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134 Cards in this Set

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