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Exam (elaborations)

FINAL EXAM BLUEPRINT

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FINAL EXAM BLUEPRINT

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FINAL EXAM BLUEPRINT
1. Cellular adaptations- expected and pathological cellular changes of tissues and cells in
which diseases or pathologic processes occur.
 Atrophy- Decreased cell size  reduced tissue mass
 Hypertrophy- Increase in cell size  enlarged tissue mass
 Metaplasia- One mature cell type replaced by another mature cell type (adaptive)
 Dysplasia- Cells vary in size and shape, large nuclei, increased mitosis (chronic
irritation, precancerous- ex: pap smear)
 Anaplasia- Undifferentiated, numerous mitotic figures- characteristic for cancer
and basis for grading aggressiveness of tumor
 Neoplasm- new growth, tumor, malignant=cancer. Benign=less serious, do not
spread.

2. Inflammation and cellular responses- edema, platelets
 Platelets
o Cellular component of inflammation
o Activated by tissue destruction and inflammation
o Activation leads to interaction with coagulation cascade
o Degranulation with serotonin release (acts like histamine)
 Edema
o Type I Hypersensitivity manifestation
o Due to increased permeability

3. Infection and cellular defense mechanisms- acute and chronic infection, White Blood
Cell’s
 Acute******
o Self limiting
o Local manifestations-result from vascular changes and corresponding
leakage of circulating components into the tissue
o Heat, swelling, redness, pain
o Exudative fluids
 Chronic
o Inflammation lasting 2 weeks or longer
o Often related to an unsuccessful acute inflammatory response
o High lipid and wax content of a microorganism
o Ability to survive inside the macrophage
o Toxins
o Chemicals, particulate matter, or physical irritants
o Dense infiltration of lymphocytes and macrophages
o Granuloma formation
o Epithelioid cell formation
o Giant cell formation
 White Blood Cells
o White blood cell adherence to the inner walls of the vessels and migration
through the vessels

,4. Immune responses- autoimmune, cellular responses, viruses, HIV,
 Autoimmune
o Disturbance in the immunologic tolerance of self-antigens
o A-diseases occur when the immune system reacts against self-antigens
that autoantibodies or T cells damage tissues
 Cellular Responses
o Immune protection afforded by the ability of cytotoxic T cells to lyse
target cells that contain antigens that bind specific receptors
 Viruses
o Attenuated virus****- live viruses that are weakened, causes limited
antigen expression w a controlled infection. ***( negatives to ab use have
initiated more vaccine development) – immune compromised.
o Many can mutate within cells where they are not available to immune and
inflammatory mechanisms
o Not available to antibodies in circulation
 Antigenic variations:
 Antigenic drift-mutations allowing new strains,Flu virus changes
every year. ****
 Antigenic shifts- major changes in antigenicity, gene switching.
Antibodies constantly have to catch up by generating new
antibodies and t cells against new antigens.
o Effects
 Inhibition of host cell DNA, RNA, or protein synthesis (herpes)
 Disruption of lysosomal membranes release enzymes that damage
host cell (herpes)
 Transformation of host cell to cancer cell results in uninhibited and
unregulated growth (HPV)
 Promotion of secondary bacterial infection
 Fusion of infected, adjacent host cells to produce giant cells (Resp
Syncytial Virus)
 Alteration of antigenic properties of host cell leading to immune
system attack of cell as foreign (hep B)
 HIV
o Syndrome caused by a viral disease
o Human immunodeficiency virus (HIV) depresses the immune system and
leads to opportunistic and recurrent infections and AIDS ****
o HIV-Depletes the bodies Th cells which is necessary for the development
of plasma cells and cytotoxic T cells
o Structure
 gp120 protein binds to the CD4 molecule found primarily on
surface of helper T cells
 Destroys CD4+ Th cells****
 Typically 800 to 1000 cell/mm3, <200 Diagnostic
 Reverses CD4/CD8 ratio these help the interaction
between T cells and APC (Antigen presenting cells) by
reacting with antigen-presenting molecules.

, o CD4s interact with MHC (antigen presenting) 2
cells
o CD8s interact with MHC 1 cells.
o BOTTOM LINE: Degree of infectivity is a
measure of Viral load and CD4 counts (<200)
o Estimated time of HIV to AIDS 10 years (99%
will progress if HIV goes untreated).
o Clinical manifestations
 Serologically negative, serologically positive but asymptomatic,
early stages of HIV, or AIDS
 Window period- time period between infection and appearance of
an antibody. (Infectious to others)
 Th cells CD4 <200 cells/mm3 diagnostic for AIDS ***
 Diagnosis of AIDS is made in association with various clinical
conditions and lab tests:
 Atypical or opportunistic infections, and cancer
 Presence of antibodies against HIV (4 to 7 weeks after
blood transmission, 6-14 months after sexual intercourse)
****
 HIV protein p24 followed by Western blot analysis
(antibodies against other HIV proteins)
o Treatment and prevention
 Highly active antiretroviral therapy (HAART)
 Reverse transcriptase inhibitors
 Protease inhibitors
 New drugs
 Entrance inhibitors
 Integrase inhibitors
 Vaccine development
 The virus is like flu, highly variant
 Even though you have antibodies, may not be an effective
response to prevent the virus.

5. Hematological abnormalities and responses- Know the normal ranges of a CBC
(Complete Blood Count)- WBC’s(and breakdowns of each of the WBC’s- ex: NLMEB,
RBC’s, HGB, HCT, Platelets) know lab values of electrolytes and what would be
effected in various diseases, disorders, pathologic processes- ex: Acute Renal Failure/
Chronic Renal Failure- what labs would be effected such as electrolytes, RBC’s,
phosphate, Calcium, Potassium and BUN and Creatnine and GFR. Ex: Pancreatitis- what
enzymes would be effected. Coagulopathies, significant and consequences of albumin
alterations.

CBC (Complete Blood Count)
Platelet 150,000-400,000 (150-400)
Hemoglobin 13.5-18.0 g/dl
Hematocrit 40-50%

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