Pathophysiology Final Study Guide

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,



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, ​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


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, ​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.




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, ​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.



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