III. Framework For Pathophysiology Flashcards
An aspect of disease where pathogenesis exposure to inciting agent to 1st appearance of sign and symptoms to recovery
Mechanism of its development
2 morphologic changes that is induced by the disease
Microscopic and macroscopic
Study of cause/reasons for the phenomena
Etiology
Identification of the causal factors
Etiology
2 major classes/etiological factors
- intrinsic/genetic
* acquired (ex: infectious, nutritional, chemical and physical)
Cause is the result of an unintended or unwanted medical treatment
Iatrogenic
2 example of iatrogenic
- chemotherapy
* radiotherapy
Having several different etiologic factors
Multifactorial
Example of a Multifactorial
CAD
1) genetic predisposition diet (high cholesterol)
2) increased BP
3) lifestyle
4) cigarette smoking (nicotine attack in the wall of the artery)
5) hormone
CAD
True or False: Is identification of the risk factors important for disease prevention
True
1) hospital acquired infections
2) hard to treat; don’t respond to some antibiotics
Nosocomial
4 examples of nosocomial diseases
- postoperative patients
- developing an incisional
- pneumonia
- staphylococcal infections
A protective response to rid the body of the cause of cell injury and the resultant necrotic cells that cell injury produces
Inflammation
4 cells and molecules involved on inflammation
- leukocytes
- endothelial cells
- cells and extracellular matrix of the surrounding tissue
- plasma proteins
3 mediators of plasma proteins
- Platelets
- inflammatory cells
- endothelial cells
2 types of inflammation
- acute inflammation
* chronic inflammation
1) rapid onset
2) last minutes to days
3) characterized by exudation of fluids and protein from vessels and emigration of neutrophils
Acute inflammation
1) longer time course (days to years)
2) involves different cell types
3) tissue repair coexist with tissue destruction
Chronic inflammation
2 cell types that involves in chronic inflammation
Lymphocytes and macrophages
6 Causes of inflammation
- infection
- trauma
- physical and chemical agents
- necrosis
- foreign bodies
- immune reaction
3 stages of acute inflammation
1) vasodilation
2) increase vascular permeability
3) movement of the WBC from the blood vessels into soft tissue at the site of inflammation
1) occurs through the release of mediators form cells
2) after a transient vasoconstriction
Vasodilation
3 Mediators in vasodilation
- histamine (produce: mast cells, basophils and platelets)
- prostaglandins (cause pain and fever)
- nitric oxide (NO)
True or False: Vasodilation decrease the hydrostatic pressure by slowing of blood flow?
False. It increases the hydrostatic pressure
True or False: Slowing of blood also causes margination of leukocytes along the wall of the blood vessels
True
True or False: The stasis of blood flow in vasodilation is fast
False. It is slow
True or False: Is rubor (redness) and calor (heat or warm) a sign of vasodilation?
True
1) it increase leakiness of vessels
2) retraction of endothelial cells
3) damage to endothelial cells
4) transcytosis
Increase vascular permeability
3 mediators of increase vascular permeability
- histamine
- bradykinin (cause dolor/pain)
- leukotrienes (CD4, D4, E4) : chemotactic
True or False: Is bronchospasm happens in asthma attack?
True. Because of leukotrienes E4 (C4 and D4)
Fluid with protein-rich
Exudate
Fluid secondary to imbalance
Transudate
3 Steps in movement of the WBC from the blood vessels into soft tissue at the site of inflammation
- rolling
- pavementing
- transmigration
1) loose, intermittent contact of WBC
2) migration of WBC from stasis of blood
Rolling
Tight, constant contact of WBC with endothelium
Pavementing
WBC crossing through the endothelial layer
Transmigration
Crossing of blood cell in the endothelial cell
Diapedesis
Process by which WBC are drawn to the site of inflammation
Chemotaxis
2 mediators in movement of WBC
- exogenous (bacterial polysaccharides)
* endogenous (C5a, leukotriene B4 and Interleukin-8/IL-8)
Roles of Leukocytes
Recognize foreign particles through mannose and scavenger receptors
1) antigen presenting cells
2) particles that bind to foreign material and signal leukocytes to remove it
Opsonin
3 types of opsonin
- IgG
- C3b
- collectins
Type of opsonin where it recognizes by Fc receptors of WBC
IgG
Type of opsonin where it recognizes by Crl, 2 & 3 on leukocytes
C3b
Type of opsonin where it is recognized by C2q on leukocytes
Collectins
3 morphology of acute inflammation
- serous
- fibrinous
- purulent inflammation
1) morphology of acute inflammation
2) mildest form
Serous
1) appearance of serous
2) content of fluid
1) relatively clear and watery
2) few cells, mostly fluid
1) protein-poor fluid
2) seen in viral infection and burn
Transudate
Specific gravity of transudate
1) appearance: finely particulate, thick fluid
2) content: much more protein and cells than serous
Fibrinous
Seen in: Uremic and Post MI pericarditis, strep throat, pneumonia
Exudate in fibrinous
Specific gravity of exudate
> 1.020
1) appearance: pus-thick, white, yellow fluid
2) content of fluid: neutrophils, proteins, necrotic cells and bacteria
3) exudate
4) seen in bacterial (staphylococcal, streptococcal and fungal infection)
Purulent inflammation
4 outcomes of acute inflammation
- resolution
- abscess
- ulcer
- fistula
1) an outcome of acute inflammation where inciting agent is removed
2) complete recovery
3) all damage done by the inciting agent and inflammatory cells is repaired
4) organ affected must be capable of regeneration
Resolution
1) an outcome of acute inflammation where walled off collection of pus (neutrophils and necrotic debris)
2) the body cannot get rid itself of the inciting agent
Abscess
4 complications of abscess
- pain (dolor)
- fever (calor)
- rupture
- swelling (tumor)
What causes abscess?
Amoebic
Loss of mucosa and deeper tissues
Ulcer
Only the mucosa is lost?
Erosion
4 layers affected by the ulcer:
- fibrins (necrotic debris)
- neutrophils
- granulation tissue
- fibrosis
Ulcer usually affects what part of the body? (2)
- stomach and duodenum
* GI tract
3 complications of ulcer
- pain (dolor)
- hemorrhage
- perforations
It is where in ulcer all is involved from mucosa to serosa?
Perforations
1) anomalous patent connection between 2 organs
2) with lumen
Fistula
1) an example of fistula
2) skin to colon
3) anywhere in anal opening
Enterocutaneous fistula aka fistula en ano
1) a dangerous kind of fistula
Aortaduodenal fistula
Folds in the small intestine
Plicae circulares
2 complications on aortoduodenal fistula
- infection can enter other organs because of the aorta
* massive hemorrhage
1) replacement of lost parenchyma with disorganized connective tissue
2) ex: collagen
Scar formation
Prolonged inflammation consisting of active inflammation and tissue destruction and repair
Chronic inflammation
4 cause of chronic inflammation
- viral
- persistent microbial infection
- prolonged exposure to infection
- autoimmune dysfunction
2 cells involved in chronic inflammation
- macrophages
* lymphocytes
1) a type of chronic inflammation
2) collection of epitheloid histiocytes
3) multinucleated giant cells
4) morphology: collection of activated macrophages
Granulomatous inflammation
2 function of epitheloid histiocytes
- to form barricade
* to prevent further inflammation
1) controls the spread of bacteria, if it is hard to eradicate
2) ex: Tuberculosis infection sputum/AFB smear
Multinucleated giant cells
5 causes of chronic inflammation
- mycobacterium
- fungi
- foreign material
- sarcoidosis
- silica
3 fungi that causes chronic inflammation
- histoplasma
- capsulatum
- blastomyces dermatitidis
Involves regeneration of the parenchyma or replacement of damaged tissue with a scar of regeneration os not possible
Repair
Regeneration of cells combined with scarring and fibrosis
Healing
6 components of healing
- induction of inflammatory process
- formation of new blood vessels (angiogenesis)
- production of extracellular matrix, collagen
- tissue remodeling
- wound contracture (5-10%)
- increasing wound strength
1) they act as scavengers
2) they remove dead tissues
3) they start deposition of extracellular matrix
Neutrophils
1) acts to contain damage
2) removing infecting substances
Induction of inflammation process
4 process in replacement by scar
1) formation of new blood vessels (angiogenesis)
2) migration and proliferation of fibroblasts
3) deposition of extracellular matrix
4) maturation and reorganization of fibrous tissue
Timeframe of scarring (4)
1) within 24 hrs of onset of acute inflammation, the process of scarring begin
2) at 3-5 days, GRANULATION TISSUE is formed
3) week 2, collagen continues to be deposited (EDEMA and inflammatory cells are absent)
4) 1 month, scar consist of collagen
Granulation tissue is
Macrophages fibroblasts??? Or fibrogen???
Healing by 1st intention
Wound that has: • clean edges • close re-approximation of margins • minimal tissue disruption Ex: healing of surgical incision
What is the result of healing by 1st intention?
Small to non-existent scar
Healing by 2nd intention
Wound that has: • unclean edges • extensive tissue disruption • tissue necrosis Ex: cutaneous ulcers and large lacerations
What is the result of healing by 2nd intention? (2)
- large, more prominent scar
* more granulation tissue is formed to bridge the gap between the edges of the wound
Reduces the wound 5-10% of its full size
Wound contraction
Where does wound contraction takes places?
Myofibrils
General wound healing and wound strength
- 1 week - 10% of normal skin (increasing in amount of strength over the following month)
- 2 or more months - scar is fully healed, but only 3/4
1) factors that may impair the process of healing
2) general factors:
• infection
• nutritional deficiency (vitamin c)
• glucocorticoid therapy (steroids)
- may result in decrease fibrosis
1) result in decrease fibrosis
2) mechanical factors:
Dehiscence
Unintentional reopening of the wound due to pressure or torsion
Dehiscence
Other factors that may impair the process of wound healing
- age
* size of the wound
Their wounds heal faster because they depend on blood supply
Children
Decrease amount of blood available for healing
Poor perfusion
Complications of cutaneous wound healing
- inadequate healing, leading to dehiscence and ulceration
* excessive scar formation, hypertrophic scar or keloid scar
They involve tissue beyond the boundaries of the wound
Keloid scars
Inadequate healing can lead to
- dehiscence
* ulceration
4 aspects of a disease process
- etiology (cause)
- mechanism of its development
- structural alterations induced by the disease
- functional consequences of morphology