Mf2 Iii Pathology

Front 1

Achondroplasia (etiology and 3 main symptoms)

Back 1

FGFR3 point mutation (gene that normally slows bone growth, the abnormal protein is more active than normal so it suppresses)
Short bones, spinal stenosis, foramen magnum stenosis

Front 2

Bisphophonates

Back 2

Inhibit osteoclasts
Treatment for OI

Front 3

Osteogenesis imperfecta and gene mutations

Back 3

Usually type I collagen
Phenotype is milder if mutation is closer to amino terminus

Front 4

Osteogenesis imperfecta: two classifications

Back 4

Type I: normal collagen but half normal amount
Type II-IV: abnormal collagen

Front 5

Blount's disease (etiology and main symptom)

Back 5

Disordered ossification of medial aspect of proximal tibial physis, epiphysi, and metaphysis so bone grows crooked
Genu varum

Front 6

Mucopolysaccharidoses

Back 6

Lysosomal enzyme deficiency for degradation of glycosaminoglycans (GAGs)
Autosomal recessive
More GAGs means thickening of tissues and GAG excretion in urine

Front 7

Morquio

Back 7

Mucopolysaccharidosis
Keratan sulfate degradation blocked
KS is primarily in cornea and cartilage
Spinal deformity, growth retardation, genu valgum

Front 8

Features of synovium (6)

Back 8

Loose connective tissue w/ lymphatics
Underneath synovial membrane
No basement membrane allowing for joints to swell quickly
Highly vascular
Fluid has hyaluronic acid
Upon damage becomes hyperplastic

Front 9

Articular cartilage features (2, composition 4, and destruction 2)

Back 9

Hyaline cartilage acts as shock absorber
Avascular
Composed of collagen II, water, proteoglycans, chondrocytes
Destruction by matrix breakdown or indigenous cells

Front 10

Osteoarthritis

Back 10

Erosion of articular cartilage
-> synovial fluid intrudes into bone
-> bone is replaced by inflammatory tissue
-> chondrocytes stop producing collagen II and instead favor catabolic activity

Front 11

Avascular necrosis (2)

Back 11

Results form ischemia -> infarct
New bone replaces infarct by creeping substitution

Front 12

Rheumatoid arthritis (2 signs)

Back 12

Chronic inflammatory disease mediated by CD4 T cells
-> destruction of articular cartilage
Pannus formation
Joint ankylosis

Front 13

Pannus

Back 13

Inflammatory, fibrotic membrane that fills joint space
Derived from synovium

Front 14

Gout and gouty arthritis

Back 14

Inflammatory arthritis caused by deposition of urate crystals in joints

Front 15

Infectious arthritis (caused by?)

Back 15

Mainly caused by TB or Lyme
Hematogenous spread or contiguous extension

Front 16

Ganglion and synovial cysts

Back 16

Ganglion - fluid-filled swelling from tissue around joint
Synovial (Baker's) - herniation of synovium through joint capsule into soft tissue

Front 17

Osteoclasts (lineage and 4 characteristics)

Back 17

Lineage: hematopoietic macrophage/monocyte lineage
Giant, multinucleated, extracellular lysosomes, ruffled border

Front 18

Osteoclast differentiation

Back 18

RANKL expressed on osteoblasts and marrow stromal cells
RANK expressed on preosteoclasts
M-CSF promotes interaction and Osteoprotegerin (OPG) blocks

Front 19

Osteoblasts (lineage and 4 characteristics)

Back 19

Lineage: mesenchymal marrow stem cells
Secrete bone matrix proteins, regulate osteoclasts, mononuclear, cuboidal

Front 20

Osteoblast differentiation

Back 20

BMP and Wnt stimulates osteoprogenitor cell -> preosteoblast

Front 21

Osteocytes (2)

Back 21

Trapped osteoblast
Secretes sclerostin which inhibits osteoblast bone formation

Front 22

Bone formation markers (3)

Back 22

Alkaline phosphatase (mineralizes bone)
Procollagen peptides
Osteocalcin

Front 23

Bone resorption markers (2)

Back 23

Urinary calcium
Hydroxyproline

Front 24

Osteoporosis (definition and risk factors6)

Back 24

Reduced bone mass and strength
Age, thin/small, hereditary, caucasion, tobacco/alcohol, early menopause

Front 25

Osteoporosis treatments (4)

Back 25

Bisphosphonates: inhibit bone resorption
Hormonal replacement therapy for prevention
Parathyroid hormone - stimulates bone formation
Selective estrogen receptor modulators - estrogens reduce bone resorption

Front 26

Vitamin D deficiency (leads to 4; and 2 causes

Back 26

Leads to decreased calcium absorption and hypocalcemia; rickets in children and osteomalacia in adults
Causes: dietary or malabsorption

Front 27

Neoplasm (6 clinical features)

Back 27

Tumor (swelling) benign or malignant
Features: fever, anemia, anorexia, cachexia, ectopic hormone production, pathology bone fracture

Front 28

Neoplasia nomenclature: epithelial tumors

Back 28

Squamous origin: benign = papilloma; malignant = carcinoma
Glandular origin: benign = adenoma; malignant = adenocarcinoma

Front 29

Neoplasia nomenclature: mesenchymal tumors

Back 29

Benign: -oma (eg lipoma)
Malignant: sarcoma (liposarcoma)

Front 30

Teratoma (benign or malignant?)

Back 30

Composed of cell types derived from more than one germ layer
Can be benign or malignant

Front 31

Hamartoma (benign or malignant?)

Back 31

Mass of normal but disorganized tissue indigenous to site of origin
Benign

Front 32

Heterotopia (benign or malignant?)

Back 32

Ectopic rest of normal tissue
Benign

Front 33

Tumor suppressor genes (3)

Back 33

Normall growth inhibiting
Both alleles must be lost
Loss of heterozygosity -> cancer

Front 34

4 aspects of carcinogenesis

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Carcinogen - agent which leads to increased incidence of neoplasms
Latency - time b/w exposure to carcinogen and neoplasm
Initiation - acquisition of IRREVERSIBLE AND TRANSMISSIBLE genetic changes
Promotion - REVERSIBLE biologic processes that favor neoplasm

Front 35

Neoplastic cell growth (proliferative pool and growth fraction)

Back 35

Proliferative pool - drives tumor growth
Growth fraction: percent of tumor that is proliferative pool

Front 36

4 pathways of tumor spreading

Back 36

Direct invasion
Lymphatic spread - carcinomas
Hematogenous spread - sarcomas
Seeding of body cavities

Front 37

Metaplasia

Back 37

NOT pre neoplastic, but cancer can arise in metaplastic epithelium

Front 38

Precursors to cancer

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Pathologic hyperplasia - atypical hyperplasia and dysplasia

Front 39

Dysplasia (3, for what systems?)

Back 39

Disordered architecture of epithelium
Proliferative state
BM still intact
Genitourinary, GI, respiratory

Front 40

Carcinoma in situ

Back 40

No maturation of cells from basal layer
Intact BM
Leads to invasive squamous cell carcinoma

Front 41

Grading malignant neoplasms + differentiation

Back 41

Well differentiated is lower grade than moderately differentiated

Front 42

Carcinoma IHC

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Cytokeratin

Front 43

Lymphoma IHC

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Leukocyte common antigen

Front 44

Melanoma IHC

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S-100

Front 45

Tumor staging

Back 45

T - site and extent of primary tumor
N - involvement of regional lymph nodes
M - distant metastases

Front 46

Mechanisms of edema (5)

Back 46

Increased hydrostatic pressure (CHF)
Decreased oncotic pressure (liver failure/hypoproteinemia)
Lymphatic obstruction (metastatic cancer)
Increased vascular permeability (inflammation)
Sodium retention

Front 47

What does right heart failure cause?

Back 47

Lower extremity edema

Front 48

What does left heart failure cause?

Back 48

Pulmonary edema

Front 49

What causes exudate vs transudate?

Back 49

Transudate - increased hydrostatic pressure
Exudate - inflammation or malignancy

Front 50

Transudate vs exudate

Back 50

Transudate - clear, low cell count, benign
Exudate - turbid, high cell count, inflammatory/malignant

Front 51

Presentation of ischemia

Back 51

Functional deficits heralded by pain (no morphologic changes in organ)
Eg: angina pectoris is caused by ischemia

Front 52

How can a person w/ CAD develop an infart?

Back 52

Thrombosis -> vessel occlusion -> myocardial infarct

Front 53

Pale/anemic vs red/hemorrhagic infarcts (3)

Back 53

Pale - occlusion of end artery (spleen, heart, kidney)
Red - when tissue is congested at time of necrosis (CHF) or in organs w/ double blood supply (intestine and lung) or organs w/ more space for escape of blood (testes)

Front 54

Gangrene (wet vs dry)

Back 54

Infarct affecting whole body part
Normally dry, if anaerobic putrefactive bacteria invade lesion -> wet

Front 55

Hemostasis vs thrombosis

Back 55

Hemostasis - response to vascular injury -> formation of hemostatic plug to control hemorrhage
Thrombosis - pathology activation of hemostatic mechanisms in uninjured vessels

Front 56

Vitamin K dependent (for synthesis) coagulation factors

Back 56

Factors II, VII, IX, X
Protein C and S

Front 57

Primary hemostatic plug (3)

Back 57

Adhesion
Secretion
Aggregation

Front 58

Coagulation factors synthesized in liver

Back 58

All except von Willebrand Factor

Front 59

Two most common causes of hereditary thrombophilia

Back 59

1. Mutation in factor V gene (factor V Leiden)
2. Mutation in prothrombin gene

Front 60

How does aspirin inhibit platelet aggregation?

Back 60

Inhibits thromboxane A2

Front 61

What is the most important factor in thrombosis?

Back 61

Endothelial injury
Exposure of subendothelial collagen tissue factor expression -> platelet adhesion and thrombus formation
Endothelium need not be physically disrupted (eg smoke can lead to endothelial dysfunction)

Front 62

Hyperemia vs congestion

Back 62

Hyperemia - active, increased blood flow
Congestion - passive, decreased blood flow

Front 63

Ischemia histology + morphology (4)

Back 63

Contraction band necrosis - dissolution of cells -> infarct -> granulation tissue
No morphological features to organs upon presentation (usually just pain)

Front 64

Osteochondroma (Age, localization in bone and body)

Back 64

During growth
Localized to physis (knee, prox humerus)

Front 65

Enchondroma (Age, localization in bone and body)

Back 65

Wider age range
Most common in localized hand bones
Metaphyseal or diaphyseal

Front 66

Osteoid osteoma (Age, localization in bone and body, radiographic signature)

Back 66

During growth
Corticocentric in diaphysis
Femur, tibia
Sclerotic mature bone surrounding woven bone

Front 67

Giant cell tumor of bone (Age, localization in bone and body)

Back 67

> 20 y.o
Epiphysis
Knee
Can produce soft tissue mass

Front 68

Osteosarcoma

Back 68

Bimodal, during growth and in elderly
Metaphyseal intramedullary

Front 69

Chondrosarcoma (Age, localization in bone and body)

Back 69

Middle-aged or older
Central skeleton
Metaphyseal intramedullary

Front 70

Ewing sarcoma (Age, localization in bone and body, histological feature)

Back 70

Small round tumor of childhood
Diaphyseal intramedullary
Translocation
Onion skin

Front 71

What condition can predispose to soft tissue tumor?

Back 71

Neurofibromatosis type I (von Recklinghausen)

Front 72

Adipose tumors

Back 72

Lipoma - superficial
Liposarcoma - deep

Front 73

Diaphyseal intramedullary tumors

Back 73

Ewing
Enchondroma

Front 74

Corticocentric diaphyseal tumors

Back 74

Osteoid osteoma

Front 75

Epiphyseal tumors

Back 75

Giant cell tumor

Front 76

Metaphyseal intramedullary

Back 76

Osteosarcoma
Chondrosarcoma
Enchondroma

Front 77

Atherosclerosis definition (what types of arteries are affected?)

Back 77

Formation of intimal lipid rich fibrous plaques (commonly at bifurcation points)
Affects muscular and elastic arteries

Front 78

Composition of fatty streaks

Back 78

Flat
Composed of lipid foam macrophages w/ T lymphocytes and extracellular lipid

Front 79

Intimal mass composition

Back 79

Smooth muscles cells
Connective tissue
NO lipids

Front 80

Components of atheromatous plaque (3)

Back 80

Cells: smooth muscle, macrophage, lymphocytes
Connective tissue, ECM
Intra/extracellular lipid deposits
(fibrous cap and necrotic center)

Front 81

Response to injury hypothesis for atherosclerosis

Back 81

Endothelial injury -> platelets -> inflammatory response -> foam cells

Front 82

Non-modifiable risk factors for atherosclerosis

Back 82

Age - older
Gender - men
Genetic