Transcript Pathophysiology

INTRODUCTION TO
Pathophysiology
Mechanisms of Disease
Diagnosis & Treatment
Inflammation & Healing
Terms Used In Pathophysiology
• Pathology = study of disease
• Pathogenesis = the development of a disease
» Diseases develops in stages
» Infectious disease example:
(A)incubation (b)disease (c)convalescence
• Pathophysiology = the study of the functional changes
associated with a specific disease
» How the disease affects specific functions of the body
• Subjective findings
» The patient’s symptoms
» Described by the patient----(the patient’s history)
• Objective findings
» Health provider’s findings---( the physical exam)
• Occurrence of disease defined by 2 factors
• Incidence = # new cases per unit of time
• Prevalence = # new & old cases per unit of time
• Disease terminology
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Etiology = cause of the disease
Idiopathic = disease with unknown cause
Iatrogenic = disease caused by human intervention
Congenital diseases = diseases occurring at birth
Syndrome = common cause of different signs & symptoms
Remission = period when symptoms & signs of disease abates
Exacerbation = period when symptoms & signs increase
Endemic disease = disease native to local area
Epidemic = many people affected in a given area
Pandemic = many people affected in large areas
Incubation = latent period of the disease before develop signs &
symptoms
Prognosis = probability for recovery
Morbidity = disease rates within a group
Mortality = death rates within a group
Epidemiology = how the disease occurs & spreads through an area
Predisposing Factors (risk factors)
• Age
• Young are prone to accidents
• Getting diseases such as diabetes, heart disease, and certain
cancers increase with age
• Very old are prone to drug interactions
• Sex
• More frequent in woman: MS, osteoporosis
• More frequent in men: gout, Parkinson’s disease
• Lifestyle
• Examples of harmful lifestyle:
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Perilous occupation
Smoking
Excess alcohol
Poor nutrition
Sedentary activity
• Environment
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Air pollution
Water pollution
Poor living conditions
Excessive noise
Chronic psychological stress
• Heredity
• Deals with genetic predisposition (inheritance)
» Genetic predisposition + certain type of environment =
mental retardation , lung cancer, etc.
• Preventive health care
• The best treatment of a disease is prevention !!
• Deals with altering risk factors that can be changed
Homeostasis
• Definition = internal constancy or a stable internal environment
• A “body in balance” is in homeostasis
• Homeostatic regulation ---- works by using feedback loops
• Feedback loops utilize 3 components
(1) receptor
(2) control center
(3) effector
– 2 types of feedback loops
(1) negative feedback
– Restores any change back to normal
– Resembles “teeter-totter”
– Stabilizing
– Most common
(2) positive feedback
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Exaggerates the change
Resembles “domino effect”
Stimulating
Least common
• Homeostasis & disease
– Disease is the failure to maintain homeostatic conditions
• Disease mechanisms
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Genetic = mutated or abnormal genes
Pathogens (microscopic organisms)
Loss of control mechanisms (e. G. Diabetes, immune problems)
Degenerative changes (normal aging)
Environmental hazards (trauma, chemicals)
Nutritional factors
Tumors (benign & malignant)
The Cell & Disease
Changes in Growth
• Changes in size of individual cell
– Atrophy = decrease in cell size
– Hypertrophy = increase in cell size
• Changes in actual number of cells
– Hyperplasia, Dysplasia, & Anaplasia = increase in rate of
reproduction
– Hyperplasia = increase in number of normal cells
– Dysplasia = increase in number of atypical cells
– Anaplasia = increase in number of frankly abnormal cells
Change in Type of Cell
• Change of one type of cell into another type (metamorphoses)
– Metaplasia =change to different mature cell type
• Cell damage is the main reason to lose homeostasis
– Deficiency of oxygen (hypoxia) = most common reason
• Mechanism of progression:
ischemia
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necrosis -to-
gangrene
• Cell death
– Once it occurs, lysis occurs with release of lysosomal enzymes
• This causes inflammation
• After inflammation, the dead cells(tissue) is either:
• Replaced by scar tissue
• Regenerated to resemble original tissue
Diagnosis & Treatment
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“SOAP” protocol:
“S” = subjective
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“O” = objective
“A” = assessment
“P” = plan
Subjective Findings = the patient’s symptoms
• Obtained by taking a medical history
– includes:
» Chief complaint (cc)
» present illness (PI)
» past history (PH) ------- med/ surg/ allergies/ lifestyles
» family history (FH)
» review of systems (ROS)
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Objective Findings = the patient’s physical manifestations
• Obtained by doing a physical exam
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Begins with opening statement (WD/WN/WW)
Then vita signs ------ T, P, BP, RR, Pain
go from head to toes!
Includes techniques of:
» inspection
» auscultation
» palpation
» percussion
• Assessment = arriving at a diagnosis
– Differential diagnoses
• Includes all possibilities
– Lab
• Basically a study of body fluids
– Diagnostic tests
• Imaging
» X-ray, US, CAT, MRI, isotope scans
• Endoscopies
• Biopsies
• Skin tests
• Plan = all possible treatments with associated complications & prognoses
• Includes a “Treatment Plan”
– individualize
– modalities available:
» do nothing (primun non nocere)
» Talk (counseling)
» Medication
» Surgery
• Includes a Prognosis
The Inflammatory Response
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Key purposes = DEFENSE
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To hunt & kill invaders
To limit their spread
To prepare tissue for repair
Key events
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Increase of vascular permeability
Recruitment (margination) & emigration (diapedesis) of WBC’s
Phagocytosis
The Inflammatory Response
• Inflammatory response = normal body defense mechanism to tissue injury
» Note: Inflammation is NOT infection
• Cells of the inflammatory response when get tissue injury
– Main groups;
• Phagocytes --- “the eaters”
– Macrophages --- become active as APC’s (antigen presenting cell)
– Neutrophils --- “little eaters”
– Monocytes --- become tissue macrophages
• T- lymphocytes (helper-T) ---- produce cytokines which “ call all to action”
• Platelets ---- release PAF (platelet activating factor) which in turn begins call
to action and release of chemical mediators
• Mast cells --- release chemical mediators that begin inflammation
Chemical Mediators
• The initial “macrophage (APC cell) – antigen complex” causes chemical
mediators to be released:
– Histamine
• From basophils & mast cells
• Cause vasodilation & increased permeability of vessels via release of
nitric oxide
– Prostaglandins
• Made in mast cell membrane from fatty acid (arachidonic)
• Cause pain & vasodilation
– Leukotrienes
• “bad” prostaglandins since cause symptoms of inflammation (pain
& swelling)
• Cause chemotaxis
• Very important for causing allergies, asthma, & anaphylaxis
Chemical Mediators
– Complement
• Coats bacterial surface; enhances phagocytosis & lyses bacteria
• Inactive plasma proteins become activated by initial An-Ab complex
– Interferon
• Proteins that are released by helper T’s & kill viruses
– Bradykinins
• From inactivated plasma protein
• Cause similar effects like histamine
• Cause pain
• Induce WBC’s into area (chemotaxis
• Local effects of inflammation
– 4 cardinal signs of inflammation
• Redness (rubor) – from increased blood supply
• Heat (calor) – from increased blood supply
• Swelling (tumor) – from increased permeability & increased proteins in
interstitial fluid
• Pain (dolar) – from chemical mediators
– Also get inflammatory exudate
• Serous – from allergic reactions & burns
• Purulent – from infections
– May lead to abscess
• Systemic effects of inflammation
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General malaise
Fatigue
Headache
Fever
• Caused by pyrogens (chemicals released from phagocytes)
• Beneficial
– Inhibits growth of pathogens
– Enhances repair process via increased metabolic rate
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Leukocytosis
Chemotaxis
Margination
Diapedesis
• Potential complications of inflammation
• Infection
• Ulceration – from chronic inflammation
– May lead to:
» perforation of viscera
» excess scar formation
• Skeletal muscle spasm
• Local tissue reactive changes
– Joints from decreased ROM become stiff
– Lungs cannot exchange gases
• Diagnostic tests for inflammation
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Leukocytosis
Differential WBC count
ESR
Cell enzymes – may or may not be tissue specific
– C-reactive protein
• Chronic Inflammation
– The acute inflammatory reaction usually subsides within 48 –72 hours as
long as the cause is removed (e.g. touching a hot stove)
– If the cause persists, you get chronic inflammation
– Clinically:
• Increase in connective tissue reaction to the chronicity
– Get more fibroblasts & more collagen
» Thus get more scar tissue
» Can get granulomas (collection of chronically inflamed tissue)
• Treatment of inflammation
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Aspirin
NSAID’s
Glucocorticoids
Heat & cold
Physiotherapy if chronic
» Prevents contractures
Healing
• 3 ways depending on the tissue involved & degree of injury
– Resolution
• Damaged cells recover in short time
• Exp = mild sunburn
– Regeneration
• Damaged cells replaced by identical cells via mitosis
• Only occurs in epithelia & connective tissue
• If complex organ, some damaged tissue replaced by regeneration
& some by scar
– Scar formation
• Key tissue = granulation tissue(highly vascular connective tissue)
» Collagen produced by fibroblasts makes granulation
tissue into scar tissue
• Scar tissue is non-functional
• Healing by primary or secondary intention
– Depend weather edges of lesion can be brought together
– Primary (first) intention gives small scar formation
– Secondary intention gives large scar formation
– Heals via granulation tissue
• Complications from large scar formation
(see next slide)
– Loss of function
– Contractures & obstructions
• Can lead to stenosis
– Adhesions
– Ulceration
• Factors promoting healing
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Nutrition
Blood supply
Cleanness of area
Lack of complications
• Factors delaying healing
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Old age
Presence of foreign material
Poor blood supply
Poor nutrition
Complications (bleeding, hematoma, excessive mobility)
Burns
• First degree burns
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Superficial partial-thickness
Involves just epidermis
Get redness but no blistering
May peel in 1-3 days
Get no scarring
• Second degree burns
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Deep partial-thickness
Involves epidermis & dermis
Get redness & blistering
Can get scarring
Can get some fluid loss
Get significant pain
• Third degree burns
– Full-thickness
– Involves all 3 layers & may
involve underlying tissue
– Get no pain
– Get serious fluid loss
• Rule of 9’s
– If burn 1st ,2nd , or 3rd &
involves more than 20% ---needs medical attention
– If burn 2nd or 3rd &
involves greater 20% =
serious
– If burn 2nd or 3rd &
involves greater 40% =
severe
• Complications
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Fluid imbalance
Dehydration
Anemia
Infection
Excess scar formation