Week 2 Flashcards

1
Q

Immune deficiency due to too few neutrophils?

A

agranulocytosis & cyclic neutropenia

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2
Q

Immune deficiency due to failure in adhesion?

A

leukocyte adhesion deficiency (LAD)

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3
Q

Immune deficiency due to slow chemotaxis?

A

“Lazy” leukocyte syndrome

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4
Q

Immune deficiency due to failure to phagocytose?

A

Bruton Agammaglobulinemia & complement deficiency

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5
Q

What are the 3 patterns of acute inflammation?

A
  • rapid onset / short duration
  • migration of leukocytes (neutrophils)
  • exudation of fluid & plasma proteins
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6
Q

What are the 3 patterns of chronic inflammation?

A
  • longer duration
  • mononuclear cells: macrophages, lymphocytes, plasma cells
  • proliferation of blood vessels & fibroblasts
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7
Q

Difference between clinical & pathological definitions of inflamation?

A

clinical: intensity & duration
pathological: histologic & appearance

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8
Q

Which type of inflammation tends to be more exudative?

A

acute

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9
Q

What type of inflammation is associated with fibrosis & scarring?

A

chronic

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10
Q

What is the difference between inflammation & immunity?

A

inflammation is the body’s response to any type of injury
&
immunity is when a living organism is present (infection)

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11
Q

T/F inflammation means there is an existing infection?

A

false: it may exist without an infection / inflammation does NOT imply infection / inflammation

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12
Q

What are the non-specific defenses?

A

physical barriers // inflammatory response (Cells/leukocytes) & (molecules (mediators)

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13
Q

What are the specific defense responses?

A

Immune Response (to living organism)
antibodies (humoral)
cytotoxic T cells (cellular)

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14
Q

What are the components of the inflammatory response?

A
  • circulating blood cells / plasma proteins
  • cells of blood vessel walls
  • cells & proteins of ECM
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15
Q

Where are most of the defensive elements located?

A

blood

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16
Q

What are the 5 Rs of the inflammatory response?

A

recognition
recruitment of leukocytes
removal
regulation (control)
resolution/repair

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17
Q

Cardinal signs of inflammation?

A

heat, redness, swelling, pain, loss of function

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18
Q

List the cellular events in acute inflammation?

A

margination
rolling
adhesion
diapedesis
chemotaxis
phagocytosis
killing

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19
Q

Systemic effects of acute inflammation?

A
  • fever (pyrogens)
  • leukocytosis (increased WBC)
  • acute phase response (cytokines stimulate hepatocytes)
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20
Q

How to determine lymphatic spread of bacterial infection?

A

painful red streak / path of spread

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21
Q

What are preformed mediators / vasoactive amines?

A

histamine (mast cell) & serotonin (platelets)

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22
Q

What is the function of histamine & serotonin?

A

vascular dilation & leakage

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23
Q

What are the outcomes of acute inflammation?

A
  • complete resolution
  • healing by CT (fibrosis)
  • progression to chronic
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24
Q

What type of inflammation is described as a ballooning of epithelium from CT?

A

serous

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25
What type of inflammation occurs around the heart after Rheumatic Fever?
fibrinous pericarditis
26
What is suppurative inflammation?
purulent (puss)
27
What is inside puss?
neutrophils & bacterial debris
28
What is a localized collection of puss?
abscess
29
What is a diffuse spread of an acute inflammatory process through facial planes of soft tissue producing cardinal signs?
cellulitis
30
What is an exudative inflammation, occurring on mucosal surfaces containing mucus-secreting cells?
catarrhal (seromucous)
31
What is an ulcer of the oral mucosa called?
recurrent aphthous stomatitis
32
What is LAD?
leukocyte adhesion deficiency - cannot adhere to endothelial cells
33
What are consequences of LAD?
severe periodontitis / infection-prone
34
What is Lazy leukocyte syndrome?
impaired chemotaxis
35
What is Chediak-Higashi Syndrome?
- AR - lysosomal inclusions from fused primary granules - BOTH chemotaxis & phagolysosome formation defect
36
What are consequences of Chediak-Higashi Syndrome?
recurrent infections platelet function abnormalities
37
What is chronic granulomatous disease of childhood?
- X-linked / AR - deficient NADPH oxidase (absent respiratory burst) --> NO hydrogen peroxide ... HOCl- cannot be made
38
Which types of bacteria can be killed / cannot with chronic granulomatous disease of childhood?
catalase - are killed (strep) catalase + not killed (staph)
39
What is myeloperoxidase deficiency?
-AR - respiratory burst normal - prevents synthesis of HOCl- *no great clinical consequences
40
Histological findings in granulomatous inflammation?
- aggregates/packets of epithelioid macrophages - multinucleated giant ells - mononuclear leukocytes - variable fibrosis
41
What are the 2 types of granulomatous inflammation?
immune & foreign body
42
What type of granuloma is coccidoides immitis?
immune (bc living organism)
43
M. tuberculosis blocks what from occurring?
fusion of phagosome with lysozome
44
What are causes of granulomatous inflammation?
- sarcoidosis - tuberculosis - infection (non-TB) - foreign body - Crohn's - immuno-deficient - cancer
45
What are the histological differences between the granulation tissue and granulamatous tissue?
granulation = reparative tissue - endothelial cells - fibroblasts -myofibroblasts granulomatous = packet - epithelioid macrophage - giant cell - lymphocytes
46
Is a pyogenic granuloma granulation or granulomatous?
granulation tissue (endothelial hyperplasia)
47
What are the 2 ways the body can repair?
regeneration OR healing
48
Describe regeneration
growth of cells & tissue to replace lost structures
49
Describe healing
variable proportions of regeneration & scarring
50
What types of regenerative cells are labile?
- derived from division of stem cells -- hematopoietic cells -- surface epithelium -- stratified squamous epithelium - skin, mouth, pharynx, esophagus, vagina, cervix -- GI epithelium
51
The most common types of cancer come from what types of tissues?
labile: because constantly dividing
52
What types of cells have a low turnover rate?
stable / quiescent
53
What types of cells are quiescent?
- viscera - endothelial cells - fibroblasts - smooth muscle cells
54
What type of cells were generated during fetal life and never divide post-natal?
permanent
55
What cell types are permanent?
cardiac myocytes & neurons
56
If a permanent tissue is damaged, what is the means of repair?
scar tissue formation / fibrosis
57
What are the reasons for fibrosis to occur?
- tissue is permanent (heart/brain) - underlying CT scaffolding disrupted - after extensive exudates
58
What type of healing occurs when wound margins are pulled together?
primary intention
59
T/F all wound healing involves inflammatory reaction?
true
60
What type of wound healing occurs when wound margins are NOT pulled together?
secondary intention
61
What type of stain allows visualization of granulation tissue?
trichome stain
62
What is an excessive scar formation within boundaries of original wound producing raised scar?
hypertrophic scar
63
What is an excessive scar formation that grows beyond the boundaries of the original wound?
keloid
64
What is required for wound healing / hydroxylation of proline & lysine?
vitamin C
65
What finding fits a tooth that is dark brown/black & does not respond to endo testing?
pulpal necrosis
66
What cells are present in acute pulpitis?
neutrophils
67
What cells are present in chronic pulpitis?
- macrophages, lymphocytes, and plasma cells
68
What is proliferation of pulpal tissue to fill cavitation and is often seen in young children?
chronic hyperplastic pulpitis
69
What is the differential diagnosis for well-defined unilocular periapical radiolucency?
- periapical cyst, granuloma, or abscess
70
What is a periapical granuloma?
- mass of chronically inflamed granulation tissue - non-vital tooth - most asymptomatic
71
What is a periapical cyst?
- pathologic cavity located in soft tissue or bone lined by epithelium - epithelial lining, lumen, & CT wall - asymptomatic, slow growing - non-vital tooth - root resorption possible
72
What is a peri-apical abscess?
- accumulation of acute inflammatory cells at apex - non-vital tooth - generally symptomatic
73
Drainage paths of acute periapical infection?
- surface of gingiva (parulis) - palate (palatal abscess) - maxillary sinus - soft tissue spaces (cellulitis) - floor of mouth (Ludwig's angina)
74
What is an acute periapical inflammation with purulent material that perforates through hard or soft tissue, epithelium, & drains through intraoral sinus?
parulis (gum boil)
75
What is a dental abscess that drains extra-orally, through the overlying skin?
cutaneous sinus tract
76
Define a fistula
an opening that connects 2 anatomical areas
77
What is Ludwig's angina?
- aggressive, rapidly spready cellulitis - involves multiple anatomic spaces - massive swelling of neck - airway obstruction
78
What is cavernous sinus thrombosis?
- spread of infection from middle third of face into deep brain structures due to valveless venous system
79
Which teeth are usually associated with cavernous sinus thrombosis?
maxillary
80
Which nerves are associated with the cavernous sinus?
CN 3: oculomotor CN 4: trochlear V1: ophthalmic V2: maxillary CN 6: abducens
81
What is osteomyelitis?
- bacterial infection of bone
82
What can cause osteomyelitis?
- odontogenic infection - trauma - developing countries??
83
What are predispositions for osteomyelitis?
- chronic systemic dx - immunodeficiency - decreased vascularity of bone
84
What is acute osteomyelitis?
- spread through medullary spaces - minimal tissue rxn
85
What is chronic osteomyelitis?
- prominent tissue rxn -- granulation tissue & fibrosis
86
With acute osteomyelitis, what would the histology look like?
- lots of neutrophils within the marrow space of bone marrow
87
What is a sequestrum?
fragment of necrotic bone separated from vital bone
88
What is an involucrum?
non-vital bone, encased by vital bone
89
What is proliferative periostitis?
- form of chronic osteomyelitis (Garre) - periosteal rxn where layers of reactive vital bone are formed --> cortical expansion
90
Which population & where is Garre osteomyelitis most common?
children/young adults mandibular molar/premolar region involving buccal cortex
91
What is chronic focal sclerosing osteomyelitis / condensing osteitis?
localized bone sclerosis associated with the apices of teeth with pulpal dx
92
Which population & where is condensing osteitis most common?
children & young adults mandibular molars & premolars
93
What is actinomycosis?
- filamentous bacterial infection most commonly involving the cervico-facial region
94
What occurs with an actinomycoses infection?
- area of trauma for entry - extension through soft tissue - disregard for facial planes & lymphatics - "woody" induration & fibrosis - draining sinus tracts - suppuration with sulfur granules
95
How does cervical facial actinomycosis appear on radiographs?
well-defined unilocular radiolucency