560A: Pathophysiology Flashcards

Pathophysiology

1
Q

Etiology:

A

cause of disease

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2
Q

Signs:

A

objective findings

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3
Q

Pathogenesis:

A

manner in which disease develops

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4
Q

Diagnosis:

A

determination of the nature and cause of a patient’s illness

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5
Q

prognosis:

A

probable outcome of a disease or disorder; outlook for recovery

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6
Q

General causes of cell injury:

A

a. congenital and hereditary diseases
b. inflammatory diseases
c. degenerative diseases
d. metabolic diseases
e. neoplastic diseases (abnormal cell growth leads to benign tumors)

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7
Q

Cells response to injury:

A

a. cell swelling (sodium + water)

b. fatty change (impaired enzyme systems that metabolize fat)

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8
Q

Cardinal signs of inflammation:

A

a. dilation (expansion) of blood vessels
b. increased vascular permeability
c. attraction of leukocytes (white blood cells) to site of injury
d. heat, redness, tenderness, swelling, pain
e. systemic response (fever, leukocytosis)

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9
Q

Causes of inflammation:

A

a. chemical agents (mediators) of inflammation that are formed & released when tissue is damaged; some are from cells; others from proteins in blood plasma
b. when antibodies and antigens (toxin or foreign bodies) interact; causes inflammatory response followed by tissue necrosis

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10
Q

Acute inflammation:

A

a. 1st line of defense in response to injury
b. nonspecific
c. may occur in response to any injury in short of one that is lethal
d. short duration
e. exudation of fluid & emigration of leukocytes
f. occurs before immune response
g. goal to remove injurious agents

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11
Q

Chronic inflammation:

A

a. non-degradable pathogens
b. lasts for several months to years
c. failure to rid whatever was causing an acute inflammation

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12
Q

Lymphocytes:

A

a. respond to foreign antigens, macrophages and related cells that process antigen and “present” it to lymphocytes;
b. important cells of immune system that communicate with one another;
c. secrete lymphokines that are chemical messengers

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13
Q

Complement system:

A

a. functions with immune system to destroy or inactivate all types of foreign antigens, including micro-organisms

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14
Q

Complement system - 2 pathways of activation

A
  1. classical pathway - triggered by antigen-antibody interactions
  2. alternative pathway - activated by bacterial cell wall material or products generated during inflammation
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15
Q

Antibodies:

A

globulins produced by plasma cells and are usually called immunoglobulins

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16
Q

5 Classes of Antibodies

A
  1. IgM
  2. IgG
  3. IgA
  4. IgD
  5. IgE
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17
Q

Components of Healing Process: Type 1 - Immediate Hypersensitivity

A

a. allergy
b. IgE antibodies
c. antigen-antibody interaction
d. antihistamines
e. desensitization w/IgA & IgG (i.e. - food allergy)
f. anaphylaxis (i.e. bee sting)
g. mediator from mast cells & basophils

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18
Q

Components of Healing Process: Type 2 - Cytotoxic Hypersensitivity

A

a. antibody attaches to antigen

b. complement activated followed by cell tissue damage

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19
Q

Components of Healing Process: Type 3 - Immune Complex Disease

A

antigen-antibody complexes form; activate complement and cause inflammatory reaction
i.e. rheumatoid arthritis

20
Q

Components of Healing Process: Type 4 - Delayed (Cell-Mediated) Hypersensitivity

A

T-lymphocytes secrete cytokines that attract lymphocytes, macrophages, and other inflammatory cells
i.e. tuberculosis, contact dermatitis

21
Q

Control and Complications of Healing: Suppression of the Immune Response

A

a. unwanted effects of immune response
(autoimmune disease, rejected transplanted organs, Rh hemolytic disease in newborn infants)
b. methods for suppressing - radiation, cytotoxic drugs, adrenal corticosteroids, antibodies
c. tissue grafts and immunity (foreign antigens; lymphocytes reject foreign antigens; immune suppression to prevent rejection)

22
Q

Control and Complications of Healing: Autoimmune Diseases

A

a. pathogenesis - antibodies formed, cross-reaction, T-lymphocytes fail to control immune response
b. treatment - corticosteroids, cytotoxic drugs
c. connective tissue diseases (autoimmune diseases)
i. e lupus erythematosus, scleroderma

23
Q

Tissue growth disorders (neoplastic diseases)

A

a. viruses - some animal tumors are caused by viruses; human tumors may be virus induced
b. gene and chromosomal abnormalities
c. failure of immunologic defenses
d. heredity and tumors

24
Q

Tumor:

A

disturbed cell growth

25
Q

Benign tumors:

A

mass of cells (tumor) that lacks the ability to invade neighboring tissue or metastasize; non-cancerous

26
Q

Malignant tumors:

A

a. cancer
b. carcinoma - arising from surface, glandular or parenchymal epithelium
c. sarcoma - solid tumor from other tissue
d. leukemia - neoplasm of blood-forming tissue

27
Q

Benign vs. Malignant

A

Benign - grow slowly, expands, stays local, cells well differentiated
Malignant - grow rapidly, grow by infiltration, metastasize, cells not well differentiated

28
Q

Hemopoiesis:

A

production of blood cells & platelets, which occurs in bone marrow

29
Q

Hemostasis:

A

complex system for causing blood to clot when and where necessary

30
Q

Factors concerned with hemostasis:

A

a. blood vessels and platelets
b. reflex contraction of blood vessels after injury
c. platelets adhere to injury
d. small breaks in capillaries are sealed by platelets
e. plasma coagulation factors

31
Q

Phases of Hemostasis

A

Phase I - generation of prothrombin activation (intrinsic & extrinsic system)
Phase II - formation of thrombin
Phase III formation of fibrin

32
Q

4 Major Categories of Bleeding Disorders:

A
  1. Abnormalities of small blood vessels
  2. Abnormalities of platelet function
  3. Deficiency of 1 or more of plasma coagulation factors
  4. Liberation of thromboplastin material into the circulation
33
Q

Erythrocyte Disorders:

A

anemia - abnormally low oxygen carrying capacity

examples: hemorrhagic anemia, hemolytic anemia, aplastic anemia

34
Q

Leukocyte Disorders:

A

leukemia - cancerous conditions involving white blood cells

35
Q

Intravascular blood clot (thrombus):

A

Pathogenesis:

  1. slowing or stasis of blood flow
  2. damage to blood vessel wall
  3. increased coagulability of blood
36
Q

Thrombosis:

A

blood clot formed withing the vascular system

37
Q

Embolus:

A

detached clot carried in circulation

38
Q

Infarct:

A

tissue necrosis caused by interruption of blood supply

39
Q

Formation of blood clots within leg veins - Predisposing factors:

A

a. stasis of blood
b. varicose veins
c. increased blood coagulability

40
Q

Formation of blood clots within leg veins - Major complication:

A

a. detachment of clot
b. embolus lodges in pulmonary artery or branches
c. clinical manifestations depend on size and location

41
Q

Large pulmonary emboli:

A
  1. obstruct main pulmonary artery or major brances
  2. obstruct blood flow to lungs, causing severe dyspnea, cyanosis, shock, sudden death
  3. lung usually not infarcted because adequate collateral blood flow is provided by the bronchial arteries
42
Q

What causes a small pulmonary emboli?

A
  1. impacted in peripheral branches of pulmonary artery

2. lung infarct may develop due to inadequate collateral circulation causing chest pain, cough, bloody sputum

43
Q

What causes a septic pulmonary emboli?

A
  1. thrombi form in pelvic vein following uterine infection
  2. bacteria invade thrombi
  3. emboli from infected thrombus travel to lungs, causing pulmonary infarct
  4. bacteria in clot invade pulmonary infarct, causing lung abscess
44
Q

Arterial Thrombosis:

A
  1. roughening of arterial wall secondary to arteriosclerosis

2. thrombi from on roughened area

45
Q

What can occur as a result of Arterial Thrombosis?

A
  1. blockage of coronary artery: myocardial infarction
  2. major artery in leg occluded: gangrene
  3. occlusion of artery to brain: stroke
46
Q

What causes intracardiac thrombosis?

A

a. clot forms (heart failure, valve injury or myocardial infarction)
b. may dislodge into circulation and cause infarction in spleen, kidneys or brain