Pathology Test 1

Front 1

acute inflammation

Back 1

*the classic response to any type of injury
*the immediate and early response to an injurious agent.

Front 2

5 things that occur at the injured site of acute inflammation

Back 2

1. swelling
2. redness
3. pain
4. heat
5. loss of function

Front 3

left shift

Back 3

immature white blood cells.
neutrafils on a blood smear mean an infection is going on
10-12k normal wbc count

Front 4

erysipleas

Back 4

involves the skin and lymphatic portions. blood cultures will be negative until treated if not treated then it will enter the blood stream.

Front 5

leukocyte, extraversion, phagocytosis

3 step process in inflammation

Back 5

1. margination, rolling and adhesion
2. trasmigration across endothelium,
3. migration toward chemotactic stimulus

Front 6

acute inflammation may have one of the four outcomes

Back 6

1. complete resoultion
2. abscess formation
3. fibrosis
4. chronic inflammation

Front 7

steps involved in phagocytosis

Back 7

1. recognition and attatchment to particle
2. engulfment with phagocytoic vacule
3. killing of degradation of the ingested material.

Front 8

neutrophil

Back 8

*1st line of defense. first thing to go and meet the pathogen.
* most numerous wbc in the circulating blood, 60 to 70% of the wbc count.

Front 9

the steps and response of the neutrophil to injury and infection

Back 9

1. margination-rolling-adhesion
2. transmigration across the edothelium
3. migration toward chemotactic stimulus.

Front 10

histamine

chemical mediator

Back 10

Dialation of the arterioloes

Front 11

serotonin

chemical mediator

Back 11

diliation of arterioloes

Front 12

Complement components; C3a, C5a, C4a

Back 12

Produced by the liver
C3a helps ingulf bacteria.
All increase vascular permeability and cause vasodilation by stimulating the release of histamine from mast cells.

Front 13

complement components; C5a

Back 13

chemotactic for neturophils, increases leukocyte adhesion.

Front 14

complement components; C3b, C3bi

Back 14

act as opsoninis that favor phagocytosis

Front 15

bradykinin

Back 15

produced by the liver
increases vascular permeability, smooth muscle contraction dilation of blood vessels, participates in pain sensation.

Front 16

leukotrienes

Back 16

vasoconstriction, bronchospasm, increased vascular permeability

Front 17

prostaglandins

Back 17

vasodialation, potentiate edema

Front 18

thromboxane

Back 18

vasoconstriction, platelet aggregation

Front 19

prostacyclin

Back 19

vasodilation, inhibits platelet aggregation

Front 20

exudate

Back 20

an inflammatory extravascular fluid that has high protein concentraion, much cellular debris, and a specific gravity > 1.020

Front 21

transudate

Back 21

a fluid with low protein content and a specific gravity of < 1.012

Front 22

purulent exudate (pus)

Back 22

exudate right in leukocytes and parenchymal cell debris

Front 23

edema

Back 23

denoates an excess of fluid in the interstitial or serous cavities.

Front 24

cytokines

Back 24

proteins produced by many cell types that alter or modulate the function of other cell types

Front 25

cytokines produced by mononuclear phagocytes are often called...

Back 25

monkines

Front 26

cytokines produced by lymphocytes are often called..

Back 26

lymphokines

Front 27

interleukins (IL)

Back 27

represent a broad family of cytokines that act primarily on leukocytes

Front 28

chemokines

Back 28

cytokines that share the ability to stimulate leukocyte movement (chemokinesis) and directed movement (chemotaxis)

Front 29

Summary of the acute inflammatory response

patterns of inflammation

Back 29

*increased blood flow to the injured area
*slowing of blood flow at area of injury
* Increased vascular permability
*leukocyte migration to area
*phagocytosis of offending agent
*potential tissue damage
*resortoration of tissue structure and function.

Front 30

serous

Back 30

blister from being bitten from a fire ant
occurs at the dermal/epidermal function

Front 31

fibrinous

Back 31

huge gaps between cells.
forms around the heart or around the pericardial sac

Front 32

outcomes of acute inflammation

Back 32

1. complete resolution
2. abscess formation
3. progression to chronic inflammation
4. Healing by connective tissue replacment (fibrosis)

Front 33

complete resolution

Back 33

neutralization and spontaneous decay of the chemical mediators, with subsequent return of normal vascular permeability, cessation of leukocytic infiltration; death of neutrophils, and finallay removal of edema fluid and protein, leukocytes, forgein agents and necrotic debris from the site.

Front 34

absess formation

Back 34

occurs with pyogenic organisms, cellular debris, protein aceous material, low pH (very acidic)

Front 35

healing by connective tissue replacement (fibrosis)

Back 35

occurs after siginificant tissue destruction in tissues that do not regenerate, or when there is abundant fibrin exudation. Also occurs in tissues or serous cavities whent eh fibrinous exudate cannot be adequately absorbed.

regeneration, scarring

Front 36

progression to chronic inflammation

Back 36

occurs when the acute inflammatory response cannot be resolved, owing to the persistence of the injurious agent or to some interference with the normal process of healing.

Front 37

chronic inflammation

Back 37

inflammation of prolonged duration (weeks, months, years) in which active inflammation, tissue destruction, and attemps to repair are proceeding simultaneously.

Front 38

chronic inflammation can arise under the following conditions

Back 38

1. persistent infection
2. prolonged exposure to potentially toxic agents
3. autoimmunity

Front 39

persistant infection

Back 39

a ganulomous reaction pattern is usually seen

Front 40

prolonged exposure to potentially toxic agents

Back 40

agents are non-degradable inanimate material

Front 41

autoimmunity

Back 41

autoimmue diseases that produce autoantigens that evoke a self-perpetuating immune response
Cells and activites involved= mononuclear cell infilitrate, tissue distruction, and connective tissue replacement

Front 42

lymphocytes

Back 42

are mobilized in non-immune mediated inflammatory reactions. lymphocytes of varying types use adhesion molecules and are influenced by chemokines to migrate to inflammatory sites. cytokines from activated macrophages, in turn activate lymphocytes, which themselves also produce inflammatory mediators.

Front 43

mast cells

Back 43

widely distributed in connective tissues. . possess receptors for igE antibody. degranulation occurs when antigen binds to IgE molecule that is attatched to mast cell. histamine is released and an anaphylactic reaction occurs.

Front 44

eosinophils

Back 44

have granules that contain major basic protein, a very toxic and injurious agen to parasites and cells.

Front 45

granulomatous inflammation

Back 45

a distinctive pattern of chronic inflammatory reaction in whcih the predominant cell type is the activated macrophage with a modified epithelioid appearance. epithelioid cells fuse to form gian cells.

Front 46

granuloma

Back 46

this is a focal area of granulomatous inflammation. it consists of micrscopic aggregation of macrphages that are transformed into epithelium-like cells (giant cells) surrounded by a collar of lymphocytes and plasma cells.

Front 47

giant cell

Back 47

a lot of macrophages that are fused together

Front 48

2 types of giant cells

Back 48

1. langerhans type
2. foreign body type

Front 49

foreign body type

giant cell

Back 49

nuclei are scattered all over the cytoplasm

Front 50

langerhans type

giant cell

Back 50

looks like a horseshoe and the nuclei are lined up around the edge. can be found in the immunineffective process.

Front 51

2 types of granulomas

Back 51

1. foreign body granuloma
2. immune granuloma

Front 52

foreign body granuloma

Back 52

incited by inert material (eg. suture material)

Front 53

immune granuloma

Back 53

incited by insoluble immogenic material

Front 54

fever

Back 54

fever is a systematic manifestation of inflammation.
mediators cause fever.
fever is one of the most prominent systemic effects of inflammation. fever depends on humoral signals from the body.

Front 55

the major forms of wound healing

Back 55

1. healing by first intention (wounds with opposed edges) by surgical scars
2. healing by second intention (wounds with seperate edges) the edges are too far apart to bring together.

Front 56

steps involved for healing by first intention

Back 56

1. within 24 hrs fibrin clot forms, neutrophils appear at the margins of the incision, mitotic activity begins in the basal layer. epithelial cells from the edges migrate and frow along cut margins.
2. in 3-7 days, epithelial cells fuse at midline beneath the surface scab, neutrophils replaced by macrophages, granulation tissue invades incision space.
3. day 5, incision space is filled with granulation tissue. collagen fibrils begin to bridge the incision. epidermis recovers normal thickness and architecture.

Front 57

healing by second intention

Back 57

the same steps that are in the first intention healing are also involved in the second intention healing but with extensive loss of cells and tissue, surface wounds that create large defects, which must be filled.

Front 58

secondary healing differs from primary healing in the following aspects

Back 58

*if involves muscles: thick scars will be left. the scars are thick because the muscles can not rejuvinate themselves.

1. inflammatory reaction is more intense. more fibrin is present, more necrotic debris and exudate must be removed.
2. much larger amounts of granulation tissues are formed
3. wound contraction also involved in myofibrils.

Front 59

2 types of immunity

Back 59

1. natural immunity (innate)
2. acquired immunity (adaptive)

Front 60

natural immunity (innate)

Back 60

natural protective mechanisms
-epidermis (mechanical layer)
-ciliary movement of bronchial epithelium (physical forces)
- lysozyme (a potent bactericidal agent found in tears)

Front 61

acquired immunity (adaptive)

Back 61

ability of the immune system to recognize and mount a defense against foreign material, bacterial or viral invaders. this response requires;
-antigen/antibody reaction that is amplified
- the body must distinguish self from non-self

Front 62

2 types of cell mediated immunity

Back 62

1. humoral response
2. cellular immunity

Front 63

humoral response

Back 63

effective in finding extracellular infections (bacteria)

Front 64

cellular immunity

Back 64

fights viral infections. combats intracellular infections

Front 65

Cell mediated immunity (CMI) intracellular microbes

Back 65

T helper cells-secrete cytokines
cytotoxic T cells-destroys altered self cells.

Front 66

natural killer cell

Back 66

1st line of defense
lyse cell invaders
no sensization
antibody dependent cell cytotoxicity

Front 67

dendritic cell

Back 67

antigen presenting cell
widely distributed.
Contains class 1 and class 2

Front 68

T Lymphocytes

Back 68

cellular immunity is mediated by thymus-derived (T) lymphocytes. Each T cell is genetically programmed to recognized a specific cell-bound antigen by means of an antigen specific T cell receptor (TCR)

Front 69

T helper cells

Back 69

CD4+ and CD3
T cells are the gate keeper of the immune system.
goes to antigen-presenting cell

Front 70

T cytotoxic cells

Back 70

CD8+ and CD3
destroys infected cells, that have been infected by a virus.
releases cytokines-which cause the cell the burst and destroy
these cells go to infected target cell.

Front 71

B lymphocytes

Back 71

become antibodies.
b cells become plasma cells that secrete antibody when stimulated by antigen and cytokines. immunoglobulins are the mediators of humoral immunity. Immunoglobulin M (IgM) constitues the antigen-binding component of B cells.
Surface antibody attatched to the membrane.

Front 72

effector cells

Back 72

basophils,
eosinophils
NK cell (natural killer)
mast cell

Front 73

eosinophils

Back 73

account for 2-3% of circulating wbc. these cells apear 2-3 days after the neurtophils.
interact with basophils and are prominant in allergic reactions. also participate in the inflammatory response to parasitic infections, and are present in chronic inflammations.

Front 74

basophils

Back 74

account for less than 1% of wbc.
most prominant in allergic reactions mediated by IgE.

Front 75

macrophages

Back 75

macrophages are derived from blood monocytes. appear at the sight of inflammation 3-4 days after the onset of infection or tissue destruction. typically present in chronic inflammation.
capable of phagocytosis, and are active in bacterial killing.
secrete mediators of inflammation (cytokines) that act locally on other cells and the body as a whole.
*Antigen presening cell Ag*
*this cell is required to process and present antigen to immunocompetent T cells. Other antigen presenting cells include langerhan cells, and follicular dendritic cells.

Front 76

Plasma cells

Back 76

make and secrete antibodies: IgG, IgM, IgE, IgA, & IgD

Front 77

types of lymphocytes

Back 77

t lymphocyte
b lymphocyte
macrophage

Front 78

order of appearance in antibody infection

Back 78

1. IgM is the primary response. first antibody present after an infection
2. IgG is part of the secondary response.
*if the person has had the virus before than IgG will be the first to respond*

Front 79

IgG

Back 79

secreted by plasma cells.
abundant, crosses placenta and facilitates phagocytosis.

Front 80

IgM

Back 80

primary response in infection or an immunization.
composed of five units that are held together by a J-chain

Front 81

IgA

Back 81

2 units held together by a J-Chain, found in mucosal secretions (found in any open area, ie nose)

Front 82

IgE

Back 82

mediates allergic and parasitic reactions

Front 83

IgD

Back 83

found only on B cells.

Front 84

antibodies (IgM, IgG, IgA, IgE, IgD)

Back 84

contain a C-terminal end that can attatch to other immune cells and an N terminal endthat binds antigen.

Front 85

antibody production

Back 85

T cell activation of B cells to become antibody secreting plasma cells is required for most antigens (T cell dependent antigens)

Front 86

Class 1 (MHC- major histocompatability complex) antigens

Back 86

Class I antigens are expressed on all nucleated cells and platelets.
found on all somatic cells, but not on macrophage or T Cells.
Class I molecules bind to those peptides derived from viral antigens assembled within the cell. This process proteolytic digestion of protein (ex. viral) transport to ER. Viral protein is association with class I molecules and transported to the cell surface for recognition by cytotoxic T cells.

Front 87

Class II (MHC) antigens

Back 87

Class II antigens are expressed on specific immune cells not on somatic cells.
Class II molecules present exogenous antigens (ex. extracellular microbes) with class II molecules assembled in the ER. This MHC peptide complex is transported to the surface where it can be recognized by T helper cells.

Front 88

major histocompatability complex (MHC)

also known as HLA markers

Back 88

the principle function of the cell surface histocompatability molecues is to bind peptide fragments of foreign proteins for presentation to appropriate antigen specific T cells.

*very important to fight viral infections*

Front 89

primary lymphoid organ

Back 89

thymus

Front 90

-once in the cell, viruses are invisible to the immune system.
-cells of the immune system are derived from stem cells.
-macrophage/dendritic cells can engulf many things.
-CD8+ T cells recognize foreign antigens (AGs) associated with MHC 1.
-mediators affect B cells

Back 90

important info.

Front 91

Asthma

Back 91

extrinsic and intrinsic mast cell activation. mast cell activation has granuales.
with asthma Ige membrane binding is required. and there is mast cell degranulation. .
-Ige membrane binding will clear whatever antigen is present.

Front 92

antigen-antibody reactions

Back 92

antigens contain sites where antibodies can bind. these sites are known as epitopes . more than one antibody can bind to their surface.
-when an immunoglobulins bound to an antigen this is known as antigen-antibody complex.

Front 93

Type I hypersensitivity

Back 93

2 types: 1. systemic 2. local.

type 1 is a rapidly developing immunologic reaction occuring within minutes after the combination of an antigen with antibody bound to mast cells or basophils in individuals previosuly sensitized to the antigen. Ex. asthma, hay fever, anaphylactic shock)

Front 94

hyper-responsive (type 1 hypersensitivity)

Back 94

over response to immune encounters/particular antigens. (location dependent)

Front 95

systemic

type 1 hypersensitivity

Back 95

takes place by antigen injected directly into the bloodstream. ex. the patient is extremely allergic to penacillin and it is given to them in an IV drip.

Front 96

local

type 1 hypersensitivity

Back 96

this is the second type of type 1 hypersensitivity.

local has 2 well defined phases
1. initial response
2. late phase.

Front 97

initial response

local-type 1 hypersensitivity

Back 97

this is characterized by vasodilation, vascular leakage and depending on the location smooth muscle spasm, and/or grandular secreations. these changes begin 5-30 minutes after exposureto an allergen and subside in about 30 minutes.

Front 98

late phase

local-type 1 hypersensitivity

Back 98

begins 2-8 hours later without further exposure and may last several days. this phase is characterized by more intense infilitration of tissues with eosinophils, neutrophils, basophils, monocytes, and CD4+ T cells. the tissue destruction in the form of mucosal epithelial damage also occurs in this phase.

Front 99

Type II hypersensitivity

Back 99

mediated antibodies (IgE or IgM) directed towards antigens present on the surface of cells or other tissue components.

there are 4 types of type II reactions
1. direct lysis
2. opsonization
3.antibody-dependent cell-mediated cytotoxicity
4. antibody mediated cellular dysfunction

Front 100

complement dependent reactions characteristics

Back 100

erthrblastis fiabois

Front 101

direct lysis

Back 101

antibodies against cell antibodies.
antibody (IgM or IgG) reacts with an antibody present on the surface of the cell, causing the activation of complement membrane attack sequence that drills holes through the lipid bilayer.

Front 102

antibody -dependent cell mediated cytotoxicity

type II hypersensitivity

Back 102

this form of antibody mediated cell injury requires cooperation from leukocytes. nonsensitized cells that have Fc receptors kill target cells, coated with low concentration of IgG antibody. cell lysis proceeds without phagocytosis.

Front 103

antibody-mediated cellular dysfunction

Back 103

antibodies that are directed against cell surface receptors impair or dysregulate function without causing cell injury or inflammation.

ex. graves disease-stimulatory hyperthyrodism.

Front 104

Example of type 2 hypersensitivity

Back 104

Rh system. Mother is rH- and the Rh is not compatible with the child Rh+ and the antibodies attack the childs circulation

Front 105

Type III Hypersensitivity

Antigen/Antibody mediated Complex

Back 105

This is also known as immune complex mediated. it is induced by antigen-antibody complexes that produce tissue damage as a result of their capacity to activate the complement system. the toxic reaction is initiated when antigen combines with antibody, whether within the circulation (deposited in cells and tissues and the area lining bloodvessels.)

ex. systemic immune complex disease (SICD)

Front 106

the pathogenesis of systematic immune complex disease can be resolved into three phases

Back 106

1. formation of antigen-antibody complexes in circulation
2. deposition of complexes in various tissues
3. an inflammatory reaction is initiated at dispersed sites throughout the body

Front 107

type IV hypersensitivity (cell mediated)

Back 107

cell-mediated hypersensitivity is initiated by specifically sensitized CD4+ T lymphocytes and involves direct cell cytoxicity mediated by CD8+ T cells.

Front 108

autoimmune disease

criteria

Back 108

-prescense of an autoimmune reaction
-not secendary to tissue damage.

a breakdown of control mechanisms that regulate self-recognition

Front 109

systemic lupus erythematosus

Back 109

this is the failure of the immune system to recognize itself. there is the production of antibodies against self-antigens. T & B Cell activiation.
this is an example of an autoimmune disease.
-There is a malfunction of suppressor T cell function and uncontrolled B lymphocyte proliferation of clones that secrete antobodies.

*T Cells turn against and attack!*

Front 110

Central tolerance

Back 110

deletion of self-reactive T and B cells

Front 111

peripheral tolerance

Back 111

activation induced cell death
T cell mediated suppression.

Front 112

Anti-dsDNA= anti-double stranded DNA. This is an antibody
Anti-SM= histone proteins. this is an antibody

Both of these antibodies are used to diagnose lupus

Back 112

imp. info

Front 113

4 of the 11 criteria that is needed for lupus diagnosis

Back 113

autoantibody directed injury:
1. kidneys
2. joints
3. serosal surface
4. skin
5. red blood cells
6. malar rash
7. discoid rash
8. photosensitivity
9. oral ulcers
10. arthritis

Front 114

M protein

Back 114

antigen. as an amino acid sequence that is similar to AA sequence that is found in heart tissue.

Front 115

Lab abnormalities

Lupus

Back 115

-Lupus prolongs PTT (partial thromboplastin time)- time it takes for blood to clot. The average time is 36 sec. Patients with lupus have prolonged PTT. This happens because lupus patients have antibodies that do not allow the blood to clot.
lupus anticoagulant is a secondary antiphospholipid antibody syndrome.
Prolonged PTT can only be found out in a test tube, and no other way.
The blood inside lupus patient's bodies does clot, but once outside the body it will not clot. Lupus patients are actually at an increased risk for forming blood clots.

Front 116

Lab abnormalities

Lupus

False/Positive test for syphilis

Back 116

this occurs only with lupus patients.

there are antibodies to cardiolipin antigen which are used in the test, which does not allow an accurate reading for syphillis in lupus patients.

Front 117

Severe combine immunodeficiency

Back 117

-defect in lymphoid stem cell in which there is no further differentiation to pre-B or pre-T cell lines. humoral as well as cell mediated immunity is hindered. There are severe life threatening infections that are possible.
-Death usually occurs in infancy unless the patient is placed in strict isolation.
*this is an autosomal recessive disease. it stios at stem cell stage. It stops bc cells are deficient of ADA (adenosine deaminase deoxyadenosine)


**Stops at lymphoid cells on the graph**

Front 118

pathogenisis

Back 118

recurrent severe infections.
a wide range of pathogens.

Front 119

Isolated IgA deficiency

Back 119

-this is the most common immunodeficiency disease
-IgA is the major immunoglobulin in mucosal secretions in the respiratory and gastrointestional tract.
-Block in terminal differentiation of IgA-secreting B cells to plasma cells.
-reccurent sinopulonary infections and diarrhea in patients.

These patients are very susceptible to respiratory, gastrointestional, and urogenitis.

Front 120

Thymic hypoplasia: DiGeorge Syndrome

Back 120

this person has:
No T helper Cells
No T Cytotoxic Cells
No T suppressor Cells

the thymus does not develop properly

there is a loss of T cell immunity and the person is susceptible to fungal and viral infections.

Front 121

Brutan disease

X Linked agammaglobulnemia

Back 121

This person has no mature B cells.

Stops at pre- B cell stage

-Failure of B Cell differentiation, absense of B & K, antibody deficient, and manifestations occur after 6 months.

This person can develop extracellular pathogens:

-H. Influenzae
-S. pneumoniae
-S. aureus
-enterovirus infections

Front 122

Common variable immunodeficiency

Back 122

-Block in B cell maturation
-Block in Plasma cell differentation
-hypogammaglbulinemia
-T Cell aberrant signal
- M& F
- common in childhood and adolscents

These people are more susceptible to H. Influenzae.

Front 123

AIDS

Back 123

AIDS is a retroviral disease that is caused by the human immondeficiency virus (HIV) and is characterized by profound immunosuppression leading to opportunistic infections, secondary neoplasms, and neurologic manifestations.

Front 124

AIDS

Sexual transmission

Back 124

Sexual transmission is the predominant mode of infection worldwide.

Front 125

Mother to infant transmission

vertical transmission

Back 125

This is the major cause of pediatric AIDS
Three routes are involved:
1. in utero by transplacental spread (accounts for most cases)
2. intrapartum- during delivery
3. via ingestion of HIV contaminated breast milk.

Front 126

AIDS immunity

Back 126

people who are immune to AIDS to not have a chemokine receptor

Front 127

AIDS dementia

Back 127

this is caused by mediators of inflammation. cytokines and mediators.

Front 128

AIDS etiology

Back 128

The viral envelope is studded by viral glycoproteins, g[120 and gp41
AIDS attacks CD4+ cells

Front 129

AIDS

immunopathogenesis

Back 129

Entry of HIV into host cells involves an intricate process between viral glycoproteins (gp120 and gp41) and host cell CD4 receptor, and chemokine receptors (CXCR4 and CCR-5)

Front 130

3 Phases of HIV infection

Back 130

1. Acute phase
2. chronic phase
3. crisis phase

Front 131

Acute Phase of HIV infection

Back 131

-this begins 3-6 weeks after infection.
-sore throat, myalgias, fever, rash, aseptic menigitis
-high level virus production
-CD4+ T cell reduction
-Virus specific immune response develops
-CD4+ T cell numbers return to normal levels
-Viremia abates, viral replication continues in specific cells.
-Flu-like symptoms

Front 132

Qualitative and quantitative loss in T cells

Back 132

apoptosis- self destruct
T Cell fusion-the cells come together and are useless.
The T cells are very important because they regulate and protect the immune system.

Front 133

Chronic Phase

Back 133

continued HIV replication lasting several years.
Lymphadenopathy develops
Minor opportunistic infections such as thrush
CD4+ cell decline
viral replication continues

Front 134

Crisis Phase

Back 134

fatigue, weightloss, diarrhea, and fever
catastrophic breakdwon of host defenses
Marked viremia
Fever that lasts more than one month
CD4+ cell count reduced below 500cells/ul
serious opportunistic infections, secondary neoplasms
neurological infections.

immune related: opportunistic infections, secondary neoplasms-AIDS dementia

Front 135

Enzyme Linked immunosorbent Assay (ELISA)

Back 135

-initial screening
-antigen/antibody assay
-99% sensitive
-repeated if positive
-p24 is readily detectable

Front 136

Western Blot

Back 136

-Confirmatory Test
-2 bands from either gag and or env region must be present for a positive test. p24, p41 g120 or g160.

if this test comes out negative, then repeat it.

Front 137

kaposi syndrom and lymophoma are common in people with aids

Back 137

imp. info

Front 138

tumor

Back 138

the proliferation of neoplastic cells that form a mass in a tissue or organ

Front 139

nomenclature

Back 139

begin tumors end with a suffix; -oma.
sarcoma denoates malignant tumors of mesenchyme or connective tissue origin.
Carcinoma denotes malignant tumors of epithelial tissue.
Sarcoma and carcinoma are malignant
The prefix adeno- when used denoates tumors composed of ducts or glands.

Front 140

benign tumors

MACROscopic features

Back 140

-benign tumors are sharply demarcated and are often encapsulated.
-growth is by expansion and compression of adjacent normal tissue
-sharp borders are distinct between tumor and normal tissue.

Front 141

benign tumors

MICROscopic tumors

Back 141

-benign tumors are composed of cells that resembe the tissue from which they have arisen.
-these tumors show a high degree of differentiation- the cells look almost normal.

Front 142

benign tumors

cellular features

Back 142

-benign tumors are composed of a uniform cell population in which all cells have the same features
- these features include, reguarly shaped nuclei and the nucleus accounts only for a small part of the total cell volume. chromatin is distributed evenly in the nucleus.
-benign tumors never metastasize

Front 143

Malignant tumors

MACROscopic features

Back 143

-lack a capsule and invade adjacent tissue by infiltration

Front 144

Malignant tumors

MICROscopic features

Back 144

-these cells show anaplasia and acquire new characteristics not inherent to the tissue of their origin.
-malignant cells are undifferentiated.

Front 145

Malignant tumors

Cellular features

Back 145

-malignant cells show marked pleomorphism (different sizes and shapes). the nuclei are of different shapes and sizes, the nuclei are hyperchromatic, nucleoli are prominant and nucleus accounts for most of the cells volume. increased nuclear to cytoplasm ratio; high N/C ratio.
-increased cellular division. chromosal abnormalities are present
- malignant tumors can metastasize

Front 146

Biology of tumors

Back 146

-the acquisition of new atypical features by malignant cells is known as anaplasia. anaplastic cells are larger than normal cells and show nuclear irregularity.
-tumor cells often regress and assume fetal features.

ex. Liver cancer cells secrete alpha fetal protein, a major secretory product of fetal liver cells, not are not synthesized by normal liver cells.

-colon cancer cells produce carcinoembryonic antigen, a glycoprotien normally found only on embryonic intestinal cells.