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NSG 5003 FINAL EXAM STUDY GUIDE / NSG5003 FINAL EXAM STUDY GUIDE (LATEST- 2020): ADVANCED PATHOPHYSIOLOGY: SOUTH UNIVERSITY

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  • SOUTH UNIVERSITY

NSG 5003 FINAL EXAM STUDY GUIDE / NSG5003 FINAL EXAM STUDY GUIDE (LATEST- 2020): ADVANCED PATHOPHYSIOLOGY: SOUTH UNIVERSITY

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  • August 25, 2020
  • 45
  • 2020/2021
  • Study guide

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  • nsg 5003 final exam study guide nsg5003 final exam study guide latest 2020 advanced pathophysiology south university

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  • SOUTH UNIVERSITY
  • NSG5003: ADVANCED PATHOPHYSIOLOGY (NSG5003)
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NSG 5003 Advanced Pathophysiology Final Study Guide


Week 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 coagulation,
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,
allergic reaction to insect proteins.
Food Poisoning
Normal Defenses of the Body
1st Line Defense
Physical Barriers: unbroken skin, mucous membranes, nasal hair, clots.
Fluids: may contain enzymes or chemicals:saliva, tears, gastric, sweat.
2nd Line Defense-non-specific
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, Phagocytosis:neutrophils & macrophages engulf cells, debris, foreign mat.
Inflammation: automatic response to cell injury.
3rd 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,releasedinflammation mediators.
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 setpoint, release of
endogenouspyrogens.
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.


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, 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- throughdermis.
4. Full thickness ulcer that includes muscle orbone.
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 ClinicalPresentation
IncompetentValves medial legarea
InefficientCalfPump edema
DistendedCapillaryBed wet wound
DecreasedFibrolysis scaring, red base
FibrinLeakage hemosiderin deposits(purple/brown on leg)
Trauma Ulcer
Documentation of Pulses
Normal: 2+
Diminished: 1+
Absent: 0
Arterial Insufficiency: decreased arterial bloodsupply.
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 no arterial occlusivedisease
.9-1 min sx in LE
.5-.9 claudication pain(leg pain w/walking)
.3-.5 ischemic restpain
<.3 ischemic w/ tissuenecrosis
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 toreturn.>30seconds
means arterial insufficiency. Will look hyperemic(brightred).

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, Week 2
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
thymus, cell mediated immunity, 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.
IgM:can activate compliment, natural antibodies ie. Involved in blood type
IgA:not in blood, is in tears, saliva & colostrums.
IgE
IgD
Compliment System:antigen-antibody complex, activated during immune rxn w/ IgG or
IgM. Causes cell damage when activated, causes macrophagestorelease enzymes.
Immune Response
Primary: 1st exposure to antigen, 1-2 weeks needed for effective antibodies
Secondary:repeat exposure to same antigen, effective response in 1-3 days
Immunity: Innate-always present. Or acquired.
Hypersensitivity Reactions
Type 1 Hypersensitivity:allergic rxn, exposed to allergen causes development of
IgE’s,activate mast cells and causes inflammation. Ie. Hay fever, allergies, asthma
Type 2 Hypersensitivity:cytotoxic hypersensitivity. Antigen oncellmembrane reacts
w/ circulating IgG’s, activates compliment, cells w/ antigen destroyed. Ie incompatible blood
type exposure.
Type 3: Immune complex hypersensitivity-antigen & antibody combine forming
immune complexes that cause inflammation & tissue destruction.
Type 4:Cell Mediated or delayed response by T-lymphocytes. No antibodies
present. Ie. Tb test, contact dermatitis.

Immune System Malfunction
Hypersensitivity: full system immune response to non-noxious stimulus.
Asthma: central windpipe or airway disorder.
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