Pathophysiology (Quiz 1)

Front 1

Pathophysiology
7/1/07

Back 1

Pathophysiology
7/1/07

Front 2

Definition:
1.Hypertrophy
2.What causes Hypertrophy
3.Hyperplasia
4.Give examples of hyperplasia

Back 2

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;

Front 3

1.Define Atrophy:
2.What are the causes of atrophy?
3.Define Metaplasia
4.It is caused by?
5.Usually seen where?

Back 3

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.

Front 4

1.Definition of Dysplasia
2.What causes cell injury?
3.Define Hypoxia

Back 4

1.Abnormal growth pattern
2.Hypoxia, physical and chemical agents, infectious agents, immunological damage, poor nutrition
3.Decreased oxygen.

Front 5

1.Define Reperfusion Injury
2.Define apoptosis:
3.What are the cell changes involved

Back 5

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

Front 6

1.Define Edema
2.What are the 2 classifications of edema
3.Most common cause of edema

Back 6

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

Front 7

1.What are the sites involved in edema

Back 7

1.a.Skin- pitting edema
b.Pulmonary edema
c.Cerebral edema
d. Body cavities
e.Anasarca (generalized edema)

Front 8

1. What are the predisposing factors of Thrombosis
2. Thrombus locations

Back 8

1.a.Endothelial injury
b.altered blood flow
c.Blood Hypercoagulability
2.Arteries
Veins
Heart chambers
Valves
Aneurysms

Front 9

1.Fate of Thrombi:
2.In pulmonary embolism, 95% arise in ____
3.In systemic embolism, 85% arise in _____

Back 9

1.Propagation (grow),Embolization(move), Dissolution(disappear), Organization/Recanalization.
2. Leg veins
3. Heart (left ventricle or atrium

Front 10

1.Causes of infarction:

Back 10

1.Thromboembolism is most common cause, plaque hemorrhage, torsion of vascular pedicles, entrapment of bowel-hernia.

Front 11

1.What is shock:
2.What are the stages of shock:

Back 11

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

Front 12

1. 3 major types of shock
2.Shock pathophysiology

Back 12

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.

Front 13

1. Define acute inflammation
2. Define chronic inflammation

Back 13

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.

Front 14

1.What are the initiators of inflammation:

Back 14

1.Infections, trauma, chemical and physical agents (endogenous and exogenous), tissue necrosis, immune reactions, foreign bodies.

Front 15

1.What are the mediators of Vasodilation
2....increased permeablitiy
3...chemotaxis along chemical gradient.
4....leukocyte activation

Back 15

1.Histamine and nitric oxide
2.Histamine and Tumor necrosis factor
3. Phospholipase C
4. Phospholipase A2

Front 16

What are the clinicopathologic outcomes of acute inflammation

Back 16

-complete resolution
-healing with fibrosis
-abcess formation
-Progression to chronic inflammation

Front 17

1.In chronic inflammation, what are the predominating cells
2. What is the key cell

Back 17

1.Lymphocytes, plasma cells, macrophages
2.Tissue macrophage: responds to chemoattractant, activation by interferon-y and endotoxin (increase metabolism and pharocytosis).

Front 18

1.Patterns in inflammation:
2.What are the 2 types of Granulomatous inflammation
3.How granuloma is formed

Back 18

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.

Front 19

1.What are the inciting agents in granuloma formation
2. Diagnosis of granuloma:

Back 19

1. Bacteria, Fungi, parasites, inorganic metals/dust, foreing bodies
2.Special stains
Culture
Polarized microscopy
Serum serology or skin test

Front 20

1. What are the systemic effects of acute inflammation.

Back 20

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.

Front 21

1.What are the components of repair

Back 21

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.

Front 22

1.Characteristics of neoplasms
2.What are the 2 key cell components of neoplasms.

Back 22

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.

Front 23

Malignant Tumors
1.Define Sarcomas
2.Define Carcinomas

Back 23

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.

Front 24

1.Define Anaplasia:
2.Define Dysplasia:

Back 24

1. Lack of differentiation, a morphologic trait of malignancy
2.An abnormal disorderly, non-neoplastic proliferation.

Front 25

1.What are the basic steps in invasion (carcinomas)

Back 25

1.a.Invasion of basement membrane
b. Attachment of cells to extracellular matrix (ECM)
c. Degradation of ECM
d. Tumor cell migration