Pathophysiology - 2 [Inflammation & Healing] Flashcards
What’s the first line of defense
Non specific
Mechanical barrier
Unbroken skin & mucous membrane
Secretions
What’s the second line of defense
Nonspecific
Phagocytosis
Inflammation
What’s the 3rd line of defense
Specific defense
Production of specific antibodies or cell mediated immunity
Explain normal capillary exchange
Arterial end - based on net hydrostatic pressure
Venous end - osmotic pressure
Example of causes of inflammation
Direct physical damage
Caustic chemicals
Ischemia/infraction
Allergic rx
Extremes of heat/cold
Foreign bodies
Infection
Difference between inflammation and infection
Inflammation- normal defence mechanism
Infection- cause of inflammation
Steps of inflammation
Release of Bradykinin
Activation of pain receptors
Mast cells+basophils release histamine
Capillary dilation
Hyperemia +capillary permeability
Bacteria enter the tissue
Neutrophil and monocytes —> injury site
Neutrophils phagocyte bacteria
Macrophages leave bloodstream to phagocytes microbes
Steps Acute inflammation
Same process as inflammation
Vasodilation
Hyperemia
Increased capillary permeability
Chemotaxis
What’re the Local effects of inflammation
Redness, warmth
Edema
Pain
Loss of function
Type of exudate
Serous - proteins, WBC
Fibrinous - high cell, fibrin
Purulent - leucocytes, cell debris
Abscess - local. Pocket purulent exudate
Hemorrhagic - damaged blood vessels
What’re the systemic effects of inflammation
Pyrexia
Malaise
Fatigue
Headache
Anorexia
Mention some diagnostic tests and findings in case of inflammation/infection
Leucocytes - increased
Erythrocytes sedimentation rate - elevated
Differential count - to detect viral vs bacterial
Circulating plasma proteins
Cell enzymes
Necrosis
What’re some potential complications with infection
Microorg. Easily penetrate edematous tissue
Phagocytosis resistance
Skeletal muscle spasm
Steps in Chronic inflammation
After acute inflammation
< swelling, exudate
> lymphocytes, macrophages, fibroblasts
Tissue destruction
> fibrous scar tissue
+/- granuloma
What’re potential complications of chronic inflammation
Deep ulcers
Perforation of vicera
Scar tissue formation
Tx of inflammation
ASA
Tylenol
NSAIDs
Glucocorticoids
Antiinflamatory effects of glucocorticoids
Decreased capillary permeability
Enhance effectiveness of epi/norepi
Reduced # leucocytes, mast cell
Reduced immune response
Adverse effects of glucocorticoids
Atrophy of lymphoid tissues
Reduced hemopoiesis
Catabolic effects
Delayed healing
Delayed growth in children
Retention Na, H2O
Increased gluconeogensis
What’s the RICE therapy for injuries
Rest
Ice
Compression
Elevation
What’re the types of healing
Resolution
Regeneration
Replacement
Scar formation
Loss of function
Contractures/ obstructions
Adhesions
Hypertrophic scar tissue
Ulceration
Type of burns
Thermal
Chemical
Radiation
Electricity
Light
Friction
Classification of burns
Superficial (1st degree)
Partial thickness (2nd degree)
Full thickness (3rd degree)
Full thickness (4th degree)
Effects of burn injury
Local/ systemic
Dehydration, edema
Shock
Respiratory problems
Pain
Infection
Hypermetabolism
Rule of nines
Healing of burns
Hypermetabolism
Immediate wound covering
Prolonged healing
Develop of scar tissue
+/- physiotherapy
+/- surgery
