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Boards 2 > MSI > Flashcards

MSI Flashcards

1
Q

Macula Adherens

A

Desmosomes attached to keratin

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2
Q

Zonula Dherens

A

Cadherins homotypic

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3
Q

ACL/PCL

A

Named for their location on the tibia

  • ACL is anterior drawer test. Normally prevents anteior displacement of the tibia on the femur
  • PCL is posterior drawer prevents posterior movement of the tibia on the femur
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4
Q

Achondroplasia

A
  • AD FGFR3 activating mutation that inhibits chondrocyte proliferation in the epiphysis leading to disorganized epiphysis
  • Impaired endochondral ossification and shortening of long bones. Other bones are fine
  • Usually associated with advanced paternal age
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5
Q

Osteoporosis

A

Normal labs and caused by an age related increase in clastic activity and a decreae in blastic activity

  • IL-1 and 6 cause decrease clasts and estrogen increases protegrin
  • One type is in post menopausla women and can respond to SERMs like raloxifen
  • Type 2 is in everybody
  • Treat with vitamin D, Ca, excercise, bisphosphonates, SERM
  • Avoid corticosteroids
  • Thinned trabechulae is histologic halmark
  • Can also give pulsatile PTH that will increase the activity of blasts (RANK-L is expressed by blasts in response to PTH adn RANK is on clasts)
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6
Q

Osteopetrosis

A
  • AR dysfucntion in Carbonic Anhydrase 2 which leads to an inability to generate acidic environment for clasts to degrade bone
  • Results in an increase in ALP activity and a decrease in Ca
  • Sclerotic thickened bone that is easy to break
  • Can present as hearing and neural impingment
  • Can be cured with a BM transplant that regenerates calsts
  • Can also get a myelophtisic process that causes pancytopmenia and EMH
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7
Q

Osteomalacia and Rickets

A

Caused by a decrease in vitamin D that impairs Ca and P metabolism

  • Low Ca and P with icnreased ALP and PTH
  • There will be unmineralized osteoid (collagen)
  • Rickets is short stature, bowing of legs and head, ribs that have beads
  • Malacia is weak bendy bones that are prone to fracutre
  • Deficent dietary or malabsorption
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8
Q

Pagets

A
  • Cause is unknown, but there is an initial increae in blastic activity that degrades bone that is then followed by an increae in clastic activity that increases bone lay down
  • Leads to a disorganized lamellar structure histologically and enlarging or changing bones grossly
  • Increase in ALP with all other lab values normal. The priamry defect is with the clasts and does not involve Ca metabolism
  • Increaed risk of osteosarcoma, especially in the older population
  • Can also have high output heart failure because of AV malformations.
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9
Q

Osteotits Fibrosis Cystica

A
  • Increase in PTH leads to subperiosteal resporption of bone that is then replaced by fibroblasts and collagen
  • Can be seen secondary to primary PTH or renal disease
  • Labs are variable, but 1 is increase in PTH and ALP and Ca with a decrease in phosphate
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10
Q

McCune Albright

A
  • Hereditery increase in GPCR signalling that elads to overactivation of a numbr of hormone pathways, most often PTH
  • Fibrosa cystica, unilateral cafe au lait spot and possible precocious puberty
  • Shortened 4th and 5th digits is classic
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11
Q

Labs

A
  • Osteoporosis all normal
  • Osteopetrosis: Increase in ALP and decrease in Ca
  • Pagets: Increase in ALP isolated
  • Osteomalacia: increase in PTH and ALP decrease in Ca and P
  • Osteotitis: Decrease in P increase in PTH, ALP and Ca
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12
Q

Giant Cell Tumor

A

Osteoclastic benign tumor most commonly located in the epiphysis

  • Will have osteoclastic markers, CD68, will be of monocyte lineage
  • Will have a soap bubble appearance on X Ray
  • Multinucleated giant cells and spindle cells
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13
Q

Osteoma

A

-Will improve with NSAIDs

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14
Q

Osteochondroma

A
  • Exophytic process from epiphyseal plate leads to chondrocyte cap
  • Generally occurs in young men
  • Pain is relieved by NSAIDs
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15
Q

Osteosarcoma

A
  • Malignant tumor of the metaphysis
  • Classically appears as Codmans triangle with a sunburst pattern
  • Is osteoblastic in origin
  • Asslocated with Rb, Pagets, Radiation
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16
Q

Ewings Sarcoma

A
  • Small blue cell neuroendocrine tumor in the diaphysis of long bones, small blue cells
  • translocation of 11;22
  • Onion skin appearance that can take up the entire bone laterally
  • Highly malignant, but generally responsive to radiation
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17
Q

Chondrosarcoma

A
  • Tumor of cartilage cells that leads to a radiolucent image in the diaphysis
  • Generally occurs in older males
  • Meddullary cavity
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18
Q

Avascular Necrosis

A

-Necrosis of scaphoid following fracture
-Pathologic fracture of femur head without osteoporosis
Associated with alcohol and steroids
-Sickle cell is aslo a common cause (dactylitis)

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19
Q

OA

A

Chronic wear and tear inflammation that leads to breakdown of collagen covering of bone, generally in large weight bearing jounts. Cartillage is normally type 2 collagen and PG

  • DIP is often involved (not in RA, but MCP is spared)
  • Osteophytes
  • Treat with NSAIDS adn intrajoint steroids
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20
Q

RA

A
  • Systemic type 3 hypersensitivity immune response
  • CCP is more specific, but RA is also likely
  • IgM to Fc IgG is RA
  • Deposition in joints and inflammation elads to pannus formation and deviation
  • Fibrnioid necrosis below teh skin is a common complaint (Rheumatoid nodules)
  • Systemic illness that can cause pleuritis, pericarditis, amyloidosis (AA)
  • Treat with DMARDs (MTX, Steroids, Sulfasalazine)
  • HLADR4
  • Invovment of PIP and MCP with sparing of DIP
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21
Q

Juvenile RA

A
  • Generally presents as a mores systemic illness and can present with fevers
  • OFten get associated uveitis
  • Systemic is predominant feature
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22
Q

Sjogrenna

A
  • Lymphocytic infiltrate into exocrine glands
  • Salivary leads to xerostomia and lacrimal to xeroopthalmia
  • Leads to infections and cavities
  • Also causes arthritis
  • RA is commonly positive
  • Ribonucleptide ssRA and ssLA are more specific. Can cross placenta and cause neonatal heart block
  • Tx: steroids and symptoms
  • Risk of marginal zone lymphoma from lyphoid aggregates
  • Can also treat with muscarinic agonist to increase eyeflow
  • Can also see cryoglobulins as you can in RA
  • Associated with HLADR/Q
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23
Q

Alkaptonuria

A
  • Defect in homogentisic oxidase that metabolizes tyrosine

- Leads to arthritis, black urine, and heart disease

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24
Q

Gout

A
  • MSU preco[itates in joints that are then phagocytosed by nneutrohils leading to inflammatin
  • Most commonly big toe
  • Due to increase in purine breakdown
  • HGPRT in lesch nyhan
  • Inhibitors of xanthine oxidase are treatment (fuboxistat and allopurinoll
  • Causes can be destruction of leukemia cells and decreased excretion
  • Decreased excretion from competition for organic anion transporter (lactate and alcohol)
  • Thiazides also cause gout
  • Tophus formation possible
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25
Q

Pseudogout

A

Larger joints with calcium pyrophosphate crystals

  • Basophilic on stain (like psammoma bodies)
  • Usually knees
  • Hypercalcemia is a risk factor
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26
Q

Osteonecrosis

A

Infarction of marrow space due to alcoholism, sickle cell, and high dose steroids

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27
Q

Seronegative Spondyloarthropathies

A
  • are all RF negative
  • Associated with HLA B27 (MHC1)
  • IBD
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28
Q

Psoriatic Arthritis

A
  • Occurs in fewer than 1/3 of patients

- Pencil in cup deformity always involving DIP and has pencil in cup appearance

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29
Q

Ankylosing spondylitis

A

Pannus and fusion of the sacro illiac joints

  • Leads to restrictive lung diseas due to kyphosis
  • Uveitis can cause blindness
  • Aoritis can cause regurg
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30
Q

Reactive arthritis

A

Urethritis, Conjunctivitis, and arhtritis that is sometimes accompanied by a rash

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31
Q

Osteomyleitis

A

-Hematogenous spread
-A Aureus
-Salmonella
-Psuedomonas
TB

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32
Q

Ankylosis Spndylitis

A
  • Fusion of sacroiliac joints
  • Aortitis can cause death
  • Uveitis can cause blindness
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33
Q

Infectous Arthritis

A

Gonorrhea

-S Aureus, Lyme, pastuerulla

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34
Q

SLE

A

-Type 3 hypersensitvity to post apoptotic nuclear fragments
-Defect in early compliment leads to inabilty to clear via C3b
-Deposition in tissue throughout the body
-Most common presenting symtoms are arthritis and macular facial rash
-Basal cell degeneration and dermal atrophy
-Also discid rash
-Pericarditis and pleuritis are possible
-Liebman sacks aeseptic endocarditis
-Antiphospholipids give false positive VDRL and also lead to hypercoagulable state that commonly causes abortions
-Mucocytis
-Neurologic symptoms
-Renal disease is the most common cause of death
Membranous leads to nephrotic syndrome early in disease course
-Diffuse proliferative gives rise to nephritis syndrome late in course and is common cause of death
-ANA and Anti-smith/anti DSDNA
-Hilar adenopathy and raynauds are common
-Hemolytic anemia

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35
Q

Drug induced lupus

A
  • Antihistone antibodies

- Commonly seen with hydralazline and procaimamide

36
Q

Sarcoidosis

A
  • Noncasseating granulomas
  • Most common is restrictive lunf disease with bilateral hilar adenopathy
  • Can effect any organ
  • Commonly effects GI and Eyes, may lead to blindness
  • Eryhthema nodosum is common skin complaint (subq fat, commonly on shins)
  • Increased ACE expression in lung tissue
  • Also elevated vitamin D levels leads to incrase in Ca levels
  • Bells Palsy
  • Ca depsoits are shumman bodies and asteroid bodies are classic
37
Q

Polymyalgia Rheumatica

A
  • Inflammation in joints and bones that involves multiple
  • Older patients with massively elevated ESR, commonly seen with temporal arteritis
  • Normal CK
  • Treat with steroids
38
Q

Fibromyalgia

A

female in middle age that has musculoskeletal compaints

-Treat with SSRI

39
Q

Polymyositis

A
  • CD8 driven endomysial inflammation
  • A component of mixed connective tissue disease
  • Elevated CK and Anti-Jo-1 antibody
  • Treat with steroids
  • Morning stiffness that most commonly effects the shoulders
  • On differential for RA
40
Q

Dermatomyositis

A
  • CD4 driven TH2 inflammation of epimysial muscle and face/hands
  • Heliotrope rash that involves area around eyes and sometimes looks like lupus rash
  • Mechanics hands
  • Commonly associated with a visceral malignancy and may be a paraneoplastic syndome
  • Anti-Jo-1 antibodies to tRNA synthase
  • Treat with steroids
41
Q

Inclusion body byositis

A

Similiar presentation with muscle pain and an elvetated CK

  • Incluision bodies will be seen and does not respond to steroids
  • Commonly seen in elderly
42
Q

MG

A

Anitbody to AchR leads to muscle weakness

  • Most commonly in small muscles and occurs at the end of the day and is worse with movement
  • Thymoma is almost always found
  • Treat with neostygmine and pyridostigmine
43
Q

Lambert Eaton

A
  • Ab to Ca Channels that are V gated
  • Leads to muscle weakness in proximal msucles commonly that gets better with exercise
  • Small Cell lung paraneoplastic
44
Q

Myositis Ossificans

A
  • Fibroblasts turn into osteoblasts

- Most commonly seen around sites of trauma, but can occur genetically

45
Q

Scleroderma

A
  • Vascular injury that leads to TH2 mediated activation of fibroblasts that leads to collagen and PG depostion in tissues
  • Most noticible in the skin that leads to thickened skin that is not wrinkled
  • Can occur in any organ
  • Lungs is the most common cause of death leading to a restrictive disease picture
  • Heart can also be invlolved
  • Kidney can also be involved, interlobular artery, change is myxoid
  • Can be diffuse that commonly has visceral involvment, characterized by anti scl-70 antibody to topoisomerase
  • CREST is characterized by anti centromere antibody
  • Calcinosis, Esophageal dysmotility, Raynauds, sclerodactyly, tel;angectasia. Minimal sclerosis of internal organs, therefore more benign presentation
46
Q

Mixed connective tissue

A
  • Has facets of SLE, Scelroderma, and Polymyositis

- U1 riboneucleotide positive

47
Q

Parakaratosis

A

Epidermal cells retain nuclei into stratum granulosum layer

-Seen along with acanthosis in psoriasis

48
Q

Albinism

A
  • Can be due to decrease in melanocyte number (s-100)

- Or decrease melanin prouction from tyrosine

49
Q

Vitiligo

A

Autoimmune destruciton of melanocytes in a particular pattern, seen in

50
Q

Melasma

A

-Change in color due to elevated estrogens (OCP) or pregnancy

51
Q

Psoriasis

A

Increase gworht of epidermis and cells retain theri nuclei

  • Acanthosis and parakeratosis
  • If scraped, ther ewill be pinpoint hemorrhages at the point of dermal papilae entry
  • Salmon coloerd plaques
  • Can treat with UVA sunlight and soralen to destory cells
  • Nuclei still present in stratum corenum
  • Increase in spinosum and decrease in granularum, more immature cells in spinosum
52
Q

Seborheic Keratosis

A
  • Lipid filled, stuck on lesions that are benign
  • Can occur all at once in leser trelaut sign which signals visceral malignancy like pancreatic cancer
  • Keratin cyst with keratin horns
53
Q

Pemphigus Vulgaris

A
  • IgG antibodies to desmoglein 3 which leads to acanthlolysis and classic reticular pattern
  • Will break easily and can be deadly, treat like burns
  • Will involve mucous membranes
  • Macula Adherens (Desmosomes) intercellular attachments to keratin
54
Q

Bullous Pemphigoud

A
  • Ab to hemidesmososes at D/E junction leads to blisters that don’t rupture easily and not acanthlysis
  • Does not involve mucosa and is less severe
55
Q

Dermatitis Herpetiformis

A
  • IgA antibodies to gliadin that lead to accumulation at derrmal papipllae
  • Pruritic vesicualr lesions on extensor surfaces
  • Celiac is HLA DR2/8
56
Q

Eryhtema Multiforme

A
  • Many causes including indcetion (HSV adn mycoplasma) drugs (beta lactams and sulfa) and cancer
  • Leads to a irregular targetoid lesion and epithelial disruption
  • There is no consistent morpholgy (Multiforme)
  • Does not involve mucous membrans and is a precursosr to stevens johnsons
57
Q

Stevens Johnsons

A
  • Continution of EM, usually due to drugs (Sulfa)
  • Widespread CD8 mediated necrosis and destruction at D/E junction leading to massiv sheding of skin
  • Involves mucous membranes
  • If greater than 30% of body involved then is TEN
58
Q

Acanthosis Nigricans

A
  • IGF mediated increase in epithelial proloferation and also collagen deposition leads to a velvety thick skin
  • Usually bilateral and commonly located at armpits
  • Sign of inuslin resistance or visceral malignancy
59
Q

Actinic Keratosis

A
  • Crusty scaly plaque that is a precursor to SCC
  • Associated with UVB exposure
  • UVA is more energy and causes burns
  • UVB is lower energy and causes thymidine dimers
60
Q

Eryhtema Nodosum

A
  • Small nodules of subq necrosis of fat, commonly presenting in skin
  • Associated with all kinds of granulomatous reactions
  • TB, Sarcoid, Fungal
61
Q

Lichen Planus

A
  • Purple Pruritic papules,polygonal commonly presenting onshings, but can present anywehre
  • Highly associated with Hep C infection
  • Sawtooth at DE junction
  • Lymphocytic infiltrate
  • Commonly invovles oral mucosa
  • Also see dystrophic naiils
62
Q

Pitarysis Rosea

A
  • Herald patch that is often misdiagnosed as RIngworm
  • Followed later by christmas tree distribution extensive rash
  • Do not treat and goes away on its own
  • Commonly occurs following a URI
63
Q

Sunburn

A

Burns and tanning are commonly associated with UVA light and UVB light is thymidine dimers
-Can lead to infections and impetigo

64
Q

Impetigo

A

Infection of the epidermis, msot commonly by S Aureus and S Pyogenes
-S Aurues may cause bullae

65
Q

Cellulitis

A

Infection of the dermis

-Pyogenes and aureus

66
Q

Necrotizing fascitis

A
  • S Pyogenes

- Clostridium perfringens - gas gangrene

67
Q

Scalded skin synddomre

A

S Aureus exotoxin to desomsomes leads to acanthllyssis and skin shedding

  • Different from TEN because doesn’t involve the DE junction just the
  • Involves the stratum granulosum
68
Q

Hairy Oral Leukoplakia

A

Associated with EBV occurs on the lateral tongue in immunocompromised individuals

69
Q

Basal Cell Carcinoma

A
  • Upper lip
  • Pearly white plaques with ulcerations and rolled edges
  • Histologically will show nests of cells with pallisading nuclei
  • Locally aggressive but rarely metastasize
  • 5-FU is a common topical treatment
70
Q

SCC

A
  • Kertin pearls, associated with UVB expsore
  • Commonly forms out of actinic keratosis
  • Scaly red, gross appearing
  • Can be keratoacanthoma that has an ulcerated keratin filled pit
  • Local invasion and may get to nodes, but mets are rare
  • Can also occur at sites of chronic inflammation such as draining sinuses
  • Increased risk with arsenic exposure and immunosupresion
71
Q

Melanoma

A
  • S-100 neural crest cells
  • ABCDE
  • BRAF kinase activtin mutaiton
  • Spread is a function of depth
  • Treat with vemerafanib
72
Q

AA pathway

A
  • AA goes to lipoxygenase that leads to leukotrienes
  • LTB4 is NO tactic
  • LTBC-E are vasodilation, leakage and bronchoconstrictin
  • COX pathway
  • 1: TXA2 and PGE, 2: PGI and Pain
  • E2 important for renal flow, gut flow and uterine contraction
73
Q

Glucocoriticouds

A

Lipocortin inhibits clevage of AA
-Also causes hypocalcemia and death to blasts and increase in clast activity leading to osteoporosis. Some effect is blurred by PTH and hypocalcemia (decrease absorption in gut)

74
Q

Aspirin

A
  • Irreversible acetylation of COX
  • Low dose is antiplatelt med is anitpain and fever, and high dose is antiinflammatory
  • Reyes
75
Q

NSAIDs

A

Reversible Cox inhibitors

  • Ulcers
  • Intersitial Nephritis
76
Q

Celecoxib

A

Specific for reversible cox 2

-Has minimal GI effect but also dose not decreae platelts

77
Q

Acetomenaphin

A

Does not effect GI and effects cox in CNS

  • Does not cause Reye’s syndrome
  • Causes toxic oxygen radical mediated necorsis of hepatocytes in response to overdose.
  • N acetlycystein will regenerate glutathione to get rid of it
  • NAPQI matabolite
78
Q

BisP

A
  • Pyrophosphate analog that binds to hydroxyappetite and decrease ability to resororb
  • Pagets, osteoporosis, hyperclacemia
  • Can cause corrosive esophagitits and osteonecrosis of the jaw
79
Q

Caliptriol

A

Vitamin D analog that can be used for psoriasis

80
Q

Allopurinol, Febuxostat

A

Inhibits Xanthine oxidase to decrease production of uric acid
-Can be used in gout and tumor lysis syndrome
-Will increase toxic concentration of 6MP
-Can also decrease rate of gout excretion
-

81
Q

Probenacid

A
  • Prevents Uric acid reabsoprtion in PCT

- Also prevents peniclin secretinon in PCT

82
Q

Colchicine

A
  • Stabalizes MT and prevents degranulation and chemotaxis of neutrophils
  • Causes GI upset
83
Q

Etanercept

A

-Decoy IgG receptor for TNF alpha

84
Q

Adalimnuab, infliximab

A

TNF Ab

-RA, ankylosing, psoriasis, crohns

85
Q

Uztezumimab

A

Ab to IL-12 and 23 that decreases differntiation into TH1 cells
-Used to treat psoriasis

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