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25 Cards in this Set

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Pathophysiology
7/1/07
Pathophysiology
7/1/07
Definition:
1.Hypertrophy
2.What causes Hypertrophy
3.Hyperplasia
4.Give examples of hyperplasia
1.Increased cell size
2. result of increased demands:mechanical, compensatory, hormones, drug induced.
3.Increased cell number (if capable of dividing)
4.hepatocyte after hepatectomy;
1.Define Atrophy:
2.What are the causes of atrophy?
3.Define Metaplasia
4.It is caused by?
5.Usually seen where?
1.Reduced size, cytoplasmic organelles
2.Denervation, disuse, pressure, aging, hormones, nutrition
3.Transformation of cell type
4.inflammation and irritation
5.in epithelium; mesenchymal tissue less common.
1.Definition of Dysplasia
2.What causes cell injury?
3.Define Hypoxia
1.Abnormal growth pattern
2.Hypoxia, physical and chemical agents, infectious agents, immunological damage, poor nutrition
3.Decreased oxygen.
1.Define Reperfusion Injury
2.Define apoptosis:
3.What are the cell changes involved
1.Oxygen restored (but reversibly damaged cells proceed to die.
2.Programmed cell death.
3.a.Caspases activated
b.Cells shrinks and break up
c.NO INFLAMMATORY RESPONSE
1.Define Edema
2.What are the 2 classifications of edema
3.Most common cause of edema
1.Distance of equilibrium between hydrostatic pressure in capillaries and plasma oncotic pressure or abnormal vessels.
2.a.Inflammatory
b.Non-inflammatory
3.back pressure in veins.
Other causes: decreased colloid osmotic pressure; lymphatic obstruction
1.What are the sites involved in edema
1.a.Skin- pitting edema
b.Pulmonary edema
c.Cerebral edema
d. Body cavities
e.Anasarca (generalized edema)
1. What are the predisposing factors of Thrombosis
2. Thrombus locations
1.a.Endothelial injury
b.altered blood flow
c.Blood Hypercoagulability
2.Arteries
Veins
Heart chambers
Valves
Aneurysms
1.Fate of Thrombi:
2.In pulmonary embolism, 95% arise in ____
3.In systemic embolism, 85% arise in _____
1.Propagation (grow),Embolization(move), Dissolution(disappear), Organization/Recanalization.
2. Leg veins
3. Heart (left ventricle or atrium
1.Causes of infarction:
1.Thromboembolism is most common cause, plaque hemorrhage, torsion of vascular pedicles, entrapment of bowel-hernia.
1.What is shock:
2.What are the stages of shock:
1.results from systemic hypoperfusion with resultant tissue and cellular hypoxia often culminating in multi-system organ failure and death.
2.a.Non progressive stage
b.Progressive stage
c.Irreversible stage
1. 3 major types of shock
2.Shock pathophysiology
1. a. Cardiogenic: Failure of myocardial pump
b.Hypovolemic: Inadequate blood or plasma volume
c.Septic: Peripheral vasodilation and pooling.
2. Myocardial dysfunction, Hypotension, perfusion, hypoxia, DIC, renal failure, ARDS, Coma, death.
1. Define acute inflammation
2. Define chronic inflammation
1.Acute inflammation
-Short duration, characterized by tumor, rubor, dolor, calor, decreased funtion
2. Chronic inflammation:
-Longer duration (days to weeks); mononuclear cell infiltrate; new capillaries and fibrosis.
1.What are the initiators of inflammation:
1.Infections, trauma, chemical and physical agents (endogenous and exogenous), tissue necrosis, immune reactions, foreign bodies.
1.What are the mediators of Vasodilation
2....increased permeablitiy
3...chemotaxis along chemical gradient.
4....leukocyte activation
1.Histamine and nitric oxide
2.Histamine and Tumor necrosis factor
3. Phospholipase C
4. Phospholipase A2
What are the clinicopathologic outcomes of acute inflammation
-complete resolution
-healing with fibrosis
-abcess formation
-Progression to chronic inflammation
1.In chronic inflammation, what are the predominating cells
2. What is the key cell
1.Lymphocytes, plasma cells, macrophages
2.Tissue macrophage: responds to chemoattractant, activation by interferon-y and endotoxin (increase metabolism and pharocytosis).
1.Patterns in inflammation:
2.What are the 2 types of Granulomatous inflammation
3.How granuloma is formed
1.Serofibrinous and Granulomatous inflammation
2.Immune and foreign body
3. offending antigen is poorly digestible; t cells secrete IF-y aand macrophages become epitheloid, these attemp to wall off offending agent.
1.What are the inciting agents in granuloma formation
2. Diagnosis of granuloma:
1. Bacteria, Fungi, parasites, inorganic metals/dust, foreing bodies
2.Special stains
Culture
Polarized microscopy
Serum serology or skin test
1. What are the systemic effects of acute inflammation.
1.a.Acute phase changes: e.g. fever, anorexia, hypotension
; It is measure in serum.(increased CRP, fibrinogen, alpha1antitripsin, C3;dec. albumin)
b.Leukocytosis (leads to left shift)
c.Leukopenia e.g. viral infx.
1.What are the components of repair
1. a.Removal of debris
b.Angiogenesis: new vessels
c.Recruitment and activation of fibroblast
d.Deposition of extracellular matrix(ECM) and collagen
e.Remodeling of fibrous tissue.
1.Characteristics of neoplasms
2.What are the 2 key cell components of neoplasms.
1.Abnormal mass of tissue, uncoordinated, purposeless growth, preys on host, autonomous.
2. a. Parenchyma (tumor cells themselves)
b.Supportive Stroma: provides blood supply, "scirrhous" nature.
Malignant Tumors
1.Define Sarcomas
2.Define Carcinomas
1.Malignancies of mesenchyme (soft tissue, cartilage, bone, muscle)
2.Carcinomas: Malignancies of epithelial origin. may be further qualififed according to origin:
-adenocarcinoma= glandular origin
-squamous cell carcinoma= squamous cells.
1.Define Anaplasia:
2.Define Dysplasia:
1. Lack of differentiation, a morphologic trait of malignancy
2.An abnormal disorderly, non-neoplastic proliferation.
1.What are the basic steps in invasion (carcinomas)
1.a.Invasion of basement membrane
b. Attachment of cells to extracellular matrix (ECM)
c. Degradation of ECM
d. Tumor cell migration