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%