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pathology Flashcards

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1
Q

etiology

A

causes of disease

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2
Q

pathogenesis

A

mechanism of disease

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3
Q

morphologic changes

A

structural alterations induced in the cells and organs that are characteristic of a disease or diagnostic of an etiologic process

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4
Q

clinical manifestations

A

functional consequences of morphological changes

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5
Q

etiology can be be broken down into two classes

A

genetic

acquired (environmental)

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6
Q

evolution of disease

A

etiology
pathogenesis
morphologic changes
clinical manifestations

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7
Q

pathogenesis breakdown

A

the sequence of cellular, biochemical, and molecular events that follow the exposure of cells or tissues to an injurious agent.

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8
Q

progress

A

clinical course and outcome

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9
Q

symptom

A

departure from normal function, appearance, or sensation. experienced by patient and indicitive of dsease. subjective

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10
Q

sign

A

any abnormally indication of disease. discoverable by clinician at examination of patient. objective

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11
Q

is a sign or symptom more objective

A

sign

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12
Q

sign or symptom, skin rash

A

sign

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13
Q

do you palpatate a sign or a symptom

A

sign

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14
Q

Hypermedia

A

Active process resulting from arteriolar dilation and increased blood inflow. Occurs at sites of inflammation or in exercising skeletal muscle.
Tissues are redder than normal because engorgement with oxygenated blood.

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15
Q

Congestion

A

Passive process resulting from impaired outflow of venous blood from a tissue.
Have n=abnormal blue red color that stems from the accumulation of deoxygenated hemoglobin.

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16
Q

Long standing chronic congestion

A

Inadequate tissue perfusion and persistent hypoxia may lead to parenchyma cell death and secondary tissue fibrosis. Elevated intravascular pressures may cause edema or rupture the capillaries

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17
Q

Edema

A

Accumulation of interstitial fluid within tissues.

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18
Q

Ansarca

A

Severe generalized edema marked by profound swelling of subcutaneous tissue and accumulation of fluid in body cavities

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19
Q

Fluid movement between vascular and interstitial spaces is governed by

A

Vascular hydrostatic pressure

Colloid osmotic pressure.

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20
Q

Increased movement of water into the interstitium

A

Increased hydrostatic pressure or decreased colloid osmotic pressure

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21
Q

How is excess edema fluid removed

A

By lymphatic drainage and returned to the bloodstream by way of the thoracic duct

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22
Q

Transudate

A

Protein poor edema fluid that accumulates because of increased hydrostatic pressure or reduced intravascular colloid

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23
Q

Exudate

A

Protein rich inflammatory edema fluid

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24
Q

Non inflammatory causes of edema

A

Increased hydrostatic pressure
Reduced plasma osmotic pressure
Lymphatic obstruction
Sodium retention

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25
Causes of increased hydrostatic pressure
Mainly caused by disorders that impair venous return.
26
What does reduction of plasma albumin concentrations lead to
Decreased colloid osmotic pressure and loss of fluid from the circulation
27
Nephrotic syndrome
Most important cause of albumin loss is from th blood. | Either by sever liver disease or protein malnutrition
28
Route fluid should normally take if things are working properly (ie no blockage)
Fluid drawn out of interstitial fluid to the lymph to the lymph duct to blood
29
What effect does excessive salt retention have to result in edema
Increases hydrostatic pressure and reduces plasma osmotic pressure.
30
Hemorrhage
Extravasation of blood from vessels, most often the result of damage to blood vessels or defective clot formation
31
Hematoma
Hemorrhage that accumulates in a tissue. | Results can range from trivial to fatal
32
Hemarthrosis
Bleeds in the joints
33
Petechiae
Minute hemorrhages in skin, 1-2 mm in diameter mucous membranes or serous always surfaces. Causes include low platelet count, defective platelet function, loss of vascular wall support
34
Purpura
Slightly larger hemorrhages 3-5 mm Can result from same disorders as petichae as well as trauma, vasculitis, and increased vascular fragility
35
Eccymoses
Larger 1-2. Cm subcutaneous hematoma Bruises Extravasated red blood cells are phagocytosed and degraded by macrophages.
36
What determines the clinical relevance of hemorrhages
Volume of blood being lost | Site of hemorrhage
37
Normal hemostasis
Series of regulated processes that culminate in the formation of a blood clot that limits bleeding from an injured vessel
38
Thrombosis
Formation of blood clot in non traumatized , intact vessels
39
What does hemostasis involve
Platelets Clotting factors Endothelium
40
Sequence of events leading to hemostasis
``` Arteriolar vasoconstriction Primary hemostasis (platelet plug) Secondary hemostasis (deposition of fibrin) Clot stabilization and resorption ```
41
Endothelium
Potent endothelium derived vasoconstrictor
42
Arteriolar vasoconstriction
Occurs immediately after injury and markedly reduces blood flow to the area. Mediated by endothelin Effect is transient and bleeding would resume if not for activation of platelets and coagulation factors
43
Neoplasia
New growth | Transformed because they continue to replicate regardless of regulatory influences that control normal cells
44
Benign tumor
Microscopic and gross characteristics remain localized
45
Malignant tumor
Lesion can invade and destroy adjacent structures and metastasize
46
Two components of tumors
Parenchyma (neoplasticism cells) Stroma (supporting, host derived non neoplastic, made up of connective tissue, blood vessels and host derived inflammation cells
47
Parenchyma of neoplasm function
Largely determines its biologic behavior | Where tumor derives its name
48
Stoma funciton
Crucial to the growth of the neoplasm. Carries blood support
49
Nomenclature benign tumors
Suffix oma to cell type from cell type tumor arises
50
Adenoma
Benign epithelial neoplasms that produce gland like structure and those derived from glands but lacking a glandular growth pattern
51
Paillomas
Benign epithelial neoplasms growing on any surface that produce microscopic or macroscopic fingerlike fronds
52
Polyp
Mass that projects above mucosal surface to form a macroscopically visible structure
53
Sarcoma
Malignant neoplasms arising in solid mesenchymal tissues or its derivatives
54
Leukemia’s and lymphomas
Malignant neoplasms arising from mesenchymal cells of the blood Leukemia is blood based Lymphoma is more solid tissue
55
Carcinomas
Malignant neoplasms of epithelial cells
56
Adenocarcinomas
Carcinomas that grow in a glandular pattern
57
Squamous cell carcinomas
Carcinomas that produce squamous cells
58
Three features benign and malignant tumors can be distinguished
Differentiation and anaplasia Local invasion Metastasis
59
Differentiation
Extent to which neoplasms resemble their parenchyma cells of origin both morphologically and functionally
60
Anaplasia
Lack of differentiation
61
Anaplastic
Tumors composed of undifferentiated cells
62
Anaplastic morphological features
Pleomorphism Nuclear abnormalities Atypical mitoses Loss of polarity
63
Pleomorphism
Variation in size and shape
64
Capsule of benign tumors
Rim of compressed fibrous tissue. Largely made of extracellular matrix deposited by stromatolites cells
65
Metastasis
Spread of tumor to sites that are physically discontinuous with primary tumor and unequivocally marks tumor as malignant
66
Metastasis pathways
Seeding within body cavities Lymphatic spread Hematogenous spread
67
Typical metastasis pathway of carcinomas vs sarcomas
Lymphatic spread is favored by carcinomas | Hematogenous spread is favored by sarcomas
68
Pattern of lymph node involvement depends on
Site of primary neoplasm and natural pathways of local lymphatic drainage
69
Paraneoplastic syndromes
Symptom complexes in cancer patients that cannot be explained by local invasion, metastasis, or elaboration of hormones
70
Hypercalcemia and paraneoplastic syndrome
Can be due to tumor production of pth related protein
71
Cushing syndrome and paraneoplastic syndrome
Arising as parneoplastic phenomenon usually related to ectopic production of acth or acth like polypeptides by cancer cells.
72
Grading
Based on degree of tumor cells and sometimes on number of mitoses or architectural features
73
Staging
Based on size of primary tumor, extent of spread to regional lymph nodes, and the presence or absence of distant metastases
74
Environmental influences of cancer
``` Smoking Alcohol consumption Reproductive history (estrogen stimulation) Diet Infectious agents ```
75
Acquired conditions that predispose cancer
Chronic inflammation Immunodeficiency Precursor lesions
76
Precursor lesions
Localized disturbances of epithelial differentiation that are associated with an elevated risk for developing carcinoma
77
Oncogenes
Genes that induce a transformed phenotype when expressed in cells by promoting increased cell growth.
78
Oncoproteins
Encoded oncogenes that serve functions similar to counterparts but are constitutively active.
79
RAS
Most commonly mutated oncogene in tumors Commonly activated by point mutations which interfere with breakdown of GTP (which is essential to inactivate RAS). Cell is forced into continuously proliferation state
80
ABL
Proto oncoprotein that has tyrosine kinase activity that is dampened by internal negative regulatory domains. Activates growth factor signaling pathways
81
MYC
Functions by activating the transcription of other genes | Genes activate include growth promoting genes whose products drive cells into the cell cycle
82
Cell cycle oncogenes | 2 categories
Gain of function mutations to promote cell cycle | Loss of function mutations (of inhibitors) promote cell cycle
83
Tumor suppressor genes
Apply brakes to cell proliferation. Disruptions of these genes render cells refractory to growth inhibitions and mimics growth promoting effects of onco genes
84
RB
Negative regulator of the cell cycle - directly or indirectly inactivated in most human cancers First tumor suppressor gene to be discovered
85
Two hit hypothesis | Familial vs sporadic
In familial cases - children inherit one defective copy of RB gene, other is normal. Then normal RB gene is lost as result of somatic mutation In sporadic cases - both alleles are lost by somatic mutation
86
TP53
Most commonly mutated gene in human cancer P53 is transcription factor that prevents neoplastic transformation by activation of temporary cell Ceylon arrest, permanent arrest, or apoptosis Maintains integrity of genome Mutant allele
87
Tumor cells evasion of cell death mechanisms
Loss of TP53 function | Overexpression of anti apoptosis members of bcl2 family
88
Quiescence
Activation of temporary cell cycle arrest
89
Senescence
Induction of permanent cell cycle arrest

Clinical Foundations (10 decks)

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