Test 2 Pathophysiology

Front 1

study of how diseases alter the normal physiological processes of the human body?

Back 1

pathophyisiology

Front 2

balance, stable internal environment gives us the ability to adapt and compensate?

Back 2

homeostasis

Front 3

atrophy?

Back 3

decrease in size resulting from decrease in workload

causes: lack of activity, hormonal, lack of blood supply

where: skeletal muscles, brain

Front 4

hypertrophy ?

Back 4

increase in cell size resulting from increase in workload

causes: increased activity, increase in blood supply

where: heart kidneys

Front 5

hyperplasia ?

Back 5

increase in # of cells resulting from the increase in workload

mechanism - increase in rate of cell division (increase in mitosis)

when in response to cell injury hyperplasia and hypertrophy many times occur together

Front 6

metaplasia ?

Back 6

replacement of one type of cell by another type that is not normal for that tissue

Front 7

dyplasia ?

Back 7

change in cell size, shape or apperance cause by an external stressor....often caused by hyperplasia...highly assosciated with neoplasm and malignancy

Front 8

types of responses?
chemical
infectious
immunologic

Back 8

chemical - CO, lead, overdoses, ingestions

infectious - bacteria, virus, fungus, parasite

immunologic - bodys own protection can lead to cell death or injury

Front 9

albumin ?

Back 9

like a sponge, pulls fluid back into the vascular system

Front 10

anabolism ?

Back 10

constructive phase

Front 11

??
catabolism

Back 11

destructive phase

Front 12

??
cellular swelling

Back 12

results from permeable or damaged cell membrane

inability to maintain intra and extracellular fluid

Front 13

??
apoptosis

Back 13

injured cell releases enzymes that engulf and destroy the cell

Front 14

??
necrosis

Back 14

pathological process, cells swell and rupture

Front 15

??
coagulative

Back 15

albumin of the cell gets denatured (liquid to solid, like a cooked egg)

Front 16

??
liquifactive

Back 16

cells become liquid and contained in the wall of cyst.....hydrolytic enzymes digest lipids in tissue

Front 17

??
fluids inside the cell

Back 17

intracellular fluid

Front 18

??
fluids outside the cell

Back 18

extracelllular

Front 19

??
extracellular fluid that is within the circulatory system

Back 19

intravascular

Front 20

??
extracelllular fluid that is outside the vascular system and in the body tissues

Back 20

interstitial

Front 21

??
describe edema

Back 21

accumulation of water in the interstitial space, caused by the disruption in forces that keep the net filtration at zero
1- decrease in plasma oncotic force
2- increase hydrostatic pressure
3- increase capillary permeability
4- lyphatic channel obstruction

Front 22

?
mastectomy

Back 22

during process lymph nodes and channels are destroyed.....poor lymph drainage on affected side

Front 23

note:
edema can cause a relative condition of dehydration

Back 23

note:
water in interstitial spaces in not available for metabolic processes

Front 24

occurs when there is a discrepancy between the blood type of the patient and the type of blood being tranfused

Back 24

transfusion reactions

Front 25

polyheme
hemopure

Back 25

hemoglobin based oxygen carrying solutions - referred to as blood substitutes

Front 26

colloid - protein containing fluid ---remains in the intravascular spaces for the long time.....have oncotic force

Back 26

crystalloids

isotonic - same tonicity as body fluid (normal saline, 0.9%NACL)

hypertonic - more particles

hypotonic - less particles (D5W)

Front 27

causes of disease?

Back 27

genetics
envionment
lifestyle
gender

Front 28

bacteria release toxins

exotoxins - secreted during bacteria growth

endotoxins - released when the bacteria die

Back 28

sepsis - systemic release of toxins

Front 29

viruses

-much harder to destroy than bacteria
-do not produce toxins
-difficult to treat, symptomatically

Back 29

mast cell - IgE

Front 30

B-Cells

-humoral immunity
-develop memory for the antigen

Back 30

T-Cells

-cell mediated immunity
- recognize and attack, no antibodies produced

Front 31

phases of inflammation

- acute inflammation
- chronic inflammation
- granuloma formation
- healing

Back 31

oncotic force - attraction of water into the intravascular space

Front 32

chemotaxis

attraction of white cells

Back 32

prostaglandins

increased vasodialation, vascular permeability, and chemotaxis

Front 33

Pathology

the study of disease and its causes

Back 33

Pathophysisology

the physiology of disordered function

Front 34

cellular swelling

caused by injury to or change in permeablity of the cell membrane resulting in unstable fluid levels

Back 34

thrombocytes

platelets -- important in blood clotting

Front 35

apoptosis

injured cell releases enzymes that engulf and destroy itself....one way the body rids itself of damaged and dead cells

Back 35

tonicity

solute concentration or osmotic pressure relative to the blood plasma or body cells

Front 36

inflammatory response

fast
nonspecific
no memory
multiple cell types - granulocytes, monocytes, macrophages

Back 36

immune response

slow
specific
long-term memory
one blood cell type - lymphocytes

Front 37

antigen

marker on the surface of cell that identifies as self or non-self

Back 37

antibody

substance produced by B-lymphocytes in response to presence of a foreign antigen

Front 38

immune response

the body's reactions that inactivate or eliminate foreign antigens

Back 38

immunity

long term condition of protection from infection or disease

Front 39

lymphocyte

type of leukocyte (white blood cell)
attacks foreign substances as part of the immune response

Back 39

B-lymphocyte

respond to presence of an antigen
produce antibodies to attack
develop memory for long term

Front 40

T-lymphocyte

do not produce antibodies or memory
attack antigens directly

Back 40

humoral immunity

long term immunity to an antigen provided by antibodies produced by B-lymphocytes

Front 41

cell-mediated immunity

short term immunity to an antigen provided by T-lymphocytes

Back 41

immunogens

antigens that are able to trigger an immune response

Front 42

ABO system

type O blood known as universal donor
AB blood known as universal receiver

Back 42

mast cells

large cells, bags of granules....when stimulated they activate the inflammatory response by degranulation (or emptying granules into extracellular environment and synthesis (construction of leukotreines and prostaglandins)

Front 43

histamine

substance released during mast cell degranulation

Back 43

serotonin

substance relesed by platelets that through constriction and dialation of the blood vessels, affects blood flow to an injured of affected site

Front 44

leukotreins

SRA-A - slow reacting substances of anaphylaxis....cause vasodialation, vascular permeability, and chemotaxis

Back 44

prostaglandins

substances synthesized by mast cells during inflammatory response...cause vasodialation, vascular permeability, chemotaxis and also cause pain

Front 45

IgE

immunoglobin involved in most alergic reactions

Back 45

Allergic reaction

first exposure to antigen stimulates B cells to produce IgE antibodies that bind to receptors on mast cells in tissues near blood vessels.....on re-exposure allergen binds to IgE on the mast cell and causes histamine release