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Pathology > Psorasis And Other Dermatitis > Flashcards

Psorasis And Other Dermatitis Flashcards

0
Q

What is the Pathogenesis of psoriasis

A
  1. Genetic factors- Certain HLA types
  2. Proposed mechanism:
    - complement mediates reaction in stratum corneum
    - damage unmasks stratum corneum antibody
    - elicits an autoantibody against stratum corneum which fixes complement- release C3a, C5a, C567
    - neutrophils activate & accumulate
    - neutrophils in stratum corneum release neutral proteases
    - unmasks more antigen
    - release proliferative factors for keratinocytes
    - epidermal hyperplasia
  3. Koebner phenomenon- genesis of new lesions at trauma sites
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1
Q

What is the morphology of psoriasis

A
  1. Acanthosis- epidermal thickening due to increased epidermal cell turnover
  2. Downward elongation of rete ridges with mitoses above basal layer
  3. Thin or absent stratum granulosum
  4. Parakeratotic scale
  5. Thin epidermis over tips of dermal papillae
  6. Tortuous blood vessels in papillae
    a. Auspitz sign
  7. Munro’s microabscesses in epidermis and stratum corneum (neuts in the horn)
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2
Q

Appearance and common locations of psoriasis

A

Appearance: salmon colored plaque covered by white-silvery scale
1. Can see erythroderma- total body erythema and scaling
2. Pustular psoriasis- small pustules on erythematous plaques
E. Most common sites: elbows, knees, scalp, lumbosacral, intergluteal cleft, glanspenis
F. Nail changes in 30%
1. Yellow-brown discoloration, onycholysis, pitting, dimpling

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3
Q

What are the blistering diseases

A

Pemphigus
Bullous Pemphigoid
Dermatitis Herpetiformis

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4
Q

What is the causes of Pemphigus and when does it occur

A

Results from loss of integrity of normal intercellular attachments within epidermis and mucosal epithelium, see acantholysis of cells, when no longer attached, cells “round up”
3. IgG antibody to intercellular cement substance of skin and mucus membrane; this can be seen in immunofluorescence testing- see net-like pattern of intercellular IgG 4. Some of the acantholysis due not only to antibody induced damage, but to
consequence of synthesis and liberation of serine protease, and plasminogen activator by epidermal cells- triggered by pemphigus antibody

  1. Superficial dermal infiltration by lymphs, histiocytes, eosinophils seen in all types of pemphigus

Occurs in the 4th - 6th decade

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5
Q

What are the different types of Pemphigus

A

Pemphigus Vulgaris
Pemphigus Vegetans
Pemphigus Foliaceus

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6
Q

Pemphigus Vulgaris - what does it look like, where does it occur

A

It’s 80% of all cases

  1. Mucosa and skin - scalp, face, axilla, groin, trunk, oral ulcers
  2. Left with shallow erosions after superficial vesicles and bullae rupture
  3. Acantholysis of cells immediately above basal layer
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7
Q

Pemphigus Vegetans- what does it look like

A
  1. Large moist verrucous vegetating plaques studded with pustules on groin,axilla, flexural surfaces
  2. Lots of epidermal hyperplasia
  3. Acantholysis of cells immediately above basal layer
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8
Q

Pemphigus Foliaceus- where and what does it look like

A
  1. Superficial bullae on scalp, face, chest, back

2. Blister involves superficial epidermis at level of stratum granulosum

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9
Q

Pemphigus Erythematosus -where

A
  • may resemble lupus- malar area of face
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10
Q

Bullous Pemphigoid- who gets it , where is it, what is it , what causes the damage and what is seen in Immunofluorescence

A

Blistering disease

  1. Autoimmune disease, patients usually elderly
  2. Tense bullae with clear fluid on inner thigh, flexor surface of forearm, axilla, groin, lower abdomen, 1/3 have oral lesions
  3. These are subepidermal, nonacantholytic blisters, can see superficial and deep perivascular inflammatory infiltrate
  4. Immunofluorescence shows linear IgG and complement along basement membrane since antigen is in lamina lucida of the basement membrane and basal basement membrane hemidesmosomes
  5. Autoantibody fixes complement, injure tissue via neutrophils and eosinophils
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11
Q

Dermatitis Herpetiformis - what does it look like, who gets it , what’s the morphology

A

Blistering disease

  1. Urticarial plaques and vesicles- bilateral, symmetrical, mainly extensor surfaces, elbows, knees, upper back , buttocks
  2. Males>females, 3rd-4th decade, association with celiac disease
  3. Grouped appearance of vesicles=herpetiform
  4. Morphology
    a. Fibrin and neutrophils accumulate at tips of dermal papillae- form small microabsceses leading to minute zones of dermo-epidermal separation - areas coalesce to form true subepidermal blister
    b. Immunofluorescence shows granular IgA in tips of dermal papillae
    c. Can develop IgA and IgG antibodies to gliadin and reticulin, particularly with HLAB8 and HLADRw3, these cases may respond to gluten-free diet
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12
Q

Noninflammatory blistering diseases

A

Porphyria

Epidermolysis Bullosa

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13
Q

Porphyria-what is its caused by, what do you see, types and histology

A

disturbance of porphyrin metabolism

  1. In general, see urticaria, vesicles that heal with scarring, exacerbated by exposure to sunlight
  2. Types of porphyria
    - Congenital erythropoietic
    - Erythrohepatic
    - Acute intermittent
    - Porphyria cutanea tarda
    - Mixed
  3. Histology- subepidermal vesicle with associated marked thickening of superficial dermal vessels
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14
Q

Epidermolysis Bullosa - when does it occur , what are the three different types

A

Non- inflammatory blistering

  1. Blisters develop at pressure sites at or soon after birth
  2. Types
    a. Junctional type- blisters in histologically normal skin at level of lamina
    lucida
    b. Scarring dystrophic type- blisters below lamina densa
    c. Simplex type- basal layer of epidermis degenerates, forms clinical bulla
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15
Q

Lichen Planus (Another chronic inflammatory dermatosis) - what does it look like, what’s its morphology , histology, and pathogenesis

A

A. Pruritic purple polygonal papules
B. Self limiting- can see zone of hyperpigmentation after 1-2 years

C. Malignant degeneration of chronic mucosal and paramucosal lesions is a possibility
D. Morphology- itchy violaceous flat topped papules- white dots/lines called
Wickham’s striae
E. Symmetric distribution- wrists, elbows, glans penis; 70% have oral lesions
F. Histology
1. Dense continuous infiltrate of lymphs along dermo-epidermal junction; necrosis of basal keratinocytes, squamatization, saw-toothed rete ridges
2. Colloid (Civatte) bodies (anucleate, necrotic basal cells in inflamed papillary
dermis

3.  With chronicity, epidermal hyperplasia, hypergranulosis, hyperkeratosis are seen   G.     Pathogenesis- ?Antigens at basal layer and D-E junction- cell mediate immune        
     response with T-lymphocytes
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16
Q

Rheumatoid Arthritis: Generalities

A
  • Chronic systemic inflammatory disorder
    - affects many tissues and organs
  • Causes nonsuppurative proliferative synovitis
    - destroys articular cartilage- can result in ankylosis
  • Affects 1% of population, seen in females 3-5x more than males, peaks at decades 3-5-Felty’s syndrome = Rheumatoid arthritis + Neutropenia + Splenomegaly
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17
Q

RA: Morphology

A
  • Synovium becomes edematous, thickened, hyperplastic, with dense perivascular lymphocytic infiltrate including lymphoid follicles, plasma cells, macrophages in stroma, increased vascularity, hemosiderin, and giant cells
  • Rice bodies- fibrin covering synovium- break off and float in joint space
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18
Q

RA: Synovial fluid

A

-Turbid, increased volume, poor mucin clot with acetic acid, contains neutrophils

And may also see pannus

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19
Q

RA: effects on skin

A
  • Rheumatoid nodules- firm, nontender, subcutaneous, occur in 25%, usually in pressure areas, eg ulnar forearm, elbow, occiput, lumbosacral
  • Rheumatoid nodules can also occur in lung, spleen, myocardium, pericardium, heart valves, aorta
  • Nodules show a characteristic central zone of fibrinoid necrosis with a rim of epithelioid histiocytes, also contains lymphocytes and plasma cells
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20
Q

RA: effects on blood vessel

A

-Usually see vasculitis in severe erosive disease with rheumatoid nodules and high rheumatoid factor (RF) titers
-Can obstruct small arteries by endarteritis obliterans and medial necrosis- results in peripheral neuropathy, ulcers, gangrene
-Can get leukocytoclastic venulitis with purpura, cutaneous ulcers, nail bed
infarcts

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21
Q

Pathogenesis of RA

A
  • Triggered by exposure of immunogenetically susceptible host to an arithritigenic microbial antigen
  • This initiates acute arthritis-but joint is ultimately destroyed by continuing autoimmune reaction with T cells releasing inflammatory mediators and lytic cytokines
22
Q

Genetic susceptibility of RA

A
  • High rate of concordance between monozygotic twins
  • Well defined familial predisposition
  • 65-80% of patients are HLADR4 or HLADR1 or both
  • These alleles share a common region of 4 amino acids in antigen-binding cleft of DR molecule adjacent to T-cell receptor
  • Binding of arthritogen initiates inflammatory synovitis
23
Q

What are the primary exogenous arthritogens

A
  • Believe arthritogen is a microbial agent
  • Suspects include Epstein Barr Virus (EBV), retroviruses, parvoviruses, mycobacteria, Borrelia, Mycoplasma
  • EBV and type II collagen might share some cross-reactive epitopes and most RA patients have antibody (autoimmunity) to type II collagen
  • Joint cartilage has lots of type II collagen
24
Q

Autoimmune reaction that occurs in RA

A

T-cells play pivotal role
-CD4 cells in affected joints early in RA
-Synovial capillary endothelial cells activated with expression of ICAM-14 leads to further attachment and transmigration of other inflammatory cells -Also release IL-1, TNFα , IFNχ
-Activated T4 cells activate monocyte-macrophages and promote
release of monokines and activate B cells4produce antibody in affected joints
-80% with rheumatoid arthritis have autoantibodies to Fc portion of autologous IgG (rheumatoid factor)- mostly IgM antibodies

25
Q

What is RF and is it found in all people with RA?

A

-RF- IgG self associate to form immune complexes in serum, synovial fluid, synovial membrane
-Circulating immune complexes responsible for extra-articular
manifestations of RA
-Some patients are RF negative (seronegative)
-Also find RF in other diseases and healthy people, so immune complexes are not critical to causing RA and their presence does not always mean RA is there
-Immune complexes in inflamed cartilage activate complement and augment synovial inflammatory reaction- degrades cartilage

26
Q

What mediators are important in RA

A
  • Sensitized T4 cells, activated B cells, macrophages elaborate cytokines within the inflammatory synovium including IL-1, IL-2, IL-3, IL-4, IL-6, IFN-χ, GM-CSF, TGF-β , TNF-α, TNF-β
  • Neutrophils and synoviocytes contribute proteases and elastases
27
Q

What do the mediators do? (TNFα)

A
  • TNFα produced by macrophages, plays central role, IL-1 does alot of the same things
  • TNFα or IL-1 induces resorption of cartilage and bone
  • Stimulate release of collagenases from synovial cells
  • Upregulate adhesion molecules eg ICAM-1, ELAM-1, VCAM
  • Expression by endothelial cells
  • Inhibits synthesis of proteoglycans in cartilage
  • Stimulate proliferation of fibroblasts via platelet derived growth factor
  • All of these actions can lead to destruction of articular cartilage and formation of pannus
  • Anti TNFα and/or IL-1 antibodies have a protective effect of a collagen- induced arthritis in mice
28
Q

Clinical course of RA - time course

A

-In ½ of patients, disease begins slowly with malaise, fatigue, generalized musculoskeletal pain, after several weeks-months, joints become
involved in a mono-, oligo-, or poly-arthritic pattern with warmth,
swelling, pain, and stiffness of joints involved
-In 10% of cases have acute onset with severe symptoms and polyarthitis developing within days
-20% of patients have periods of remission, but then symptoms return in new joints
-Pattern of involvement is generally one of small joints first, larger joints later

29
Q

Clinical course of RA : joint involvement , X-ray characteristics and deformities

A
  • Hand and feet mcp and pip joints-wrists and ankles-elbows and knees
  • X-ray shows joint effusion, juxta-articular osteopenia with erosions, narrowing of joint space and loss of articular cartilage
  • Characteristic deformities include: radial deviation of wrist, ulnar deviation of fingers, flexion-hyperextension abnormalities of fingers
  • Due to destruction of tendons, ligaments, and joint capsules, the deformed joints have no stability and minimal range of motion
  • Baker’s cyst- posterior knee synovial cyst from increased intra-articular pressure causes outpouchings of synovium
30
Q

How to diagnosis RA

A

Need to have 4 of the following:

  1. Morning stiffness
  2. Arthritis in 3 or more joint areas
  3. Arthritis of hand joints
  4. Symmetric arthritis
  5. Rheumatoid nodules
  6. Serum rheumatoid factor
  7. Typical X-ray changes
    - REMEMBER, Rheumatoid factor is positive in most RA patients but not all, and rheumatoid factor is positive in persons with other conditions
    - Synovial fluid in RA patients shows a non-specific inflammatory picture
31
Q

Juvenile rheumatoid arthritis - general . Age of onset, male vs female

A
  • Major cause of functional disability in children
  • Usually diagnosed in early childhood, before age 16 to consider it juvenile
  • Females twice as likely to have, except M=F with systemic onset
32
Q

JRA vs RA

A

Differs from adult RA

  • Oligoarthritis more common
  • Systemic onset more frequent
  • Large joints>small joints
  • Rheumatoid factor and rheumatoid nodules usually absent-ANA positivity is common
33
Q

JRA- pathogenesis, morphology, extra-articular , prognosis

A

Pathogenesis

  • Genetic susceptibility
  • Abnormal immunoregulation
  • Cytokine production
  • Viral infection
  • Morphology of joint- marked synovitis- similar to adult RA
  • Usually slow gradual onset- knees, wrists, elbows, ankles- symmetric, warm, swollen joints
  • Extra-articular- pericarditis, myocarditis, pulmonary fibrosis, glomerulonephritis, uveitis, growth retardation
  • Abrupt systemic onset with high fever, rash, serositis, hepatosplenomegaly can occur
  • 70-90% with the disease recover, 10% left with severe joint deformities
34
Q

What are the Seronegative Spondyloarthropathies (Lack RF)

A
  • Ankylosing spondyloarthritis = rhematoid spondylitis=Marie-Stumpell disease
  • Reactive Arthritis (formerly known as Reiters syndrome)
  • Psoriatic arthritis
  • Enteropathic Arthritis
  • Infectious Arthritis
  • Osteoarthritis = Degenerative Joint Disease (DJD)
35
Q

Ankylosing spondyloarthritis = rhematoid spondylitis=Marie-Stumpell disease - who does it effect more ,what is it, what joints , presentations

A
  • Chronic inflammatory joint disease of axial joints- especially sacroiliac
  • Usually male, begins in adolescence
  • 90% HLA B27
  • Can have autoantibody against joint elements after infection

Histology

  • Chronic synovitis causes articular cartilage destruction and bony ankylosis, especially sacroiliac and apophyseal joints
  • Inflame tendinoligamentous insertion sites leads to bony outgrowths and ossification of annulus fibrosus which compounds fibrous and bony ankylosis leading to severe spinal immobility

Presentation- low back pain, often progressive

  • 1/3 have peripheral joint involvement of hip, knee or shoulder
  • extra-articular manifestations can include uveitis, aortitis, amyloidosis
36
Q

Psoriatic arthritis- who gets it, histology,what joints

A

-Affects 5% of psoriatics, usually not as severe as RA, remissions more frequent,
less joint destruction than RA
-Male-female distribution is even, peak around age 35-45
-Genetic predisposition, but no specific pattern
-Synovium with papillary hyperplasia- dense chronic inflammation like RA
-Synovial vessels- prominent endothelial cells, thick walls, transmural inflammation -Joint symptoms, slow onset in 2/3, acute onset in 1/3
-More than 50% have involvement of first DIP joint
-20-40% have sacroiliac/spinal disease
-Extra-articular manifestation uncommon except for conjunctivitis/uveitis

37
Q

Reactive arthritis( Reiters syndrome) - what causes it , what are some extra-articular manifestations, who usually gets it ,prognosis

A
  • Triad = Arthritis + nongonoccocal urethritis/cervicitis + conjunctivitis
  • Most patients are male, peak in 3rd-4th decade, 80% are HLAB27+
  • Origin- autoimmune reaction initiated by prior infection

-Candidate infections include:
-GI- Shigella, Salmonella, Yersinia, Campylobacter
-GU- Chlamydia
-Several weeks after inciting infection (urethritis, diarrhea) patient develops
asymmetric joint stiffness of ankles, knees, feet and low back pain
-“Sausage finger” can develop as a result of synovitis of the digital tendon sheath
-Calcaneal spurs can be seen

-Extra-articular manifestations include: Keratoderma blennorrhagicum 
    Conjunctivitis 
    Balanitis circinata 
    Cardiac conduction abnormalities  
    Aortic regurgitation

-Natural history of Reactive Arthritis -usually waxes and wanes over weeks/months-50% have recurrent symptoms- functional disability

38
Q

Enteropathic Arthritis- associated diseases, what joints

A
  • Associate with/induced by various inflammatory disorders of bowel
  • Usually HLAB27+
  • 10-20% with Ulcerative Colitis or Crohn’s have migratory oligoarthritis of large joints/spine for months/years
  • Bacterial infection- postenteric arthritis- abrupt- usually knees and ankles; sometimes affects wrists, fingers, toes
39
Q

Infectious Arthritis - modes, agents

A
  • Modes
    • Hematogenous dissemination- microorganisms seed joints
    • Direct inoculation of articular structure
    • Contiguous spread to joint from soft tissue abscess or osteomyelitis
    • Potentially serious- can cause rapid destruction of joint- may cause permanent deformity

-Agents-
Bacterial-acute suppurative arthritis
-seed joint during bacteremia, except in neonate which have higher incidence of contiguous spread from epiphyseal osteomyelitis
-Most common bacteria include:
-Gonococcus- late adolescent, young adult
-Staphylococcus- older child & adults
-Streptococcus
-Hemophilus influenza- children under 2
-Gram negative bacilli- E. coli, Salmonella, Pseudomonas

40
Q

Infectious arthritis - who gets infected, predisposing factors , presentation

A
  • In bacterial arthritis, M=F except gonococcus is seen more in sexually active female
  • Predisposing factors include immune deficiency, debilitating illness, joint trauma, chronic arthritis, IV drug use

-Presentation- suddenly develop acutely painful and swollen infected
joint- restricted range of motion
-Systemic effects include fever, leukocytosis, elevated ESR
-90% of nongonococcal arthritis, only one joint is affected:
knee>hip>shoulder>elbow>wrist>sternoclavicular

41
Q

Gonococcal arthritis

A

oligoarticular, skin rash, genetic deficiency of C5,C6,C7- need prompt and effective treatment

42
Q

Tuberculous Arthritis

A

-Chronic, progressive, monoarticular- all ages
-Usually from adjoining osteomyelitis or hematogenous dissemination from pulmonary infection
-Insidious onset, gradual progressive pain
-May or may not have systemic symptoms
-Form confluent granulomas with central caseous necrosis
-Affected synovium can grow as pannus over articular cartilage- erode into bone along joint margins
-Chronic disease- severe destruction- fibrous ankylosis and obliteration
of joint space
-Distribution: hips>knees>ankles

43
Q

Lyme Arthritis- Borrelia burgdorferei- general, morphology

A
  • Skin infection followed by dissemination of organism to other sites including joints within days to weeks
  • 80% get joint symptoms within weeks to years

-Arthritis is remitting and migratory, usually affects large joints:
knees>shoulders>elbows>ankles, usually 1-2 joints at a time for
weeks-months
-Morphology-Chronic papillary synovitis- synoviocyte hyperplasia, fibrin deposition, mononuclear cell infiltrates (especially CD4+),
onionskin thickening of arterial walls
-Can resemble RA- 10% chronic arthritis with pannus formation
leading to deformity
-In 25%, silver stain for organisms is positive

44
Q

Morphology of DJD

A
  • Early OA- chondrocytes proliferate, form clones
  • Water content of matrix increases, proteoglycan concentration decreases
  • Superficial layers of cartilage degrade leading to vertical and horizontal fibrillation and cracking of matrix
  • At this point see softer than normal granular articular surface
  • Continued friction eventually causes full thickness portions of cartilage to slough, get new articular surface of subchondral bone plate which gets polished (bone eburnation) - meanwhile subchondral bone plate thickens (rebuttresses) and sclerose underlying cancellous bone -Small fractures through articulating bone are common, dislodged pieces of cartilage and subchondral bone form loose bodies (joint mice)
  • Fluid is forced into gaps in cartilage and into subchondral regions by one-way mechanism
  • then the fluid collection forms fibrous walled cysts
  • Get osteophytes at margins of articular surface -cap by fibrocartilage and hyaline cartilage - gradually ossifies
  • Synovium becomes congested and fibrotic, may have scattered chronic inflammatory cells
45
Q

Is DJD just wear and tear?

A

NO
-Chondrocytes in OA cartilage- produce IL-1- initiate matrix breakdown-Other mediators- prostaglandins, TNFα,_TGFΒ induce release of lytic enzymes from chondrocytes- inhibits matrix synthesis

46
Q

Who gets OA and what joints

A

-5% of osteoarthritis is seen in younger persons predisposed by macrotraumatic or repeated microtraumatic injuries to a joint, congenital joint deformity or systemic disease, e.g. diabetes, ochronosis, hemochromatosis, marked obesity; this is
termed “secondary osteoarthritis”
-Joints affected most often: knees and hands in women; hips in men
-Exponential increase in prevalence after age 50
-80-90% of men and women have evidence of OA by age 65
-With aging see alterations in proteoglycans and collagen, decreased tensile strength of cartilage

47
Q

Clinical symptoms of OA

A

-Deep achy pain worsening with use
-Morning stiffness
-Crepitus
-Limited range of movement
-Cervical/lumbar nerve root compression- osteophytes impinging on foramina-get radicular pain, muscle spasms, muscle atrophy,
neurological defects
-Usually only mono- or oligo- articular
-Commonly affects hips, knees, lower lumbar cervical vertebrae, PIP, DIP, first MCP, and first TMT
-Heberdens nodes- females- prominent osteophytes at DIP
-Wrists, elbows, shoulders usually spared
-Uncertain how to prevent or halt progression

48
Q

What is Central tolerance

A

Clonal deletion of self-reactive T and B lymphocytes during their
maturation in the central lymphoid organs. Negative selection of
developing T cells that express high-affinity receptors for self-antigens

49
Q

What is Peripheral tolerance and what mechanisms are in place as its back up

A

-Self reactive T cells that escape intrathymic negative selection can inflict tissue damage unless they are deleted or controlled in peripheral tissue

  • Use the following backup mechanisms to keep these cells from doing damage
    1. Clonal deletion by activation-induced cell death
    2. Clonal anergy
    3. Peripheral suppression by T cells
50
Q

What’s involved in Clonal deletion by activation-induced cell death

A

Apoptotic death of activated T cells by the Fas-Fas ligand system(Fas = CD95- a member of the TNF-receptor family). Get rid of self-antigen-specific T cells because they are constantly being activated by self-tissue antigens.

51
Q

What is clonal anergy

A

-Functional inactivation of lymphocytes induced by encounter with antigens under certain conditions
-T cell-bearing receptors for self-antigen encounters antigen on
a cell that doesn’t express MHC class II molecules (e.g. thyroid
cells)
-Also affects B cells- if encounter antigen before fully mature, never re-express Ig receptor

52
Q

How do t cells cause Peripheral suppression

A

-Suppressor T cells, CD8+ May work by secreting cytokines, eg TGF-B, downregulates immune response

Pathology (12 decks)

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