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Pathology > Week 2 > Flashcards

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
Q

What type of inflammation occurs around the heart after Rheumatic Fever?

A

fibrinous pericarditis

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26
Q

What is suppurative inflammation?

A

purulent (puss)

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27
Q

What is inside puss?

A

neutrophils & bacterial debris

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28
Q

What is a localized collection of puss?

A

abscess

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29
Q

What is a diffuse spread of an acute inflammatory process through facial planes of soft tissue producing cardinal signs?

A

cellulitis

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30
Q

What is an exudative inflammation, occurring on mucosal surfaces containing mucus-secreting cells?

A

catarrhal (seromucous)

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31
Q

What is an ulcer of the oral mucosa called?

A

recurrent aphthous stomatitis

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32
Q

What is LAD?

A

leukocyte adhesion deficiency
- cannot adhere to endothelial cells

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33
Q

What are consequences of LAD?

A

severe periodontitis / infection-prone

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34
Q

What is Lazy leukocyte syndrome?

A

impaired chemotaxis

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35
Q

What is Chediak-Higashi Syndrome?

A
  • AR
  • lysosomal inclusions from fused primary granules
  • BOTH chemotaxis & phagolysosome formation defect
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36
Q

What are consequences of Chediak-Higashi Syndrome?

A

recurrent infections
platelet function abnormalities

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37
Q

What is chronic granulomatous disease of childhood?

A
  • X-linked / AR
  • deficient NADPH oxidase (absent respiratory burst)
    –> NO hydrogen peroxide … HOCl- cannot be made
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38
Q

Which types of bacteria can be killed / cannot with chronic granulomatous disease of childhood?

A

catalase - are killed (strep)
catalase + not killed (staph)

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39
Q

What is myeloperoxidase deficiency?

A

-AR
- respiratory burst normal
- prevents synthesis of HOCl-
*no great clinical consequences

40
Q

Histological findings in granulomatous inflammation?

A
  • aggregates/packets of epithelioid macrophages
  • multinucleated giant ells
  • mononuclear leukocytes
  • variable fibrosis
41
Q

What are the 2 types of granulomatous inflammation?

A

immune & foreign body

42
Q

What type of granuloma is coccidoides immitis?

A

immune (bc living organism)

43
Q

M. tuberculosis blocks what from occurring?

A

fusion of phagosome with lysozome

44
Q

What are causes of granulomatous inflammation?

A
  • sarcoidosis
  • tuberculosis
  • infection (non-TB)
  • foreign body
  • Crohn’s
  • immuno-deficient
  • cancer
45
Q

What are the histological differences between the granulation tissue and granulamatous tissue?

A

granulation = reparative tissue
- endothelial cells
- fibroblasts
-myofibroblasts

granulomatous = packet
- epithelioid macrophage
- giant cell
- lymphocytes

46
Q

Is a pyogenic granuloma granulation or granulomatous?

A

granulation tissue
(endothelial hyperplasia)

47
Q

What are the 2 ways the body can repair?

A

regeneration OR healing

48
Q

Describe regeneration

A

growth of cells & tissue to replace lost structures

49
Q

Describe healing

A

variable proportions of regeneration & scarring

50
Q

What types of regenerative cells are labile?

A
  • derived from division of stem cells
    – hematopoietic cells
    – surface epithelium
    – stratified squamous epithelium
    • skin, mouth, pharynx, esophagus,
      vagina, cervix
      – GI epithelium
51
Q

The most common types of cancer come from what types of tissues?

A

labile: because constantly dividing

52
Q

What types of cells have a low turnover rate?

A

stable / quiescent

53
Q

What types of cells are quiescent?

A
  • viscera
  • endothelial cells
  • fibroblasts
  • smooth muscle cells
54
Q

What type of cells were generated during fetal life and never divide post-natal?

A

permanent

55
Q

What cell types are permanent?

A

cardiac myocytes & neurons

56
Q

If a permanent tissue is damaged, what is the means of repair?

A

scar tissue formation / fibrosis

57
Q

What are the reasons for fibrosis to occur?

A
  • tissue is permanent (heart/brain)
  • underlying CT scaffolding disrupted
  • after extensive exudates
58
Q

What type of healing occurs when wound margins are pulled together?

A

primary intention

59
Q

T/F all wound healing involves inflammatory reaction?

A

true

60
Q

What type of wound healing occurs when wound margins are NOT pulled together?

A

secondary intention

61
Q

What type of stain allows visualization of granulation tissue?

A

trichome stain

62
Q

What is an excessive scar formation within boundaries of original wound producing raised scar?

A

hypertrophic scar

63
Q

What is an excessive scar formation that grows beyond the boundaries of the original wound?

A

keloid

64
Q

What is required for wound healing / hydroxylation of proline & lysine?

A

vitamin C

65
Q

What finding fits a tooth that is dark brown/black & does not respond to endo testing?

A

pulpal necrosis

66
Q

What cells are present in acute pulpitis?

A

neutrophils

67
Q

What cells are present in chronic pulpitis?

A
  • macrophages, lymphocytes, and plasma cells
68
Q

What is proliferation of pulpal tissue to fill cavitation and is often seen in young children?

A

chronic hyperplastic pulpitis

69
Q

What is the differential diagnosis for well-defined unilocular periapical radiolucency?

A
  • periapical cyst, granuloma, or abscess
70
Q

What is a periapical granuloma?

A
  • mass of chronically inflamed granulation tissue
  • non-vital tooth
  • most asymptomatic
71
Q

What is a periapical cyst?

A
  • 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
Q

What is a peri-apical abscess?

A
  • accumulation of acute inflammatory cells at apex
  • non-vital tooth
  • generally symptomatic
73
Q

Drainage paths of acute periapical infection?

A
  • surface of gingiva (parulis)
  • palate (palatal abscess)
  • maxillary sinus
  • soft tissue spaces (cellulitis)
  • floor of mouth (Ludwig’s angina)
74
Q

What is an acute periapical inflammation with purulent material that perforates through hard or soft tissue, epithelium, & drains through intraoral sinus?

A

parulis (gum boil)

75
Q

What is a dental abscess that drains extra-orally, through the overlying skin?

A

cutaneous sinus tract

76
Q

Define a fistula

A

an opening that connects 2 anatomical areas

77
Q

What is Ludwig’s angina?

A
  • aggressive, rapidly spready cellulitis
  • involves multiple anatomic spaces
  • massive swelling of neck
  • airway obstruction
78
Q

What is cavernous sinus thrombosis?

A
  • spread of infection from middle third of face into deep brain structures due to valveless venous system
79
Q

Which teeth are usually associated with cavernous sinus thrombosis?

A

maxillary

80
Q

Which nerves are associated with the cavernous sinus?

A

CN 3: oculomotor
CN 4: trochlear
V1: ophthalmic
V2: maxillary
CN 6: abducens

81
Q

What is osteomyelitis?

A
  • bacterial infection of bone
82
Q

What can cause osteomyelitis?

A
  • odontogenic infection
  • trauma
  • developing countries??
83
Q

What are predispositions for osteomyelitis?

A
  • chronic systemic dx
  • immunodeficiency
  • decreased vascularity of bone
84
Q

What is acute osteomyelitis?

A
  • spread through medullary spaces
  • minimal tissue rxn
85
Q

What is chronic osteomyelitis?

A
  • prominent tissue rxn
    – granulation tissue & fibrosis
86
Q

With acute osteomyelitis, what would the histology look like?

A
  • lots of neutrophils within the marrow space of bone marrow
87
Q

What is a sequestrum?

A

fragment of necrotic bone separated from vital bone

88
Q

What is an involucrum?

A

non-vital bone, encased by vital bone

89
Q

What is proliferative periostitis?

A
  • form of chronic osteomyelitis (Garre)
  • periosteal rxn where layers of reactive vital bone are formed –> cortical expansion
90
Q

Which population & where is Garre osteomyelitis most common?

A

children/young adults
mandibular molar/premolar region involving buccal cortex

91
Q

What is chronic focal sclerosing osteomyelitis / condensing osteitis?

A

localized bone sclerosis associated with the apices of teeth with pulpal dx

92
Q

Which population & where is condensing osteitis most common?

A

children & young adults
mandibular molars & premolars

93
Q

What is actinomycosis?

A
  • filamentous bacterial infection most commonly involving the cervico-facial region
94
Q

What occurs with an actinomycoses infection?

A
  • 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
Q

How does cervical facial actinomycosis appear on radiographs?

A

well-defined unilocular radiolucency

Pathology (9 decks)

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