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Solutions | Grade A+
• Cellular Chemotaxis -✓✓body releases chemical that dispatch WBC's & platelets
• Systemic Responses -✓✓FEVER*, pain, sleepiness, lethargy, anemia, & weight loss
• Titer -✓✓the level of antibody within the bloodstream, usually corresponds with to the
level of exposure to the microbe
TB, rubella, any vaccines...
Positive means you have been exposed through infection or vaccine!
• HIV -✓✓attacks CD4 cells- normal range 800-1200 cells/mm^3
Becomes significant when below 500, below 200= aids
• E-coli -✓✓bacteria are acquired by the fecal-oral route, usually in food or contaminated
water. The bacteria live in the intestines of healthy cattle.
• Immunocompetence -✓✓an individual's ability to protect oneself from infectious agents
because of a strong immune system
From a young age builds immune defenses & swiftly eliminates many microorganisms
as threats of infection
• immunosuppression -✓✓indicates that there is a defective immune system that is
placing a person at risk for infections.
• opportunistic infection -✓✓which is an infection caused by a microorganism that
flourishes because of a host's deficient immune system
• hospital-acquired infection -✓✓A patient infection caused by microorganisms that
originated within the clinical environment
Difficult to treat bc often caused by antibiotic-resistant bacteria
• Type I immediate hypersensitivity -✓✓Allergy; person produces many IgE antibodies
against a specific allergen
Occurs minutes after contact with allergen; histamine is released
Symptoms include hives, hay fever, asthma, eczema, gastric disturbances, and
anaphylactic shock (a life-threatening severe form)
, • Type II cytotoxic hypersensitivity -✓✓Igs attack antigens on cell surface
Antibody-mediated cell lysis results
Blood transfusion reaction is an example of a Type II hypersensitivity
• Type III immune complex disorders -✓✓occur when antigen combines with Ig within
circulation and these complexes are then deposited in tissues
autoimmine disorders
• Type IV delayed hypersensitivity -✓✓T cell mediated
Previous exposure to antigen primes the T cells
T cell attack does not occur until days after initial exposure (delayed)
Example: poison ivy, transplant rejection
Mantoux test for tuberculosis demonstrates a Type IV hypersensitivity
• SLE (systemic lupis erythemantous)-Etiology -✓✓Cause unknown, risk factors- genetic
predisposition and environmental, estrogen hormones (commonly occurs in women 14-
45-SN), and immunological elements
• SLE (systemic lupis erythemantous)- patho -✓✓Antibodies form immune complexes
that are deposited in organs & tissues such as the skin, heart, joint synovial
membranes, glomeruli of the kidney & lungs
This deposit of immune complexes triggers an inflammation reaction that damages
small blood vessels and various organ membranes
The kidneys are particularly susceptible to inflammation in SLE, termed as
Lupus nephritis.
The lungs also commonly succumb to inflammatory changes such as pneumonitis,
pleuritic, and pulmonary hypertension.
Cardiac involvement in individuals with SLE can cause pericarditis,
endocarditis, and coronary artery disease.
• SLE (systemic lupis erythemantous)- clinical manifestations -✓✓S/S- butterfly rash
(cheeks & nose), fever (higher than 100F- REPORT), joints- painful & swollen (SN)
Labs- (SN)
Creatinine over 1.3 = bad kidney (kidneys hit the hardest)
Decreased WBC (norm 5000-1000) so below 5000 normal for these pt- suppressed
immune system
• SLE (systemic lupis erythemantous)- triggers -✓✓Triggers (4 S's): sun exposure,
smokin, stress, sepsis (infection)
• HIV/AIDS etiology -✓✓HIV-1 affects most people in the US
HIV-2 most common in West Africa