Pat of Is

Disease and Illness concept
Pathogenesis
Both are used interchangeably, but not the same
Definition : a disease’s development or
Illness definition : change of individual cause the evolution
person was no longer in the state of perceived Most disease progress are according to a
“normal” health. typical pattern of symptom
Illness refers to subjective symptom that may Some disease are self limiting disease
not indicate the presence of disease. Other diseases are chronic disease , may
Disease : occurs when homeostasis isn’t undergo remissions or exacerbations
maintained. Other diseases are never resolve
Personal perception about disease was related Manifestations
with body failure to do the dayli living activity. Definition : a change in metabolism or cell division
that
Example : someone with diabetes disease. causes signs, lab data interpretation and symptoms.
Disease Subclinic condition
Disease doesn’t represent the new Subjective : Symptoms, reported by patient
development of life but express the Objective : Signs, disease’s identification by clinicians
distorsion of individual’s normally life. Lesi : structural change is caused by disease progress
Etiology Sequele : result of inflammation process
Definition : the cause of a disease Complication : new process or condition caused
Intrinsic and extrinsic factor secondary by first or original disease.
Intrinsic : inheritance, age, gender, nutritional Resolution : Patient can resolve from the disease

status without
complication or sequele.
Extrinsic : enviroment
What is this?
Idhiopatic : unknown causal
Nausea
Example : What is etiology of tuberculosis?
Fever
Intrinsic factor? Extrinsic factor ?
Edwien calm and cool student! Never give up until Finish! Cayo.........!!!
Sskin inflammation Stress can cause the release of epinephrine and
Bacterial pneumonia glucocorticoids, the release of epinephrine can
Disease is a dynamic process not a static cause panic or agression.
process
Disease relate with stress : heart, brain, lung. The
Manifestation of the disease was vary
energy of these organs were redirect by stress
every time. respon.
Disease stages
Immune system
Exposure or injury: target tissue is exposed by
causative Immunodeficiency infections. Ex AIDS
agent or injury
Tumors; on the other hand, a hyperactive
Latency or incubation period: no sign or symptoms are immune system may cause fatal disease, as in
evident the case of an overwhelming allergic reaction to
the sting of a bee.
Prodromal period :signs and symptoms are mild and The immune system may lose its normal
non specific capacity to distinguish self from nonself,
resulting in immune reactions against one's own
Acute phase : the disease reaches full intensity, tissues and cells (autoimmunity). Ex ITP
possibly resulting complications
Immune system
Remission :second latent phase occurs in some
disease, is often followed by another Responsible for safeguarding the body from
acute phase disease causing microorganism. It is a part of a
complex system of Host Defense
Convalescenc: the patient progresses toward recovery
after the termination of the disease Host defense : Innate/natural and
Recovery :the patients regains health or normal acquired/adaptive
function
Innate defense : physical (skin) and chemical barriers
Stress and disease (Lysozyme found in mucus, saliva, tears
and HCl), complex defense, cells, and natural
When a stressor such as life change occurs, a killer lymphocyte. Innate immunity is the first
line of defense, because it is always ready
person can respond in 2 ways :
Acquired defense : caused by foreigners
Succesfully to adapt encounter the body ( virus or bacteria)
1.
Failure to adapt, it can cause disease Immune respons
2. There are two main types of adaptive immunity—cell
mediated (or cellular) immunity _T cell, which is bearing cells, such as virusinfected or cancer
responsible for defense against intracellular microbes, cells. Cancer cells also have nonself proteins.
and humoral immunity B cell, which protects against Cytotoxic T cells are responsible for socalled
extracellular microbes and their toxins.
Cellular immunity is mediated by T (thymusderived) cellmediated immunity
lymphocytes, mature in Thymus Helper T (Th) cells regulate immunity by
Humoral immunity is mediated by B (bone marrow secreting cytokines, the chemicals that enhance
derived, mature in marrow) lymphocytes and their the response of other immune cells.
secreted products such as lymphokine (IL2, IL4,
MHC
Interferon8)
The T cell antigen receptor only in
Hummoral immunity = antibody mediated response ascociation with specific cell surface
molecules. Also known as HLA
Antigen
Every person receives one set of MHC
Substance can induce immune respons genes from each parent. Both sets are
expreesed on individual cells
T and B lymphocyte have specific
Natural Killer Cells
receptors to specific antigen molecular
Natural killer (NK) cells kill virus
shapes (epitop) infected cells and tumor cells by cellto
cell contact. They are large, granular
In B cells, the receptors are called by lymphocytes with no specificity and no
antibody (an immunoglobuline) memory. Their number is not increased by
prior exposure to any kind of cell.
Hapten?Carrier?
Complement system
Macrophage
Composed of a number of blood plasma proteins
Macrophages are immune and designated by the
inflammatory response letter C and a subscript. A limited amount of activated
complement
Macrophages lack receptors of specific protein is needed because a cascade effect occurs:
antigens, but they have specific receptors Each activated
for c region of immunoglobuline (Fc) protein in a series is capable of activating many other
Macrophages ingest and process the proteins.
antigen
The complement proteins are activated when
T cell pathogens enter the
body. The protein “complement” certain immune
Types of T Cells responses, which
accounts for their name.
The two main types of T cells are cytotoxic T
cells and helper T cells. Cytotoxic T (Tc) cells Certain other complement proteins join to form a
can bring about the destruction of antigen membrane attack
complex that produces holes in the walls and plasma result from such
membranes of second exposure exogenous antigens take a variety of
bacteria. Fluids and salts then enter the bacterial cell forms, such
to the point as itching of the skin, to potentially fatal diseases,
that it bursts. such as bronchial
asthma. The various reactions produced are called
Complement system includes 20 serum proteins hypersensitivity
reactions, and tissue injury in these reactions may be
There are 2 pathways : classic and alternate caused by
humoral or cellmediated immune mechanisms.
Classis : Ig M and IgG binds with the antigen and
activate C1 next Injurious immune reactions may be evoked not only by
turn to activates C4, C2 and C3 exogenous
environmental antigens, but also by endogenous tissue
Alternate : bacterial cell membranes activates C3, and antigens.
next to C5
and C9 Some of these immune reactions are triggered by
homologous
Cytokines and Immunity antigens that differ among individuals with different
genetic
LMWP involved in communications berween backgrounds. Transfusion reactions and graft
rejection are examples
macrophage and lymphocyte of immunologic disorders evoked by homologous
antigens.
Whenever cancer develops, it is possible that
cytotoxic T cells have not been activated. Type 1 Systemic Anaphylaxis
With this possibility in mind, cytokines have Systemic anaphylaxis is characterized by vascular

shock, widespread
been used as immunotherapeutic drugs to edema, and difficulty in breathing. In humans,
enhance the ability of T cells to fight cancer. systemic anaphylaxis may
occur after administration of foreign proteins (e.g.,
Interferon, and also interleukins, which are antisera), hormones,
cytokines produced by various white blood cells, enzymes, polysaccharides, and drugs (such as the
are also being administered for this purpose. antibiotic penicillin
Pathophysiology manifestation The severity of the disorder varies with the level of
sensitization.
There are 3 basic reactions : Extremely small doses of antigen may trigger
anaphylaxis, for example, the
hypersensitivity, autoimmune response tiny amounts used in ordinary skin testing for various
forms of allergies.
and alloimmune response
Within minutes after exposure, itching, hives, and skin
HypersensitivityExogenous antigens occur in dust, erythema appear,
pollens, foods, drugs, followed shortly thereafter by a striking contraction of
microbiologic agents, chemicals, and many blood respiratory
products used in bronchioles and respiratory distress. Laryngeal edema
clinical practice. The immune responses that may results in
hoarseness. Vomiting, abdominal cramps, diarrhea, veritable virus factory and
and laryngeal reservoir, whose output remains largely protected
obstruction follow, and the patient may go into shock from host defenses.
and even die within
the hour. The risk of anaphylaxis must be borne in Second, macrophages provide a safe vehicle for HIV
mind when certain to be transported to
therapeutic agents are administered. Although
patients at risk can generally various parts of the body, including the nervous
be identified by a previous history of some form of system.
allergy, the absence of
such a history does not preclude the possibility of an Third, in late stages of HIV infection, when the CD4+
anaphylactic reaction. Tcell numbers
Type 2Type 3Type 4Autoimmune diseaseBody’s decline greatly, macrophages may be an important site

normal defense become self of continued viral
destructive, recognizing self antigen as a
foreign replication.In contrast to tissue macrophages, the
number of monocytes in
The causes are not clearly understood
circulation infected by HIV is low, yet there are
Alloimmune responseCommonly happens in unexplained functional
transplantation or
transfusion defects that have important consequences for host
defense. These defects
The recipients react to antigens, primarily
include impaired microbicidal activity, decreased
the HLA of the donor cells chemotaxis, decreased
Commonly ascociated with type 2 secretion of IL1, inappropriate secretion of TNF, and,
hypersensitivity reaction most important, poor
Immunodeficiency capacity to present antigens to T cells.
An absent or depressed immune response
increses susceptability to infection. RADANGINFLAMMATION
Defect of T cell, B cell, lymphoid tissue DAP
Disorder Definition
In vascularized tissues, some stimuli can provoke a
AIDS host
response called inflammation.
Caused by gradual destruction of T cell
nflammation agents such as microbes and damaged,
HIV infection of macrophages has three important usually
implications. necrotic cells that consists of vascular responses,
migration and
First, monocytes and macrophages represent a activation of leukocytes, and systemic reactions.
The inflammatory response is closely interwined with phagolysosome but also into the extracellular space.
the process The
of repair. Inflammation serves to destroy, dilute, or most important of these substances in neutrophils and
wall off the macrophages are lysosomal enzymes, present in the
injurious agent, and it sets into motion a series of granules; reactive oxygen intermediates; and products
events that try of
to heal and reconstitute the damaged tissue. Repair arachidonic acid metabolism, including
begins prostaglandins
during the early phases of inflammation but reaches and leukotrienes.
completion
usually after the injurious influence has been These products are capable of causing endothelial
neutralized. injury
and tissue damage and may thus amplify the effects of
During repair, the injured tissue is replaced through the initial injurious agent.
regeneration
of native parenchymal cells, by filling of the defect Products of monocytes/macrophages and other
with fibrous leukocyte types have additional potentially harmful
tissue (scarring) or, most commonly, by a products
combination of these
two processes. Phospholipid
Acute InflammationDefinition Arachidonat acid
Direct response of the body to the injury or cyclooxigenase lipooxigenase
death cells.
Hidroxy and
Sign : rubor, kalor, dolor, tumor, functio laesa
endoperoxide
Exudation : cellular and non cellular, caused
by protein leakage hydroperoxy fatty acid

Cellular Exudation : neutrophyl exudation and tromboxan prostaglandine leucotrien
mixed exudation
TERMINATION OF THE ACUTE
Noncellular exudation : serosa, fibrinosa, INFLAMMATORY RESPONSE
musinosa
It is predictable that such a powerful system of host
Lymphatic system (limphangitis, limphadenitis) defense, with
its inherent capacity to cause tissue damage, needs
Cellular aspect tight controls
to minimize the damage.
1. Margination and Emigration of leucocyte
In part, inflammation declines simply because the
2. PhagocytosisRelease of Leukocyte Products and mediators of
Leukocyte inflammation have short halflives, are degraded after
Induced Tissue Injury their
release, and are produced in quick bursts, only as long
During activation and phagocytosis, leukocytes release as the
microbicidal and other products not only within the stimulus persists.
organization.
In addition as inflammation develops, the process also
triggers a 3. Progression of the tissue response to chronic
variety of stop signals that serve to actively terminate inflammation (discussed below). This
the may follow acute inflammation, or the response may
reaction. be chronic almost from the
onset. Acute to chronic transition occurs when the
These active mechanisms include a switch in the acute inflammatory response
production of proinflammatory leukotrienes to cannot be resolved, owing either to the persistence of
antiinflammatory lipoxins from the injurious agent or to
arachidonic acid , the liberation of an anti some interference with the normal process of healing.
inflammatory cytokine, transforming growth factorb
(TGFb), from macrophages and For example, bacterial infection of the lung may
other cells; and neural impulses (cholinergic begin as a focus of acute inflammation
discharge) that (pneumonia), but its failure to resolve may
inhibit the production of TNF in macrophages. n lead to extensive tissue destruction and
Inflammation mediatorsOutcome of acute formation of a cavity in which the inflammation
inflammation continues to smolder, leading eventually to a
chronic lung abscess. Another example of
1. Complete resolution. In a perfect world, all chronic inflammation with a persisting stimulus
inflammatory reactions, once they have is peptic ulcer of the duodenum or stomach.
succeeded in neutralizing and eliminating the Peptic ulcers may persist for months or years
injurious stimulus, should end with and, as discussed below, are manifested by
restoration of the site of acute inflammation to both acute and chronic inflammatory reactions.
normal. This is called resolution
and is the usual outcome when the injury is limited or Chronic InflammationClinical Data Interpretation
shortlived or when there has been little tissue
destruction and the damaged parenchymal cells can T
regenerate. Resolution involves neutralization or
spontaneous decay of the WBC
chemical mediators, with subsequent return of normal
vascular permeability, LED
cessation of leukocytic infiltration, death (largely by
apoptosis) of neutrophils, and Endocrine and metabolism : malaise,
finally removal of edema fluid and protein,
leukocytes, foreign agents, and anorexia, drowsiness
necrotic debris from the site of inflammation
2. Healing by connective tissue replacement Bacterial Infection

(fibrosis). This occurs after substantial
tissue destruction, when the inflammatory injury
involves tissues that are Definition
incapable of regeneration,or when there is abundant
fibrin exudation. When the • Invasion and multiplication of microorganisms in
fibrinous exudate in tissue or serous cavities (pleura, body tissues that produce sign and symptoms
peritoneum) cannot be such as an immune response
adequately cleared, connective tissue grows into the
area of exudate, converting • The severity of infections depends on :
it into a mass of fibrous tissue—a process also called pathogenicity, number of microorganism,
strength of host defenses
Pathophysiology change• Inflammation
• Weakened defense mechanism :
• Red, heat, pain, edema, loss of function
immunodeficiency (low level of T cell and B cell,
• Fever (many microorganism are unable to
disfunction of WBC)
survive in a hot environtment)
• Microbes can enter the host by inhalation, ingestion,
sexual transmission, insect or animal bites, or • Leucosytosis (neu, eos, baso, lymp, mono)
injection.
The first barriers to infection are intact host skin and • Chronin inflammation
mucosal surfaces and their secretory products. In • ESR

general, respiratory, gastrointestinal, or genitourinary
tract infections occur in healthy persons and are • Stained smear
caused
by relatively virulent microorganisms that are capable HOW MICROORGANISMS CAUSE DISEASE
of
damaging or penetrating intact epithelial barriers. In • Infectious agents establish infection and damage
contrast, most skin infections in healthy persons are
caused by less virulent organisms entering the skin tissues in three ways:
through damaged sites (cuts and burns).
1. They can contact or enter host cells and directly
• Bacteria damage body tissues by interfering
cause cell death.
with essential cell function or by releasing
2. They may release toxins that kill cells at a
exotoxins or endotoxins which cause cell
distance, release enzymes that degrade tissue
damage.
components, or damage blood vessels and
• During bacterial growth, the cells release
cause ischemic necrosis.
axotoxins, enzymes thata damage host cell,
3. They can induce host cellular responses that,
altering it functions or killing it.
although directed against the invader, cause
• Enterotoxins are a specific type of exotoxins
additional tissue damage, usually by immune
secreted by bacteria that infect the gi tract,
mediated mechanisms.
affect the vc and cause gastroenteritis.
SKin
• Endotoxins are contained in the walls of
• The dense, keratinized outer layer of skin is a natural
gram negative bacteria, released during the barrier to infection,
lysis of bacteria and the low pH of the skin (about 5.5) and the
presence of fatty acids organisms, whereas volunteers given Vibrio cholerae
and
inhibit growth of microorganisms other than sodium bicarbonate have a 10,000fold increase in
residents of the normal flora. susceptibility to cholera.
Human skin is normally inhabited by a variety of • In contrast, some ingested agents, such as Shigella
bacterial and fungal and
species, including some potential opportunists, such Giardia cysts, are relatively resistant to gastric acid;
as Staphyloccus
epidermidis and Canadida albicans. Although skin is hence, as few as 100 organisms of each are sufficien
usually an effective to
barrier, certain types of fungi (dermatophytes) can
infect the stratum cause illness.
corneum, hair, and nails, and a few microorganisms
are able to traverse the Respiratory
unbroken skin.
• Some 10,000 microorganisms, including viruses,
• For example, Schistosoma larvae released from
freshwater snails penetrate bacteria, and fungi, are inhaled daily by every city
swimmers' skin by releasing collagenase, elastase,
and other enzymes that inhabitant. The distance these microorganisms travel
dissolve the extracellular matrix. Most
microorganisms, however, penetrate into the respiratory system is inversely proportional
through breaks in the skin, including superficial to
pricks (funga infections),
wounds (staphylococci), burns (Pseudomonas their size
aeruginosa), and diabetic and
pressurerelated foot sores (multibacterial infections). • Large microbes are trapped in the mucociliary
Intravenous catheters blanket
in hospitalized patients can produce local or systemic
infection that lines the nose and the upper respiratory tract.
(bacteremia).
Microorganisms are trapped in the mucus secreted by
GI
goblet cells and are then transported by ciliary action
• Most gastrointestinal pathogens are transmitted by to
food the back of the throat, where they are swallowed and
or drink contaminated with fecal material. Where
cleared. Organisms smaller than 5 μm travel directly
hygiene fails, diarrheal disease becomes rampant. to
the alveoli, where they are phagocytosed by alveolar
• Acidic gastric secretions are important defenses
within macrophages or by neutrophils recruited to the lung
the gastrointestinal tract and are lethal for many by
gastrointestinal pathogens. Healthy volunteers do not
cytokines.
become infected by Vibrio cholerae unless they are
fed • Damage to the mucociliary defense results from
repeated insults in contrast to 20 cm in men.
smokers and patients with cystic fibrosis, while acute
injury occurs • Obstruction of urinary flow and/or reflux can
in intubated patients and in those who aspirate gastric compromise normal defenses
acid. and increase susceptibility to UTIs. UTIs can spread
retrogradely from the
• Successful respiratory microbes evade the bladder to the kidney and cause acute and chronic
mucociliary defenses in pyelonephritis, which is
part by attaching to epithelial cells in the lower the major preventable cause of renal failure.
respiratory tract and
pharynx. • From puberty until menopause, the vagina is
protected from pathogens by
• For example, influenza viruses possess a low pH resulting from catabolism of glycogen in the
hemagglutinin proteins that normal epithelium by
project from the surface of the virus and bind to sialic lactobacilli. Antibiotics can kill the lactobacilli and
acid on the make the vagina
surface of epithelial cells. This attachment induces susceptible to infection. To be successful as
the host cell to pathogens, microorganisms
engulf the virus, have developed specific mechanisms for attaching to
vaginal or cervical
• leading to viral entry and replication within the host mucosa or enter via local breaks in the mucosa during
cell. However, sex (genital warts,
sialic acid binding prevents newly synthesized viruses
from leaving syphilis).
the host cell. Influenza viruses have another cell
surface protein,
neuraminidase, which cleaves sialic acid and allows
virus to release
from the host cell.
Urogenital
• The urinary tract is almost always invaded from the
exterior via the urethra
• The regular flushing of the urinary tract with urine
serves as a defense
against invading microorganisms.
• Urine in the bladder is normally sterile, and

successful pathogens (e.g.,
gonococci, E. coli) adhere to the urinary epithelium.
Anatomy is an
important factor for infection. Women have more than
10 times as many
urinary tract infections (UTIs) as men, because the
distance between the
urinary bladder and skin (i.e., the length of the
urethra) is 5 cm, in

Pat of Is

Transféré par

Informations du document

Description originale:

Copyright

Formats disponibles

Partager ce document

Partager ou intégrer le document

Options de partage

Avez-vous trouvé ce document utile ?

Ce contenu est-il inapproprié ?

Droits d'auteur :

Formats disponibles

Pat of Is

Transféré par

Droits d'auteur :

Formats disponibles

Disease and Illness concept

Intrinsic : inheritance, age, gender, nutritional Resolution : Patient can resolve from the disease

With this possibility in mind, cytokines have Systemic anaphylaxis is characterized by vascular

Type 2Type 3Type 4Autoimmune diseaseBody’s decline greatly, macrophages may be an important site

2. Healing by connective tissue replacement Bacterial Infection

mucosal surfaces and their secretory products. In • ESR

• Urine in the bladder is normally sterile, and

Vous aimerez peut-être aussi