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EXAM 1

Lines of defense:
1st line – mechanical and chemical barriers
 Cellular response
o phagocytosis by:
 neutrophils
 monocytes
 macrophages
2nd line – non-specific (inflammation and phagocytosis)
 vascular response
o Increased capillary permeability
 Vasodilation
3rd line – specific immunity (humoral and cell-mediated immunity)
 humoral immunity
o B cells and Ab’s
 Cell mediated
o T cells
Inflammation
Local effects:
Redness (rubor or erythema), heat, swelling, pain (vascular)
- Redness and warmth are caused by increased flow into the damaged area
- Edema is caused by the shift of protein and fluid into the interstitial space
- Pain is from increased pressure
Systemic effects: (cellular)
Mild fever, malaise, fatigue, headache, and anorexia

Chemical mediators Actions

histamine Immediate vasodilation and increased capillary permeability to form


exudate
bradykinins Vasodilation and increased capillary permeability, pain, and chemotaxis
chemotactic factors For example, attract neutrophils to site
cytokines Serve as communicators in the tissue fluids, sending messages to
lymphocytes and macrophages, the immune system, or the
hypothalamus to induce fever
prostaglandins Vasodilation and increased capillary permeability, pain, fever,
potentiate histamine effect

Diagnostic tests for inflammation/infection


Culture and sensitivity (sputum, blood, wound):
- Sample of body fluid taken to identify the presence of pathogen (organism) causing an
infection or illness
o Sample is added to a substance to help promote growth of the organism in a lab
setting
- Drug sensitivity may be preformed to determine the antibiotic that will work best to treat the
infection
Complete blood count (CBC) with WBC differential:
- CBC: basic screening test of the blood, most common ordered lab tests
o Provides info about the total number, variety, percentage, concentration and quality
of the blood cells (erythrocytes, leukocytes, and thrombocytes)
- WBC: specific patterns of leukocytes expressed as a percentage of the total number of
leukocytes
o Relative value (%) x WBC (cells/mm3) = absolute value (cells/mm3)
o Normal range: 4,500-10,500/mm3
C-reactive protein:
- A protein produced primarily by the liver during an acute inflammatory process
o A blood test that is positive for the presence of CRP indicates the presence of
inflammation but not the cause
o Non specific test for the presence of inflammation
Erythrocyte sedimentation rate:
- Measurement of the rate of the red blood cells settle in test tube over a period of time
o Diagnostic for inflammation but NOT for a specific disease
o Inflammation increases the protein (fibrinogen) in the plasma, causing the RBC’s to
clump together and this weight of the clumps settles faster than the individual cells
o Increased ESR is positive for inflammation
Types of healing
- Resolution: minimal tissue damage
- Regeneration: damaged tissue replaced with cells that are functional
- Replacement: function tissue replaced by scar tissue and loss of function

Healing process following tissue injury


Stage 1:
- Hemostasis: platelet aggregation. Clotting factor activation
Stage 2:
- Phagocytosis
- Angiogenesis and formation of granulation tissue
- Mitosis of nearby cells (epithelialization)
- Collagen formation: strengthen of wound bed
Stage 3:
- Scab retraction
- Wound contraction

Healing by first intention:


Refers to the process involved when the wound is clean, free of foreign material and necrotic tissue,
and the edges of it are held close together, creating a minimal gap between the edges.
- This type of healing is seen in some surgical incisions
Healing by second intention:
Refers to a situation in which there is a large break in the tissue and consequently more
inflammation, a longer healing period, and formation of more scar tissue
- A compound fracture would heal this way

Complication related to scar formation


Loss of function:
- Results from the loss of normal cells and lack of specialized structures or normal
organization in scar tissue
Contractures and obstructions:
- Scar tissue is non-elastic and shrinks over time, this process may limit movement range and
eventually lead to fixation and deformity of the joint (contraction)
- Shrinking may also cause shortening and narrowing (stenosis)
Adhesions:
- A band of scar tissue joining two surfaces that are normally separated
o common examples are the adhesions between loops of intestines or plueral
membranes
Hypertrophic scar tissue:
- an overgrowth of fibrous tissue consisting of excessive collagen deposit, leading to hard
ridges of scar tissue or keloid formation, can cause more sever contractures
Ulceration:
- blood supply may be impaired around the scar, resulting in further tissue breakdown and
possible ulceration
o this may occur when scar tissue develops in the stomach following surgery or healing
of an ulcer
o this scar tissue interferes with blood flow in nearby arteries

Types of hypersensitive reactions


Type I- allergic (A)
- Clinical manifestations: target areas become red and swollen, edema, pruritus, vesicles
forming, erythema, airway edema, increased IgE and eosinophils
o Examples: hay fever, anaphylaxis
Type II- Cytotoxic (B)
- Clinical manifestations: airway edema, pruritus, and decreased blood pressure
o Examples: ABO incompatibility, rheumatic fever
Type III- Immune complex ©
- Clinical manifestations: inflammation and tissue destructions
o Examples: Autoimmune disorders like SLE, glomerulonephritis, rheumatoid
arthritis
Type IV- cell mediated or delayed (D)
- Clinical manifestations: edema, redness, vesicles, pruritus
o Example: contact dermatitis, transplant rejection, TB test delayed response

Differentiation (specialization)
- Cells vary in their degree of development depending on differentiation required for a
particular cells function
Cancer
Risk factors (carcinogen):
- Genetic factors: oncogenes that regulate all growth
- Viruses: oncogenic viruses alter host cell DNA
- Radiation: UV rays (sun), x-rays, gamma rays, and radioactive chemicals cause cumulative
chromosomal damage in cells
- Chemicals: exposure to both natural and synthetic products in excess can be dangerous; the
effects of carcinogenic agents depend on the amount and duration of exposure
- Biological factors: chronic irritation and inflammation with increased mitosis
- Age: increasing
- Diet: natural substances, additives, or processing methods
- Hormones
Etiology:
- Carcinogenesis is the process by which normal cells are transformed into cancer cells

Pathogenesis:

Apoptosis: programmed cell death


Proto-oncogene: A normal gene which, when altered by mutation, becomes an oncogene that can
contribute to cancer
Oncogene: a gene that in certain circumstances can transform a cell into a tumor cell.
Tumor suppressor gene: or anti-oncogene, is a gene that protects a cell from one step on the path to
cancer
Staging cancer:
- Used to estimate prognosis
- Most common system used is the TMN system:
 Size of primary tumor (T)
 Involvement of regional lymph nodes (N)
 Spread (metastasis) of tumor (M)
Benign:
- Benign tumors have tissue name plus the suffix -oma (e.g., adenoma)
- Usually differentiated cells that reproduce at a higher rate than normal
- Encapsulated
- Tissue damage
 This is a result of compression of adjacent structures.
 It can be life-threatening in the brain.
Malignant:
- Malignant tumors (cancers) have the tissue name plus the suffix -carcinoma (e.g.,
adenocarcinoma)
- Undifferentiated, nonfunctional cells
- Rapid reproduction—abnormal mitotic figures
- Infiltrate or spread into surrounding tissue
- Spread to distant sites

Spread of malignant tumors:


- Invasion
 Local spread
 Tumor cells grow into adjacent tissues
 Example: Uterine carcinoma invades the vagina.
- Metastasis
 Spread to distant sites
 Via blood or lymph or other body fluids
 Example: Carcinoma of the colon spreads to the liver.

Spread of cancer:
In situ: cell growth and reproduction, such as cancer, remaining at the original site, not invasive or
spreading
Invasive: local spread
Metastasis: spread of the cancer cells to distant sites by the blood or lymphatic’s; secondary
malignant tumor
Seeding: refers to the spread of cancer cells in the body fluids or along membranes, usually in body
cavities
Primary tumor:
Secondary tumor:

Clinical manifestations of tumors:


Local effects of tumors:
- Pain
 Occurs when tumor is well advanced
 May be absent until late stages
- Obstruction
 When tumor compresses a duct or passageway
 Blood supply or lymphatic flow may be restricted
 Digestive tract
 Airflow in bronchi
- Tissue necrosis and ulceration
 May lead to bleeding or infection around the tumor

Systemic effects of malignant tumors:


- Weight loss and cachexia
 Anorexia, fatigue, pain, stress
 Increased demands on the body from tumor cells
- Anemia
 Caused by blood loss at tumor site
 Nutritional deficits may reduce hemoglobin synthesis.
- Severe fatigue
 Caused by inflammatory changes, cachexia, anemia
 Stress of treatment schedule
 Psychological factors
- Effusions
 Inflammation causes fluid buildup in body cavities.
- Infections
 Occur frequently as resistance declines
- Bleeding
 Tumor cells may erode the blood vessels.
- Paraneoplastic syndrome
 Associated with certain tumor types
 Tumor cells release substances that affect neurological function and may have
hormonal effects.

Diagnostic tests for cancer detection and monitoring:


CBC with WBC differential:
Histologic and cytologic exams collected by:
- Biopsy (tumor or bone marrow)
- Exfoliative cell sample
Tumor markers (prostate specific antigen-PSA)
Genetic marker (BRCA-1 for breast cancer)
Endoscopic exam
Imaging studies
- Radiological (x-ray)
- Computed tomography (CT)
- Ultrasound
- Magnetic resonance imaging (MRI)

Terms related to prognosis


- “Cure” for cancer: defined as a 5-year survival without reoccurrence after diagnosis and
treatment
- Remission: no clinical signs
- Terminal: leading to death

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