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NUR 3031 PATHOPHYSIOLOGY FINAL EXAM REVIEWED STUDY GUIDE LATEST UPDATE

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NUR 3031 PATHOPHYSIOLOGY FINAL EXAM REVIEWED STUDY GUIDE LATEST UPDATE Cellular Injury Reversible  Although impairing cell function, does not result in cell death. Two patterns under microscope: 1 Cellular swelling: occurs with impairment of Na+/K+ pump, usually as a result of hypoxic cell injury 2 Fatty change: linked to intracellular accumulations of fat; reversible, usually indicatessevere injury. Irreversible  Cell death or necrosis can occur. Apoptosis (Programmed cell death): a form of cell death necessary to make way for new cells; NORMAL PROCESS IN THE BODY Necrosis: cell death and degradation; UNREGULATED death; cellswells and ruptures; inflammation results. Cells may undergo liquefaction, coagulation, infarction, or caseous necrosis Gangrene  Large area of necrotic tissue; Three types: 1 Dry gangrene: lack of arterial blood supply but venous flow can carry fluid OUT of tissue 2 wEt gangrene: lack of venous flow lets fluid ACCUMULATE in tissue (Efluid can ‘E’nter) 3 Gas gangrene: Clostridium infection produces toxins and bubbles Cellular stressors  Hypoxia: lack of oxygen in air, respiratory disease, ischemia, anemia, edema, or inability of cells to use oxygen. Causes: ATP DEPLETION or “POWER FAILURE”; AEROBIC metabolism STOPS, less ATP is produced, Na+/K+ pump is impeded, cell swells up, lactic acid is produced due to ANAEROBIC metabolism. Heat and Cold: extremes of heat and cold cause damage to the cells Electricity: can cause extensive tissue injury and disruption of neural/ cardiac impulses Chemical agents: injures cell membrane, block enzymatic pathways, and disrupt osmotic/ionic balance Biologic agents: are able to replicate and continue to produce injurious effects Radiation: ionizing radiation, ultraviolet radiation, nonionizing radiation Nutritional imbalances: Nutritional excess/deficiency can predispose cellsto injury Atrophy  decrease cell size causing reduce oxygen consumption and other cellular functions. General causes: 1 Disuse: reduction in muscle use 2 Denervation: atrophy in muscles of paralyzed limbs 3 Loss of endocrine stimulation: in relationship with disuse atrophy 4 Inadequate nutrition and ischemia: cells decrease size and energy requirements due to lack of nutrition and oxygen. Hypertrophy  increase cell size and with it an increase in the amount of functioning tissue mass.  Pathogenic Hypertrophy: thickening of urinary bladder and myocardial hypertrophy. Hyperplasia  increase in the number of cells in an orga

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Pathophysiology Final Exam


NUR 3031 PATHOPHYSIOLOGY FINAL EXAM
REVIEWED STUDY GUIDE LATEST UPDATE
Cellular Injury

Reversible  Although impairing cell function, does not result in cell death.
 Two patterns under microscope:
1 Cellular swelling: occurs with impairment of Na+/K+ pump, usually as a result of hypoxic cell injury
2 Fatty change: linked to intracellular accumulations of fat; reversible, usually indicates severe injury.

Irreversible  Cell death or necrosis can occur.
 Apoptosis (Programmed cell death): a form of cell death necessary to make way for new cells;
NORMAL PROCESS IN THE BODY
 Necrosis: cell death and degradation; UNREGULATED death; cell swells and ruptures; inflammation
results. Cells may undergo liquefaction, coagulation, infarction, or caseous necrosis

Gangrene  Large area of necrotic tissue; Three types:
1 Dry gangrene: lack of arterial blood supply but venous flow can carry fluid OUT of tissue
2 wEt gangrene: lack of venous flow lets fluid ACCUMULATE in tissue (E fluid can ‘E’nter)
3 Gas gangrene: Clostridium infection produces toxins and bubbles

Cellular stressors  Hypoxia: lack of oxygen in air, respiratory disease, ischemia, anemia, edema, or inability of cells
to use oxygen. Causes: ATP DEPLETION or “POWER FAILURE”; AEROBIC metabolism STOPS, less
ATP is produced, Na+/K+ pump is impeded, cell swells up, lactic acid is produced due to
ANAEROBIC metabolism.
 Heat and Cold: extremes of heat and cold cause damage to the cells
Electricity: can cause extensive tissue injury and disruption of neural/ cardiac impulses
Chemical agents: injures cell membrane, block enzymatic pathways, and disrupt osmotic/ionic
balance
Biologic agents: are able to replicate and continue to produce injurious effects
Radiation: ionizing radiation, ultraviolet radiation, nonionizing radiation
Nutritional imbalances: Nutritional excess/deficiency can predispose cells to injury

Atrophy  decrease cell size causing reduce oxygen consumption and other cellular functions.
 General causes:
1 Disuse: reduction in muscle use
2 Denervation: atrophy in muscles of paralyzed limbs
3 Loss of endocrine stimulation: in relationship with disuse atrophy
4 Inadequate nutrition and ischemia: cells decrease size and energy requirements due to
lack of nutrition and oxygen.

Hypertrophy  increase cell size and with it an increase in the amount of functioning tissue mass.
 Pathogenic Hypertrophy: thickening of urinary bladder and myocardial hypertrophy.

Hyperplasia  increase in the number of cells in an organ or tissue.
 Occurs in tissues such as epidermis, intestinal epithelium, and glandular tissue.
 2 types of PHYSIOLOGICAL HYPERPLASIA:
1 Hormonal hyperplasia: Breast and uterine enlargement during pregnancy, due to estrogen.
2 Compensatory hyperplasia: Regeneration of the liver that occurs after partial hepatectomy, or
with the removal of a kidney.

1

,  Most forms on NONPHYSIOLOGICAL HYPERPLASIA are due to excessive hormonal or the effects of
growth factors on target tissues.

Metaplasia  Reversible change in which a cell type is replaced by another cell type, occurs in response to irritation




2

, and inflammation. (‘M’ is like mix-and-match)

Dysplasia  deranged cell growth of a specific tissue, results in cells that varies in size, shape, and organization
 Strongly implicated as a precursor of cancer; reversible change

Hypoxia  lack of oxygen supply to the tissue despite of good perfusion of blood.

Ischemia  Decreased blood supply to a body organ or part usually due to functional constriction or obstruction.
 ISCHEMIA commonly depends on blood flow through limited numbers of blood vessels and produces
LOCAL TISSUE injury

 IMMUNE DISORDERS AND IMMUNODEFICIENCY

HIV  retrovirus selectively attacks CD4+ T lymphocytes; pt. infectious even when asymptomatic
Unprotected sexual activity; blood, semen, vaginal fluids, oral intercourse; Contaminated blood; infectedmother
to child, breast milk, placenta, needles, blood transfusions

Stage 1  Occurs shortly after infection, high viral load
 Symptoms: flu like symptoms; GI issues; Lymphoadenopathy, rash; viral replication, CD4+ cell count

Stage 2  Latent Period, lowest viral load
 Symptoms: Asymptomatic of illness; CD4+ count drops progressively ; 200-499 cells/ᵤL; Risk for
opportunistic infections; Inflammation in more than 2 areas for > 3 months

Stage 3  AIDS phase, caused by HIV infection of cells, viral load increases, suppressed immune system and
opportunistic infections, malignancies, wasting and CNS degeneration.
 Symptoms: Occurs when CD4+ cell count is less than 200 cells
 Respiratory: pneumocystis carinni pneumonia (PCP), pulmonary TB (can migrate anywhere in the body)
 GI: esophageal candidiasis, CMV infection, herpes simple virus, diarreah, gastroenteritis
Nervous System: taxoplasmosis (cat poo)
 Malignancies: Kaposi sarcoma, non-hodgkins, lumphoma

Diagnostic HIV tests
1. ELISA  enzyme-linked immunosorbent assay (ELISA) screens for HIV antibodies.
2. Western blot  test to confirm a positive Elisa test.
3. Polymerase Chain Reaction (PCR)  most accurate, most expensve

Nursing Assessment Weight analysis, LOC, Reports of pain
 Skin; palpation of lymph nodes, VS, lung sounds, oral cavity, rectal and vaginal exam

 HEMATOLOGIC DISORDERS

MVC  Normocytic: normal size; normal MVC
 Macrocytic: large size; high MVC
 Microcytic: small size; low MVC

MCHC  Normochromic: normal amount of Hb; normal MCHC
 Macrochromic: concentrated amount of Hb; high MCHC
 Microchromic: diluted amount of Hb; low MCHC


3

, Hypercoagulability  Increased platelet function
 Diabetes Mellitus: if they develop CHF at risk for clots.
 Smoking and oral contraceptives directly correlated in developing clots
 Arterial Thrombi, Atherosclerosis, atrial fibrillation, blood clots arise from heart cause
strokes, and murmurs
 Venous Thrombi: incompetent valves w/in veins

Thrombocytopenia  Platelet less than 100,000, most common cause of abnormal bleeding and loss of bone
marrow function occurs
 Excessive consumption of platelet (DIC chews up platelets, usually occurs from sepsis)
 Excessive pooling of platelets in spleen
 Causes: drug induced Thrombocytopenia; Heparin Induced Thrombocytopenia (HIT); Patients
allergic to heparin: platelets drop by more than 10%; Immune Thrombocytopenia Purpura (ITP)

Signs and Symptoms  mucus membranes bleeding: nose, mouth, GI, and uterine cavity. Occurs in small vessels
 Acute ITP most common bleeding disorder in children
 Chronic ITP most common in adults
 Excess destruction of platelets by body, platelet production decreased 1-3 days
 Petechiae (purplish red spots), Purpura (purple areas of bruising in large areas)

DIC Disseminated intravascular coagulation; complication of other disorders, bleeding and clotting at the same
time, seen in septic pts or severe trauma, cancers, and hematologic conditions
 Treated w/ heparin as blood is transfused as well
Post partum: amniotic emboli can occur along with DIC
H1N1 also caused DIC in some pts

Hodkin Lymphomareplacement of normal cell by Reedsternberg cells, mutation of T- lymphocyte.
 starts in single lymph node and spreads to neighboring lymph node. Eventually infiltrates
liver, spleen, lungs, bone marrow, and ureters.
 2 Categories:
1. Nodular lymphocyte predominant Hodgkin lymphoma, unique form that exhibits a nodular
growth pattern
2. Classical Hodgkin lymphoma is characterized by clonal proliferation of typical mononuclear
Hodgkin cells
 Unknown etiology, but exposure to carcinogens and viruses, genetics and immune
mechanisms has been proved to be the involved.
 Common in early adulthood (15-40) and in older adulthood (>55); Most common in men

Signs and Symptoms  Painless enlargement of a single node or group of nodes; initial lymph above the diaphragm
 Chest discomfort with cough and dyspnea.
 Fever, night sweats
 Weight loss
 Pruritus (itching)
 Advance stages of HL: liver, spleen, lungs, digestive tract, and CNS are involved.

Diagnostic Test  presence of Reed Sternberg cells in biopsy
 CT scans of chest and abdomen.
 Thrombocytosis, leukocytosis, eosinophilia, elevated erythrocyte sedimentation rate (ESR),
elevated alkaline phosphatase


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