Introduction to Rheumatology Flashcards

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1
Q

What are the functions of connective tissue?

A
  • (bones, tendons, cartilage) Binds together, supports, and strengthens other body tissue
  • (adipose)Protects and insulates internal organs
  • Compartmentalises structures such as skeletal muscles
  • (Blood)-major transport system within the body
  • (adipose) site of stored energy resources

-Main site of IMMUNE RESPONSE

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2
Q

What are the things that make connective tissue connective tissue?

A

common embryological origin, they come from MESINKINE which orginates from the mesoderm -variability in vascularity(some connective tissues have a good blood supply but some don’t

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3
Q

What are the 3 components of connective tissue?

A

Cells: -Fibroblast -Macrophages -Mast cells -Plasma Cell -Lymphocytes -Leukocytes -Adipose cell

Fibres(ECM): -Reticular -Elastic -Collagen

Ground substance(ECM): -large rubbery jelly like material -made of of starches, proteins and water, multiadhesive Glycoproteins(gives structural support to connective tissues) and macromolecules

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4
Q

Describe the 3 main fibres of connective tissue?

A

Collagen: -Stongest, resistant, flexible, made of COLLAGEN

Elastic: -Smaller in diameter than collagen -Branch to form network -Made of protein called ELASTIN -Flexible -Found in blood vessels and skin

Reticular fibres: -Provide support for the walls of blood vessels -Reticulo refers to NET/MESH STRUCTURE -Made of COLLAGEN (but tends to be smaller diameter) and has a GLYCOPROTEIN COVERING

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5
Q

What are the roles of different cells in connective tissue?

A

Fibroblasts: -large flat cells with branching processes -Migrate throughout the connective tissue secreting the FIBRES and GROUND SUBSTANCES

Macrophages: -Develop from white blood cells =surround and engulf material by phagocytosis

Mast Cells: -Alongside blood vessels that supply connective tissue -Produce HISTAMINE(chemical that dialates blood vessels

Adipocytes: -fat cells -Store triglycerides

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6
Q

What is the main function of connective tissue matrix fibres?

A

Provides strength and support

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7
Q

What are the 4 main connective tissues?

A
  • Proper connective tissue
  • Cartilage
  • Bone tissue
  • Blood
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8
Q

What are the 2 types of proper connective tissue?

A

LOOSE: -Areolar(most common) -Adipose -Reticular

DENSE(tends to have more collagen): -Regular (tight collagen fibres e.g tendons and ligaments) -Irregular(skin dermis) -Elastic

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9
Q

What is the function of proper connective tissue?

A
  • Binding tissue
  • Resists mechanical stress esp, tension
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10
Q

What cells are in proper connective tissue?

A
  • Fibroblasts
  • Fibrocytes
  • Defense cells
  • Fat cells
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11
Q

What is the function of the cartilage?

A
  • Strengthen and support connective tissue
  • Resists compression
  • Cushions and supports body structures
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12
Q

Is cartilage avasclar or vascular?

A

AVASCULAR and it has NO nerve supply

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13
Q

What cells are in the cartilage?

A

CHONDROBLASTS-in growing cartilage

-responsible for the development of the cartilage Chondrocytes

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14
Q

What is the most common form of cartilage in the body?

A

Hyaline cartilage

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15
Q

Where is hyaline cartilage?

A

end of long bones to cushion joints and at epiphyseal plates

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16
Q

How strong is hyaline cartilage?

A

weakest of the 3 types of cartilage as it doesn’t contain many collagen fibres

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17
Q

Which type of cartilage is the strongest?

A

FIBROCARTILAGE- because it has lots of THICK COLLAGEN fibres

This strength makes it a good shock absorber

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18
Q

What are the features of fibrocartilage?

A
  • No PERICHONDRIUM (connective tissue that envelops cartilage)
  • Chondrocytes scattered among visible bundles of collagen fibres
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19
Q

Where is fibrocartilage commonly found?

A

Invertebral discs

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20
Q

What are the features of Elastic cartilage?

A

-Provides strength and elasticity and maintains the shape of certain structures like the external ears

-CHONDROCYTES located in a threadlike network of elastic fibres

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21
Q

What are the different types of bone tissue and what are they composed of?

A

COMPACT: -Osteon-basic unit of compact bone -Lamellae-Concentric circles of matrix -Lacunae-spaces in the matrix that house cells -Osteocytes-Mature bone cells

SPONGY: -Trabeculae-columns of bone filled with red bone marrow

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22
Q

What are 3 main types of Rheumatological Disorder?

A

RHEUMATOID ARTHRITIS-autoimmune disorder effecting the joints resulting in warm INFLAMMED swollen painful joints. Symtoms typically get worse after est

SYSTEMIC LUPUS erythematosus- autoimmune disorder of the connective tissue. Affects multiple organ systems and joints

VASCULITIS-Is a group of disorders that destroy blood vessels by inflammation

23
Q

What are the 2 broad categories of arthritis?

A
  • Osteoarthritis
  • Rheumatoid arthritis
24
Q

What is thought to cause rhematoid arthritis?

A
  • Genetic predispostition
  • environmental triggers(Smoking etc)
25
Q

What is the incidence of rheumatoid arthritis in the uk?

A

1%

26
Q

Who gets Rheumatoid arthritis?

A

-older people -female -affects young people age 20-40 mainly

27
Q

What happens in rheumatoid arthritis

A

-Inflammation of the synovial membrane leads to it and over a longer period of time can lead to erosion of the hyaline cartilage - if left untreated you can get narrowing of the joint space, bone erosion, bone destruction and very severe joint deformity

28
Q

What cytokines are involved in regulating your inflammatory response in Rheumatoid arthritis?

A

TNF-alpha

IL-1

IL-6

IL-17

29
Q

What things are thought to contribute to cartilage destruction?

A

MMP’s(Enzyme) Nirogen oxide

30
Q

What does RANKL do ?

A

expressed by osteoblast, resulting in the formation of Osteoclasts = can cause bone destruction

31
Q

What are the symptoms of Rheumatoid arthritis?

A

-Pain -Stiffness -JOint swelling

32
Q

What are the key features of Rheumatoid arthritis?

A

Symptoms- often last the remainder of the persons life Inflammatory synovitis-palpable synovial swelling, Morning stiffness, symptoms get better throughout the day Polyarthritis-more than 3 joints being affected Symmetrical-If you have fingers and wrists affected on one side than they will be affected on the other

33
Q

What are the differences between Rheumatoid arthritis and Osteoarthritis

A

Age: RA=30-50 OA=50+

Speed of Onset: RA-Rapid OA-Slow

Joint Pattern: RA-Bilateral, Symmetrical OA-Asymmetric

Movement: RA-Often better OA-often worse AM

stiffness: RA-over an hour OA-uncommon

Hand joints: RA-PIP, MCP OA-DIP, thumb, CMC

Wrist, ankle, elbow: RA-Common OA-uncommon Systematic symptoms: RA-common OA-uncommon

Joint Swelling: RA-Effusion, red warm OA-bony ESR/CRP: RA-elevated OA-Normal

Serology: RA-positive OA-negative RA-Inflammatory OA-degenerative RA-Autoantibodies OA-No antibodies RA-small joints OA-large weight bearing joints RA-poligoarthritsi OA-oligo arthritis(1 joint affected)

34
Q

Where is swelling confined to in RA and how does it feel?

A

area of the joint capsule Synovial thickening feels like a firm sponge

35
Q

What is a key visible problem caused by Rheumatoid arthritis?

A

Deformities Noduales- at elbows and hands, assosiated with severe RA that causes erosion Also assosiated with RHematoid Factor antibody: -45% positive in first 6 months -85% positive with established disease

36
Q

What are the auto antibodies associated with RA?

A

Rheumatoid Factor AntiCCP Assosiated with nodules

37
Q

What x ray changes do you see in Rheumatoid arthritis?

A

-Soft tissue swelling -Erosions -joint space loss -Subluxation -Erosions

38
Q

Historically what is the typical course of RA?

A

Damage occurs early in most patients: -50% show joint space narrowing or erosions in the first 2 years -By 10 years, 50% of young working patients are disabled

39
Q

What is the life expectancy of people with RA?

A

Lower: -Women 10 years less -Men 4 years less Many causes for this, most likely sue to cardiovascular disease which is increased alongside inflammation with RA pateints

40
Q

What is the typical pattern of pain and stiffness in RA?

A

Inflammatory pattern- affects multiple joints, symmetrical, small joints, stiffness is early morning

41
Q

How do we investigate RA?

A

-Blood tests (Check autoantibodies) -Check inflammatory markers -x-rays -ultrasound to check inflammation in soft tissue and joints that you cant see with x-rays

42
Q

What are the principles of treating RA?

A

1)Diagnose -confirm diagnosis 2)Severity -Determine where the patient stands in the spectrum of disease 3) Treatment -When damage begins early start agressive treatment early 4)Monitor -Treatment for adverse effects -Disease activity, revise Rx as needed

43
Q

How do you assess RA during the treatment process?

A

Assess current activity: -Morning stiffness, synovitis, fatigue, ESR Document the degree of damage: -ROM and deformities -Joint space narrowing and erosions on x-ray Document extra-articular manifestations: -Nodules, pulmonary fibrosis, vasculitis Assess prior Rx responses and side affects

44
Q

What are the 3 therapies in the treatment plan of RA?

A

EDUCATION: -Use resources from the arthritis foundation and the ACR -Assistive devices -Multidisciplinary team EXERCISE: -ROM(range of motion), conditioning, and strengthening exercises MEDICATIONS: -Analgestic and/or anti-inflammatory -to relieve pain -immunosupressants, cytotoxic and biologic -steroids(short term) -Balance efficancy and safety with the activity

45
Q

How do we treat RA long term?

A

Use DISEASES MODIFYING ANTI-RHEUMATIC DRUGS (DMARDs)

46
Q

Give examples of some DMARDS traditional?

A

-MINOCYCLINE(may work best early) -Sulfasalazine, hyroxychloroquine(moderate effect, low cost) -Intramuscular gold(slow onset, decreases progression, rare reminisision, requires close monitoring)

47
Q

What are some examples of new DMARDs used?

A

LEFLUNOMIDE: -pyrimidine inhibitor -Effect and side effects similar to those of MTX ETANERCEPT: -soluble TNF receptor,blocks TNF -Rapid onset, quite effective in refractory patients in short term trails and in combo with MTX -injection site reactions, long term effects unknown, expensive

48
Q

What are 3 drug treatment options for RA?

A

NSAIDS: -symptomatic relief, improved function -No change in disease progression Low-dose prednisone: -May substitute for NSAID -Used as bridge therapy -If used long term consider prophylactic treatment for osteoporosis INTRA-ARTICULAR STEROIDS: -useful for flares

49
Q

What are 4 immunosuppressive drugs used to treat RA?

A

Methotrexate: -Most effective single DMARD -Good benefir to risk ratio Azathioprine: -Slow onset, reasonably effective Cyclophosphamide -Effective for vasculitis, less so fro arthritis Cyclosporine: -Superior to placebo, renal toxicity Not commonly used anymore can be effective when combined with each other

50
Q

What has a big effect on RA and other autoimmune conditions?

A

BIOLOGICAL THERAPIES: Work by working on specific biological targets e.g targeting cytokines therefore reducing inflammation by a lot e.g. TNF- alpha inhibitors

51
Q

What side effects and complications are assosiated with RA medication?

A

Lots of these medicines work by dampening down your immune response, therefore increasing there risk of infection

52
Q

Why and how do you monitor the treatment of RA with DMARDs?

A

-Need frequent monitoring as the blood, liver, lung, kidney are frequent sites of adverse effects -Most patients need to be seen 3-6 times a year

53
Q

What other sites can RA effect

A

Liver Cardiovascular Neurological Musculoskeletal Bone marrow Spleen Dry/inflammed eyes Kidney damage due to protein accumulation

54
Q

What are the 3 main undifferentiated connective tissue diseases and what are the symptoms?

A

Systemic lupus erythematosus(SLE): -Alopecia Malar rash(looks like a butterfly) -Arthralgia -Oral ULcers -Photosensitivity Scleroderma: -Reflux -Raynauds -Digital -Ulcerations RA: -Arthritis -Sicca symptoms