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PHCY220 > MSK > Flashcards

MSK Flashcards

1
Q

Indicators of RA

A

Persistent inflammation affecting joints that are:

  • Peripheral
  • Polyarthritic
  • Symmetrical
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2
Q

Etiology of RA

A
  • Exact cause unknown
  • genetic factors + environmental factors + chance
  • 50% genetic
  • 50% environmental + chance
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3
Q

Etiology of RA cont.

Genetic factors:

A

Genetic factors:

  • MHC class II alleles HLA-DR4/DR1 serotypes
  • Newly discovered PTPN22, PADI4, STAT4
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4
Q

Etiology of RA cont.

Environmental factors:

Chance:

A

Environmental factors:

  • Cigarette smoking
  • Infectious agents
  • Occupational exposures (Silica dust, mineral ols)
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5
Q

Proposed mechanism of cause of RA

A
  • Exposure of genetically susceptible host to unknown antigen triggering immune response
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6
Q

Proposed mechanism of cause of RA

  • L1, pg 13
A

frgtrew

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7
Q

RA pathogenesis

Normal joint:

Rheumatoid joint:

  • L1, pg 14
A

Normal joint:

  • Thin synovial membrane
  • Provides lubrication
  • Lack immune cells

Rheumatoid joint:

  • Synovial membrane inflammation
  • Antigen presenting cells, activated T & B cells
  • Pannus formation
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8
Q

RA Pathogeneses cont’d

Step 1:

Step 2:

Step 3:

  • L1, pg 16
A

Step 1:
- Exposure of genetically susceptible host to unknown antigen

Step 2:
- Antigen presenting cells activate T-cells (MHC II - CD4+ T), activation of B-cells

Step 3:
- Local release of proinflammatory cytokines by mo, T-cells

= Joint inflammation

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9
Q

RA pathogenesis cont’d

Step 4:

Step 5:

L1, pg 18

A

Step 4:
- Proinflammatory cytokines cause mo and fibroblasts to release matrix metalloproteinases (MMPs) degrade cartilage

Step 5: Proinflammatory cytokines cause fibroblasts to release RANKL. RANKL activates osteoclasts. Degrade bone

= Joint destruction

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10
Q

RA pathogenesis cont’d

Step 6:

L1, pg 20

A

Step 6:
- Pannus: hypertrophied synovial tissue with inflammatory cells, cytokines, and fibroblasts growing over articular cartilage and causing erosion

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11
Q

Signs and symptoms of RA

  • RA is a systemic disease with articular and extr-articular manifestations

Non-specific symptoms:

A

Non-specific symptoms:

  • Fatigue
  • Anorexia (loss of appetite)
  • Weakness
  • Low grade fever
  • Vague musculoskeletal symptoms (muscle pain, joint soreness)
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12
Q

RA signs and symptoms

Articular:

L1, pg 22

A

Articular:

  • Symmetric polyarthritis
  • Joint pain, swelling, warmth
  • Morning stiffness of joints, and after rest
  • Reduced range of motion, grip strength
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13
Q

RA signs and symptoms

Extra-articular:

L1, pg 23

A

Extra-articular:

  • Cutaneous
    • Rheumatoid nodules
    • Vasculitis
    • Palmar erythema
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14
Q

RA Classification Criteria - Serology

Rheumatoid factor (RF):

A

Rheumatoid factor (RF):

  • RF is an IgM auto-antibody reactive with the FC portion of the patients own IgG
  • The presence of RF is not specific for RA so CAN NOT be used for diagnosis or screening of RA
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15
Q

RA Classification Criteria - Serology

Anti-citrullinated protein antibodies (ACPA):

A

Anti-citrullinated protein antibodies (ACPA):

  • Serum autoantibodies
  • More specific for RA than Rheumatoid factor
  • Detectable in early disease
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16
Q

RA Classification Criteria - Acute phase reactants

Erythrocyte sedimentation rate (ESR):

C-reactive protein (CRP):

A

Erythrocyte sedimentation rate (ESR):

  • Increased in nearly all patients with RA
  • Very non-specific

C-reactive protein (CRP):

  • Usually increased during acute inflammation
  • Also non-specific
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17
Q

Other RA test

  • L1, pg 30
A

edrfgthyuj

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18
Q

RA goals of treatment

A
  • There is no cure for RA

Main goals:

  • Achieve disease remission
  • Control disease activity (inflammation and joint destruction)
  • Maintain functional ability and quality of life

DMARDs, biologics

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19
Q

OA epidemiology

A
  • In patients > 55 y.o

- Hip OA is more common in males

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20
Q

OA at specific joints

OA of the knee:

OA of the hip:

OA of the hands:

OA of the neck/back:

OA of the foot:

A

OA of the knee:
- More common in females

OA of the hip:
- Occurs in males and females

OA of the hands:
- Mainly affects woman

OA of the neck/back:

  • Called sponylosis
  • Often asymptomatic with no problems

OA of the foot:

  • Joint at base of big toe
  • Interphalangeal joints
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21
Q

The important articular changes in OA

  • Early stage
  • Progression of OA
  • Late stage
A

Early stage:
- The cartilage is thicker than normal

Progression of OA:

  • joint surface is breached and vertical clefts develop (fibrillation)
  • Cartilage is metabolically active
  • Chondrocytes replicate and form clusters

Late stage:
- Cartilage becomes hypocellular

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22
Q

Pathogenesis of OA

The extracellular matrix of normal cartilage contains:

A
  • Proteoglycans (PGs): responsible for compressive stiffness of tissue and ability to withstand load
  • Collagen: provides tensile strength and resistance to shear force
  • Matrix metalloproteinases (MMPs): degrade all extracellular matrix components
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23
Q

Pathogenesis of OA

A
  • Primary changes occur in the cartilage
  • Matrix metalloproteinases (MMPs) have an important role in the loss of cartilage matrix in OA
  • Synthesis and secretion of MMPs might be stimulated by IL-1 or other factors (ie mechanical stimuli)
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24
Q

Symptoms of OA

A
  • Pain (worse with activity, improved with rest)
  • Stiffness after inactivity or in the morning
  • Swelling, usually mild
  • Reduced range of motion
  • Giving way or sensation of instability
  • Muscle spasm
  • Sleep disturbance
  • Fatigue
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25
Q

Signs of OA

A
  • Gait abnormalities
  • Osteophytes (bony enlargements)
  • Crepitus
  • Tenderness on palpation
  • Deformity
  • Muscle weakness
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26
Q

Diagnosis

L2, pg 19 & 20

A
  • Radiographic findings in OA
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27
Q

Lab tests for OA

A
  • No specific lab test available for diagnosis of OA
  • Lab findings may help to identify the underlying cause of secondary OA
  • ESR, CBC, urine analysis are usually normal
  • Synovial fluid analysis is important in excluding other conditions (ie gout, septic arthritis, or RA
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28
Q

Treatment goals for OA

A
  • reduce pain
  • Improve function/minimise disability
  • Improve quality of life
  • Arrest (or reverse) joint destruction
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29
Q

Differences b/w OA and RA

A

ujyhgt

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30
Q

Describe the general structure of a classical NSAIDs

L3, pg 6

A
  • Classical NSAIDs are generally made up structurally of an ACIDIC moiety (carboxylate, enol) attached to a PLANAR, AROMATIC group
  • Some contain a polar linking group to an additional lipophilic group
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31
Q

Mechanism of action of NSAIDs

L3, pg 8 & 9

A

Majority of NSAIDs act as reversible inhibitors of the enzyme CYCLOOXYGENASE (COX)

  • COX also known as prostaglandin synthase
  • Aspirin irriversibly acylates the COX enzyme

COX catalyses the conversion of Arachidonic acid (AA) to prostaglandin H2
- Prostaglandins are mediators of inflammation

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32
Q

NSAIDs are acidic … except?

A

Paracetamol

  • It is Analgesic and antipyretic but NO anti-inflammatory activity
  • Paracetamol and ibuprofen can be dosed together
  • Different MoA
  • Not a true NSAID
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33
Q

MoA of paracetamol

  • pretty sure dont need to know as not in the assessable tasks
  • L3, pg 12 & 13 & 14
A

jhuyy

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34
Q

Describe the basis of paracetamol toxicity

Metabolism:

L3, pg 17

A
  1. Normal levels of glutathione (GSH). Therapeutic doses of paracetamol
    • Non-toxic conjugates. Renal excretion. Normal.
    • Protein adducts -> Hepatic necrosis & renal failure
  3. N-acetylcysteine. Treatment for overdose (and inc. production of GSH)
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35
Q

Relate structure and metabolism of NSAIDs to pharmacokinetic properties

Oxicams:

L3, pg 27

A

Tenoxicam (funded) and Meloxicam

: Enols - pKa 6.3

  • Non-classical
  • Enolate stabilised by intramolecular H-bond with amide
  • Ionised at physiological pH (acidic)
  • Higher COX-2 selectivity
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36
Q

Oxicams metabolism

A
  • Meloxicam - Slow oxidation
    • hence dosed once daily
  • Long half-life (20-50 hrs) due partly to lack of carboxylic acid
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37
Q

Understand the basis of COX-1 vs COX-2 selectivity

L3, pg 30 & 31

A
  • Isoleucine in COX 1 replaced with smaller Valine in COX 2

- Smaller size (V) allows access to a side pocket of the main substrate channel in COX2 sterically blocked in COX1

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38
Q

Describe the origins of endogenous steroids

A

Cholesterol

  • Important component of all cell membranes
  • Precursor for bile acids
    • Main function of bile acid - to facilitate the formation of micelles, where they emulsify dietary lipids and fat-soluble vitamins promoting absorption
  • Precursor for androgens, estrogens, progesterone, adrenocorticoids
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39
Q

Cyclooxygenase isoforms

COX-1:

COX-2:

A

COX-1:

  • Constitutively expressed
  • Small amounts of prostanoids (basal production)
  • “homeostatic” or housekeeping functions
  • Renal, gastric blood flow, gastric cytoprotection, platelet aggregation

COX-2:

  • Low basal expression
  • Rapidly upregulated by cytokines
  • Pathological”
  • Large amounts of prostanoids (pain, inflammation, fever)
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40
Q
  1. Understand the role of cyclooxygenase in actions of NSAIDs
  2. Relate actions and (unwanted) effects of NSAIDs to mechanism of action
  3. Start to predict the most appropriate NSAID for different patients (children/elderly/CV or renal disease) based on above knowlege
A

hhbftdcrcvy

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41
Q

Epidemiology of OA

A
  • Most common form of arthritis
  • Onset in 40’s and 50’s
  • Over half of people in 70s have OA
  • Women&raquo_space; Men
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42
Q

OA Treatment goals

A
  • Educate patients about disease & treatment
  • Alleviate symptoms
  • Prevent or slow progression
  • Maintain function & maximize QoL
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43
Q

OA Treatment

A
  • Nonpharmacologic treatment
    • Exercise (weight loss)
    • Thigh weakness inc. knee arthritis
  • Paracetamol
    • 1st choice
    • Can combine with low dose NSAIDs
  • Recommendations:
    • ROM, strength, aerobic, wt bearing, isometric, aquatics
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44
Q

Topical agents for OA

A

Topical NSAIDs & capsaicin

  • Suboptimal relief with acetaminophen, or who cannot tolerate or are reluctant to use systemic agents
  • Intitial NSAID therapy should be topical rather than oral in persons >75 years old
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45
Q

Topical therapies may also be tried as adjunct to systemic agents where pain relief is not adequate

A
  • Both agents should be applied 3-4 times daily

- Maximal effect can take up to 2 weeks for topical NSAIDs and 4 weeks for topical capsaicin

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46
Q

NSAIDs for OA

A
  • Due to their risk of serious adverse effects NSAIDs are considered 2nd line therapy after failure of acetaminophen
  • NSAIDs are often preferred by OA patients due to better pain relief
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47
Q

NSAIDs monitoring OA

A

Prior to starting long-term NSAID therapy
- assess patients for their risk of cardiovascular, GI and renal complications

If patient has no risk factors

  • ibuprofen 200-400 mg Q8H or naproxen sodium 220 mg Q12H
  • Over a 1- to 2- week trial, the dose can be titrated until adequate pain relief is achieved or the maximum dose is reached
  • Avoid long-term therapy, but if continued therapy is needed, use the lowest effective dose
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48
Q

NSAIDs toxicities

L5, pg 16, 17, 18

A
  • Gastrointestinal
  • Cardiovascular & renal
  • Thrombosis
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49
Q

Duloxetine

A
  • Duloxetine is an antidepressant approved for use in osteoarthritis of the knee
  • Duloxetine may be used as monotherapy or in combination with acetaminophen of NSAIDs for OA of the hip and knee if treatment with these agents has not provided adequate pain relief
  • Common side effects include nausea, fatigue and constipation
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50
Q

Intra-articular steroids

A

Limited to acute knee pain with local signs of inflammation and joint effusion

  • Aspiration of fluid followed by intra-articular injection of corticosteroid has a small and temporary effect (4-6 weeks) on pain and function
  • Repeated injection may damage cartilage
  • The same site should not be injected more than 3-4 times per year

Not studied in hand and hip OA

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51
Q

Hyaluronic acid for OA

A
  • Hyaluronan is a linear polysaccharide found in synovial fluid
  • 3 weekly injections have a comparable effect to 5 weekly injections
  • Reserved for patients who have failed other therapies as costs are high
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52
Q

Summary of OA treatment

A
  • Non-drug therapy is place to start
    • weight loss, exercise
  • Paracetamol 1g po qid
  • Progress if no response
  • NSAIDs are effective but potentially toxic
    • Monitor efficacy and safety
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53
Q

Methotrexate

  • MoA:
A

MoA:

  1. Inhibition of aminoimidazolecarboxamide (AICAR) trabsformylase. Inhhibits degradation of adenosine. anti-inflammatory effects
  2. Inhibition of proinflammatory cytokine production
  3. Inhibition of dihydrofolate reductase. anti-proliferative effects of immune cells
  4. Inhibition of thymidylate synthetase. with secondary effects on polymorphonuclear chemotaxis
  5. Induction of apoptosis?
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54
Q

Methotrexate

  • Side effects:

pic on L6, pg 15

A
  • Stomatitis

GI:

  • Diarrhoea
  • Hepatotoxixity

Teratogenic: contraindicted in pregnancy

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55
Q

Methotrexate

  • Route of administration:
  • Onset of action:
A

Route of administration:
- PO, SC

Onset of action:
- 2-3 weeks

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56
Q

Hydroxychloroquine

  • Proposed MOA:
  • Onset of action:
  • Route:
A

Proposed MOA:
- Suppression of T-cells, inhibition of leukocyte chemotaxis, inhibition of DNA and RNA synthesis

Onset of action:
- 6 weeks

Route:
- PO

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57
Q

Hydroxychloroquine

  • Side effects
A

CNS:
- Dizziness, headache, insomnia, dreams

Ocular toxicities:

  • Blurred vision
  • Dec. accommodation

GI:
- N, V, D (dec. by taking with food)

  • May be used in pregnancy
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58
Q

Sulfasalazine

  • Proposed MOA:
  • Onset of action:
  • Route:
A

Proposed MOA:

  • Sulfapyridine component. antirheumatic properties
  • Dec. IgA and IgM RF production
  • Inhibition of in vitro B cell proliferation

Onset of action:
- 2 months

Route:
- PO

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59
Q

Sulfasalazine

  • Side effects:
A

GI
- N/V/D, anorexia

Derm:
- hypersensitivity reactions

Skin & urin may turn yellow-orange

Safe for pregnancy

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60
Q

Leflunomide

  • MOA:
  • Onset of action:
  • Route:
A

MOA:

  • Inhibits dihydroorotate dehydrogenase
  • Inhibits protein synthesis
  • Competitive inhibitor of pyrimidine synthesis. Dec. lymphocyte proliferation & modulation of inflammation

Onset of action:
- 4-6 weeks

Route:
- PO

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61
Q

Leflunomide

  • Side effects
A
  • Hepatotoxicity
  • Hypertension
  • HEME: bone marrow toxicity
  • GI: diarrhoea
  • DERM: Alopecia
  • Teratogenicity
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62
Q

Etanercept

  • MOA:
  • Onset of action:
A

MOA:
- Binds TNF-a in the circulation and in the joint, preventing interaction with cell surface TNF,a receptors. Dec. TNF activity

Onset of action:
- 1-4 weeks

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63
Q

Etanercept

  • Side effects:
A

CNS
- Demyelinating syndromes

ID:
- Inc URTI

Heme:
- Blood dyscrasis

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64
Q

Infliximab

  • MOA:
  • Onset of action:
A

MOA:
- Binds TNF-a in the circulation and in the joint, preventing interaction with cell surface TNF-a receptors. Dec. TNF activity

Onset of action:
- Days to weeks

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65
Q

infliximab

  • Side effects
A

Infusion related:

  • “cytokine release syndrome” A clinical syndrome of fever, chills and headache
  • Manage by slowing the infusion rate

Sepsis and disseminated TB and other opportunistic infections

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66
Q

Adalimumab & Golimumab

  • MOA:
  • Onset of action:
A

MOA:
- Binds TNF-a in the circulation and in the joint, preventing interaction with cell surface TNF-a receptors. Dec. TNF activity

Onset of action:
- Weeks to months

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67
Q

Adalimumab & Golimumab

  • Side effects:
A

CNS:
- Demyelinating syndromes

ID:

  • Inc URTI, bronchitis, UTI
  • Inc. risk for serious and opportunistic infection (ie TB)
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68
Q

Tocilizumab (Actemra)

  • MOA:
  • Onset of action:
  • Side effects:
A

MOA:
- Binds membrane bound and soluble IL-6 receptor, inhibit binding of IL-6 to receptor and downstream signalling effects including T-cell activation, OC activation

Onset of action:
- 3 months

Side effects:

  • Elevated liver enzymes
  • Elevated lipids & triglycerides
  • Neutropenia
  • GI perforation
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69
Q

Rituximab

MOA:

Rituximab depletes B-cells through three different mechanisms:

A
  1. Complement-mediated B-cell lysis
  2. Cell-mediated cytotoxicity via macrophages and natural killer (NK) cells
  3. Apoptosis by activation of different caspases
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70
Q

Rituximab (Rituxan)

  • MOA:
  • Onset of action:
  • Side effects:
A

MOA:
- Binds CD20 expressed on surface of B cells and depletes them via multi mechanisms, depletion of B cells suppresses the RA disease process

Onset of action:
- 2 months

Side effects:
- Infusion reactions

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71
Q

The goals of therapy of RA:

A
  • Achieve remission
  • Control disease activity
  • Maintain functional ability
  • Quality of life
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72
Q

Why treat RA early?

A
  • Treat RA early to prevent irreversible joint damage
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73
Q

Treat-to-target strategy for RA

  • L8, pg 9
A
  • Treat early and aggressively until target is reached

- Target = remission (or low disease activity)

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74
Q

Commonly used DMARDs

A

L8, pg 13

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75
Q

Methotrexate

  • Why is this a ‘go-to’
A
  • This is our ANCHOR drug unless containdicated
  • PO or SC (SC preferred as less toxicity
  • Folic/folinic acid supplementation reduces ADRs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Biologics: common adverse effects

A
  • upper respiratory infections (colds, sinusitis, bronchitis, etc)
  • Injection site reactions (SC agents)
  • Infusion reactions (IV agents) - itching, hives, headache, palpitations
  • Skin rash
  • Dizziness
  • Nausea, diarrhoe
  • Headache
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Biologics: Rare / serious toxicities

A
  • Bacterial infections (pneumonia)
  • Unusual infections (TB, fungal, PML)
  • Leukopenia, neutropenia, thrombocytopenia, anemia, pancyttopenia
78
Q

A good summary slide

  • L8, pg 29
A

uygt

79
Q

Patients considering biologics are

Recommended:

Not recommended:

A

Recommended:
- Inactivated/killed vaccines (influenza, Pneumococcal, HBV)

Not recommended:
- Live Attenuated vaccines (herpes Zoster)

80
Q

If live Vaccines must be given

when to administer?

A
  • Administer at least 2 weeks (preferably 4 weeks) prior to starting biologic
81
Q

Joints affected by gout

Most common:

Common:

Rare:

A

Most common:
- Metatarsophalangeal joint (90%)

Common:
- Ankle, knee & elbow

Rare:
- Shoulder and hip joints

82
Q

Causes of gout

A
  • Associated with hyperuricaemia
  • Uric acid
    • produced naturally in the body
    • A waste product of purine breakdown
    • Excreted primarily by the kidneys
83
Q

Causes of gout

  • L8 or 9, pg 6
A

dfregthgtre

84
Q

Causes of gout

Uric acid balance depends on:

Gour L, pg 7

A
  • Dietary intake
  • Synthesis
  • Excretion
  • Ethnicity
85
Q

Gout causes: Dietary intake

Dietary influences:

Gout L, pg 8

A

Dietary influences:

  • Advice is consistent with healthy eating pyramid except for fish intake
  • Avoid soft drinks and fruit juices
    • High fructose corn syrup (HFCS)
    • Fructose is converted to purines and uric acid
86
Q

Gout causes: Synthesis and excretion

A
  • Increased uric acid production 10%

- Decreased renal clearance 90%

87
Q

Gout causes: Ethnicity

A
  • GLUT9 polymorphisms are associated with gout risks
  • Maori people have a higher level of the GLUT9 variant within the GLUT9 gene which encodes for a glucose transporter
  • Increased susceptibility to hyperuricaemia and gout
  • Prevalence of gout in Maori men is the highest in the world ~ 12%
88
Q

How does gout develop?

gout L, pg 12

A

Hyperuricaemia -> MSU crystallization -> MSU crystal growth –> MSU crystal deposition -> MSU crystal release in joint fluid –> Phagocytosis of MSU crystal –> Triggers acute gout flare

89
Q

Gout stages

A
  1. High Uric acid
    - Symptoms: None
  2. Acute Flares
    - Symptoms: joint inflammation
  3. Intercritical Periods:
    - Symptoms: none
  4. Advanced Gout:
    - Symptoms: Frequent or constant joint pain, lumps and bumps
90
Q

Gout pharmacology

Treatment for Acute attack:

Longterm prevention with ULT*:

A

Treatment for Acute attack:

  • NSAIDs
  • Glucocorticosteroid
  • Colchicine

Longterm prevention with ULT*:

  • Xantine-oxidase inhibitors: Allopurinol, Febuxostat
  • Uricosurics: Probencid, Benzbromarone
  • Urate oxidase: Rasburicase
91
Q

Adverse effects of NSAIDS

Major adverse effects

A
  • GI - Gastrointestinal bleeding
  • MI - Myocardial infraction (cardivascular)
  • RI - Renal impairment

“GIMIRI”

92
Q

Colchicine

MoA:

A
  • inhibit intracellular signalling molecules (tyrosine kinases and phospholipases)
  • Binds to tubulin during mitosis, inhibits spindles formulation

AS A RESULT

  • Inhibit leukocyte migration to inflamed site
  • Dec. secretion of cytokines and lysosomal enzymes
  • Inhibit phagocytosis
  • Inhibit cell division, ultimate cell death
  • Colchicine does not dec. urate production, increae renal urate excretion or posses any analgesic properties
93
Q

Colchicine toxicity

Early symptoms:

Delayed symptoms:

A

Early symptoms:
- Gi symptoms

Delayed symptoms:

  • Tachypnoea, seizure, shock, renal failure, liver damage etc
  • Death due to multiple organ failure (usually within 48hrs) and sepsis (usually within 7 days)
94
Q

Colchicine drug interactions

A
  • CCP3A4 & P-glycoprotein inhibitors

- Chemotherapy agents

95
Q

Glucocorticosteroids

MoA:

A

MoA:
- Dec. arachidonic acid production by inhibiting phospholipase A2 resulting in decreased prostaglandin synthesis

  • Dec. transcription of pro-inflammatory genes - dec. production of cytokines
  • Inhibition of pro-inflammatory pathways
  • Reduce the numbers of circulating lymphocytes, eosinophils and monocytes
  • Ultimately reduce inflammation
96
Q

Clinical risks with glucocorticoids

A
  • Fractures
  • cardiovascular risk
  • Hyperglycaemia and worsening of glycaemic control in patients with diabetes
  • GI bleeding
  • Infection
97
Q

Long-term preventrion with Urate Lowering therapy (ULT)

Gout L, pg 30 to 41

A

wehydefr

98
Q

What is pain

  • Idk if I want to learn this definition
A
  • An unpleasant sensory and emotional experience associated with actual or potential tissue damage
99
Q

Types of pain

A

Nociceptive Pain
- (sprains, bone fractures, burns, bruises) - special nerve ending which heal with time. (somatic or visceral)

Neuropathic Pain (shingles, neuralgia) nervous system dysfunction pain

Mixed category Pain (migraine headaches) - Complex mixture of niciceptive and neuropathic

Central Pain - caused by dysfunction of nervous system such as fibromyalgia

100
Q

Quality Nocicieptive: Visceral Pain

Descriptors:

Distribution/Examples:

A

Descriptors:
- Cramping, squeezing, pressure

Distribution/Examples:

  • Referred
    • heart attack, kidney stone
  • Colicky
    • Bowel obstruction, gallstone
  • Diffuse
    • Peritonitis
101
Q

Quality Nociceptive: Somatic pain

Descriptors:

Distribution/Examples:

A

Descriptors:
- Aching, deep, dull, gnawing

Distribution/Examples:

  • Well localized - patients can often point with one finger to the location of their pain
    • bone mets, strained ankle, toothace
102
Q

Quality nociceptive: referred pain

A
  • Both somatic and visceral pain travel along the same pathways. Pain stimuli arising from the viscera is perceived as somatic in origin
  • This can be confused by the brain and is often described as referred pain
103
Q

Neuropathic pain

A
  • abnormal sensations
  • Hyperaesthesia - an increased sensitivity to stimulation
  • Hyperalgesia - increased response to a stimulus that is normally painful
  • Allodynia - pain caused by a stimuli that is not normally painful
104
Q

Neuropathic pain feeling

Neuralgia:

Parasthesia:

Tight feeling:

A

Neuralgia:
- Pain in the distribution of the nerve, lancing, shooting, jumping, electricity

Parasthesia:
- An abnormal sensation, tingling, pins and needles

Tight feeling:
- Vice like tightness, gripping, cramping

105
Q

Transduction, Transmission, perception & modulation of pain

A

Pain L, pg 17 - 21

106
Q

Factors influencing pain

A

Developmental
- Age

Physiological
- Fatigue

Social

  • Attention
  • Previous experience

Psychological

  • Anxiety
  • Coping style
107
Q

general principles of management - for pain

A

Pain L, pg 29 - 30 & 12-36

108
Q

Available Opioids

Natural:

Semisynthetic:

Fully synthetic:

A

Natural:

  • Morphine
  • Codeine

Semisynthetic:

  • Oxycodone
  • Diacetylmorphine (heroin)
  • Naloxone (antagonist)

Fully synthetic:

  • Pethidine
  • Tramadol
  • Methadone
  • Fentanyl
109
Q

Opioids can be classified as:

Strong opioids used for severe pain:

Weak opioids used for moderate pain:

A

Strong opioids used for severe pain:

  • Morphine
  • Oxycodone
  • Pethidine
  • Fentanyl

Weak opioids used for moderate pain:

  • Codeine
  • Tramadol
110
Q

Opioid Receptor

A
  • Opioids act by binding to opioid receptors
  • G protein-coupled receptors
  • There are three different opioid receptors - u, s, k
  • Analgesic properties are mediated mainly via m receptors and k receptors of the dorsal horn of the spinal cord
  • Enkephalins interact more selectively with the receptors in the periphery
111
Q

Opioid MoA

1.
2.
3.
4.
5.

Opioid L, Pg 9, 10

A
  1. Opioids bind to opioid receptors
  2. Activate intracellular signalling events
  3. All 3 families are G protein-coupled receptors and inhibit adenylate cyclase
  4. They are involved in hyperpolarisation (Incr K+ efflux) or reducing presynaptic C++ influx; this inhibits neuronal activity and dec. transmission of nociceptive impulses
  5. Resulting in reduction of pain perception
112
Q

Morphine

  • idk if need to know
  • Opioid L, pg 12
A

wefrgt

113
Q

Codeine phosphate

  • Opioid L, pg 14 & 15 &16
  • Idk if need to know
A
  • Is a weak opioid

- Codeine is a prodrug, metabolised to morphine

114
Q

Tramadol

A
  • Weak opioid
  • Inhibits the reuptake of serotonin and noradrenaline at the descending inhibitory pathway
  • Time to effect is around 30 minutes and can last 5-6 hours
115
Q

Tramadol metabolism

A
  • Tramadol is metabolized by the liver and excreted by the kidneys
  • Tramadol has an active metabolite (O-desmethyltramadol) - That is also excreted by the kidney
  • The daily dose should be reduced in the presence of chronic renal failure
116
Q

Oxycodone + Fentanyl

Opioid L, pg 19

A

freg

117
Q

Methadone

A
  • Supplied as a racemic mixture
    • L methadone is mu agonist
    • D methadone is NMDA receptor antagonist
  • May have greater efficacy in neuropathic pain
  • Half life variable but average is 24 hours
  • highly lipophilic - good in renal dialysis
118
Q

Opioid related side effects

A
  • GI
    • nausea and vomiting
    • Constipation
  • Sedation
  • Respiratory depression in overdose
  • Pruritus
  • Cough suppression
119
Q

Opioids and tolerance

A

Tolerance is defined as reduction of the pharmacological effect of an opioid

  • When the same dose produces a lesser effect
  • Increasing doses of drug is required to produce the same effect
  • The mechanisms of the development of tolerance are complex
120
Q

Physical dependence:

Addiction:

A

Physical dependence:
- Is a state of adaption by the body with extended use of an opioid

Addiction:
- To opioids is drug seeking behaviour where the person is looking for opioids for its euphoric action rather than pain relief alone

121
Q

Some boring shit on Opioid L, pg 24-30

A

deikuyhgtfr

122
Q

Epidemiology of gout

A
  • Gout is the most common form of inflammatory arthritis
  • Prevalence is western developed countries is 3-6% in men and 1-2% in women
  • Prevalence steadily increases with age - plateaus after 70 years of age
123
Q

Risk factors for gout

A
  • Long term hyperuricaemia
  • Chronic kidney disease
  • Male sex (Male vs female 4:1)
  • Obesity
  • Maori and Pacific ethnicity
124
Q

Signs and symptoms of gout

Symptoms:

Signs:

A

Symptoms:

  • Severe pain
  • Swelling
  • Symptoms intensifies within 6 to 12 hours

Signs:

  • Red, warm, and swollen joint(s)
  • May have mild fever
  • Advanced gout: presence of Tophi
125
Q

Describe the diagnosis of gout

  • The American College of Rheumatology (ACR):
  • Gold standard: presence of MSU under polarised microscopy
A

Gout L2, pg 9, 10, 11

126
Q

Gout Treatment goals

A
  • To achieve rapid and effective pain relief
  • To improve quality of life
  • To maintain joint function
  • To prevent disease complications
  • To avoid treatment-related adverse effects
  • To provide cost effective therapy
127
Q

Non-pharmacological treatment for gout

A
  • Not effective when used alone
  • used with medicine
  • Apply ice packs: highly effective in reducing pain and swelling

Lifestyle factors

  • Regular exercise to reduce weight
  • Stop smoking
  • Diet
128
Q

NSAIDs for gout

A
  • Treatment of choice in reducing pain and inflammation associated with an acute attack
  • Most effective when given within the first 24 hours of the onset of pain
129
Q

Take care with Colchicine

A
  • Patients need clear instructions + lowest effective dose
  • If nausea, vomiting, diarrhoea or abdominal pains: Stop colchicine: seek immediate medical attention
  • Avoid with CYP3A4 and/or p-glycoprotein inhibitors
130
Q

Preventing future attacks for gout

A

Start ULT early:

  • Patients with hyperuricaemia should start ULT when they have:
    • Two or more flares per year
131
Q

Tips on ULT

Help patient understand:

A
  • ULT medicines need to be taken EVERY day and LIFE-LONG to stop gout flares returning
  • If ULT stops, most pts have flares again within four years. Even after yrs of being symptom free
132
Q

Allopurinol

A
  • First-line ULT
  • Start at a low dose. Slowly titrate upwards, to the target serum urate level. Helps minimize adverse effects
  • Allopurinol is safe in pts with dec. renal function; Lower starting dose, slower titration
133
Q

Allopurinol + Flare prophylaxis medicines

A
  • Flare prophylaxis medicines are recommended for the first 6 months of ULT
134
Q

Treatment options for flare prophylaxis include:

A
  • Naproxen 250 mg, twice daily for up to 6 months
  • Colchicine, 500 mcg, twice daily for up to six months
  • Prednisone 5mg, once daily, for up to 6 months
135
Q

Probenecid

GOUTL2, pg 29 & 30

A
  • Increases the exrection of uric acid (uricosuric)

- Contraindication: in patients with kidney stones, history of blood disorder, acute gout attack

136
Q

Benzbromorone:

Fevuxostat:

A

GOUTL2, pg 31 - 33

137
Q

Urate lowering treatment table summary

A

Gout Lecture 2, pg 34

138
Q

Controlled Drugs

A
  • Risk of harm to individual or society
  • Class A eg heroin
  • Class B eg morphine
  • Class C eg codeine
139
Q

Misuse of Drugs Act (MDA)

  • Controlled drugs L, pg 7 & 8
A

defrtgyh

140
Q

What can Medical practitioners & Nurse prescribe?

What is the limit on period of supply?

What about dentists?

A

Medical Practitioners & Nurse Practitioners

  • Class A & B = 1 month
  • Class C = 3 months

Dentists
- All classes = 7 days

141
Q

The prescription

A
  • controlled drugs L, pg 15 & 16 & 17 & 18 & 19
142
Q

Dispensing prescriptions & prescription expiry & repeats exceptions to baseline rule

A

Controlled drugs L, pg 20 -21 - 24 & 25 & 26 & 27

143
Q

Phone/ Oral prescriptions

A
  • Require original within two businesss days
144
Q

Pharmacist requirements when dispensing

A

Controlled drugs L, pg 29

145
Q

Supplying a CD prescription

A

Controlled drugs L, pg 30

146
Q

Records and storage of controlled drugs

A

Controlled drugs L, pg 31 - 34

147
Q

Complementary and Alternative Medicine (CAM)

  • Read through this lecture
  • L15
A

cdfvghbyj

148
Q

Rongoa

An important part of healthcare for many Maori and is based on a holistic approach to health.

It includes native:

A

It includes native:

  • Plant-based remedies
  • Physical therapies
  • Spiritual healing
149
Q

Unani / Greek / Middle Eastern Medicine

Therapy / Ways of treatment

A
  1. regimental therapy
    - Massage, cupping
  2. Dietotherapy
    • Special diet, regulation of quality and quantity of food
  3. Pharmacotherapy
    • Drugs from herbal or animal origin in raw form
150
Q

L15 Summary

A
  • Many different treatments available outside of ‘western medicine’
  • Often treatments ok to use with western medicine - but always check
  • Complementary and alternative medicine users are more likely to be female, better educated, have poorer health status
  • Arguments over what constitutes evidence
  • Many seem to work (clinical or placebo effect??)
  • ALWAYS be respectful of peoples beliefs
151
Q

What is advertising?

L16, pg 8? and 9?

A
  • Promotion of goods or services
  • On TV, in newspapers, in pamphlets, on radio, on billboards, on buses, in magazines
  • Not always clear it is advertising - may seem to be articles in a magazine, infomercials, interviews
152
Q

What is a medicine?

A
  • Substance or article that is sold/supplied for administering to human beings for a therapeutic purpose AND
  • Achieves (or is likely to) its intended action by pharmacological, immunological, or metabolic means
153
Q

Is it making a therapeutic claim?
- Yes? its a medicine

Is it a registered medicine?

  • Yes? great, it can make a therapeutic claim
  • No? - cannot make a therapeutic claim
A

frbghvfrg

154
Q

Dietary supplements

A
  • No therapeutic claim
  • Can be advertised with a health cliam
  • Very common in community pharmacies
155
Q

Claims of therapeutic purpose vs ‘health claims’

A

Health claims

- Claims which support normal physiological function - not claims for therapeutic purpose

156
Q

Advertisements for Medicines

A

L16, pg 20 - 21 - 22 - 23 - 24

157
Q

PCNZ PSNZ advertising Guidelines

A

L16, pg 27 - 28 - 29

158
Q

Bone homeostasis

Osteoblasts (bone-forming):

Osteoclasts (bone-resorbing):

Osteocytes:

A

Osteoblasts (bone-forming):
- Derived from precursor cells in the bone marrow

Osteoclasts (bone-resorbing):
- Multinucleated cells derived from precursor cells of the macrophage/monocyte lineage.

Osteocytes:

  • Derived from osteoblasts
  • Form a connected cellular network that, along with the nerve fibres in bone, can sense mechanical strain and cracking and respond by triggering bone remodelling
159
Q

Bone homeostasis (cont’d)

A
  • Osteoid (collagen) is the organic matrix of bone. Also, proteoglycans, osteocalcin and various phorphoproteins (PP)
  • Calcium phosphate crystals (hydroxyapatite) are deposited in the osteoid, converting it into hard bone matrix
160
Q

Bone remodelling (cont’d)

Bone remodelling involves:

A

Bone remodelling involves:

  • Activity of the osteoblasts and osteoclasts
  • Turnover of bone minerals (calcium and phosphate)
  • Actions of several regulators: PTH, calcitonin, vit D, oestrogen, growth hormone, steroids, and various cytokines
161
Q

Parathyroid hormone

A

Acts on PTH receptors in bone, kidney, and the gastrointestinal tract to maintain the plasma {Ca2+}

  • Mobilises Ca2+ from bone
  • Promotes its reabsorption by the kidney
  • Stimulates the synthesis of calcitriol; Ca2+ absorption from the intestine

PTH promotes phosphate excretion, its net effect is to increase [Ca2+] in the plasma and lower phosphate

162
Q

Vitamin D

A

Vitamin D (calciferol) is a lipophilic pre-hormone converted into a number of biologically active metabolites that function as true hormones.

Their main action is the maintenance of plasma Ca2+ by:

  • Its absorption in the intestine
  • Mobilising it from bone
  • Dec. its excretion
163
Q

Vitamin D (cont’d)

A

Two sources of vitamin D:

  • Dietary ergocalciferol (D2), derived from ergosterol in plants
  • Colecalciferol (D3) generated in the skin from 7-dehydrocholesterol by the action of ultraviolet irradiation

Colecalciferol is converted to calcifediol in the LIVER, and this is converted to a series of other metabolites of varying activity in the KIDNEY, the most potent of which is CALCITRIOL

164
Q

Vitamin D (cont’ddd)

A

The synthesis of calitriol from calcifediol is regulated by PTH, and is also influenced by the phosphate concentration in the plasma and by the calcitriol conc. itself through negative feedback

165
Q

Vitamin D (cont’ddddddddd)

A
  • Its effect on bone involves promotion of maturation of osteoclasts and indirect stimulation of their activity. It decreases collagen synthesis by osteoblasts
  • The effect on bone is complex and not confined to mobilising Ca2+; in clinical vitamin D deficiency in which the mineralisation of bone is impaired, administration of vitamin D restores bone formation
166
Q

Drugs used in bone disorders

A
  • Antiresorptive drugs that decrease bone loss eg bisphosphantes
  • Anabolic agents that increase bone formation eg. teriparatide
  • Vitamin D
    • In rickets and osteomalacia which are nutritionally induced deficiencies in bone mass and result from vitamin D deficiency
167
Q

Bisphosphonates

A
  • Enzyme-resistant analogues of pyrophosphate, a normal constituent of tissue fluids that accumulates in bone and has a role in regulating bone resorption
  • Inhibit bone resorption by inhibiting osteoclasts
  • Form tight complexes with calcium in the bone matrix, and are released slowly as bone is resorbed
168
Q

Bisphosphonates (Cont’d)

Can be grouped into two classes:

A
  • Simple compounds that are very similar to pyrophosphate (etidronate) incorporated into ATP analogues that accumulate within osteoclasts and promote apoptosis
  • Potent, nitrogen-containing bisphosphonates (eg alendronate, zoledronate). These prevent bone resorption by interfering with the anchoring of cell surface proteins to the osteoclast membrane by prenylation, necessary for their attachment to bone (prevent ruffling)
169
Q

Bisphosphonates (Cont’ddddd)

A
  • Given orally although poorly absorbed (ac). May be given intravenously in malignancy
170
Q

Oestrogens and SERMs

A
  • Decline in oestrogen can cause postmenopausal OP
  • HRT can ameliorate OP
  • Non-hormonal agent (eg selective oestrogen receptor modulators, SERMs) exhibit agonist actions on bone
  • Raloxifene stimulates osteoblasts and inhibits osteoclasts; agonist actions on the cardiovascular system; and antagonist activity on mammary tissue and the uterus
171
Q

Teriparatide (PTH)

A
  • A fragment of PTH (given SC once daily); in small doses paradoxically stimulates osteoblast activity (and reduce apoptosis) and enhance bone formation; used to treat OP

ADRs: dizziness, headache, and arthralgias

  • A bisphosphonate should be given at the end of a course of teriparatide to prevent bone loss due to teriparatide withdrawal
172
Q

Vitamin D

A
  • All preparations can be given orally and are well absorbed from the intestine
  • Fat soluble
  • Excessive intake of vitamin D causes hypercalcaemia causing kidney stones
173
Q

Calcium salts

A
  • Calcium gluconate (PO, IV) and calcium lactate (PO)
  • Calcium carbonate poorly absorbed in the gut, used to bind phosphate in GI tract to treat hyperphosphataemia. Also, as an antacid
  • ADRs: GI disturbance
174
Q

Medication Error:

Near Misses:

A

Medication Error:
- “Any preventable event that may cause or lead to inappropriate medication use or patient harm while the medication is in the control of the health care professional, patient, procedures, and systems, including prescribing, order communication, product labelling, packaging, and nomenclature, compounding, dispensing, distribution, administration, education, monitoring, and use

Near Misses:
- “ An event that could have resulted in unwanted consequences, but did not because either by CHANCE or through timely INTERVENTION the event DID NOT REACH THE PATIENT

175
Q

What is medication-related harm?

A
  • Patient Morbidity
  • Patient Morality
  • Social Harm
  • Financial Burden
176
Q

Where do errors happen?

A
  1. Prescribing
    - Patient information
    - Drug selection = EBP
    - Correct dose and frequency
  2. Dispensing
    - Patient information
    - Interpretation of script
    - Drug selection
    - Labelling
    - Compounding
    - Giving the script to the correct patient
  3. Administration
    - Five rights
177
Q

Understand why elderly and young are more vulnerable:

Identify types of high risk drugs

A

Error L, pg 7

178
Q

Why do errors happen

Two broad categories:

Error L, pg 10 & 11

A
  1. Practitioner Error

2. System failure

179
Q

Swiss cheese model

Error L, pg 11

A

dsfrgt

180
Q

Reporting errors and near misses

Error L, pg 15

A

frgt

181
Q

Open disclosure

Error L, pg 15

A

cdfvgty

182
Q

Root cause analysis:

Error L, pg 19

A

fvgb

183
Q

Define osteomyelitis,

A
  • AN infection of the bone:
    • Acute
    • Chronic
  • The inflammatory response associated with acute osteomyelitis can then lead to bone necrosis and subsequently on to chronic infections
  • Bones are usually resistant to infection, but under certain conditions can become susceptible
184
Q

Demonstrate understanding of the pathophysiology, including the common pathogens involved

A

The most common pathogen =
Staphylococcus aureus (S. aureeus)
- Methicillin-resistant S. aureus (MRSA) infections are becoming more common
- Usually bacterial. fungal OM is possible but wont be discussed in this lecture

185
Q

Identify risk factors of Osteomyelitis

A

Predisposition to serious infections in general

  • Indwelling catheters
  • IV drug use
  • Poor vascularity
  • Immunocompromised

Sickle cell disease

Age under 5: increased blood flow to bones

Trauma - unintentional or intentional

186
Q

Identify common symptoms of osteomyelitis

A
  • Local pain and tenderness over the affected bone
  • Reduced range of motion
  • Inflammation
  • Erythema
  • Oedema
  • Fever, chills and malaise
187
Q

Understand treatment principles and challenges for osteomyelitis

A

Acute Osteomyelitis - Treatment

  • Surgical debridement
  • Empiric IV antibiotics should be started based on the likely causative pathogen, patient risk factors and route of infection
  • All patients should have cover for S. aureus
  • Deescalate therapy when sensitivities back
  • Duration: 3-8 weeks
  • Flucloxacillin 2g IV q6h
  • Oral therapy not appropriate
  • 6 weeks - consult - consider oral switch
  • MRSA: vancomycin IV
188
Q

Identify monitoring required and preventative measures for osteomyelitis

How do we know if the treatment has worked (efficacy)

A

Look at what you used to diagnose the condition

  • Signs and symptoms, resolving?
  • Microbiology and imaging
  • Lab tests?

How do we know if the treatment is safe and appropriate?

  • Monitor for side effects of antibiotics
  • LFTs (must do with flucloxacillin)
  • U&Es
  • TDM (eg. vancomycin
189
Q

Define septic arthritis (SA)

A

Definition: An infection of a joint usually by bacteria, but can also arise from fungi or mycobacteria

190
Q

Demonstrate understanding of the pathophysiology, including the common pathogens involved in septic arthritis

A

Septic arthritis can arise from:

  • Haematogenous spread (from blood)
  • Bites or other trauma
  • Direct inoculation during joint surgery
  • Pre-existing bony infection into the joint space

Bacteria enter the joint and produce an acute inflammatory response in the synovial membrane. inflammatory cells cause cartilage breakdown and bone loss

In addition, bacterial DNA and toxins can have a direct effect on bone structure causing damage

191
Q

common pathogens involved in septic arthritis

A
  • S. aureus (including MRSA) is the most common cause in adults, as well as streptococci
  • Polymicrobial infections are uncommon! Only usually from penetrating trauma or IVDU

PHCY220 (5 decks)

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