1. INTRODUCTION TO Pathophysiology
Mechanisms of Disease
Diagnosis & Treatment
Inflammation & Healing

2. 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

3. Disease terminology 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

4. 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:
Perilous occupation
Smoking
Excess alcohol
Poor nutrition
Sedentary activity

5. Preventive health care
Environment
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

6. Homeostasis & disease Disease mechanisms
Disease is the failure to maintain homeostatic conditions
Disease mechanisms
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)

7. The Cell & Disease Changes in Growth Change in Type of Cell
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

9. Cell damage is the main reason to lose homeostasis
Deficiency of oxygen (hypoxia) = most common reason
Mechanism of progression:
ischemia -to- 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

10. Diagnosis & Treatment “SOAP” protocol:
“S” = subjective “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)
Objective Findings = the patient’s physical manifestations
Obtained by doing a physical exam
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

11. 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

12. The Inflammatory Response
Key purposes = DEFENSE
To hunt & kill invaders
To limit their spread
To prepare tissue for repair
Key events
Increase of vascular permeability
Recruitment (margination) & emigration (diapedesis) of WBC’s
Phagocytosis

13. 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

14. 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

15. 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

16. 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
General malaise
Fatigue
Headache
Fever
Caused by pyrogens (chemicals released from phagocytes)
Beneficial
Inhibits growth of pathogens
Enhances repair process via increased metabolic rate

17. Leukocytosis
Chemotaxis
Margination
Diapedesis

18. 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
Leukocytosis
Differential WBC count
ESR
Cell enzymes – may or may not be tissue specific
C-reactive protein

19. Thus get more scar tissue
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
Aspirin
NSAID’s
Glucocorticoids
Heat & cold
Physiotherapy if chronic
Prevents contractures

20. 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

21. 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

22. Complications from large scar formation
(see next slide)
Loss of function
Contractures & obstructions
Can lead to stenosis
Adhesions
Ulceration
Factors promoting healing
Nutrition
Blood supply
Cleanness of area
Lack of complications
Factors delaying healing
Old age
Presence of foreign material
Poor blood supply
Poor nutrition
Complications (bleeding, hematoma, excessive mobility)

24. Burns First degree burns Rule of 9’s Second degree burns Complications
Superficial partial-thickness
Involves just epidermis
Get redness but no blistering
May peel in 1-3 days
Get no scarring
Second degree burns
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
Fluid imbalance
Dehydration
Anemia
Infection
Excess scar formation