Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

clin med > inflammatory rheumatic disease > Flashcards

inflammatory rheumatic disease Flashcards

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’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

What are some acute inflammatory endogenous and exogenous reponces?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the initiating force of chronic inflammatory diseases?

A

Remote and unrecognizable
Disease phenotype is fully established

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the best case senserio for acute inflammation pathogenesis?

A

pathogen is killed and cells and tissues are repaired

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What might endothelial activation contribute to?

A

contributes to atherosclerosis- more build up becomes own pathogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Upregulation in the complement pathway is what type of response?

A

abnormal responce

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

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

A

drug reactions, serum sickness, and infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are capable of destroying target cells?

A

Cytotoxic T lymphocytes - capable of destroying target cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What type of cellular cytotoxity is this?

A

Antibody-Dependent Cellular Cytotoxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the cytotoxic mechanism?

A

Cytotoxic mechanism: cytoplasmic granules containing perforin and granzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the characteristics of Rheumatic diseases?

A

InflammatoryAutoimmuneDegenerativeMSK, Neuro, Cardiac, Pulm, Inte

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Gout

A

Crystal-induced inflammation of synovial joints

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Where might gout happen?

A

synovial joints

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the crystals in gout made of?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Does gout happen in proximal or distal joints?

A

more distal small joints are more suceptable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Where are the most common locations for gout to occur?

A

Most common locations: great toe, midfoot, ankle, and knee

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What have studies shown about patients with gout?

A

60% more likely to develop kidney stones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Over time what occurs when gout is constant?

A

Over time ‘flares’ can become more frequent and more painful- resulting in a chronic destructive condition = JOINT DEFORMITY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the initiating factor of gout?

A

Initiating Factor: monosodium urate crystal formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what does hyperuricemia mean?

A

Body supersaturated with uric acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the difference between underexcretion and overexcretion that causes gout?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the pathophysiology of gout?

A

Crystal formation (primary factor) influenced by secondary local physical factors
Temperature
Blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the mechanisms of gouts immune responses?

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Exam: what type of inflammatory response is gout?

A

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
Q

What does podagra mean?

A

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
Q

What is the differential diagnosis seen?

A

D/Dx: Episodic Oligoarticular Arthritis, most common type of juvenile arthritis
Olio-affecting a few joints

35
Q

What are the pharmacology assistance for gout?

A

Pharmacology:
NSAIDs: anti-inflammatory drug
Colchicine: anti-inflammatory  gout prophylaxis
Corticosteroids: anti-inflammatory

36
Q

How would one conform the diagnosis of gout?

A

synovial fluid aspiration histology

37
Q

What does tophi formation mean?

A

Chronic gout- firm, irregular, subcutaneous deposits
Most often occurs along tendinous tissues on the extensor surfaces of joints and tendons

38
Q

What is chronic Erosive polyarthritis?

A

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
Q

What is the treatment for gout?

A

Decrease inflammatory cell recruitment - anti-inflammatory medication
Activation of involved joints -AROM/PROM

40
Q

Why is AROM and PROM good or bad for gout?

A

AROM and PROM are good for gout because of the activation that is caused in the joint

41
Q

How does one prevent gout?

A

Decrease serum uric acid levels  Diet

42
Q

What is the clinical presentation of IMMUNE COMPLEX VASCULITIS?

A

Acute inflammatory disease of the small blood vessels
Palpable purpura, arthritis, abdominal pain

43
Q

What is the difference between exogenous and endogenous?

A

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
Q

What are the initiators of immune complex vascuilitis?

A

Antigen elicits an ongoing humoral response due to abundant quantities - initiators

45
Q

Why is immune complex vascuilitis self limiting?

A

Typically self-limiting - Immune response upregulated - potential to effectively clear deposited immune complexes

45
Q

What are the propagators of immune complex vascuilitis?

A

Deposition of immune complexes (antigen:antibody molecule) in vessel endothelium - triggers ongoing immune response - propagator

46
Q

what is serum sickness in terms of immune complex vascuilitis?

A

Serum Sickness - Serum sickness is a reaction that is similar to anallergy. Theimmune system reactsto medicines that contain proteins used to treat immune conditions.

47
Q

what is the classic example of hypersensitivity resulting in immune complex vascuilitis?

A

Classic example: penicillin-induced hypersensitivity vasculitis

48
Q

What is the clinical presentation?

A

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
Q

What type of rheumatic disease is lupis?

A

systemic autoimmune

49
Q

What is the epidemiology?

A

30 cases per 100,000 in the general populations in the US
Females 9X»>Males
Most prevalent in black and African America populations

50
Q

What is the etiology for lupis?

A

Complex- Genetic susceptibility and poorly defined environmental factors

51
Q

What are the environmental triggers of lupis?

A

Sunlight
Viral Infection
Certain medications

52
Q

How does the body view the apotic cells?

A

Unique form of apoptotic cell death stimulates immune response

53
Q

What is the intiator of lupis?

A

Hyperactive autoantibody response to ‘self-antigens’ (complement pathway)

54
Q

What is the hallmark of lupis?

A

Auto-amplification

auto-amplification connect this to the systemic change that occurs in all tissues of the body

55
Q

What is the combined result of lupis?

A

continued immune response and tissue damage due to response derived from apoptotic cells and damaged cells

55
Q

What is the propagator of lupis?

A

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
Q

What is the universal feature of lupis?

A

Production of autoantibodies

56
Q

What are the clinical manifestations of lupis?

A

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
Q

What is the most common clinical manifestations of lupis?

A

skin rash

57
Q

What type of inflammatory disease is RA?

A

Chronic systemic inflammatory disease

58
Q

If a patient has RA in the right hand will have RA in the left hand?

A

bilateral patient will show symptoms in both hands

59
Q

What joints does RA normally occur in?

A

diarthrodial joints

60
Q

Overtime with inflammatory flares what occurs in the cartilage?

A

Characterized by chronic inflammatory proliferation of the synovial linings of diarthrodial joints- aggressive cartilage destruction and bony erosions

61
Q

What is the epidemiology of RA?

A

1% in the general population in the US
Females 3X»>Males
Peak onset 60s

62
Q

What is the onset?

A

in the 60s

63
Q

What is the etiology of RA?

A

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
Q

Where does the destruction occur?

A

Majority of destruction occurs in joint synovium lungs, skin and blood vessels can be affected

65
Q

What is the pathophysiology of RA?

A

Pathophysiology: centered around the synovial linings of the joint

66
Q

Explain the expansion that occurs with RA?

A

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
Q

What is joint pannus that occurs with RA?

A

High concentration of B cells, T cells, and macrophage

68
Q

What is the end feel a patient will feel with RA?

A

spongy

69
Q

Where will RA invade?

A

RA synovium can invade adjacent tissue such as cartilage and bone

70
Q

What is the genetic initiator of RA?

A

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
Q

What is the environmental initiator of RA?

A

Most strongly implicated: cigarette smoking and infection

72
Q

What is the hallmark feature of RA?

A

development of antigen-driven autoantibodies

73
Q

What is the propagator of RA?

A

Autoantigens interact with immune cells amplify disease process

73
Q

What are the clinical manifestations of RA?

A

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
Q

What is the treatment for RA?

A

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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions