an individuals perception of their state of health 

"how they feel"

Signs

and

Examples

- objective

-obvious to someone other than the affected person

Example: fever or skin rash

Symptoms

and

examples

- subjective

Example: pain or nausea 

clinical evidence or effects

the signs and symptoms of disease

the tendencies that promote development of a disease

"high risk" but not certain development 

potential unwanted outcomes of the primary condition

Example: paralysis after recovery from stroke

- short term

-develops quickly

-marked signs (severe fever or pain etc.)

insidious onset 

-gradual progression

-vague or very mild signs

atrophy 

and 

example

decrease in cell size

example: not using the muscle, menopause

Hypertrophy

Cause

example

increase in cell size

cause: homrones, exercise

example: breasst enlarge in pregnancy 

hyperplasia

cause

example

increase in number of cells

cause: irritation

example: puberty 

metaplasia

example

one cell type is replaced by another cell type

example: smoking 

dysplasia 

example

cells take on different sizes and shapes

example: abnormal pap smear

the growth of new cells

anaplasia = malignancy 

- apoptosis

-necrosis 

- loss of function

- change in morphology 

- ischemia (no blood to tissue)

-physical agents (heat, cold, radiation)

-mechanical (trauma, crush injury)

-chemicals/toxins 

◊exogenous - pollution, heavy metals, overdose, some drugs

◊endogenous - free radicals

- microorganisms

-abnormal metabolites

- nutritional deficites

-imbalance of fluid and electrolytes

-ischmic injury

-seen in localized bacterial infections

-dead cells release hydrolytic enzymes which digest and liquefy tissue

-area is walled off forming cyst or abscess

example: brain tissue dies 

-usually seen in kidney, heart, adrenal glands

-result of hypoxia

-cellular proteins are denatured "fried egg" effect

example: myocardial infarction 

-affects adipose tissue

-gross appearance is chalky white deposits

-common in abdominal structures

-commonly secondary to inflammation or trauma

-characteristic of TB infection of the lungs

-initiates chronic inflammatory response - forms walled off structure

-partial coagulation necrosis occurs in center 

-coagulative necrosis

-due to hypoxia from severe interference with arterial blood supply

-associated with DM, arteriosclerosis, smoking, severe frostbite

-skin turns dark brown or black

-slow progression

-liquefaction necrosis

-associated with bacterial infections

-interrupts venous drainage

- area is cold, swolling and pulseless

-can follow dry gangrene

-risk of sepsis 

- type of wet gangrene

-due to infection with bacteria that produces gas in tissues

-associated with trauma, DM, atherosclerosis, colon cancers

-cessation of respiration and cardiac activity

-lowering of body temp

-absent corneal reflex and papillary light reflex

- no brain wave activity on EEG

-no intracranial blood flow by arteriography

-non-specific

-mechanical barriers

-unbroken skin and mucous membranes

-tears and gastric juices etc. 

-non-specific

-phagocytosis

-inflammation

-"immunity"

-specific defense

-production of specific antibodies or cell-mediated immunity 

-tissue (not single cells)

-only occurs in living tissue

-localize injurious agent

-removes injurious agent

- initiates healing process (ultimate goal, if healing doesn't occur = chronic inflammation may ensue)

-infection

-physical damage

-chemical damage

-ischemia/infarction

-allergic rxn

-extremes in temp

-foreign bodies 

-vascular

-cellular

-chemical

-vasodilation

-increased permeability 

• allows cells and proteins to move out of vessels into injured tissues

- fibrinogen

-antibodies

-complement

• allows plasma to dilute toxins in tissue 

-mast cells

-neutrophils

-monocytes

-macrophages

they live in tissue

- degranulation of pre-formed chemicals (histamine and chemotactic factor)

-synthesis of mediators that perpetuate inflammatory response

*phagocytosis

- prepares site for healing

-neutrophils arrive 1st and end up in pus

-monocyte comes later (by 24 hours)

* macrophages - tissue dwelling phagocytes

*regulate the vascular mediators released by mast cells

- limit/control inflammation 

-release vascular mediators

-release chemotactic mediators 

-immediate vasodilation

-increased capillary permeability to form exudates

-activate neutrophils

-platelet aggregation

-increase plama proteins and ESR

-induce fever, chemotaxis and leukocytosis

*later response

-vasodilation and increased capillary permeability

-chemotaxis 

-vasodilation

-increased capillary permeability

-pain

-chemotaxis 

-vasodilation and increased capillary permeabiity

-pain

-chemotaxis 

-vasodilation and increased capillary permeability

-chemotaxis

-increased histamine response

-dilute toxins from bacteria and toxic chemicals relased by dying cells

-deliver SBC, antibodies, clotting factors and complement

-remove wastes

-transport nutrients 

-thin and watery

-small amount of protein/WBCs

example: blister fluid, burns, allergic rxn

-tick, sticky, clotted

-occur with more severe inflammation

-increased risk of scarring

example: strep throat, bacterial pneumonia, bacterial pericarditis 

-large content of leukocytes, cell debri and bacteria

-yello-green color

example: abcess 

-fever

-malaise

-fatigue

-headache

-anorexia

-leukocytosis = increased WBCs

-differential count = proportion of WBC altered depending on cause

-increased fibrinogen and prothrombin

-c-reactive protein present

-increased ESR

-cell enzymes present 

-infection

-deep ulcers

-skeletal muscle spasm

-local complications (obstruction, loss of sensation, decreased cell function)

-non-pharmacological (RICE)- (rest, ice, compression, elevation)

-Aspirin

-Tylenol

-NSAIDs

-glucocorticoids

-decreased capillary permeability

-enhanced effectiveness of epinephrine and norepinephrine

-decreased number of leukocytes and mast cells

- decreased immune response 

-atrophy of lymphoid tissue and decreased hemopoesis

-catabolic effects

-delayed healing

-delayed growth in kids

-retention of sodium and water due to aldosterone like affect in kidneys 

-resolution

-regeneration

-replacement 

-best outcome

-complete return to normal

-source of injury is eliminated

-removal of chemical mediators

-damaged tissue/organ capable of replacign necrotic area with same cell type

- not possible in all organs/tissues

-scar tissue

-occurs with extensive destruction

-function is lost

- damage is minor and there are no complications in healing

example: papercut, sutured surgical incision 

-occurs with large tissue loss or when wounds are left open

example: stage IV ulcer

tertiary intention 

-delayed primary intention healing

-seen with wounds left open and then sutured

-typicall leaves large scar

-youth

-good nutrition

-adequate hydration

-effective circulation

-clean, undisturbed wound

-no infection or further trauma

-advanced age

-poor nutrition/hydration

-anemia

-circulatory problems

-medical disorders

-irritation, bleeding, excessive mobility

-chemotherapy

-prolonged use of glucocorticoids

-epidermis and part of dermis

-little, if any blistering

-epidermis and part of dermis

-blister formation

- human leukocyte antigens

*genetically determined

*matched in transplants

*self-antigens

-major histocompatability complex antigens

*self-antigens

*gentically determined

*matched in transplants

macrophages

-originate in bone marrow --> monocytes

-live in organs and tissue

-functions:

*phagocytosis

*inflammation (secrete monokins and interleukins)

*antigen presenting cell

-immunocompetent

*specific response

-T cells and B cells

-mature in thymus

-cell mediated immunity

-includes:

*CD*- cytotoxic or killer T cells

*CD4 - helper T cells

suppressor T cells

memory T cells

cytotoxic or killer T cells

-destroy foreign cell membrane

-release monokines and lymphokinds

-attack cancer and virus infected cells

Helper T cells

-secrete cytokines which regulate all cells in the immune system

- "reserves"

-respond to antigen on 2nd exposure 

- mature in bone marrow

-target bacteria and viruses outside of body cells

-plasma cells (stimulated B cells) provide humoral immunity and produce antibodies

-B memory cells

natural killer cells

-target tumor cells and virus infected cells

-kill without prior exposure to antigen

-produced by plasma cells

-provide humoral (fluid in body) immunity

-IgG, IgA, IgM, IgE, and IgD

G - good going!

- most abundant ~85%

-only one that crosses placenta and gives passive immunity, the majority is transferred in last weeks of pregnancy putting pre-terms at greater risk of infection

-functions include:

*activates complement

-active against bacteria, virus and toxins

A - Ah Choo!!

-2nd most abundant

-found in secretions such as tears, saliva, respiratory, GI, vaginal, prostatic and breast milk

-functions include:

*prevents bacteria and virus from attaching to epithelial cells

M - Mega 

-largest

-1st to appear in circulation in response to foreign antigen, it's presence indicates infection

-1st one to be produced in newborn

-functions include:

*activates complement

*neutralizes microorganisms

*invovled in ABO incompatibility 

E - Egg allergy

- attaches to mast cells and basophils located in tissues

-binding of antigen to IgE attached to mast cells causes release of histamine

-function:

*mediates type 1 rxn (allergy)

*inflammation

- cell membrane bound found exclusively on B cells

-function:

*participates in antigentic activation of B-cells

-is not found in serum or body fluids

group of inactive proteins circulating in blood

C1 to C9

-classical pathway

-lectin pathway

-alternative pathway

-activated during immune rxn involving IgG or IgM when Ag-Ab complex binds to C1

-primary mediator of humoral immune system

-activated by gram-negative bacterial polysaccharides (endotoxin)

-activated by fungal cell wall polysaccharides (zymosan)

-opsonization

-anaphylatoxin activity

-cell lysis

-leukocyte chemotaxis

the secretion of chemicals that mark the invading organisms saying "eat me" 

- increases phagocytosis 

-relased by mast cells and basophils

-chemical mediator

-vasodilation, increased vascular permeability, pruitis, contraction of bronchiolar smooth muscle

-chemical mediator

-vasodilation, increased vascular permeability, pain

-chemical mediator

-type of lipid from mast cells and basophils

-contraction of bronchiolar smooth muscle

-inflammation

-chemical mediator

-released by macrophages and activated T cells

-lymphokines, monokines, interferons, interleukins

-activate and cause proliferation of T and B cells

-cellular communication

-inflammation, fever, leukocytosis

-chemical mediator

-tumor necrosis factor (type of cytokine)

-inflammation, fever, tissue wasting, septic shock (drop in BP, tumor necrosis 

-chemical mediator

-attract phagocytes

-measures levels of serum antibodies

-detect presence of infection

-enzyme linked immnosorbent assay

-detects for HIV antibodies

-used for a number of other diseases

-species specific

example: fish dont get rabies 

-gene specific

-r/t ethnicity

example: north american aboriginal people are more susceptible to TB

-primary (first exposure)

-secondary (repeat exposure)

-pathogen enters body and causes illness

-antibodies formed in host

example: chicken pox

-vaccine

-no illness

-antibodies formed in host

-from mother to child

-temporary protection

example: placental passage and ingestion of breast milk

-cyclosporine

-azathiprine

-prednisone

(homograft)

- species to species 

autograft

(heterograft)

two different species 

-hyperactive

-acute

-chronic/late

-immediately after transplant

-seen in ABO incompatible transplants

-must remove transplant

-after several weeks

-involves humoral and cell mediated immunity to un-matched HLA antigens

-uncommon after 1 year

-occurs after months or years

-see degeneration of blood vessels and loss of graft

-pt. often dies

-seen most often with bone marrow transplants

-donors lymphocytes initiate cell mediated type IV rxn against host cells

-severe dermatitis, diarrhea, fever, jaundice

-immune response to normal, harmless substances which usually results in some degree of damage to the body

type I - anaphylactoid or atopic rxn

type II - cytotoxic antibody mediated rxn

type III - immune complex mediated rxn

type IV - cell mediated, delayed rxn

-anaphylactoid or atopic rxn

-IgE mediated

-exposure to allergy (antigen)

-production of IgE --> binds to mast cells/basophils

-re-exposure = release of histamine (1st phase)

-2nd phase is 4-6 hours later with production of SRS-As which results in worsening signs and symptoms

-example of type 1 rxn

-sensitized mast cells release large amount of histamine into general circulation

-life threatening, severe systemic response to allergen

-overwhelming relase of histamine and other vasoactive chemicals into circulation 

-leads to shock

-generalized itching or tingling

-coughing

-difficulty breathing, stridor, wheezing

-feelings of weakness

-dizziness or fainting

-sense of fear or panic

-edema (eyes, lips, tongue, hands, feet)

-hives

-loss of consciouness with collapse

-epinephrine

-O2

-benadryl (H1 blocker)

-cimetidein, zantac (H2 blocker)

-albuterol (beta adrenergic)

-corticosteroids (blunt long term effects)

-fluid resuscitation

-cytotoxic hypersensitivity 

-cytotoxic antibodies, IgG or IgM react with antigen

-binding of IgG or IgM to antien forms a complex which can 

*activate complement or attrack NK, macrophages or neutrophils

*block receptor on cells surface so that function of cell is affected

-hemolytic anemia

-graves disease

-myasthenia gravis

-hay fever/allergic rhinitis

-food allergy

-atopic dermatitis/eczema

-asthma

-anaphylaxis

-immune complex hypersensitivity

-antibody binds to antigen and forms complex in circulation

-complex deposited in tissue or blood vessel wall

-complement activated

-inflammation

type IV rxn

(cell mediated)

-cell mediated

-not due to antibodies

-due to T-cells

*cytotoxic T cells attack and destroy directly

*cytokine producing T cells activate macrophages which cause tissue damage

Type IV rxn

(delayed)

-delayed response of sensitized T cells to antigen

-initiates inflammatory response

example: poison ivy, latex allergy (can also be type I), TB skin test

-hashimoto thyroiditis

-system lupus erythematosis

-rheumatic fever

-myasthenia gravis

-scleroderma

-pernicious anemia

-HIV

-marked by remissions and exacerbations

-polyarthritis with swollen painful joints, without damage

-butterly fash, photosensitivity, ulcers in mouth, hair loss

-glomerulonephritis

-pleurisy

-carditis - raynauds phenomenon

-psychoses, depression, seizures

-anemia, leucopenia, thrombocytopenia

-genetics

-common between ages 20-40 years

-10 times more common in women

-higher incidence in african americans, asians, hispanics and native americans

-estrogen

-recurrent EBV increases risk

-systemic lupus erythematosus

-autoimmune disease

-complexes form in circulation

-complexes are too large to be filtered

-elicits inflammation in specific organs

-NSAIDs, immunosuppression (predinsone, MTX)

-avoid triggers (sun exposure, fatigue, emotional upset)

-treat individual organs/systems affected

-basic developmental failure (often genetic or congenital diseases)

examples: Di Georges syndrome, X-linked hypogammglobulinemia

- loss of immune response due to specific causes

example: infections, splenectomy, malnutrition, liver disease, drugs, radiation, chemotherapy, HIV-AIDS, severe stress

-used to confirm infection if ELISA is positive

-if serum Ab binds to viral proteins pt. is HIV+

-polymerase chain rxn

-looks for RNA or DNA in WBC

-can detect as early as 5 days after infection

-drop in CD4 count and change in CD4/CD8 ratio

-presence of opportunistic infections/cancers

-2-4 weeks after exposure

-large viral load

-flu-like illness

-may be asymptomatic

"latent phase

+/- signs and symptoms

decreased viral load

-acute illness - AIDS

-CD4 T cell count = <200/ul

-memory loss, confusion, dementia

-candidiasis, herpes

-generalized lymphadenopathy

-TB, pheumocystis carinii pneumonia

-chronic diarrhea, infections of GI tract, wasting of GI, anorexia

-dermatitis, Kaposi's sarcoma

-Viremia - HIV

-decreasing count of CD4 helper T cells

-HAART - high active anti-retro virus therapy

-combo therapy of: reverse transcriptase inhibitors, protease inhibitors, ingtegrase inhibitors, entry inhibitors

-prokaryotes

-no neucleus, complex cell wall structure, unicellular

-function metabolically and reproduce

-divide by binary fission

-do not require living tissue

-vary in size and shape

-Bacilli (rod shaped)

-spirochetes (includes spiral forms and vibrio)

-cocci (spherical forms)

-rigid cell wall

*gram-positive stain purple

*gram-negative stain red

-external capsule or slime layer

-flagellae

-pili or fimbraie 

-release of toxins

-cell membrane

-enzymes

-cytoplasm

-binary fission

-spores

-usually produced by gram positive 

-relased as bacteria grows

-damage cells, inhibit protein synthesis

-cause immune response with production of anti-toxins

endotoxins

-present in cell wall of gram negative

-released on death of bacterium

-vasoactive compounds that can cause septic shock

-activate complement

-activate coagulation cascade

-act as pyrogens and initiate inflammation

-require living host

-lack enzymes

-bind to receptor on cell membrane of "host cell"

-can mutate

- common cause of STD

-can result in PID and infertility

-worldwide leading cause of blindness

-gram negative

-transmitted by insect vectors

-lack of cell wall

-cause of atypical pneumonia (walking pneumonia)

-eukaryotic (contain nucleus)

-fungal or mycotic infection (single celled yeast or multicellular molds)

-only a few are pathogenic

-cause primary infection on skin or mucous membranes

examples: histoplasmosis, pneumocystis carinii

-eukaryotic

-unicellular, lack cell wall

-pathogens are usually parasites

ex: trichomoniasis, malaria, amebic dysentery

-entomebea histolytica

exist in active form, secrete proteolytic enzymes which damage tissues

exist in hardy, resistant formed cysts and shed in feces

-flat or round worms

-ovum --> larva --> adult

-enter body through skin or ingestion

-more common in young children

-change shape of proteins in host cell

-transmitted by contaminated meats, blood or donor organs

-degenerative disease of nervous system

-creutzfelt-jacob disease

-variant creutzfelt jacob disease

three areas of body that are sterile

-brain

-bladder

-stomach

-age

-pregnancy

-genetic susceptibility

-immunodeficiency

-malnutrition

-chronic disease

-stress

-inflammatino or trauma

-immunosuppression

-chemicals

-autoclave

-must be cleaned before sterilized

-used on skin and tissues

-reduce number of organisms

-time between entry of organism and appearnce of clinical signs and symptoms

-organism is reproducing

fatiue, loss of appetite, headache

non-specific "coming down with something"

more evident in some infections than others

-disease fully develops

-manifestations reach peak

-length depends on virulence of organism and host factors

-infection is not fully eradicated

-organism continues to reproduce

-s/s usually milder

-periodic acute episodes may occur

-bacteria in blood

-small numbers for short time

-destroyed by phagocytes but may lead to septiciemia

-fever may be present

-fatigue and weakness

-headache

-nausea

-drugs derived from organism

-some newer drugs are synthetic

-antibacterial

-antiviral

-antifungal

-decreased rate of reproduction

-host then has ability to destroy organism

-drugs do not destroy virus

*host defenses kick in

*does not work on latent viral infections

-drugs may act by:

*blocking entry

*inhibit gene expression

*inhibiting assembly of virus

-interfere with mitosis in fungi

-interfere with fungal membrane permeability

-most are topical