Pathology Flashcards – First Aid for the USMLE STEP 1

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  • What is apoptosis and what are the two pathways
    "programmed cell death, intrinsic or extrinsic"
  • What is the energy requirement for apoptosis
    ATP
  • In which scenarios does apoptosis occur via the intrinsic pathway
    "embryogenesis, hormone induction (menstruation), atrophy (endometrial lining during menopause), result of injurious stimuli like radiation, toxins, hypoxia)"
  • "What changes occur, and what do they lead to"
    levels of anti and pro apoptotic factors leading to inc mito permeability and release of cytochrome c
  • What are the signals for the extrinsic pathway
    ligand receptor interactions -Fas ligand binding Fas (CD95) or killer T cells
  • What substances mediate the effects of the extrinsic pathway
    perforin and granzyme
  • Both pathways activate which cytosolic enzymes that mediate cellular breakdown
    caspases
  • What are the characteristics of apoptosis
    "cell shrinkage, nuclear shrinkage and basophilia (pyknosis), membrane blebbing, pyknotic nuclear fragmentation (karyorrhexis), nuclear fading (karyolysis), and formation of apoptotic bodies, which are phagocytosed - no inflammation"
  • What is the term for enzymatic degradation and protein denaturation of a cell resulting from exogenous injury
    necrosis
  • What happens to intracellular components in necrosis
    extravasate
  • What kind of process is necrosis
    inflammatory
  • Where does coagulative necrosis occur
    "heart, liver, kidney"
  • Where does liquefactive necrosis occur
    "brain, bacterial abscess, pleural effusion"
  • When does caseous necrosis occur
    "TB, systemic fungi"
  • Where does fatty necrosis occur
    pancreas (saponification)
  • Where does fibrinoid necrosis occur
    blood vessels
  • When does gangrenous necrosis occur
    "dry in ischemic coagulative, wet with bacteria: common in limbs and GI tract"
  • What are the pro/anti apoptotic proteins and which is which
    Bax is pro and Bcl-2 is anti
  • What cell injuries are reversible with O2
    "dec ATP synth, cellular swelling from a lack of ATP (no Na/K pump), nuclear chromatin clumping, dec glycogen, fatty change, ribosomal detachment (dec protein synthesis)"
  • What cell injuries are irreversible
    "nuclear pyknosis, karyolysis, karyorrhexis; Ca2+ influx leading to caspase activation; plasma membrane damage; lysosomal rupture; mitochondrial permeability"
  • What kind of infarcts are red and where do they occur
    "hemorrhagic, occur in loose tissues or with collaterals, such as liver, lungs intestine or following reperfusion"
  • Where do pale infarcts occur
    "solid tissues with single blood supply such as heart, kidney, and spleen"
  • What is reperfusion injury due to
    damage by free radicals
  • What is atrophy and what are the causes
    "reduction in the size or number of cells - dec in hormones, dec innervation, dec blood flow, dec nutients, inc pressure, occlusion of secretory ducts"
  • In which organs does atrophy occur because of a lack of hormones
    uterus and vagina
  • In what scenario does atrophy occur via dec innervation
    motor neuron damage
  • In which scenario does atrophy occur via inc pressure
    nephrolithaisis
  • In which scenario does atrophy occur via occlusion of secretory ducts
    CF
  • What are the characteristic findings in inflammation
    "rubor, dolor, calor, tumor and functio laesa"
  • What aspects of the inflammatory process cause fluid exudation
    "inc vasc perm, vasodltn, endothelial injury"
  • What aspects of the inflammatory process cause fibrosis
    fibroblast emigration and proliferation; deposition of extracellular matrix
  • What occurs in the resolution of an inflammatory process
    restoration of nl structure
  • What is granulation tissue
    "highly vascularized, fibrotic"
  • What is an abscess
    fibrosis surrounding pus
  • What is a fistula
    abnl communication
  • What is scarring
    collagen deposition resulting in altered structure or fxn
  • What cells/substances mediate acute inflammation and what is the time of onset and how long does it last
    "PMNs, eosinophils, antibody - rapid onset, lasts minutes to days"
  • What cells mediate chronic inflammation and how is characterized
    "mononuclear cells, persistent destruction and repair, assocaited with blood vessel proliferation, fibrosis and granuloma"
  • What is a granuloma
    nodular collections of epitheliod MACS and giant cells
  • What is the first step of leukocyte extravasation what molecules mediate on the vasc/stroma and the leukocyte
    "rolling, E/P selectin, sialyl lewisX"
  • What is the second step of leukocyte extravasion and what molecules mediate on the vasc/stroma and the leukocyte
    "tight binding, ICAM-1, LFA-1 (integrin)"
  • What is the 3rd step of leukocyte extravasation and what molecules mediate on vasc/stroma and the leukocyte
    "diapedesis, PECAM-1, PECAM-1"
  • What is diapedesis
    leukocyte travels between endothelial cells and exits blood vessels
  • What is the 4th step of leukocyte extravasation and what molecules mediate on the vasc/stroma and leukocyte
    "migration, bacterial products and CILK (C5a, IL-8, LTB4, Kallikrein) and various leukocyte binders"
  • What happens in leukocyte migration
    leukocyte travels through interstitium to site of injury or infection guided by chemotactic signals
  • How do free radical damage cells
    "membrane lipid peroxidation, protein modification, DNA breakage"
  • How are free radicals initiated
    "radiation exposure, metabolism of drugs in phase 1, redox reaction, nitric oxide, transition metals, leukocyte oxidative burst"
  • How are free radical eliminated
    "enzymes = catalase, superoxide dismutase, glutathione peroxidase; spontaneous decay, antioxidants like vit ACE"
  • In what pathology of the eye is free radical injury the cause
    Retinopathy of prematurity - O2 toxicity
  • In what pathology of the lungs is free radical injury the cause
    bronchopulmonary dyslpasia
  • What free radical damage leads to liver necrosis
    CCi4 leading to fatty change
  • What drug can cause free radical injury
    Acetominphen
  • Overload of what metal can cause free radical injury
    Iron
  • Reperfusion free radical injury can occur after what scenario
    "anoxia, especially aftery thrombolytic therapy"
  • What are the 8 granulomatous diseases
    "TB, fungal infnx, syphillis, leprosy, cat scratch fever, sarcoidosis, crohns, berylliosis"
  • What substance do Th1 cells secrete to activate MACS and what do MACS secrete to maintain granuloma formation
    "IFN-gamma, and TNF alpha"
  • What drugs can lead to disseminated disease in patients with granulomas
    anti-TNF
  • Which is hyocelluar - transudate or exudate
    transudate
  • Which is protein rich - transudate or exudate
    exudate
  • Which has a specific gravity > 1.020
    exudate
  • What are the causes of a transudate
    "inc hydrostatic pressure, dec oncotic pressure, Na retention"
  • What are the causes of an exudate
    "lymphatic obstruction, inflammation"
  • What causes an elevated ESR
    products of inflammation coat RBCs and cause aggregation - when aggregated fall at a faster rate within the test tube
  • What are the causes of elevated ESR
    "infections, inflammation (temporal arteritis), cancer, pregs, SLE"
  • What are the causes of e decreased ESR
    "sickle cell, polycythemia (too many), CHF (unknown)"
  • What is a leading cause of fatality from toxilogic agents in children and what is the MOI
    "iron poisoning, cell death due to peroxidation of membrane lipids"
  • What are the symptoms of iron poisoning in acute and chronic
    "acute - gastric bleeding, chronic - metabolic acidosis, scarring leading to GI obstruction"
  • beta pleated sheets demonstratable by apple green birefringence of Congo red stain under polarized light
    amyloidosis
  • How does the affected tissue appear in amyloidosis
    waxy
  • What is the protein in primary amyloidosis and where is it derived from
    "ligh chain, Ig light chains (multiple myeloma)"
  • What is the protein in secondary amyloidosis and where is it derived from
    "acute phase reactant, serum amyloid-associated protein (chronic inflammatory disease)"
  • What is the protein in senile cardiac amyloidosis
    transthyretin
  • What is the protein in amyloidosis with DM type 2
    amylin
  • What is the protein in amyloidosis with medullary carcimona of the thyroid and what is it derived from
    "A-CAL, calcitonin"
  • What is the protein in amyloidosis with alzheimers and what is it derived from
    "beta amyloid, amyloid precursor protein"
  • What is the protein in dialysis associated amyloidosis and what is it derived from
    "beta2 microglobulin, MHC class 1 proteins"
  • "What are the findings in hypovolemic/cadiogeneic shock in terms of ouput, TPR, CO, skin temp"
    "low-output TPR, inc TPR, low CO, cold clammy"
  • "What are the findings in septic shock in terms of output, TPR, venous return skin temp"
    "high output failure, dec TPR, dilated arterioles, high venous return, hot pt"
  • What are the hallmarks of cancer
    "evading apoptosis, self-sufficiency in growth signals, insensitivity to antigrowth signals, sustained angiogenesis, limitless replicative potential, tissue invasion and metastasis"
  • What is it called when cells have increased in number
    hyperplasia
  • "abnl proliferation of cells with lozz of size, shape and orientation"
    dysplasia
  • Have neoplastic cells invaded the BM in carcinoma in situ
    no - preinvasive
  • What is the N/C ration in neoplastic changes
    high
  • "In carcinoma in situ, what amount of thickness do neoplastic cells represent and are the cells polyconal or monoclonal"
    "entire thickness, monoclonal"
  • What do cells use to invade the BM in invasive carcinoma
    collagenases and hydrolases
  • At what point are invasive carcinomas able to metastasize
    once they reach a lymph or blood vessel
  • What is the seed and soil theory of metastasis
    "seed = tumor embolus, soil = target organ; angiogenesis allows tumor survival"
  • "What changes in cadherin, integrin, and integrin receptors occur in metastatic disease"
    "dec cadherin, inc laminin, inc integrin receptors"
  • Is hyperplasia reversible or irreversible
    reversible
  • What happens in metaplasia and is it reversible
    "one adult cell type is replaced by another, often 2ndary to irritation and/or environmental exposure like sqamous metaplasia in trachea and bronchi of smokers; reversible"
  • What happens in dysplasia and is it reversible
    "abnl growth with loss of cellular orientation, shape, and size in comparison to nl tissue; commonly perneoplastic; reversible"
  • What happens in anaplasia and is it reversible
    "abnl cells lacking differentiation; primitive cells of same tissue, often equated with undiff malignant neoplasms - little or no resemblence to tissue of origin; irreversible"
  • What happens in neoplasia and is it reversible
    clonal differentiation of cells that is uncontrolled and excessive; irreversible
  • What happens in desmoplasia and is it reversible
    fibrous tissue formation in response to neoplasm; irreversible
  • What is the tumor grade
    degree of cellular differentiation based on histologic appearance of the tumor
  • How are tumors graded
    "I-IV; degree of differntiation and number of mitoses per high power field, character of tumor itself"
  • What is tumor stage
    "degree of localization/spread based on site and size of primary lesion, spread to regional lymph nodes, presence of metastases; spread of tumor in a specific patient"
  • "Which usually has more prognostic value, grade or stage"
    stage - usually
  • What neoplasm is associated with Down syndrome
    "ALL, AML"
  • "What neoplasm is associated with XP, albinism"
    "melanoma, basal cell carcinoma - esp sqaumous cells carcinoma of the skin"
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