III. Framework For Pathophysiology Flashcards
(105 cards)
1
Q
An aspect of disease where pathogenesis exposure to inciting agent to 1st appearance of sign and symptoms to recovery
A
Mechanism of its development
2
Q
2 morphologic changes that is induced by the disease
A
Microscopic and macroscopic
3
Q
Study of cause/reasons for the phenomena
A
Etiology
4
Q
Identification of the causal factors
A
Etiology
5
Q
2 major classes/etiological factors
A
- intrinsic/genetic
* acquired (ex: infectious, nutritional, chemical and physical)
6
Q
Cause is the result of an unintended or unwanted medical treatment
A
Iatrogenic
7
Q
2 example of iatrogenic
A
- chemotherapy
* radiotherapy
8
Q
Having several different etiologic factors
A
Multifactorial
9
Q
Example of a Multifactorial
A
CAD
10
Q
1) genetic predisposition diet (high cholesterol)
2) increased BP
3) lifestyle
4) cigarette smoking (nicotine attack in the wall of the artery)
5) hormone
A
CAD
11
Q
True or False: Is identification of the risk factors important for disease prevention
A
True
12
Q
1) hospital acquired infections
2) hard to treat; don’t respond to some antibiotics
A
Nosocomial
13
Q
4 examples of nosocomial diseases
A
- postoperative patients
- developing an incisional
- pneumonia
- staphylococcal infections
14
Q
A protective response to rid the body of the cause of cell injury and the resultant necrotic cells that cell injury produces
A
Inflammation
15
Q
4 cells and molecules involved on inflammation
A
- leukocytes
- endothelial cells
- cells and extracellular matrix of the surrounding tissue
- plasma proteins
16
Q
3 mediators of plasma proteins
A
- Platelets
- inflammatory cells
- endothelial cells
17
Q
2 types of inflammation
A
- acute inflammation
* chronic inflammation
18
Q
1) rapid onset
2) last minutes to days
3) characterized by exudation of fluids and protein from vessels and emigration of neutrophils
A
Acute inflammation
19
Q
1) longer time course (days to years)
2) involves different cell types
3) tissue repair coexist with tissue destruction
A
Chronic inflammation
20
Q
2 cell types that involves in chronic inflammation
A
Lymphocytes and macrophages
21
Q
6 Causes of inflammation
A
- infection
- trauma
- physical and chemical agents
- necrosis
- foreign bodies
- immune reaction
22
Q
3 stages of acute inflammation
A
1) vasodilation
2) increase vascular permeability
3) movement of the WBC from the blood vessels into soft tissue at the site of inflammation
23
Q
1) occurs through the release of mediators form cells
2) after a transient vasoconstriction
A
Vasodilation
24
Q
3 Mediators in vasodilation
A
- histamine (produce: mast cells, basophils and platelets)
- prostaglandins (cause pain and fever)
- nitric oxide (NO)
25
True or False: Vasodilation decrease the hydrostatic pressure by slowing of blood flow?
False. It increases the hydrostatic pressure
26
True or False: Slowing of blood also causes margination of leukocytes along the wall of the blood vessels
True
27
True or False: The stasis of blood flow in vasodilation is fast
False. It is slow
28
True or False: Is rubor (redness) and calor (heat or warm) a sign of vasodilation?
True
29
1) it increase leakiness of vessels
2) retraction of endothelial cells
3) damage to endothelial cells
4) transcytosis
Increase vascular permeability
30
3 mediators of increase vascular permeability
* histamine
* bradykinin (cause dolor/pain)
* leukotrienes (CD4, D4, E4) : chemotactic
31
True or False: Is bronchospasm happens in asthma attack?
True. Because of leukotrienes E4 (C4 and D4)
32
Fluid with protein-rich
Exudate
33
Fluid secondary to imbalance
Transudate
34
3 Steps in movement of the WBC from the blood vessels into soft tissue at the site of inflammation
* rolling
* pavementing
* transmigration
35
1) loose, intermittent contact of WBC
| 2) migration of WBC from stasis of blood
Rolling
36
Tight, constant contact of WBC with endothelium
Pavementing
37
WBC crossing through the endothelial layer
Transmigration
38
Crossing of blood cell in the endothelial cell
Diapedesis
39
Process by which WBC are drawn to the site of inflammation
Chemotaxis
40
2 mediators in movement of WBC
* exogenous (bacterial polysaccharides)
| * endogenous (C5a, leukotriene B4 and Interleukin-8/IL-8)
41
Roles of Leukocytes
Recognize foreign particles through mannose and scavenger receptors
42
1) antigen presenting cells
| 2) particles that bind to foreign material and signal leukocytes to remove it
Opsonin
43
3 types of opsonin
* IgG
* C3b
* collectins
44
Type of opsonin where it recognizes by Fc receptors of WBC
IgG
45
Type of opsonin where it recognizes by Crl, 2 & 3 on leukocytes
C3b
46
Type of opsonin where it is recognized by C2q on leukocytes
Collectins
47
3 morphology of acute inflammation
* serous
* fibrinous
* purulent inflammation
48
1) morphology of acute inflammation
| 2) mildest form
Serous
49
1) appearance of serous
| 2) content of fluid
1) relatively clear and watery
| 2) few cells, mostly fluid
50
1) protein-poor fluid
| 2) seen in viral infection and burn
Transudate
51
Specific gravity of transudate
52
1) appearance: finely particulate, thick fluid
| 2) content: much more protein and cells than serous
Fibrinous
53
Seen in: Uremic and Post MI pericarditis, strep throat, pneumonia
Exudate in fibrinous
54
Specific gravity of exudate
> 1.020
55
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
56
4 outcomes of acute inflammation
* resolution
* abscess
* ulcer
* fistula
57
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
58
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
59
4 complications of abscess
* pain (dolor)
* fever (calor)
* rupture
* swelling (tumor)
60
What causes abscess?
Amoebic
61
Loss of mucosa and deeper tissues
Ulcer
62
Only the mucosa is lost?
Erosion
63
4 layers affected by the ulcer:
* fibrins (necrotic debris)
* neutrophils
* granulation tissue
* fibrosis
64
Ulcer usually affects what part of the body? (2)
* stomach and duodenum
| * GI tract
65
3 complications of ulcer
* pain (dolor)
* hemorrhage
* perforations
66
It is where in ulcer all is involved from mucosa to serosa?
Perforations
67
1) anomalous patent connection between 2 organs
| 2) with lumen
Fistula
68
1) an example of fistula
2) skin to colon
3) anywhere in anal opening
Enterocutaneous fistula aka fistula en ano
69
1) a dangerous kind of fistula
Aortaduodenal fistula
70
Folds in the small intestine
Plicae circulares
71
2 complications on aortoduodenal fistula
* infection can enter other organs because of the aorta
| * massive hemorrhage
72
1) replacement of lost parenchyma with disorganized connective tissue
2) ex: collagen
Scar formation
73
Prolonged inflammation consisting of active inflammation and tissue destruction and repair
Chronic inflammation
74
4 cause of chronic inflammation
* viral
* persistent microbial infection
* prolonged exposure to infection
* autoimmune dysfunction
75
2 cells involved in chronic inflammation
* macrophages
| * lymphocytes
76
1) a type of chronic inflammation
2) collection of epitheloid histiocytes
3) multinucleated giant cells
4) morphology: collection of activated macrophages
Granulomatous inflammation
77
2 function of epitheloid histiocytes
* to form barricade
| * to prevent further inflammation
78
1) controls the spread of bacteria, if it is hard to eradicate
2) ex: Tuberculosis infection sputum/AFB smear
Multinucleated giant cells
79
5 causes of chronic inflammation
* mycobacterium
* fungi
* foreign material
* sarcoidosis
* silica
80
3 fungi that causes chronic inflammation
* histoplasma
* capsulatum
* blastomyces dermatitidis
81
Involves regeneration of the parenchyma or replacement of damaged tissue with a scar of regeneration os not possible
Repair
82
Regeneration of cells combined with scarring and fibrosis
Healing
83
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
84
1) they act as scavengers
2) they remove dead tissues
3) they start deposition of extracellular matrix
Neutrophils
85
1) acts to contain damage
| 2) removing infecting substances
Induction of inflammation process
86
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
87
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
88
Granulation tissue is
Macrophages fibroblasts??? Or fibrogen???
89
Healing by 1st intention
```
Wound that has:
• clean edges
• close re-approximation of margins
• minimal tissue disruption
Ex: healing of surgical incision
```
90
What is the result of healing by 1st intention?
Small to non-existent scar
91
Healing by 2nd intention
```
Wound that has:
• unclean edges
• extensive tissue disruption
• tissue necrosis
Ex: cutaneous ulcers and large lacerations
```
92
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
93
Reduces the wound 5-10% of its full size
Wound contraction
94
Where does wound contraction takes places?
Myofibrils
95
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
96
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
97
1) result in decrease fibrosis
| 2) mechanical factors:
Dehiscence
98
Unintentional reopening of the wound due to pressure or torsion
Dehiscence
99
Other factors that may impair the process of wound healing
* age
| * size of the wound
100
Their wounds heal faster because they depend on blood supply
Children
101
Decrease amount of blood available for healing
Poor perfusion
102
Complications of cutaneous wound healing
* inadequate healing, leading to dehiscence and ulceration
| * excessive scar formation, hypertrophic scar or keloid scar
103
They involve tissue beyond the boundaries of the wound
Keloid scars
104
Inadequate healing can lead to
* dehiscence
| * ulceration
105
4 aspects of a disease process
* etiology (cause)
* mechanism of its development
* structural alterations induced by the disease
* functional consequences of morphology
