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127 Cards in this Set

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  • Back
  • 3rd side (hint)
changes in body fluid levls and osmolarity with cholera
"isotonic contraction:" decreased ECV, no change in osmolality
oncogenes on 18q: DCC causes ColonCancer, DPC causes PancreaticCancer
tumor suppressors / oncogenes on c17
17q: NF1, BRCA-1; 17p: p53
pigmented macules on buccal mucosa, lips, palms, soles, skin not exposed to skin
peutz-jeghers! (colonic JAMMertomas + Peutz all over (her) face, hands, genitals)
treatment of hypernatremia
water replacement, but slowly (2mEq/L/hr) -- avoid cerebral edema
measurement of interstitial fluid vol
plasma volume via albumin, ECF volume using inulin, subtract
measuring fluid volmes: inulin, albumin, heavy water
inulin: ECF; albumin: plasma volume; heavy water: total body volume
nuclear shrinking and basophilia from DNA condensation ("pykno ~ pico = small nuc and DNA")
loss of nuclear basophilia -- "lyse the karyo (nucleus) and the color leaks out"
type of necrosis seen in an abscess
liquefactive (same as brain?)
"RHECKING" the nucleus (fragmentation)
type of amyloidosis in cardiac tissue
usu primary amyloidosis (AL or ATTR); manifests as restrictive cardiomyopathy
islet amyloid polypeptide (type 2 DM)
port wine stain
vascular lesions a/w Sturge-Weber disease (which also includes leptomeningeal angiomatosis -- similar lesions of meninges)
sturge-weber disease
"sturge-chuck-weber:" port-wine stains (capillary hemangiomas), meningeal hemangiomas; eye involvement: glaucoma, retinal detachment; cns: MR, convulsions
MCC aortic stenosis in a 25 yo
congenitally malformed valve (mono- or bicuspid)
vasculitis of the aortic arch
takayasu arteritis (chronic inflam changes --> stenosis --> upper body ischemia, aka pulseless disease)
widened pulse pressure
AR (decreased diastolic pressure) or arteriosclerosis (increased systolic pressure)
alkphos in kids vs adults
kids have much higher alk phos (needed for growth), usu up to 5x greater
Legg-Calve-Perthes disease
idiopathic aseptic necrosis of femoral head; boys > girls, 3-10yo; can lead to osteoarthritis
posterior wall of heart formed by
LA (can compress esophagus)
left border of heart formed by
protein mixture (type I collagen) secreted by osteoblasts; can mineralize to become bone
failure of osteoid mineralization
osteomalacia / rickets
sparse trabeculae
osteoporosis (bony trabeculae are in normal abundance in osteomalacia, just not mineralized)
harsh systolic murmur
VSD murmur is harsh, systolic; PDA is continuous and machinery like; VSD causes increased O2sat of RV, PDA can eventually cause R-->L shunt (once pulm vasc resistance increases), so no change in RV O2sat
diastolic pressure gradiant between atrium and ventricle
AV stenosis (mitral, tricuspid)
GI diseases a/w arthropathy
MCC: IBD (UC and Crohn's); others: bypass surgery, Whipple disease, celiac disease
cardiac myxoma
most frequent primary cardiac tumor: benign, 90% in atria (LA), "ball-valve" obstructions --> MS
Prinzmetal's angina
coronary artery spasm at rest, usu with fixed obstruction near site of spasm; tend to be younger than pts with unstable angina (due to atherosclerosis)
artery frequently injured in knee dislocation
popliteal (extension of superficial femoral artery, ends below the knee in a 'trifurcation:' ant tib, post tib, and peroneal)
subendocardial vs transmural infarct
subendocardial usu in setting of shock, affects most EKG leads; transmural is more common, ST elev in a few leads (due to coronary artery occlusion)
thenar vs hypothenar innervation
thenar: median n; hypothenar: ulnar n;
congenital defect a/w osteium primum ASD (often accompanied by tricupsid/mitral valve malformations)
down syndrome
firing rate of IX and X nerves with respect to blood pressure
increases with increasing blood pressure, causes increased sympathetic outflow; IX = carotid sinus baroreceptors, X = aortic arch baroreceptors
bullous pemphigoid vs pemphigus vulgaris
PV: anti-desmosomal Abs (intrapeidermal bullae), BP: anti-BM Abs (subepidermal bullae); PV: 1st lesion in oral mucosa --> skin --> denuded surface --> infection --> death, BP: blistering, pruritic, but spares oral mucosa and less serious than PV
intramembranous vs. endochondral bone growth
intramembranous: spontaneous bone formaton w/o pre-existing cartilage; endochondral: ossification of cartilaginous molds (eg long bones)
unhappy triad
ACL, medial collateral ligament (MCL), medial meniscus
which side of leg is fibula on
anterior and posterior in ACL / PCL refer to
sites of TIBIAL attachment (=> ACL tear allows tibia to move forward -- anterior drawer sign)
sign of MCL tear
abnormal massive aBduction (no ligament to restrain motion)
rotator cuff muscles
SItS (Supraspinatus, Infraspinatus, Teres minor, Subscapularis)
Role of Supraspinatus
helps deltoid aBduct arm
role of teres minor
laterally rotates and aDducts arm (along w/ subscapularis)
role of subscapularis
medially rotates and aDducts arm (along w/ teres minor)
role of infraspinatus
laterally rotates arm
name the muscular dsytrophies and their inheritence
all involve progressive muscle degeneration, increased CPK (unlike congenital myopathies): duchennes/beckers (XR); fascioscapulohumeral (AD); limb-girdle (AR); myotonic (AD, CTG repeat)
myotonic dystrophy
AD, CTG repeats (anticipation), wasting of muscles + cataracts and heart conduciton defects
myasthenia gravis vs lambert eaton syndrome
MG: improves with rest, 1' affects head/neck, Abs against nAChR, a/w thymomas; LE improves with USE, does NOT 1' affect face, Abs against presynaptic CALCIUM channels, a/w paraneoplastic tumors (eg small cell of lung);
changes in 'bands' during muscle contraction
HIZ shrinks: H band, I band, Z-band
calcium channels in t-tubules
dihydropyradine receptors (opened by depolarization of postsynaptic -muscle- cell)
conduction to contraction of skeletal muscle
presynaptic NT release --> small depol of postsynaptic (muscle) cell --> depol travels down to t-tubules --> opens voltage-gated Ca++ channels (dihydropyradine receptors) --> small Ca++ influx --> opens calcium-gated ryanodine receptor/channels on SR --> big increase in intracytoplasmic Ca++ --> bind Troponin C --> move tropomyosin (via Troponin I) out of the way, allow myosin-actin binding
conduction to contraction of smooth muscle
requires increased intracell Ca; 2 methods: 1) AP --> voltage-gated Ca++ channels open, or 2) alpha1/M3 stim --> Gq --> IP3 --> inc Ca++; once calcium increases, get unified pathway: Ca++ binds calmodulin --> activates myosin light chain kinase --> phosphorylates (activates) myosin --> cross-bridge formation and contraction
hormonal regulators of smooth muscle contraction
alpha1 (vasculature) and M3 (sweat glands) both cause contraction via Gq --> IP3 --> Ca++; beta2 (vasodilation) causes relaxation via Gi --| cAMP --> myosin light chain kinase activation (ie beta2 prevents activation of MLCK)
skeletal vs smooth muscle
skeletal has Z-lines, uses Ca++ - TropnoninC complexes to facilitate bindin, striated, multinucleated, and AP upstroke is driven by SODIUM; smooth has no Z-lines, is single nucleated, not striated, AP upstroke is driven by CALCIUM and Ca++ binds calmodulin to activate myosin light chain kinase
pannus formation
RA: tissue flap (inflammatory?), causes cartilage and bone destruction
jointspace in RA vs OA
increased in RA (inflammation), decreased in OA (wear-and-tear destruction of cartilage brings bones closer together)
systemic sx in RA / OA
none in OA (it’s a mechanical wear and tear process); fever, fatigue, pleuritis and pericarditis in RA
joints affected in RA / OA
RA: synoval joints, MCP/PIP (boutenierres, swan neck, z-thumb); OA: weight-bearing joints (hip), PIP/DIP (Bouchard's and Heberden's nodes)
age of onset of RA/OA
RA in middleage women (F 20-50) -- same as most AI diseases; OA: old people (disease of wear and tear)
change with rest in RA/OA
OA improves with rest (worse at end of the day); RA improves with movement (characterized by morning stiffness)
infectious causes of arthritis (septic arthritis)
MCC: S.Aureus; in sexually active young people: gonococcus--monoarticular; others: lyme disease: a/w ECM, polyarticular. See **IgM**
Seronegative arthrititides
a/w HLA-B27 (unlike RA: HLA-DR4): 1) ANKYLOSING SPONDYLITIS (spine and sacroiliac, uveitis); 2) REITER SYNDROME (urethritis, conjuncitivitis, arthritis); 3) PSORIATIC ARTHRITIS (10% of psoriasis patients); 4) IBD
tx for osteoporosis
bisphophonates --| bone resoprtion (also used for paget's disease, bone mets, multiple myeloma)
2 types of osteoporosis
1: post-menopause --> dec estrogen; 2: senile, M/F > 70yo
failure of bone marrow resorption (osteoclastic failure); can cause: 1) anemia, 2) cranial nerve dysfunction (impingment of neural foramina), 3) blindness, 4) deafness
increased thickness of epiphyseal plates
rickets (osteomalacia of kids): dec Vit D --> dec Ca++ --> dec mineralization of osteoid --> "Soft bones"
brown tumor
cystic space lined with osteoclasts and filled with fibrous stroma / blood (seen in osteitis fibrosa cystica = Von Recklinghausen's Dz of bone)
osteitis fibrosa cystica
primary increase in PTH --> inc Vit D, inc Ca++, dec Phosphorus; --> inc osteoclast activity, inc alk phos
paget's disease
inc osteoclast and blast activity --> elevated alk phos (rest normal); mosaic pattern of bone (disorganized), "cap won't fit" b/c of increased bone density, but poor structural integrity --> increased fractures; common in elderly, and can lead to osteosarcoma (rarely, but the only time you see osteosarcoma in elderly)
osteosarcoma in elderly
2' to paget's disease
McCune Albright syndrome
polyostotic fibrous displasia in little girls: café au lait spots, short stature, precocious puberty
consequences of paget's disease
1) bone pain from fractures (poor structural integrilty); 2) high output heart failure (shunts in highly vascular bone); 3) hearing loss; 4) osteosarcoma (rare, but only cause of osteosarcoma in elderly)
osteomyeleitis in: 1) neonates; 2) kids; 3) adults; 4) sickle cell; 5) IVDU
1) neonates: e.coli/grp B strep --> heme spread; 2) kids: s.aureus --> heme spread; 3) adults: surgery/fracture complication; 4) sickle cell: salmonella; 5) IVDU: pseudomonas
histiocytosis x
clonal proliferation of langerhans cells; see birbeck granules in cells (tennis-racket shaped cytoplasmic structures)
types of histiocytosis x
from worse to better: 1) Letterer-Siwe (multiorgan, multifocal); 2) Hans-Schuller-Christian (unisystem, multifocal): skull, DI, exophthalmus; 3) Eosinophilic Granuloma (unifocal, usu bone), best prognosis
polymyalgia rheumatica
muscle pain, stiffness, NO WEAKNESS; a/w temporal arteritis (elev ESR); usu >50yo, tx w/ prednisone
polymyositis vs dermatomyositis
both a/w anti-Jo-11 1, elev CK and aldolase, progressive proximal muscle weakness caused by CD8+ T-cell injury; dermatomyositis adds rash (in pattern of woman's shawl)
anti-RNP Abs
mixed connective tissue disease
bone tumors around knee
epiphysis: giant cell tumor (benign); metaphysis: osteochondroma (aka exostosis; benign), osteosarcoma (osteogenic carcinoma; malignant)
giant cell tumor of bone
FEMALES 20-40 yo (only bone tumor more common in females); occurs in epiphyseal end (knee), locally aggressive but benign; "soap bubble" on xray, spindle shaped cells with multinucleated giant cells histologically
osteochondroma (exostosis)
males < 25yo; most common benign bone tumor
benign cartilaginous tumor found in intrameddulary bone, distal extremities (hands and feet)
3 main types of malignant bone tumors and locations
osteosarcoma (metaphysis around knee, M 10-20y); Ewing's sarcoma (intramedullary, M < 15yo); Chondrosarcoma (intramedullary, M 30-60)
most common malignancy of bone, found in metaphysis near knee; M 10-20yo; Rad findings: Codman triangle, sunburst pattern; early heme spread; PREDISPOSING factors: Paget's dz (elderly), Rb gene mutation;
malig intramedullary cartilaginous tumor; M 30-60yo; can be 1' or from osteochondroma
ewing sarcoma
intramedullary tumor; boys < 15yo; t(11;22); *extremely malignant*, early mets; histo: small blue cells, onion skin on xray; "Patrick Ewing dribbling a small blue onion; he's a little kid, but still so tall that the tumor cant get to the end of his bone (intramedullary)"
malig tumor of skeletal muscle, most common soft tissue sarcoma of kids; tx with dactinomycin
anti-histone antibodies
drug-induced lupus
what precipitates gouty attack
alcohol, large meal
linear staining on immunofluorescence
goodpasture's (anti-BM IgG)
non-caseating granulomas
sarcoidosis -- cause increased ACE, increased Vit D --> inc Ca++, bilateral hilar adenopathy, erythema nodosum, Bell's palsy
psoriasis vs eczema
psoriasis is on EXTENSOR surfaces and NON-pruritic; eczema on FLEXOR surfaces and PRURITIC
psoriasis: epidermal changes
epidermal hyperplasia (acanthosis); increased stratum spinosum, DECREASED stratum granulosam (psoriasis gets you more STRINGs, less GIRLS)
auspitz sign
a/w psoriasis: bleeding punctate spots when lesoin scraped off
dermatitis herpetiformis
a/w celiac disease; group (herpetiformis) of pruritic papules and vesicles
lichen planus
Pruritic Planar Purple Polygonal Papules; lymphocytes
erythema multiforme
target lesions (multiple types of lesions: macules, papules, vesicles); stevens-johnson is a very serious type
stevens-johnson syndrome
major form of erythema multiforme, high mortalitiy rate (necrosis and ulceration of skin)
albinism vs vitiligo
vitiligo is acquired, autoimmune (a/w graves, addisons), and patchy; albinism is usu result of tyrosinase deficiency (impaired tyrosine --> L-DOPA --> melanin)
spitz nevus
juvenile melanoma (but MISNOMER -- benign!); spindle shaped cells
basal cell vs squamos cell carcinomas
BASAL cell: upper face, pearly papule w/ overlying telangiectasia, pallisading nuclei; SQUAMOUS cell: lower face, sheets of cells with KERATIN PEARLS, a/w arsenic and actinic keratosis
congenital hypothyroidism
lethargic, poor feeding, prolonged jaundice, muscle hypotonia, macroglossia, MR (T4 needed for brain dev); inc risk of ASD/VSD
sporothrix infection
dimorphic fungus, xmit by thorbrick --> subq mycosis, nodules along lymphatics
apocrine vs eccrine glands
both used for sweat; apocrine glands "rip off piece of membrane" --> fatty, smelly (sweat); eccrine glands secrete NaCl ('sweat') directly to skin via exocytosis
apocrine vs eccrine glands
essential for formation/differntiation of osteoclasts (they have RANK-receptors); hypoestrogen --> overexpression --> osteoporosis
"gluteus medius gait"
hip drops downoward when ipsilateral foot lifted -- caused by injury to superior gluteal nerve or gluteus medius muscle
acute: within 1wk of procedure, mediated by CD4 and CD8 T cells (B Cells don't really play any role)
2 most imp factors for osteoclast differentiation
M-CSF and RANK-L (osteoclasts, mature and precursors, possess receptors for both)
roles of FGF
nevascularization, wound healing, and bone matrix formation (FGF-R mutation --> achondroplasia)
parvovirus in kids and adults
kids: erythema infectiousum (5th disease); adults: arthritis
antibodies against neutrophil myeloperoxidase
p-ANCA (PAN, Churg-Strauss)
endothelial injury --> endothelial dysfunction / collagen exposure --> platelet adhesion/aggregation/release of {PDGF, TGF-beta} --> migration of SMC from media to intima, SMC proliferation
hemangiosarcoma (angiosarcoma) a/w what toxins
thorotrast, PVC, arsenic
pulseless disease
takayasu arteritis: granulomatous thickening of aortic arch, elevated ESR, azn females < 40yo
which organ is rarely involved in PAN
fatty streaks
earliest lesion of athersclerosis, present after age 10; lipid-laden foam cells in intima
vasculitis a/w HBV
malignant HTN vs diabetic hyaline arteriolosclerosis
malignant HTN causes hyperplastic arteriolosclerosis (homogenous, onion-like, concentric thickening of arterial walls); diabetic hyaline arteriolosclerosis causes intimal thickening with homogeneous hyaline deposition in intima
temporal arteritis is morphologically most similar to?
takayasu arteritis (pulseless disease)
most specific sx of giant cell (temporal) arteritis
jaw claudication
takayasu vs giant cell (temporal) arteritis
usu distinction is size and location (takayasu: aorta, proximal aortic branches; temporal: distal carotids); however, both can present similarly so distinction often made based on AGE (takayasu: < 40; temporal: elderly)
temporal arteritis vs PAN
temporal (and takayasu) are GIANT CELL arterititides --> involve giant cells and mononuclear infiltrates; PAN is characterized by immune complexes, complement, and plasma proteins --> fibrinoid necrosis
main mechanisms for dev of varicose veins
incompetent venous valves
vascular effects of tertiary syphilis
vaso vasorum endarteritis / obliteration --> weakened adventitia --> aortic aneurysm --> AR