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inflammatory rheumatic disease Flashcards

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1
Q

What does it mean if the acute response is self limiting?

A

Acute episodes are self-limited due to inflammatory response
Removal of stimulus
Re-exposure causes ‘flares’

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1
Q

What are some acute inflammatory endogenous and exogenous reponces?

A

Endogenous- crystal deposition (gout)
Exogenous- new medication or infection

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2
Q

What is the initiating force of chronic inflammatory diseases?

A

Remote and unrecognizable
Disease phenotype is fully established

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3
Q

What does propagation mean?

A

Autoimmune response - self-amplified cycle of damage
Autoimmune diseases are characteristically driven by ‘self-antigens’
Can elicit innate and adaptive immune responses

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4
Q

What is the best case senserio for acute inflammation pathogenesis?

A

pathogen is killed and cells and tissues are repaired

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5
Q

What are the mechanisms of pathogensis of inflammation?

A
  1. cytokines
  2. endothelial activation
  3. complement pathway
  4. immune complex formation
  5. cellular cytotoxicity up regulation
    a. lymphocyte mediated
    b. antibody dependent cytotoxicity
  6. host tissue differentiation
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6
Q

What happens when during inflammation with cytokines

A

Type and pattern of cytokines determine immune effector pathway = cellular function
Upregulation of cytokine production

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7
Q

When there is pro inflammatory cytokines what will occur?

A

Pro-inflammatory cytokines - promote inflammation - triggers adhesion-promoting receptors on blood vessel endothelium

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8
Q

What might endothelial activation contribute to?

A

contributes to atherosclerosis- more build up becomes own pathogen

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9
Q

Upregulation in the complement pathway is what type of response?

A

abnormal responce

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10
Q

Amplification of inflammatory responses

A

Serum proteins that cooperates with both the innate and the adaptive immune systems to eliminate pathogens = Amplification of inflammatory response

both innate and adaptive immune systems

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11
Q

What occurs in the immune complex formation?

A

Macrophage and Neutrophil complexes

damage healthy tissue if released in large amounts

follows upregulation of complement pathway

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12
Q

What are some clinical conditions that be seen in immune complex formation?

A

drug reactions, serum sickness, and infections

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13
Q

What are capable of destroying target cells?

A

Cytotoxic T lymphocytes - capable of destroying target cells

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14
Q

What type of cellular cytotoxity is this?

A

Antibody-Dependent Cellular Cytotoxicity

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15
Q

What is the cytotoxic mechanism?

A

Cytotoxic mechanism: cytoplasmic granules containing perforin and granzymes

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16
Q

What happens during host tissue differentiation

A

Inflammatory mediators and T cells stimulate cells unrelated to the immune response to change function chronic inflammatory response

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17
Q
A
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18
Q

What are the characteristics of Rheumatic diseases?

A

InflammatoryAutoimmuneDegenerativeMSK, Neuro, Cardiac, Pulm, Inte

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19
Q

Gout

A

Crystal-induced inflammation of synovial joints

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20
Q

What are the clinical presentations of gout?

A

Crystal-induced inflammation of synovial joints
Presents in ~4% of adults in the US
Males 3x&raquo_space;> Females
Studies have shown that patients with gout are 60 percent more likely to develop kidney stones

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21
Q

Where might gout happen?

A

synovial joints

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22
Q

What are the crystals in gout made of?

A

Monosodium urate crystals in joint space = severe acute joint pain and swelling

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23
Q

Does gout happen in proximal or distal joints?

A

more distal small joints are more suceptable

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24
Where are the most common locations for gout to occur?
Most common locations: great toe, midfoot, ankle, and knee
25
What have studies shown about patients with gout?
60% more likely to develop kidney stones
26
Over time what occurs when gout is constant?
Over time ‘flares’ can become more frequent and more painful- resulting in a chronic destructive condition = JOINT DEFORMITY
27
What is the initiating factor of gout?
Initiating Factor: monosodium urate crystal formation
28
what does hyperuricemia mean?
Body supersaturated with uric acid
29
What is the difference between underexcretion and overexcretion that causes gout?
Underexcretion - 90% of patients Overproduction- 10% of patients Underexcretion = most often due to impaired renal function or diuretics Overproduction = diet, medication, defects in pathway leading to increased uric acid production
30
What is the pathophysiology of gout?
Crystal formation (primary factor) influenced by secondary local physical factors Temperature Blood flow
31
What are the mechanisms of gouts immune responses?
Monosodium crystals are efficient activators of the immune response - Triggers Complement pathway : attracts neutrophils - Vasodilators : pain and swelling - Macrophage destruction of crystals : increased adhesion molecules and localized endothelium response
32
Exam: what type of inflammatory response is gout?
acute inflammatory response Self-limiting- typically resolves in a week Excellent example of the acute inflammatory response- high focused, localized, self-limiting with tissue destruction
33
What does podagra mean?
Podagra = severe inflammatory arthritis at the first metatarsophalangeal joint most frequent first episode occurs when walking in the middle of the night, most intense form of arthritis
34
What is the differential diagnosis seen?
D/Dx: Episodic Oligoarticular Arthritis, most common type of juvenile arthritis Olio-affecting a few joints
35
What are the pharmacology assistance for gout?
Pharmacology: NSAIDs: anti-inflammatory drug Colchicine: anti-inflammatory  gout prophylaxis Corticosteroids: anti-inflammatory
36
How would one conform the diagnosis of gout?
synovial fluid aspiration histology
37
What does tophi formation mean?
Chronic gout- firm, irregular, subcutaneous deposits Most often occurs along tendinous tissues on the extensor surfaces of joints and tendons
38
What is chronic Erosive polyarthritis?
Result of uric acid supersaturation over years- multiple joint sites Remodeling of thin synovial membrane into thick inflammatory tissue Destructive and irreversible joint deformities- bone and cartilage erosions
39
What is the treatment for gout?
Decrease inflammatory cell recruitment - anti-inflammatory medication Activation of involved joints -AROM/PROM
40
Why is AROM and PROM good or bad for gout?
AROM and PROM are good for gout because of the activation that is caused in the joint
41
How does one prevent gout?
Decrease serum uric acid levels  Diet
42
What is the clinical presentation of IMMUNE COMPLEX VASCULITIS?
Acute inflammatory disease of the small blood vessels Palpable purpura, arthritis, abdominal pain
43
What is the difference between exogenous and endogenous?
Antigen from exogenous source - streptococcal skin infection, Hep B virus, seasonal allergies Antigen from endogenous source - systemic lupus, vascular immunoglobulins (protein) Both result in an intense inflammatory response
44
What are the initiators of immune complex vascuilitis?
Antigen elicits an ongoing humoral response due to abundant quantities - initiators
45
Why is immune complex vascuilitis self limiting?
Typically self-limiting - Immune response upregulated - potential to effectively clear deposited immune complexes
45
What are the propagators of immune complex vascuilitis?
Deposition of immune complexes (antigen:antibody molecule) in vessel endothelium - triggers ongoing immune response - propagator
46
what is serum sickness in terms of immune complex vascuilitis?
Serum Sickness - Serum sickness is a reaction that is similar to an allergy. The immune system reacts to medicines that contain proteins used to treat immune conditions.
47
what is the classic example of hypersensitivity resulting in immune complex vascuilitis?
Classic example: penicillin-induced hypersensitivity vasculitis
48
What is the clinical presentation?
Systemic autoimmune rheumatic disease Chronic inflammatory injury = damage to multiple organs Episodic in nature, highly variable in severity Most commonly affected - skin, joints, kidneys, blood cells, serosal surfaces, brain
48
What type of rheumatic disease is lupis?
systemic autoimmune
49
What is the epidemiology?
30 cases per 100,000 in the general populations in the US Females 9X>>>Males Most prevalent in black and African America populations
50
What is the etiology for lupis?
Complex- Genetic susceptibility and poorly defined environmental factors
51
What are the environmental triggers of lupis?
Sunlight Viral Infection Certain medications
52
How does the body view the apotic cells?
Unique form of apoptotic cell death stimulates immune response
53
What is the intiator of lupis?
Hyperactive autoantibody response to ‘self-antigens’ (complement pathway)
54
What is the hallmark of lupis?
Auto-amplification auto-amplification connect this to the systemic change that occurs in all tissues of the body
55
What is the combined result of lupis?
continued immune response and tissue damage due to response derived from apoptotic cells and damaged cells
55
What is the propagator of lupis?
Propagation Antigen derived from self & apoptotic cell - forms immune complexes that are deposited in subendothelial tissue Autoantibodies bind to extracellular molecules in target organs Autoantibodies directly induce cell death
56
What is the universal feature of lupis?
Production of autoantibodies
56
What are the clinical manifestations of lupis?
Multisystem autoimmune disease - predominantly affects women during childbearing years Characterized by periodic exacerbations (flares) Symptoms are highly varied-constant with an individual Universal feature- Production of autoantibodies Skin rash most common Renal disease- frequent cause of morbidity and mortality Hematologic disturbances- anemia, thrombocytopenia, leukopenia Inflammation of serosal surfaces- pleuritic chest pain, peritonitis Neurologic syndromes- seizures
57
What is the most common clinical manifestations of lupis?
skin rash
57
What type of inflammatory disease is RA?
Chronic systemic inflammatory disease
58
If a patient has RA in the right hand will have RA in the left hand?
bilateral patient will show symptoms in both hands
59
What joints does RA normally occur in?
diarthrodial joints
60
Overtime with inflammatory flares what occurs in the cartilage?
Characterized by chronic inflammatory proliferation of the synovial linings of diarthrodial joints- aggressive cartilage destruction and bony erosions
61
What is the epidemiology of RA?
1% in the general population in the US Females 3X>>>Males Peak onset 60s
62
What is the onset?
in the 60s
63
What is the etiology of RA?
Systemic autoimmune disease abnormal activation of B cells, T cells, and innate immune cells Damage to ‘self’ Majority of destruction occurs in joint synovium lungs, skin and blood vessels can be affected Cause- unknown Genetic: dysregulated pathways Environmental factors appear to contribute
64
Where does the destruction occur?
Majority of destruction occurs in joint synovium lungs, skin and blood vessels can be affected
65
What is the pathophysiology of RA?
Pathophysiology: centered around the synovial linings of the joint
66
Explain the expansion that occurs with RA?
Significantly expansion of cellular lining composed of activated cells High concentration of B cells, T cells, and macrophage = joint pannus Increased vascular supply RA synovium can invade adjacent tissue such as cartilage and bone
67
What is joint pannus that occurs with RA?
High concentration of B cells, T cells, and macrophage
68
What is the end feel a patient will feel with RA?
spongy
69
Where will RA invade?
RA synovium can invade adjacent tissue such as cartilage and bone
70
What is the genetic initiator of RA?
Studies show a 15-35% match among identical twins MCH class II - antigen presenting to T cells Suspected to initiate and drive disease progression
71
What is the environmental initiator of RA?
Most strongly implicated: cigarette smoking and infection
72
What is the hallmark feature of RA?
development of antigen-driven autoantibodies
73
What is the propagator of RA?
Autoantigens interact with immune cells amplify disease process
73
What are the clinical manifestations of RA?
Typically persistent, progressive disease Fatigue and joint inflammation- pain, swelling, warmth, and morning stiffness Small and large joints – bilateral Joint deformities Lower spine spared, cervical spine can be involved Highly active cases- extra-articular manifestations can occur
74
What is the treatment for RA?
Prompt and aggressive treatment to control inflammation- slow progressive joint erosion Immunomodulatory Medications have been shown to be beneficial NSAIDs RA appears to respond best to the use of multiple treatment agents

clin med (19 decks)

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