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
2
Q
What microorganism is most commonly found on the surface of the tongue?
A
Streptococcus salivarius
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
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
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)
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
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
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
9
Q
What are the three main items that caries need for their formation?
A
- Cariogenic bacteria
- A susceptible surface
- A fermentable carbohydrate source
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
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
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
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
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
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
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
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
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
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
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
21
Q
What are chemical-induced cell injuries caused by?
A
Carbon monoxide (CO)
Carbon tetrachloride (CCl4)
Mercury
Cyanide
Methanol
Lead
22
Q
What chemical-induced cell injury causes the following:
- Systemic hypoxia
A
Carbon monoxide (CO) poisoning
Systemic hypoxia
23
Q
What chemical-induced cell injury causes the following:
- Hepatocellular damage (“fatty liver”)
A
Carbon tetrachloride (CCl4)
Hepatocellular damage (“fatty liver”)
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
25
What **chemical-induced cell injury** causes the following:
- Prevents cellular oxidation
- Odor of bitter almonds
***_Cyanide_***
Causes:
- Prevents cellular oxidation
- Odor of bitter almonds
26
What **chemical-induced cell injury** causes the following:
- Blindness
***_Methanol_***
Causes
Blindness
27
What **chemical-induced cell injury** causes:
- Basophilic stippling of RBC's
***_Lead_***
causes:
- Basophilic stippling of RBC's
28
Explain Free Radical Injury
- Induced by
- Initiated reactions
- Cellular damage
- Generated form
- Antioxidants
***_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
29
Name and describe the two types of cell injury
***_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
30
Name the cellular reactions to injury
Name
* Definition
* Results
***_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
Explain what Gingival overgrowth is often related to
***_Gingival overgrowth_*** is often _drug_ _related_:
* Phenytoin (Dilantin)
* Ca2+ channel blockers (eg. nifedipine\_
* Cyclosporin
32
Explain the two types of Enzymatic cellular degradation
**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
State the 5 types of Endogenous Pigmentation
***_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
Name the **Endogenous Pigmentation** that is associated with the following pathology: (Also describe its characteristics)
- Brown atrophy
- Age
***_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
Name the **Endogenous Pigmentation** that is associated with the following pathology: (Also describe its characteristics)
- Hemosiderosis
- Hemochromatosis
***_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
Name the **Endogenous Pigmentation** that is associated with the following pathology: (Also describe its characteristics)
- Hemolytic anemias
- Hepatocellular injury
***_Bilirubin_***
**_Characteristics_**
* Yellowish color
* Major bile pigment
* Derived from heme
* ***Jaundice***: Bilirubin accumulation
**_Associated Pathology_**
* Hemolytic anemias
* Hepatocellular injury
* Biliary tree obstruction
37
Name the **Endogenous Pigmentation** that is associated with the following pathology: (Also describe its characteristics)
- Physiologic pigmentation
- Suntan
- Addison's disease
- Albinism
- Vitiligo
***_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
Name the **Endogenous Pigmentation** that is associated with the following pathology: (Also describe its characteristics)
- Hepatocellular injury (only) and is derived from lipofuscin
***_Ceroid_***
**_Characteristics:_**
* Derived from lipofuscin (via auto-oxidation)
* Accumulates in hepatic Kupffer cells
**_Associated Pathology:_**
* Hepatocellular Injury
39
What are the two processes for Hemosiderin Accumulation?
Name the process
Definition of the process
Associations
Tissue injury Y/N
***_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
What are Pathologic calcifications?
What are the two types?
***_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
Explain the pathogenesis of **Dystrophic** Pathologic Calcification
- explain serum Ca2+ levels
- Common locations
***_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
Explain the pathogenesis of **Metastatic** Pathologic Calcification
- explain serum Ca2+ levels
- Common locations
***_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
What is **Eggshell calcification**
***_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
What is **Calcinosis**
**Calcinosis**
* Calcification in or under the skin
* Associated with scleroderma and dermatomyositis
45
What is Sialolithiasis
***_Sialolithiasis_***
* Formation of **salivary stone** (sialolith) within salivary gland or duct
* Pain more severe when eating
46
What is **Necrosis** - Cell death
- Histological characterization
- Cellular degradation types
- Name the three major forms of necrosis
* 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
Which type of necrosis is characterised by the following definition:
* Enzymatic degestion
* Suppuration
* Loss of tissue architecture
* Adipose liquefaction
* Fatty acid released
**Liquefactive**
- Fat
Examples:
* Brain abscess
* Acute pancreatitis
48
Which type of **necrosis** is characterised by the following definition:
* Granulomatous inflammation
* Clumped cheesy material
Caseous
Examples:
* Tuberculosis
49
Which type of **necrosis** is characterised by the following definition:
* Ischemia
* Protein denaturation
* Tissue architecture preserved
* Infarct area is triangular shaped
* Ischemic coagulation
* Putrefaction
***_Coagulative_***
- Gangrenous
Examples:
- Myocardial infarction
- Gangrene
\*\*\*NOTE: **Coagulative necrosis is the most common form of necrosis**
50
Explain the three types of Nuclear changes associated with cell death
- Pyknosis
- Karyolysis
- Karyorrhexis
***_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
Explain Apoptosis - Cell death
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
Explain the definition of inflammation State the two types of responses
***_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
Explain the characteristics of ***_Acute inflammation_***
**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
What are the five clasic signs of acute inflammation?
***_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
What are the two stages of acute inflammation
* - name the stage
* - Events
* - Characteristics
**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
Explain the two types of Edema
***_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
Describe the general definition for Chronic inflammation and state the three stages of chronic inflammation
***_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
Compare Acute and Chronic inflammation
59
Explain Granulomatous Inflammation
***_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
What are the systemic effects of inflammaiton
***_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
Name the Major Inflammatory Mediators
**_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
What cells in the body DO NOT have the ability to regenerate?
Neruons (**CNS**), alveolar (**Lungs**), cardiac (**heart**), and skeletal and smooth (**muscle**) cells DO NOT have the ability to regenerate
63
What are Cytokines - inflammatory mediators
Name and describe the 4 major categories
What are Lymphokines?
***_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
Explain the secretion and function of the following Cytokines:
* IL-1
* IL-2
* IL-3 (CSF)
* IL-4
* IL-5
* IL-6
***_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
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What is a good method for remembering IL 1 through IL 5 cytokines?
**H**ot **T**-**B**one st**EA**k
*_IL-1:_* Fever (**H**ot)
*_IL-2:_* **T** cell activation
*_IL-3:_* **B**one marrow stimulation
*_IL-4_*: Ig**E** stimulation
*_IL-5:_* Ig**A** stimulation
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What inflammatory cytokines do activated macrophages secrete?
IL-1
IL-6
IL-8
IL-12
TNF-alpha
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Explain the secretion and function of the following Cytokines:
* IL-8
* IL-10
* IL-12
* INF-gamma
* TNF-alpha
* TNF-beta
* TGF-beta
***_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_***
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What is Hageman factor?
**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
Name and state the details of the three stages in wound repair
***_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
What is contract inhibition?
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
What are the two methods of wound healing?
**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
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Discuss organ/tissue regeneration
- which tissues does actively regenerate and which tissues do not regenerate
**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
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