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Concepts in Pathology and Tissue Morphology > Week 4 > Flashcards

Week 4 Flashcards

1
Q

whats the most common soft tissue tumor of adulthood?

A

lipoma

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2
Q

what gene might be involved in the formation of a lipoma

A

HMGA2 gene rearrangement

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3
Q

where do liposarcomas frequently occur?

A

deep soft tissue of proximal extremities and retroperitoneum

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4
Q

what ancillary study might be helpful in diagnosing a liposarcoma

A

FISH positive for amplification of MDM2 on chromosome 12

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5
Q

what is the most common neoplasm in women?

A

uterine leiomyomas

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6
Q

where do leiomyomas commonly occur?

A
  • uterus
  • erector pili muscles
  • muscularis of gut
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7
Q

what would an IHC test on a leiomyoma and leiomyosarcoma show

A

positive for muscle-specific actin, desmin, caldesmon

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8
Q

leiomyosarcoma and occurrence by gendeer

A

W>M

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9
Q

where do leiomyosarcomas occur

A

uterus, deep soft tissues of extremities, and retroperitoneum

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10
Q

Rhabdomyomas are rare, but where would you find them?

A
  • most often in head and neck of men 25-40

* heart of children (hamartoma)

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11
Q

what would an IHC study show for a rhabdomyoma or rhabdomyosarcoma?

A

positive for muscle specific actin, desmin, and myoglobin/myogenein/myoD1

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12
Q

what is the most common sarcoma of childhood and adolescence?

A

rhabdomyosarcoma

*can be seen in adults too

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13
Q

what is a genetic abnormalities seen in synovial sarcoma

A

t(X,18)

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14
Q

what is the pathophysiology of damage in osteoarthritis

A

mechanical wear and tear of joint/cartilage (avascular) -> loss of cartilage and joint space -> bone on bone wear (eburnation)

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15
Q

what are some risk factors for osteoarthritis

A
  • female
  • obese
  • trauma
  • advanced age
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16
Q

Osteoarthritis typically does not have significant inflammation or systemic symptoms. what are some key characteristic of pain associated with osteoarthritis?

A
  • worse with use, worse as day progresses

* alleviated with rest

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17
Q

when does reactive arthritis occur

A

post-GI or GU infection, usually young adults, esp males

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18
Q

whats the classic triad of reactive arthritis?

A
  • conjunctivitis
  • urethritis
  • arthritis
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19
Q

what are common bacteria involved in reactive arthritis?

A
  • shigella
  • yersinia
  • chlamydia
  • campylobacter
  • salmonella
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20
Q

what protein is associated with reactive arthritis?

A

HLA-B27

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21
Q

what is reactive arthritis?

A
  • a seronegative spondyloarthropathy

* an autoimmune condition caused by cross-reactivity with bacterial antigens

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22
Q

What protein is associated with rheumatoid arthritis

A

HLA-D4

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23
Q

classic features of pain with rheumatoid arthritis

A
  • symmetric

* improves with use; morning stiffness

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24
Q

what is rheumatoid arthritis

A

autoimmune disease characterized by mainly chronic inflammatory cells in the synnovium and deposition of antigen complexes

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25
Q

what is the mechanism of joint destruction in rheumatoid arthritis

A

release of cytokines and inflammatory factors (including IL-1, IL-6, TNF-α) -> tissue damage and eventually erosion of adjacent bone and cartilage

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26
Q

what is a key joint that is spared in rheumatoid arthritis?

A

DIP

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27
Q

unlike osteoarthritis, Rheumatoid arthritis does have systemic signs and symptoms. What are they?

A
  • rheumatoid nodules
  • interstitial lung disease
  • pericarditis
  • anemia
  • amyloidosis
  • vasculitis
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28
Q

what testing can be used to diagnoses rheumatoid arthritis?

A
  • rheumatoid factor (RF)

* Anti-cyclic citrullinated peptide (anti-CCP) antibody (more specific than RF)

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29
Q

what is the cause of gout

A

hyperuricemia (underexcretion or overproduction) -> precipitation of monosodium urate crystals in joint

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30
Q

Who/what does gout typically affect?

A
  • usually older men

* typically one joint, especially MTP join

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31
Q

risk factors for gout

A
  • obesity
  • HTN
  • diet (red meat, EtOH)
  • DM
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32
Q

in polarized light, what will the crystals look like for gout

A
  • yellow under parallel light

* blue under perpendicular light

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33
Q

what kind of crystals are deposited in gout

A
  • monosodium urate crystals

* needle shaped

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34
Q

what kind of crystals are deposited in pseudo gout?

A
  • calcium pyrophosphate

* rhomboid shaped

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35
Q

demographic of pseudo gout

A

older patients, males and females

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36
Q

cause of pseudo gout

A

mostly idiopathic

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37
Q

most common joint to be affected by pseudogout

A

knee

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38
Q

what is osteogenesis imperfecta

A

disorder characterized by brittle bones, usually due to absent or low collagen Type I, or abnormal collagen

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39
Q

what mutations account for most cases of osteogenesis imperfecta

A

COL1A1 and COL1A2 genes

others include SERFINF1 and PPIB

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40
Q

what are some signs of osteogenesis imperfecta

A
  • blue sclera
  • dentinogenesis imperfects
  • hearing loss (abnormal/fractured ossicles)
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41
Q

inheritance of osteogenesis imperfecta

A

autosomal dominant, most are de novo

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42
Q

what is a sign of vertebral compression in osteoporosis

A

kyphosis

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43
Q

what is a common diagnostic test for osteoporosis

A
  • DEXA (dual energy xray absorptiometry) scan

* clinical - hx fx of hip or vertebrae +/- radiologic findings

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44
Q

what happens in osteoporosis

A

loss of trabecular and coritcal bone mass

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45
Q

What is primary osteoporosis

A
  • age related
  • type I - post menopausal women -> loss of estrogen
  • type II - old age (men and women)
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46
Q

what is secondary osteoporosis?

A

due to drugs (ie steroids), hyperparathyroidism, or hyperthyroidism

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47
Q

pathophysiology of osteoporosis

A

•increased osteoclastic activity relative to osteoblastic activity

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48
Q

what happens in post-menopausal women who get osteoporosis

A

decreased estogen -> decreased osteoprotegerin (OPG) -> increased RANKL/RANK -> upregulated osteoclast activity

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49
Q

what is osteomalacia

A

defective mineralization of osteoid due to low vitamin D levels

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50
Q

risk factors for osteomalacia

A
  • kidney and liver failure
  • diet/malabsorption
  • dark-skinned populations
  • northern latitudes/low sunlight
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51
Q

pathophysiology of paget’s disease

A
  • abnormal osteoclast activity -> abnormally formed and weak bones
  • osteoblasts activity and overcompensation -> disorganized bone formation -> osteosclerosis
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52
Q

long term paget’s disease can lead to

A
  • arteriovenous shunts in bone

* high output cardiac failure

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53
Q

patients with paget’s disease are at increased risk for

A

osteosarcoma

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54
Q

what are lab values that will be seen with pagets disease

A
  • alkaline phosphatase ELEVATED
  • PTH normal
  • calcium normal
  • PO4 normal
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55
Q

histologic features seen in paget’s disease

A

irregular mosaic pattern of bone formation

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56
Q

patients with paget’s disease may complain of (esp men)

A

increased hat size

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57
Q

rickets can be seen in children. what is it?

A

defective mineralization of osteoid due to low vitamin D and defective mineralization of cartilage in growth plate - weak/soft bones

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58
Q

what are some clinical findings in rickets

A
  • epiphyseal widening
  • bowing of bones (genu varum)
  • rachitic (ribcage) rosary
  • fxs
  • soft skull (craniotabes)
  • frontal bossing
  • pigeon breast defromity
  • muscle spasms
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59
Q

what are some risk factors for rickets?

A
  • diet/malabsorption
  • dark-skin
  • northern latitudes/ low sunlight
  • breast feeding w/o vit d supplementation
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60
Q

what is osteomyelitis

A

infection of bone and bone marrow; majority are bacterial

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61
Q

risk factors for osteomyelitis

A

DM, vascular disease, IV drug use

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62
Q

how does infection spread to bone in osteomyelitis for children

A

•hematogenous spread, associated with bacteremia

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63
Q

what bones are most affected in osteomyelitis for children

A

long bone, especially metaphysis

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64
Q

how does infection spread to bone in osteomyelitis for adults

A
  • often caused by injury exposing bone to infectious organism
  • or spread of nearby soft tissue infection (contiguous)
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65
Q

bones most affected by osteomyelitis in adults

A
  • vertebrae (esp in tuberculosis)
  • pelvis
  • feet
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66
Q

what is the most common organism responsible for osteomyelitis?

A

staph. aureus (80-90%)

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67
Q

what organism might be implicated in osteomyelitis for patients affected by sickle cell disease?

A

salmonella

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68
Q

what organism might be implicated in osteomyelitis for patients who are young and sexually active?

A

N. gonnorhea

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69
Q

what organisms might be implicated in osteomyelitis for patients affected by diabetes, IV drug use, GU infections?

A

pseudomonas and E. coli

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70
Q

what organism might be implicated in osteomyelitis for patients who have had animal bites/scratches?

A

pasturella

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71
Q

what organism might be implicated in osteomyelitis for neonates?

A

H. influenza or group b streptococcus

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72
Q

what are some radiologic findings you might see in osteomyelitis?

A
  • cloaca
  • sequestrum
  • involucrum
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73
Q

what is a cloaca

A
  • possible radiologic finding in osteomyelitis

* cortical defect formed due to increased pressure in bone from abscess formation/suppurative inflammation

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74
Q

what is a sequestrum

A
  • possible radiologic finding in osteomyelitis

* fragment of dead infected bone, which is resistant to treatment by abx and immune cells

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75
Q

what is a involucrum

A
  • possible radiologic finding in osteomyelitis

* reactive bone and inflammatory cells and reactive tissue surrounding sequestrum

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76
Q

what mutation is found in achondroplasia

A

FGFR3 mutation

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77
Q

what happens with the FGFR3 mutation in achondroplasia

A

it is an activation mutation that leads to premature closure of growth plate

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78
Q

what bones are affected in achondroplasia

A

long bones, which undergo endochondral ossification

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79
Q

what bones are spared in achondroplasia

A

bones which undergo membranous ossification (eg skull and pelvis)

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80
Q

most common inheritance of achondroplasia

A
  • Autosomal dominant

* most are inherited from unaffected father as de novo mutation

81
Q

what are histologic findings associated with osteopetrosis

A
  • lack of bone marrow elements (hematopoietic cells)

* replacement of bone marrow by dense, irregular bone

82
Q

mutations associated with osteopetrosis lead to functional abnormalities in what cell type

A

osteoclast (lack of function)

83
Q

what is osteopetrosis

A

defect in bone resorption leading to thick, dense, yet fragile bone

84
Q

what are some mutations associated with osteopetrosis

A
  • carbonic anhydrase II
  • CLCN7
  • TCIRG1
85
Q

what is the CLCN7 gene important for

A
  • part of HCl ion exchange channel

* mutated in most cases of pure osteopetrosis

86
Q

what gene is second most commonly mutated in osteopetrosis

87
Q

a mutation in carbonic anhydrase II is part of a syndrome of

A

osteopetrosis and renal tubular acidosis

88
Q

signs and symptoms of osteopetrosis include

A
  • broken bones
  • anemia, thrombocytopenia, leukopenia (replacement of bone marrow)
  • vision and hearing problems
  • facial paralysis
  • short stature
89
Q

what is the treatment for osteopetrosis

A

bone marrow transplant

90
Q

examples of benign tumors of the epiphysis

A
  • chondroblastoma

* giant cell tumor

91
Q

examples of benign tumors of diaphysis

A
  • endochondroma

* fibrous dysplasia

92
Q

examples of malignant tumors of diaphysis

A
  • ewing sarcoma

* chondrosarcoma

93
Q

examples of malignant tumors of metaphysis

A
  • osteosarcoma

* juxtacortical osteosarcoma

94
Q

examples of benign tumors of metaphysis

A
  • osteoblastoma
  • osteochondroma
  • non-ossifying fibroma
  • osteoid osteoma
  • chondromyxoid fibroma
  • giant cell tumor
95
Q

most common cancer types to metastasize in bone

A 
BLT with a Kosher Pickle
•breast
•lung
•thyroid
•kidney
•prostate
96
Q

what kind of bone tumors are usually seen in metastatic disease

A
  • usually osteolytic

* but can be osteoclastic (sclerotic), esp prostate

97
Q

enchondroma (or chondroma) is a type of primary bone tumor of cartilage (intraosseous cartilage). What mutations are associated?

A

IDH1 and IDH2

98
Q

osteochondroma is a primary bone tumor (cartilage-capped tumor with bony stalk). What mutations are associated?

A

EXT1 and EXT2

99
Q

Chondrosarcoma is a primary bone tumor of cartilage. What mutations are associated?

A

IDH1 and IDH2

100
Q

what is fibrous dysplasia

A

a benign tumor with normal bone components that don’t mature (key word* look like chinese characters)

101
Q

what mutation might be associated with fibrous dysplasia

A

GNAS mutation, monostotic vs polyostotic

102
Q

McCune Albright syndrome can be associated with cafe au lait spots, precocious puberty in girls, hyperthyroidism and acromegaly. What bone abnormality can occur?

A

fibrous dysplasia, monostotic or polyostotic

103
Q

What bone benign tumor can be found with gardner syndrome?

A

osteoma

Gardner syndrome = FAP with osteomas and epidermal cysts

104
Q

Aside from osteomas and fibrous dysplasia, what are some other benign tumors that produce bone/osteoid

A
  • osteoid osteoma

* osteoblastoma

105
Q

ewing sarcoma is classified as a primary bone tumor without matrix formation (bone or cartilage). What mutation is associated?

106
Q

Giant cell tumor of bone is classified as a primary bone tumor that does not form matrix (bone or cartilage). What mutation is associated?

107
Q

what would be seen on a radiologic image of chondrosarcoma

A

stippled or popcorn-like calcification and endosteal scalloping

108
Q

common sites for chondrosarcoma

A
  • pelvis/shoulder/ribs
  • femur
  • humerus
109
Q

where in a bone would you expect to find chondrosarcoma

A

begins in metaphysis and extends to diaphysis

110
Q

what symptoms would be seen with chondrosarcoma

A

constant pain that is not relieved with rest

111
Q

what would be seen histologically in chondrosarcoma

A
  • disordered arrangement of chondrocytes within clear lacunae, surrounded by a bluish matrix
  • increased cellularity and atypia
112
Q

what’s the demographic most affected by osteoid osteoma, which is a benign bone forming tumor?

A

males in teens and 20s

113
Q

bones most commonly affected by osteoid osteoma

A

femur or tibia; tumor is <2 cm

114
Q

presentation of osteoid osteoma

A

pain, esp at night, relieved with aspirin/NSAIDS

115
Q

what is the cause of pain in osteoid osteoma?

A

prostaglandins produced by the tumor, which is why aspirin helps the pain

116
Q

what would be seen on a radiologic image of osteoid osteoma

A

small radiolucent nidus surrounded by sclerotic bone

nidus is the tumor, sclerotic bone is reactive

117
Q

what is seen histologically in osteoid osteoma

A

interlacing trabeculae of woven bone lined by osteoblasts

118
Q

how can osteoblastoma be differentiated from osteoid osteoma?

A 
in osteoblastoma
•tumor is >2cm
•often in posterior spine 
•does not have sclerotic border
•pain not relieved by aspirin
119
Q

Giant cell tumors are benign, but locally aggressive. What is the demographic typically affected

A

F>M, 20s to 40s

120
Q

typical locations of giant cell tumors

A

usually in epiphyses of long bones (distal femur, proximal tibia, and distal radius)

121
Q

giant cell tumors can become malignant in 2-3% of cases. Where might metastases occur

A

in 1-9% of cases, distant mets occur. most often in lungs - “benign pulmonary implants”

122
Q

what is the presentation of giant cell tumors

A

usually pain and swelling

123
Q

what would be seen in radiologic image of giant cell tumor

A

expanding lytic lesion without sclerotic rim

124
Q

what would be seen histologically in giant cell tumor

A

multinucleated cells (not neoplastic) in background of uniform mononuclear cells (neoplastic primitive mesenchymal cells)

125
Q

t(11,22) is present in ewing sarcoma. What important gene movement occurs

A

EWS gene moved from chromosome 22 to the FLI1 gene on chromosome 11

126
Q

Ewing sarcoma is a malignant tumor with primitive round cells (no differentiation) what demographic does it affect

127
Q

where does ewing sarcoma occur

A

usually diaphysis of long bones

128
Q

presentation of ewing sarcoma

A

painful, enlarging mass; may be warm and tender (mimic infection)

129
Q

what would be seen on a radiologic image of ewing sarcoma

A

destructive lytic tumor with moth-eaten margins, extending into soft tissues

130
Q

what would be seen histologically in ewing sarcoma

A

sheets of primitive, small round blue cells

131
Q

What ancillary studies could be used in diagnosis of ewing sarcoma

A
  • IHC positive for CD99

* FISH positive for EWSR1 gene rearrangement, usually t(11,22), EWSR1 and FLI1

132
Q

osteosarcoma is a malignant bone tumor that produces bone matrix. What is the primary demographic affecgted

A
  • <20 year olds
  • M>F
  • second peak in older adults, with predisposing conditions (paget disease, bone infarcts, prior radiation)
133
Q

presentation of osteosarcoma

A
  • painful, enlarging masses

* may present with pathologic fracture

134
Q

location of osteosarcoma

A

usually in metaphysis of long bones (esp around knee)

135
Q

radiologic findings in osteosarcoma

A
  • large infiltrative destructive mass

* mass often breaks through cortex and lifts periosteum (codman triangle) or extends into soft tissue

136
Q

histologic findins in osteosarcoma

A

pleomorphic cells with hyperchromatic nuclei which make bone

137
Q

how does aspiring work?

A

irreversibly inhibits prostaglandin biosynthesis by acetylating cyclooxygenase (COX)

138
Q

What are DMARDs

A
  • Disease-modifying antirheumatic drugs

* mitigate (and possibly reverse) damage due to reduction in inflammatory mediators

139
Q

Biologics are a type of DMARD. what types are there

A
  • cytokine blokers
  • inhibitors of T cell activation
  • inhibitors of B cell function
140
Q

how does methotrexate work in cancer

A

competitively inhibits dihydrofolate reductase (DHFR) an enzyme that participates in tetrahydrofolate synthesis (folic acid needed for purine synth)

141
Q

what does methotrexate do in treatment of RA (and other autoimmune diseases)?

A
  • inhibits enzymes involved in purine metabolism
  • inhibition of T cell activation and suppression of intracellular adhesion molecule expression by T cells
  • selective down regulation of B cells
142
Q

Leflunomide can be used in treatment of RA. what does it do

A

•inhibition of dihydroorotate hydrogenase, which inhibits uridine monophosphate synthesis and ultimately pyrimidine synthesis

143
Q

side effects of leflunomide

A
  • liver damage (esp if on methotrexate too)
  • lung disease
  • birth defects
144
Q

Infliximab can be used in RA treatment. what does it do

A

cytokine blocker; it is a chimeric anti-TNF-α monoclonal antibody

145
Q

Etanercept can be used in RA treatment. what does it do

A

cytokine blocker (specifically anti-TNF agent); human TNF receptor linked to the Fc portion of a human IgG1

146
Q

infliximab administration has been associated with an increased risk for

A

developing tuberculosis

147
Q

anti-TNF therapy may have increased incidence of

A
  • infection
  • lupus
  • exacerbation of demyelinating diseases (eg MS)
  • heart failure
  • increased incidence of lymphoma (may/may not be assoc)
148
Q

what is the goal in therapy for osteoporosis

A

downregulating osteoclast activity

149
Q

bisphosphonates can be used in treatment of osteoporosis, pagets disease, primary hyperparathyroidism, osteogenesis imperfecta, and metastatic carcinoma. How does it work?

A
  • localized in calcium (bone), taken up by osteoclast
  • then inhibits enzymes that induce apoptosis
  • and alter pathways for intracellular protein trafficking, aspects of cytoskeleton, and maintenance of cell contact with bone
150
Q

side effects of bisphosphonates

A

GI upset, esophagitis, osteonecrosis of jaw, atypical femoral fractures

151
Q

how does denosumab work

A
  • monoclonal antibody targeting RANKL on osteoblast

* reduces RANKL-RANK interaction -> reduces osteoclastogenesis

152
Q

what might cause decreased uric acid secretion

A
  • idiopathic
  • renal failure
  • diuretics
153
Q

what might cause increase uric acid in blood

A
  • diet
  • tumor lysis
  • trauma
  • lesch-Nyhan
154
Q

what is the treatment of an acute flare of gout

A

symptomatic relief and reduction of inflammation

-> NSAIDs, steroids, colchicine

155
Q

Long term management of gout has the goal of

A

reduction of uric acid levels

156
Q

how does colchicine work

A
  • inhibits microtubule polymerization and neutrophil chemotaxis
  • degranulation
157
Q

role of aspirin in gout

A
  • High dose aspirin can help treatment -> inhibits tubular reabsorption of uric acid
  • low dose aspirin can cause flare
158
Q

what does allopurinol inhibit

A

xanthine oxidase, which catalyzes hypoxanthine -> xanthine -> plasma uric acid

159
Q

how does probenecib work?

A

inhibits tubular reabsorption of uric acid

160
Q

what are type 1 muscle fibers

one slow red ox

A
  • slow contraction; capable of endurance
  • high in oxidative activity; low in glycolytic activity
  • red bc high myoglobin and high mitochondrial content
161
Q

what are type 2 muscle fibers

two fast white sugar

A
  • fast contraction; fatigue quickly
  • low oxidative activity; high in glycolytic activity
  • white grossly
162
Q

histopathological features of neurogenic atrophy

A
  • fiber type grouping

* group atrophy

163
Q

histopathological features of disuse/steroid atrophy

A

type II myofiber atrophy

164
Q

histopathological features of dystrophin related myopathy

A
  • myofiber size variability
  • necrosis
  • regeneration
  • endomysial fibrosis
  • fatty replacement
165
Q

histopathological features of inflammatory myopathy

A
  • inflammation (usually T cells)
  • necrosis
  • regeneration
166
Q

histopathological features of congenital myopathy

A
  • wide variety of specific changes, inclusions, etc
  • nemaline rods
  • central cores
167
Q

histopathological features of channelopathies

A

may be normal

168
Q

clinical clues for neurogenic atrophy

A

nerve damage (often associated with sensory features)

169
Q

clinical clues for disuse/steroid atrophy

A
  • bedridden/icu
  • corticosteroids
  • hyperthyroidism
170
Q

clinical clues for dystophin related myopathy

A

childhood onset

171
Q

clinical clues for inflammatory myopathy

A
  • adult onset

* associated rheumatologic features

172
Q

clinical clues for congenital myopathy

A

onset at birth; floppy infant

173
Q

clinical clues for channelopathies

A
  • myotonia

* intermittent symptoms

174
Q

etiology of neurogenic atrophy

A

moto nerve damage

175
Q

etiology of disuse/ steroid atrophy

A

atrophy of fast twitch (type 2) fibers

176
Q

etiology of dystrophin related myopathy

A

hereditary abnormalities of dystrophin related proteins

177
Q

etiology of inflammatory myopathies

A

autoimmune

178
Q

etiology of congenital myopathy

179
Q

etiology of channelopathies

A

muscle sodium channel protein SCN4A defect

180
Q

myopathic pattern often associated with

A

scattered myofiber necrosis and regeneration

181
Q

inflammatory myopathy patterns are myopathic, but also characterized by

A

inflammatory infiltrates and/or intracellular inclusions

182
Q

cushing syndrome cause endogenous exposure to

A

glucocorticoid -> steroid atrophy

183
Q

hyperthyroidism can cause what type of atrophy

A

type II myofiber atrophy (like disuse and glucocorticoid)

184
Q

what is the dystophin-glycoprotein complex

A

skeletal muscle membrane associated proteins involved in the mechanical stabilization and signaling interactions between cytoskeleton, membrane, and ECM

185
Q

what is gower’s sign and what is it a key clinical sign of

A
  • sign of duchenne muscular dystrophy

* pt uses hands to “walk” up their own body to stand from a sitting position due to muscle weakness in thigh and hip

186
Q

congenital myopathies often result in relatively static deficits. Examples of these deficits include

A
  • central core disease
  • nemaline myopathy
  • centronuclear myopathy
187
Q

ion channel myopathies are familial disorders that are characterized by

A
  • myotonia

* relapsing episodes of hypotonic paralysis associated with abnormal serum potassium levels

188
Q

hyperkalemic periodic paralysis is an inherited disorder involving mutations in

A

skeletal muscle sodium channel protein (SCN4A, chromosome 7) -> regulates sodium entry during contraction

189
Q

malignant hyperthermia is a rare syndrome, but can result in death from

A

anesthetic agents or succinylcholine during surgery

190
Q

mitochondrial myopathies can stem from mitochondrial or nuclear inheritance. usually manifest

A
  • early adulthood

* proximal muscle weakness and sometimes severe involvement of ocular musculature

191
Q

what is polymositis

A
  • inflammatory myopathy
  • associated with T-cell and increased expression of MCH 1 on myofibers
  • successful treatment with corticosteroids
192
Q

dematomyositis is most common inflammatory myopathy in

193
Q

dematomyositis is believed to have an autoimmune basis.f what happens

A

myofiber damage in a paraseptal or perifascicular pattern

194
Q

inclusion body myositis is most common inflammatory myopathy in

A

patients older than 60

195
Q

morphologic hallmark of inclusion body myositis

A

rimmed vacuoles that contain aggregates of same proteins that accumulate in brains of pts with neurodegenerative disorders

196
Q

key in treatment of inclusion body myositis

A

does not respond well to immunosuppressive agents

197
Q

thyrotoxic myopathy

A
  • acute or chronic proximal muscle weakness

* myofiber necrosis and regeneration

198
Q

ethanol myopathy

A
  • after binge drinking
  • complain of acute muscle pain
  • myocyte swelling, necrosis, and regeneration
199
Q

drug myopathy

A
  • statins common

* affected muscles usually show evidence of myopathic injury, usually without inflammatory component

Concepts in Pathology and Tissue Morphology (10 decks)

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