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Block 4 > Pathophysiology > Flashcards

Pathophysiology Flashcards

0
Q

What is pseudogout?

A

Aging cartilage degeneration: age related OA - calcium pyrophosphate crystals into joint cavity. Common in the elderly
Mineralisation around chondrocytes
Mainly asymptomatic

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1
Q

What is gout? and what causes it?

A

Crystal arthropathy, Hyperuricaemia
Presents with a acute red swollen joint and soft tissue lesions (similar to septic arthritis)
Multiple attacks lead to chronic damage
Uric acid is breakdown product of purines, gout if not excreting it or producing too much of it
Excreted by kidneys so gout in CKD, Taken in in diet - red meat
Acute leukemia - high turnover of cells so high levels of uric acid

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2
Q

What are Seronegative spondyloarthropathies?

A

Inflammatory systemic disease involving axial skeleton (spine and sacroilliac joints), also peripheral joints. Negative to rheumatoid factor
Oligoarthritis commonly involving large joints in lower limbs
Familial clustering, & linkage to HLA-B27
Characterized by inflammation at sites of attachment of ligament, tendon, fascia, or joint capsule to bone (enthesopathy)
Includes Reiter’s syndrome, ankylosing spondylitis, psoriatic arthritis, & arthritis of inflammatory bowel disease
Occurs more third decade, commonly young men
Genetic factors important role in susceptibility
Initial event involves interaction between genetic & environment factors, particularly bacterial infections
Reiter’s syndrome may follow GI/ GU infections
Bowel inflammation implicated in pathogenesis of Reiter’s syndrome, psoriatic arthritis, & ankylosing spondylitis

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3
Q

What is Ankylosing spondylitis?

A

Erosion of sites where ligaments and tendons attach to bone at sacroiliac joint and lumbar spine. Eventual posterior fusion of spine and possible involvement of upper spine and large joints. 5x more common in men. 90% have HLA-B27 antigen

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4
Q

What are Reactive arthropathies?

A

Inflammatory joint disorders with an infective cause but distant in time and place from the infection

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5
Q

What is Psoriatic arthritis?

A

Inflammation of the joints in 5-7% of psoriasis sufferers
Most have extra spinal disease
Silver/grey scaly spots on scalp, elbows, knees and lower spine
Pitting fingernails/toenails
Pain & swelling in one or more joints
Dactylitis of fingers/toes gives “sausage” appearance

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6
Q

What are 3 types of autoimmunity?

A

Organ-specific: type 1 diabetes
Tissue-specific: myesthenia gravis
Systemic: lupus

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7
Q

Which cells mainly mediate autoimmunity?

A

B cells

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8
Q

Why can diagnosis of autoimmunity be difficult?

A

Presence of auto-antibodies in healthy patients

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9
Q

What are the mechanisms underlying autoimmunity?

A

Inappropriate access to self- antigens by antigen presenting cells (normally immuno-priviledged site exposed)
Inappropriate/increased local expression of co-stimulatory molecules (infection or inflammation)
Alterations in way in which molecules are presented to immune system
(MHC changes)
Molecular mimicry (infective agent)

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10
Q

What are the types of arthropathy?

A

Degenerative: OA
Inflammatory: Seropositive e.g. RA, Seronegative e.g. Ank Spond, Psoriatic, Inflammatory bowel disease, Gout, Infection

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11
Q

What are risk factors for rheumatoid arthritis?

A

Genetic predisposition: HLA-DR4 associated
2-3x women than men
Increases with age
Caucasians

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12
Q

What are symptoms of rheumatoid arthritis?

A

Systemic: fatigue, anorexia, weight loss, low grade fever, anaemia
Articular- joint aching and stiffness
Extra-articular: pericarditis, valve problems, atherosclerosis, pleural effusions, rheumatoid nodules, pulmonary fibrosis, anaemia, splenomegaly, osteoporosis, rheumatoid nodules, vasculitis, leg ulcers, C1/C2 atlanto-axial subluxation, nerve compression scleritis, xerophthalmia

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13
Q

What are clinical features in the hands of a rheumatoid patient?

A

Metacarpophalangeal joint & proximal interphalangeal joint arthritis with ulnar deviation

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14
Q

Describe the pathogenesis of rheumatoid arthritis

A

Rheumatic factor autoantibodies attack synovium
Inflammation of synovium: angiogenesis, proliferation
Secondary changes occur in cartilage: enzymes and prostaglandins destroy articular cartilage and underlying bone, pannus invasion destroys cartilage at joint periphery

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15
Q

What can cause ankylosis of joints in rheumatoid arthritis?

A

Reduced movement of joint due to collagen scarring building up in the joint. This can mineralise and fix the joint

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16
Q

Describe visible differences in the joint between RA and OA

A

RA: inflammation, pannus, eroding cartilage, bony & fibrous ankylosis
OA: Osteophytes, bony spur, no ankylosis, subchondral cyst, subchondral sclerosis, thinned fibrillated cartilage

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17
Q

What investigations can be done to diagnose rheumatoid arthritis?

A

Bloods
FBC : anaemia (chronic disease / haemolytic)
ESR : raised
CRP : moderately raised
Immunology: RhF : raised in ~70% of cases (also some healthy people), Anti CCP more specific marker
Radiology :
US, MR or isotope bone scans (early changes)
Radiographs of hands & feet (later changes), soft tissue swelling, juxta-articular osteopenia, joint space narrowing, periarticular erosions, subluxation, deformity

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18
Q

What are treatment options for rheumatoid arthritis?

A

Symptomatic relief: Pain killers, Glucocorticosteroids
Treatment of underlying disease process: DMARDS (Disease modifying anti-rheumatic drugs), Normally at least two
Biological agents after DMARDS have been unsuccessful

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19
Q

How do corticosteroids help to treat rheumatoid?

A

Inhibition of transcription factors
Reduced transcription of many cytokine genes e.g. ↓IL1, IL2 and TNF
Reduced clonal proliferation of T helper Cells

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20
Q

What are DMARDs?

A

Mimic endogenous compounds, Anti-cancer and immunosuppressant effects
Anti-proliferatives: Methotrexate (against folate activity), azathioprine (against purine synthesis)
Suppressive: sulphasalazine (against IL-1 & TNF), penicillamine (against MΦs, T cells, IL-1)
Gold injections = uncertain mechanism

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21
Q

Describe how methotrexate works

A

Folic acid antagonists. Inhibits dihydrofolate reductase activity which prevents conversion of dihydrofolate to tetrahydrofolate which is not all used for the production of purines and amino acids and therefore DNA and protein synthesis
Inhibits S phase
Renal excretion
Side effects - mainly affects tissues which are highly proliferative - Gi tract, liver due to anti proliferative effects

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22
Q

Describe how azathioprine works

A

Anti proliferative effects
Purine analogue
Reduce DNA & RNA synthesis so can’t go through cell cycle
Reduce guanine and adenine synthesis
Adverse effects: cholestasis, liver necrosis

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23
Q

What Biological Agents can be used to treat rheumatoid arthritis?

A

mAbs (monoclonal antibodies): infliximab = anti-TNF cytokine, rituximab = anti-CD20 on B lymphocytes

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24
Q

What is the prognosis for rheumatoid arthritis patients?

A

10% will become severely disabled, majority of damage in first 5 years
70% will have variable symptoms with flair ups requiring drug therapy 20% mild disability and symptoms
Complications: Reduced immunity, Complications of drug treatments

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25
Q

What questions need to be asked in a history addressing lumps and bumps?

A 
How long have you had this? 
Exacerbating/alleviating factors 
Pain in swelling location or elsewhere 
History of trauma 
Any previous or recent treatment/intervention/surgery 
Site-dependent questions 
Neurological disturbance/distribution 
Temporally-associated systemic symptoms
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26
Q

What additional factors need to be considered when forming a diagnosis on lumps and bumps?

A 
Age 
Gender 
Social history 
Occupation 
Medical history
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27
Q

What are 2 methods for lump examination?

A 
SSSCCATTTT
Site, Size, Shape, Consistency, Colour, Auscultate, Tenderness, Tissue layer, Thrills/Fluctuance, Transillumination 
SPACE TIT
Size, Shape, Surface 
Position 
Attachments 
Consistency & Colour 
Edge 
Thrills/pulsation/fluctuance 
Inflammation 
Transillumination
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28
Q

What are methods for determining the origin/content of a lump?

A

Transillumination - fluid filled
Fluctuance - fluid filled
Auscultate - air, bowel sounds, pulsation, bruits

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29
Q

What does annular mean in relation to lumps?

A

Ring shaped

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30
Q

What does arcuate mean in relation to lumps?

A

Curved

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31
Q

What does nodule or papule mean in relation to lumps?

A

Palpable mass of specific size

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32
Q

What does macule mean in relation to lumps?

A

Flat region of surface colour change

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33
Q

What does pustule mean in relation to lumps?

A

Small pocket of pus

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34
Q

What techniques can be used to determine the tissue layer location of a mass?

A

Bone masses are immobile
Muscle/tendon masses can be moved, or have their movement limited, by muscle contraction
Neural masses only tend to move left-to-right
Pressing on a neural mass can cause pain/tingling/sensory loss
Lumps within the skin can be moved with the skin

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35
Q

What ways can you describe a skin cancer?

A

A – Asymmetry
B – Borders
C – Colour
D - Dimensions

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36
Q

How does lymphadenopathy present?

A

Palpable relatively non-mobile mass

Enlargement can be unilateral during cancer or infection

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37
Q

What are Sister Mary Joseph Nodules?

A

Cancer metastasis in umbilicus

Spread up urachus from bladder

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38
Q

What needs to be considered with groin lumps?

A

Can you get above the swelling? Yes: not a hernia, No: likely a hernia
Reduce a hernia and test cough impulse
Is it solid or fluid-filled? - fluid, hydrocele
Where is the lump relative to the testicle? - above: spermatocele, on testicle: Cancer
Where is the testicle? - within swelling: hydrocele
Does it look/feel like a ‘Bag of worms’? - varicocele

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39
Q

What is testicular pain?

A

Torsion until proven otherwise

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40
Q

What is a hydrocele? And how can you diagnose it?

A

Fluid in tunica vaginalis
Will transilluminate and sits at the level of the testicle
May not be able to palpate the testicle

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41
Q

How would a patent processus vaginalis present?

A

Young boy
Swelling not there in the morning but appears during the day, then disappears when lying down
Swelling transilluminates but can’t get hand above it
Peritoneal fluid communicating, gravity means it accumulates through the day

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42
Q

What is a hernia?

A

Protrusion of a tissue or organ through its retaining tissue

43
Q

What are the 4 abdominal wall area hernias?

A

Inguinal: Males more than females, Above & medial to pubic tubercle
Femoral: Females more than males, Below & lateral to pubic tubercle
Incisional (post operative)
Umbilical: Normally in newborn / young

44
Q

What is Lumbar (Petit) triangle?

A

Site for herniation

Bordered by iliac crest, latissimus dorsi and external oblique

45
Q

What is the inguinal canal?

A

Passageway through anterior abdominal wall

46
Q

What is the deep inguinal ring?

A

Invagination of transversalis fascia

Lies between the midpoint of inguinal ligament & the midinguinal point (1cm above the inguinal ligament)

47
Q

What is the superficial inguinal ring?

A

Lies supero-lateral to the pubic tubercle

Point of emergence of spermatic cord (male) or round ligament of uterus and coverings (female)

48
Q

What are the contents of the female inguinal canal?

A

Round ligament of uterus
Lymphatics from uterus
Ilioinguinal nerve
Genital branch of genitofemoral nerve

49
Q

What are the contents of the male inguinal canal?

A

Spermatic cord & contents
Ilioinguinal nerve
Genital branch of genitofemoral nerve

50
Q

What is a direct inguinal hernia?

A

Medial to inferior epigastric artery
Weakness of conjoint tendon
Presses on the superficial inguinal ring

51
Q

What is an indirect inguinal hernia?

A 
Lateral to inferior epigastric artery 
Passes through processus vaginalis via deep & superficial inguinal rings 
Travels into scrotum 
Congenital type 
Common in males
52
Q

What is Hesselbach’s triangle?

A

Region of bulging with a direct inguinal hernia

Bordered by rectus abdominis, inguinal ligament and inferior epigastric artery

53
Q

Describe the examination of an inguinal herniae

A 
Patient lying down & standing 
Observe site and direction 
Make other regional observations
Compare sides 
Test cough impulse 
Reducible/irreducible 
Pressure over alternate inguinal rings 
May need to stand 
Auscultate for bowel sounds
54
Q

What types of groin swelling can occur in females?

A

Canal of Nuck (female equivalent of processus vaginalis)
Bartholin gland cyst
Femoral hernia

55
Q

What swellings can occur in femoral triangle?

A

Saphenous vein pierces roof (can dilate here saphena varix)
Inguinal lymph nodes sit in triangle (lymphadenopathy)
Femoral hernia presents as swelling in the triangle

56
Q

Where are superficial inguinal lymph nodes?

A

Sit in two groups, proximal & distal

Gross lymphadenopathy can present as a groin lump

57
Q

Which structure lies outside femoral sheath & deep to iliac fascia?

A

Femoral nerve
Femoral artery, vein & lymphatics located inside the fascia
Artery and vein sit in femoral sheath & lymphatics sit in femoral canal

58
Q

What is the femoral canal?

A

Fascial compartment for lymphatics (weak spot)

59
Q

Why are women at higher risk of femoral hernia?

A

Wider pelvic girdle so femoral canal larger

60
Q

What forms the femoral ring?

A

Lacunar ligament
Inguinal ligament
Pectineal ligament
High chance of hernial sac contents strangulation due to rigid borders of femoral ring

61
Q

What are Branchial cysts?

A

Remnants of the embryological branchial sinus which should obliterate
If it remains open it can form a branchial fistula that opens & discharges onto the lower neck

62
Q

What are rheumatological diseases?

A

Characterized by pain & inflammation in joints & connective tissues
Sometimes referred to as collagen-vascular diseases
May affect many different parts of the body
Over 200 different conditions

63
Q

What are Non Immunological Inflammatory Diseases?

A

Osteoarthritis (OA)
Gout
Pseudogout

64
Q

What form of immunity underlies the non inflammatory rheumatological diseases?

A

Innate

65
Q

What are Immunologically-Mediated rheumatological Diseases?

A 
Rheumatoid Arthritis (RA) 
Systemic Lupus Erythematosus  (SLE/ Lupus) 
Spondyloarthropathies 
Ankylosing spondylitis 
Reactive Arthritis (Reiter’s Syndrome) 
Psoriatic Arthritis 
Spondylitis associated with Inflammatory Bowel Disease
Sjogren’s Syndrome 
Polymyositis/Dermatomyositis 
Behcet’s Syndrome 
Systemic Sclerosis (Scleroderma) 
Giant Cell Arteritis
66
Q

What is the Function of Normal Synovium?

A

Maintenance of intact non-adherent tissue surface
Lubrication of cartilage
Control of synovial fluid volume & composition (plasma & hyaluronan)
Nutrition of chondrocytes within joint

67
Q

What is athralgia?

A

Joint pain

68
Q

What are characteristics of joint Arthritis?

A 
Pain 
Redness 
Swelling 
Increased warmth 
Fluid accumulation (synovial effusion)
Stiffness (especially in morning/ inactivity)
69
Q

Describe the Pathogenesis of Rheumatoid Arthritis

A 
Inflammed synovial tissue (synovitis)
Villous hyperplasia 
Intimal cell proliferation 
Inflammatory cell infiltration: T & B cells, macrophages & plasma cells 
Production of cytokines & proteases 
Increased vascularity 
Self-amplifying process
70
Q

What are Key cytokines in Chronic Inflammatory Arthritis?

A 
TNF-alpha
IL-1 
IFN-gamma 
IL-6 
OPGL (RANK-ligand) 
IL-17 
IL-23
71
Q

What T cell subtypes contribute to pathogenesis of RA?

A

Synovial naive T cells
Regulatory T cells
T helper cells: release cytokines to activate leukocytes and mesenchymal cells, recruit B cell help, cytotoxicity CD8 cells, cell contact mediated activation of macrophages, fibroblasts & endothelium

72
Q

What signs of RA can be seen on xray?

A

Early Arthritis - soft tissue swelling, especially around PIP joints Chronic inflammation in joint leads to bone destruction evident as erosions
Prolonged severe chronic arthritis leads to deformity & disability

73
Q

What is the Immune Response Directed Against in RA?

A

Type II collagen
IgG (rheumatoid factor)
Citrullinated proteins (arginine residues modified)

74
Q

What is the immune response targeted against in SLE?

A

Nuclear: Ribonuclear proteins, Histones, dsDNA
Leukocyte cell surface antigens
Cardiolipin

75
Q

What are Susceptibility genes for rheumatological conditions?

A 
MHC class II in RA, HLA DR4
MHC class I in seronegative spondyloarthropathy   
Complement deficiency genes in SLE
Gender due to oestrogen involvement
76
Q

Describe Genetic Basis of Rheumatic Diseases

A

Genotype contributes to rheumatic disease susceptibility
Rheumatic diseases are polygenic
Genotype predisposes an individual to disease, but does not make disease development certain

77
Q

What Environmental factors may contribute to rheumatological disease?

A

Viral (hepatitis B and C, mumps, EBV)
Bacterial (Streptococci, Salmonella, Shigella)
UV light in SLE

78
Q

What factors of Immune System Status are important in the development of rheumatological conditions?

A 
Relative state of activation 
Relative balance of Th1:Th2 cells  
History of previous immune responses
Level of expression of autoantigen 
Level of expression of MHC 
Co-stimulatory molecules  
Ongoing inflammation
79
Q

Describe the 3 phases of RA development

A

Environment and genetics feed into this
Pre-articular phase: autoimmunity, anti CCP, RhF, collagen specific response
Transition phase: microbial insult, biomechanical events, neurological events, microvascular dysfunction
Articular phase: articular localisation, CV disease, osteoporosis, functional decline

80
Q

Describe differences between acute and chronic inflammatory arthritis

A

Acute Arthritis: Rapid onset (hours/days), Severe symptoms, innate immune response, neutrophils (proteases, leukotrienes, prostaglandins)
rapid joint destruction, Can evolve into chronic disease
Examples: Gout & Infectious Arthritis
Chronic Arthritis: gradual onset (days/weeks), Symptoms more moderate, adaptive immune response, T cells & macrophages, Cytokines & chronic inflammation lead to joint remodeling &
destruction via erosion
Examples: Rheumatoid Arthritis, Ankylosing Spondylitis

81
Q

Give examples of monoarticular inflammatory arthritis

A

Gout
Infection
Reactive

82
Q

Give examples of polyarticular inflammatory arthritis

A

RA

SLE

83
Q

Which joints are affected in RA and SLE?

A

PIPs and MCPs

84
Q

Which joints are affected in Osteoarthritis and Psoriatic arthritis?

A

DIPs

85
Q

Which joint is affected in gout?

A

MTP - big toe

86
Q

Give examples of symmetrical inflammatory arthritis

A

RA and SLE

87
Q

Give examples of asymmetrical inflammatory arthritis

A

Psoriatic and reactive

88
Q

What is the clinical picture of someone presenting with RA?

A 
Morning stiffness 
Arthritis of 3 or more joints
Arthritis of hand joints 
Symmetrical
Rheumatoid nodules 
Anti CCP/RhF 
Radiographic changes
Diagnostic criteria: 4 of 7 present for at least 6 weeks
89
Q

What can be complications of RA?

A 
Carpal tunnel syndrome 
Baker’s cyst 
Vasculitis 
Subcutaneous nodules 
Secondary Sjögren’s syndrome 
Peripheral neuropathy 
Cardiac & pulmonary involvement
Felty’s syndrome 
Anaemia of chronic disease
90
Q

What are therapeutic strategies for RA?

A

Reduce inflammation: NSAIDs, Steroids (prednisolone)
Disease Modifying Anti-Rheumatic Drugs (DMARDs): Sulfasalazine, Methotrexate, Hydroxychloroquine, Steroids, Azathioprine, Cyclosporine, Cyclophosphamide
More selective biologics: TNF antagonists, IL-6R antagonists, anti-B cell (CD20) therapy, costimulatory inhibitors (CTLA4-Ig), (IL-1R antagonists)

91
Q

How does etanercept exert its therapeutic effects?

A

Binding of inflammatory cytokines like TNF to its receptor leads to the production of inflammatory effector molecules. Soluble TNF receptor fusion proteins like etanercept prevent this binding
MAbs have similar effect by binding directly to the cytokine

92
Q

What are surgical options for RA treatment?

A

Removal of inflamed synovium

Arthroplasty

93
Q

What systems can be effected in RA?

A 
Joints (arthritis) 
Vessels (vasculitis) 
Eyes (scleritis & episcleritis) 
Haematologic (anaemia, thrombocytosis)
Pulmonary (pleurisy, alveolitis)
94
Q

Which systems are involved in SLE?

A 
Joints (arthritis) 
Skin (photosensitive rash) 
Serosa (pericardium & pleura) 
Haematology (anaemia, thrombocytopenia)
Kidneys (glomerulonephritis) 
Lungs (interstitial disease, alveolitis) 
CNS (cognitive dysfunction, seizures)
95
Q

What is SLE?

A

Autoimmune connective tissue disease, immune system primarily attacks parts of the cell nucleus
Affects tissues throughout body M:F 1: 9 Most often develops between 15 & 40yrs , although can develop any age
More common in afrocarribean and Asian populations

96
Q

What risk does pregnancy pose to someone with SLE?

A

Chances of miscarriage, premature birth, & inter-uterine death high if disease poorly controlled
Ro or La positive mother - pass to baby and cause heart problems, baby can be born with malar rash which settles 3-6 months

97
Q

What are treatment options for Seronegative spondyloarthropathies?

A

Early diagnosis & treatment, pain, stiffness & fusion controlled
In women, AS often mild &hard to diagnose
Exercise
Medications: NSAIDs, Sulfasalazine, MTX, Biologics
Posture management

98
Q

What is Reiter’s Syndrome?

A

Inflammatory Arthritis can affect spine, joints of spine & sacroiliac joints
Characteristic inflammation of joints, urinary tract, eyes, & ulceration of skin &mouth
Fever, weight loss, skin rash
Often begins following inflammation of the intestinal or urinary
tract. Sets off a disease process involving joints, eyes, urinary tract, & skin. Many people have periodic attacks that last from 3-6 months Some have repeated attacks, usually followed by symptom-free periods

99
Q

What are treatments for psoriatic arthritis?

A 
Skin care 
Light treatment (UVB or PUVA) 
Corrective cosmetics 
Medications: NSAIDs, DMARDs 
Biologics  IL- 23 
Exercise 
Splints 
Surgery (rarely)
100
Q

What is Inflammatory Bowel Disease? And how does it link to arthritis?

A

2 separate diseases: inflammation of bowel & can cause arthritis
Crohn’s Disease: inflammation of colon or small intestines
Ulcerative Colitis: ulcers & inflammation of lining of the colon
Severity IBD influences severity of arthritis
Other areas affected by IBD include spine, hips ankles, knees, liver, skin, eyes

101
Q

Describe osteoarthrititis

A

Most common rheumatic disease
Progressive loss of cartilage & reactive changes at margins of joint & in subchondral bone
Begins at 40/50, increases with age; mainly aged 65 & older
Affects weight-bearing joints eg knees, hips, & lumbosacral spine
May be consequence of earlier damage or overuse of joint
Obesity frequently associated, Genetic factors play a role in development, Dominant in females, incidence 10x greater than in men
Final outcome is full-thickness loss of cartilage down to bone

102
Q

What is treatment for osteoarthrititis?

A

Joint Replacement Surgery -Primarily of knee & hip, also available in hands, shoulders,& elbows
Indications: pain at rest, instability, patients benefit from aggressive PT before & after surgery

103
Q

What are treatment options for IBD?

A

Diet
Exercise
Medication: Corticosteroids, Immunosuppressants, NSAIDs, Sulfasalazine, Biologics (anti- TNF)
Surgery

104
Q

Who would be in the MDT of a rheumatology patient?

A 
Consultants & trainees 
Rheumatology Nurse practitioner
Biologics Nurse practitioner  
Occupational Therapist 
Physiotherapist
105
Q

Why are cutaneous nerve innervation areas different to dermatomes?

A

Named nerve can carry several root values and innervate parts of several dermatomes

Block 4 (8 decks)

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