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MMB > MMB (022) Red Hot Joint > Flashcards

MMB (022) Red Hot Joint Flashcards

1
Q

Cardinal signs of acute inflammation ?

A
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2
Q

Types of Reactions of acute inflammation ?

A

-Vascular

-Cellular

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3
Q

Order of Vascular changes in acute inflammation ? B

A
  1. Transient, insignificant, vasoconstriction
  2. Arteriolar vasodilatation&raquo_space; increased blood flow with engorged capillaries.

3.Increased vessel permeability&raquo_space;SWELLING

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4
Q

Three characteristic microscopic features of this blood vessel ?

A

• A dilated BV

• Engorged with RBCs

• Leukocytes at the periphery of the blood stream

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5
Q

What are the immediate causes of increased vascular permeability?

A
  • chemical mediators (histamine, bradykinin, NO, C5a, L PAF) [transient]
  • severe direct vessel injury [sustained]
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6
Q

What are the delayed causes of increased vascular permeability?

A

Endothelial cell injury (e.g. bacterial endotoxins) [prolonged]

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7
Q

Cellular events of inflammation mainly revolve around recruitment of… ?

A

Leukocytes

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8
Q

What is the most important function of inflammatory response?

A

• Deliver leukocytes to the site of injury

• Activate leukocytes

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9
Q

What is the function of leukocytes?

A

• Ingest the microbe

• Kill it

• Eliminate necrotic tissues and foreign substances

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10
Q
A
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11
Q

the type of leukocyte emigrating to the site of infection depends on the…… and the….

A

duration of inflammation ,, type of stimulus

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12
Q

…cells :
when recruited to inflammation site ; are short lived and die by apoptosis

A

PNLs

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13
Q

…cells :
when recruited to inflammation site ; survive longer than PNLs

A

monocytes

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14
Q

…cells :
Are recruited to inflammation sites in the 1st 6-24 hours

A

PNLs

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15
Q

…cells :
Are recruited to inflammation sites in 24-48 hours

A

monocytes

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16
Q

General infections lead to ….. recruitment

A

continuous PNLs

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17
Q

Viral infections lead to ….. recruitment

A

lymphocytes

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18
Q

Hypersensitivity reactions lead to ….. recruitment

A

eosinophils

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19
Q

When are Leukocytes activated ?

A

Once they reach site of infection

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20
Q

How are Leukocytes activated ?

A

Through microbes, necrotic products & mediators

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21
Q

Some mediators of acute inflammation ?

A

• Vasoactive amines

• Complement components

• Eicosanoids

• Clotting cascade

• Kinin cascade

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22
Q

Beneficial effects of acute inflammation ?

A

-dilution of toxins

-entry of antibodies and drugs

-cell nutrition and oxygenation

-start of immune response

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23
Q

Harmful effects of acute inflammation ?

A

-Damage to normal tissues (enzymatic digestion, abscess cavities, vascular damage)

-Swelling in critical sites (epiglottis, brain)

  • Immune hypersensitivity reactions (causing tissue damage and even life-threatening consequences, e.g. asthma
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24
Q

What are the common causes of a red hot joint?

A
  1. Infection
  2. Crystal deposition
  3. Flare in activity of chronic arthritis
  4. Trauma
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25
Q

Routes of infection ; of Septic arthritis ?

A
  • Hematogenous (blood borne infection)

-Direct extension from a soft-tissue abscess or osteomyelitis

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26
Q

Risk factors ; of Septic arthritis ?

A
  • Existing joint problems (e.g. osteoarthritis, gout, rheumatoid arthritis, an artificial joint, previous joint surgery)

-Joint trauma

-Weak immune system ( diabetes, kidney and liver diseases, drugs suppressing immunity)

-Increased skin fragility and poor healing of wounds

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27
Q

How to diagnose a case of septic arthritis?

A

-Examination of synovial fluid :
• White cell count, which is usually very high.

• Culture for bacteria or other organisms

  • X-rays:
    done only to look for damage or to rule out other causes
  • Blood tests :
    to monitor inflammation
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28
Q

What’s the abnormality in this Synovial fluid smear ?

A
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29
Q

What is GOUT ?

A

-Gout is a disorder of purine metabolism. Its final metabolite, uric acid, crystallizes in the form of monosodium urate, precipitating in joints, tendons, and tissues

-The crystals then trigger a local immune mediated inflammatory reaction

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30
Q

The final metabolite of purine is ….

A

uric acid

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31
Q

uric acid crystallizes in the form of…. In tissue

A

monosodium urate

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32
Q

Name the lesion and the disease

A

Disease : Gout

Lesion : tophi

33
Q

Genetic factors of Gout?

A

20 to 80 percent have a family history

34
Q

Gender factors of Gout?

A

more common in men than in women

35
Q

weight factor of Gout?

A

Obesity Increases the risk of developing hyperuricemia because there is more tissue available for turnover or breakdown, which leads to excess uric acid production

36
Q

Alcohol consumption factor of Gout?

A

Beer contains purines

37
Q

Diet factor of Gout?

A

Eating much food that is rich in purines can cause or aggravate gout in some people

38
Q

Lead mineral effect on Gout?

A

Inhibits purine excretion

39
Q

Drugs related to Gout?

A

like Niacin and diuretics

40
Q

Organs and meat PURINE-RICH ?

A

Brains, Kidneys, Liver, thymus, pancreas, calves’ tongues, stomach) Some sea food: Anchovies, Sardines, Oysters, Lobster

41
Q

What’s preferred for consumption to prevent Gout ?

A

Plenty of liquid, low- fat dairy products, coffee, cereals, fruits and cherry juice

42
Q
A
43
Q

the most common site affected with Gout ?

A

first MTP joint

44
Q

Tophi (white masses of MUC) get deposited in:

A
  1. Joints (appear in the articular cartilage of joints, periarticular tendons, ligaments and soft tissues)
  2. Cartilage of nose and ear
  3. Interstitial tissue of kidney
  4. Cardiac valves.
45
Q

A serum urate level of approximately…. mg/dl indicates gout will devolop

A

6.8

46
Q

the radiographic hallmark findings of chronic gout ?

A

-classic marginal erosions (red arrow)

  • overhanging cortex (blue arrow)

-preservation of bone density ,, and maintenance of the joint space are apparent

47
Q
A

X-ray shows:

  1. Juxta-articular erosive changes around the first MTP joint
  2. with overhanging edges
  3. soft tissue swelling
  4. the joint space is maintained
  5. No evidence of osteopenia

Diagnosis:

GOUTY arthritis

48
Q

Radiographic features of gouty lesions in the fingers ?

A
49
Q

this is a microscopy of a red-hot joint dissorder

What is it and describe what you see

A
  • 1)Needle- shaped sodium urate crystals

-2) surrounded by a FB granuloma ( fibroblasts, mononuclear cells and giant cells)

50
Q

Treating the acute Gout attack ?

A

NSAIDs, ? Colchicine, corticosteroids, i articular injections of steroids, possible combinations according to patient ’s health condition and kidney function)

51
Q

Treatment of chronic gout ?

A

therapy to reduce serum uric acid level to AT LEAST 6mg/dl ?

52
Q

What is Rheumatoid arthritis ?

A

-A systemic, chronic inflammatory, autoimmune disease affecting many tissues, mainly the joints.

-It results in a non- suppurative synovitis frequently progressing to destroy articular cartilage and underlying bone&raquo_space; disabling arthritis

53
Q

Male : to Femal Ratio of Rheumatoid arthritis ?

A

M:F =
1:3

54
Q

Relation of smoking to Rheumatoid arthritis ?

A

Smokers 2-3x > non-smokers

55
Q

Pathogenesis of rheumatoid arthritis ?

A

RA is initiated in a genetically predisposed person by activation of CD4+ helper T cells responding to some arthritogenic agent, possibly microbial or to a self-antigen.

56
Q

Rheumatoid arthritis is activated through ….. cells

A

CD4+ helper T cells

57
Q

What is Rheumatoid factor ?

A

Rheumatoid factor is IgM directed to the altered Fc fragment of IgG

58
Q

Two types of Pathological lesions : of rheumatoid arthritis ?

A

-Articular lesions

-Extra –articular lesions (systemic)

59
Q

Articular lesions of rheumatoid arthritis ?

A

-Synovial inflammation - pannus

-Destruction of articular cartilage

-Erosion of adjacent bone

-Fibrous fusion (ankylosis)

60
Q

Extra –articular lesions of rheumatoid arthritis ?

A

-Rheumatoid nodules

-Vasculitis

61
Q

How is rheumatoid arthritis triggered ?

A

Modification of autoantigens

62
Q

microscopic features of Rheumatoid Arthritis ?

A
  1. Synovial cell hyperplasia
  2. Dense inflammatory
  3. Angiogenesis
  4. Fibrinopurulent exudate on the synovial and joint surfaces
  5. Osteoclastic activity in underlying bone&raquo_space; synovium penetrates bone&raquo_space; periarticular erosions and subchondral cysts.
63
Q

What is Ankylosis ?

A

Bony joint fusion

64
Q

What’s the pannus ?

A

Joint lesion of Rheumatoid Arthritis ;
-edematous synovium
-inflammatory cells
-granulation tissue
-fibroblasts

65
Q

What is the following gross picture

A

PANNUS

66
Q

How does Rheumatoid Arthritis progress from Pannus to ankylosis ?

A
67
Q

Systemic symptoms of rheumatoid arthritis ?

A

-low grade fever

-weakness

-malaise

-weight loss

68
Q

Cuttanious affections of rheumatoid arthritis ?

A

Rheumatoid nodules

69
Q

How can rheumatoid arthritis be detected in blood

A

Positive Rheumatoid factor and anti-CCP (cyclic citrullinated peptide Ant.B)

70
Q

What are the joints commonly affected in RA ?

A

Small joints of hand affected first (metacarpophalangeal, proximal interphalangeal joints of hands and feet), then wrist, elbow, knee.

71
Q

….joints are usually spared by RA

A

RA generally spares the distal interphalangeal joints of the fingers

72
Q

Signs of joint acute inflammation ?

A
  • Joint Pain
  • Joint warmth
  • Joint swelling
  • Morning stiffness
  • Joint symptoms become worse after periods of disuse
  • Joint deformity
73
Q

rheumatoid hand disease can include two types of deformities , what are they ?

A

• Boutoniere deformity

• Swan- Neck deformity

74
Q

Explain Boutoniere deformity

A

The finger is bent toward palm at knuckle (first Interphalangeal joint)

75
Q

Explain Swan- Neck deformity

A

Observed at distal interphalangeal joint ;

-The distal portion of the finger is bent permanently toward palm

  • The middle joint is bent in opposite direction resulting in finger looking like Swan Neck
76
Q

What is Ulnar deviation ?

A

When the joints in the wrist and hand to shift so that the fingers bend toward the ulna bone

77
Q
A

.

78
Q
A
79
Q
A

MMB (72 decks)

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