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PATHOLOGY > ARTHRITIS > Flashcards

ARTHRITIS Flashcards

1
Q

OSTEOARTHRITIS IS _____ OF CARTILAGE

A

DEGENERATION

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2
Q

OSTEOARTHRITIS ALWAYS OCCUR AT WHICH AREA IN MEN AND FEMALE?

A

MEN AT HIPS WHILE FEMALE AT KNEE OR HANDS JOINTS

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3
Q

DESCRIBE THE PATHOGENESIS OF OA.

A
  • OA IS A DEGENERATION OF THE ARTICULAR CARTILAGE AND ITS DISORDERED REPAIRED.
  • IT INVOLVES THE COMPLEX PATHOLOGIC CHANGES IN CHONDROCYTES AND MATRIX.
  • IN OA, THERE ARE 3 PHASES WHICH ARE:
    1. CHONDROCYTES INJURY WHICH RELATED TO THE GENETIC FACTOR AS WELL AS BIOCHEMICAL FACTOR SUCH AS AGING.
    2. EARLY OA IN WICH THE CHONDROCYTES STARTS TO PROLIFERATE AND SECRETE INFLAMMATORY MEDIATORS, COLLAGENS, PROSTEOGLYCANS, PROTEASES WHICH LATER WILL INITIATE THE SECONDARY INFLAMMATORY CHNAGES.
    3. LATE OA IS WHERE THERE IS REPETITIVE INJURY AND THIS WILL LEAD TO CHONDROCYTE DROP OUT. THIS MARKS THE LOSS OF THE CARTILAGE AND EXTENSIVE SUBCHONDRAL BONE CHANGES
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4
Q

TRUE/FALSE:
A. IN RA, ANTIGEN- ANTIBODY COMPLEXES CONTAINING CITRULLINATED FIBRINOGEN AND A-ENOLASE.
B. PANNUS CAN BE FOUND IN GROSS MORPHOLOGY OF RA
C. IN HISTOLOGY, INFILTRATION OF INFLAMMATORY IS ONE OF THE FEATURES OF RA.
D. RA ALWAYS OCCUR IN MEN THAN WOMEN
E. PANNUS IN RA SHOWED A FINGERLIKE PROJECTION OF SYNOVIUM THAT ARE INFILTRATED BY CHRONIC INFLAMMATORY CELLS.

A

A. TRUE (IT CONTAINS CITRULLINATED FIBRINOGEN, COLLAGEN TYPE II, A- ENIOLASE, VIMENTIN DEPOSIT IN THE JT)
B. TRUE (OA ONLY HAVE A LIL BIT PANNUS, SOMETIMES CANNOT BE OBSERVED)
C. TRUE
D. FALSE (FEMALE > COMMON MALE)
E. TRUE

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5
Q

STATE THE CLINICAL COURSE OF OA.

A
  1. DEEP, ACHY PAIN WORSENS WITH USE
  2. MORNING STIFFNESS
  3. CREPITUS, AND LIMITATION OF RANGE OF MOVEMENT
  4. IMPINGEMENT ON SPINAL FORAMINA BY OSTEOPHYTES RESULTS IN CERVICAL AND LUMBAR NERVE ROOT COMPRESSION AND RADICULAR PAIN, MUSCLE SPASM.
  5. HEBERDEN’S NODE
  6. BOUCHARD’S NODE
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6
Q

STATE THE HISTOLOGY OF RA

A
  • SYNOVIAL CELL HYPERPLASIA AND PROLIFERATION
  • DENSE INFLAMMATORY INFILTRATES OF CD4+ HELPE T CELLS, B CELLS, PLASMA CELLS, DENDRITIC CELLS, AND MACROPHAGES
  • INCREASED VASCULARITY D/T ANGIOGENESIS
  • FIBRINOPURULENT EXUDATES ON THE SYNOVIAL AND JOINT SURFACES
  • OSTEOCLASTIC ACTIVITY IN UNDERLYING BONE ALLOWING THE SYNOVIUM TO PENETRATE INTO THE BONE AND CAUSE PERIARTICULAR EROSIONS AND SUBCHONDRAL CYSTS
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7
Q

WHAT IS RHEUMATOID ARTHRITIS?

A

RHEUMATOID ARTHRITISIS:
- AN AUTOIMMUNE DISEASE
- CHRONIC INFLAMMATORY DISORDER
- PRINCIPALLY ATTACK THE JOINT, PRODUCING A NON SUPPURATIVE PROLIFERATIVE AND INFLAMMATORY SYNOVITIS
- THE DISEASE PEAKS IN THE SECOND TO FOURTH DECADES
- FEMALE < COMMON THAN MALE

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8
Q

STATE THE MICROSCOPIC FEATURES OF RHEUMATOID NODULES.

A
  1. CENTRAL FIBRINOID NECROSIS
  2. SURROUNDED BY A PROMINENT RIM OF ACTIVATED MACROPHAGES AND NUMEROUS LYMPHOCYTES AND PLASMA CELLS
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9
Q

DESC THE PATHOGENESIS OF RHEUMATOID ARTHRITIS.

A

-RHEUMATOID ARTHRITIS IS DUE TO ANTIBODIES AGAINST SELF ANTIGENS SUCH AS SPECIFIC HLA-DRB1 ALLELES AND PTPN22 GENE.
- AS A RESULT, CYTOKINE MEDIATED INFLAMMATION OCCUR AND PREDOMINANTLY SECRETE CD4+ T CELLS.
- THE CYTOKINE INCLUDES:
1. IFN-Y FROM THE TH1 CELLS TO ACTIVATE THE MACROPHAGES AND RESIDENT SYNOVIAL CELLS.
2. IL17 FROM TH17 TO RECRUIT THE NEUTROPHILS AND MONOCYTES
3. TNF AND IL1 FROM MACROPHAGES TO STIMULATE RESIDENT SYNOVIAL CELLS TO SECRETE PROEASES THAT DESTROY HYALINE CARTILAGE
4. RANKL EXPRESSED ON THE ACTIVATED T CELLS STIMULATES BONE RESORPTION

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10
Q

OTHER THAN PANNUS, WHAT OTHER FINDINGS THAT CAN BE SEEN IN GROSS MORPHOLOGY?

A
  1. PANNUS
  2. BONY ANKYLOSIS
  3. FIBROUS ANKYLOSIS
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11
Q

WHAT IS RHEUMATOID NODULE?

A
  • RHEUMATOID NODULE ALWAYS ARISE FROM THE ULNAR ASPECTS OF THE FOREARM, ELBOW, OCCIPUT, AND LUMBOSACRAL AREA.
  • IT IS LESS COMMONLY TO OCCUR IN THE LUNGS, PERICARDIUM, MYOCARDIUM AND OTHER VISCERA ORGANS.
  • THE NODULES ARE FIRM, NON TENDER AND OVAL TO ROUND IN SHAPE, AND IS LOCATED IN THE SUBCUTANEOUS TISSUES UNDER THE SKIN.
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12
Q

OBSTRUCTION BY AN OBLITERATING ENDARTERITIS RESULTING IN ______

A

PERIPHERAL NEUROPATHY, ULCERS AND GANGRENE

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13
Q

LEUKOCYTOCLASTIC VASCLITIS PRODUCE _____

A

PURPURA, CUTANEOUS ULCERS AND NAIL BED INFARCTION

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14
Q

LEUKOCYTOCLASTIC VASCLITIS PRODUCE _____

A

PURPURA, CUTANEOUS ULCERS AND NAIL BED INFARCTION

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15
Q

STATE THE CLINICAL COURSE OF RHEUMATOID ARTHRITIS.

A
  • GENERALLY SYMMETRICAL
  • SMALL JOINTS > AFFECTED THAN LARGE JOINTS
  • USUALLY SYMTPOMS DEVELOP IN THE HANDS OR FEET THEN PROCEEDED TO THE WRIST, ANKLES AND ELBOW
  • UPPER SPINE RARELY INVOLVED AND USUALLY THE LUMBOSACRAL REGION AND HIPS ARE SPARED.
  • JTS ARE SWOLLEN, WARM, PAINFUL, STIFF IN THE MORNING AND WHEN DURING INACTIVITY.
  • PROGRESSIVE JT ENLARGEMENT, DECREASED RANGE OF MOTION EVOLVING TO COMPLETE ARTHRITIS.
  • INFLAMMATION IN THE TENDONS, LIGAMENTS AND THE ADJACENT SKELETAL MUSCLES.
  • BOUTONNIERE DEFORMITY OF HAND
  • SWAN NECK DEFORMITY OF THE FINGERS
  • ULNAR DEVIATION OF METACARPOPHALANGEAL JT
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16
Q

WHAT CAN BE OBSERVED IN RADIOGRAPHY

A
  • JOINTS EFFUSIONS AND JUXTA ARTICULAR OSTEOPENIA WITH EROSIONS
  • NARROWING OF THE JOINT SPACE
  • ULNAR DEVIATION
17
Q

HOW TO RA?

A
  • PAIN RELIEVE SUCH AS CSS, STEROID SPARINGS DRUGS
  • ANTI- INFLAMMATORY SUCH AS METHOTREXATE
  • SLOW DOWN OR STOP JT DESTRUCTION
  • ANTI TNF AGENTS ARE NOT CURATIVE
  • OTHER BIOLOGIC AGENTS THAT INTERFERE WITH T AND B LYMPHOCYTES RESPONSES ARE APPROVED.
18
Q

WHAT IS THE COMPLICATION OF RA?

A
  • LONG TERM COMPLICATION: SYSTEMIC AMYLOIDOSIS
  • INFECTION WITH OPPORTUNISTIC ORGANISMS IN PATIENT WHO RECEIVE LONG TERM ANTI TNF OR OTHER IMMUNOSUPPRESSIVE AGENTS
19
Q

WHAT IS THE COMPLICATION OF RA?

A
  • LONG TERM COMPLICATION: SYSTEMIC AMYLOIDOSIS
  • INFECTION WITH OPPORTUNISTIC ORGANISMS IN PATIENT WHO RECEIVE LONG TERM ANTI TNF OR OTHER IMMUNOSUPPRESSIVE AGENTS
20
Q

WHAT IS GOUT?

A
  • GOUT IS THE TRANSIENT ATTACK THAT IS INTIATED BY THE CRYSTALLIZATION OF THE MONOSODIUM URATE.
  • PEOPLE WHO HAVE GOUT ALWAYS A/W HYPERURICEMIA BUT PEOPLE WITH HYPERURICEMIA DOES NOT ALWAYS A/W GOUT.
21
Q

DESC THE PATHOGENESIS OF GOUT.

A
  • HIGH PURINE INTAKE WILL CAUSES THE HYPERURICEMIA TO OCCUR.
  • HYPERURICEMIA WILL CAUSES THE PRODUCTION OF URATE CRYSTALS AT THE JOINT.
  • THE PRECIPITATION OF URATE CRYSTALS AT THE JT WILL CAUSES THE INFLAMMATORY CELLS TO INFILTRATE AND SECRETE CYTOKINES TO RECRUIT LEUKOCYTES.
    -MACROPHAGES WILL THEN PHAGOCYTOSE THE CRYSTAL THUS ACTIVATING THE CYTOSOLIC SENSOR AND INFLAMMASOMES PATHWAY.
  • THE ACTIVATION OF INFLAMMASOMES PATHWAYS CAUSING THE ACTIVATION OF THE CASPASE-1 WHICH IN TURN ACTIVATING THE IL-1B.
  • ACTIVATION OF THE IL-1B WILL CAUSES THE SECRETION OF NEUTROPHILS AS WELL AS MACROPHAGES SO IT CAN SECRETE MORE CHEMOKINES AND CYTOKINES.
  • MACROPHAGES ALSO WILL RELEASE PROTEASE SO IT CAN INGEST THE CRYSTALS AND EVENTUALLY DAMAGE THE MEMBRANE OF THE PHAGOLYSOSOME SO THERE WILL BE LEAKAGE OF ALTERNATIVE PATHWAY.
  • PRECIPITATION OF URATE CRYSTALS ALSO WILL ACTIVATE THE COMPLEMENT PATHWAY WHICH WILL CAUSES THE NEUTROPHILS CHEMOTAXIS TO OCCUR.
  • THEREFORE, NEUTROPHILS WILL TRY TO PHAGOCYTOSE THE CRYSTALS.
  • UNFORTUNATELY, NEUTROPHILS WILL EVENTUALLY BECOMES LYSED AND THIS WILL CAUSES THE CONTENTS OF THE NEUTROPHILS SUCH AS LYSOZYME TO LEAK OUT.
  • HENCE, THE LYSOZYME WILL CAUSES THE INFLAMMATION AS WELL AS TISSUE INJURY TO OCCUR.
22
Q

STATE THE RISK FACTOR OF GOUT.

A
  • AGE OF THE INDIVIDUAL, AND THE DURATION OF THE HYPERURICEMIA, USUALLY PEOPLE WHO HAVE HYPER URICEMIA FOR ABOUT 20- 30 YEARS WILL RESULT IN GOUT.
  • HIGH ALCOHOL CONSUMPTION
  • OBESITY
  • DRUGS SUCH AS THIAZIDE
  • GENETIC PREDISPOSITION SUCH AS HGPRT, GLUT9, URAT1
  • LEAD TOXICITY
23
Q

WHAT IS ACUTE ARTHRITIS?

A
  • ACUTE ARTHRITIS IS A DENSE NEUTROPHILIC INFILTRATE THAT PERMEATES THE SYNOVIUM AND SYNOVIAL FLUID.
  • ACUTE ARTHRITIS HAVE CRYSTALS THAT ARE LONG, SLENDER IN SHAPED, APPEARS LIKE NEEDLE, AND NEGATIVELY BREFRINGENT.
  • REMISSION IS WHEN CRYSTALLISATION ABATE AND THE CRYSTALS ARE RESOLUBILISED.

ABATE= TO LESSEN OR DECREASE

24
Q

WHAT IS CHRONIC TOPHACEOUS ARTHRITIS?

A
  • CHRONIC TOPHACEOUS ARTHRITIS ARE REPTITIVE PRECIPITATION OF URATE CRYSTALS DURING ACUTE ATTACK
  • THE MSU ENCRUST THE ARTICULAR SURFACE AND FORMS VISIBLE DEPOSITS IN THE SYNOVIUM
  • THE SYNOVIUM BECOMES HYPERPLASTIC, FIBROTIC, AND THICKENED BY INFLAMMATORY CELLS FORMS A PANNUS
  • IN SEVERE CASES, FIBROUS OR BONY ANKYLOSIS ENSUES, RESULTING IN LOSS OF JT F(X).
25
Q

WHERE DOES TOPHI OCCUR?

A

IN THE LIGAMENTS, TENDONS, BURSAE, ARTICULAR CARTILAGE
RARELY IN THE EARLOBES, FINGERTIPS AND KIDNEYS
SUPERFICIAL TOPHI CAN ULCERATE THROUGH THE OVERLYING SKIN

26
Q

HOW DOES TOPHI OCCUR?

A

TOPHI ARE FORMED BY LARGE AGGREGATION O URATE CRYSTALS SURROUNDED BY AN INTENSE INFLAMMATORY REACTION OF FOREIGN BODY GIANT CELLS

27
Q

TRUE/FALSE:
A. THE FIRST STAGE OF GOUT IS ACUTE GOUT
B. IN GOUT PT, WE CAN FIND JUXTA-ARTICULAR OSTEOPENIA AS THE RADIOLOGY FINDINGS.
C. THE RADIOLOGY FINDINGS OF GOUT INCLUDE BONE EROSION AND SCLEROSIS
D. GOUT NEPHORPATHY IS ONE OF THE COMPLICATIONS OF GOUT
E. ACUTE ARTHRITIS LOOKS LIKE A NEEDLE LIKE SHAPED AND APPEARS SPINDLE.

A

A. FALSE (THE FIRST STAGE IS HIGH URIC ACID LEVEL, THEN SECOND STAGE IS ACUTE GOUT, THEN INTERCRITICAL GOUT, LASTLY CHRONIC GOUT)
B. FALSE (JUXTA-ARTICULAR OSTEOPENIA CAN BE FOUND IN RA)
C. TRUE
D. TRUE
E. TRUE

28
Q

TRUE/FALSE
THE FOLLOWING ARTHRITIS AND THE CHARACTERISTIC FEATURES ARE CORRECTLY MATCHED:
A. FIBROUS ARTHRITIS: A/W RAISED ESR
B. GOUTY ARTHRITIS: EXARCABATE BY HEAVY ALCOHOL CONSUMPTION
C. RA: HAS FORMATION OF BONY AKYLOSIS
D. SEPTIC ARTHRITIS: TISSUE BIOPSY IS ESSENTIAL FOR LAB DIAGNOSIS
E. OA: SYNOVIUM IS THE INITIAL SITE OF LESION

A

A. TRUE
B. TRUE
C. TRUE
D. FALSE
E. FALSE

29
Q

WHAT IS PSEUDOGOUT?

A
  • PSEUDOGOUT IS A CALCIUM PYROPHOSPHATE CRYSTAL DEPOSITION DISEASE.
  • IT IS ALSO KNOWN AS CHONDROCALCINOSIS
  • IT OCCURS IN INDIVIDUALS THAT AGED MORE THAN 50 YEARS OLD AND THE SEXES AS WELL AS RACES ARE EQUALLY AFFECTED.
  • CPPD IS DIVIDED INTO 3 PARTS WHICH ARE
    1. IDIOPATHIC
    2. HEREDITARY
    3. SECONDARY
30
Q

WHAT IS MEANT BY HEREDITARY PSEUDOGOUT?

A
  • HEREDITARY PSEUDOGOUT IS AN AUTOSOMAL DOMINANT DISORDER THAT CAUSES THE CRYSTALS TO BE DEVELOPED EARLY IN LIFE AND ARE A/W SEVERE OA.
  • THE DISEASE IS CAUSED BY THE MUTATION OF THE GERMLINE IN THE PYROPHOSPHATE TRANSPORT CHANNEL.
31
Q

WHAT IS MEANT BY SECONDARY PSEUDOGOUT?

A
  • SECONDARY PSEUDOGOUT IS A/W VARIOUS DISORDERS INCLUDING PREVIOUS JT DAMAGE, HYPERPARATHYROIDISM, HYPOTYROIDISM, DIABETES, HEMOCHROMATOSIS, HYPOMAGNESEMIA, AND OCHRONOSIS.
32
Q

STATE THE CLINICAL COURSE OF PSEUDOGOUT.

A
  • ASYMPTOMATIC
  • MAY PRODUCE ACUTE, SUBACUTE OR CHRONIC ARTHRITIS THAT CAN BE CONFUSED WITH OA OR RA.
  • THE JT INVOLVEMENT MAY LAST FROM SEVERAL DAYS TO WEEKS AND MAYBE MONOARTICULAR OR POLYARTICULAR, THE KNEES THEN FOLLOWED BY THE WRIST, ELBOW, SHOULDER AND ANKLES ARE MOST COMMONLY AFFECTED
33
Q

STATE THE INFECTIOUS ARTHRITIS.

A
  • SUPPURATIVE ARTHRITIS
  • MYCOBACTERIAL ARTHRITIS
  • LYME ARTHRITIS
  • VIRAL ARTHRITIS
34
Q

SUPPURATIVE ARTHRITIS IS AN _____ SUPPURATIVE ARTHRITIS AND IT WAS _________ SPREAD.

A

ACUTE
HAEMATOGENOUSLY

35
Q

TRUE/FALSE
REGARDING SUPPURATIVE ARTHRITIS:
A. IN NEONATES, THERE IS AN INCREASED INCIDENCE OF CONTIGUOUS SPREAD FROM UNDERLYING EPIPHYSEAL OSTEOMYELITIS
B. H. INFLUENZA ARTHRITIS PREDOMINATES IN ADULT
C. S. AUREUS IS THE MAIN CAUSATIVE AGENT IN CHILDREN YOUNGER THAN 2 YEARS OF AGE
D. SALMONELLA OCCUR AT ANY AGE
E. GONOCOCCUS IS PREVALENT DURING LATE ADOLESCENCE AND YOUNG ADULTHOOD.

A

A. TRUE
B. FALSE (PREDOMINATE IN CHILDREN YOUNGER THAN 2 Y/O)
C. FALSE (OLDER CHILDREN AND ADULTS)
D. TRUE
E. TRUE

36
Q

TRUE/FALSE
REGARDING SUPPURATIVE ARTHRITIS:
A. IN NEONATES, THERE IS AN INCREASED INCIDENCE OF CONTIGUOUS SPREAD FROM UNDERLYING EPIPHYSEAL OSTEOMYELITIS
B. H. INFLUENZA ARTHRITIS PREDOMINATES IN ADULT
C. S. AUREUS IS THE MAIN CAUSATIVE AGENT IN CHILDREN YOUNGER THAN 2 YEARS OF AGE
D. SALMONELLA OCCUR AT ANY AGE
E. GONOCOCCUS IS PREVALENT DURING LATE ADOLESCENCE AND YOUNG ADULTHOOD.

A

A. TRUE
B. FALSE (PREDOMINATE IN CHILDREN YOUNGER THAN 2 Y/O)
C. FALSE (OLDER CHILDREN AND ADULTS)
D. TRUE
E. TRUE

37
Q

INDIVIDUAL WITH DEFICIENCIES IN ___,____,____ ARE SUSCEPTIBLE TO GONOCOCCAL INFECTIONS

A

C5,C6,C7

38
Q

STATE THE CLINICAL COURSE OF SUPPURATIVE ARTHRITIS.

A
  • SUDDEN ACUTE PAIN AND SWOLLEN JT THT HAS RESTRICTED RANGE OF MOTION
  • FEVER, LEUKOCYTOSIS AND ELEVATED ESR
  • IN NON GONOCOCCAL INFECTION, MAINLY IT INVOLVES A SINGLE JT
  • AXIAL JT ARE OFTEN IN IDU
  • JT ASPIRATION IS DIAGNOSTC IF IT YIELDS PURULENT FLUID IN WHICH THE CASUAL AGENT CAN BE IDENTIFIED
39
Q

BRIEFLY DESC
- MYCOBACTERIAL ARTHRITIS
- LYME ARTHRITIS
- VIRAL ARTHRITIS

A
  1. MYCOBACTERIAL ARTHRITIS
    - MONOARTICULAR INFECTION THAT IS CAUSED BY M. TUBERCULOSIS AND IT CAN OCCUR AT ANY AGE
  2. LYME ARTHRITIS
    - SPIROCHETES BORRELIA BURGDORFERI WHICH IS TRANSMITTED BY DEER TICKS
  3. VIRAL ARTHRITIS
    - IT CAN BE D/T MANY VIRUS SUCH AS HEP B AND C, ALPHAVIRUS, PARVOVIRUS B19 AND RUBELLA

PATHOLOGY (13 decks)

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