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Clinical Foundations > pathology > Flashcards

pathology Flashcards

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
Q

Causes of increased hydrostatic pressure

A

Mainly caused by disorders that impair venous return.

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26
Q

What does reduction of plasma albumin concentrations lead to

A

Decreased colloid osmotic pressure and loss of fluid from the circulation

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27
Q

Nephrotic syndrome

A

Most important cause of albumin loss is from th blood.

Either by sever liver disease or protein malnutrition

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28
Q

Route fluid should normally take if things are working properly (ie no blockage)

A

Fluid drawn out of interstitial fluid to the lymph to the lymph duct to blood

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29
Q

What effect does excessive salt retention have to result in edema

A

Increases hydrostatic pressure and reduces plasma osmotic pressure.

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30
Q

Hemorrhage

A

Extravasation of blood from vessels, most often the result of damage to blood vessels or defective clot formation

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31
Q

Hematoma

A

Hemorrhage that accumulates in a tissue.

Results can range from trivial to fatal

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32
Q

Hemarthrosis

A

Bleeds in the joints

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33
Q

Petechiae

A

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

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34
Q

Purpura

A

Slightly larger hemorrhages
3-5 mm
Can result from same disorders as petichae as well as trauma, vasculitis, and increased vascular fragility

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35
Q

Eccymoses

A

Larger 1-2. Cm subcutaneous hematoma
Bruises
Extravasated red blood cells are phagocytosed and degraded by macrophages.

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36
Q

What determines the clinical relevance of hemorrhages

A

Volume of blood being lost

Site of hemorrhage

37
Q

Normal hemostasis

A

Series of regulated processes that culminate in the formation of a blood clot that limits bleeding from an injured vessel

38
Q

Thrombosis

A

Formation of blood clot in non traumatized , intact vessels

39
Q

What does hemostasis involve

A

Platelets
Clotting factors
Endothelium

40
Q

Sequence of events leading to hemostasis

A 
Arteriolar vasoconstriction
Primary hemostasis (platelet plug)
Secondary hemostasis (deposition of fibrin)
Clot stabilization and resorption
41
Q

Endothelium

A

Potent endothelium derived vasoconstrictor

42
Q

Arteriolar vasoconstriction

A

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
Q

Neoplasia

A

New growth

Transformed because they continue to replicate regardless of regulatory influences that control normal cells

44
Q

Benign tumor

A

Microscopic and gross characteristics remain localized

45
Q

Malignant tumor

A

Lesion can invade and destroy adjacent structures and metastasize

46
Q

Two components of tumors

A

Parenchyma (neoplasticism cells)
Stroma (supporting, host derived non neoplastic, made up of connective tissue, blood vessels and host derived inflammation cells

47
Q

Parenchyma of neoplasm function

A

Largely determines its biologic behavior

Where tumor derives its name

48
Q

Stoma funciton

A

Crucial to the growth of the neoplasm. Carries blood support

49
Q

Nomenclature benign tumors

A

Suffix oma to cell type from cell type tumor arises

50
Q

Adenoma

A

Benign epithelial neoplasms that produce gland like structure and those derived from glands but lacking a glandular growth pattern

51
Q

Paillomas

A

Benign epithelial neoplasms growing on any surface that produce microscopic or macroscopic fingerlike fronds

52
Q

Polyp

A

Mass that projects above mucosal surface to form a macroscopically visible structure

53
Q

Sarcoma

A

Malignant neoplasms arising in solid mesenchymal tissues or its derivatives

54
Q

Leukemia’s and lymphomas

A

Malignant neoplasms arising from mesenchymal cells of the blood
Leukemia is blood based
Lymphoma is more solid tissue

55
Q

Carcinomas

A

Malignant neoplasms of epithelial cells

56
Q

Adenocarcinomas

A

Carcinomas that grow in a glandular pattern

57
Q

Squamous cell carcinomas

A

Carcinomas that produce squamous cells

58
Q

Three features benign and malignant tumors can be distinguished

A

Differentiation and anaplasia
Local invasion
Metastasis

59
Q

Differentiation

A

Extent to which neoplasms resemble their parenchyma cells of origin both morphologically and functionally

60
Q

Anaplasia

A

Lack of differentiation

61
Q

Anaplastic

A

Tumors composed of undifferentiated cells

62
Q

Anaplastic morphological features

A

Pleomorphism
Nuclear abnormalities
Atypical mitoses
Loss of polarity

63
Q

Pleomorphism

A

Variation in size and shape

64
Q

Capsule of benign tumors

A

Rim of compressed fibrous tissue. Largely made of extracellular matrix deposited by stromatolites cells

65
Q

Metastasis

A

Spread of tumor to sites that are physically discontinuous with primary tumor and unequivocally marks tumor as malignant

66
Q

Metastasis pathways

A

Seeding within body cavities
Lymphatic spread
Hematogenous spread

67
Q

Typical metastasis pathway of carcinomas vs sarcomas

A

Lymphatic spread is favored by carcinomas

Hematogenous spread is favored by sarcomas

68
Q

Pattern of lymph node involvement depends on

A

Site of primary neoplasm and natural pathways of local lymphatic drainage

69
Q

Paraneoplastic syndromes

A

Symptom complexes in cancer patients that cannot be explained by local invasion, metastasis, or elaboration of hormones

70
Q

Hypercalcemia and paraneoplastic syndrome

A

Can be due to tumor production of pth related protein

71
Q

Cushing syndrome and paraneoplastic syndrome

A

Arising as parneoplastic phenomenon usually related to ectopic production of acth or acth like polypeptides by cancer cells.

72
Q

Grading

A

Based on degree of tumor cells and sometimes on number of mitoses or architectural features

73
Q

Staging

A

Based on size of primary tumor, extent of spread to regional lymph nodes, and the presence or absence of distant metastases

74
Q

Environmental influences of cancer

A 
Smoking
Alcohol consumption
Reproductive history (estrogen stimulation)
Diet
Infectious agents
75
Q

Acquired conditions that predispose cancer

A

Chronic inflammation
Immunodeficiency
Precursor lesions

76
Q

Precursor lesions

A

Localized disturbances of epithelial differentiation that are associated with an elevated risk for developing carcinoma

77
Q

Oncogenes

A

Genes that induce a transformed phenotype when expressed in cells by promoting increased cell growth.

78
Q

Oncoproteins

A

Encoded oncogenes that serve functions similar to counterparts but are constitutively active.

79
Q

RAS

A

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
Q

ABL

A

Proto oncoprotein that has tyrosine kinase activity that is dampened by internal negative regulatory domains.
Activates growth factor signaling pathways

81
Q

MYC

A

Functions by activating the transcription of other genes

Genes activate include growth promoting genes whose products drive cells into the cell cycle

82
Q

Cell cycle oncogenes

2 categories

A

Gain of function mutations to promote cell cycle

Loss of function mutations (of inhibitors) promote cell cycle

83
Q

Tumor suppressor genes

A

Apply brakes to cell proliferation.
Disruptions of these genes render cells refractory to growth inhibitions and mimics growth promoting effects of onco genes

84
Q

RB

A

Negative regulator of the cell cycle - directly or indirectly inactivated in most human cancers
First tumor suppressor gene to be discovered

85
Q

Two hit hypothesis

Familial vs sporadic

A

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
Q

TP53

A

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
Q

Tumor cells evasion of cell death mechanisms

A

Loss of TP53 function

Overexpression of anti apoptosis members of bcl2 family

88
Q

Quiescence

A

Activation of temporary cell cycle arrest

89
Q

Senescence

A

Induction of permanent cell cycle arrest

Clinical Foundations (10 decks)

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