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MD4001 > Week 11 > Flashcards

Week 11 Flashcards

1
Q

What is the origin of the adrenal medulla?

A

Neural crest

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2
Q

What is the origin of the adrenal cortex?

A

Mesodermal

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3
Q

What is the physiology/function of mineralocorticoids?

A
  • Regulate salt/electrolyte & water balance

- Na+ retention in kidney to maintain BP

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4
Q

What is the main mineralocorticoid?

A

Aldosterone

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5
Q

What is the physiology/function of glucocorticoid?

A
  • Affect carbohydrate & protein metabolism

- Potent effects on host defence mechanisms (immunosuppressive & anti-inflammatory)

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6
Q

What is the main glucocorticoid in humans?

A

Hydrocortisone (also called cortisol)

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7
Q

Why are hydrocortisone actions not completely separate from mineralocorticoid actions?

A

Because hydrocortisone has equal potency for the mineralocorticoid & glucocorticoid receptors so can have effects on water & electrolyte balance

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8
Q

What 3 things are glucocorticoids used most commonly for?

A
  1. Replacement therapy
  2. Anti-inflammatory
  3. Immunosuppressive
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9
Q

What does ACTH (from anterior pituitary) stimulate?

A

Synthesis & secretion of glucocorticoids & mineralocorticoids from adrenal cortex

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10
Q

What does the renin-angiotensin system aid ACTH to promote?

A

Mineralocorticoid secretion

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11
Q

What synthetic analogue is used instead of recombinant ACTH?

A

Tetracosactide

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12
Q

What drug is used to mimic the mineralocorticoid effect?

A

Fludrocortisone

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13
Q

What drug is used to mimic the glucocorticoid effect?

A

Prednisolone

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14
Q

What is the rate limiting step in the biosynthesis of corticosteroids, mineralocorticoids & sex hormones?

A

Conversion of cholesterol to pregnenolone (regulated by ACTH)

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15
Q

What drug inhibits the conversion to pregnenolone (rate limiting step)?

A

Aminoglutethimide

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16
Q

What does the drug Trilostane do?

A

Blocks 3 beta-dehydrogenase

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17
Q

What is Trilostane used to treat?

A

Cushing’s & primary hyperaldosteronism

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18
Q

What does the drug Metapyrone do?

A

Prevents the beta-hydroxylation of C11

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19
Q

What does the drug Carbenoxolone do?

A

Inhibits the conversion of hydrocortisone to cortisone in the kidney

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20
Q

What is the mechanism of action of Glucocorticoids?

A
  • Bind intracellular receptors migrate to nucleus, dimerize & regulate gene transcription
  • Rapid non-genomic effects mediated through signalling systems in cytosol
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21
Q

What are the 3 common glucocorticoids drugs used systematically?

A
  1. Hydrocortisone
  2. Prednisolone
  3. Dexamethasone
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22
Q

What are the metabolic effects of glucocorticoids mediated by?

A

By enzymes such as cAMP-dependent protein kinase (PKA) but not all the target genes are known

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23
Q

Describe glucocorticoids regulatory actions on the hypothalamus & pituitary?

A

Negative feedback on CRF & ACTH leading to reduced release of endogenous glucocorticoids

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24
Q

Describe glucocorticoids regulatory actions of the cardiovascular system?

A

Reduced vasodilation & fluid exudation

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25
Q

Describe glucocorticoids regulatory actions of the musculoskeletal system?

A

Decreased osteoblast & increasing osteoclast activity to give a tendency for osteoporosis

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26
Q

Describe glucocorticoids metabolic actions on carbohydrates?

A
  • Decreased uptake & utilisation of glucose accompanied by increased gluconeogenesis to cause hyperglycaemia
  • Increased glycogen storage
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27
Q

Describe glucocorticoids metabolic actions on proteins?

A

Increased catabolism & reduced anabolism particularly in muscle, leading to muscle waste

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28
Q

Describe glucocorticoids metabolic actions on lipids?

A

Permissive effect on lipolytic hormones & redistribution of fat

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29
Q

Describe glucocorticoids acute inflammatory effect?

A

Decreased influx & activity of leukocytes

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30
Q

Describe glucocorticoids chronic inflammatory effects?

A

Decreased activity of mononuclear cells, decreased angiogenesis & fibrosis

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31
Q

Describe glucocorticoids effects on lymphoid tissue?

A
  • Decreased clonal expansion of T & B cells & decreased activation of cytokine-secreting T cells
  • Switch from Th-1 & Th-2 responses
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32
Q

Describe/List glucocorticoids actions on mediators of inflammatory & immune responses?

A
  • Decreased production & action of cytokines (interleukins, TNF-α, cell adhesion factors & induced nitric oxide)
  • Reduced eicosanoids due to decreased COX-2
  • Reduced IgG & complement components in blood
  • Increased anti-inflammatory factors (IL-10 & Annexin-1)
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33
Q

Describe the overall action of glucocorticoids on immune systems?

A

Reduction in activity of innate & acquired immune systems

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34
Q

When would you use glucocorticoids for replacement therapy?

A

Adrenal failure (Addison’s disease)

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35
Q

When would you use glucocorticoids for anti-inflammatory/ immunosuppressive therapy?

A
  • Hypersensitivity & Asthma
  • Topically in inflammatory conditions of skin, eye, ear & throat
  • Rheumatoid arthritis, IBD, haemolytic anaemias, idiopathic thrombocytopenia
  • Prevent graft-versus host disease
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36
Q

When would you use glucocorticoids for treating cancer?

A
  • Combination with cytotoxic drugs for Hodgkin’s disease & acute lymphocytic leukaemia
  • Reduce oedema in tumours (Dexamethasone)
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37
Q

List the adverse/unwanted effects of glucocorticoid therapy?

A
  • Suppress response to infection & injury
  • Opportunistic infections can be problematic
  • Oral fungal/yeast infections can occur
  • Wound healing is impaired
  • Osteoporosis
  • Hazard of fractures
  • Hyperglycaemia
  • Muscle wasting & weakness
  • Inhibition of growth in children
  • Euphoria, depression & psychosis
  • Glaucoma
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38
Q

When are adverse/unwanted effects of glucocorticoid therapy commonly found?

A

Mainly after prolonged systemic use but not following replacement therapy

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39
Q

Describe the potential causes of Cushing’s syndrome?

A
  • Excessive exposure to glucocorticoids

- Disease (tumour) or prolonged administration of glucocorticoid drugs

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40
Q

How common is a pituitary tumour the cause of Cushing’s syndrome?

A

70% of endogenous cases

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41
Q

How common is an adrenal tumour the cause of Cushing’s syndrome?

A

15% of endogenous cases

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42
Q

What are the physical signs/symptoms of Cushing’s syndrome?

A
  • Euphoria/ depression
  • Buffalo hump
  • Thinning of skin
  • Thin arms & legs (muscle wasting)
  • Osteoporosis
  • Hyperglycaemia
  • Easy bruising
  • Poor wound healing
  • Increased abdominal fat
  • Moon face, red cheeks
  • Cataracts
  • Benign intracranial hypertension
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43
Q

What is the main treatment for iatrogenic Cushing’s syndrome?

A

Decrease/ withdraw use of corticosteroids gradually

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44
Q

What is the main treatment for endogenous Cushing’s syndrome?

A
  • Surgery to remove tumour
  • If surgery unsuccessful, or not possible to remove the tumour safely, medication can be used to counter the effects of the high cortisol levels
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45
Q

What happens if Cushing’s syndrome is left untreated?

A

High blood pressure which increases risk of heart attack & stroke

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46
Q

What is the main clinical use of mineralocorticoids?

A

Replacement therapy as in Addison’s disease where there is decreased aldosterone secretion

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47
Q

What is the most common mineralocorticoid drug?

A

Fludrocortisone (oral)

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48
Q

What is the mechanism of action of Fludrocortisone?

A
  • Increases Na+ reabsorption in distal tubules & increases K+ & H+ efflux
  • Acts on intracellular receptors that modulate DNA transcription
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49
Q

What is spironolactone?

A

Competitive antagonist of mineralocorticoids & is a potassium-sparing diuretic

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50
Q

What 4 things is Spironolactone used for?

A
  1. Hyperaldosteronism
  2. Resistant hypertension
  3. Heart failure
  4. Oedema
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51
Q

What is Addison’s disease?

A

Adrenal glands are dysfunctional & lead to cortical insufficiency

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52
Q

Describe the epidemiology of Addison’s disease?

A
  • Rare
  • Most 30-50yrs old
  • Can occur at any age
  • 7 in 10 cases due to autoimmune disease
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53
Q

Describe autoimmune Addison’s disease?

A

Antibodies destroy adrenal cortex cells which make cortisol & aldosterone

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54
Q

How can TB cause Addison’s disease?

A

Can spread to & gradually destroy adrenals

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55
Q

What are 4 other causes of Addison’s disease?

A
  1. Metastatic cancers
  2. Atrophy due to prolonged steroid therapy
  3. Hemochromatosis
  4. Amyloidosis
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56
Q

List the symptoms of Addison’s disease?

A
  • Anorexia
  • Nausea/vomiting
  • Weakness
  • Hypotension
  • Skin pigmentation (due to ACTH)
  • Low sodium/high potassium
  • Chronic dehydration
  • Sexual dysfunction.
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57
Q

What is the treatment for Addison’s disease?

A
  • Corticosteroid (steroid) replacement therapy for life
  • Hydrocortisone used to replace cortisol (tablet 2-3x day)
  • Prednisolone/ Dexamethasone
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58
Q

What treatment should you give in Addison’s disease if greater mineralocorticoid effects are needed?

A

Aldosterone is replaced with fludrocortisone, a more selective analogue

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59
Q

What is a cause of primary hyperaldosteronism?

A

Adrenal adenoma / Conn’s syndrome (80%+)

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60
Q

Describe the treatment for Adrenal adenoma / Conn’s syndrome causing hyperaldosteronism?

A
  • Prior to surgery use aldosterone antagonists (Spironolactone) usually for 4 weeks
  • Surgical adrenalectomy, laparoscopic surgery is preferred
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61
Q

Why might hypertension persist after removal of the adenoma in hyperaldosteronism?

A

Due to effects of previous hypertension on vasculature

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62
Q

Describe how an Adrenal hyperplasia can cause primary hyperaldosteronism?

A

In bilateral adrenal hyperplasia (BAH) adrenal cells become hyperplastic, resulting in excessive secretion of aldosterone (15%)

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63
Q

How is the rare unilateral adrenal hyperplasia treated?

A

Adrenalectomy

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64
Q

Describe adrenal carcinoma causing primary hyperaldosteronism?

A
  • Rare

- Only diagnosed once adrenal adenoma removers & examined histologically

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65
Q

Describe congenital adrenal hyperplasia?

A
  • Genetic disorder where C-21 hydroxylase enzyme is missing

- Non-hydroxylated versions of cortisol, corticosterone & aldosterone are made

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66
Q

Why are non-hydroxylated versions of cortisol, corticosterone & aldosterone bad?

A

Lack normal activity & do not negatively feedback on HPA axis

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67
Q

What does high levels of ACTH cause?

A

Constant stimulation of production of C-19 androgens

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68
Q

How do you treat congenital adrenal hyperplasia?

A
  • Cortisol to replace missing cortisol & cause negative feedback
  • Replace mineralocorticoid
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69
Q

How many different types of arthritis & rheumatic disease are there?

A

Over 200

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70
Q

What is Rheumatoid arthritis?

A
  • Chronic, systemic autoimmune disease

- Inflammation of lining/synovium of the joints

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71
Q

What may rheumatoid arthritis lead to?

A

Long-term joint damage resulting in chronic pain, loss of function & disability

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72
Q

Describe the epidemiology of rheumatoid arthritis?

A
  • 3x more common in women
  • 30-50yrs, can also affect young
  • All ethnic groups & parts of the world
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73
Q

Describe the symptoms of rheumatoid arthritis?

A
  • Inflamed joints are warm, tender, swollen, red & painful & difficult to move
  • Fatigue
  • Loss of appetite, weight loss, flu-like symptoms, depression, anemia
  • Vasculitis
  • Sjogren’s syndrome
  • Inflammation surrounding heart & lungs
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74
Q

Describe the foot, knee & ankle when affected by rheumatoid arthritis?

A

Effusions & synovial thickening of knee usually detected easily

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75
Q

How commonly is the hip affected by rheumatoid arthritis?

A

Common, but early manifestations are not apparent

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76
Q

How commonly are the hands & wrists affected by rheumatoid arthritis?

A

Affected in virtually all people with RA

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77
Q

Describe the elbow when affected by rheumatoid arthritis?

A
  • Effusion difficult to detect on physical exam

- Only objective finding is loss of motion

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78
Q

Describe the shoulders when affected by rheumatoid arthritis?

A

Neck stiffness & general loss of motion

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79
Q

Describe how blood is affected by rheumatoid arthritis?

A

Hypochromatic-microcytic anemia with low serum ferritin & low/normal iron-binding capacity almost universal
in patients with active RA

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80
Q

Describe how nerves are affected by rheumatoid arthritis?

A

Results from cervical spine instability, peripheral nerve entrapment & vasculitis resulting in mononeuritis multiplex

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81
Q

Describe how the heart is affected by rheumatoid arthritis?

A

Pericardial effusion present in ~50%, but clinical symptoms are rare

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82
Q

Describe how the lungs are effected by rheumatoid arthritis?

A

Interstitial lung disease common, but may be asymptomatic

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83
Q

Describe how the eyes are affected by rheumatoid arthritis?

A

Keratoconjunctivitis sicca, episcleritis, scleritis

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84
Q

Describe how the skin is affected by rheumatoid arthritis?

A

Rheumatoid nodules in 50%, dermal vasculitic lesions

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85
Q

What are Major histocompatibility complex (MHC)?

A

Membrane glycoproteins on the cell surface that display peptide antigens to T cells

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86
Q

What is the function of MHC II?

A

Bind peptides derived from proteins from extracellular sources that have been internalised into intracellular vesicles (DC, macrophage/ phagocytic cells & B cells)

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87
Q

What does class II MHC present?

A

Peptides to CD4+ T helper cells

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88
Q

What does Th1 produce in general?

A

Cell mediated immunity

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89
Q

What does Th2 produce in general?

A

Antibody responses

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90
Q

What do the Th1 cytokines activate?

A

Macrophages

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91
Q

What do the Th2 cytokines activate?

A

B cells

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92
Q

What have been found to be associated with rheumatoid arthritis?

A

Specific human leukocyte antigen (HLA)-DR genes

93
Q

What is present in 2/3’s of caucasians with rheumatoid arthritis?

A

HLA-DR4

94
Q

Where are Specific human leukocyte antigen (HLA)-DR genes located?

A

Reside in the MHC & participate in antigen presentation

95
Q

What are the 3 potential roles of HLA-DR genes?

A
  1. Binds to arthritogenic peptides
  2. Serves as target for auto reactive T cells
  3. Closely linked to other genes in MHC
96
Q

What help mediate autoimmunity?

A

Regulatory T (Treg) cells by suppressing autoreactive T cells by secreting inhibitory cytokines (IL-10 & TGF-Beta)

97
Q

What is tolerance?

A

Process that keeps the immune system from attacking “self”

98
Q

Describe deletional tolerance (recessive)?

A
  • Self-reactive T cells are deleted in thymus.

- Occasionally, may escape deletion and in periphery can cause tissue damage

99
Q

Describe regulatory tolerance (dominant)?

A
  • T cell specific for self antigen becomes a regulatory T cell
  • Cytokines (IL-10 & TGF-beta) produced by Treg inhibit other self-reactive T cells
100
Q

What are cytokines?

A

Proteins made by cells that affect the behavior of other cells (i.e. interleukins)

101
Q

What are chemokines?

A

Small chemoattractant proteins that stimulate the migration & activation of cells

102
Q

What are synovial fibroblasts activated by?

A
  • IL-1
  • TNF-alpha
  • IL-15, 16, 17, 18, 22, 23
103
Q

What can synovial fibroblasts do?

A

Invade cartilage & bone & regulate monocyte differentiation into osteoclasts

104
Q

How do you diagnose rheumatoid arthritis?

A
  • Medical history
  • Physical examination
  • Lab tests
105
Q

List 3 different types of lab tests for rheumatoid arthritis?

A
  1. Imaging studies- Erythrocyte Sedimation Rate
  2. Blood tests- (CRP)
  3. Rheumatoid factor- Antinuclear Antibodies (ANA)
106
Q

What 4 factors does the treatment of rheumatoid arthritis focus on?

A
  1. Relieving pain
  2. Reducing inflammation
  3. Stopping/ slowing joint damage
  4. Improving functioning & sense of well-being
107
Q

What are the 3 symptomatic medications for rheumatoid arthritis?

A
  1. NSAIDs
  2. Analgesics
  3. Corticosteroids
108
Q

What are the 4 disease modifying drugs for rheumatoid arthritis?

A
  1. Methotrexate
  2. Sulfasalazine, Azathioprine
  3. Cyclosporine, Hydroxychloroquine
  4. Minocycline
109
Q

What are the 3 biologic modifiers for rheumatoid arthritis?

A
  1. Infliximab (anti-TNF)
  2. Rituximab (anti-CD20)
  3. Combination DMARD Therapy
110
Q

How are people with rheumatoid arthritis likely to be affected?

A
  • 75% joint pain, swelling & flare-ups
  • 20% always have mild rheumatoid arthritis
  • 5% develop severe disease with extensive disability
111
Q

What is Ankylosing Spondylitis (AS)?

A

Chronic inflammatory arthritis predominantly affecting the joints of the spine

112
Q

Describe the epidemiology of Ankylosing Spondylitis (AS)?

A

3 Males: 1 Females

113
Q

Describe the treatment for Ankylosing Spondylitis (AS)?

A
  • 1st usually NSAID
  • Aspirin, ibuprofen,
    indomethacin,
    Diclofenac, ketoprofen (COX-2 inhibitors)
  • Anti-TNF mAb (infliximab) proved very effective
114
Q

What is Ankylosing Spondylitis (AS) associated with?

A

Human class I MHC molecule HLA- B27 (90% of patients)

115
Q

Describe the symptoms/signs of Ankylosing Spondylitis (AS)?

A
  • Back pain
  • Bone grows out from both sides of vertebrae & may join them together
  • “Bamboo spine”/ locked spine
116
Q

What is B27 also linked to?

A

Reactive Arthritis (ReA), but at lower level (~50%)

117
Q

What is Reactive Arthritis triggered by?

A

Bacterial infection, usually of gut/urinary tract (salmonella, campylobacter, chlamydia)

118
Q

List signs of reactive arthritis?

A
  • Eye inflammation
  • Diarrhoea
  • Lower back pain
  • Scaly skin patches on genitalia
  • Flaky skin patches on sole
  • “Sausage” toes
  • Swelling in knee, heel or ball of foot
119
Q

What are the theories for B27 peptide and Ankylosing Spondylitis (AS)?

A
  • Peptide from bacteria presented by B27, looks like host peptide in spine
  • Autoreactive T cells target joint (however, you can remove CD8 T cells & still get disease)
120
Q

What is the theory for B27 misfolds & Ankylosing Spondylitis (AS)?

A
  • Misfolds insides cells & causes cells to be stressed & secrete cytokines
  • Or, misfolded at cell surface & recognised incorrectly by Natural Killer cells
121
Q

What is coeliac disease?

A

Gut condition where small intestines become inflamed losing the villi (diarrhoea, abdo pain & bloating)

122
Q

What are the complications associated with Coeliac disease?

A
  • Osteoporosis
  • Iron, vit B12, folate deficiency anaemia
  • Bowel cancer
123
Q

Describe the epidemiology of coeliac disease?

A
  • 2-3x higher in females
  • 1 in 100 in UK
  • Onset within 1st year but diagnosis may take longer
  • Adulthood 40-60yrs
  • 1st degree relatives should be tested
124
Q

What is gluten made up of?

A

Long strings of gliadin molecules which contain glutamine

125
Q

What bit of gluten is coeliac disease reactive to?

A

33-mer peptide

126
Q

What is the function of the parathyroid gland chief cells & oxyphilic cells?

A
  • CHIEF CELLS: parathyroid hormone (PTH)

- OXYPHILIC CELLS: unknown

127
Q

What is the primary action of the parathyroid hormone?

A

Maintenance of plasma [Ca2+]

128
Q

What is the action of PTH + Vit D3?

A

Increase plasma Ca2+

129
Q

What is the action of calcitonin?

A

Decreases plasma Ca2+

130
Q

Where is the Ca2+ located in the body?

A
  • 99% bone/teeth

- 1% mainly intracellular

131
Q

What is CaPO4 converted to?

A

Hydroxyapatite

132
Q

Describe the breakdown of Ca2+ in plasma 2.3-2.6mM (0.1% of body calcium)?

A
  • 50% free
  • 45% bound to protein
  • 5% chelated to dicarboxylic acids ie. citrate/lactate
133
Q

Describe the 6 physiological functions of Ca2+?

A
  1. Prosthetic group for many enzymes & structural proteins
  2. Structure of plasma membrane
  3. Excitation-contraction coupling in muscle
  4. Excitation-secretion coupling at axonal terminals & endocrine & exocrine glands
  5. Blood coagulation
  6. Major intracellular second messenger
134
Q

How much calcium is in our extracellular fluid?

A

1000mg

135
Q

How much ECF phosphorus pool is there?

A

500mg

136
Q

What regulates parathyroid hormone (PTH) secretion?

A

Increased [Ca2+]o causes stimulation of PKC, increased PKC & [Ca2+]i inhibits PTH synthesis & release

137
Q

What is the Pre-proparathyroid 115 residue made up of?

A
  • Signal sequence
  • Pro-sequence
  • Biologically active sequence
  • C-terminal fragment sequence
138
Q

Describe the processing of pre-proparathyroid hormones?

A
  • It enters the endoplasmic reticulum and signal sequence is cleaved off = Proparathyroid 90 residues
  • Enters Vesicle secretion and pro sequence is cleaved off = parathyroid (secreted) 84 residues
139
Q

Describe the processing of pro-calcitonin in the parafollicular C cells within the thyroid?

A
  • Primary transcript undergoes RNA processing & losses CGRP = mature mRNA
  • mRNA translation causes loss of A or B
  • Proteolytic processing splits it up into N terminal peptide, Calcitonin & CCP (mature peptides)
140
Q

Describe the processing of pro-calcitonin in the brain neurones?

A
  • Primary transcript undergoes RNA processing & losses Calcitonin & CCP
  • mRNA translation causes loss of A or B, C & D
  • Proteolytic processing splits it up into N terminal peptide, CGRP & C-terminal peptide
141
Q

Describe how osteocytes are stimulated/produced to cause bones resorption?

A
  • PTH & Vit D act on osteoblasts to secrete growth factors (macrophage colony-stimulating factor & IL-6)
  • M-CSF causes stem cells to become osteoclast precursors –> mononuclear osteoclast
  • IL-6 RANK ligand stimulates osteoclasts (multi nucleated) to reabsorb bone
142
Q

Describe how osteoblasts cause bone formation?

A

They secrete Ca2+ and phosphate to cause nucleation and lay down new bone

143
Q

What do interns on the osteoclast mate with?

A

Vitronectins on the bone to seal off the area

144
Q

Describe the metabolism of vitamin D?

A

7-dehydrocholesterol –> Cholecalciferol (Vit D3) –> 25-Hydroxycholecalciferol (25-OHD3) –> 1,25-(OH)2D3

145
Q

What is the active form of Vitamin D which stimulates osteoblasts?

A

1,25-(OH)2D3

146
Q

What is Ergocalciferol (vit D isoform) also known as?

A

Vitamin D2

147
Q

Describe the intestinal absorption of Ca2+?

A
  • Vit D allows Ca2+ from intestinal lumen to move into epithelial cell & bind to calbindin
  • Ca2+ moves into interstitial space & allows H+ to enter
  • Ca2+ moves into interstitial space & allows 2 Na+ to enter
148
Q

Describe the intestinal absorption of phosphate?

A
  • 2 Na+ & NaPi enter epithelial cell from intestinal lumen
  • Protein synthesis allows for HPO4 or H2PO4- to leave into interstitial space
  • It also allows for 3 Na+/2 K+ ATP channel to be activated
149
Q

Describe what chief cell of parathyroid releasing PTH does to control plasma [Ca+]?

A
  1. Increases bone Ca reabsorption
  2. Inhibits tubule Pi reabsorption
  3. Increases conversion of 25-OH-vitamin D to active form 1,25(OH)2-vit D
  4. Increases kidney tubule Ca reabsorption
150
Q

What is the definition of long term conditions?

A

Condition that requires ongoing medical care, limits what one can do & is likely to last longer than 1 year

151
Q

What how much do long term conditions use up NHS resource, GP consultations & hospital bed days (%)?

A
  • NHS resource: 78%
  • GP consultations: 80%
  • Hospital bed days: 60%
152
Q

Describe the epidemiology of Long term conditions?

A
  • ~2million Scots have atleast 1 LTC
  • 1/3 of households
  • 61% of 75-84yrs have 1 LTC
  • 22% of 75-84yrs have 2+ LTC
153
Q

Describe the 3 points to Scotland’s mutual care model for LTC?

A
  1. Culture which supports people with LTC & their carers to be lead partners in decisions about health
  2. Workforce with awareness, environment, knowledge & capability to enable LTC living well
  3. Health, housing, social services, community & voluntary partners work together with people & families with LTC
154
Q

What help does the lower risk people with LTC get?

A
  • Supporter self-care (70-80%)

- Professional care

155
Q

What help does the high risk people with LTC get?

A
  • Disease management (15-20%)

- MIU, A&E, emergency

156
Q

What help does the individuals with complex LTC needs get?

A

Case management (3-5%)

157
Q

What does SPARRA stand for?

A

Scottish Patients at Risk of Readmission & Admission

158
Q

What does SPARRA do?

A
  • Identify patients aged over 65 most at risk of emergency admission in the coming year
  • Feedback probabilities & details of patients to front-line teams
159
Q

What does SPARRA act as a basis for?

A

Further assessment to identify those patients who will benefit most from preventive interventions ie. intensive case management

160
Q

What is Shared Medical appointments (SMA) & what does it aim to do?

A
  • 1:1 patient-centred consultation (60mins) with a clinician-provider in presence of other patients & other healthcare providers
  • Aim to improve health & wellbeing
161
Q

What are the possible benefits of group consultations/shared medical appointments (SMA)?

A
  • People living with diabetes improved HbA1c up to 1 year
  • Less complications for baby & mother in group antenatal care
  • Older people improved continence
  • Improved patient knowledge
  • Improved quality of life in COPD
  • Improved patient satisfaction
162
Q

What are the whole system benefits of group consultations/shared medical appointments (SMA)?

A
  • Efficiency gains (clinician time) 40% productivity gain
  • Reduced A&E use & emergency admissions
  • Reduced bed days
  • 50% reduction psychiatric bed days
  • Lower care & societal costs
  • Reduced waiting times 3 months to 3 weeks
  • Improved patient & staff satisfaction
163
Q

Describe the epidemiology of diabetes in Scotland?

A
  • Prevalence 5%
  • 88% have type 2
  • 88% of those are overweight/obese
  • 10,000 new cases per year
164
Q

At 40yrs of age, what are the years lost due to a BMI>30 compared to a BMI<25 in men and women?

A
  • MEN: 5.8yrs lost

- WOMEN: 7.1yrs lost

165
Q

Describe the relationship between insulin resistance and obesity?

A
  • Insulin resistance closely linked to abdominal obesity

- Weight increases, insulin resistance increases

166
Q

What is a 5% (4.5kg) weight loss equal to?

A

22% of excess weight = 40% of excess abdominal fat

167
Q

What does weight loss do among obese diabetic patients?

A
  • Reduced Blood pressure
  • Improves lipid profile
  • Glycaemic control
168
Q

What do we tell our obese patients to do for weight maintenance?

A

Reduce intake by 50-100kcal per day for weight maintenance

169
Q

What are the 3 successes associated with weight monitoring?

A
  1. Sustained weight, no increase
  2. Minor weight loss with dietary change to reduce risk of complications
  3. Weight normalisation- rare
170
Q

How much body fat is there in a caucasian compared to south asian with both BMI 22.3?

A
  • Caucasian: 9.1%

- South Asian: 21.2%

171
Q

What is an obesogenic environment?

A
  • Imbalance calories consumed & burned

- Static leisure, transport, employment

172
Q

Describe the Healthy Weight Communities (EPODE)?

A
  • Cut childhood obesity by 1/4
  • All sectors: breastfeeding, walking clubs, gala days, community centres, parks, schools, shops etc.
  • Total environment approach
173
Q

What else can be used as a tool to facilitate healthier lifestyles & prevent obesity?

A

Law to regulate harms

174
Q

Describe the changes in rules for marketing & labelling foods?

A
  • 24 Oct 2012: consistent from of pack labelling, voluntary but food industry on board
  • 11 Oct 2012: food choices not fully conscious “Impulse marketing”
175
Q

What 4 things should we encourage to try decrease levels of obesity in society?

A
  1. Greater personal responsibility
  2. Greater personal & societal responsibility without legislation
  3. Greater persoanl & societal responsibility including legislation
  4. Societal responsibility & legislation
176
Q

What are 3 ideas for compulsory improvements in food & drink labelling?

A
  1. Regulation to ban marketing of foods high in sugar, salt & fat before 9pm watershed on TV to protect children
  2. Creation of a 20% per L sugar sweetened beverages
  3. Prioritise & fund health services to address weight in obese patients, in a similar way to smoking cessation
177
Q

What are the 4 different pathologies causing adrenal hyperfunction?

A
  1. Cushing’s syndrome
  2. Conn’s syndrome
  3. Adrenogenital syndrome & Congenital adrenal hyperplasia
  4. Adrenocortical neoplasms
178
Q

Describe Cushing’s syndrome?

A
  • Excessive secretion of cortisone
  • Also mineralocorticoid effectds
  • Female>Male
179
Q

Describe the features of Cushing’s syndrome?

A
  • Muscle catabolism
  • Abdominal Fat
  • Abnormal collagen maturation
  • Hypertension
  • Osteoporosis
  • Impaired glucose tolerance
  • Hirsutism
  • Buffalo hump (fat neck)
  • Depression/psychosis
180
Q

What causes approx 2/3 of Cushing’s syndrome?

A

Pituitary adenoma producing ACTH –> adrenal hyperplasia

181
Q

What causes approx 1/6 of Cushing’s syndrome?

A

Primary adrenal neoplasm- benign & malignant 50:50

182
Q

What causes approx 1/6 of Cushing’s syndrome?

A
  • Ectopic ACTH or related peptides –> adrenal hyperplasia

- Iatrogenic –> adrenal atrophy

183
Q

What is Conn’s disease?

A

Primary hyperaldosteronism

184
Q

Describe the sign’s of Conn’s disease?

A
  • Hypokalaemia
  • Muscle weakness & cramps
  • Metabolic alkalosis
  • High aldosterone
  • Low renin
185
Q

What is the gender ratio for Conn’s?

A

Females 4 : Males 1

186
Q

What do 80% of Conn’s have?

A

Adrenal adenoma (tends to be benign)

187
Q

What do 20% of Conn’s have?

A

Bilateral hyperplasia of zona glomerulosa but unknown cause

188
Q

What can cause secondary hyperaldosteronism?

A

Increased renin-angiotensin activity ie. as a result of renal ischaemia (associated with renal artery stenosis)

189
Q

How common is Congenital adrenal hyperplasia?

A
  • Uncommon but not impossible

- 1 in 15,000

190
Q

What are 2 causes of Congenital adrenal hyperplasia?

A
  1. 21 hydroxylase deficiency (CYP21)

2. 11-beta hydroxylase deficiency

191
Q

List the 3 different types of adrenal neoplasia?

A
  1. Benign
  2. Primary malignant (cortex, medulla)
  3. Secondary malignant (lung, breast, kidney, colon, melanoma, lymphoma)
192
Q

Describe an Adenoma?

A
  • Not infrequent at autopsy but only diagnosed in life if functional
  • Low malignant potential so treat conservatively (do nothing)
  • Most adenomas non-functional!
193
Q

Describe an Adrenal carcinoma?

A
  • Rare
  • Poor outlook as aggressive with necrosis & rapid growth
  • More often secrete sex steroids
  • Surgery is only hope
194
Q

What are the 2 purposes of monitoring molecular changes in adrenal pathology?

A
  1. Possible use in distinguishing adenoma from carcinoma (limited)
  2. Identification of familial syndromes
195
Q

Describe a Phaeochromocytoma?

A
  • Chromaffin cells
  • Intermittent production of catecholamines
  • Not easy to say if benign or malignant (10% benign, 10% malignant)
196
Q

Describe the episodic/stress induced presentation of Phaeochromocytoma?

A
  • Hypertension
  • Sweating
  • Collapse
  • Glycosuria
197
Q

What can cause Phaeochromocytoma?

A

20% familial, may be part of MEN (genetic predisposition)

198
Q

Describe a neuroblastoma?

A
  • Very rare
  • Commonest malignant tumour in children
  • N-myc (oncogene) amplification or adrenal site worse prognosis
199
Q

What is a cause of acute adrenal hypofunction?

A

Meningococcal septicaemia

200
Q

What are 4 causes of chronic adrenal hypofunction?

A
  1. Addison’s disease
  2. Amyloid
  3. Tuberculosis
  4. Metastasis
201
Q

What is the cause of Addison’s disease 75% of the time?

A

Autoimmune adrenalitis

202
Q

What are the 2 illnesses associated with Addison’s disease?

A
  1. Vitiligo

2. Diabetes

203
Q

What is the ratio of type 1 & type 2 diabetes mellitus?

A

DM2 10: DM1 1

204
Q

What is the usual cause of type 1 diabetes mellitus?

A

Insulitis (may be triggered by viral infection)

205
Q

What is the usual association of type 2 diabetes mellitus?

A

Beta-cell failure correlates with the formation of pancreatic islet amyloid deposits

206
Q

Describe type 1 diabetes mellitus?

A
  • Under 40, childhood
  • Thin
  • 1 in 500
  • Danger of ketosis
  • 40% concordance in monozygous twins
  • Destruction of beta cells
207
Q

Describe type 2 diabetes mellitus?

A
  • Over 40y
  • Obese
  • 1:50
  • Hyperosmolar not ketosis
  • No MHCII linkage
  • Not autoantibodies to islets
  • Beta cells persist
208
Q

What are 3 other causes of diabetes?

A
  1. Pancreatitis (destroy islets)
  2. Cystic fibrosis (scarring, inflammation)
  3. Tumour
209
Q

What are the 4 theories of the placebo effect?

A
  1. Endogenous opiates- Naloxone-sensitive results
  2. Conditioning- Pavlov’s dog
  3. Expectancy- wine & placebo alcohol, dopamine & money
  4. Motivation- more compliant patient?
210
Q

What are the 2 examples of blinding & acupuncture?

A
  1. Sham acupuncture locations- variation anyway, could hit meridians “by chance”, practitioner blinding
  2. Sham acupuncture needles- practitioner/patient blinding
211
Q

What are 3 orthodox explanations for acupuncture?

A
  1. Gate control theory of pain
  2. Opioid release
  3. Placebo effect
212
Q

How can we test the claims of complementary alternative medicine (CAM)?

A

Emily Rosa & therapeutic touch

213
Q

Describe chiropractic on trial?

A
  • Comparative treatments ie. physiotherapy

- Massage often part of chiropractic assessment

214
Q

What 3 things are not possible to confirm/refute for treatment in lower back pain?

A
  1. Painkillers
  2. Exercise
  3. Physiotherapy
215
Q

What did Simon Singh say about the British Chiropractic Association (BCA) & what happened?

A
  • Said chiropractic treatment “happily promotes bogus treatment”
  • BCA sued him for libel (false information) in June 2008, case was dropped in April 2010
216
Q

What did the Cochrane review conclude for Acupuncture & osteoarthritis?

A
  • Sham-controlled trials show statistically significant benefits but don’t meet thresholds
  • Atleast partially due to placebo effects from incomplete blinding
  • Waiting list-controlled trials of acupuncture suggests statistically significant, much of which due to expectation/placebo
217
Q

What did the Cochrane review conclude for Chiropractic interventions for low-back pain?

A
  • Combined chiropractic interventions slightly improve pain & disability in short/med-term for acute & subacute LBP
  • Future research is very likely to change estimate of effect & confidence in results
218
Q

What are the 4 questions we ask regarding if CAM interventions work?

A
  1. Is there a placebo effect?
  2. Something within the body that explains how a placebo effect occurs?
  3. CAM effect over & above what can be attributed to the placebo effect?
  4. Something within the body that could explain how 1+ CAM effects occurs?
219
Q

List the reasons why people use CAM?

A
  • Health promotion/disease prevention
  • Exhausted conventional options
  • Conventional option side effects/risks
  • No conventional therapy
  • Conventional approach emotionally/spiritually bereft
  • Do they know its CAM?
220
Q

Why can/can’t CAM appear effective?

A
  • Some MAY be effective: herbal remedies could contain active ingredients
  • Some CAM clearly have NO plausible scientific explanation/inherent efficacy
221
Q

What are the 3 factors that can make CAM treatment appear effective?

A
  1. Disease-associated
  2. Patient-focussed
  3. CAM-based
222
Q

List the natural impediments to making valid inferences/conclusions?

A
  • Placebo effect
  • Natural history of disease
  • Causal inferences
  • Reluctance to admit when wrong
  • Simple optimism
  • Respect for authority
  • Conspiracy-orientated view of the world
223
Q

What are the 2 ethical issues around CAM’s working?

A
  1. It it’s nothing more than a placebo, is that a bad thing?

2. Do we need to know how a treatment works?

224
Q

What are the 2 ethical issues around CAM’s being safe?

A
  1. Regulation of practitioners/ substances

2. Direct vs indirect harm

225
Q

How can you balance patient choice against the 1st duty of a doctor?

A
  • Make the care of your patients your first concern
  • Patient autonomy
  • Informed choice
226
Q

What are the 2 ethical questions regarding if CAM should be researched?

A
  1. Worthwhile finding active ingredient in herbal meds?

2. As worthwhile researching homeopathy?

227
Q

What is the ethical question for if there is a fair allocation of money regarding CAM?

A

Diversion of funds from science-based therapies?

228
Q

What are the 2 ethical questions for CAM being a fair exploration of choice?

A
  1. Or weakening commitment to the scientific method?

2. Undermining or enhancing public trust?

MD4001 (11 decks)

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