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MSK Part 2 > Pathology > Flashcards

Pathology Flashcards

1
Q

Explain Gout

A

Crystal-induced arthritis

Systemic disease that presents in one or more joints.

Most common form of inflammatory arthritis (4% of US population)

Primarily in men ages 30-50. Rare in pre-menopausal women (uricosuric effects of estrogen). After 60 women get it as much as men.

See yellow and blue crystals in a microscope.

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2
Q

What is seen in people with gout, and how is it diagnosed?

A

90% of patients under-excrete Uris acid while 10 are over producers.

Hyperuricemia necessary but no sufficient for clinical manifestation of Gout. (Over 6.8mg/dL)

BMI adds to prevalence. Under 30 is 1-2%
-Over 35 is 7% prevalence.

There is a multifactorial etiology (genetics, alcohol/seafood, high fructose corn syrup intake, obesity, diabetes, hyperlipidemia, and hypertension.

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3
Q

Which enzyme was lost that helps excrete Uric acid?

A

Uricase

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4
Q

What are Clinical Presentations of Gout?

A

Gold standard is aspiration of visible crystals from joint. You can also use a diagnosing chart because toe joints are hard to aspirate.

Podagra: 80% of first flares are monoarticular usually involving 1st MTP.

Can affect mid foot, ankle, knee

Often begins in the middle of the night. (I can’t stand the sheets touching my skin.). Resolve spontaneously in 3-10 days without treatment.

4 phases:
Asymjptomatic Hyperuricemia

Acute Gout attack

Interval Gout (asymptomatic): interval flares within 2 years

Chronic Gouty Arthritis/Tophaceous Gout. Develops within 10-20 years of untreated gout.

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5
Q

What is the treatment of Gout?

A

NSAID therapy
-Contraindicated to those with kidney disease, heart failure, gastric ulcers, or Coronary artery disease.

Colchicine: 1.2 mg taken at onset and .6 mg taken 1 hr later on first day.

Glucocorticoids for those intolerant or unable to take NSAIDS or Cochicine

CHRONIC PREVENTION:
Xanthine Oxidase Inhibitors (decrease uric acid production.

Uricosuric agents (not as effective as xanthine oxidase inhibitors.

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6
Q

What is CPPD?

A

Mimicker: will present like gout, OA, RA, and septic arthritis

Calcium Pryophosphate Deposition Disease

Psuedogout or Chondrocalcinosis

Knee is primary location of this Calcium deposit, but it is mostly asymptomatic with only X-ray findings of calcified cartilage.

It can coexist with other joint diseases to make it even more confusing.

White lines within the knee joint space.. More flat crystals.

Etiology is unknown, but age is best theory.

Risk Factors: Age, hypothyroidism, hyperparathyroidism, hypomagnesemia.

Do establish with joint fluid analysis. If you are over 65 with acute/subacute monoarthritis and xrays of chondrocalcinosis it is probably CCPD

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7
Q

What is Psuedo-Osteoarthritis?

A

Progressive CPPD that causes new valgus deformity in the elderly

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8
Q

What is treatment for CCPD

A

No specific treatment for CCPD

Acute attacks:

  • Intra-articular steroids
  • Cochicine (dosed same for gout)
  • Oral corticosteroids

Can use NSAIDS, but extra caution because renal toxicity and cardiac concerns appear.

Chronic:

  • Colchicine
  • Low dose NSAID
  • Hydroxychlorquine
  • Methotrexate
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9
Q

What is the etiology of Septic Arthritis?

A
  1. Hematogenous
  2. Extension from localized soft tissue infections
  3. Direct introduction (trauma)
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10
Q

What are the Clinical Presentations for Septic Arthritis?

A

Non-Gonoccal:

  • Decreased ROM
  • Fever, pain, with swelling
  • Up to 20% mortality rate and 40% permanent reduction in joint function

Gonoccal:
-In young sexually active teen females (more than 4x more likely). From primary infection site (genital, or oral) may present with rash

BOTH are medical emergencies that need to be treated. When in doubt, aspirate and treat***

Staph and Neisseria

Joint space loss or widening in xrays before joint destruction.

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11
Q

How do we treat Septic Arthritis

A

Non-Gonococcal:
-Drainage of joint fluid aspirated or surgery. May need surgery to fix joint.

Prosthetic-Associated: May need removal of prosthesis and IV antibiotics.

Gonococcal: IV/IM antibiotic

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12
Q

Which disease causes Herberden’s nodes?

A

Osteoarthritis

Most common

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13
Q

Which monoarthropathies require a joint tap for definitive diagnosis?

A 
Gout- yes
CPPD- yes
Septic Arthritis-Yes
OA-maybe
Traumatic joint problems-No
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14
Q

What is inside Synovial membranes?

A

Type A and B synoviocytes and synovial fluid

A: macrophages with phagocytic activity

B: Similar to fibroblasts that synthesize hyaluronic acid and various proteins

Fluid: Has hyaluronic acid to act as a viscous lubricant and provide nutrition to articular cartilage.

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15
Q

Explain the pathogenesis of OA

A

Repeated biomechanical stress and genetic factors may predispose to chondrocyte injury which leads to alteration of the ECM

Degradation exceeds chondrocyte synthesis.

Matrix metalloproteinases (MMPs) are secreted by chondrocytes to degrade type 2 collagen network. ECM becomes severely degraded.

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16
Q

What is the Morphology of OA

A

There are fissures and clefts in cartilage

Pieces of (joint mice) loose bodies tumble into the joint.

The friction of the bone on the cartilage causes a polished ivory appearance (bone eburnation)

Also get small fractures or outgrowths on the articular surface.

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17
Q

What is the Clinical course of OA

A

Hips, Knees, Low Lumbar, Cervical, and interphalangeal joints and first carpo and tarsometatarsal joints are most common

Herberden nodes appear on DIP joints in women.

Joint pain that worsens with use, Stiffness will resolve with use, morning stiffness, crepitus (creaky joints, and limitation of range of motion. Can get impingement on nerves

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18
Q

What is the Pathogenesis of RA?

A

Autoimmune origin

Can progress to destruction of articular cartilage. Can get extra articular lesions too.

Peak incidence in 3rd to fifth decade of life.

Has genetic predisposition and environmental factors.
Smoking or smoking can cause citrullination

ASSOCIATED with HLA class ll locus*** (DRB)

CD4 + T helper cells initiate autoimmune response. IFN-y activate macrophages
IL-17 recruits neutrophils. RANKL expressed on activated T cells that stimulate osteoclasts for bone resorption.

TNF and IL-1 from macrophages stimulate synovial cells to secrete protease that destroy hyaline cartilage.

Serum autoantibodies are specific many times to citrullinated peptides with are converted to citrulline and they are deposited in the joints.

Rheumatoid factor (RF) bind to Fc receptors of their own IgG. ESR and CRP elevated. Prescience of Anti-CCP

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19
Q

What is the Morphology of RA?

A

Symmetric and affects more of the small joints of hands and feet.

Includes synovial cell hyperplasia and proliferation. Dense CD4 infiltrates. More vascularity. Osteoclast activity.

These changes produce a pannus. A mass of everything happening

Pannus in bad RA can make fibrous ankylosis which can ossify to bony ankylosis that can lock a joint.

Rheumatoid nodules are infrequent manifestation of RA in the subcutaneous tissue

20
Q

What is the Clinical Course of RA?

A

Anticitrullinated protein antibodies are characteristic of RA. After several weeks to months the joints become involved.

Symmetrical. Can get tendon and ligament inflammation that gives ulnar deviation and flexion-hyperextension of the fingers. (Swan neck and boutonnière deformities)

Joint becomes stiff when rising in the morning or following inactivity. More inflammatory than OA. Have decreased ROM in waxing and waning course.

Treatment is corticosteroids, methotrexate, and TNF antagonists.

Late complications are Cardiovascular Disease (highest cause of mortality in RA pts.). Pulmonary, cutaneous, and ocular involvement.

21
Q

What is the Pathogenesis of Seronegative Spondyloarthropathies

A

Absence of rheumatoid factor.

Involvement of sacroiliac joints

ASSOCIATION of HLA-B27****

Bony proliferation leading to ankylosis

It is an immune mediated response by T cells against an undefined antigen that can cross-react with antigens expressed on bodily cells.

22
Q

What is Ankylosing spondylitis?

A

Prototypical spondyloarthritis

2nd and 3rd decade of life as lower back pain and spinal immobility.

Limited ROM in axial spine (schober test) and Sacroilitis.

Involvement of peripheral joints such as the hips, knees, and shoulders.

Have HLA-B27 positive alleles.

Bamboo spine

23
Q

What is reactive arthritis?

A

Triad of arthritis, nongonococcal urethritis or cervicitis, and conjunctivitis.

HLA-B27 positive. Men in 20s or 30s

Comes from previous infection of the GU system or GI tract.

Patients with severe chronic disease have involvement of sine that is indistinguishable from akylosing spondylitis. Asymmetric pattern

24
Q

Psoriatic Arthritis

A

Associated with psoriasis that affects peripheral and axial joints and ligaments and tendons.

HLA-B27 and HLA-Cw6
30-50 age wise

Not as severe as RA. Interphalangeal joints of hands and feet are affected in asymmetric in pencil cup deformity

25
Q

Gout Pathogenesis

A

Hyperuricemia is necessary but not sufficient for gout.

Primary gout: elevated uric acid is from reduced excretion with unknown cause

Secondary gout: increased production during chemotherapy: or decreased excretion from a renal disease.

Inflammation is triggered by precipitation of urate crystals in the joints. Stimulates cytokines and acute arthritis. Repeated attacks lead to tophi or aggregates of urate crystals.

Genes, alcohol, obesity, drugs, and age (duration of hyperuricemia). Not just hyperuricemia alone.

26
Q

Gout Morphology

A
  1. Acute arthritis
  2. Chronic tophaceous arthritis
  3. Tophi in various sites
  4. Gouty nephropathy

Urate crystals in needle shapes. Negatively birefringent are red****. Perpendicular are blue

Chronic tophaceous arthritis come from repetitive precipitation of crystals. Can cause pannus.

27
Q

Gout Clinical Course

A

Asymptomatic stage of hyperuricemia around puberty

Acute arthritis after several years as sudden onset of joint pain.

Asymptomatic intercritical period. Without treatment attacks become less frequent but polyarticular.

Chronic tophaceous gout after about 12 years of initial attack.

Treatment is to help with lifestyle choices. And lower urate levels.

28
Q

CPPD?

A

Pseudogout
Calcium Pyrophosphate Crystal Deposition Disease

More common over 50

Has sporadic, hereditary, and secondary types.

Autosomal dominant variant results early with crystal deposition.

Articular cartialage Proteoglycans are degraded to allow crystallization around chondrocytes.

Frequently asymptomatic. Affects knees, wrists, elbow, shoulders, and ankles.

Therapy is supportive, but there is no known treat emend that prevents or slows crystal formation.

29
Q

Sjogren’s Syndrome

What is disease?
Presentation, age of onset, risk factors
Immune mechanism underlying disease

A

Dry eyes and mouth with prolonged fatigue. Also causes dry skin, rashes and persistent cough.

Over 40, Being a woman is risk factor.

Mechanism Autoimmune disease of T and B cells infiltrating salivary and lacrimal glands that impales their function.
Large numbers of autoantibodies such as rheumatoid factor are present

Antibodies against Ro/La ribonucleotide (Anti-SSA and SSB) complex is diagnostic hallmark***

30
Q

Myasthenia Gravis

What is disease?
Presentation, age of onset, risk factors
Immune mechanism underlying disease

A

(Muscle weakness severe)

Eyelid droop, double vision, peek sign, dysphasia, speech difficulty.

Autoantibodies that target acetylcholine receptor at neuromuscular junction. Target muscle specific tyrosine kinase as well.

Idiopathic, most common in women under 40 and women over 60. Can occur any time.

31
Q

Scleroderma

What is disease?
Presentation, age of onset, risk factors
Immune mechanism underlying disease

A

Hardening of the skins by immune response triggering cells to overproduce collagen. The extra collagen is deposited and replaces normal tissue.

Hard and tight skin
30-50 years, risk factors include: women, family history, Native American of Choctaw descent.

Raynaud’s phenomenon is noted in 95% of patients.

32
Q

Lambert-Eaton Myasthenic Syndrome

What is disease?
Presentation, age of onset, risk factors
Immune mechanism underlying disease

A

Fatiguable Muscle weakness (begins in upper legs, hips, and upper arms). (DRY MOUTH COMMON)

50% associated with small cell lung cancer, no sensory or CNS signs.

Autoantibodies bind to UGCC which decreases calcium influx into presynaptic neuron leading to decreased ACh released leading to muscle weakness.

35 yrs with genetics, 60 with lung cancer
Risk factor: Small cell lung cancer

33
Q

Reactive Arthritis

What is disease?
Presentation, age of onset, risk factors
Immune mechanism underlying disease

A

Joint inflammation due to infection

TRIAD arthritis, conjunctivitis, and urethritis

Pt. Presents with joint pain, dysuria, and eye inflammation. Attacks knees, ankles, and feet

Presents days to weeks after an infection. Mechanism is unknown but B and T cells attack self antigen in joints. MHC HLA B-27 becomes the auto-antigen.***

25-40, Risk factor: infection, STI, men more common

34
Q

Seronegative Spondyloarthritis

What is disease?
Presentation, age of onset, risk factors
Immune mechanism underlying disease

A

Infection that isn’t detectable in the blood and causes inflammation of the spine (especially lumbar and sacral lumbar joints). Can detect autoantibodies in serum either, like RF.

Innate immune attack. HLA-B27, and TNFa are involved

Present with spine pain, eye inflammation, psoriasis.

Teens to 40s, most common in males, these with crowns, whipped or intestinal bypass surgery

35
Q

Rheumatoid Arthritis

What is disease?
Presentation, age of onset, risk factors
Immune mechanism underlying disease

A

Having to do with painful joints

Tender, warm, and swollen joints that present symmetrically.

As disease progresses, inflamed synovium invades cartilage and bone that leads to joint erosions and destruction.

Risk factors: Smoking, Drinking, Females, HLA-DRB. Happens in early adulthood, but sometimes earlier.

36
Q

Ankylosing Spondylitis

What is disease?
Presentation, age of onset, risk factors
Immune mechanism underlying disease

A

Bent spine

Back pain and stiffness

Too much IL-6, IL-17 and IL-23. Causes chronic inflammation of spinal joints with no rheumatoid factors

Risk factors: HLA-B27 ( in 98%), European descent. Gradual onset between 20 and 30

Bamboo Spine (Patho)

37
Q

Systemic Juvenile Idiopathic Arthritis

What is disease?
Presentation, age of onset, risk factors
Immune mechanism underlying disease

A

Total body inflammation of unknown cause for people under 16.

Increased erythrocytes sedimentation rate, increased C-reactive protein, and ANA. 10-20% of pts will have cytokines storm. No association of autoantibodies. Lots of TNFa, IL1 and IL6

Presentation: Fever, Fatigue, Swelling, Stiff joints, Swollen lymph nodes and Spleen

Risk factor: psoriasis in family, Japan or Indian descents, dactylits. 1-5 years old

38
Q

What are the Seronegative polyarthropathies?

A 
Spondyloarthritis
Ankylosis spondylitis
Psoriatic arthritis
Reactive arthritis
Enteropathic (GI disease)
Negative RF (rheumatoid factor)
Most are Positive for HLA-B27
39
Q

Describe Osteosarcomas in pediatrics

A

Highly malignant, pleomorphic, spindle cell, neoplasm.

Cause unknown.

Active adolescents

Derive from primitive bone forming mesenchymal cells. Located in the epiphysis or metaphysis of distal femur, proximal tibia.

SUNBURST pattern

40
Q

Ewing Sarcoma pediatrics

A

Peak 10-20 years old

Thought to be of neural crest origin.

Small round cell undifferentiated tumors

T(11:22)

Fever and weight loss are associated.

Femur and pelvis are most common sites.

41
Q

Osteochondroma Pediatrics

A

Bony outgrowth.

Painless, hard, non tender and can be excised.

42
Q

Osteoid Osteoma pediatrics

A

Pain relieved by NSAIDS

Femur and Tibia. Dense sclerosis surrounds small radiolucent nidus

43
Q

Osteoblastoma pediatrics

A

Prolonged period of back pain ESPECIALLY at night.

Can evolve into stiffness or a painful scoliosis but it is rare.

NSAIDS don’t work well.

44
Q

Diskitis

A

Infection/inflammation of intervertebral joint space that doesn’t cause associated vertebral Osteomyelitis

Staph Aureus

More common in lumbar spine (50-60%)

Tuberculosis can cause it, and always consider it if first line antibiotics aren’t improving infection

Salmonella: consider in sickle cell anemia patients

Symptoms are back pain, AB pain, irritability to walk or sit. Typically holds spine in a straight or stiff position. They will lose lumbar lordosis due to paravertebral muscle spasm.

45
Q

Is back pain normal in kids?

A

NO

Back pain lasting more than a week requires a detailed investigation

MSK Part 2 (8 decks)

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