Patho Exam 1

First line of defense

nonspecific or general mechanism such as skin or mucous-membrane; blocks the entry of bacteria

Second line of defense

innate immune system mechanism; non-specific process ofphagocytosis

Third line of defense

specific mechanism in the body; stimulate production of antibodies, synthesized lymphocytes

Normal capillary exchange

* generally, capillary bed is not opened, it is based on the metabolic needs thecells or need of removal of wastes
* Arterial end: Movement of fluid electrolytes, oxygen, and nutrients exchange, based on net hydrostatic pressure; high pressure
* Venous end: osmotic pressure facilitates movement of fluid, carbon dioxide, and other wastes; low pressure

Capillary exchange during inflammation

* Injury to the site
* Chemical mediators: Histamine is released and causes vasodilation
* Vasodilation increases the blood flow, increased capillary permeability, opens capillary beds
* Swelling comes from continuous blood flow from increased release of histamine
* Leukocytes move to site of injury: fibrinogen makes network over injury
* Phagocytosis: removal of debris to prep for healing
* Everything then sent back through venous

Local effects of inflammation

erythema and warmth

edema

pain

loss of function

exudate

Serous exudate

watery, consists of proteins and WBC

Fibrinous exudate

thick and sticky; high cell and fibrin content; increased riskof scar tissue

Purulent exudate

thick, yellow green in color; cell debris, microorganisms, leukocytes

Abscess exudate

localize packet of purulent exudate or pus in solid tissue

Systemic effects of inflammation

* fever
* leukocytosis: increased number of leukocytes
* Elevated values: c-reactive proteins, ESR, cell enzymes
* Malaise, fatigue, headache anorexia

Chemical Mediators in inflammatory response

* Histamine: vasodilation and increased capillary permeability
* Cytokines: increase plasma proteins, ESR, induce fever, leukocytosis
* Prostaglandins: vasodilation, increased capillary permeability, pain,

Effects of chronic inflammation

* Diseases: : diabetes, cancer, cardiovascular (inflammation of the heart), Alzheimer’s disease, arthritis, pulmonary diseases, autoimmune disease
* tissue destruction
* chronic inflammation develops if acute inflammation not completely eradicated

Resolution Healing

minimal damage, damaged cells recover, damaged tissue returns to normal

Ex: sunburn

Regeneration healing

Damaged tissue is replaced by cells that are functional in mitosis; new cells are formed but do not contribute to the function of the organ

Ex:

Replacement Healing

extensive tissue damage or cells can’t be replaced on its own, can result in loss of function; wound has to be healed or covered by a new tissue

First degree burn (superficial partial thickness)

involves epidermis and upper part of dermis; little to no blister formation

* Red, painful, heal rapidly with no scar tissue

Second degree burn (deep partial thickness)

epidermis and part of dermis; blister formation

* Red, edematous, blistered, hypertensive within inflammatory stage; can leave scar tissue and be infected easily

Third and fourth degree burns (full thickness)

destruction of all skin layers and underlying tissues

* Burn area is charred, no initial pain because of destruction of nerves; edematous tissue is under the dead/charred skin, cuts into damaged skin maybe required to release pressure; requires skin grafts over burn region

Possible complications occuring the first few days after a burn

Dehydration

edema

Shock

Respiratory problems

Pain

Infection

Increased metabolic needs for healing period

Excessive burn fluid shift

inflammatory response results in a massive shift of water, proteins and electrolytes into tissues causes fluid excess or edema

results in decreased circulation of blood volume, low BP and shock

Why do third/fourth degree burns require skin grafts to heal

there are no cells available for the skin to heal on its own as all the skin layers and underlying tissues have been burn/damaged

Bacteria

prokaryotic, no nuclear membrane, function metabolically, divide by binary fission, do not require living tissue to survive

* Major groups: cocci (spheres), bacilli (rod-shapes), spirochete (coiled/wavy-lines), strepto (chains), staph (clusters)

Viruses

obligates intercellular organisms, requires living host for reproduction

* has active or latent stage
* protein coat/capsid allows for quick mutation
* nucleic acid core

Chlamydia

primitive forms, common cause of sexually transmitted infection, can result in infertility, related to bacteria

* Elementary Body (EB): infectious
* Reticulate body (RB): noninfectious, attacks host cells to repro

Rickettsia

gram negative bacteria that live inside host cell, obligates intercellular parasite

* transmitted by insect vector: lice, ticks

Fungi

eukaryotic organisms (contain nucleus), only a few pathogenic usually causing primary infections

* fungal infection- single celled yeast or multicellular mo

Prions

protein like agents that change the shape of proteins with host cells

* transmitted by contaminated tissue

Helminths

flat worms or parasites

Mycoplasma

common cause of pneumonia, lack cell walls

Resident flora locations

skin

nasal cavity

mouth

gut

vagina

urethra

Resident flora advantages

helpful in preventing other microorganisms from establishing a colony

Resident flora disadvantages

if resident biota from one body region invades another region, could inflect infection from foreign bacteria of that region

* easier for opportunistic infections to happen

Sporadic infection

in a single individual

Endemic infection

contagious transmission within a population

Epidemic

higher than normal transmission within a population

Pandemic

transmission has occurred on most continents

Direct contact

no intermediary; touching infectious lesions, sexual activity, contact with infected blood or bodily secretions

Indirect Contact

intermediary object or organism; contaminated food or hand, fomite/inanimate object

Droplet tranmission

respiratory or salivary secretions are expelled from infected individual

Aersol transmissinon

involves small particles from respiratory tract; suspended in air, and can travel faster than droplets

Vector borne transmission

insect or animal immediate host

Nosocomial infections

acquired infections, occur in health care facilities

Factors determining host resistance

age

pregnancy

genetic susceptibility

immunodeficiency

malnutrition

chronic disease

severe physical or emotional stress

inflammation or trauma

Pathogenicity

the capacity of a microbe to cause disease

Virulence

degree of pathogenicity

Virulence factors

invasive abilities

motility

enzymes

toxins; adherence to tissue by pili, fimbriae

specific receptor sites

ability to avoid host defenses

Superinfection

multi-drug resistant form of common infections

methods of preventing and controlling infection

Source and contacts must be identified in controlling infections

* Methods: sterilization of equipment
* Chemicals, heat, clean equipment prior to sterilization
* Use of chemicals: Antiseptics used on skins and tissues; disinfectants used on surfaces or objects

Incubation period

time between entry of organisms into the body and appearance of clinical signs and disease

Prodromal period

\n non-specific- “coming down with something”; fatigue loss of appetite, headache

Acute Period

Infectious period develops fully, and the clinical manifestations reach a peak; length depends on depends on virulence of the pathogen and host resistance

Convalescent period

when the signs subside, and body processes return to normal

Local signs of infection

organism enters the body and remains confined to a specific location; warmth, pain, tenderness, swelling, redness,

* Bacterial: purulent exudate


* Viral: serous, clear exudate

Systemic signs of infection

fever may present

fatigue and weakness

headache

nausea

Subclinical infection

microbe reproduces in body but does cause sign or symptoms

Blood tests

CBC to assess - variations in numbers of leukocytes

* Leukocytosis: bacterial infection
* Leukopenia: viral infection

Differential count

C-reactive protein

Erythrocyte sedimentation rate (ESR)

Immunological testing of bodily fluids

antigen identification

antibody titer

Nonspecific immune response

phagocytosis

inflammation

Specific immune response

production of specific antibodies against foreign substances

Lymphoid structures

lymph nodes

spleen

tonsils

intestinal lymphoid tissue

lymphatic circulation

Self antigens

HLA proteins label cells of the individual, immune system ignores self-cells

Non-self

immune system recognizes specific non-self-antibodies as foreign; memory cells produced to respond quickly to antigen

T lymphocytes

from bone marrow stem cells, further differentiation inthymus, cell mediated immunity

B lymphocytes

responsible to for produce antibodies, humoral immunity, mature in bone marrow, plasma cells, B memory cells

Macrophages

initiates immune response through phagocytosis (engulf foreign material); process and present antigen to lymphocytes for immune response, develop from monocytes; secretes chemicals (monokines, interleukins)

Bone marrow

origination of all immune cells

thymus

maturation of T lymphocytes

IgA

found in colostrum, secretions, tears, saliva and mucous membranes

IgG

most common in blood

* crosses placenta, creates passive immunity in new borns
* antibacterial, antiviral

IgM

first to increase in immune response; activates complement, involved in ABO incompatibility reactions

IgE

allergic response, causes release of histamine and other chemicals, results in inflammation

Active natural immunity

natural exposure to antigen, development of antibodies

* Person has infection and then develops antibodies

Active artificial immunity

antigen purposefully introduced to body; stimulation of antibody production

* Immunization, booster immunization

Passive natural immunity

IgG transferred from mother to fetus

* Across placenta, through breast milk
* Protection of infant for the first few months of life or until weaned

Passive artificial immunity

injection of antibodies, short-term protection

* Administration of rabies antiserum

Hyperacute transplant rejection

immediately after transplantation

Acute transplant rejection

develops after several weeks

Type 1 Hypersensitivity: allergic reactions

Clinical effects: skin rashes, hay fever, caused by allergen

Causative mechanism: exposure to allergen, development of IgE’s, mast cells

Complications: anaphylaxias

Type 2 Cytotoxic Hypersensitivity

Causative Mechanism: antigen is present on the cell membrane, may be normal or exogenous component; circulating IgGs or IgMs react with antigen activating complement

Type 3 immune complex hypersensitivity

Causative mechanism: Antigen combines with antibody, forms immune complexes, deposited in tissue, activation of complement system

Clinical effects: process causes inflammation and tissue destruction

autoimmune diseases

Ex: glomerulonephritis, rheumatoid arthris, lupus

type 4 mediated or delayed hyper sensitivity

Causative mechanism: delayed response by sensitized T lymphocytes, release of lymphokines, destruction of the antigen

Clinical effects: inflammatory response, contact dermatitis, allergic skin rash

Anaphylaxis

severe, life threatening, systematic hypersensitivity reaction result increased blood pressure, airway obstruction, and severe hypoxia

causes: latex materials, insect stings, nuts, shellfish, various drugs

Anaphylaxis symptoms

Generalized itching or tingling, especially in oral cavity

coughing

difficulty breathing

feeling of weakness, dizziness or fainting

sense of fear and panic

Edema around eyes, lips, tongue, hands, feet

Hives

Collapse with loss of consciousness

Anaphylaxis treatment

* First aid response (administer EpiPen)
* ER: epinephrine, glucocorticoids, antihistamines, oxygen, stabilize BP

Anaphylaxis effects

Vasodilation and increased capillary permeability: decreased blood pressure, faint, weak

Nerve endings irritated: itching

Constriction of bronchioles; release of mucous: airways obstructed, cough, dyspnea

Nervous system: anxiety, fear, dizziness, loss of consciousness

Severe oxygen deficit to the brain

Mechanisms of autoimmune disorders

* Individuals develop antibodies to their own cells or cellular material; the antibodies then attack the individuals tissue
* When self-tolerance is loss of one’s own antigens the immune system cannot differentiate self from foreign material, immune system leads to inflammation and tissue necrosis

Systemic Lupus Erythematosus patho

chronic inflammatory disease

presence of large number of circulating autoantibodies against DNA, platelets and erythrocytes, nucleic acids

* immune complexes are deposited into connective tissue in the body activated the complement, causing inflammation and necrosis
* Vasculitis (inflammation of the blood vessels) develops in organs, impairing blood supply to tissues

Systemic Lupus Erythematosus clinical manifestations

skin rash or joint inflammation; inflammation in specific organs that are affected

Systemic Lupus Erythematosus diagnostic tests

Antibody serum: presence of ANA in blood

ESR is high: indicating inflammatory response

Systemic Lupus Erythematosus treatment

* Glucocorticoids (prednisone): reduces inflammatory and immune response
* treatment specified to affected area

Causes of Immunodeficiency

loss of function, or total of one or more components of immune system leading increased risk

* primary: basic developmental failure somewhere in the system
* Secondary (acquired deficiencies): loss of immune response from specific causes

Immunodeficiency effects

predisposition to the development of opportunistic infections; arise form resident normal flora in the body

HIV-AIDs course

caused by HIV, HIV helper T cells (CD4 cells) are destroyed by the virus

* transmission: body fluids, semen, vaginal secretions, blood

HIV-AIDs effect

loss of immune response, increase susceptibility to secondary infections and cancer

HIV-AIDS complications

opportunistic infections, lymphoma, wasting syndrome, dementia

Vegetative state

loss of awareness and mental capacities, result of diffuse brain damage; person unresponsive to external stimuli

Locked-in syndrome

individual is aware and capable of thinking but is paralyzed and cannot communicate, use eye movement for yes or no response

Criteria for brain death

cessation of brain function:

* including function of the cortex and brainstem
* Flat or inactive electrotroencephalogram (EEG)

Absence of brainstem reflexes or responses

Absence of spontaneous respirations when ventilator assistance is withdrawn

Establishment of certainty of irreversible brain damage by confirmation of cause of the dysfunction

Evaluation twice by different physicians

Decorticate

responses include rigid flexion in the upper limbs, with adducted arms and internal rotation of the hands; lower limbs extended