Pathophysiology Final Study Guide
Patho Section 1
Cell & Tissue Function/Dysfunction
Atrophy: decrease in size of cells.
Hypertrophy: increase in cell size.
Hyperplasia: increase in number of cells.
Metaplasia: mature cell type is replaced by a different mature cell type.
Dysplasia: cells vary in size & shape within a tissue.
Anaplasia: undifferentiated cells with variable nuclear & cell structure.
Neoplasm: tumor.
Cell Damage
Ischemia: oxygen deficit due to respiratory or circulatory problems.
Hypoxia: reduced oxygen in tissue.
Oxygen Deficit: decreased energy production, loss of Na pump ↑ intracellular Na.
Temperature: inactivation of some enzymes, damages organelles, protein c oagulation,
disruption of cell membrane.
Micro-organisms
Abnormal Metabolites: caused by genetic disorders or altered metabolism.
Nutritional Deficits
Cell Death
Apoptosis:programmed cell death controlled by genetics.
Necrosis:lysis of a cell, cell components leak into blood.
Liquification:dead cells liquefy due to release of enzymes.
Coagulation:cell proteins are altered or denatured causing coagulation.
Caseous:form of coagulation necrosis, thick, yellowish, cheesy.
Fat: fatty tissue is broken down into fatty acids.
Tissue Damage from Chemicals
Exogenous: from environment.
Endogenous: from inside the body,
Tissue Damage from Physical Agents
Hypothermia: vasoconstriction, ↑ blood viscosity, hypovolemic shock ↓ blood
pressure.
Hyperthermia: causes general vasodilatation, decrease in circulating blood volume.
Radiation: primarily affects actively dividing cells
Biological Agents
Insects/Animals: direct injection of toxin, transmission of infectious agent,
https://kupt2013comps.wikispaces.com/file/view/Pathophysiology+Final+Study+Guide.doc 7/6/17, 5F04 PM
Page 1 of 40
, allergic reaction to insect proteins.
Food Poisoning
Normal Defenses of the Body
1 st
Line Defense
Physical Barriers: unbroken skin, mucous membranes, nasal hair, clots.
Fluids: may contain enzymes or chemicals:saliva, tears, gastric, sweat.
2 nd
Line Defense-non-specific
Phagocytosis:neutrophils & macrophages engulf cells, debris, foreign mat.
Inflammation: automatic response to cell injury.
3 rd
Line Defense-specific defense produced by
Antibodies
Cell Mediated Immunity
Cellular Defenses
Mast Cells: located in tissue & release histamine & bradykinin.
Macrophages: monocytes that enter tissue & act as phagocytes.
Interferons: small proteins made by lymphocytes to prevent virus replication.
White Blood Cells
Granulocytes
Neutrophils: work by phagocytosis.
Basophils: release histamine leading to inflammation.
Eosinophils:combat the effects of histamine.
Agranulocytes
Monocytes:can enter tissue to become macrophages which
function as phagocyte.
Lymphocytes: B & T
Acute Inflammation
Vascular Response: vasodilatation & increased capillary permeability.
Cellular Response: migration of inflammatory cells through chemotaxis to injury site to
destroy ineffective organism, remove damaged cells, released inflammation ediators.
m
Exudate
Serous: watery, mostly fluids, some proteins and WBC’s.
Fibrinous: thick, sticky, high fibrin content.
Purulent: thick, yellow-green, contains leukocytes, cell debris & microorganisms.
Abscess: Pocket of purulent exudates or pus in a solid tissue.
Local Effects of Inflammation-Cardinal Signs of Inflammation
Redness & Warmth: due to increased blood flow to area.
Swelling: shift of protein & fluid into interstitial space.
Pain: pressure on free nerve endings, chemical mediators irritate nerves.
Loss of Function: edema may restrict movement.
Systemic Effects of Inflammation
Mild Fever: due to resetting of hypothalamic thermoregulatory set point, release
https://kupt2013comps.wikispaces.com/file/view/Pathophysiology+Final+Study+Guide.doc 7/6/17, 5F04 PM
Page 2 of 40
, of endogenous pyrogens.
Malaise
Fatigue
Headache
Anorexia
Treatment of Inflammation: drugs may decrease capillary permeability, reduce number of
leukocytes & mast cells.
Types of Healing
Resolution: minimal tissue damage, cells can repair themselves.
Regeneration: damaged tissue is replaced by identical tissue.
Replacement: functional tissue replaced by scar or fibrous tissue.
1st Intention: wound is clean, edges are close together with minimal gap.
2nd
Intention: large break in tissue, longer healing process with more scar tissue.
Scar Formation: fibroblasts proliferate, abnormal amount of collagen.
Hypertrophic: overgrowth of fibrous tissue, keloid.
Ulceration: blood supply around scar is impaired resulting in tissue
breakdown.
Wound Staging
1. Partial thickness ulcer-red or pink ie. Sunburn.
2. Partial thickness ulcer-blister, scrape, abrasion.
3. Full thickness ulcer- through dermis.
4. Full thickness ulcer that includes muscle or bone.
Drainage
Transudate: clear & watery.
Serosanginous: clear w/ tinge of red/brown. Contains serum/blood thin & watery.
Exudate: creamy yellowish. Contains proteins & WBC’s Thick.
Purulent: yellowish. Contains leukocytes and necrotic debris, thick.
Infected Pus: hues of yellow, green or blue. Contains pathogens, thick.
Venous Insufficiency linical Presentation
C
I ncompetent Valves edial leg area
m
I nefficient Calf Pump e dema
istended Capillary Bed
D et wound
w
ecreased Fibrolysis
D s caring, red base
ibrin Leakage
F emosiderin deposits(purple/brown on leg)
h
rauma
T lcer
U
Documentation of Pulses
Normal: 2+
Diminished: 1+
bsent: 0
A
Arterial Insufficiency: decreased arterial blood supply.
https://kupt2013comps.wikispaces.com/file/view/Pathophysiology+Final+Study+Guide.doc 7/6/17, 5F04 PM
Page 3 of 40
, Acute(thrombosis) vs Chronic(arteriosclerosis)
Characteristics
Dry Gangrene: nonviable dry tissue.
Wet Gangrene: tissue necrosis + bacterial infection. Drainage w/ odor.
Black Gangrene: gangrenous borders, mummified skin.
Pain w/ walking=Claudication
Skin is atrophic(no hair) slow nail growth & Diminished Pulse
Ankle Pressure Index: SBP LE/SBP UE
1 n o arterial occlusive disease
>
. 9-1 m in sx in LE
. 5-.9 c laudication pain(leg pain w/ walking)
. 3-.5 i schemic rest pain
.3 i schemic w/ tissue necrosis
<
Assessment of arterial flow, skin color w/ elevation/dependency
1. LE Elevation to 60º for 1 minute. Normal=no color change.
2. Lower the LE & record time for color to return.>30seconds
means arterial insufficiency. Will look hyperemic(bright red).
Immune Response-Third Body Defense
Humeral Immunity: antibodies are produced to protect body & stored in blood.
Cell Mediated Immunity:lymphocytes are programmed to attack non-self cells.
Antigens:immunogens, proteins, polysaccharides, glycoproteins on cell surface.
Cells
Macrophages:present throughout the body, derived from monocytes,
initiate immune response, engulf foreign materialprocess & display
foreign antigens & present them to lymphocytes, secrete monokines &
interleukins .
Lymphocytes:primary cell in immune response,
T: has 3 subgroups made in bone marrow & differentiate in
t hymus, cell mediated i mmunity, can target certain cells.
1.Cytotoxic T:cells destroy cells bind to antigen & release enzymes
2.Helper T: facilitate immune response by activating & regulating
3.Memory T: remember antigens.
B:Made in bone marrow, located in spleen & lymphoid tissue,
produce antibodies.
Natural Killer:kill tumor or virus infected cells w/o prior exposure
Antibodies
IgG:most common, can activate compliment, cross placenta, primary &
secondary immune response.
https://kupt2013comps.wikispaces.com/file/view/Pathophysiology+Final+Study+Guide.doc 7/6/17, 5F04 PM
Page 4 of 40
Patho Section 1
Cell & Tissue Function/Dysfunction
Atrophy: decrease in size of cells.
Hypertrophy: increase in cell size.
Hyperplasia: increase in number of cells.
Metaplasia: mature cell type is replaced by a different mature cell type.
Dysplasia: cells vary in size & shape within a tissue.
Anaplasia: undifferentiated cells with variable nuclear & cell structure.
Neoplasm: tumor.
Cell Damage
Ischemia: oxygen deficit due to respiratory or circulatory problems.
Hypoxia: reduced oxygen in tissue.
Oxygen Deficit: decreased energy production, loss of Na pump ↑ intracellular Na.
Temperature: inactivation of some enzymes, damages organelles, protein c oagulation,
disruption of cell membrane.
Micro-organisms
Abnormal Metabolites: caused by genetic disorders or altered metabolism.
Nutritional Deficits
Cell Death
Apoptosis:programmed cell death controlled by genetics.
Necrosis:lysis of a cell, cell components leak into blood.
Liquification:dead cells liquefy due to release of enzymes.
Coagulation:cell proteins are altered or denatured causing coagulation.
Caseous:form of coagulation necrosis, thick, yellowish, cheesy.
Fat: fatty tissue is broken down into fatty acids.
Tissue Damage from Chemicals
Exogenous: from environment.
Endogenous: from inside the body,
Tissue Damage from Physical Agents
Hypothermia: vasoconstriction, ↑ blood viscosity, hypovolemic shock ↓ blood
pressure.
Hyperthermia: causes general vasodilatation, decrease in circulating blood volume.
Radiation: primarily affects actively dividing cells
Biological Agents
Insects/Animals: direct injection of toxin, transmission of infectious agent,
https://kupt2013comps.wikispaces.com/file/view/Pathophysiology+Final+Study+Guide.doc 7/6/17, 5F04 PM
Page 1 of 40
, allergic reaction to insect proteins.
Food Poisoning
Normal Defenses of the Body
1 st
Line Defense
Physical Barriers: unbroken skin, mucous membranes, nasal hair, clots.
Fluids: may contain enzymes or chemicals:saliva, tears, gastric, sweat.
2 nd
Line Defense-non-specific
Phagocytosis:neutrophils & macrophages engulf cells, debris, foreign mat.
Inflammation: automatic response to cell injury.
3 rd
Line Defense-specific defense produced by
Antibodies
Cell Mediated Immunity
Cellular Defenses
Mast Cells: located in tissue & release histamine & bradykinin.
Macrophages: monocytes that enter tissue & act as phagocytes.
Interferons: small proteins made by lymphocytes to prevent virus replication.
White Blood Cells
Granulocytes
Neutrophils: work by phagocytosis.
Basophils: release histamine leading to inflammation.
Eosinophils:combat the effects of histamine.
Agranulocytes
Monocytes:can enter tissue to become macrophages which
function as phagocyte.
Lymphocytes: B & T
Acute Inflammation
Vascular Response: vasodilatation & increased capillary permeability.
Cellular Response: migration of inflammatory cells through chemotaxis to injury site to
destroy ineffective organism, remove damaged cells, released inflammation ediators.
m
Exudate
Serous: watery, mostly fluids, some proteins and WBC’s.
Fibrinous: thick, sticky, high fibrin content.
Purulent: thick, yellow-green, contains leukocytes, cell debris & microorganisms.
Abscess: Pocket of purulent exudates or pus in a solid tissue.
Local Effects of Inflammation-Cardinal Signs of Inflammation
Redness & Warmth: due to increased blood flow to area.
Swelling: shift of protein & fluid into interstitial space.
Pain: pressure on free nerve endings, chemical mediators irritate nerves.
Loss of Function: edema may restrict movement.
Systemic Effects of Inflammation
Mild Fever: due to resetting of hypothalamic thermoregulatory set point, release
https://kupt2013comps.wikispaces.com/file/view/Pathophysiology+Final+Study+Guide.doc 7/6/17, 5F04 PM
Page 2 of 40
, of endogenous pyrogens.
Malaise
Fatigue
Headache
Anorexia
Treatment of Inflammation: drugs may decrease capillary permeability, reduce number of
leukocytes & mast cells.
Types of Healing
Resolution: minimal tissue damage, cells can repair themselves.
Regeneration: damaged tissue is replaced by identical tissue.
Replacement: functional tissue replaced by scar or fibrous tissue.
1st Intention: wound is clean, edges are close together with minimal gap.
2nd
Intention: large break in tissue, longer healing process with more scar tissue.
Scar Formation: fibroblasts proliferate, abnormal amount of collagen.
Hypertrophic: overgrowth of fibrous tissue, keloid.
Ulceration: blood supply around scar is impaired resulting in tissue
breakdown.
Wound Staging
1. Partial thickness ulcer-red or pink ie. Sunburn.
2. Partial thickness ulcer-blister, scrape, abrasion.
3. Full thickness ulcer- through dermis.
4. Full thickness ulcer that includes muscle or bone.
Drainage
Transudate: clear & watery.
Serosanginous: clear w/ tinge of red/brown. Contains serum/blood thin & watery.
Exudate: creamy yellowish. Contains proteins & WBC’s Thick.
Purulent: yellowish. Contains leukocytes and necrotic debris, thick.
Infected Pus: hues of yellow, green or blue. Contains pathogens, thick.
Venous Insufficiency linical Presentation
C
I ncompetent Valves edial leg area
m
I nefficient Calf Pump e dema
istended Capillary Bed
D et wound
w
ecreased Fibrolysis
D s caring, red base
ibrin Leakage
F emosiderin deposits(purple/brown on leg)
h
rauma
T lcer
U
Documentation of Pulses
Normal: 2+
Diminished: 1+
bsent: 0
A
Arterial Insufficiency: decreased arterial blood supply.
https://kupt2013comps.wikispaces.com/file/view/Pathophysiology+Final+Study+Guide.doc 7/6/17, 5F04 PM
Page 3 of 40
, Acute(thrombosis) vs Chronic(arteriosclerosis)
Characteristics
Dry Gangrene: nonviable dry tissue.
Wet Gangrene: tissue necrosis + bacterial infection. Drainage w/ odor.
Black Gangrene: gangrenous borders, mummified skin.
Pain w/ walking=Claudication
Skin is atrophic(no hair) slow nail growth & Diminished Pulse
Ankle Pressure Index: SBP LE/SBP UE
1 n o arterial occlusive disease
>
. 9-1 m in sx in LE
. 5-.9 c laudication pain(leg pain w/ walking)
. 3-.5 i schemic rest pain
.3 i schemic w/ tissue necrosis
<
Assessment of arterial flow, skin color w/ elevation/dependency
1. LE Elevation to 60º for 1 minute. Normal=no color change.
2. Lower the LE & record time for color to return.>30seconds
means arterial insufficiency. Will look hyperemic(bright red).
Immune Response-Third Body Defense
Humeral Immunity: antibodies are produced to protect body & stored in blood.
Cell Mediated Immunity:lymphocytes are programmed to attack non-self cells.
Antigens:immunogens, proteins, polysaccharides, glycoproteins on cell surface.
Cells
Macrophages:present throughout the body, derived from monocytes,
initiate immune response, engulf foreign materialprocess & display
foreign antigens & present them to lymphocytes, secrete monokines &
interleukins .
Lymphocytes:primary cell in immune response,
T: has 3 subgroups made in bone marrow & differentiate in
t hymus, cell mediated i mmunity, can target certain cells.
1.Cytotoxic T:cells destroy cells bind to antigen & release enzymes
2.Helper T: facilitate immune response by activating & regulating
3.Memory T: remember antigens.
B:Made in bone marrow, located in spleen & lymphoid tissue,
produce antibodies.
Natural Killer:kill tumor or virus infected cells w/o prior exposure
Antibodies
IgG:most common, can activate compliment, cross placenta, primary &
secondary immune response.
https://kupt2013comps.wikispaces.com/file/view/Pathophysiology+Final+Study+Guide.doc 7/6/17, 5F04 PM
Page 4 of 40
