Patho Test 2.txt

• Innate Resistance
• (Natural or Native Immunity)

• Examples-
• Physical and mechanical barriers-sloughing off of cells, coughing/sneezing, flushing, vomiting, mucus/cilia
• Skin
• Linings of GI, GU, and respiratory tracts
• Biochemical barriers-saliva, tears, earwax, sweat, mucus

Inflammation

Inflammatory response activated to protect body from further injury, prevent infection of injured tissue, and promote healing

• Trauma
• Infection
• Surgery
• Caustic chemicals
• Heat and cold extremes
• Ischemic damage

• 1. Vasodilation- slower blood velocity increases blood flod flow to injured site
• 2. Increased vascular permeability-fluid escapes outside of vessel causing edema,
• Edema
• Increased concentration of red blood cells (warmth and redness)
• 3. White blood cell adherence to the inner walls-migrate thru enlarged juctions in vessel

• Limit and control tissue damage
• Prevent and limit infection and further damage
• Initiates adaptive immune response
• Initiates healing thru removal of bacterial products, dead cells, and other products of inflammation

Mast cell

Pg. 125:Figure 5-3

• Skin
• Digestive lining
• Respiratory tract

• physical injury
• chemical agents
• immunologic processes
• toll-like receptors

• 1. Degranulation-release granules
• 2. Synthesis-new production and release of mediators in response to stimulus

Histamine-vasoactive amine that causes temporary, rapid constriction of large blood vessels and dilation of postcapillary venules. Retraction of endothelial cells lining capillaries

• Chemotactic Factors-attration "recruit"
• Neutrophil chemotactic factor:Predominant cells need to kill bacteria in early stages of inflammation
• Eosinophil chemotactic factor of anaphylaxis-help regulate inflammatory response

• Leukotrienes
• Prostaglandins=pain
• Platelet-activating factor

(Review pg 126 in text for functions)

• Complement
• Coagulation
• Kinin

• Can destroy pathogens directly
• Activates or collaborates with every other componenet of inflammatory response

Forms fibrinous meshwork at injured or inflamed site

Functions to activate and assist inflammatory cells

Primary kinin is bradykinin

Causes dilation of blood vessels, pain, smooth muscle contraction, vascular permeability, and leukocyte chemotaxis

pgs. 129-134

• Rubor=redness
• tumor=swelling (histamine releases)
• calor=heat
• Dolor=Pain (bradykinin, prostaglandins)

Results from vascular changes and corresponding leakage of circulating components into tissue

• Serous-watery exudate from plasma indicating early inflammation
• Fibrinous-thick, clotted exudate indicating more advanced inflammation
• Purulent-contains pus, WBC, protein, tissue debris indicating bacterial infection (yellow, green)
• Hemorrhagic-leakage of RBC from capillaries indicating bleeding

• Fever-caused by exogenous and endogenous pyrogens. Pyrogens act directly on hypothalamus, portion of brain that controls body's thermostat
• Leukocytosis-increased number of circulating leukocytes or white blood cells. Shift to the left refers to ratio of immature to mature neutrophils. Bacteria causes shift to the left and called bands.
• Increased plasm portein synthesis-increased during inflammation, increased fibrinogen increases Erythrocyte Sedimentation Rate (ESR)

Consist of central area of amorphous caseous (cheeselike) necrosis that is surrounded by zone of activated macrophages, in which multinucleate macrophages (langerhans giant cells) are present. A wall of fibrin is laid down around granuloma, and the contents eventually breakdown and liquefy.

Chronic inflammation

Often related to an unsuccessful acute inflammatory response.

Chronic inflammation is characterized by dense infiltration of lymphocytes and macrophages. If macrophages are unable to protect the host from tissue damage, the body attempts to wall off and isolate the infected area, thus forming a granuloma

• splinters
• sutures
• viral
• bacterial
• TB lesion

• Filling in the wound
• Sealing the wound
• Shrinking the wound

• Primary intention
• Paper cut
• Sutured surgical wound

• Secondary intention
• Abdominal infection
• Pressure ulcers

Begins 3 to 4 days after injury and continues for as long as 2 weeks

• Fibroblast proliferation-lay foundation
• Collagen synthesis by fibroblasts
• Epithelialization
• Contraction of wound
• Cellular differentiation

Fibroblasts

Collagen

Maturation phase

Maturation phase

During remodeling, cappillaries disappear, leaving scar avascular

• Hemorrhage
• Fibrous adhesions
• Infection
• Steriods
• Hypovolemia
• Wound Sepsis

Impaired collagen matrix assembly- keloid scar, hypertrophic scar, scurvy

Impaired epithelialization-steroids, hypoxemia, nutritional deficiency

Impaired contraction-burns, can occur in liver constricting vascular flow

dehiscence-pulls apart

• Strain
• Obesity
• Increased risk of sepsis

Adaptive (acquired) Immunity

Often called immune response. Develops more slowly than the inflammatory response and is specific and has memory.

• Involves:
• Antigen/Antibody

Humoral and cell-mediated immunity

Active and passive Immunity

Cell Mediated T and B lymphocytes

B lymphocytes- B cells- produce antibodies that enter blood and react with antigen

T lymphocytes- T cells- attack antigen directly

Both are extremely speciif and recognize only one specific antigen

Active immunity

Long lived

Passive Immunity

Only temporary because donor's antibodies or T cells are eventually destroyed

Allergens

hypersensitivity

Type I: IgE mediated

Type II: Tissue-specific reactions

Type III: Immmune complex mediated

Type IV: Cell Mediated

IgE mediated reaction

Rate of development-Immediate

Antibody involved-IgE

Effector cells involved-Mast cells

Participation of complement-NO

Tissue specific reaction

Rate of development-Immediate

Antibody involved- IgG and IgM

Effector cells involved-Macrophages in tissues

Participation of complement-Frequently

Immune complex mediated reaction

Rate of development-Immediate

Antibody involved-IgG and IgM

Effector cells involved- Neutrophils

Participation of complement-Yes

Cell-mediated reaction

Rate of development-Delayed

Antibody involved-None

Effector cells involved-lymphocytes and macrophages

Participation of complement-No

IgE mediated-result of excessive or inappropriate production of IgE antibodies after exposure to some type of environmental antigen.

With initial exposure to antigen, IgE (immunoglobulin) binds to Fc receptor on surface of mast cell. Individual now sensitized to antigen. Antigens cause allergic responses called allergens. With subsequent exposure to antigen, tiny sacs in mast cells called granules break open and release histamine, which then triggers inflammatory response

Histamine

• Contracts Bronchial smooth muscles
• Increases Vascular permeability
• Increases blood flow to affected area
• Increased gastric acid secreation (N/V)

• Hay fever
• Food and drug allergies
• Bee stings
• Asthma
• Anaphylaxis

• Sudden onset
• GI symptoms
• Urticaria-hives
• ENT and respiratory symptoms
• Anaphylaxis-rapid onset, urticaria, cramps, difficulty breathing. Caused by bronchospasm, angioedema, hypotension, shock. Can be Lethal

• Predisposition to develop allergies
• Genetic tendency
• Higher quantities of IgE
• More Fc receptors on mast cells which connect IgE

Blood transfusions-red blood cell reaction

Specific cell or tissue (tissue specific antigens) is target of immune response. Direct interaction b/t IgG and IgM class antibodies and tissue or cell surface antigens.

• 1. Cell is destroyed by antibodies and complement
• 2. Antibody may cause cell destruction through phagocytosis
• 3. Toxic products produced by neutrophils
• 4. Antibody dependent cell mediated cytotoxicity (ADCC)
• 5. Cell malfunctions

Erythroblastosis Fetalis-Rh or Abo incompatibility b/t blood of mother and fetus

Hemolytic anemia-antibodies produced against red blood cells could be drug induced

Transfusion reaction-Antibodies produced against donor cells

Abnormal creation that forms. ex-autoimmune disorder

caused by antigen antibody immune complexes formed in circulation and deposited later in vessel walls and other tissue.

Size influences whether remain in plasma or lodge in tissues where they result in tissue damage.

Complement activated and neutrophils degranulate enzymes damage tissue. can damage and destroy healthy tissue

• Serum sickness
• Systemic lupus erythematosus
• arthus reaction-local reaction
• Acute glomerulonephritis that follows strept infection

• Mediated by Sensitized T lymphocytes
• Don't involve antibody
• Reaction delayed-24-72 hours after exposure

• Graft rejection
• Skin test for TB
• Allergic contact dermatitis- poison ivy and metals

Breakdown of tolerance to own antigens

• Examples-pg 171 other examples
• SLE
• Chronic multisystem inflammatory disease-abnormal antibodies attack RBC's

Autoantibodies against nucleic acids, erythrocytes, Coagulation porteins, platelets

Deposition of circulating immune complexes containing antibody against host DNA

More common in females

Clinical manifestation-Butterfly rash, Lupus

• facial rash
• discoid rash
• photosensitivity
• Oral or nasophyaryngeal ulcers
• arthritis
• serositis
• renal disorders
• neurologic dis
• hematologic disorder
• immunologic disorder
• Presence of antinuclear antibody-blood test of ANA-titer. some reaction going on in body if ANA is elevated

Immunse sys reacts w/antigens on tissue of genetically dissimilar members of same species

• ex.
• graft rejection
• transplant rejection classified to time:hyper, acute, chronic
• Hyperacute;immediate rejection

cellular immune system of transplant tissue can attach unrelated recipient tissue

Failure of immune mechanisms of self defense

Primary (congenital) immunodeficiency (Pg 196:Table 7-13)

Secondary (acquired) immunodeficiency-caused by another illness (cancer, infection) More common

Acquired Immunodeficiency Syndrome (AIDS)

Blood borne pathogen. Increasing faster in women than men.

• Depletes CD4 Th cells
• Incidence:Worldwide 5 mill/yr
• US 31K/yr

Retrovirus

Genetic information stored in RNA rather than DNA

Contains reverse transcriptase to convert RNA into double stranded DNA

Integrase inserts new DNA into infected cells genetic material

Structure:GP 120 proteins bind to CD$ molecule found on surface of CD4 Th cells

800-1000 cells/mm3

• Antibody 4-7 wks after blood products
• Antibody 6-14 mo after sexual transmission
• Window period
• Can still be infectious

Early signs-flu symptoms, swollen lymph glands, diarrhea, fatigue

Organisms produce infection in persons w/impaired immune function

• Encephalopathy
• Myelopathy
• Neuropathy
• Viral meningitis
• Opportunistic infections
• Neoplasms
• Bleeding

symptoms associated with many disorders (itching)

• Histamine
• Protease
• Heat
• Cold
• Chemical

Ischemic ulcers resulting from pressure, shearing forces, friction, moisture

• Sacrum
• Heels
• Ischia
• Greater Trochanter

result in the endothelial cell lining capillaries becoming disrupted with platelet aggregation

1-Persistant redness in light pigmented skin, persistant redness w/ blue or purple hues in dark pigment

2- Partial thickness skin loss involving the epidermis or dermis or both, Abrasion, blister, shallow crater

3-Full thickness skin loss involving damage or necrosis of subcutanous tissue : Deep Crater w/ or w/o undermining of underlying tissue

4- Full thickness skin loss with extensive destruction, tissue necrosis or damage to muscle bone or supporting structures

• scars that are progressively enlargeing due to excessive collagen
• shiny, hairless, elevated scars
• more common in African Americans and Orientals, ages 10-30

within 1 year of trama

• Allergic Contact Dermatitis
• Irritant Contact Dermatitis
• Atopic Dermatitis
• Stasis Dermatitis
• Seborrheic Dermatitis

• Common form of cell mediated or delayed hypersensitivity
• s/s-Erythema, prurites, vesticles

poison ivy, metals, latex

• Nonimmunologically mediated inflammatino of the skin
• Severity R/T concentration and exposure time
• Lesions similar to allergic type

Acids, soaps, detergents

Eczema

• more common in Infancy and childhood
• has increase serum IgE
• Family history of asthma, hay fever, atopic dermatitis
• s/s- skin is dry sensitive, itchy, skin pruritus

• occurs as a result of venous stasis and edema
• Associated with varicosities, phlebitis and vasucular trauma
• Erythema, pruritus, scaling, petechiae, hyperpigmentation, may progress to ulcerations

• Chronic inflammation
• on scalp, eyebrows, eyelids, ear canals, axilla, chest, back
• Infants=cradle cap
• Scaly, whitish, yellow, plaques
• Pruritus

• Disorders charasterized by papules, scales, plaques, and erythema
• Ex-Psoriasis

• Furuncles (Boils)
• Carbuncle
• Cellulitus
• Impetigo

• (Boil)
• Inflammation of hair follicle, single
• Red, firm nodule that may progress to a cystic nodule
• will see pus and necrotic tissue

• Collection of infected hair follicles-multiple
• See them on back of neck, upper back, lateral thighs

• infection of dermis and subcutaneous tissue
• Extension of a skin wound, ulcer, furuncles, carbuncles
• Will see Erythema, warmth, edema, pain

• caused by Staph, group A B-hemolytic streph
• Common in infants and childern-in summer season
• Vesicles and pustules weep and crust
• honey color serous liquid
• Pruritus
• Communitable

• HSV-1
• HSV-2
• Herpes Zoster

• Cold sore or fever blister
• Nongenital sites--mouth and cornea
• Vesicles rupture and form crust
• Dormant in nerve ganglia
• Recurrence stress, hormones

• Genital infections
• Large number are sexually transmitted
• Vesicles that progress to ulceration

Shingles

• Varicella occurs as a primary infection followed years later by herpes zoster
• Burning pain, paresthesia localized to the affected dermatome
• Vesicular eruptions
• Find Face, cervical, thoracic dermatome

• Tinea Corporis
• Tinea Capitis
• Tinea Pedis
• Candida

• fungal infections of the skin and are classified according to thier location on the body
• can get from animal

• Body
• (Ring Worm)

Scalp

• Feet
• (Athlets Foot)

• caused by yeastlike fungus Candida Albicans
• Normally found on mucous membranes, skin , GI tract and Vagina
• s/s Burning, itching, whitich yellow curdlike substance
• ex-thrush

• moist warm environment
• antibiotics
• pregnancy
• cushing disease
• diabetes mellitus
• debilitated states
• <6 months of age
• Immunosuppression

• Tumors of the skin are normally associated with aging
• Seborrheic Keratosis
• Actinic Keratosis

• Benign proliferation of the basal cells that produce smooth or waxy elevated lesions
• more common in older adults
• on chest, back, face
• Shades of tan, yellow, flesh colored, brown-black lesions

• precancerous tumors associated with exposure to UV radiation of the sun
• risk=individuals w/ unprotected light skin
• pigments patchese of rough skin

• Mole
• pigments and nonpigmented
• Flat and elevated
• watch for malignant transformation

fair complexion, excessive exposure to the sun, tanning salons, or ultraviolet radiation predisposes a person

• caused by sunlight exposure
• on face, neck
• slow growth
• metastatic spread rate
• more common in men then women

• start as nodule
• Pearly/Ivory
• Depressed Center and rolled borders
• progressess to ulceration with waxy borders

• A tumor of the epidermis
• Malignant potential
• sun exposure and fair complexion
• Red, scaly, elevated, irregular borders
• shallow chronic ulcer

• A tumor originating from the melanocytes
• Rapidly progressive, metastatic
• intermittent intense sun exposure

Raised, black, brown most from Nevi or moles shades of red, blue or white

cells that synthesize the pigment melanin

• A=Asymmetry
• B=Border Irregularity
• C=Color variation
• D= diameter >6mm
• E=Evolving Change

• Vascular Malignancy
• Endothelial Cell
• Purplish brown macules-develop into plaques and nodules
• Immunosuppression, transplant recipient, AIDS, African middle aged blacks, Jewish descent

• Inflammatory disease with cutaneous manifestations
• Discoid (cutaneous) is limited to the skin and can lead to SLE
• Lesions are often located on light-exposed areas of the skin, and photosensitivity is common
• most common site=face "Butterfly Rash"

altered immune responce to an unknown antigen

• flat, circumscribed area that is a change in the color of the skin
• ex-freckle

• An elevared firm area circumscribed are less than 1 cm in diameter
• ex-wart

• A flat nonplable, irregular shaped macule more than 1 cm in diameter
• ex-port-wine stain

• Elevated, firm and rough lesion with flat top surface more than 1 cm in diameter
• ex-psoriasis

• elevated irregular shaped area of cutaneous edema
• ex-insect bite

Elevated firm circumscribed lesion; deeper in dermis that a papule

Elevated solid lesion, may be clearly demarcated; deeper in dermis, more than 2 cm in diameter

• Elevated, circumscribed superficial not into dermis, filled with serous fluid- less than 1 cm in diameter
• ex-chickpox

• vesticle more than 1 cm in diameter
• ex-blister

• elevated superficial lesion similar to a vesicle but filled with purulent fluid
• ex-acne

• Elevated circumscribed encapsulated lesion, in dermis or subcutaneous layer, filled with liquid or semisold material
• ex-sebaceous cyst

• Fine, irregular red lines produced by capillary dilation
• ex- Telangiectasia in rosacea

heaped up, keratinized cell, flaky skin, irregular thick or thin

• rough, thickened epidermis secondary to persistent rubbing, itching, or skin irrritation
• ex-chronic dermatitis

• loss of the epidermis, linear, hollowed out, crusted area
• ex-abrasion, scabies

linear crack or break from the epidermis to the dermis

loss of part of the epidermis, depressed, moist, glistening, follows rupture of a vesicle or bulla

loss of epidermis and dermis, concave, varies in size

• thinning of the skin surface and loss of skin markings, skin appears translucent and paper like
• ex=Aged skin, striae