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Prelim: Histopathology > III. Framework For Pathophysiology > Flashcards

III. Framework For Pathophysiology Flashcards

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

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2
Q

2 morphologic changes that is induced by the disease

A

Microscopic and macroscopic

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3
Q

Study of cause/reasons for the phenomena

A

Etiology

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4
Q

Identification of the causal factors

A

Etiology

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5
Q

2 major classes/etiological factors

A
  • intrinsic/genetic

* acquired (ex: infectious, nutritional, chemical and physical)

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6
Q

Cause is the result of an unintended or unwanted medical treatment

A

Iatrogenic

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7
Q

2 example of iatrogenic

A
  • chemotherapy

* radiotherapy

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8
Q

Having several different etiologic factors

A

Multifactorial

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9
Q

Example of a Multifactorial

A

CAD

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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

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11
Q

True or False: Is identification of the risk factors important for disease prevention

A

True

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12
Q

1) hospital acquired infections

2) hard to treat; don’t respond to some antibiotics

A

Nosocomial

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13
Q

4 examples of nosocomial diseases

A
  • postoperative patients
  • developing an incisional
  • pneumonia
  • staphylococcal infections
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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

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15
Q

4 cells and molecules involved on inflammation

A
  • leukocytes
  • endothelial cells
  • cells and extracellular matrix of the surrounding tissue
  • plasma proteins
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16
Q

3 mediators of plasma proteins

A
  • Platelets
  • inflammatory cells
  • endothelial cells
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17
Q

2 types of inflammation

A
  • acute inflammation

* chronic inflammation

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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

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19
Q

1) longer time course (days to years)
2) involves different cell types
3) tissue repair coexist with tissue destruction

A

Chronic inflammation

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20
Q

2 cell types that involves in chronic inflammation

A

Lymphocytes and macrophages

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21
Q

6 Causes of inflammation

A
  • infection
  • trauma
  • physical and chemical agents
  • necrosis
  • foreign bodies
  • immune reaction
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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

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23
Q

1) occurs through the release of mediators form cells

2) after a transient vasoconstriction

A

Vasodilation

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24
Q

3 Mediators in vasodilation

A
  • histamine (produce: mast cells, basophils and platelets)
  • prostaglandins (cause pain and fever)
  • nitric oxide (NO)
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25
Q

True or False: Vasodilation decrease the hydrostatic pressure by slowing of blood flow?

A

False. It increases the hydrostatic pressure

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26
Q

True or False: Slowing of blood also causes margination of leukocytes along the wall of the blood vessels

A

True

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27
Q

True or False: The stasis of blood flow in vasodilation is fast

A

False. It is slow

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28
Q

True or False: Is rubor (redness) and calor (heat or warm) a sign of vasodilation?

A

True

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29
Q

1) it increase leakiness of vessels
2) retraction of endothelial cells
3) damage to endothelial cells
4) transcytosis

A

Increase vascular permeability

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30
Q

3 mediators of increase vascular permeability

A
  • histamine
  • bradykinin (cause dolor/pain)
  • leukotrienes (CD4, D4, E4) : chemotactic
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31
Q

True or False: Is bronchospasm happens in asthma attack?

A

True. Because of leukotrienes E4 (C4 and D4)

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32
Q

Fluid with protein-rich

A

Exudate

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33
Q

Fluid secondary to imbalance

A

Transudate

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34
Q

3 Steps in movement of the WBC from the blood vessels into soft tissue at the site of inflammation

A
  • rolling
  • pavementing
  • transmigration
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35
Q

1) loose, intermittent contact of WBC

2) migration of WBC from stasis of blood

A

Rolling

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36
Q

Tight, constant contact of WBC with endothelium

A

Pavementing

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37
Q

WBC crossing through the endothelial layer

A

Transmigration

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38
Q

Crossing of blood cell in the endothelial cell

A

Diapedesis

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39
Q

Process by which WBC are drawn to the site of inflammation

A

Chemotaxis

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40
Q

2 mediators in movement of WBC

A
  • exogenous (bacterial polysaccharides)

* endogenous (C5a, leukotriene B4 and Interleukin-8/IL-8)

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41
Q

Roles of Leukocytes

A

Recognize foreign particles through mannose and scavenger receptors

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42
Q

1) antigen presenting cells

2) particles that bind to foreign material and signal leukocytes to remove it

A

Opsonin

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43
Q

3 types of opsonin

A
  • IgG
  • C3b
  • collectins
44
Q

Type of opsonin where it recognizes by Fc receptors of WBC

A

IgG

45
Q

Type of opsonin where it recognizes by Crl, 2 & 3 on leukocytes

A

C3b

46
Q

Type of opsonin where it is recognized by C2q on leukocytes

A

Collectins

47
Q

3 morphology of acute inflammation

A
  • serous
  • fibrinous
  • purulent inflammation
48
Q

1) morphology of acute inflammation

2) mildest form

A

Serous

49
Q

1) appearance of serous

2) content of fluid

A

1) relatively clear and watery

2) few cells, mostly fluid

50
Q

1) protein-poor fluid

2) seen in viral infection and burn

A

Transudate

51
Q

Specific gravity of transudate

A
52
Q

1) appearance: finely particulate, thick fluid

2) content: much more protein and cells than serous

A

Fibrinous

53
Q

Seen in: Uremic and Post MI pericarditis, strep throat, pneumonia

A

Exudate in fibrinous

54
Q

Specific gravity of exudate

A

> 1.020

55
Q

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)

A

Purulent inflammation

56
Q

4 outcomes of acute inflammation

A
  • resolution
  • abscess
  • ulcer
  • fistula
57
Q

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

A

Resolution

58
Q

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

A

Abscess

59
Q

4 complications of abscess

A
  • pain (dolor)
  • fever (calor)
  • rupture
  • swelling (tumor)
60
Q

What causes abscess?

A

Amoebic

61
Q

Loss of mucosa and deeper tissues

A

Ulcer

62
Q

Only the mucosa is lost?

A

Erosion

63
Q

4 layers affected by the ulcer:

A
  • fibrins (necrotic debris)
  • neutrophils
  • granulation tissue
  • fibrosis
64
Q

Ulcer usually affects what part of the body? (2)

A
  • stomach and duodenum

* GI tract

65
Q

3 complications of ulcer

A
  • pain (dolor)
  • hemorrhage
  • perforations
66
Q

It is where in ulcer all is involved from mucosa to serosa?

A

Perforations

67
Q

1) anomalous patent connection between 2 organs

2) with lumen

A

Fistula

68
Q

1) an example of fistula
2) skin to colon
3) anywhere in anal opening

A

Enterocutaneous fistula aka fistula en ano

69
Q

1) a dangerous kind of fistula

A

Aortaduodenal fistula

70
Q

Folds in the small intestine

A

Plicae circulares

71
Q

2 complications on aortoduodenal fistula

A
  • infection can enter other organs because of the aorta

* massive hemorrhage

72
Q

1) replacement of lost parenchyma with disorganized connective tissue
2) ex: collagen

A

Scar formation

73
Q

Prolonged inflammation consisting of active inflammation and tissue destruction and repair

A

Chronic inflammation

74
Q

4 cause of chronic inflammation

A
  • viral
  • persistent microbial infection
  • prolonged exposure to infection
  • autoimmune dysfunction
75
Q

2 cells involved in chronic inflammation

A
  • macrophages

* lymphocytes

76
Q

1) a type of chronic inflammation
2) collection of epitheloid histiocytes
3) multinucleated giant cells
4) morphology: collection of activated macrophages

A

Granulomatous inflammation

77
Q

2 function of epitheloid histiocytes

A
  • to form barricade

* to prevent further inflammation

78
Q

1) controls the spread of bacteria, if it is hard to eradicate
2) ex: Tuberculosis infection sputum/AFB smear

A

Multinucleated giant cells

79
Q

5 causes of chronic inflammation

A
  • mycobacterium
  • fungi
  • foreign material
  • sarcoidosis
  • silica
80
Q

3 fungi that causes chronic inflammation

A
  • histoplasma
  • capsulatum
  • blastomyces dermatitidis
81
Q

Involves regeneration of the parenchyma or replacement of damaged tissue with a scar of regeneration os not possible

A

Repair

82
Q

Regeneration of cells combined with scarring and fibrosis

A

Healing

83
Q

6 components of healing

A
  • 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
Q

1) they act as scavengers
2) they remove dead tissues
3) they start deposition of extracellular matrix

A

Neutrophils

85
Q

1) acts to contain damage

2) removing infecting substances

A

Induction of inflammation process

86
Q

4 process in replacement by scar

A

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
Q

Timeframe of scarring (4)

A

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
Q

Granulation tissue is

A

Macrophages fibroblasts??? Or fibrogen???

89
Q

Healing by 1st intention

A 
Wound that has:
• clean edges 
• close re-approximation of margins
• minimal tissue disruption 
Ex: healing of surgical incision
90
Q

What is the result of healing by 1st intention?

A

Small to non-existent scar

91
Q

Healing by 2nd intention

A 
Wound that has:
• unclean edges 
• extensive tissue disruption 
• tissue necrosis
Ex: cutaneous ulcers and large lacerations
92
Q

What is the result of healing by 2nd intention? (2)

A
  • large, more prominent scar

* more granulation tissue is formed to bridge the gap between the edges of the wound

93
Q

Reduces the wound 5-10% of its full size

A

Wound contraction

94
Q

Where does wound contraction takes places?

A

Myofibrils

95
Q

General wound healing and wound strength

A
  • 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
Q

1) factors that may impair the process of healing

2) general factors:

A

• infection
• nutritional deficiency (vitamin c)
• glucocorticoid therapy (steroids)
- may result in decrease fibrosis

97
Q

1) result in decrease fibrosis

2) mechanical factors:

A

Dehiscence

98
Q

Unintentional reopening of the wound due to pressure or torsion

A

Dehiscence

99
Q

Other factors that may impair the process of wound healing

A
  • age

* size of the wound

100
Q

Their wounds heal faster because they depend on blood supply

A

Children

101
Q

Decrease amount of blood available for healing

A

Poor perfusion

102
Q

Complications of cutaneous wound healing

A
  • inadequate healing, leading to dehiscence and ulceration

* excessive scar formation, hypertrophic scar or keloid scar

103
Q

They involve tissue beyond the boundaries of the wound

A

Keloid scars

104
Q

Inadequate healing can lead to

A
  • dehiscence

* ulceration

105
Q

4 aspects of a disease process

A
  • etiology (cause)
  • mechanism of its development
  • structural alterations induced by the disease
  • functional consequences of morphology

Prelim: Histopathology (3 decks)

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