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
Routes of infection ; of Septic arthritis ?
- Hematogenous (blood borne infection) -Direct extension from a soft-tissue abscess or osteomyelitis
26
Risk factors ; of Septic arthritis ?
- 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
27
How to diagnose a case of septic arthritis?
-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
28
What’s the abnormality in this Synovial fluid smear ?
29
What is GOUT ?
-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
30
The final metabolite of purine is ….
uric acid
31
uric acid crystallizes in the form of…. In tissue
monosodium urate
32
Name the lesion and the disease
Disease : Gout Lesion : tophi
33
Genetic factors of Gout?
20 to 80 percent have a family history
34
Gender factors of Gout?
more common in men than in women
35
weight factor of Gout?
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
Alcohol consumption factor of Gout?
Beer contains purines
37
Diet factor of Gout?
Eating much food that is rich in purines can cause or aggravate gout in some people
38
Lead mineral effect on Gout?
Inhibits purine excretion
39
Drugs related to Gout?
like Niacin and diuretics
40
Organs and meat PURINE-RICH ?
Brains, Kidneys, Liver, thymus, pancreas, calves’ tongues, stomach) Some sea food: Anchovies, Sardines, Oysters, Lobster
41
What’s preferred for consumption to prevent Gout ?
Plenty of liquid, low- fat dairy products, coffee, cereals, fruits and cherry juice
42
43
the most common site affected with Gout ?
first MTP joint
44
Tophi (white masses of MUC) get deposited in:
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
A serum urate level of approximately…. mg/dl indicates gout will devolop
6.8
46
the radiographic hallmark findings of chronic gout ?
-classic marginal erosions (red arrow) - overhanging cortex (blue arrow) -preservation of bone density ,, and maintenance of the joint space are apparent
47
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
Radiographic features of gouty lesions in the fingers ?
49
this is a microscopy of a red-hot joint dissorder What is it and describe what you see
- 1)Needle- shaped sodium urate crystals -2) surrounded by a FB granuloma ( fibroblasts, mononuclear cells and giant cells)
50
Treating the acute Gout attack ?
NSAIDs, ? Colchicine, corticosteroids, i articular injections of steroids, possible combinations according to patient ’s health condition and kidney function)
51
Treatment of chronic gout ?
therapy to reduce serum uric acid level to AT LEAST 6mg/dl ?
52
What is Rheumatoid arthritis ?
-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 >> disabling arthritis
53
Male : to Femal Ratio of Rheumatoid arthritis ?
M:F = 1:3
54
Relation of smoking to Rheumatoid arthritis ?
Smokers 2-3x > non-smokers
55
Pathogenesis of rheumatoid arthritis ?
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
Rheumatoid arthritis is activated through ….. cells
CD4+ helper T cells
57
What is Rheumatoid factor ?
Rheumatoid factor is IgM directed to the altered Fc fragment of IgG
58
Two types of Pathological lesions : of rheumatoid arthritis ?
-Articular lesions -Extra –articular lesions (systemic)
59
Articular lesions of rheumatoid arthritis ?
-Synovial inflammation - pannus -Destruction of articular cartilage -Erosion of adjacent bone -Fibrous fusion (ankylosis)
60
Extra –articular lesions of rheumatoid arthritis ?
-Rheumatoid nodules -Vasculitis
61
How is rheumatoid arthritis triggered ?
Modification of autoantigens
62
microscopic features of Rheumatoid Arthritis ?
1. Synovial cell hyperplasia 2. Dense inflammatory 3. Angiogenesis 4. Fibrinopurulent exudate on the synovial and joint surfaces 5. Osteoclastic activity in underlying bone >> synovium penetrates bone >> periarticular erosions and subchondral cysts.
63
What is Ankylosis ?
Bony joint fusion
64
What’s the pannus ?
Joint lesion of Rheumatoid Arthritis ; -edematous synovium -inflammatory cells -granulation tissue -fibroblasts
65
What is the following gross picture
PANNUS
66
How does Rheumatoid Arthritis progress from Pannus to ankylosis ?
67
Systemic symptoms of rheumatoid arthritis ?
-low grade fever -weakness -malaise -weight loss
68
Cuttanious affections of rheumatoid arthritis ?
Rheumatoid nodules
69
How can rheumatoid arthritis be detected in blood
Positive Rheumatoid factor and anti-CCP (cyclic citrullinated peptide Ant.B)
70
What are the joints commonly affected in RA ?
Small joints of hand affected first (metacarpophalangeal, proximal interphalangeal joints of hands and feet), then wrist, elbow, knee.
71
….joints are usually spared by RA
RA generally spares the distal interphalangeal joints of the fingers
72
Signs of joint acute inflammation ?
- Joint Pain - Joint warmth - Joint swelling - Morning stiffness - Joint symptoms become worse after periods of disuse - Joint deformity
73
rheumatoid hand disease can include two types of deformities , what are they ?
• Boutoniere deformity • Swan- Neck deformity
74
Explain Boutoniere deformity
The finger is bent toward palm at knuckle (first Interphalangeal joint)
75
Explain Swan- Neck deformity
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
What is Ulnar deviation ?
When the joints in the wrist and hand to shift so that the fingers bend toward the ulna bone
77
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