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134 Cards in this Set
- Front
- Back
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Metaplasia (from what? Is it reversible?)
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From chronic irritation. Named according to New cell type. Increased risk of malignant transforamtion but is reversible
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Pyknosis
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Chromatin clumping and shrinking
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Karyorrhexis
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Fragmentation of chromatin
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Karyolysis
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fading of chromatin
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Coagulative Necrosis
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from sudden cutoff of blood supply to organ. Architecture preserved except for nuclear changes. Eosinophilia. Any solid organ except brain.
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type of Necrosis of heart or kidney
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Coagulative necrosis
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Liquefactive necrosis
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enzymatic liquefaction of tissue. In CNS injury and some bacterial infections, abscess
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type of Necrosis in brain
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Liquefactive necrosis
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Caseous necrosis - characteristic
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granulomatous
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Fat necrosis (cause and examples)
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Due to trauma (injury in breast) or enzymatic digestion (pancreatitis)
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type of necrosis in breast or pancreatitis
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Fat necrosis
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Gangrenous necrosis
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Dry (Coag. Necrosis) vs. wet (Coag. Necrosis with superimposed infection). Usually extermiites, sometimes used interchangably with organ necrosis ("Gangrenous bowel")
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type of necrosis of extermeties (organ)
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Gangrenous necrosis
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Fibrinoid necrosis
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protein/immune complex deposition in vessel walls
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Apoptosis - extrinsic death receptors (2)
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Fas/Fas Ligand or TNF
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Apoptosis - intrinsic-increased mitochondrial permeability (factors -2)
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Decreased Bcl-2, release of cytochrome C
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Apoptosis: what does both extrinsic and intrinsic pathways lead to?
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activation of CASPASES
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Caspases
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involved in Apoptosis
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Steatosis (is it reversible?)
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Accumulation of fat (triglycerides), reversible
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What is the initiating factor of Atherosclerosis?
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Endothelial injury
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Atherosclerosis
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Hypercholesterolemia leads to fibrous plaque build up within the intima of arteries.
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What does α-1-antitrypsin deficiency lead to?
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Cirrhosis, emphysema
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What is mallory bodies related to?
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Liver dz
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Neurofibrillary tangles are seen in?
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Alzheimer's
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Hyaline Change (characteristic, cause, reversible?)
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Homogenous, glassy, pink appearance. Caused most often by accumulation of protein (usually HTN). Is reversible.
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How does Glycogen accumulation look like in a cell?
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It appears as clear vacuole
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Von Gierke's dz?
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Glucose-6-phosphatase deficiency. Hepato/renomegaly with profound hypoglycemia
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McArdle's dz
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Muscle phosphorylase deficiency. Cramping with exercise and no increase in lactic acid
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What is Anthracosis?
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Carbon dust accumulation
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What is Lipofuscin?
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wear and tear, yellowish pigment seen in older people's cells
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Hemosiderin (how does it show? Systemic causes?)
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Accumulation of iron. Local-bruise. Primary - hereditary hemochromatosis / Secondary - transfusions
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Difference b/w dystrophic and metastatic calcification?
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Dystrophic accurs in damaged tissue, may see psammoma bodies, normal serum Ca level vs. Metastatic occurs in previously normal tissue, caused from hypercalcemia
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What are the common causes of Hypercalcemia that causes metastatic calcifications?
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hyperparathyroidism, osteolytic tumors, hypervitaminosis D, excess calcium intake
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Cardinal signs of cell injury
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Rubor (redness from vessel dilitation), Dolor (pain from increased pressure and mediators - bradykinin), Calor (heat from increased blood flow), Tumor (swelling due to fluid accumulation), Function laesa
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What are the 3 main components of Acute inflammation?
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1. Increased blood flow; 2. Increased vascular permeability (proteins leukocytes leak out); 3. Emigration, accumulation, and activation of leukocytes
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Exudate (local or systemic/ cause)
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high in protein. Abnormal permeability due to local problem. Due to lymphatic obstruction or inflammation
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Transudate? (local or systemic/cause)
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Low in protein. Think about Starling. Usually from systemic problems (edema, ascites), ultrafiltrate. Due to altered ostmotic or hydrostatic pressure (Cirrhosis, nephrosis, CHF)
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Steps in Acute inflammation
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1. Vasodilation --> 2. Permeability --> 3. Stasis from increased blood viscosity --> 4. Emigration of leukocytes
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What is the immediate mediator of Vasodilation in Acute inflammation?
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Histamine.
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(Leukocyte in inflammation) What cytokines upregulate Adhesion molecules?
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TNF & IL-1
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What does Integrin bind to?
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ICAM & VCAM of endothelium
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PECAM-1?
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Responsible for diapedesis
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C5a, LTB4, IL-8?
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Responsible for chemotaxis
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LTB4
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Responsible for chemotaxis
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C5a
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Responsible for chemotaxis
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IL-8
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Chemokines. Responsible for chemotaxis. Attract leukocytes
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Name enzymes that are involved in Phagocytosis (that kills microbe)
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NADPH Oxidase, H2O2 (SOD), O2 superoxide (myeloperoxidase), lysosomal enzymes
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Leukocyte Adhesion Defect (Defective LFA-1 aka CD18)
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Delayed umbilical separation. Recurrent bacterial infections with absent pus formation, neutrophilia
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Chediak Higashi syndrome
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AR inheritance. Abnormal microtubule forming leads to impaired chemotaxis and migration. WBCs have large cytoplasmic granules (represent abnormal lysosomes). Neutropenia, albinism, neuropathy, repeated infections
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Chronic Granulomatous Disease (CGD)
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X-linked. Deficient NADPH oxidase activity. Phagocytes can ingest but can't kill catalase positive organisms (S. aureus). Enzyme-deficient neutrophils can't produce H2O2 that is needed as a substrate for myeloperoxidase
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Myeloperoxidase deficiency
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Susceptible to yeast infxns by Candida albicans
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Acute inflammation -- Serous
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Clear fluid (blister)
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Acute inflammation -- Fibrinous
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Fibrin deposition. Charateristic in body cavity linings (pericardium, pleura, menigines). Can result in organization/adhesions if not resolved
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Acute inflammation -- purulent (pus)
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Neutrophils, necrotic cells. From infections, can result in abscess
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Acute inflammation -- ulcers
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Mostly in GI and GU tracts
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Acute inflammation -- Pseudomembranous
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Bacterial toxins induce mucosal damage. Classic ex: C. Diff colitis
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Histamine
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Immediate cause of vasodilation/increase in vascular permeability during inflammation. Dilation of arterioles. Causes mast cell degranulation
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Serotonin
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vasodilation, increase vascular permeability. Serotonin is present in platelets
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C1-C9
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Classical complement mediators. Stimulated by AB
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C3b, Bb, C5-9
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Alternative complement mediators. Stimulated by bacteria
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Lectin
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Stimulated by bacteria (MBP, C3b, C5-9)
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C5a, C3a
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Anaphylatoxins
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C5a
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Chemotaxis, Anaphylatoxins
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C3b
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Anaphylatoxins, opsonin
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Bradykinin
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Increases permeability, dilation, pain
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Factor XIIa (Hageman factor)
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activates kinin, clotting, fibrinolytic and complement cascades
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Arachidonic acid metabolites
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Cleaved from membrane by phospholipase A2. Prostaglandind, Thromboxane, Lipoxygenase
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Prostaglandin
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vasodilation, decrease pain threshold and pyrogen (fever)
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Thromboxane (TXA2)
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Vasoconstriction, platelet aggregation
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Lipooxygenase
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Leukotrienes
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PAF
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Derived from basophil. Platelet aggregation, vaso and bronchoconstriction
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IL-1, TNF
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from macrophages. Fever, acute phase protein release, activate leukocytes and endothelium, shock if too much
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MCP-1
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attract leukocytes
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MIP-1-alpha
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attract leukocytes
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RANTES
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attract leukocytes
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NO
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from endothelial cells. Increase cGMP. Vasodilation, reduce inflammatory response (compensate), microbicidal
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Vasodilation (inflammatory mediators)
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Histamine, Prostaglandind, NO
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Increased permeability (inflammatory mediators)
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Histamine, Bradykinin, Leukotriens, PAF, C3a, C5a
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Chemotaxis, activation of leukocytes
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IL-8, LTB4, C5a, IL-1, TNF, PAF
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Fever
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Prostaglandins, IL-1 & TNF
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Pain
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Bradykinin, Prostaglandin
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Chronic inflammation -- cause?
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Unresolved acute inflammation (chronic infections, toxic agents), or autoimmune reactions
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Chronic inflammation -- features?
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Mononuclear cells (macrophages, lymphocytes), tissue destruction, connective tissue healing (fibrosis)
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Eosinophils -- features
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Seen in allregies and parasitic infxns. High IgE titer. "NAACP" - neoplasm, allergies, asthma, collagen vascular dz, parasites
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Mast cells (in inflammation)
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Chronic inflammation. Releases Histamine --> could lead to Anaphylaxis
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Granulomatous Inflammation (cause, characteristics)
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Due to infxns, foreign bodies, sarcoidosis, TB. Accumulation of epithelial-like cells from cell mediated immune response. Outside are lymphocytes stimulating macrophages (IFN-gamma mediated). Giant cells. Central-necrotic tissue.
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Explain Systemic effect of inflammation - related to fever
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IL-1& TNF stimulate COX2 induction --> PGE2 production in hypothalamus --> altered hypothalamic set point --> fever
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Leukocytosis
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Increase in bloodstream to fight organisms
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Neutrophilia
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Bacterial infxn with left shift (increase in immature PMN's)
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Leukomoid Rxn
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WBC > 50K. Consider Pertussis or Leukemia
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Lymphocytosis (where?)
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Usually viral
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Eosinophilia
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NAACP -- neoplasm, allergies, asthma, collagen vascular dz, parasites
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Acute phase proteins -- systemic effects of inflammation
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CRP (C-reactive protein), Fibrinogen, SAA (serum amyloid A), ESR, platelets
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Sepsis (cause & clinical)
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occurs from high levels of TNF usually during bacterial infxn. Profound Hypotension due to vasodilation, high cardiac output state, tachycardia, warm/flush skin, DIC, ARDS
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Post-infarct changes -- 0-24hrs
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Nuclear pyknosis, myocardial hypereosinophilia, early coagulative necrosis (how many days after infarct?)
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Post-infarct changes -- 1-3 days
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Coagulative necrosis progresses, neutrophil infiltration and liquefaction of dead tissue (how many days after infarct?)
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Post-infarct changes -- 3-10 days
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Macrophage infiltration, necrotic tissue phagocytosed (how many days after infarct?)
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Post-infarct changes -- 10-30 days
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Necrosis replaced by granulation tissue (fibroblasts & angioblasts proliferate, collagen deposition) (how many days after infarct?)
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Post-infarct changes -- > 1 month
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Fibroblasts and new blood vessels recede, collagenous scar becomes progressively acellular and more dense. Scar maturation and remodeling (how many days after infarct?)
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Complication of 2nd intention healing
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Keloid scar due to excess collagen deposition (common in African Americans)
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Keloid scar (cause and common race)
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due to excess collagen deposition. Common in African americans
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Neoplasm (def)
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Abnormal proliferation of cells that is excessive, uncontrolled, irreversible and heritable
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-carcinoma
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Epithelial malignant neoplasm
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-sarcoma
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Mesenchymal malignant neoplasm. Mesenchymal tissue -- fibroblasts, adipocytes, smooth/skeletal muscle, bone, cartilage, blood vessels
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Difference b/w primary and mestastatic tumor?
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Single lesion vs. multiple lesions
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Teratoma
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Multiple germ layer (ectoderm, endoderm, mesoderm)
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Blastoma
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immature cells (neoplasia)
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Carcinosarcoma
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both malignant epithelial and mesenchymal tissues
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Polyp
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Mass that projects from surface
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Polyp -- sessile vs. pendunculated
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Sessile (broad base) is worse than Pendunculated (slender stalk)
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Hamartoma
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Disorganized mature tissue in site where it arises
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Choristoma
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Mature tissue in site not normally seen
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Dysplasia
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Abnormal growth pattern of tissue. Still within epithelium, not necessarily whole width of epi. Increased risk of cancer
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Carcinoma in situ
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Neoplasm still confined to BM. Full thickness dysplasia. Confined to glands without invasion into lamina propria or muscularis mucosa in glandular epithelium (intestines)
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2 important features of Malignancy
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ability to invade and metastasize
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What is the basis for tumor grading?
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Differentiation. Morphologic features including differentiation, number of mitoses, necrosis. Low, Med, high grade
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Malignancy related to maturity of cell
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More immature the cell, the more malignant
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What is the reaction of stroma to cell in neoplasia
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Desmoplasia in malignancy
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What is the basis for tumor staging?
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Level of local invasion. TNM -- tumor size, nodal involvement, metastasize
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Tumor grading vs. staging
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Differentiation vs. local invasion
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3 routes of Metastasis
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1. Direct seeding of surrounding structures; 2. Lymphatic spread; 3. Hematogenous
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Lymphatic spread in Metastasis
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Route of most carcinomas. Enter lymph nodes and grow there. Sentinal node = 1st draining node
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What is the Metastatic route for carcinomas? Sarcomas?
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lymphatic spread vs. Hematogenous spread
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What is Sentinal node? (ex)
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1st draining node in Mestastasis - lymphatic spread. Axillary node for breast cancer
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Paraneoplastic syndrome -- ex.
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Symptoms or biochemical disturbances caused by tumors but not because of invasion. (like hormones) Small cell carcinoma --> Cushing's, SIADH, Eaton lambert syndrome / Lung SCC --> hypercalcemia / Thymoma --> Myasthenia gravis / Pancreatic carcinoma --> migratory thrombophlebitis
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Cachexia
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Fat and muscle wasting due to excess cytokines (TNF suppresses hunger area in hypothal)
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Nasopharyngeal cancer
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Highest incidence in Asian countries. Related to EBV exposure
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Hepatocellular cancer
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Highest incidence in SE Asia. Related to hepatitis B, alfatoxins
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FAP - Familial Adenomatous Polyposis (cause, tx)
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Hundreds of polyps in colon. Caused by mutation of the APC gene on chromsoms 5q21 (Beta-catenin accumulates causing uncontrolled growth of adenomas). 100% will transform to cancer. Must have prophylactic collectomy
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Li Fraumeni syndrome
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P53 responsible for cell cycle arrest and apoptosis following DNA damage --> inherited P53 mutation. Predisposes to many different cancers at early age.
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BRCA1 / BRCA2
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Tumor suppressor gene. BRCA1 - mc in families with breast & ovarian cancer / BRCA2 - mc in families with male and female breast cancer
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HNPCC (cause)
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Mismatch repair. Increased risk of colon, endometrial, ovarian cancer. AR
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Xeroderma Pigmentosum
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Nucleotide excision repair. Can't repair thymine dimers caused by UV exposure
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Defective DNA repair syndromes
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Usually AR (except HPNCC which is AD). "Two hit hypothesis" -- need mutations or deletions in both alleles
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