Pathology - Exam 2 - Objectives Only

Front 1

Accumluation of interstitial fluid w/ in tissues?

Back 1

edema

Front 2

Edema formation:

Back 2

40% solids, 60% water ---> 2/3rd intracellular fluid & 1/3rd interstitial fluid --> inter. fluid 80% & plasma 20%

Front 3

Left side of the heart is connected to _________ the heart and right side of the heart is connected to anything _______ the heart.

Back 3

left side = below heart

right side = above heart

Front 4

Types of Edema:

Back 4

1. Inflammatory: acute, chronic and angioedema

2. Non-inflammatory: hydro/plasma pressure & lymph obstruction

Front 5

Non-inflammatory 1 edema contains:

Back 5

1. congestive heart failure

2. ascites

3. venous obstruction (thrombosis, external pressure, dependency of lower limbs)

Front 6

Non-inflammatory 2 edema contains:

Back 6

1. decrease in synthesis (hypoproteinemia, liver cirrhosis, protein malnutrition)

2. increase loss (nephrotic syndrome, protein-losing gastroenteropathy)

Front 7

Non-inflammatory 3 edema contains:

Back 7

1. peau d'orange appearance

2. resected axillary nodes, scarring nodes, filariasis (worms)

Front 8

Excess of blood in vessels supplying oxygen is -

Back 8

hyperemia

Front 9

Abnormal/excessive accumulation of body fluid is called -

Back 9

congestion

Front 10

What kind of process does hyperemia have?

Back 10

active

Front 11

What kind of process does congestion have?

Back 11

passive

Front 12

T/F: Hyperemia and Congestion both have an increase in blood volume.

Back 12

TRUE

Front 13

What color tissue does hyperemia contain?

Back 13

red

Front 14

What color tissue does congestion contain?

Back 14

blue-red

Front 15

(Hyperemia/Congestion) has excess of oxygenated blood.

Back 15

Hyperemia

Front 16

(Hypermia/Congestion) has poorly oxygenated blood.

Back 16

Congestion

Front 17

(Hypermia/Congestion) has a physiologic process (arterial dilation diring exercise).

Back 17

Hyperemia

Front 18

(Hypermia/Congestion) has a pathologic process --> heart failure, venous obstruction, hypoxia and long-standing stasis.

Back 18

Congestion

Front 19

Escape of blood from BV into surrounding tissue -

Back 19

hemmorage

Front 20

Process of thrombus formation inside a BV -

Back 20

thrombosis

Front 21

Solid mass of blood constitients formed w/ in vascular system during life -

Back 21

thrombus

Front 22

Explain the growth formation of Thrombus:

Back 22

1. Red cells settle out before clot forms, forming 2 layers: Lower deeper layer (resembles jelly) & Upper clearer layer (resembles chicken fat)

2. Takes on shape of vessel in which it is formed in.

Front 23

Obstruction of artery, typically by blood clot or air bubble is called -

Back 23

embolism

Front 24

What is a detached intravascular mass?

Back 24

emoblus

Front 25

Types of Embolism: (2)

Back 25

1. Pulmonary (most common; from DVT, right side of heart)

2. Systemic (arterial; left side of heart, major arteries)

Front 26

3 types of Non-Thrombotic Embolism and what they cause?

Back 26

1. Fat= sever trauma w/ bone fracture, severe burns, pulmonary insufficiency, neurologic symptoms, renal impairment, skin petechiae.

2. Air (gas)= chest wall injury, nitrogen bubbles ---> Caisson disease.

3. Amniotic= respiratory distress, triggers clotting cascade.

Front 27

Ischemic death (necrosis) of tissue is called -

Back 27

infarction

Front 28

List some causes of infarction: (5)

Back 28

1. arterial thrombosis/embolism

2. atheromatous plaque, dissecting aortic aneurysm

3. external compression (tumor)

4. testicular/ovary torsion, bowel volvulus

5. venous obstruction (less common) & congestion (more common)

Front 29

List the factors for Primary Immunity: (4)

Back 29

1. defense mechanisms require no previous sensitization

2. quick/non-specific acute inflammatory response

3. phagocytize offending agent

4. ***innate/non-specific***

Front 30

List the factors for Secondary Immunity: (3)

Back 30

1. activated lymphocytes produce antibodies specific to each antigen

2. has memory; able to recognize/mount stronger attack to antigen

3. ***adaptive/aquired***

Front 31

What causes a bridge between primary and secondary immunity?

Back 31

macrophages

Front 32

List factors for Petechiae: (3)

Back 32

1. (1-2mm)

2. FOCAL hemmorage

3. pinpoint, NON-RAISED, round, purplish red spot hemmorhages into skin, mucous membranes/serosal surfaces.

Front 33

List main causes of Petechiae:

Back 33

- increase pressure, clotting disease, low platelet count (thrombocytopenia), defective platelet count, clotting factor defenciences, loss of vessel wall support (vitamin C deficiency).

Front 34

List factors of Purpura: (3)

Back 34

1. (3-5mm)

2. Focal hemmorage

3. Flat/non-raised, purplish red spot hemmorrhages into skin,mucous membranes/serosal surfaces.

Front 35

T/F: Petechiae, Purpura and Ecchymosis all have the same main causes.

Back 35

TRUE

Front 36

List factors for Ecchymosis: (3)

Back 36

1. (1-2 cm)

2. widespread surface petechiae

3. non-elevated, rounded or irregular, blue or purplish patch

Front 37

List factors for Hematoma: (3)

Back 37

1. localized collection of blood

2. usually clotted w/in tissue/organ/space due to break in BV wall

3. usually protuberant or mass-like

Front 38

Main causes of Hematoma: (4)

Back 38

1. trauma (most common)

2. vessel disease (aneurysm)

3. warfarin (coumadin)

4. bleeding disorders

Front 39

Which cells recognize antigens, memory, killer cells, and helper cells?

Back 39

T-cells

Front 40

Which cells contain histamine/serotonin and heparin, release granules in allergic reaction?

Back 40

basophil

Front 41

Which cells become plasma cells --> antibodies (bind to specific antigen)?

Back 41

b-cells

Front 42

Which cells deal with allergies, anti-parasite cell ans has IgE receptors?

Back 42

eosinophil

Front 43

What cells are the main B-cell, makes almost all antibodies and deals with allergies?

Back 43

plasma cells

Front 44

Immunoglobulins are also known as ____________; which are produced by B-cells.

Back 44

antibodies

Front 45

List factors for Humoral immune response: (3)

Back 45

1. antibody (Ab) driven

2. Abs helps neutralize extracellular pathogen/toxins.

3. not effective in neutralizing intracellular pathogens

Front 46

List factors for Cell-mediated immune response: (3)

Back 46

1. cellular response driven

2. effective against intracellular pathogens; (pathogens that reside & replicate inside cells where the ab can't reach them)

3. also tumor/cancer cells

Front 47

What are major cells in humoral response?

Back 47

B lymphocytes

Front 48

Describe Initial (primary response) for Humoral Immunity: (5)

Back 48

1. Activation of B-cell stimulate cell-division.

2. Increase in Ab production (2-3 weeks to produce enough cirulating abs to neutralize Ag).

3. Memory B cells created as primary immune response terminates.

4. Memory cells swiftly recognize on second exposure to same Ag.

5. Stimulates an immediate, full response to Ag.

Front 49

What are the 5 major groups of antibodies (immunoglobulins)?

Back 49

1. IgG

2. IgM

3. IgA

4. IgE

5. IgD

Front 50

Main characterisitic of IgG -

Back 50

active in secondary immune response

Front 51

Main characteristic of IgA -

Back 51

found in body secretions and primary in defense mechanism

Front 52

Main characteristic of IgM -

Back 52

largest antibodies

Front 53

Main characteristic of IgE -

Back 53

stimulate release of histamine from mast cells

Front 54

Main characteristic of IgD -

Back 54

large amounts found in serum

Front 55

3 major cellular components in Cell-Mediated Immunity:

Back 55

1. T-lymphocytes (CD4 or T-helper cell & CD8 or T-cytotoxic cell)

2. Natural killer cells (NK)

3. Macrophages

Front 56

This cell releases cytokines that regulate action of all other immune system cells (b-cells, macro, nk cells) & has twice as many CD4 as CD8 in circulation:

Back 56

CD4 or T-helper cell

Front 57

This cells kills cells infected w/ viruses, cancer cells, and normal cells confused as non-self; must be first activated by a T-helper cell/macrophage prior to binding/destroying an Ag; plays important role in organ/tissue rejection:

Back 57

CD8 or T-cytotoxic cell

Front 58

This cell is similar to cytotoxic Tcells; prior to sensitization by APC not necessary; destroys virus infectted, cancer, damaged cells; respond immediately to presence of antigen; often affected by immunodeficiency disorders such as AIDS:

Back 58

NK cells

Front 59

T/F: In cell-mediated immunity, macrophages require sensitization to destroy antigens.

Back 59

FALSE; no prior sensitization required to destroy antigens.

Front 60

What is active immunity?

Back 60

exposure of Ag --> production of Abs in response to the Ag.

Front 61

2 types of Active immunity:

Back 61

1. Natural active immunity (infective disease --> chicken pox/herpes)

2. Artificial active immunity (vaccines/booster shots --> polio, tetanus, hep A/B, measles, mumps)

Front 62

What is passive immunity?

Back 62

individual receives performed Abs from another source (usually gamma globulin, IgG)

*immune system doesn't produce any of it's own Abs, still subject to infection; short lived as no memory cells are created.*

Front 63

2 types of passive immunity:

Back 63

1. Natural passive immunity (transfer of maternal Abs across placenta to infant and in breast milk)

2. Artificial passive immunity (injection of performed Abs from a second source, often a horse; post exposure prophylaxis given to health worker to boost immune response following needlestick injury)

Front 64

Exaggerated immune response against a foreign substance (allergies) is called -

Back 64

hypersensitivity reaction

Front 65

Exagerated immune response against a part of the person's own body (which the body now considers a foregn (self allergy)) is called -

Back 65

autoimmune disease

Front 66

Partial or total failure of immune response (AIDS/Diabetes) is called -

Back 66

immune deficiency disease

Front 67

4 types of hypersensivity reactions:

Back 67

1. Type 1: allergic, anaphylactic, immediate. --> antibody/rapid/acute

2. Type 2: cytotoxic, ADCC --> antibody,rapid,acute

3. Type 3: immune complex, arthur reaction --> antibody,rapid,acute

4. Type 4: cell-mediated ---> T-cell/delayed/chronic

Front 68

DiGeorge Syndrome is a failure of the 3rd and 4th _____________ pouches development. The main problem is the __-cells.

Back 68

- pharyngeal

- T-cells

Front 69

Are T-cells in extra or intra cellular?

Back 69

intracellular

Front 70

What is the most common malignant neoplasm in the oral cavity?

Back 70

carcinoma

Front 71

What is important when referring to prognosis? (staging or grading)

Back 71

staging

Front 72

_______ is a way of classifying the spread/size of a malignancy; shows severity of clinical/histological features of the tumor.

Back 72

staging

Front 73

________ is an increase in size of cells.

Back 73

hypertrophy

Front 74

_________ is an increase in cell numbers.

Back 74

hyperplasia

Front 75

_________ is a neoplasm that is non-cancerous, slow rate of growth, has an expansile type of growth and no signs/symptoms.

Back 75

benign

Front 76

________ is a neoplasm that is cancerous, relatively rapid rate of growth, has an invasive w/ or w/out expansile type of growth, and has signs/symptoms ---> ulceration, bleeding, induration/fixation.

Back 76

malignant

Front 77

List factors of identifying -carcinoma: (3)

Back 77

- malignant (epithelial)

- common in older pt's

- spread via lymphatic

Front 78

List factors of identifying -sarcoma: (3)

Back 78

1. malignant (connective tissue)

2. common in young pt's

3. spread via hematogenous route

Front 79

3 main cancer treatments are -

Back 79

1. surgery

2. radiation therapy

3. chemotherapy

Front 80

Other types of cancer treatment are - (3)

Back 80

1. combination therapies: neoadjuvant --> given BEFORE primary therapy to shrink tumors; adjuvant --> given AFTER primary therapy to increase chances of long-term survival.

2. hormonal therapy

3. monoclonal antibody therapy/targeted drug therapies

Front 81

Grading of tumors:

Grade 1=

Grade 2/3=

Grade 4=

Back 81

Grade 1 = cells are well differentiated

Grade 2/3= moderately differentiated

Grade 4= poorly differentiated