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NBDE Part 1 > Microbiology Oral and Pathology > Flashcards

Microbiology Oral and Pathology Flashcards

1
Q

How is periodontal health characterized?

A

Periodontal health is characterized by the predominant inhabitants of the oral cavity, mostly gram positive facultative species such as streptococcus sanguis, Streptococcus mitis, streptococcus salivarius, actinomyces viscosus, actinomyces naeslundii, and a few beneficial gram negative species such as veillonella parvula and Capnocytophaga ochracea

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2
Q

What microorganism is most commonly found on the surface of the tongue?

A

Streptococcus salivarius

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3
Q

Describe the composition, adhesion location and organization of Plaque

A
  • An organized biofilm consisting of 80% water and 20% solids: 95% microorganisms; and 5% organic components (calcium, phosphorus), desquamated cells (epitheial cells, leukocytes) and food debris
  • It adheres to teeth, dental prostheses, and oral mucosal surfaces and is also found in the gingival sulcus and periodontal pockets
  • Dental plaque is classified as supragingival and subgingival based on its position along the tooth surface
    • Supragingival = G+ cocci
    • Subgingival = G - Bacilli and spirochetes
  • As plaque matures, there is a transition from the early aerobic environment characterized by gram-positive facultative species to an exceedingly oxygen deprived milieu in which gram negative anaerobes predominate.
  • It is the key etiologic agent in the initiation of both caries and periodontal diseases
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4
Q

Explain the series of steps for plaque formation

A
  • Pellicle formation: Salivary and GCF glycoproteins bind to oral mucosal, tooth, and dental prosthesis surfaces almost immediately via electrostatic and van der Waals forces. It prevents tissue desiccation and provides surface lubrication, but also promotes bacterial adherence.
  • Bacterial colonization: Occurs within a few hours of pellicle formation. Gram-positive facultative species (streptococcus sp. Actinomyces sp., Lactobacillus sp.) are the first to colonize through the binding of their adhesins and fimbriae to the pellicle.
  • Maturation: Multiplication and coaggregation of bacterial species that do not inititally colonize tooth and gingival epithelial surfaces
  • Mineralization: Calculus formation. Plaque becomes 50% mineralized in about 2 days, and 90% mineralized in about 12 days
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5
Q

Explain the composition, adhesion and location of calculus formation

A
  • Calcified bacterial plaque that forms on teeth and dental prostheses
  • 70-90% of calculus is composed of inorganic components (calcium, phosphorus), the majority of which are crystalline (hydroxyapatite)
  • The remaining 10-30% of calculus is organic, consisting of protein- carbohydrate complexes, desquamated cells (epithelial cells, leukocytes), and microorganisms
  • Saliva is the main mineral source for supragingival calculus, but GCF (gingival cervicular fluid) provides most of the mineral for subgingival calculus
  • The most common locations for supragingival calculus are the lingual of mandibular anterior teeth and the buccal of maxillary molars (due to their proximity to salivary ducts)
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6
Q

What is the calculus formation epitatic concept?

A

Epitactic Concept:

  • The predominant theory of calculus formation, which suggests that seeding agents (protein-carbohydrate complexes or bacteria) induce small foci of mineralization, which ultimately enlarge and coalesce to form a calcified mass

Calculus does NOT directly cause gingival inflammation, but provides a rough surface for the continued accumulation of perio-pathogenic bacterial plaque

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7
Q

What is materia alba

A

Material Alba

Loosely adherent matter largely composed of desquamated cells, food debris, and other components of dental plaque that is easily washed away

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8
Q

Explain the characteristics of cariogenic bacteria and how it synthesises material that leads to caries

A
  • Cariogenic bacteria synthesize glucan (dextrans) and fructans (levans) from their metabolism of dietary sucrose (via glucosyltransferase), which contribute to their adherence to tooth structure
  • As a consequence, lactic acid is formed, reducing salivary pH and creating sites of enamel demineralization and cavitation
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9
Q

What are the three main items that caries need for their formation?

A
  1. Cariogenic bacteria
  2. A susceptible surface
  3. A fermentable carbohydrate source
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10
Q

Explain Stephan Curve for oral pathology

State common microbes for early colonizers and where they likely colonize

What are recurrent caries?

A

Stephan Curve

  • Rapid drop in salivary pH within a few minutes after fermentable carbohydrate (eg. sucrose) intake
  • Enamel demineralization occurs once the pH falls below 5.5
  • Recovery to a normal salivary pH can take 15-40 minutes
  • The frequency of carbohydrate intake is more detrimental than the quantity because it maintains a prolonged decrease in pH

Common microbs for early colonizers:

  • Strepococcus (S. mutans, S. sanguis, S. salivarius) generally cause pit and fissure, smooth-surface and root caries
  • Lactobacillus sp (L. casei, L. acidophilus) generally cause pit and fissure caries
  • Actinomyces sp (A. viscosus, A. naeslundii) generally cause root caries
    • They are acidogenic (make acid) and aciduric (tolerate living in acid)

Recurrent caries: occurs around an existing restoration. It may occur on the crown or the root

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11
Q

Explain plaque-induced gingivitis characterizations and predominant microbial flora

A

Plaque-Induced Gingivitis

Characteristics

  • Presence of plaque
  • Absense of attachment loss
  • Gingival inflammation, starting at the gingival margin
  • Can be modified by systemic factors, medications, or malnutrition
  • Reversible with removal of plaque (and modifying factors)

Predominant Microbial Flora

  • Variable microbial pattern containing predominantly gram-positive and gram-negative facultative and anaerobic cocci, bacilli, and spirochetes such as Streptococcus sanguis, streptococcus mitis, Actinomyces viscosus, Actinomyces naeslundii, Peptostreptococcus micros, Fusobacterium nucleatum, Prevotella intermedia, and Campylobacter rectus
    • Gingivitis associated with sex steroid fluctuations (pregnancy, puberty, menstrual cycle, oral contraceptive use) is associated with elevated proportions of Prevotella intermedia, which uses these steroids as growth factors
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12
Q

Explain Chronic Periodontitis characterizations and predominant microbial flora

A

Chronic periodontitis

Formerly known as adult periodontitis

Characteristics

  • Presence of plaque
  • Presence of attachment loss
  • Amount of periodontal destruction is consistent with prescence of microbial deposits (subgingival plaque and calculus)
  • Most prevalent in adults but can occur in children and adolescents
  • Generally progresses at a slow to moderate rate but may have periods of rapid progression
  • Can be modified by other local factors, systemic factors, medications, smoking, or emotional stress

Predominant Microbial Flora

  • Variable microbial pattern containing predominantly gram-negative, anaerobic bacilli and spirochetes such as Prophyromonas gingivalis, Tanerella forsythensus (formally Bacteroides forsythus), Treponema denticola, Prevotella intermedia, Fusobacterium nucleatum, Eikenella corrodens, and Campylobacter rectus
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13
Q

What is the difference between Recurrent periodontits and Refractory periodontitis?

A

Recurrent periodontitis:

  • Describes a recurrence of periodontitis after successful treatment

Refractory periodontitis:

  • describes periodontitis that does not respond to treatment
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14
Q

Explain Aggressive Periodontitis characterizations and predominant microbial flora

Describe the difference between localized and generalized

A

Aggressive Periodontitis

Formaly known as juvenile periodontitis or early-onset periodontitis

Characterisitcs

  • Presence of plaque
  • Presence of attachment loss
  • Amount of periodontal destruction is generally inconsistent with presence of microbial deposits
  • Familial aggregation
  • Usually affects individuals younger than 30 yrs but can occur in older patients
  • Generally progresses rapidly but may be self-arresting
  • Phagocyte abnormalities are common
  • Hyper-responsive monocyte/macrophage phenotype is common
  • Can be modified by other local factors, systemic factors, medications, smoking or emotional stress

Classification

  • Localized: Localized to first molars and/or incisors. Typically a circumpubertal onset. Often self-limiting (“burns out”) in 20s
  • Generalized: Affects at least three permanent teeth other than first molars and incisors. Usually affects people < 30years old, but patients may be older. Often associated with systemic diseases (neutropenias, leukemias, etc)

Predominant Microbial Flora

  • Similar to chronic periodontitis with often elevated proportions of Aggregatibactor actinmomycetemcomitans (formerly Actinobacillus actinmomycetemcomitans) and/or Porphyromonas gingivalis
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15
Q

Explain Necrotizing Periodontal disease Characteristics, Classifications, and Predominant Microbial flora

A

Necrotizing Periodontal disease

Formerly known as trench mouth or Vincent’s disease

Characteristics

  • Presence of plaque
  • Interproximal gingival necrosis (“punched out” papillae)
  • Marginal gingival pseudomembrane formation
  • Attachment loss may or maynot be present
  • Gingiva bleeds easily
  • Pain when brushing or eating
  • Bad breath (fetor oris)
  • Commonly associated with emotional stress, malnutrition, smoking or immunosuppression (HIV)

Classification:

  • Necrotizing ulcerative gingivitis (NUG): No attachment loss
  • Necrotizing ulcerative periodontitis (NUP): attachment loss present

Predominant Microbial Flora

  • Variable microbial flora with elevated proportions of spirochetes (Treponema sp), Prevotella intermedia, Fusobacterium sp, and Selenomonas sp
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16
Q

Explain Candidiasis Characteristics, Classifications, and Predominant Microbial flora

A

Candidiasis

Characteristics

  • An opportunistic fungal infection
  • Commonly associated with immunosuppresion (HIV), ill-fitting dentures, chronic xerostomia (Sjogren’s syndrome), or prolonged use of antibiotics

Classification

  • Pseudomembranous candidiasis (thrush): Whitish patches of desquamative epithelium, which can be easily wiped off,* leaving a slighly bleeding surface. *most common form
  • Atrophic (erythematous) candidiasis: Painful brigh-red, smooth, “beefy” lesions on the tongue, palate, or other mucosal surfaces, usually associated with ill-fitting dentures
  • Chronic hyperplastic candidiasis: Asymptomatic* whitish plaques commonly found on the buccal mucosa near the commissures that *cannot be removed, resembling oral leukoplakia

Predominant Microbial Flora

  • Candida albicans
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17
Q

Expain the mechanical means for plaque control

A
  • Toothbrushing and flossing are proven methods to remove plaque
  • However, they cannot remove subgingival plaque in pockets > 3 mm deep (as in cases of periodontal disease)
  • Dental professionals must scale teeth and root plane in order to remove the subgingival plaque and calculus
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18
Q

Expain the chemical means for plaque control

A

Chemical Plaque Control

  • Chemical means of plaque control is often used as an adjunct to mechanical cleaning
  • Two mouthrinses are ADA approved for the treatment of gingivitis:
    • Rx- only chlorhexidine gluconate and an OTC phenolic/essential oil compound
  • Chlorohexidine gluconate is the most effective antiplaque mouth rinse due to its substantivity
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19
Q

What are the modes of cell injury

A

Modes of Cell Injury

  • Hypoxia and ischemia
  • Physical trauma: Burns, frostbite, radiation, electric shock, etc
  • Microorganisms: Bacteria, viruses, fungi, parasites, etc
  • Immunologic reactions: Autoimmunity and anaphylaxis
  • Chemical/pharmacologic insulat: Poisons, drugs, alcohol, etc.
  • Nutritional imbalances: Vitamin deficiency, obesity, etc
  • Genetic defects: Hemoglobinopathies, storage diseases, etc.
  • Aging: Increases telomerase activity, inaccurate repaire of DNA, etc
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20
Q

What tissues are the most vulnerable to hypoxia and what does it result from

A

Heart, brain and lungs are very vulnerable to hypoxia.

Results from:

  • Vascular ischemia
  • decreased blood oxygen (eg. anemia, pulmonary disease)
  • decreased tissue perfusion (eg. shock, cardiac failure)
  • CO poisoning
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21
Q

What are chemical-induced cell injuries caused by?

A

Carbon monoxide (CO)

Carbon tetrachloride (CCl4)

Mercury

Cyanide

Methanol

Lead

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22
Q

What chemical-induced cell injury causes the following:

  • Systemic hypoxia
A

Carbon monoxide (CO) poisoning

Systemic hypoxia

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23
Q

What chemical-induced cell injury causes the following:

  • Hepatocellular damage (“fatty liver”)
A

Carbon tetrachloride (CCl4)

Hepatocellular damage (“fatty liver”)

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24
Q

What chemical-induced cell injury causes the following:

  • Renal tubular necrosis
  • Pneumonitis
  • GI ulceration

Gingival lesions

A

Mercury

Causes

  • Renal tubular necrosis
  • Pneumonitis
  • GI ulceration

Gingival lesions

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25
Q

What chemical-induced cell injury causes the following:

  • Prevents cellular oxidation
  • Odor of bitter almonds
A

Cyanide

Causes:

  • Prevents cellular oxidation
  • Odor of bitter almonds
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26
Q

What chemical-induced cell injury causes the following:

  • Blindness
A

Methanol

Causes

Blindness

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27
Q

What chemical-induced cell injury causes:

  • Basophilic stippling of RBC’s
A

Lead

causes:

  • Basophilic stippling of RBC’s
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28
Q

Explain Free Radical Injury

  • Induced by
  • Initiated reactions
  • Cellular damage
  • Generated form
  • Antioxidants
A

Free Radical Injury

  • Induced by activated oxygen species
  • Inititate autocatalytic reactions
  • Cellular damage:
    • membrane lipid peroxidation
    • Nucleic acid denaturation
    • Cross-linking of proteins
  • Generated from:
    • Redox reactions
    • Radiation (UV light)
    • Drugs and chemicals
    • Reperfusion injury
  • Antioxidants:
    • Superoxide dismutase (make peroxide)
    • Catalase (degrades peroxide)
    • Vitamine E
    • Ceruloplasmin: carries copper in blood
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29
Q

Name and describe the two types of cell injury

A

Types of Cell Injury

Reversible Cell Injury

  • Cellular and organelle swelling (due to Ca2+ influx)
  • Bleb formation
  • Ribosomal detachment from ER
  • Clumping of chromatin (due to decreased pH)
  • Increased lipid deposition (due to decreased protein synthesis)

Irreversible cell injury

  • Extensive plasma membrane damage
  • Massive Ca2+ influx
  • Diminished oxidative phosphorylation within mitochondria (due to accumulation of Ca2+ rich densities)
  • Release of lysosomal enzymes into the cytoplasm (due to lysosomal rupture)
  • Nuclear fragmentation (karyorrhexis)
  • Cell death (necrosis)

The outcome of cell injury depends largely on the severity and duration of the insult, but also on the cell type and its adaptive mechanism

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30
Q

Name the cellular reactions to injury

Name

  • Definition
    • Results
A

Cellular Reactions to Injury

  • Atrophy
    • Decrease in cell size
      • Decrease in tissue or organ size (usually secondary to decreased workload, neurovascular supply, nutrition, endocrine stimulation, and increase in age)
  • Hypertrophy
    • Increase in cell size
      • Increase in tissue or organ size (usually secondary to increased tisseu workload or endocrine stimulation)
  • Aplasia
    • Complete lack of cells
      • Agenesis (tissue or organ absence)
  • Hypoplasia
    • Decrease in cell numbers
      • Decrease in tissue or organ size
  • Hyperplasia
    • Increase in cell numbers
      • Increase in tissue or organ size (eg. glandular breast proliferation associated with pregnancy)
  • Metaplasia
    • Reversible, morphological change from one cell type to another
      • Usually occurs in response to stress (eg. conversion of columnar epithelium to stratified squamous)

Hypertrophy and hyperplasia can occur simultaneously (eg. uterine enlargement during pregnancy)

31
Q

Explain what Gingival overgrowth is often related to

A

Gingival overgrowth is often drug related:

  • Phenytoin (Dilantin)
  • Ca2+ channel blockers (eg. nifedipine_
  • Cyclosporin
32
Q

Explain the two types of Enzymatic cellular degradation

A

Enzymatic Cellular Degradation

  • Autolysis:
    • Cellular degradation caused by intracellular enzymes indigenous to the cell itself
  • Heterolysis
    • Cellular degradation caused by enzymes extrinsic to the cell
33
Q

State the 5 types of Endogenous Pigmentation

A

Comparison of Endogenous Pigments

  • Lipofuscin
    • Yellow-brown color “wear and tear”
  • Bilirubin
    • Yellowish color - Jaundice
  • Hemosiderin
    • Golden brown color - from heme/iron
  • Melanin
    • Brown-black color - tyrosine
  • Ceroid
    • Lipofuscin - hepatic kupffer
34
Q

Name the Endogenous Pigmentation that is associated with the following pathology: (Also describe its characteristics)

  • Brown atrophy
  • Age
A

Lipofuscin

Characteristics:

  • Yellow-brown color
  • “wear and tear” pigment
  • Derived from lipid peroxidation
  • Has no effect on cell function
  • Accumulates in heart, liver, brain

Associated Pathology

  • Brown atrophy
  • Age
35
Q

Name the Endogenous Pigmentation that is associated with the following pathology: (Also describe its characteristics)

  • Hemosiderosis
  • Hemochromatosis
A

Hemosiderin

Characteristics:

  • Golden brown color
  • Derived from heme
  • Aggregates of ferritin micelles (iron storage sites)
  • Identified with Prussian blue stain
  • Accumulates in phagocytes of:
    • Bone marrow, Liver, Spleen

Associated Pathology:

  • Hemosiderosis
  • Hemochromatosis
36
Q

Name the Endogenous Pigmentation that is associated with the following pathology: (Also describe its characteristics)

  • Hemolytic anemias
  • Hepatocellular injury
A

Bilirubin

Characteristics

  • Yellowish color
  • Major bile pigment
  • Derived from heme
  • Jaundice: Bilirubin accumulation

Associated Pathology

  • Hemolytic anemias
  • Hepatocellular injury
  • Biliary tree obstruction
37
Q

Name the Endogenous Pigmentation that is associated with the following pathology: (Also describe its characteristics)

  • Physiologic pigmentation
  • Suntan
  • Addison’s disease
  • Albinism
  • Vitiligo
A

Melanin

Characteristics

  • Brown-black color
  • Derived from tyrosine
  • Synthesized in melanocytes
  • Accumulates in skin, eyes, hair

Associated Pathology

  • Increased melanin:
    • Physiologic pigmentation
    • Suntan
    • Addison’s disease
  • Decreased melanin
    • Albinism
    • Vitiligo
38
Q

Name the Endogenous Pigmentation that is associated with the following pathology: (Also describe its characteristics)

  • Hepatocellular injury (only) and is derived from lipofuscin
A

Ceroid

Characteristics:

  • Derived from lipofuscin (via auto-oxidation)
  • Accumulates in hepatic Kupffer cells

Associated Pathology:

  • Hepatocellular Injury
39
Q

What are the two processes for Hemosiderin Accumulation?

Name the process

Definition of the process

Associations

Tissue injury Y/N

A

Hemosiderin Accumulation

Hemosiderin = an insoluble, iron-containing protein derived from ferritin. It is detected histologically by Prussian blue stain

  • Hemosiderosis
    • Increased hemosiderin accumulation (in tissue macrophages)
    • Association:
      • Hemorrhage
      • Thalassemia
    • Tissue Injury: NO
  • Hemochromatosis (Bronzed disease)
    • More extensive hemosiderin accumulation (throughout body)
    • Associations:
      • Increased iron absorption
      • Decreased iron utilization
      • Hemolytic anemias
      • Blood transfusions
    • Tissue injury: YES
40
Q

What are Pathologic calcifications?

What are the two types?

A

Pathologic calcifications

  • Abnormal deposition of calcium salts in normal noncalcified tissue
  • Types of Calcifications:
    • Dystrophic
      • Calcification of degenerate or necrotic tissue
        • Normal Serum Ca2+
    • Metastatic
      • Calcification of normal tissue
        • Abnormal Serum Ca2+
41
Q

Explain the pathogenesis of Dystrophic Pathologic Calcification

  • explain serum Ca2+ levels
  • Common locations
A

Dystrophic

  • Definition: Calcification of degenerate or necrotic tissue
  • Serum Ca2+: Normal
  • Pathogenesis:
    • Enhanced by collagen and acidic phosphoproteins (eg. osteopontin)
  • Common locations:
    • Hyalinized scars
    • Degenerated leiomyoma foci
    • Caseous nodules (Tb)
    • Damaged heart valves
    • Atherosclerotic plaques
42
Q

Explain the pathogenesis of Metastatic Pathologic Calcification

  • explain serum Ca2+ levels
  • Common locations
A

Metastatic

  • Definition: Calcification of normal tissue
  • Serum Ca2+: Abnormal
  • Pathogenesis:
    • Percipitation caused by tissue acidity and increased Ca2+ concentration
    • Associated with:
      • Hyperparathyroidism
      • Vitamine D intoxication
      • Bone destruction (eg. metastatic cancer)
      • Sarcoidosis
  • Common locations:
    • Stomach
    • Lungs
    • Kidneys
43
Q

What is Eggshell calcification

A

Eggshell calcification

  • Thin layer of calcification around intrathoracic lymph nodes
  • Seen on chest x-ray
  • Associated with silicosis
    • Lung fibrosis caused by the inhalation of dust containing silica.
44
Q

What is Calcinosis

A

Calcinosis

  • Calcification in or under the skin
  • Associated with scleroderma and dermatomyositis
45
Q

What is Sialolithiasis

A

Sialolithiasis

  • Formation of salivary stone (sialolith) within salivary gland or duct
  • Pain more severe when eating
46
Q

What is Necrosis - Cell death

  • Histological characterization
  • Cellular degradation types
  • Name the three major forms of necrosis
A
  • Most common form of cell death resulting from irreversible injury
  • Characterized histologically by a vacuolated cytoplasm, calcification, and nuclear changes
  • Cellular degradation:
    • Autolysis: Caused by intracellular enzymes of necrotic cell
    • Heterolysis: Caused by enzymes outside the necrotic cell
  • Three major forms of necrosis:
    • Coagulative = ischemia
    • Liquefactive = Suppuration
    • Caseous = Cheesy/clumpy
47
Q

Which type of necrosis is characterised by the following definition:

  • Enzymatic degestion
  • Suppuration
  • Loss of tissue architecture
  • Adipose liquefaction
  • Fatty acid released
A

Liquefactive

  • Fat

Examples:

  • Brain abscess
  • Acute pancreatitis
48
Q

Which type of necrosis is characterised by the following definition:

  • Granulomatous inflammation
  • Clumped cheesy material
A

Caseous

Examples:

  • Tuberculosis
49
Q

Which type of necrosis is characterised by the following definition:

  • Ischemia
  • Protein denaturation
  • Tissue architecture preserved
  • Infarct area is triangular shaped
  • Ischemic coagulation
  • Putrefaction
A

Coagulative

  • Gangrenous

Examples:

  • Myocardial infarction
  • Gangrene

***NOTE: Coagulative necrosis is the most common form of necrosis

50
Q

Explain the three types of Nuclear changes associated with cell death

  • Pyknosis
  • Karyolysis
  • Karyorrhexis
A

Nuclear Changes Associated with Cell Death

  • Pyknosis =
    • Nuclear shrinkage and chromatin condensation
  • Karyolysis =
    • Nuclear dissolution and chromatin fading (basophilia)
  • Keryorrhexis =
    • Nuclear fragmentation; completely disappears in 1-2 days
51
Q

Explain Apoptosis - Cell death

A

Apoptosis

  • Programmed cell death that occurs in both physiologic and pathologic states
  • Does not result in an inflammatory response
  • Induced by several cytosolic proteases
  • There is no breakdown in the mechanisms that supply cellular energy
  • Leads to nuclear pyknosis and karyorrhexis, cell shrinkage, and ultimately phagocytosis by macrophages or neightboring parenchymal cells
  • There is no rupture of the cell membrane
  • Normal cell volume is maintained
52
Q

Explain the definition of inflammation State the two types of responses

A

Inflammation

  • A vascular and cellular response to tissue injury, resulting in the isolation of the causative agent, elimination of necrotic cells and tissues, and host tissue repair
  • There are two basic types of inflammatory response
    • Acute
    • Chronic

Acute inflammation generally precedes chronic inflammation, although some types of injury can directly induce a chronic inflammatory response

53
Q

Explain the characteristics of Acute inflammation

A

Acute inflammation

  • The initial response to tissue injury, largely consisting of leukocytes infiltration, which rids the affected area of infectious agents (mostly bacteria) and degrades necrotic tissues resulting from the damage
  • PMNs are the first leukocytes to respond
  • Will elicit increased antibody titer
  • The presence of monocytes and macrophages marks the transition from acute to chronic inflammation
  • Its outcome may include the following:
    • Regeneration: Complete resolution of affected tissues
    • Repair: Fibrosis (scarring) of affected tissue
    • Abscess: Formation of pus (neutrophils, necrotic cells, and exudate)
    • Chronic inflammation
54
Q

What are the five clasic signs of acute inflammation?

A

Acute Inflammation

  1. Redness (rubor):
    1. from vasodilation and increased vascular permeability
  2. Heat (calor):
    1. From vasodilation and increased vascular permeability
  3. Swelling (tumor):
    1. From edema
  4. Pain (dolor):
    1. From inflammatory mediators and pressure due to edema
  5. Loss of function (functio laesa):
    1. From swelling and pain
55
Q

What are the two stages of acute inflammation

    • name the stage
        • Events
            • Characteristics
A

Acute Inflammation

  • Vascular Stage
    • Vasodilation and increased vascular permeability, predominantly mediated by histamine-producing cells (mast cells, basophils, and platelets)
      • Formation of an exudative edema (a straw-colored protein-rich exudate of extravascular fluid)
      • Increased blood flow (hyperemia) may lead to vascular congestion
  • Cellular Stage
    • Margination, adhesion, diapedesis, and chemotaxis of leukocytes (predominantly polyorphonuclear neutrophils (PMNs) toward the site of injury
      • Phagocytosis and leukocyte degranulation leads to microbial cell lysis, but also host tissue damage
56
Q

Explain the two types of Edema

A

Edema

  • Exudate
    • Cause: Inflammatory increase in vascular permeability
    • Characteristics:
      • Cell-rich (WBC’s, cellular debris)
      • High plasma protein
      • high specific gravity
      • Flushes away foreign material
  • Transudate
    • Cause: Noninflammatory alteration of vascular hydrostatic or osmotic pressure
    • Characteristics:
      • Few cells
      • Low plasma protein
      • Low specific gravity
57
Q

Describe the general definition for Chronic inflammation and state the three stages of chronic inflammation

A

Chronic inflammation

  • A prolonged inflammatory response consisting of continuous inflammatory cell infiltrates, tissue injury and wound healing
  • Can be caused by persistent infections, foreign bodies, immune reactions, or unknown reason

The Three Stages of Chronic Inflammation:

  • Mononuclear cell infiltration
    • Migration of macrophages, lymphocytes, plasma cells and eosinophils
  • Granulation tissue formation
    • Healing tissue consisting largely of fibrosis (fibroblasts), angiogenesis (new capillaries), and inflammatory cells
  • Host tissue destruction
    • Mediated by cytokines of host leukocytes
58
Q

Compare Acute and Chronic inflammation

A
59
Q

Explain Granulomatous Inflammation

A

Granulomatous Inflammation

A granuloma consists of granulation tissue (fibrosis, angiogenesis, and inflammatory cells) frequently containing epithelioid cells and multinucleated giant cells

  • A specific type of chronic inflammation characterized by macrophages that have been transformed into epithelioid cells and are surrounded by lymphocytes, fibroblasts, and local parenchymal cells
  • Associated with tuberculosis, leprosy, sarcoidosis, syphilis, blastomycosis, histoplasmosis, coccidioidomycosis, crohn’s disease, and foreign body containment (eg. sutures
60
Q

What are the systemic effects of inflammaiton

A

Systemic Effects of Inflammation

  • Fever
  • Leukocytosis
    • Neutrophilia: Largely associated with bacterial infections
    • Eosinophilia: Largely associated with parasitic infections
    • Lymphocytosis: Associated with some viral infections (mumps, rubella)
61
Q

Name the Major Inflammatory Mediators

A

Major Inflammatory mediators

  • Histamine -> Primary mediator of anaphylaxis (vasodilation)
  • Prostaglandins -> Vasodilation, Pain, Fever
  • Leukotrienes (SRS-A) -> Primary mediator of asthma, Vascular permeability, chemotaxis
  • Cytokines -> Fever, chemotaxis
  • Serotonin -> Vascular permeability
  • Bradykinin -> Pain, Vascular permeability
  • Nitric oxide -> Vasodilation, tissue damage
  • Complement proteins -> Vascular permeability, chemotaxis
  • Lysosomal enzymes -> Bacterial killing, tissue damage
  • f-met-leu-phe (FMLP) -> Chemotaxis
62
Q

What cells in the body DO NOT have the ability to regenerate?

A

Neruons (CNS), alveolar (Lungs), cardiac (heart), and skeletal and smooth (muscle) cells DO NOT have the ability to regenerate

63
Q

What are Cytokines - inflammatory mediators

Name and describe the 4 major categories

What are Lymphokines?

A

Cytokines

  • Small peptides secreted by many cell types
  • Most are involved in host defense and immunity
  • Lymphokines: Cytokines secreted by T cells

​​There are four major categories of cytokines:

  1. Interleukins (IL): largest group of cytokines. Regulate leukocyte activity
  2. Interferons (INF): interfere with viral replication. Anti-proliferative effects (protect cells that haven’t been infected yet). Associated with nonspecific immune system
  3. Tumor necrosis factor (TNF): regulate tumor suppression
  4. Colony stimulating factor (CSF): Regulate differentiation and growth of bone marrow elements
64
Q

Explain the secretion and function of the following Cytokines:

  • IL-1
  • IL-2
  • IL-3 (CSF)
  • IL-4
  • IL-5
  • IL-6
A

Inflammatory Cytokines

Recall: IL = Interleukins = regulate leukocyte activity; CSF = colony stimulating factor = regulated differentiation and growth of bone marrow elements

  • IL-1
    • Secreted by: Monocytes, Macrophages, PMNs, Fibroblasts, Epithelial Cells, Endothelial cells
    • Function: Produce fever, Stimulates Th cells, Stimulates Osteoclasts
  • IL-2
    • Secreted by: Th-1 cells
    • Function: Stimulates other Th cells and Tc cells
  • IL-3 (CSF)
    • Secreted by: Th cells, NK cells
    • Function: Stimulated hematopoietic stem cells
  • IL-4
    • Secreted by: Th-2 cells
    • Function: Stimulates B cells and IgE
  • IL-5
    • Secreted by: Th-2 cells
    • Function: Stimulates B cells and IgA; Stimulates Eosinophils
  • IL-6
    • Secreted by: Monocytes, macrophages, fibroblasts, Th cells
    • Function: Produces fever, Stimulates B cells, Stimulates Th cells, Stimulates osteoclasts
65
Q

What is a good method for remembering IL 1 through IL 5 cytokines?

A

Hot T-Bone stEAk

IL-1: Fever (Hot)

IL-2: T cell activation

IL-3: Bone marrow stimulation

IL-4: IgE stimulation

IL-5: IgA stimulation

66
Q

What inflammatory cytokines do activated macrophages secrete?

A

IL-1

IL-6

IL-8

IL-12

TNF-alpha

67
Q

Explain the secretion and function of the following Cytokines:

  • IL-8
  • IL-10
  • IL-12
  • INF-gamma
  • TNF-alpha
  • TNF-beta
  • TGF-beta
A

Inflammatory Cytokines

Recall: IL = Interleukins = regulate leukocyte activity; CSF = colony stimulating factor = regulated differentiation and growth of bone marrow elements

INF = Interfere with viral replication = Assocated with viral replication. nonspecific immune system

TNF = Tumor necrosis factor = regulates tumor suppression

  • IL-8
    • Secreted by: Monocytes, Macrophages
    • Function: Chemotaxis of PMNs
  • IL-10
    • Secreted by: Th-2 cells
    • Function: Inhibits Th-1 cells
  • IL-12
    • Secreted by: Monocytes, Macrophages
    • Function: Stimulates Th-1 cells
  • INF-gamma
    • Secreted by: Th-1 cells
    • Function: Stimulates monocytes, macrophages, NK cells and PMNs
  • TNF-alpha and TNF-Beta
    • Secreted by: Monocytes (alpha), Macrophages (alpha), T cells (Beta)
    • Function: Stimulates adhesion molecules, stimulates Th cells, Stimulates osteoclasts, Cachexia (wasting syndrome)
  • TGF-beta** **= Transforming growth factor​
    • Secreted by: Monocytes, Macrophages, T cells, B cells
    • Function: The “anti-cytokine”, Inhibits T cells, B cells, PMNs, monocytes, macrophages, NK cells, Stimulates collagen formation and wound healing
68
Q

What is Hageman factor?

A

Hageman factor (Factor XII) is necessary in the production of bradykinin

Recall: Bradykinin is secreted in plasma, vasodilates, Bronchial dilates, and its major function is PAIN and vascular permeability

69
Q

Name and state the details of the three stages in wound repair

A

Wound Repair

**Although there are three sequential stages, they are not mutually exclusive; their events commonly overlap

  1. Inflammatory Stage
    • Starts immediately after tissue injury and lasts 3-5 days
    • The vascular and cellular phages of acute inflammation are activated
    • Fibrin clot formation
    • Epithelial migration starts from opposing wound margins
    • Local mesenchymal cells differentiate into fibroblasts
  2. Fibroplastic Stage
    • Starts 3-4 days after tissue injury and lasts 2-3 weeks
    • Epithelial migration is completed and its thickness increases
    • Collagen formation occurs as fibroblasts migrate across the fibrin network
    • Angiogenesis and new capillary formation starts from the wound margin
    • Fibrinolysis occurs as more connective tissues is formed
  3. Remodeling Stage
    • Starts 2-3 weeks after tissue injury and continues indefinately
    • Epithelial stratification is restored
    • Collagen remodeling, re-orientating the fibers to provide better tensile strength
    • Wound contraction and scar formation
70
Q

What is contract inhibition?

A

During epithelialization, the free edges of the wound epithelium migrate toward each other until they meet, signaling a stop in lateral grwoth. This is known as contact inhibition

71
Q

What are the two methods of wound healing?

A

Methods of wound healing

  • Primary intention
    • Occurs when wound margins are closely re-approximated
      • Faster healing with minimal scarring and risk of infection
  • Secondary intention
    • Occurs when there is a gap between the wound margins because close re-approximation cannot occur
      • Slower healing with granulation tissue formation and scarring. More prone to infection

Tensile strength of a healing wound is dependent on collagen fiber formation

72
Q

Discuss organ/tissue regeneration

  • which tissues does actively regenerate and which tissues do not regenerate
A

Regeneration

  • Adaptive mechanism for restoring a tissue or organ
  • Occurs in several tissue types:
    • Liver
    • Bone
    • Cartilage
    • Intestinal mucosa
    • Surface epithelium
  • Does NOT occur in several tissue types:
    • Skeletal muscles
    • Cardiac muscles
    • Lung alveoli
    • Neruons (CNS)

Liver is a very uncommon site for infarction because of its regenrative capacity; can remove as much as 70% of hepatic tissue. Hepatocyte mitosis peaks at 33 hours

73
Q
A

NBDE Part 1 (7 decks)

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