

What 3 things should you remember to consider regarding psychospiritual distress?

A
  1. Uncontrolled physical symptoms
  2. Depression
  3. Other medical causes ie. hyperthyroidism
190
Q

What are the possible management techniques for psychospiritual distress?

A
  • Counselling/ psychology/ cognitive behavioural therapy

- Medication if clinically indicated

191
Q

What is the common property of antipsychotics/ neuroleptics/ anti schizophrenic drugs/ major tranquillisers?

A

Antagonising actions of dopamine in the brain

192
Q

What are the 3 positive symptoms of schizophrenia?

A
  1. Delusions
  2. Hallucinations
  3. Thought disorders
193
Q

What are the 2 negative symptoms of schizophrenia?

A
  1. Withdrawal from social contact

2. Flattening of emotional responses

194
Q

What does the clinical potency of antipsychotics correlate with?

A

D2 blocking action

195
Q

Describe the dopamine theory?

A
  • ↑ dopamine content in restricted area of temporal lobe of schizophrenics (amygdala)
  • ↑ dopamine synthesis & release in striatum of schizophrenics
196
Q

Describe the Glutamate theory?

A
  • ↓ glutamate & receptor density in post-mortem schizophrenic brains
  • Mice with ↓ NMDA receptor expression show stereotypic schizophrenic behaviours & ↓ social interactions. Also respond to antipsychotics
197
Q

What do glutamate & dopamine do to GABAergic striatal neurones?

A

Excitatory & inhibitory effects on GABAergic striatal neurones which project to thalamus & constitute a sensory ‘gate’

198
Q

Too _____ glutamate or too _____ dopamine disables the “gate”?

A
  1. Little

2. Much

199
Q

What does a disabled “gate” do?

A

Allowing uninhibited sensory input to reach the cortex

200
Q

What is excess dopamine responsible for?

A

Positive symptoms of schizophrenia

201
Q

What is reduced glutamate responsible for?

A

Negative symptoms of Schizophrenia

202
Q

List the 3 types of 1st generation or “Classical” Antipsychotics?

A
  1. Phenothiazines
  2. Butyrophenones
  3. Thioxanthines
203
Q

What are 3 examples of Phenothiazines (1st generation antipsychotics)?

A
  1. Chlorpromazine
  2. Fluphenazine
  3. Pipotiazine
204
Q

What is an example of Butyrophenones (1st generation antipsychotics)?

A

Haloperidol

205
Q

What are 2 examples of Thioxanthines (1st generation antipsychotics)?

A
  1. Flupentixol

2. Clopenthixol

206
Q

List the 3 types of 2nd generation or “Atypical” Antipsychotics?

A
  1. Benzamides
  2. Dibenzodiazepines
  3. Others
207
Q

What is an example of a Benzamides (2nd generation antipsychotic)?

A

Amisulpride (selective D2 & D3 receptor antagonist)

208
Q

What are 2 examples of Dibenzodiazepines (2nd generation antipsychotic)?

A
  1. Clozapine
  2. Olanzapine
    (unselective receptor blocking profile)
209
Q

What are 4 examples of Others types of 2nd generation antipsychotic drugs?

A
  1. Risperidone, paliperidone (mixture of receptor types blocked)
  2. Quetiapine (α adrenoceptor blocker)
  3. Aripiprazole (Dopamine & 5-HT antagonist)
210
Q

What are the PROS of ‘Atypical’ or 2nd generation antipsychotics?

A
  • Overcome some of the problems of the classical antipsychotics
  • Efficacy in treatment-resistant patients
  • Improve negative & positive symptoms
211
Q

Is there evidence that 2nd generation antipsychotics are more effective than 1st generation in controlling symptoms?

A

NO

212
Q

What 4 factors does the distinction between typical & atypical antipsychotics rest on?

A
  1. Receptor profile
  2. Incidence of extrapyramidal side-effects
  3. Efficacy in treatment-resistant group of patients
  4. Efficacy against negative symptoms
213
Q

What group of antipsychotics shows less extrapyramidal side effects?

A

Atypical 2nd generation antipsychotics

214
Q

What 6 receptors do antipsychotic drugs act on?1

A
  1. Dopamine 1 (D1)
  2. Dopamine 2 (D2)
  3. α1
  4. H1
  5. mACh (muscarinic ACh receptor)
  6. 5-HT2A (histamine receptor)
215
Q

What are the behavioural effects of antipsychotics?

A
  • Apathy & reduced initiative
  • Few emotions, drowsy (can be easily stirred from this)
  • Aggressive tendencies inhibited
216
Q

What 2 main types of disturbances to antipsychotics cause?

A
  1. Acute, reversible Parkinson-like symptoms due to block of nigro-striatal dopamine receptors
  2. Slowly developing Tardive dyskinesia (serious problem)
217
Q

Describe Tardive Dyskinesia?

A
  • Involuntary movements of face & limbs
  • After months/years of treatment
  • Associated with proliferation of dopamine receptors in corpus striatum
  • Treatment generally unsuccessful
  • Less common with newer antipsychotics
218
Q

What are the endocrine unwanted effects of antipsychotics?

A

Increased prolactin secretion (male/female) by blocking D2 receptors in the pituitary

219
Q

What are the anti-muscarinic unwanted effects of antipsychotics?

A
  • Blurring of vision, dry mouth & eyes, constipation

- Can help attenuate extrapyramidal actions

220
Q

What is the α-adrenoreceptor blocking unwanted effect of antipyschotics?

A

Orthostatic hypotension

221
Q

What are the H1-receptor blocking unwanted effects of antipsychotics?

A

Sedative & anti-emetic actions

222
Q

List the Unwanted effects of antipsychotics?

A
  • Postural hypotension
  • Sedation
  • Weight gain
  • Endocrine actions
  • Diabetes
  • Autonomic actions (atropine-like)
  • Extrapyramidal actions
  • Jaundice
  • Leucopoenia & agranulocytosis
  • Skin reactions (itchy rash)
  • Neuroleptic malignant syndrome
223
Q

How would you go about prescribing an antipsychotic for 1st episode schizophrenia?

A
  • Choice should consider side-effect profile
  • Titrate to minimum effective dose
  • Adjust dose according to response & tolerability within BNF limits
  • Evaluate over 6-8 weeks
224
Q

What should you do if the antipsychotic drug prescribed is effective?

A

Continue at established dose, don’t change the brand of drug!

225
Q

What should you prescribe if both 1st & 2nd generation antipsychotic drug’s are not effective?

A

Clozapine

226
Q

What should you do if the schizophrenic patient is not tolerating or has poor compliant for antipsychotic drug?

A

Prescribe a depot or compliance aid

227
Q

What antipsychotics can be used for acute behavioural emergencies & mania?

A
  • Chlorpromazine

- Haloperidol

228
Q

What antipsychotic can be used for treatment of emesis?

A

Prochlorperazine

229
Q

What antipsychotics can be used for treatment of Huntington’s disease?

A
  • Olanzapine
  • Risperidone
  • Quetiapine
230
Q

What antipsychotic can occasionally be used to treat depression?

A

Flupentixol

231
Q

What is the definition of Complementary Alternative Medicine (CAM)?

A

Group of diverse medical & health care systems, practices & products that are not generally considered part of conventional medicine

232
Q

What is Complementary or Integrative medicine?

A

Refers to use of CAM together with conventional medicine

233
Q

What is Alternative medicine?

A

Referes to use of CAM in place of conventional medicine

234
Q

List the different Alternative medical systems?

A
  • Traditional Chinese Medicine (TCM)
  • Ayurvedic Medicine
  • Homeopathy
  • Naturopathy
  • Indigenous healing systems
235
Q

List the different mind-body interventions?

A
  • Meditation
  • Yoga
  • Deep-breathing exercises
  • Qi gong
  • Tai chi
  • Guided imagery
  • Biofeedback
  • Dream therapy
236
Q

List the different biological based therapies?

A
  • Herbal medicine
  • Bach flower remedies
  • Bee venom therapy
  • Chelation therapy
  • Vegetable juice therapy
237
Q

List the different manipulative & body-based methods?

A
  • Osteopathy
  • Chiropractic
  • Craniosacral therapy
  • Alexander technique
  • Acupuncture
  • Rolfing
  • Kinesiology
238
Q

List the different energy therapies?

A
  • Therapeutic touch
  • Healing touch
  • Reiki
  • Magnet therapy
  • Light therapy
  • Crystal therapy
  • Qi gong
239
Q

How do you make a homeopathic preparation?

A
  • Principle of similars

- Preparations must undergo potentiation: serial dilutions of mother tincture, succession

240
Q

What is the common homeopathic dilution?

A

30C = 1 in 100*30

241
Q

What is the annual public spend on homeopathy?

A

~£45m

242
Q

What are the direct & indirect risks associated with homeopathy?

A
  • DIRECT harm: no risk of interactions with “high potency” medicines
  • INDIRECT harm: delay in receiving appropriate treatment, attitudes of practitioner
243
Q

What are the regulations for homeopathy?

A
  • No legal regulation of homeopaths in the UK: Society of Homeopaths, Faculty of Homeopathy, British Homeopathic Association
  • Homeopathic products regulated by EU directive
244
Q

What is the difference between herbal & homeopathic medicines?

A
  • Both are natural
  • Homeopathic is unlikely to have an active ingredient
  • Herbal medicine is likely to have an active ingredient that can interact with other medications
245
Q

List other drugs that St John’s Wort (Hypericum for depression) interacts with?

A
  • Hormonal contraceptives
  • Anti-depressives
  • Anti-coagulants
  • Anti-epilepsy agents
  • Heart medications
  • Anti-cancer agents
  • Anti-virals for HIV
    etc. ..
246
Q

What are the direct & indirect risks associated with herbal medicine?

A
  • DIRECT harm: Adverse drug reactions, Drug interactions, Quality control
  • INDIRECT harm: Delay in receiving appropriate treatment
247
Q

What regulates herbal medicines in the UK market?

A

MHRA regulations

248
Q

What 3 things does the MHRA monitor to regulate herbal medicines?

A
  1. Safety, quality, efficacy as per any regular medicine- Marketing Authorisation (MA)
  2. Safety & quality (not efficacy) based on traditional usage- Traditional Herbal Medicines Registration (THR)
  3. The “herbalist exemption”- Regulation 3 of The Human Medicines Regulations 2012
249
Q

What does DD Palmer (straight Chiropractor) state about disease?

A

95% of all diseases are caused by displaced vertebrae

250
Q

Describe Chiropractic?

A
  • Straight vs Mixer
  • Detect “subluxations” & block flow of “innate intelligence”, use of X-rays or gadgets
  • Spinal manipulations including high velocity, low-amplitude thrusts, audible “crack”
251
Q

What gadgets are used in Chiropractic?

A
  • BJ Palmer & Neurocalometers

- E meters & the Church of Scientology

252
Q

What are the direct & indirect risks of Chiropractic & Osteopathy?

A
  • DIRECT harm: 50% of chiropractic patients suffer an adverse reaction, tearing of artery wall leading to stroke, injury to the spinal cord, Chiropractic X rays
  • INDIRECT harm: Delay in receiving appropriate treatment, Attitudes of practitioner, Anti-vaccination
253
Q

What are the only 2 CAM modalities under statutory regulation?

A
  1. General Chiropractic council (GCC)

2. General Osteopathic Council (GOsC)

254
Q

Describe Acupuncture?

A
  • Ch’i (Qi, “ch-ee”) as a ‘vital energy’: Flows through ‘meridians’ associated with major organs, illness due to disrupted flow of Ch’i
  • Insertion of needles along meridians: restores flow of Ch’i, 1-10cm in depth, with/without rotation, left in place for sec/hrs
255
Q

Describe the diagnosis process during Acupuncture?

A
  • Inspection
  • Auscultation
  • Olfaction
  • Palpitation
  • Inquiring
256
Q

What are the direct & indirect risks of acupuncture?

A
  • DIRECT harm: Infections, Pneumothorax

- INDIRECT harm: Delay in receiving appropriate treatment, Attitudes of practitioner

257
Q

How can you become a registered acupuncture?

A

Premises & practitioners must be licensed via local authority (same as tattooing/body piercing)

258
Q

What are the regulations for Acupuncture?

A

Voluntary regulation via several organisations ie. British Acupuncture council

259
Q

What 2 things are tightly controlled in the body’s fluid compartments?

A
  1. Volumes

2. Composition

260
Q

What are the 2 major divisions of the body’s fluid compartments?

A
  1. Intracellular

2. Extracellular

261
Q

What can the extracellular be divided further into?

A
  1. Plasma
  2. Interstitial
    (synovial, intra-ocular, CSF etc)
262
Q

What is composition determined by?

A

Movement across the plasma membrane

263
Q

Describe the volume in the major compartments for a 70kg man?

A
  • Total body fluid: 42L
  • Intracellular fluid: 28L (incl. ~2L blood cells)
  • Interstitial fluid: 11L
  • Plasma: 3L
264
Q

What is the barrier between plasma & interstitial fluid?

A

Capillary wall

265
Q

What is the barrier between extracellular fluid & intracellular fluid?

A

Plasma membrane

266
Q

How does the body get a gain in fluid?

A
  • Food & water intake

- Oxidation of food

267
Q

How does the body get losses in fluid?

A
  • Urine (1500ml)
  • Faeces (100ml)
  • Sweat (50mls)
  • Insensible losses (900ml)
268
Q

What is the average total losses of body fluid’s?

A

2550ml

269
Q

What is insensible water loss?

A
  • Transepidermal diffusion: water that passes through the skin & is lost by evaporation
  • Evaporative loss from respiratory tract
  • Insensible losses are solute free
270
Q

What are the types of sensor’s which regulate body fluid?

A
  • Osmoreceptors in hypothalamus
  • Low pressure baroreceptors in right atria & great veins
  • High pressure sensors in carotid sinus/aorta
271
Q

What happens if the total sodium drops & osmolality start the same?

A

Total volume falls (including plasma volume)

272
Q

What happens if the total sodium rises & osmolality stays the same?

A

Total volume will rise

273
Q

What are compensatory mechanisms really linked to?

A

Low volume (low GFR, stimulation of JGA) or high volume (increased GRF & release of ANP)

274
Q

If you eat too much/too little salt, where is the only controllable route of loss?

A

Via urine (hormonal control)

275
Q

What’s the possible non-hormonally controlled increased losses of NaCl?

A
  • Exercise/heat causing increased sweating

- Diarrhoea causing increased loss via faeces

276
Q

Describe the intake of NaCl?

A

Normally in excess of need (hedonistic)

277
Q

Describe the control of plasma Na+?

A
  • Hormones must act on the kidney
  • DCT is the area of control in nephron
  • No receptors detecting Na+
  • Controlled indirectly via volume sensors
  • Changes in Na+ lead to changes in blood volume
278
Q

What is the equation for working out Net sodium excretion?

A

Na+ filtered (changed via GFR) - Na+ reabsorbed (changed via rate of flow, aldosterone, ANP etc)

279
Q

What 4 things occur if osmolality rises?

A
  1. Increase in thirst
  2. Increase in release of ADH
  3. Increase in water intake/retention
  4. Increase in volume
280
Q

What 5 things occur if increase in volume leads to an increase in stretch of vascular system?

A
  1. Baroreceptors
  2. Decrease in renin release
  3. Decrease in aldosterone release
  4. Increased release of ANP (cardiac myocytes)
  5. Decreased sodium & water retention
281
Q

What 7 things occur if decrease in volume leads to a decrease in stretch of vascular system?

A
  1. Baroreceptors
  2. If pressure falls (decreased vol.), influences ADH release & thirst centres
  3. Increase renin release
  4. Increased angiotensin II
  5. Increase aldosterone release
  6. Decreased release of ANP
  7. Increased sodium & water retention
282
Q

What should you remember about K+?

A

Its an intracellular ion

283
Q

How is K+ lost?

A

Predominantly via urine, little lost in sweat/faeces in normal conditions

284
Q

Describe the control of K+?

A
  • Control at the kidney
  • K+ is freely filtered
  • Predominantly reabsorbed again in PCT with controlled secretion at the DCT
  • Secretion linked to Na+ reabsorption (sodium pump)
285
Q

What % of K+ is inside cells?

A

98%

286
Q

What do we get a significant & variable intake of K+?

A

From diet

287
Q

What does intracellular K+ act as?

A

Reservoir (attenuates change)

288
Q

What does an increased K+ in plasma do?

A
  • Increases activity of basolateral sodium pump
  • More K+ enters
  • Increased secretion across simple diffusion channels on apical membrane
  • Increased secretion of aldosterone
289
Q

What are the effects of K+ plasma driven by?

A

Direct detection of raised K+ levels by the aldosterone-secreting cells of the adrenal cortex

290
Q

What is the effects of aldosterone on the DCT?

A
  • Increases activity of sodium pump (basolateral)
  • Increases no. of Na+ pumps (basolateral)
  • Increases no. of Na+ & K+ channels in apical membrane
291
Q

What is the result of aldosterone on the DCT?

A

Increased reabsorption of sodium & increased secretion of potassium

292
Q

Describe Conn’s syndrome?

A

Hyperaldosteronism leading to 1. hypertension from increased

fluid volume & 2. hypokalaemia

293
Q

List the 4 types of IV crystalloids fluids?

A
  1. 5% Dextrose (glucose)
  2. 0.18% NaCl 4% Dextrose
  3. 0.9% NaCl (isotonic saline)
  4. Plasmalyte
294
Q

Describe the distribution of IV 5% Dextrose?

A
  • Initially through ISF & plasma, glucose
    metabolised so effectively adding just water
  • Further distributes into cells, ISF & plasma
295
Q

Describe the distribution of IV Plasmalyte?

A

Through ISF & plasma, does not enter cells

296
Q

List the 3 types of IV colloid fluids?

A
  1. 4.5% Albumin
  2. Hydrolysed Gelatin
  3. Blood
297
Q

Describe IV 4.5% albumin fluid?

A
  • Supplied in 0.9% NaCl
  • Tends to stay in plasma, does not enter cells
  • Blood product
298
Q

Describe IV hydrolysed gelatin fluid?

A
  • Supplied in 0.9% NaCl
  • Initially tends to stay in plasma, does not enter cells
  • Protein metabolised over time, so equivalent to 0.9% NaCl
299
Q

Describe the distribution of IV blood fluids?

A

Stays in vasculature & increases blood volume

300
Q

What are the 4 questions to ask before prescribing fluids?

A
  1. In terms of volume where is my patient starting from?
  2. Does my patient need IV fluid?
  3. Am I prescribing
    maintenance/ Replacement/ Resuscitation fluid?
  4. Want volume & what type of fluid?
301
Q

What are the clinical features of Diabetes ketoacidosis?

A
  • Hyperglycaemia: dehydration, tachycardia, hypotension, clouding of vision
  • Acidosis: air hunger (Kussmaul’s respiration) acetone breath, abdominal pain, vomiting
302
Q

What are 4 reasons why a patient may be dehydrated?

A
  1. Hyperglycaemia
  2. Vomiting
  3. Kaussmaul respiration
  4. Altered conscious level (reduced intake)
303
Q

What 3 treatments would you give for a dehydrated adult patient?

A
  1. Start: 1000mls 0.9% saline over 1st hr
  2. IV insulin infusion 6 units/hr
  3. K+ IV (slowly)
304
Q

What happens to the K+ during dehydration?

A
  • Potassium has shifted out of cells (serum K+ may be normal)
  • Excreted by kidneys (total loss)
  • May be additional losses if vomiting
305
Q

Where does audit come from?

A
  • Department of Health, 1989, ‘Working for Patients’
  • Quality improvement in delivery of health care
  • Part of the clinical governance agenda
306
Q

What is your role as a newly qualified doctor in regards to an audit?

A
  • More than tick box exercise
  • Audits can improve practice / quality / patient experience
  • Audits can be published
307
Q

What 3 things does the audit do for clinical governance agenda?

A
  1. Personal responsibility
  2. Organisational culture
  3. Reduce variation between providers
308
Q

Define the purpose of a clinical audit?

A

Quality improvement process that seeks to improve patient care & outcomes through systematic review of care against explicit criteria & implementation of change

309
Q

Define the purpose of research?

A

Attempt to derive generalisable new knowledge by addressing clearly defined questions with systematic & rigorous methods

310
Q

Describe how clinical audits & research can interconnect?

A
  • Audit can be the final stage of research project
  • Research findings identify areas for audit
  • Audit helps with dissemination of research findings
  • Audit identify’s gaps in research evidence
311
Q

What are the questions you ask when performing research or an audit?

A
  • RESEARCH: what should we be doing?

- AUDIT: are we doing it right (does it reach a predetermined standard)?

312
Q

List the 7 common elements of clinical audit’s & research?

A
  1. Professionally led
  2. Influence on clinical practice
  3. Formal data collection
  4. Methodological rigour
  5. Data analysis / interpretation
  6. Publishable?
  7. Ethics
313
Q

Is there ethics involved in research & clinical audits?

A
  • RESEARCH: YES!

- AUDIT: NO, may be needed if it’s judged to put patients at risk, if uncertain, seek advice from ethics committee

314
Q

What are the 2 key factors in distinguishing research & audit according to National Research Ethics service?

A
  • INTENT: to generate new knowledge (research) to measure performance against a standard of care (audit)
  • ALLOCATION OF TREATMENT SERVICE if by protocol (research)
315
Q

What question do we ask in qualitative research?

A

What is the patient experience of receiving this service?

316
Q

What is the quantitative research hypothesis test?

A

How do patient outcomes compare between this service (or treatment) & an alternative?

317
Q

What does PICO (parts to a quantitative research question) stand for?

A
  • Patient/ Precipitants
  • Intervention
  • Comparison
  • Outcome
318
Q

Define Service Evaluation?

A

Review process undertaken solely to define/judge current service with the intention of benefiting those who use it, used to inform local practice

319
Q

What are the 3 components of Service Evaluation?

A
  1. Structure (what you need- infrastructure, staff)
  2. Process (what to do)
  3. Outcome (what you expect)
320
Q

What are the 3 service evaluation questions?

A
  1. Does the service achieve its objectives?
  2. Does the service (still) meet pt’s needs?
  3. Is the service equitable?
321
Q

What are the 2 main parts of an audit?

A
  1. Retrospective- notes review (beware missing data)

2. Prospective- ongoing data collection (beware the “Hawthorne effect”)

322
Q

List the 8 steps to doing an audit?

A
  1. Identify a topic/ problem
  2. Identify local resources (local audit dept)
  3. Choose standard, create the audit proforma
  4. Define the sample
  5. Collect data
  6. Compare data with the standard
  7. Develop & implement change
  8. Re-audit
323
Q

What does the “Johnston et al Quality in Health Care 2000” state are the 5 main barriers?

A
  1. Lack of resources
  2. Lack of expertise/ advice in project design & analysis
  3. Problems between group members
  4. Lack of an overall plan for audit
  5. Organisational impediments
324
Q

What does the “Johnston et al Quality in Health Care 2000” state are the 6 key facilitators?

A
  1. Modern medical records systems
  2. Effective training
  3. Dedicated staff
  4. Protected time
  5. Structured programmes
  6. Shared dialogue between purchasers & providers
325
Q

List the different criteria for choosing a topic?

A
  • High cost, volume, or risk to staff or users?
  • Evidence of a serious quality problem?
  • Evidence available to inform standards ie. systematic reviews/ national clinical guidelines?
  • Is problem amenable to change?
  • Is the topic a priority?
  • Potential for involvement in national audit project?
326
Q

List the different criteria for choosing a standard?

A
  • Agree the standard (minimal, ideal or optimal)

- Is it evidence based & related to aspects of care?

327
Q

Describe the minimal, ideal & optimal standards?

A
  • MINIMAL: lowest acceptable level of performance
  • IDEAL: care possible under ideal conditions
  • OPTIMAL: realistic under normal conditions of practice
328
Q

List the 4 perceived benefits of an audit?

A
  1. Improved communication among colleagues
  2. Improved pt care
  3. Increased professional satisfaction
  4. Better admin & data recording
329
Q

List the 4 disadvantages of an audit?

A
  1. Diminished clinical ownership
  2. Fear of litigation
  3. Hierarchical & territorial suspicions
  4. Professional isolation
330
Q

Who do you contact in the NHS regarding Audit or Service Evaluation?

A

Clinical Effectiveness Department- Clinical Effectiveness Manager / Coordinator

331
Q

Who do you contact in the NHS regarding research?

A

Research & Development Office:

  • R&D Manager
  • Research Governance Officer
  • Research Advisor (academic support)
332
Q

Can a study have components of audit, research & service evaluation?

A

YES

333
Q

Describe what is involved/what isn’t involved in an audit?

A
  • Never involves a new treatment
  • Never involves allocation of pts to groups
  • Should not involve anything being done to pts beyond their normal care
  • Simple stats
  • Results of local relevance
  • Influence on clinical practice locally
  • Some aspects may require review by an ethics committee
334
Q

Describe what is involved/what isn’t involved in research?

A
  • May involve pts getting new treatment
  • May involve pts being allocated to different groups
  • May involve pts receiving experimental interventions
  • Can involve complex stats
  • Results generalisable
  • Influence on clinical practice everywhere
  • Always requires ethics review
335
Q

What level of glycated haemoglobin gives a diagnosis of diabetes mellitus?

A

≥48mmol/mol

336
Q

What level of fasting blood glucose gives a diagnosis of diabetes mellitus?

A

≥7.0mmol/L

337
Q

What level of 2hr blood glucose gives a diagnosis of diabetes mellitus?

A

≥11.1mmol/L following OGTT

338
Q

What level of random blood glucose gives a diagnosis of diabetes mellitus?

A

≥11.1mmol/L in presence of symptoms

339
Q

What are the 4 different classifications of diabetes mellitus & how common are they (%)?

A
  1. Type 1 diabetes (ß cell destruction) - 10%
  2. Type 2 diabetes (insulin resistance & deficiency, secretory defect) - 85%
  3. Other types (genetic, pancreatic/endocrine disease, drugs) - 5%
  4. Gestational diabetes
340
Q

When do type 1 diabetes symptoms occur?

A

When 80% ß cell mass lost

341
Q

Give an example of an environmental factor with leads to ß cell destruction in type 1 diabetes?

A

Viral infection

342
Q

List the 4 areas that autoantibodies act on in Type 1 diabetes (autoimmune)?

A
  1. Islet cells
  2. Insulin
  3. GAD (GAD65)
  4. Tyrosine phosphatase
343
Q

What are the 2 strong HLA associations in Type 1 diabetes?

A
  1. Linkage to DQA & DQB genes

2. Influences by DRB genes

344
Q

What are the 3 environmental factors for Type 2 diabetes?

A
  1. Obesity
  2. Stress
  3. Reduced physical activity
345
Q

Describe the classical presentation of Type 1 Diabetes Mellitus?

A
  • Thirst, polyuria
  • Malaise, fatigue
  • Infections ie. candidiasis
  • Blurred vision
  • Complications
  • Incidental finding
  • More visceral fat distribution
346
Q

Describe Monitoring for diabetes mellitus

A
  • Monitor blood glucose

- Test for ketones

347
Q

What is Diasend?

A

Web-based diabetes management system that allows you to store, review & print insulin pump, CGM & blood glucose meter data on the diasend website for monitoring patterns

348
Q

Describe glycated haemoglobin (HbA1c)?

A

Form of hemoglobin that is measured primarily to identify the 3-month average plasma glucose concentration

349
Q

What is CS11?

A

Continuous subcutaneous insulin infusion

350
Q

What are the acute complications of diabetes mellitus?

A
  • Diabetic Ketoacidosis
  • Hypoglycaemia
  • Other emergencies
351
Q

What are the chronic complications of diabetes mellitus?

A
  • Microvascular: keys, kidneys, nerves (feet)

- Macrovascular: heart, brain, (feet)

352
Q

What combination of things in the liver make Ketone bodies?

A
  1. Amino acids Leucine, Lysine

2. Free fatty acids

353
Q

In diabetic ketoacidotic patients what electrolyte loss should you monitor and be most concerned about?

A

The huge Potassium loss/shift, this often kills patients!

354
Q

Describe the treatment of diabetic ketoacidosis?

A
  • Insulin IV 6U/hr then by sliding scale
  • N/Saline initially (4-6L)
  • Dextrose 5% subsequently to replace water losses
  • Careful monitoring of K+ & replace as required
355
Q

Describe the symptoms of hypoglycaemia?

A
  • Adrenergic: tachycardia, palpitations, sweating, tremor, hunger
  • Neuroglycopaenic: dizziness, confusion, sleepiness, coma, seizures
356
Q

What is the formal definition of hypoglycaemia?

A

Blood glucose <= 2.2mmoll-1

357
Q

What are the 3 possible causes of hypoglycaemia?

A
  1. Too much insulin
  2. Too little food
  3. Unusual exercise
358
Q

What is the human counter-regulatory mechanism for fall in blood glucose?

A

Vagal stimulation –> parasympathetic –> glucagon release –> glycogen release by liver

359
Q

What is the human counter-regulatory mechanism for neuroglycopaenia?

A

Adrenal medulla stimulation –> sympathetic –> Adrenaline release –> glycogen release by liver

360
Q

What is the treatment for hypoglycaemia?

A

IV 50% dextrose

361
Q

Describe the emergency- HyperOsmolar Non-Ketotic coma (HONK)?

A
  • Elderly patients
  • Often undiagnosed
  • Intercurrent stress (MI, chest infection etc)
362
Q

Describe why Metformin Associated Lactic Acidosis (MALA) is an emergency?

A

Causes Renal impairment

363
Q

Describe the process of glycation?

A

Protein –> Glucose Schiff base –> Ketoamine –> 5-Hydroxymethylfurfural —> Increased cross linking & browning of proteins

364
Q

What are the 5 stages of nephropathy?

A
  1. Hyperfiltration
  2. Normal
  3. Microalbuminuria
  4. Overt nephropathy
  5. Chronic renal failure
365
Q

What screening would you do for nephropathy?

A
  • Albustix
  • Microalbuminuria
  • Creatinine
366
Q

How would you manage nephropathy?

A
  • Blood pressure: aggressive treatment ACEI/AIIRA, 130/80 or lower
  • Hyperlipidaemia: statin
  • Good glycaemic control
  • Diet
367
Q

Describe diabetic microangiopathy?

A

Debris in lumen causes blockage of normal blood supply –> ischaemia –> pain & lack of function

368
Q

What would you look at on examination of the foot?

A
  • General appearance
  • “Architecture”
  • Pulses
  • Sensation (neurosthesiometer, monofilament)
  • Education (patient)
369
Q

List the 4 stages of diabetic retinopathy?

A

Background –> Preproliferative –> Proliferative –> Advanced eye disease

370
Q

What are the 3 types of maculopathy?

A
  1. Exudative
  2. Oedematous
  3. Ischaemic
371
Q

Describe the management of diabetic retinopathy?

A
  • Screening: annual if no previous DR
  • Methods: ophthalmoscope, retinal camera
  • “System”
  • Blindness audit

MD4001 (11 decks)

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