Pathology Exam 1

Front 1

What is the most common cause of acquired, physical etiology?

Back 1

Trauma

Front 2

Macule

Back 2

a discolored spot on the skin or mucosa that isn't elevated above the surface

Front 3

Papule

Back 3

small, circumscribed, superficial, solid elevation of the skin or mucosa, measuring less than 1.0mm in diameter

Front 4

Plaque

Back 4

a small, circumscribed, superficial, solid elevation of the skin or mucosa, equal to or greater than 1.0mm in diameter

Front 5

Wheal

Back 5

smooth, slightly elevated area on the skin which is redder or paler than the surrounding area; usually associated w/ itchiness (pruritus)

Front 6

Nodule

Back 6

a small, protruding bump that is felt on the surface of an organ, skin or mucosa

Front 7

Mass

Back 7

a collection of solid tissue; may be sessile or pedunculated; endophytic or exophytic; very general term; anything that's a big collection of tissue

Front 8

Cyst

Back 8

an epithelial line cavity that appears as a mass; it is a type of mass that is closed

Front 9

Vesicle

Back 9

a clear, fluid-filled blister that is less than 5mm in diameter

Front 10

Bulla

Back 10

a clear, fluid-filled blister that is greater than 5mm in diameter

Front 11

Pustule

Back 11

a visible collection of pus within or beneath the epithelium

Front 12

Ulcer

Back 12

a local defect of the surface of an organ or tissue, which is produced by the sloughing of inflammatory necrotic tissue

Front 13

Leukoplakia

Back 13

a white area on the oral mucosa that will not rub off

Front 14

Erythroplakia

Back 14

an erythematous (red) area on the mucosa

Front 15

Sclerosis

Back 15

an indurated or hardened piece of tissue or organ

Front 16

Pathognomonic

Back 16

a particular sign whose presence means that a particular disease is present beyond any doubt; diagnostic quality

Front 17

What is the pathognomonic sign of Erythema multiform

Back 17

Target lesion; the defining feature of this disease

Front 18

What is the Diagnostic Sequence for Differential Diagnosis

Back 18

1. Chief complaint

2. History of Present Illness (duration of process)

3. Medical, social, family histories

4. Complete clinical examination

5. Evaluation and classification of disease/lesion

6. Develop list of differential diagnoses

7. Develop working or tentative diagnosis

8. Lab and special exams

9. Formulate final diagnosis

10. Tx plan and Tx

Front 19

What is the Pathogenesis of a disease

Back 19

Sequence of events in cells or tissues in response to the etiologic agents from the initial stimulus to the functional and structural abnormalities that characterize the disease

Front 20

What are the four adaptive responses that cells can have to stress

Back 20

Atrophy

Hypertrophy

Hyperplasia

Metaplasia

Front 21

What are the two characteristics that determine a cell type's stress/adaptive responses

Back 21

Ability to turnover

Regenerative capacity

Front 22

What is a cell's adaptive response if it has high turnover ability and high regenerative capacity

Back 22

Hyperplasia - still divide and replace cells

Front 23

What cells of the body adaptively respond to stress with hyperplasia (have high turnover)

Back 23

Bone marrow

Epithelium

Hepatocytes

Fibroblasts

Oral cavity tissues (buccal mucosa, tongue)

Front 24

What cells of the body exhibit low turnover and are responsive to stimuli

Back 24

Endothelium (blood vessel lining)

Supportive cells (in bone, cartilage, smooth muscle)

Front 25

What cells of the body exhibit little or no ability to turnover

Back 25

Neurons

Skeletal myocytes

Cardiac myocytes

Front 26

Atrophy

Back 26

loss of cellular organelles and cellular size

(a reversible and adaptive response of cell to reduce mass of its functional cytoplasm by decreasing number/volume of organelles; decrease in cell size and then cell number)

Front 27

What is involution of the uterus after birth an example of

Back 27

Physiologic Atrophy (due to loss of hormonal stimulation after parturition)

Front 28

What is the loss of secondary sex characteristics with age an example of

Back 28

Physiologic atrophy (due to decrease in hormonal stimulation)

Front 29

What is decrease in muscle size of your calf after breaking your ankle an example of

Back 29

Pathologic atrophy (due to reduced functional demand)

Front 30

What has happened to the myocytes on the right slide if the cells on the left are normal

Back 30

Cells in the center have atrophied due to reduced functional demand (Pathologic Reversible Atrophy)

Front 31

Is it possible to reverse physiologic or pathologic atrophy

Back 31

Yes, you can reverse either through hypertrophy

Front 32

What has happened to the myocytes on the right if the myocytes on the left are normal

Back 32

Neurogenic atrophy (due to loss of innervation); Some myocytes have atrophied and some have hypertrophied (a compensatory mechanism)

atrophy --> hypertrophy of adjacent tissue

Front 33

Autophagy

Back 33

not getting an adequate supply of nutrients/O2 so cells respond by using less energy/use own energy

Front 34

What are the possible causes of pathologic atrophy

Back 34

Reduced functional demand

Loss of innervation

Inadequate supply of O2

Inadequate nutrition

Loss of endocrine stimulation (testicular, breast)

Aging (senile atrophy - brain/heart)

Front 35

What are the possible causes of physiologic atrophy

Back 35

Developmental change (thymus)

Physiologic change (uterus after parturition)

Aging change (involution of secondary sex traits)

Front 36

What has happened to these muscle cells

Back 36

Irreversible/Extreme atrophy after long period of immobilization; cell loss/death; white areas = fat inside muscle that was washed away

Front 37

What are the mechanisms of atrophy

Back 37

Decreased protein synthesis

Increased protein degradation (ubiquitin ligase activation, proteasome digestion)

Organelle recycling via Autophagy

Cell death (extreme)

Front 38

What is the mechanism that underlies atrophy

Back 38

Autophagy - self-eating

Front 39

What is hypertrophy

Back 39

increase in organelle/cell SIZE

(increase in cell size leading to increase in organ size due to increase in organelle number/size; result of increased functional demand, hormonal stimulation; can be physiologic or pathologic; reversible if stimulus removed)

Front 40

What are the possible causes of hypertrophy

Back 40

Increased functional demand (lifting weights)

Hormonal stimulation (increase in uterus size during pregnancy)

Front 41

What are the mechanisms behind hypertrophy

Back 41

Increased protein synthesis

Front 42

What can happen to the heart as a result of systemic hypertension

Back 42

Hypertrophy; (increased functional demand due to HTN leads to heart muscle hypertrophy in order to get blood to the system, which eventually leads to reduced functionality b/c of too much demand on the heart and CHF)

Front 43

What has happened to these cardiac myocytes from the top slide to the bottom slide and why

Back 43

Hypertrophy; the cells on the bottom are larger and the nuclei are farther apart; due to increased functional demand

Front 44

Hyperplasia

Back 44

increase in cell NUMBER

(due to proliferation; cell growth both physiologic and pathologic; it is a controlled process, even if proliferation is abnormal; cells respond to a signal; when the signal is gone cells will stop proliferation; it is NOT cancer, but you do have increased risk of cancer)

Front 45

What two adaptive stress responses does the uterus undergo during pregnancy

Back 45

Hypertrophy and Hyperplasia (increase in cell size and increase in cell number)

Front 46

Neoplasia

Back 46

Uncontrolled proliferation of cell number; CANCER; you have increased risk of this with hyperplasia

Front 47

What are the possible causes of hyperplasia

Back 47

Hormonal Stimulation (uterus during pregnancy, lactating breast)

Compensatory (blood donation, liver regeneration)

Excessive Hormonal Stimulation (pathologic; benign prostatic hyperplasia)

Excessive Growth Factor Stimulation

Front 48

What has happened to these prostate cells

Back 48

Benign Prostatic Hyperplasia; pathologic; NOT cancer, but increased risk of cancer; expanded glandular elements; uneven hyperplastic growth areas (the whole tissue is not enlarged evenly like in lactating breast hyperplasia)

Front 49

Metaplasia

Back 49

replacement/reprogramming of cells

(replace of one adult cell type with another through an adaptive process - reprogram stem cells of normal tissue; reversible to an extent)

Front 50

What are the possible causes of metaplasia

Back 50

Chronic Irritation (smoker's tracheal epithelium, esophagus w/ GERD)

Vitamin A deficiency (essential for bronchial epithelium)

Front 51

What adaptive cellular response often occurs to the tracheal epithelium of smokers or those with a Vitamin A deficiency

Back 51

Metaplasia; changed from ciliated columnar epithelium with functional goblet cells and cilia to stratified squamous epithelium (tougher but lacks functionality - more prone to infections of the lung)

Front 52

What adaptive cellular response has occurred from the esophageal epithelium on the left to that on the right

Back 52

Metaplasia due to GERD (gastroesophageal reflux disease); change from normal stratified squamous epithelium to epithelium that looks like glandular lining of the gut

can lead to Barrett's esophagitis if left untreated

Tx with Prilosec

Front 53

What is chondroplasia

Back 53

Type of metaplasia where you have cartilagnious growth in place of normal tissue; e.g. - extra growth on gingiva when you remove denture (cartilaginous growth); chronic irritation from denture makes tissue that's stronger

Front 54

What are intracellular accumulations

Back 54

cells deal with materials they're unable to eliminate by intracellular digestion

Front 55

What are the possible causes of intracellular accumulations

Back 55

Abnormal metabolism (fatty liver in alcoholism - fat accumulates inside cells)

Defect in Protein Processing (accumulation of proteins)

Lack of Enzyme Processing (accumulation of endogenous materials)

Ingestion of Indigestible materials (anthracosis - breathe in CO2 - coalminers - black lung)

Front 56

What has caused the normal liver cells on the left to change to those on the right in someone with chronic alcoholism/alcohol poisoning

Back 56

Intracellular Accumulations/Fatty Change/Steatosis

triglyceride accumulation in parenchymal cells; appears as clear vacuoles in the cells

Front 57

What has occurred here to the macrophages in smooth muscle in someone with atherosclerosis

Back 57

Intracellular Accumulations - phagocytic cells ingesting cholesterol but it cant be digested; clear cells formed with nuclei and nothing else; left with foam cells - major contributor to atherosclerosis

Front 58

What are four pigments that frequently accumulate in cells - intracellular accumulation

Back 58

1) Carbon - exogenous pigment; anthracosis

Endogenous:

2) Melanin (from oxidation of tyrosine in melanocytes; brown-black)

3) Lipofuscin ("wear and tear" - golden-brown; increases with age; in terminally differentiated, neuron, or infrequently cycling cells, hepatocyte)

4) Hemosiderin (excess iron - yellow/brown)

Front 59

What are five common types of intracellular accumulations

Back 59

1) Fatty Change (steatosis; triglycerides)

2) Protein (Russell Bodies - IgG accumulation in plasma cells; hyaline change)

3) Glycogen (hyperglycemic/uncontrolled diabetes)

4) Inherited lysosomal storage disease (incomplete breakdown of complex lipids b/c of lysosomal enzyme issues - Gaucher (cerebrosides), Tay-Sachs (gangliosides), Hunter diseases (mucopolysaccharides)

5) Pigments

Front 60

What are heat-shock proteins

Back 60

stress proteins made to help protect the cell from a particular stress (heat, oxidants, etc); some help to re-fold denatured proteins, some unfold proteins to allow transport into organelles; limits tissue necrosis by rescuing cells

Examples:

chaperones = folding proteins

ubiquitin - facilitates degradation of proteins denatured beyond repair

Front 61

What three things cause Cellular Aging

Back 61

1) DNA damage (ROS - oxidative stress; mutations in DNA repair enzymes)

2) Decreased replicative capacity/Cellular Senescence (telomere length/reduced telomerase activity)

3) Defective protein homeostasis (unfolded protein /ER/integrated stress response activated w/ defective protein folding - lose this with age)

Front 62

What are three possible ways to reverse cellular aging

Back 62

1) Reduce insulin/IGF signaling (stop eating)

2) Reduce activation of kinases (TOR and AKT)

3) Activation of Deacetylase

Increased metabolism leads to aging

Front 63

What is a reversible injury

Back 63

Injury where you can remove the injurious agent and the cell returns to normal

Front 64

What is an irreversible injury

Back 64

Cell does not return to normal after an injurious stimulus; either necrosis or apoptosis occurs

Front 65

Ischemia

Back 65

Loss of blood supply

Front 66

Which cell death pathway stimulates an inflammatory response: necrosis or apoptosis

Back 66

Necrosis - always pathologic and stimulates inflammatory response

(apoptosis can be pathologic or physiologic - does NOT stimulate an inflammatory response)

Front 67

What are the steps of a reversible injury

Back 67

1) ER and mitochondrial swelling, chromatin condense, form membrane blebs, form myelin figures

2) Recovery (when injurious stimulus removed)

Front 68

What are the steps of an irreversible injury that leads to necrosis

Back 68

1) ER and mitochondrial swelling, chromatin condense, form membrane blebs

2) Myelin figures form (phospholipid growths), amorphous densities in mitochondria, lysosome releases proteases

3)Plasma membrane ruptures, Nucleus contents leak (Cell death/Necrosis) - causes inflammatory response

Front 69

What are the steps of an irreversible injury that leads to apoptosis

Back 69

1) NO SWELLING; chromatin condense, form membrane blebs; cell SHRINKS

2)Cellular fragmentation - form apoptotic bodies (Apoptosis)

3) Apoptotic fragments Phagocytosed - NO inflammatory response

Front 70

What are the possible causes of Cell Injury

Back 70

Oxygen deficiency/Hypoxia

Chemical agents

Physical agents

Nutritional Imbalances

Infectious agents

Immunological reactions

Genetic factors

Aging

Front 71

What is the one cause of Cell Injury that usually results in apoptosis rather than necrosis

Back 71

Genetic factors

Front 72

What is the most important cause of hypoxia

Back 72

Ischemica (loss of blood supply) causes hypoxia (oxygen deficiency)

Front 73

What three factors about a cell injury does the cellular response depend on

Back 73

Type

Duration

Severity

Front 74

How does ischemia effect the skeletal muscle and cardiac muscle differently

Back 74

2-3 hr for skeletal muscle cell injury could be reversible; 20-30 mins for cardiac muscle cells is irreversible

Front 75

What are the four main mechanisms behind cell injury and do they result in necrosis or apoptosis

Back 75

Result in Necrosis:

1. Mitochondrial damage - ability to generate ATP and ROS

2. Disturbance to Ca++ homeostasis

3. Membrane damage (plasma, mitochondrial, lysosomal)

4. Genetic damage; DNA damage and misfolding of proteins (only one that can result in apoptosis)

Front 76

What are the two major effects of mitochondrial damage that result in cellular necrosis

Back 76

Decrease in ATP generation

Improper control of ROS

Front 77

What two injurious effects result from increase in Ca++ entry/disturbances in Ca++ homeostasis

Back 77

1) Increased mitochondrial permeability (decreased ATP production)

2) Activation of multiple cellular enzymes (membrane damage, nuclear damage, decreased ATP production)

Front 78

What results from plasma membrane damage and what results from lysosomal membrane damage

Back 78

Plasma membrane damage - loss of cellular components

Lysosomal membrane damage - enzymatic digestion of cellular components

Front 79

What is the name of the major event that causes mitochondrial damage, and in extreme cases, necrosis

Back 79

Ischemia (loss of blood supply)/Hypoxia (decreased oxygen supply) - mitochondria need nutrients/O2 to function

Front 80

What are three main examples of ROS

Back 80

superoxide anion (O2-)

hydrogen peroxide (H2O2)

hydroxyl anion (OH-)

Front 81

What is formed as a natural byproduct of normal metabolism of oxygen, but can damage the cell if not properly controlled

Back 81

Reactive Oxygen Species (ROS)

Front 82

When does a phagosome form, how, and what is its funtion

Back 82

Formed in response to bacterial infection; forms when a neutrophil engulfs bacteria; contains phagocyte (NADPH) oxidase, which generates radicals that kill the microbes in the phagosome

Front 83

What is the process of a phagosome (ROS) killing microbes known as

Back 83

Respiratory/oxidative burst

Front 84

How are the ROS from phagocytic leukocytes (phagosomes) different from the ROS in mitochondria

Back 84

Phagosome ROS function is to kill microbes

Mitochondria ROS function is to produce energy

Front 85

Under what circumstances and how do ROS cause tissue injury

Back 85

Depends on rate of production and rate of removal

Front 86

How are ROS's normally removed

Back 86

By several enzymes in the mitochondria; eventually all converted to either H2O2 or H2O and then removed

Front 87

What are three different ways that free radicals cause injury

Back 87

1. Lipid peroxidation - membrane damage

2. Protein damage - breakdown, misfolding

3. DNA strand breaks - mutations, breaks

Front 88

What is it called when you observe small, clear vacuoles in the cytoplasm and cell swelling; is this reversible or irreversible

Back 88

Hydropic Swelling/Vacuolar degeneration; Reversible

Front 89

What is it called when you see lipid vacuoles in the cytoplasm and what cells does this typically occur in; is this reversible or irreversible

Back 89

Fatty change; occurs in cells that have fat metabolism, like hepatocytes and myocardial cells; Reversible

Front 90

What are the names of the two processes that have occurred in these liver slides from a reversible injury (normal liver is leftmost slide)

Back 90

Hydropic Swelling and Fatty Change

Front 91

What are the distinguishing features of cells that have undergone reversible injury (as opposed to normal cells and cells undergoing irreversible injury)

Back 91

Normal cells - homogenous, uniform spaces, nuclei and cell size

Reversible injury cells - empty spaces due to water/fluid, membrane blebs, lots of protein, cells swollen/larger

Irreversible injury cells - plasma membrane wouldn't be intact

Front 92

What are distinguishing morphological traits of a reversible cell injury manifested at the organ level

Back 92

Increased weight (Swollen/larger) - fluid accumulation in many cells

Pallor (Lighter color) - cells compressing on capillaries so blood supply compromised

Front 93

What has occurred to this kidney

Back 93

Reversible cell injury at organ level - increased weight (larger) and change in pallor (lighter)

Front 94

Damage to what parts of the cell signal that the damage is no longer reversible, and now irreversible

Back 94

Mitrochondrial or plasma membranes

Front 95

What two major things make a cell injury irreversible

Back 95

Mitochondria damage

Plasma membrane ruptured

Front 96

What are the three types of Nuclear/DNA breakdown that indicate cell death

Back 96

Karyolysis

Karyorrhexis

Pyknosis

Front 97

What is karyolysis

Back 97

Nucleus has undergone lysis and no contents are observed; indicates cell death

Front 98

What is karyorrhexis

Back 98

Fragmentation of DNA within the nucleus; indicates cell death

Front 99

What is pyknosis

Back 99

Nucleus becomes smaller and stains very dark; indicates cell death

Front 100

In which of the following instances is the cell dead: pyknosis, karyorrhexis, karyolysis

Back 100

Cell is dead in all cases

Front 101

What nuclear status is depicted in cell #1

Back 101

Pyknosis (small cell and nucleus)

Front 102

What nuclear status is depicted in cells #2

Back 102

Karyorrhexis (DNA present but fragmented)

Front 103

What nuclear status is depicted in cell #3

Back 103

Normal; Alive

Front 104

What nuclear status is depicted in cell #4

Back 104

Karyolysis; no DNA

Front 105

Three different states of kidney tubules are depicted. Describe each one

Back 105

Left: Normal

Center: Reversible Injury (membranes still intact, swelling, lots of protein, empty spaces/fluid)

Right: Irreversible Injury (most cells in karyolysis - no nuclei; segment of kidney is dying)

Front 106

What is the type of necrosis most commonly associated with hypoxia

Back 106

Coagulative necrosis

Front 107

What are two causes of hypoxia aside from ischemia

Back 107

1. Hypoxemia - deficient oxygenation of blood

2. Hemoglobin problems

Front 108

What is a localized area of coagulative necrosis due to loss of blood supply called

Back 108

Infarct (ischemic necrosis)

Front 109

What is a defining structural feature of coagulative necrosis

Back 109

Architecture/structure remains intact (ex: can still tell kidney tubules are tubules in coagulative necrosis); can occur in any tissue except brain tissue

Front 110

What has happened to this kidney

Back 110

Coagulative necrosis; in white, triangular area, pale and firm, tissue retains basic outline

Front 111

What has happened to the right side of this slide if the left is normal kidney tubules

Back 111

Coagulative necrosis: Right shows tubules missing nuclei, but can still determine the architecture of the cells/tubule

Left shows normal part of kidney with glomeruli, tubules, and neutrophils

Front 112

What has happened to the white area of this heart

Back 112

Coagulative necrosis - due to occlusion of the coronary artery and resulting ischemia; white area is dead tissue

Front 113

What type of necrosis involves the complete digestion of tissue; autolysis and heterolysis

Back 113

Liquefactive Necrosis; occurs following microbial infection and also in brain tissue/infarct

Front 114

In which type of necrosis is the tissue no longer recognizable: Coagulative or Liquefactive

Back 114

Liquefactive - tissue converted into a semi-liquid mass

Front 115

Which type of necrosis is often associated with microbial infection and a strong inflammatory stimulus

Back 115

Liquefactive

Front 116

What is the difference between neutrophil function in Coagulative vs liquefactive necrosis

Back 116

Coagulative - neutrophils remove dead cells and then repair tissue

Liquefactive - neutrophils release proteolytic enzymes and ROS and liquefy the tissue, you form an abscess

Front 117

In what type of necrosis do you form an abscess

Back 117

Liquefactive

Front 118

What type of necrosis is pictured here

Back 118

Liquefactive - VERY strong inflammatory response

Front 119

What type of necrosis is pictured here

Back 119

Liquefactive - VERY strong inflammatory response

Front 120

What has occurred to this lung tissue

Back 120

Liquefactive necrosis - has many abscesses

Front 121

What two types of necrosis does gangrene include

Back 121

Coagulative - on bottom (dry)

Liquefactive - on top (wet)

Front 122

What part of gangrenous necrosis is associated with a foul smell

Back 122

Wet gangrene - liquefactive necrosis with bacteria

Front 123

What condition is depicted here and what disorder does it often result from

Back 123

Gangrene (dry)

Diabetes

Front 124

What characteristics describe caseous necrosis

Back 124

Immune injury; seen in granulomatous diseases (Tb and some fungal infections); cheese-like, white appearance; has a necrotic center enclosed within a granuloma; tissue architecture obliterated

Front 125

What condition is shown here resulting from tuberculosis

Back 125

Caseous necrosis

Front 126

What type of necrosis is shown here and in what tissue type does it occur

Back 126

Caseous necrosis; in lung tissue; pictured are lung alveoli; large pink areas are granulomas with necrotic center

Front 127

Why is fibrinoid necrosis not actually a type of necrosis

Back 127

cell death doesn't occur; walls of arteries are damaged, allows plasma proteins to leak out; associated with immune injury and malignant HTN

Front 128

What type of necrosis only occurs in fat tissue and what is the mechanism behind it

Back 128

Fat Necrosis

Results from injury that releases lipases that attack the plasma membranes of fat cells, hydrolyze triglycerides yielding free fatty acids, become calcium soaps

usually associated w/ pancreatitis

Front 129

What are the two types of pathologic calcification and where do they occur

Back 129

Dystrophic

Metastatic

Occur in necrotic tissue

Front 130

Where does dystrophic calcification occur and how does it occur

Back 130

locally, at areas of necrosis

in presence of normal calcium-phosphorous metabolism; interferes w/ normal organ fxn

formation of calcium phosphate mineral (similar to bone)

Front 131

Where does metastatic calcification occur and how does it occur

Back 131

in normal tissue, when there's hypercalcemia (e.g. - in hyperparathyroidism)

occurs globally/not at one site

formation of calcium phosphate mineral (similar to bone)

Front 132

What materials are released into the surroundings/ECM in apoptosis

Back 132

NOTHING; everything remains contained within apoptotic bodies then macrophages come to phagocytose the bodies

Front 133

Can necrosis and apoptosis be: physiologic, pathologic or either

Back 133

Necrosis - only pathologic

Apoptosis - can be physiologic or pathologic

Front 134

What are the physiologic causes of apoptosis

Back 134

Embryogenesis

Involution of hormone-dependent tissues

Elimination of cells that served their purpose

Removal of potentially self-reactive lymphocytes

Killing of virus infected and neoplsatic cells by cytotoxic T cells

Front 135

What are the pathologic causes of apoptosis

Back 135

Cells damaged beyond repair (DNA damage and Misfolded proteins)

Front 136

What is involved in the extrinsic pathway of Apoptosis

Back 136

death-receptor initiated; cell surface receptors TNF and Fas ligand activated, activated adapter proteins, activate caspase cascade (eventually results in formation of apoptotic bodies)

Front 137

What is involved in the intrinsic pathway of Apoptosis

Back 137

mitochondrial pathway; activated by cell injury, activates Bcl-2 family, activates Bax and Bak (regulated by Bcl-2 and Bcl-x), interact w/ mitochondria to increase permeability, releases cytochrome C and pro-apoptotic proteins, both activate parts of caspase cascade (eventually results in formation of apoptotic bodies)

Front 138

What is the result of the caspase cascade

Back 138

Initiator caspases activated, then executioner caspases activated, then endonucleases activated which results in DNA fragmentation AND cytoskeleton breakdown (eventually results in formation of apoptotic bodies)

Front 139

What are the cardinal signs of inflammation

Back 139

Redness

Swelling

Pain

Heat

Loss of Function

Front 140

What are the two responses involved in inflammation, which comes first

Back 140

Vascular then Cellular

Front 141

What is the most common and most important cause of inflammation

Back 141

Infection (bacterial)

Front 142

What must tissue be in order to undergo inflammation

Back 142

Living

Front 143

What are the two most important reasons for inflammation

Back 143

Control Infection (destroy and eliminate cause/remove dead tissue)

Initiate wound healing

Front 144

What is the purpose of inflammation when caused by bacteria versus necrotic tissue

Back 144

Bacteria - destroy and eliminate

Necrotic tissue - remove dead tissue

Front 145

What are two reasons why inflammation might backfire and hurt the host, give clinical examples

Back 145

Reaction too powerful (bacterial meningitis, staph pneumonia)

Inappropriate response (hay fever, asthma, anaphylaxis, arthritis, autoimmune diseases)

Front 146

What are the steps that occur during the vascular phase of inflammation

Back 146

Injury/Stimulus

Transient, reflex vasoconstriction

Vasodilation (due to mast cells/histamines)

Increased blood flow (through arterioles)

THEN

Increased blood volume (hyperemia) - leads to redness and heat

AND

Increased vascular permeability (to protein) Edema/Exudate in extravas spaces - leads to swelling

Front 147

What cells are most important during the vascular response of inflammation

Back 147

Mast cells

Front 148

What cells predominate the cellular phase of inflammation

Back 148

Neutrophils

Front 149

What role do mast cells play in inflammation

Back 149

Activated almost immediately by anything that causes inflammation; have granules, histamines, and leukotrienes and release contents VERY rapidly - cause vasodilation and increase vascular permeability

Front 150

Why are women more likely to develop gingivitis when pregnant than when not

Back 150

Increased hormonal effect; hormones cause an increase in bacteria in gingival crevices

Front 151

What is the difference in blood flow in microvascular beds in normal versus inflamed tissue

Back 151

Normal - blood flow is intermittent; arteriolar/pre-capillary sphincters normally opening and closing in response to mediators

Inflamed - sphincters remain open, blood volume increases (active hyperemia)

Front 152

What is it called when more blood is brought to an affected area due to dilation of arterioles

Back 152

Hyperemia

Front 153

What does Starling's Law explain and what is the purpose

Back 153

Exchange of substances between blood and tissues:

Hydrostatic Pressure = Osmotic Pressure + Lymphatic Drainage (in normal tissue)

Keeps water from accumulating in tissues

Front 154

What are normal capillaries freely permeable to

Back 154

water, gases and electrolytes (only semi-permeable to proteins; about 90% retained)

Front 155

What do capillaries become permeable to during inflammation that they are not normally freely permeable to

Back 155

Plasma proteins

Front 156

What morphological characteristics of inflammation result from hyperemia

Back 156

Redness and Heat

Front 157

What is edema primarily caused by

Back 157

the Loss of Barrier Functions of capillaries and venules

Front 158

What is exudate

Back 158

protein-rich edema fluid; occurs when plasma proteins accumulate in tissues due to increased permeability of venules and capillaries to protein (result of inflammation)

Front 159

What components of Starling's law change during inflammation

Back 159

Hydrostatic pressure - marked increase; forces more fluid out from capillaries into tissues

Osmotic pressure - decreases due to leakage of plasma proteins into tissues (draw more fluid out of vessels and favor fluid retention in tissues)

Lymphatics try to compensate for changes but can't

Result is protein-rich edema fluid/exudate in tissue

Front 160

What are the three different types of exudate

Back 160

Serous

Fibrinous

Purulent

Front 161

What is the content of serous exudate

Back 161

High in fluid

Few proteins

No WBCs

Front 162

What is the content of fibrinous exudate

Back 162

High protein number

Some fluid

Few or no WBCs

Front 163

What is the content of purulent exudate

Back 163

High WBC number

Some proteins

Some fluid

Front 164

What are the physical characteristics of serous exudate/inflammation

Back 164

yellow, straw-like color; ex: skin blister resulting from a burn

Front 165

What are the physical characteristics of fibrinous exudate/inflammation

Back 165

fibrin is dominant feature; whitish material, like wet paper; ex: bread and butter pericarditis

Front 166

What are the physical characteristics of purulent inflammation

Back 166

Yellow-green color; PUS; usually associated w/ bacterial infection within a thin membrane; filled with neutrophils; mostly liquefactive necrotic tissue; ex: bacterial meningitis - in meninges of brain

Front 167

Which type of exudate is associated with death

Back 167

Purulent; usually occurs in brain cavity (bacterial meninges) - too much pressure causes death

Front 168

What condition does this heart depict

Back 168

Fibrinous exudate/inflammation (bread and butter pericarditis)

Front 169

What condition does this brain depict

Back 169

Purulent exudate/inflammation (due to bacterial meningitis)

Front 170

What condition does this ruptured colon depict

Back 170

Purulent exudate/peritonitis

Front 171

What is an abscess

Back 171

Localized collection of pus (purulent exudate is NOT localized) - caused by pyogenic organisms or infection from necrotic tissue (liquefactive necrosis)

Front 172

What is transudate

Back 172

Edema associated with non-inflammatory conditions; has NO protein (no vascular permeability)

Front 173

What are some of the mechanisms that result in transudate

Back 173

Abnormal Fluid Dynamics:

Increased hydrostatic pressure (not compensated for by osmotic pressure or lymphatics)

Problems with lymphatic drainage

Problems with osmotic pressure

Front 174

What are five clinical conditions that have production of transudate

Back 174

1) Congestive Heart Failure

2) Kwashiorkor/Malnutrition

3) Liver Cirrhosis

4) Breast Cancer (scarring OR obstruction of lymph nodes)

5) Filariasis/Elephantiasis

Front 175

Why is transudate produced in congestive heart failure

Back 175

Increased hydrostatic pressure (b/c of left or right sided heart failure)

Front 176

Where does transudate manifest in left and right sided heart failure respectively

Back 176

Left: transudate in lungs

Right: transudate in lower limbs

Front 177

Why is transudate produced in Kwashiorkor and Liver Cirrhosis and what are the clinical manifestations of transudate in these conditions

Back 177

Malnourishment and liver damage result in low level of plasma proteins - leads to reduced Osmotic pressure

Ascites - fluid accumulation in peritoneal cavity (can also include exudate accum from infection)

Front 178

Why is transudate produced in lymphatic obstruction (either from breast cancer tx and damage of lymph nodes or obstruction of lymph nodes by cancer)

Back 178

Lymphatic drainage cannot function effectively

Front 179

Why is transudate produced in Filariasis/Elephantiasis

Back 179

Lymphatic drainage cannot function effectively

Filariasis = worm infection that invades lymph nodes

results in fluid drainage to lower extremities (Elephantiasis)

Front 180

What is the difference between active and passive hyperemia

Back 180

Active - blood accum due to dilation of arterioles/mast cells and mediators

Passive - blood accum due to increased blood pressure and gradual accum of fluid

Front 181

What important mediator of vascular permeability is preformed in secretory granules

Back 181

Histamine

Front 182

What are the two most important cell types that produce histamine

Back 182

1) Mast cells

2) Basophils

Front 183

What are the four primary cell-derived mediators of vascular permeability

Back 183

Histamine

Prostaglandins

Leukotrienes

Cytokines

Front 184

What are the primary plasma protein-derived mediators of vascular permeability

Back 184

Complement (C3a, C5a, C3b, C5b)

Factor XII (Kinin and Plasmin system)

Front 185

What cell(s) produce prostaglandins/leukotrienes

Back 185

All leukocytes

Mast cells

Front 186

What cell(s) produce cytokines

Back 186

Macrophages, lymphocytes, EC, mast cells

Front 187

From what organ are plasma proteins typically derived

Back 187

Liver

Front 188

In what order are the five major mediators of vascular permeability released

Back 188

1) Histamines

2) Prostaglandins/Leukotrienes

3) Plasma

4) Cytokines

5) ROS

Front 189

Which mediators of vascular permeability take the longest to to be synthesized of prostaglandins/leukotrienes, cytokines and histamines

Back 189

Cytokines

Front 190

During what phase of the inflammation process does histamine play the largest role

Back 190

earliest during permeability change; during acute inflammation

Front 191

Where are mast cells typically located in the skin

Back 191

dermal layer; surrounding blood vessels and close to nerve cells

Front 192

What stimuli trigger the release of histamine from mast cell granules

Back 192

Physical injury/trauma

Neuropeptides/Substance P

Complement fragments

Front 193

What are anti-microbial peptides (AMPs)

Back 193

peptides released by epithelial cells to kill microbes; provide first layer of defense during infection; also activate mast cells to release mediators

Front 194

What two substances play a role in immediate defense after initial infection and help to activate mast cells/histamine release

Back 194

Anti-microbial peptides

Complement (C3a and C5a)

Front 195

In what scenario is histamine release unfavorable

Back 195

In response to an allergen/synthesis of IgE

Front 196

What type of cell is this

Back 196

Mast cell - prominent nucleus; contains granules; tissue resident

Front 197

What is the mechanism of a mast cell

Back 197

First - rapid, transient release of histamine

released contents, other released mediators, cause increased dilation of arterioles, active hyperemia, increased vascular permeability to proteins, formation of exudate

Front 198

How is arachidonic acid formed

Back 198

formed when phospholipases activated and hydrolyze membrane phospholipids

Front 199

What are the two pathways by which arachidonic acid is metabolized

Back 199

Cyclooxygenase - produce prostaglandins and thromboxanes

Lipoxygenase - produce leukotrienes

Front 200

What are the names of the two lipid-derived mediators of vascular permeability that follow release of histamine, and what additional functions do they have

Back 200

Prostaglandins - Vasodilation (same effects as histamine, just later); inhibits platelet aggregation

Leukotrienes - Neutrophil chemotaxis; bronchospasm

Front 201

What are the potent inhibitors of prostaglandins and leukotrienes

Back 201

Corticosteroids

Front 202

What is the function of aspirin and NSAIDs

Back 202

anti-inflammatory drugs; inhibit all upstream cyclooxygenase activity - no inflammation

Front 203

What is the purpose of drugs that block cysteinyl leukotrienes (LTC4)

Back 203

Manage asthma - prevent bronchospasms

Front 204

What are the three major plasma protease systems

Back 204

1) Kinin

2) Fibrinolytic/Plasmin

3) Complement

Front 205

What do plasma protease systems depend on

Back 205

Formation of biologically active peptide fragments in body fluids by the action of proteolytic enzymes on their substrates

Normally proteases are inactive; upon activation they produce peptide fragments that mediate permeability and other inflammatory changes

Front 206

What is the name of the proteases (and their inactive form) that act to form bradykinin

Back 206

Kallikreins (from inactive Pre-K)

Front 207

What is the name of the proteases (and their inactive form) that act to form peptides

Back 207

Plasmins (from inactive plasminogen)

Front 208

What does Factor XII do and where is it produced

Back 208

Activates the proteases (forming kallikrein and plasmin) that eventually form bradykinin and peptides

Liver

Front 209

What does bradykinin do in the inflammation process

Back 209

Causes pain and increased vascular permeability

Front 210

What do peptides do in the inflammation process

Back 210

Increase vascular permeability, mediate WBC chemotaxis, activate the complement system

Front 211

What are the two major cytokines involved in endothelial activation during inflammation

Back 211

Tumor necrosis factor-alpha (TNF-alpha)

Interleukin-1 (IL-1)

Front 212

What is the principle function of cytokines in inflammation

Back 212

Endothelial activation - cause upregulation of cell surface adhesion molecules, promotes adhesion of neutrophils and monocytes

Front 213

What cells are TNF-alpha and IL-1 mainly produced by

Back 213

Mast cells and macrophages

Front 214

What is an inflammasome

Back 214

a molecular complex involved in the activation of inflammatory caspases resulting in processing of immature pro-IL-1 into mature IL-1

Front 215

Describe the two pathways that result in the production of cytokines

Back 215

1) Bacterial cell wall lipids activate Toll-like receptor (on plasma membrane, endosomal membrane or in cytosol), (e.g. produces TNF)

2) Inflammasome pathway activated by extracellular pathogenic ATP - inflammatory caspases activated by K+ efflux or production of ROS (e.g. converts immature pro-IL-1 to mature IL-1)

Front 216

What are the primary functions of Vascular Endothelial Growth Factor (VEGF)

Back 216

Increases vascular permeability: transcytosis of proteins across the endothelium AND stimulates formation of new microvessels (inherently leaky)

Front 217

In what blood vessels do most of the vascular permeability changes occur

Back 217

Venules (except when cause is direct injury - could be any blood vessel)

Front 218

What is the most important cause/mechanism of vascular permeability

Back 218

Gaps/Endothelial Contraction; involves the rapid, transient response of histamines and leukotrienes; endothelial cells move away from one another, creating gaps in the venules

Front 219

What growth factor increases transcytosis of proteins across the endothelium AND stimulates formation of new microvessels

Back 219

Vascular Endothelial Growth Factor (VEGF)

Front 220

What is a clinical example of a delayed prolonged mechanism behind vascular permeability

Back 220

mild sunburn (sun damage to endothelial cells releases cytokines which take a long time to appear)

thermal injury, UV radiation

Front 221

What mechanism of vascular permeability causes an immediate transient response

Back 221

Gaps/Endothelial Contraction; immediate release of histamines and leukotrienes

Short-lived, after mild injury; reversible

Front 222

What mechanisms of vascular permeability cause an immediate prolonged response

Back 222

Endothelial contraction, Endothelial retraction and Leukocyte-dependent injury

response to bacterial infection; biphasic because you have histamine release, cytokine release, and neutrophil recruitment

moderate injury; can last for hours or days

Front 223

What mechanism of vascular permeability causes and immediate sustained response

Back 223

Direct injury; injury to the blood vessel causes leakage that will be sustained until the blood vessel is repaired

severe injury; can last for hours or days

Front 224

What mediator system only produces vascular permeability

Back 224

None; all mediator systems have multiple inflammatory effects

Front 225

What are the four major systemic protective effects of inflammation

Back 225

1) Fever (cytokines work on brain)

2) Increased plasma levels of acute-phase proteins (cytokines work on liver)

3) Leukocytosis (cytokines work on bone marrow)

4) Increased HR and BP

Front 226

What mediator is primarily responsible for the systemic effects of inflammation

Back 226

Cytokines

Front 227

Does most antimicrobial defense occur in the bloodstream or in the tissues

Back 227

Tissues - most infections originate in the tissues outside the bloodstream - inflammatory response goes to tissue and attempts to prevent microbial spreading beyond initial site of infection

Front 228

What are the major systemic pathologic effects of inflammation

Back 228

Low cardiac output

Low peripheral resistance

Blood vessel injury

Thrombosis

ARDS

SEPSIS

Front 229

What is the purpose of producing fever, more acute-phase proteins in plasma and more neutrophils (leukocytosis) during inflammation

Back 229

All systemic protective effects of inflammation

Fever - tells body something is wrong

Acute-phase proteins - help fight infection

Neutrophils - help fight infection

Front 230

What is the mechanism behind a fever

Back 230

LPS released from cell wall - causes release of TNF-alpha and IL-1, metabolize AA, produce Prostaglandin E2 - releases NTs in hypothalamus - resets body's thermostat to a higher temp

Front 231

What happens during rouleaux and what is the purpose

Back 231

(+) Fibrinogen binds to (-) RBCs, RBCs clump together

this increases Erythrocyte Sedimentation Rate (ESR)

Front 232

What is the normal number of WBCs in the blood and what number does this increase to when fighting infection

Back 232

4,500-11,000 to 15,000-20,000

Front 233

What are some of the systemic effects of increased HR and BP during inflammation

Back 233

Decreased sweating

Shivering (reduced blood supply to skin)

Malaise

Anorexia

Front 234

What are examples of acute-phase proteins

Back 234

C-reactive Proteins and Serum Amyloid (microbe elimination)

Fibrinogen (rouleaux)

All work to fight microbial infection; number increased 100-fold during infection

Front 235

In what stage of the inflammatory response are neutrophils most important

Back 235

Acute inflammation

Front 236

What are the most predominant cell type found in the blood

Back 236

Neutrophils

Front 237

What types of cells stain pink and blue respectively

Back 237

Eosinophils (pink), Basophils (blue)

Front 238

What three cell types are considered granulocytes

Back 238

Neutrophils, basophils, eosinophils

All contain granules; but have different nuclei and granule characteristics

Front 239

What color do neutrophils stain

Back 239

Don't stain/neutral

Front 240

What characterizes an eosinophil and what percent of WBCs do they constitute

Back 240

stain pink; lobulated nucleus, horseshoe shape; granulocyte

1-4% of WBCs

Front 241

Besides fighting infection/inflammatory what other roles do eosinophils play in the body

Back 241

fight infection against worms and protozoa; impt role in allergic diseases and asthma

Front 242

What characterizes a neutrophil and what percent of WBCs do they constitute

Back 242

Polymorphonuclear Leukocyte - multilobular nuclei; granulocyte

40-60% of WBCs

Front 243

What characterizes a basophil and what percent of WBCs do they constitute

Back 243

stain blue with H&E stains; share many characteristics of mast cells (release histamine when activated) - associated wtih allergic rxn; granulocyte

0.5-1% of WBCs

Front 244

What two cell types are considered mononuclear/round cells

Back 244

Monocytes

Lymphocytes

Front 245

What characterizes a monocyte and what percent of WBCs do they constitute

Back 245

prominent nucleus, kidney-bean shaped; largest cell; eventually leave bloodstream and become macrophages; impt in induction of immune response and wound healing

2-8% of WBCs

Front 246

What type of cell is capable of differentiating once it leaves the bloodstream and enters the tissue

Back 246

Monocyte (to macrophage)

Front 247

What types of cells besides macrophages do monocytes serve as precursors to

Back 247

Kupffer cells in liver

Osteoclasts in bone

Front 248

What characterizes a lymphocyte and what percent of WBCs do they constitute

Back 248

Subtypes: T & B cells, plasma cells, NK cells, T helper cells, T suppressor cells; regulate immune response and guard against mycobacteria, viruses; primarily involved in chronic inflammation

20-40% of WBCs

Front 249

What "cells" are not true cells/leukocytes

Back 249

Platelets; involved in clot formation and wound healing

Front 250

What type of cell is pictured here

Back 250

Lymphocyte - round nucleus

Front 251

What type of cell is pictured here

Back 251

Neutrophil - multilobular nucleus

Front 252

What type of cell is pictured here

Back 252

Monocyte - kidney bean shaped nucleus

Front 253

What type of cell is pictured here

Back 253

Basophil - blue stained granules

Front 254

What type of cell is pictured here

Back 254

Eosinophil - pink stained granules

Front 255

Which of the cardinal signs of inflammation does vasodilation cause

Back 255

Redness

Front 256

Which of the cardinal signs of inflammation does increased blood flow (hyperemia) cause

Back 256

Heat

Front 257

Which of the cardinal signs of inflammation does fluid exudation cause

Back 257

Swelling

Front 258

What is the purpose of: red and white blood cells transported as a lubricated column and positioned toward the center of the stream

Back 258

Laminar Flow

Front 259

Why does bloodflow slow down in the microcirculatory bed during inflammation

Back 259

RBC concentration in the vessels increases b/c of increased vascular permeability and mvmt of proteins and fluid to tissue - blood becomes more viscous

Front 260

What is the presence of numerous dilated small blood vessels packed with RBCs and slow flowing blood called

Back 260

Stasis

Front 261

What is it called when RBCs stick together to form clumps and what does this lead to

Back 261

Rouleaux, leads to increased Erythrocyte sedimentation rate (ESR)

Front 262

What is the space between columns of blood cells and platelets called and what does it do

Back 262

Plasma - acts as a lubricant to assist laminar flow

Front 263

What acute phase protein clumps together with RBCs during rouleaux

Back 263

Fibrinogen

Front 264

What action by RBCs assists with the margination of WBCs

Back 264

Rouleaux - clumping of RBCs pushes WBCs toward the endothelial wall

Front 265

When vascular permeability is coming to an end, what can get through still and what can't

Back 265

Cells/leukocytes can get through, proteins can't anymore

Front 266

What is diapedesis and what cells undergo this process

Back 266

Transmigration - crossing from blood vessel to tissue; Leukocytes do this

Front 267

What are the three major steps of the leukocyte-endothelial cell adhesion cascade

Back 267

Rolling

Adhesion

Transmigration

Front 268

What are the three types of selectin, where do they occur, and what is the purpose of selectin

Back 268

E-selectin: endothelium

P-selectin: platelets and endothelium

L-selectin: lymphocytes

Adhesion molecules

Front 269

Why is the initial adhesion process of leukocytes to the endothelial surface described as rolling

Back 269

Leukocytes bind to selectins via carbohydrate ligands (sialyl-lewis X) through low-affinity interactions with a fast off-rate; adhesion easily disrupted by blood flow; leukocytes detach and bind again - "roll" along endothelial surface

Front 270

What type of selectin is first stimulated to go to the endothelial cell surface by mediators like histamine, thrombin and platelet activating factor (PAF) in order to recruit leukocytes

Back 270

P-selectin - redistribute from W-P bodies (intracellular store in granlues) to surface of endothelial cell

Front 271

What type of selectin is expressed within 1-2 hours after injury on endothelial cells by macrophage/mast cell release of TNF-alpha and IL-1 (cytokines)

Back 271

E-selectin

Front 272

What are the two endothelial adhesion molecules of the immunoglobulin family and what is their function

Back 272

ICAM-1 and VCAM-1 (intracellular/vascular cell adhesion molecules) - found on endothelial cells

serve as ligands for integrins found on leukocytes

Front 273

What is Sialyl-Lewis X and where is it found

Back 273

Glycoprotein found on leukocytes; selectins bind to this - leads to rolling/slight adhesion

Front 274

What integrins bind to ICAM-1

Back 274

Beta-2 integrins; LFA-1 (CD11a and CD18) and Mac-1 (CD11b and CD18)

Front 275

What integrins bind to ICAM-2 and where is this integrin expressed

Back 275

Beta-1 integrins; VLA-4

mostly in granulocytes, but also in monocytes and macrophages

Front 276

What are integrins

Back 276

glycoproteins made of alpha and beta chains that are expressed on many cell types and bind to ligands (adhesion molecules) on endothelial cells

Front 277

What are Sialyl-Lewis X and integrins attached to vs what are adhesion molecules (selectins and ICAM/VCAM) attached to

Back 277

Sialyl-Lewis X and integrins presented on leukocytes

Adhesion molecules presented on endothelial cells

Front 278

Integrins are normally expressed on leukocytes in a low-affinity state, what induces their expression in a high-affinity state

Back 278

Chemokines - produced at site of injury that enter the blood vessel, bind to the endothelial cells, and are displayed at high concentrations on endothelial cell surface - induce change to high affinity state (receptor shape changes)

Front 279

What do integrins presented on leukocytes have affinity for

Back 279

ICAM-1 and VCAM-1 (on endothelial cells)

Front 280

What is the difference between affinity and avidity

Back 280

Affinity is a single protein-protein interaction

Avidity is interaction between multiple ligands and receptors at the same time (tighter overall interaction)

Front 281

What do chemokines do to induce a higher affinity state of integrins for adhesion molecules

Back 281

Change conformation/shape of integrin receptor (increased avidity)

Front 282

What does the increased avidity between integrins and adhesion molecules do to the leukocytes attached to the endothelial cells

Back 282

Stop rolling, create firm adhesion, leukocytes flatten

Front 283

What mediators act on adherent leukocytes to stimulate the cells to migrate through interendothelial spaces toward site of injury/infection

Back 283

Chemokines

Front 284

What is the name of homophilic adhesion molecules and where are they located

Back 284

PECAM-1 (platelet endothelial cell adhesion molecules)/CD31

Intercellular junction of endothelium AND Leukocyte surfaces

Front 285

Must there be vascular permeability in order for leukocytes to transmigrate

Back 285

No. But they do typically correlate

Front 286

What happens to leukocytes after PECAM-1 molecules bind to each other

Back 286

Migrate across endothelium

Front 287

How do leukocytes most likely pierce the basement membrane of endothelium

Back 287

secrete collagenases

Front 288

What is the net result of leukocyte transmigration

Back 288

leukocytes accumulate where they're needed

Front 289

What do leukocytes do temporarily after they transmigrate/leave circulation

Back 289

Surround/Cuff the vessel

Front 290

All the leukocytes express integrins and endothelial cells have ligands for them, which cells appear first and which appear later

Back 290

Depends on age of inflammatory response and nature of etiology

In acute inflammation: neutrophils appear first (6-24 hrs)

As injury ages: monocytes appear (24-48 hrs)

Infection by pseudomonas organism: neutrophils may continue to be recruited for several days

Viral infection: lymphocytes

Allergy/asthma: eosinophils

Front 291

What stage of an inflammatory response is this/what stage of transmigration are the leukocytes in and what type of WBCs are they

Back 291

Cuffing the BV - after transmigration

Neutrophils

Front 292

The large pink cells are myocytes that have undergone karyolysis; what other cells are present here and why/what stage of inflammatory response is this

Back 292

Mostly monocytes (prominent, round nuclei) - later stage of inflammatory response because monocytes have replaced neutrophils and come to clean up the mess

Front 293

What types of cells are (1) and what is happening to them

What types of cells are (2-4) and what is happening to each

What type of cell is (5) and what has happened to it

Back 293

(1) - Red blood cells; in Rouleaux

(2-4): Neutrophils

(2): marginating/rolling

(3): firm adhesion

(4): just transmigrated

(5): myocyte - karyolysis

Front 294

Which disease is a rare autosomal recessive disease that causes reduced expression of CD18 on the surface of leukocytes; and what is the pathogenesis

Back 294

LAD-I; decrease in firm adhesion to the endothelium

Front 295

What disease manifests as: delayed separation of the umbilical cord, recurrent bacterial infection, gingivitis/periodontitis, absence of pus formation and impaired wound healing, leukocytosis/neutrophilia

Back 295

LAD-1 (severity depends on extend of CD18 deficiency)

Front 296

What percent CD18 deficiency constitutes severe deficiency

Back 296

98% deficiency in CD18

Front 297

What percent CD18 deficiency constitutes mild/moderate deficiency

Back 297

70-98% deficiency in CD18

Front 298

How are neutrophils in tissue usually dealt with after they have served their purpose

Back 298

Efferocytosis of apoptotic neutrophils in tissue by macrophages (after 1-2 hours)

Front 299

What is the pathway of mediators that acts as a thermostat and is inhibited when neutrophils are undergoing efferocytosis

Back 299

IL-23 to IL-17 to G-CSF (which results in production of neutrophils in bone marrow and release of mature neutrophils to circulation)

Front 300

With LAD-1 what happens to the cytokine pathway that mediates the production and release of neutrophils

Back 300

In LAD-1 there are no/few neutrophils in the tissues because they are unable to transmigrate from the blood b/c deficient CD-18; therefore no neutrophils are undergoing efferocytosis, and the cytokine mediator pathway cannot be inhibited, so there's an increased production of neutrophils from the bone marrow that are circulating in the blood (Neutrophilia)

Front 301

What is the result of the upregulation of IL-17 in the gingival areas (due to LAD-I)

Back 301

Bone resorption/Periodontal bone loss; TH-17 cells secrete cytokine IL-17 which produces increased amounts of neutrophil in the blood but they can't function properly

Front 302

This person has LAD-I, what is the clinical diagnosis of their tissue

Back 302

Dysplastic Eschar - dead tissue sloughing off; develops b/c there's a wound and neutrophils can't get there to remove dead tissue

Front 303

What is the clinical diagnosis of this situation - elevated neutrophil count in the blood but neutrophils unable to leave blood vessel

Back 303

LAD-I (gingivitis/periodontitis)

Front 304

What are proposed treatments for LAD-I and how would they work

Back 304

Antibiotics - antibody against IL-17 to protect from bone loss

Bone marrow/hematopoetic cell transplantation; replace the dead bone marrow tissue

Front 305

What is the disease that is a rare autosomal disease in which the expression of Sialyl-Lewis X is completely deficient, meaning they fail to interact with selectins

Back 305

LAD-II

Front 306

What results from LAD-II deficiency of expression of Sialyl-LewisX mechanistically

Back 306

Defective rolling; E and P selectins don't adhere, but neutrophils still able to adhere and transmigrate via integrins/ICAM under conditions of reduced sheer force; allows for some defense against bacterial infections

Front 307

What are the clinical manifestations of LAD-II

Back 307

Less severe than LAD-I; no delay in umbilical cord separation; bacterial infection NOT life-threatening

Add'l: children have delayed motor development, mentally retarded, short in stature

Front 308

What is disease is a rare genetic disease in which there is a genetic loss in activation of beta-integrin by chemokines (mutation in kindlin) and in which patients have a defect in chemokines

Back 308

LAD-III

Front 309

What are the clinical manifestations of LAD-III

Back 309

Similar to LAD-I b/c defect in neutrophil adherence mechanism; (add'l defect in platelet aggregation can cause cerebral hemorrhage at birth and bleeding disorders)

Front 310

In diagnosis, how can you distinguish LAD-I from LAD-III

Back 310

In LAD-III: integrin expression is intact but activation impaired; genetic analysis for mutation in kindlin

Front 311

What is granulopoiesis

Back 311

when neutrophils produced in the bone marrow are released into circulation

Front 312

What are all of the steps neutrophils must accomplish in order to kill bacteria and prevent infection

Back 312

Adherence

Transmigrate

Chemotaxis

Phagocytosis

Front 313

In what organ are neutrophils produced

Back 313

bone marrow

Front 314

What percent of neutrophils are reserved in bone marrow; where are the remaining neutrophils located

Back 314

93% in bone marrow

3% circulating in blood

4% marginating on surface of endothelial cells

Front 315

About how many neutrophils does a normal individual produce in a day and how many does an infected person produce

Back 315

100 billion - normal

Over 1 trillion - serious infection (mobilized reserve of mature neutrophils)

Front 316

What two factors stimulate bone marrow to produce neutrophils

Back 316

G-CSF and GM- CSF (glycoproteins)

Front 317

What are the cells stages involved to produce a mature neutrophil

Back 317

Stem Cell

Myeloblast

Promyelocyte

Myelocyte

Metamyelocyte

Band PMN

Segmented PMN

Front 318

What is the name of this cell in the neutrophilic series

Back 318

Myeloblast - originates from stem cells; relatively undifferentiated with a high nuclear:cytoplasmic ratio; prominent nucleoli (immature nucleus)

Front 319

What is the name of this cell in the neutrophilic series

Back 319

Promyelocyte - the biggest cell in the neutrophilic series; characterized by the production and accumulation of primary (azurophil) granules plus MPO; nucleus is still immature (can see nucleoli)

Front 320

What is the name of this cell in the neutrophilic series

Back 320

Myelocyte - appearance of MPO-negative specific secondary granules, smaller and finer than primary granules

Front 321

What is the name of this cell in the neutrophilic series

Back 321

Metamyelocyte - looks like a mature neutrophil except for its nucleus (larger and kidney bean shaped - looks like a monocyte); cell surface receptors begin to be expressed

Front 322

What is the name of this cell in the neutrophilic series

Back 322

Band PMN - smaller than the metamyelocyte and nucleus appears U-shaped; begin synthesis of gelatinase

Front 323

What is the name of this cell in the neutrophilic series

Back 323

Segmented PMN - a mature neutrophil

Front 324

What is the name of this cell in the neutrophilic series

Back 324

Stem cell - completely undifferentiated

Front 325

At what stage in the neutrophilic series does granule formation begin

Back 325

Promyelocyte (continues to segmented cell stage)

Front 326

During what stages of the neutrophilic series can the cells proliferate and at what stage do the cells become end cells

Back 326

Proliferation possible from stem cells to myelocyte stage; Ends cells at Metamyelocyte stage

Front 327

About how many days does it take for neutrophils to be produced and mature in bone marrow

Back 327

12 days

Front 328

What is the neutrophil lifespan in the blood

Back 328

5-10 hours; then apoptose and removed by monocyte/macrophage system

Front 329

What is the neutrophil lifespan in tissue

Back 329

1-2 hours

Front 330

What causes a "shift to the left"

Back 330

Depletion of reserve pool of mature neutrophils; less mature neutrophils (band cells) enter the blood

Bad - immature cells not as efficient/effective at attacking microbes as mature cells

Front 331

What is the name of the cytokines that form a neutrophil production regulatory system

Back 331

Colony-stimulating factors (CSFs); e.g. G-CSF

Front 332

What neutrophil blood count means a person is susceptible to infection

Back 332

less than 1500 mm^3; host defense mechanism compromised, won't be able to fight infection if encountered

Front 333

What neutrophil blood count means a person has an infection

Back 333

less than 500 mm^3; have infection, can't fight it

Front 334

What are the possible causes of neutropenia

Back 334

Neutropenia is decrease in blood neutrophil count

Bone Marrow Pathology (congenital, malignancies, radiation, drugs - anti-cancer antibiotics, infection - hep a and b, measles)

Ineffective Production of Folic Acid or Vitamin B12

Enhanced Destruction (Septicemia, Hypersplenism - neutrophils removed and stored in spleen/overactive spleen)

Front 335

What are the two most common clinical signs of infection in Neutropenia

Back 335

Oral Ulcerations (Stomatitis)

Severe Gingivitis/Periodontitis

Front 336

During neutropenia, is there a way for oral mucosa breakdown to be reversed

Back 336

Yes, when neutrophil count begins to rise again the oral status usually begins to improve

Front 337

What part of the oral mucosa is most effected by decrease in neutrophil number

Back 337

Gingiva - gingival sulcus heavily populated with neutrophils in health b/c of great bacterial load; decrease in neutrophils - loss of protection

Front 338

What are the different ways to treat oral manifestations of neutropenia

Back 338

Antibiotics

Improved Oral Hygiene

G-CSF supplementation

Front 339

What parts of the body are very susceptible to bacterial infection because of neutropenia

Back 339

Middle ears, Oral cavity, Perirectal area, Lungs

Front 340

How does cyclic neutropenia differ from neutropenia

Back 340

Recurrent, opportunistic infection; have 3-6 days of severe neutropenia in 21 day period; asymptomatic during off days; on days - ulceration of tongue, gingivitis, stomatitis, cellulitis, sometimes death (10%), severe perio bone loss

Front 341

What is the neutrophil count during the on days of cyclic neutropenia

Back 341

<200 mm^3

Front 342

What causes cyclic neutropenia

Back 342

mutation of gene elastase; neutrophil arrested at promyelocyte stage

Front 343

How do you diagnose neutropenia and how do you diagnose cyclic neutropenia

Back 343

Neutropenia - blood count

Cyclic neutropenia - observe period of normal neutrophil count and abnormal - have to take sequential WBC count 2-3x/week for 8 weeks

Front 344

What is agranulocytosis

Back 344

Granulocytes (particularly neutrophils) are absent; due to decreased production or increased destruction

Front 345

What are most cases of agranulocytosis caused by

Back 345

Anticancer chemotherapeutic agents - inhibit normal mitosis and division

some cases are idiopathic

Front 346

Following transmigration, what process causes leukocytes to emigrate toward the site of injury

Back 346

Chemotaxis - trigger/stimulus causes neutrophils to move against concentration gradient (stop when there is no longer a gradient)

Front 347

What are the exogenous triggers for leukocyte chemotaxis

Back 347

1) Bacterial products

2) N-formyl-methionyl peptide

Front 348

What are the endogenous triggers for leukocyte chemotaxis

Back 348

1) Complement pathway (C3a and C5a)

2) Lipid-derived mediators (leukotriene B4)

3) Cytokines - esp in chemokine family

Front 349

What may cause abnormal chemotaxis and what is the result

Back 349

Bacterial toxins (e.g. leukotoxin from P. gingivalis); prevents migration and can cause increased risk of aggressive infection

P. gingivalis has proteases that break down C5a - causes perio disease

Front 350

What do granules contain that are very important in neutrophil ability to phagocytose

Back 350

Lysozymes

Front 351

How do neutrophils produce energy

Back 351

Glycolytic pathway; very short-lived so don't need complicated protein synthesizing apparatus or a lot of mitochondria

Front 352

What is the function of the ROS produced by neutrophils

Back 352

Help kill microbes (NOT for ATP production) - respiratory burst

Front 353

What is degranulation

Back 353

Release granules (part of digesting microbes)

Front 354

Activation of Toll-like receptors by what on microbes leads to the amplification of the inflammatory response

Back 354

Pathogen-associated molecular patterns (PAMPs) - induces cytokines

Front 355

What must neutrophils do in order to phagocytose microbes

Back 355

Adhere

Front 356

What can bacteria have to make it difficult for neutrophils to adhere

Back 356

Capsules - prevents neutrophil recognition; S. pneumonia/pneumococci, H. influenza, P. gingivalis

Front 357

What happens to bacteria to prepare them to be phagocytosed

Back 357

Opsonization - complement and antibodies (opsonins) bind to bacteria and prepare it to be phagocytosed

Front 358

What are the two types of opsonin used in the process of phagocytosis

Back 358

Complement (C3b)

Antibodies (IgG)

Front 359

How does opsonization work

Back 359

Opsonins bind to bacteria and neutrophils must have receptors to be able to recognize the opsonins in order to phagocytose

Front 360

What are the two types of neutrophil opsonin receptors

Back 360

Fc (antibody)

C3b

Front 361

What is formed when a neutrophil phagocytoses bacteria

Back 361

Phagosome

Front 362

What is present in the phagosome membrane that generates ROS and what is it sometimes known as

Back 362

NADPH oxidase/phagocyte oxidase

Front 363

What do NADPH oxidase and oxygen produce

Back 363

H2O2 (hydrogen peroxide) - oxygen-dependent process

Front 364

What is the oxygen-independent pathway necessary to produce HOCl-

Back 364

Granules contain MPO, combined with Cl-

Front 365

When you combine the oxygen-dependent and oxygen-independent pathways of phagocytosis, what do you produce

Back 365

HOCl- (causes fragmentation of bacteria and killing)

Front 366

Phagolysosome

Back 366

Phagosome including HOCl- combined with lysosome

Front 367

What are the two proteins produced by neutrophils that assist with phagocytosis

Back 367

Bacterial Permeability Increasing protein (BPI)

LL-37 (cationic protein)

they bind to bacteria and create holes in it to facilitate killing

Front 368

What are the four major components that come together to kill/degrade bacteria

Back 368

1) NADPH oxidase

2) Granules

3) Additional proteins (BPI and LL-37)

4) Lysozyme - degrades bacterial coat

occurs intracellularly - inside phagolysosome

Front 369

What is produced during phagocytosis and contributes to killing some types of bacteria, like pneumococci

Back 369

Lactic acid

Front 370

What is the extracellular mechanism by which bacteria are killed by neutrophils

Back 370

Neutrophil Extracellular Traps (NETS) - beneficial suicide; formation of ROS intracellularly - disintegration of nuclear and granular membranes and mixing/release of contents - release of NETs - trap bacteria and kill

fail-safe mechanism if intracellular mechanisms aren't functioning properly

Front 371

What are the potential negative consequences of NETs

Back 371

may cause autoimmune diseases - possible source of antigens

Front 372

What disease involves abnormal lysosome formation due to mutation, is autosomal recessive, has melanocytes with large granules, has neutrophils with giant azurophilic granules

Back 372

Chediak-Higashi Syndrome

Front 373

What diseases involves clinical manifestations identified in infancy/childhood, oculocutaneous albinism, photophobia, grey hair color, recurrent bacterial infection (gingivitis, oral ulceration, perio diseases)

Back 373

Chediak-Higashi Syndrome

Front 374

What is happening to this cell/what are the clinical implications

Back 374

Chediak-Higashi Syndrome; multilobular nucleus - so cell is neutrophilic, but has prominent granules

Front 375

What disease involves a defect in NADPH oxidase due to mutation and formation of a granuloma

Back 375

Chronic Granulomatous Disease; genetic defect in NADPH oxidase, don't generate sufficient amount - catalase positive bacteria remove H2O2; impaired ROS production; granuloma formation from reduced efferocytosis and activation of monocytes

Front 376

What disease clinically manifests as recurrent bacterial infection, is most susceptible to catalase positive bacteria, has superficial skin infections, abscesses, cellulitis, gingivitis

Back 376

Chronic Granulomatous Disease - have normal recruitment of neutrophils, they just don't function properly; have abnormal respiratory bursts

Front 377

What do long-term repeated infections, like CGD, likely result from

Back 377

lack of NETs formation

Front 378

What disease involves the mutation and loss of cathepsin C gene (LL-37 not produced), skin defect, and neutrophil function, keratosis in palms and soles

Back 378

Papillon-Lefevre Syndrome

Front 379

What type of bacteria produces leukotoxins and is assoicated with perio disease

Back 379

A. actinomycetemcomitans (Aa)

Front 380

What bacteria produces proteases that inactivate the complement pathway and prevent neutrophil from being recruited to site of infection

Back 380

P. gingivalis

Front 381

What bacteria produces protein A, which binds to the antibody receptor of neutrophils so the bacteria can't be opsonized

Back 381

S. aureus

Front 382

What does DNAse do

Back 382

dissolves NET (produced by some bacteria)

Front 383

What do leukocytes change their lipoxygenase-derived products from and to in the change from inflammation to resolution of inflammation

Back 383

COXs (pro-inflammatory) to lipoxins (resolve inflammation)

Front 384

How do lipoxins work to resolve inflammation

Back 384

Bind to specific cell surface receptors on neutrophils to inhibit chemotaxis and ROS generation and promote neutrophil apoptosis

ALSO - promote monocyte chemotaxis and do NOT induce cytokine production by monocytes/macrophages (don't wan to recruit inflamm cells)

Front 385

What is largely the cause of the extensive cellular and tissue destruction seen in purulent exudate

Back 385

proteolytic enzymes and other factors released by neutrophils

Front 386

What are the two process that can heal injured tissue

Back 386

Regeneration

Repair

Front 387

What determines whether injured tissue undergoes regeneration or repair

Back 387

The type of cells the tissue is made of (labile, stable, permanent)

Front 388

What happens to injured tissue in regeneration vs repair

Back 388

Regeneration - replace damaged or lost cells with identical cell type (via stem cells in basement membrane)

Repair - replace injured/dead cells with fibrous/collagenous scar

Front 389

When does fibrosis occur and what is it

Back 389

Extensive deposition of collagen, occurs in tissues as a consequence of chronic inflammation (usually in lung, liver, kidney or heart)

Front 390

When does scar tissue interfere with organ function

Back 390

If the scar tissue is extensive (e.g. in infarcts - may lead to thinning of muscle walls and complications/loss of function)

Front 391

What has occurred from the slide on the left to that on the right; this is heart tissue

Back 391

Left: cells undergoing karyolysis following inflammatory response

Right: replacement of dead tissue with fibrotic tissue; white areas where cells lost due to severe damage and replaced by collagenous scar

Front 392

Do you get regeneration or repair with: labile, stable and permanent cells

Back 392

Labile - most likely regenerate; usually cells that turnover rapidly (skin)

Stable - can either regenerate or repair, depends on severity of injury (liver, kidney)

Permanent - almost always repair with scar tissue (neuron, heart)

Front 393

What percent of cells are dividing/undergoing mitosis in tissues that contain labile cells; what are examples of these tissue types

Back 393

1.5% - give you regeneration

hematopoetic tissue, lymphoid tissue, surface epithelium (skin, mucous membranes, GI, urinary and respiratory tracts, salivary glands)

Front 394

How do stem cells, which are labile cells, divide

Back 394

They divide continuously; with injury - one daughter cell becomes another daughter cell and the other becomes a terminally differentiated cell

Front 395

What two things does regeneration of any tissue require

Back 395

1. Intact basement membrane

2. Sufficient stem cells to promote regeneration (need asymmetrical division to maintain integrity of basal cell layer/have enough stem cells)

Front 396

In what clinical situations will you develop a scar if the basement membrane of the surface epithelium is damaged, but won't scar if basement membrane left intact

Back 396

Chicken Pox

Acne

Front 397

What cell type is long-lived, has low turnover, are quiescent and have minimal replicative activity in their normal state

Back 397

Stable cells - proliferate in response to injury or tissue loss

Front 398

What are examples of stable cells

Back 398

Parenchymal cells - liver, pancreas, thyroid, salivary glands, adrenal cortex, renal tubular epithelium

Connective tissue and mesenchymal cells - osteoblasts, fibroblasts, vascular endothelial cells, smooth muscle cells

Front 399

What percent of cells are dividing/undergoing mitosis in tissues that contain stable cells

Back 399

less than 1.5%; but this number does not determine an organ's ability to regenerate; always have ability to divide with appropriate stimulus/injury

Front 400

What biological action does the mythical story of Prometheus and the eagle give an example

Back 400

Regeneration of liver cells (stable cells) with damage to the liver

Front 401

What must not be damaged in order for liver cells to regenerate instead of repair

Back 401

Extracellular matrix (like basement membrane can't be damaged in epithelial cells)

Front 402

What has happened to the liver here

Back 402

Undergone cirrhosis (can happen with chronic alcoholism); liver nodules and fibrosis, it's hard and has lots of connective tissue; smaller than normal liver because the scar tissue contracts

normal liver is soft and tender, normal size is fairly large

Front 403

What has happened to these liver cells

Back 403

Surrounded by collagen because of damage to ECM - has undergone repair due to a severe injury

Front 404

What has happened to some of the kidney cells/tubules pictured here

Back 404

Coagulative necrosis/karyolysis; cells are dead and you can't distinguish nuclei, can also see much protein stained pink by eosin, but basic architecture of the tubules is still intact

Front 405

What has happened to the kidney cells here, and what types of cells have caused this

Back 405

Glomeruli surrounded by blue-stained collagen (undergo fibrosis more readily than tubules); caused by severely damaged stable cells - lost regenerative capacity

Front 406

If the first slide is normal lung parenchyma, what has most likely occurred to the lung parenchyma in the other two slides

Back 406

1) Empty spaces, no fluid in cells; probably due to pneumonia; lots of collagen/fibrosis (H&E stain)

2) Fibrosis - due to persistent injury (Trichrome stain)

Front 407

What type of cell cannot replicate after birth, give examples

Back 407

Permanent cell (neurons, skeletal muscle, cardiac muscle); once destroyed - lost forever; scar formation occurs

Front 408

Why does the heart increase in size with age

Back 408

Due to Hypertrophy (increase in cell size) NOT hyperplasia (increase in cell number) because heart cells can't multiply/divide

Front 409

What are the three things that exit the blood vessels and enter the extravascular space during inflammatory response, and in what order

Back 409

1) Edema - with vascular/cellular response

2) Neutrophils - early acute inflammation

3) Monocytes/macrophages - late acute inflammation

Front 410

What is a clinical example of exudate resolution after injury (etiology promptly destroyed, no or minimal cell necrosis)

Back 410

Mild heat injury

Front 411

What is a clinical example of exudate organization after injury (etiology promptly destroyed, no or minimal cell necrosis)

Back 411

Fibrinous exudate - Fibropurulent Pericarditis; have fibrotic layer on top of exudate which leaves a fibropurulent scar on top

Front 412

What is a clinical example of the framework remaining intact (after etiology NOT destroyed, in tissue of labile/stable cells)

Back 412

Lobar pneumonia

Basement membrane of skin intact, ECM of liver cells intact

Front 413

What is a clinical example of the framework being destroyed (after etiology NOT destroyed, in tissue of labile/stable cells)

Back 413

Liver Cirrhosis - scarring when ECM of liver cells destroyed

Front 414

What is a clinical example of necrosis of the tissue of permanent cells (after etiology NOT destroyed)

Back 414

Myocardial Infarct - scarring (from ischemic necrosis - permanent damage to cardiac myocytes)

Front 415

What does regenerative medicine involve, give an example

Back 415

regeneration and repopulation of damaged organs using stem cells; induced pluripotent stem cells (iPS cells) - expose genes that confer stem cell properties to pt's differentiated cells - resulting iPS cells can be induced to differentiate

Front 416

What are the predominant examples used to describe labile cells and stable cells

Back 416

Labile - Skin/epithelial cells

Stable - Liver cells

Front 417

What are the three things that must be resolved in order for proper healing to occur

Back 417

1) Bleeding

2) Loss of tissue

3) Infection

Front 418

What are the four phases of wound healing

Back 418

1) Early

2) Intermediate

3) Late

4) Terminal

Front 419

What happens during the early phase of wound healing and how long does it last

Back 419

Platelets activated - form clot

Neutrophils and macrophages recruited

rapid, transient

Front 420

What happens during the intermediate phase of wound healing

Back 420

Activation of resident cells - cells normally present in the tissue (fibroblasts, mast cells, endothelial cells)

Proliferative response of resident cells - form new blood vessels (angiogenesis), re-epithelialization

Front 421

What happens during the late phase of wound healing

Back 421

Collagen synthesis

Front 422

What happens during the terminal phase of wound healing

Back 422

Remodeling; increase wound strength by replacing original collage deposited with stronger collagen

takes months

Front 423

What are the two major categories skin wounds can be grouped into

Back 423

Healing by First Intention - edges held close together by sutures, clips or tape to help heal

Healing by Second Intention - edges are widely separated

Front 424

What occurs during healing by first intention

Back 424

Minimal tissue loss, wound edges held close together, no infection and little scarring

Front 425

What occurs during healing by second intention

Back 425

Extensive tissue loss, ulcer/large wounds, extensive scarring

Front 426

What is the response that occurs within seconds after skin incised by a scalpel blade

Back 426

Hemostatic response - arrests hemorrhage and initiates healing

platelets release 5-HT from granules (plug defects in vessel wall and release factors into immediate wound area and activate clotting cascade), TxA2 activated, fibrin and fibrinogen (clotting proteins)

Front 427

What protein forms a clot to stop bleeding

Back 427

Fibrin

Front 428

What functions does a clot have

Back 428

Stabilizes platelet plug so it can't be dislodged

Cements cut margins of wound

Generate chemotactic peptides to attract leukocytes, resident fibroblasts and endothelial cells

Forms a scaffold of fibrils - facilitate migration of leukocytes and mesenchymal cells to wound

Discharge vasoactive compounds into wound (prostaglandins, PAF, proteolytic enzymes, VEGF)

Front 429

Are platelets required for wound healing

Back 429

Yes, must have platelets to stop bleeding

Front 430

In what type of wounds are neutrophils important

Back 430

Infected wounds - eliminate contaminating microbes

Front 431

What is a clinical example of a situation where neutrophils can't be recruited to site of injury and won't heal

Back 431

LAD-I - defect in neutrophil transmigration process so neutrophils don't get to wound and it can't heal (e.g. Dysplastic Eschar, Stump of umbilical cord)

Front 432

What is the difference between macrophage recruitment in acute inflammation and that in wound healing

Back 432

In acute inflammation - macrophages do NOT secrete cytokines, don't want to initiate an inflammatory response; cytokines required in wound healing for chemotaxis of fibroblasts AND angiogenesis and remodeling

Front 433

When do macrophages appear and how long do they remain during wound healing

Back 433

24-72 hours after injury; remain for 5-7 days

Front 434

What type of cell is recruited in wound healing that is not recruited in acute inflammation

Back 434

T-lymphocytes; produce cytokines that help with healing

Front 435

During wound healing, what process involves basal epidermal keratinocyte transformation from sedentary to migratory phenotype, under influence of cytokines

Back 435

Epithelialization

Front 436

What does re-epithelialization involve mechanistically

Back 436

Mitotic activity 4-5 cells from leading edge (where cells are exhibiting phagocytic activity and digesting their way through the clot); eventually the migrating cells contact and you have restoration of epithelium

Front 437

What is angiogenesis, in what stage of wound healing does it occur, and why is it important in wound healing

Back 437

formation of new blood vessels during intermediate stage - critical at injury site for collateral circulation and to bring in nutrients (plasma proteins) for next phase; process mainly mediated by VEGF

Front 438

What is the name of tissue that includes leaky, newly produced blood vessels during wound healing

Back 438

Granulation tissue - highly vascular; mass of migrating and proliferating fibroblasts and capillaries; contains many new blood vessels, fibroblasts, some monocytes, and few neutrophils; underneath the now thin epithelial layer - bleeds easy if traumatized

Front 439

What is degraded and then reformed in order to produce new blood vessels during angiogenesis in wound healing

Back 439

Basement membrane of endothelial cells

Front 440

What tissue changes occur from the intermediate stage of wound healing to the late stage

Back 440

Granulation tissue devascularized and turns into scar tissue

Front 441

What two stages of the wound healing process do these two tissue slides depict

Back 441

Intermediate stage (granulation tissue) and Late stage (scar tissue/fibrosis)

Front 442

What do the arrows point to in this intermediate stage of wound healing

Back 442

Many blood vessels in granulation tissue

Front 443

What stage of wound healing is depicted here

Back 443

Late stage - lots of collagen/scar tissue

Front 444

What are the most and second most abundant cells in connective tissue (i.e. scar tissue)

Back 444

Fibroblasts, and then mast cells

Front 445

What are the cells needed for wound healing (in order) and what is their primary function

Back 445

EARLY

1) Platelets - clot formation

2) Neutrophils - kill bacteria, digest ECM/basement membrane, remove dead tissue

INTERMEDIATE

3) Macrophages - clean up mess, secrete cytokines for fibroblast chemotaxis; secrete cytokines for angiogenesis and epithelialization

LATE

4) Fibroblasts - secrete collagen

5) Mast cells - interact with fibroblasts to stimulate collagen synthesis

TERMINAL

6) Fibroblasts leave

7) Myofibroblasts - wound contraction

Front 446

What type of cells commonly cause tissue injury during inflammatory response

Back 446

Neutrophils

Front 447

What cells mediate healing by second intention

Back 447

Myofibroblasts - myocontractile and collagen synthesizing abilities

Front 448

What is wound contraction

Back 448

Process where wound edges begin to move towards each other to the center of the wound; results in mechanical reduction in size of wound; especially important in healing by second intention

Front 449

What does the terminal stage of wound healing involve

Back 449

maturation and increase in tensile strength of the wound (re-modeling) - replace original Type III collagen with Type I collagen - increased cross-linking between collagen fibrils increases strength

Front 450

Does tissue that undergoes wound healing ever reach the strength of normal skin

Back 450

No. 80% of original strength after ~6 weeks; 90% of original strength after ~6 months

Front 451

What replaces the epidermal and dermal layers of skin after the terminal stage of wound healing

Back 451

Epidermal - epithelial cells (regeneration - labile cells)

Dermal - scar tissue (repair of basement membrane - stable cells)

Front 452

What type of collagen is originally produced in wound healing and what type of collagen replaces it during the terminal stage of wound healing

Back 452

Type III to Type I

Front 453

What is the defining feature, histologically, of a skin ulcer

Back 453

Loss of epithelial cell layer

Front 454

What type of skin condition is observed here

Back 454

Skin ulcer - no epithelial layer

Front 455

What stage of the wound healing process is shown here

Back 455

Intermediate - Granulation tissue with lots of blood vessels and thin epithelial layer (angiogenesis and re-epithelialization occurring)

Front 456

What stage of the wound healing process is shown here

Back 456

Intermediate/Late stage - Not a ton of blood vessels, wound contraction occurring in epithelial layer

Front 457

What process is depicted here in the change from the first picture to the second

Back 457

Wound healing by second intention - extensive scar tissue forms underneath epithelial layer; occurs with ulcers/large wounds

Front 458

What are the major differences in the vascular and cellular responses between inflammation and wound healing

Back 458

Inflammation:

- Vascular response increases vascular permeability; initiated by mast cells

- Neutrophils and macrophages impt for cellular response

Wound Healing

- Vascular response causes angiogenesis - initiated by platelets/neutrophils

- Macrophages for proliferative response

- Fibroblasts for actual healing

Front 459

What is chronic inflammation

Back 459

a continuation of wound healing - if scar tissue becomes so big that it interferences with function of the organ then chronic inflammation occurs (e.g. myocardial infarct)

Front 460

How do growth factors function during wound healing

Back 460

proliferative response - promote survival, proliferation and migration

use cell surface receptors - activate signaling pathways and transcription factors in the nucleus through tyrosine-kinase activity (PDGF, VEGF) - except GPCR (no tyrosine-kinase activity)

Front 461

What type of receptor is utilized by certain chemokines (IL-8) and cytokines (IL-4, IL-2)

Back 461

G protein coupled receptors; receptors don't have tyrosine-kinase activity; they activate adapter proteins and result in transcription of genes that promote cell cycle entry, prevent apoptosis, etc

Front 462

What are the three different ways in which cytokines can function with receptors to initiation gene expression

Back 462

Autocrine - cell produces particular cytokines and has receptors for the cytokine on the same cell

Paracrine - one cell produces cytokine that acts on receptors on a different, adjacent cell

Endocrine - growth factors secreted into blood

Front 463

What are two examples of an autocrine system

Back 463

Lymphocyte proliferation by cytokines - T cells release cytokines and has receptors for those cytokines on the cell

Compensatory hyperplasia - part of liver removed, cytokines produced remaining liver cells act to produce more liver cells

Front 464

What is an example of a paracrine system

Back 464

Recruitment of inflammatory cells - macrophage produces cytokines that act on other inflammatory cells to recruit them

Front 465

What growth factor initiates a healing response after clot formation during wound healing

Back 465

PDGF (platelet derived growth factor) - produced by platelets mostly, also macrophages, endo cells and keratinocytes; chemoattractant for neutrophils, monocytes, fibroblasts; important for synthesis and remodeling of ECM

Front 466

What does recombinant PDGF (regranex) treat clinically

Back 466

Diabetic ulcers

Front 467

What is the most important growth factor for epithelialization during wound healing

Back 467

EGF (epidermal growth factor) - promotes proliferation and migration of epithelial cells; also promotes proliferation of fibroblasts and induces granulation tissue formation

Front 468

What growth factor is the most important for angiogenesis during wound healing

Back 468

VEGF (vascular endothelial growth factor) - produced in response to PDGF, TGF-beta, and hypoxia by epithelial cells; also promotes migration and proliferation of endo cells (epithelialization)

Front 469

What growth factor should you develop antibodies against in order to stop growth of tumor cells in some cancers

Back 469

VEGF - reduce nutrient delivery to tumor

Front 470

What is the mesh beneath epithelial, endothelial or smooth muscle structures called

Back 470

Basement membrane

Front 471

What is the primary collagen type found in basement membrane

Back 471

Type IV - sheet-like collagen; doesn't form bonds between different fibrils; also includes proteoglycans and laminins

Front 472

What is the matrix between basement membrane and blood vessels called, what's included in this matrix

Back 472

Interstitial matrix - fibroblasts, integrins, adhesive glycoproteins, cross-linked collage (rope-like); reservoir for growth factors

Front 473

What is important for the production of collagen cross-linking and what happens if collagen can't cross-link

Back 473

Vitamin C - without cross-linking the area will bleed easily and the wound won't heal as well

Front 474

What growth factor is important for ECM deposition and scar formation

Back 474

Transforming growth factor beta (TGF-beta); chemoattractant for fibroblasts, promotes collagen/ECM synthesis, inhibits collagen degradation; induces TIMPs; results in fibrosis in kidney/lung/liver after chronic inflamm; has anti-inflammatory effects as well

Front 475

What does TIMP do during wound healing

Back 475

Tissue inhibitor of metalloproteinases - prevent metalloproteinases from degrading collagen

Front 476

In what situation is TGF-beta expressed transiently

Back 476

Fetal healing - healing occurs without scar formation; TGF-beta undesirable

Front 477

What can be administered to reduce scarring

Back 477

Antibodies to TGF-beta

Front 478

What three things does scar tissue formation depend on the balance between

Back 478

TGF-beta (promote collagen formation)

MMPs - metalloproteinases (degrade Type III collagen during remodeling)

TIMPs (inhibit degradation of Type I collagen)

Front 479

In what types of tissues do you see labile cells/regeneration after wound healing

Back 479

Skin (epidermis)

Bone

Oral Mucosa

Fetal wound

Front 480

In what types of tissues do you see stable cells/regeneration or repair depending on severity of injury during wound healing

Back 480

Liver

Lung

Kidney (regeneration in cortical tubules, scar tissue/repair in medullary tubules and glomeruli)

Front 481

In what types of tissues do you see permanent cells/repair and scar tissue formation during wound healing

Back 481

Heart

Nervous System (except some parts of peripheral - regeneration of axons)

Front 482

What type of necrosis do you here see (after myocardial infarct)

Back 482

Coagulative necrosis - nuclei look abnormal, but basic architecture still intact

Front 483

What is happening to this cardiac tissue

Back 483

Early acute inflammation: Karyolysis of cardiac myocytes (no nuclei); lots of neutrophils present

Front 484

What is happening to this cardiac tissue

Back 484

Late acute inflammation: macrophages cleaning up mess from neutrophils

Front 485

What stage of wound healing is this

Back 485

Intermediate stage - granulation tissue with lots of new blood vessels

Front 486

What stage of wound healing is this

Back 486

Late stage - lots of collagen produced, healing/repairing damaged tissue with scar tissue (replaced granulation tissue)

Front 487

What is a traumatic neuroma

Back 487

reactive proliferation of neuronal tissue after damage of nerve bundles (e.g. damaged axon); NOT a neoplasm; have scar tissue, can't reestablish innervation; tumor-like mass develops at site of injury

Front 488

What are the most common sites for traumatic neuromas

Back 488

mental foramen, tongue, lower lip

Front 489

What is the only case in which you have regeneration of neuronal tissue

Back 489

Traumatic neuroma - damaged axon

Front 490

What two types of ossification occur during bone formation/fracture repair

Back 490

Intramembranous ossification

Endochondral ossification

Front 491

What occurs during intramembranous ossification and how do bones grow, what types of bones

Back 491

differentiation of mesenchymal cells into osteobalsts; osteoid formation (collagen and organic ECM), combined wtih Ca++ and phosphates results in mineralized bone matrix; also need osteoclasts for bone remodeling

bones grow in WIDTH (skull, maxilla, mandible)

Front 492

What occurs during endochondral ossification, how do bones grow, what types of bones

Back 492

differentation of mesenchymal cells into hyaline chondrocytes then replacement of hyaline cartilage with bone

Long bones grow in LENGTH

Front 493

What are the steps of bone regeneration after fracture

Back 493

1) Hematoma - clot

2) Provisional callus - angiogenesis/granulation tissue; fibrocartilage - soft

3) Hard callus - endochondral ossification; woven bone replaces soft callus

4) Remodeling - cortical bone replaces woven bone; healing without scar

Front 494

How can you tell a bone has been broken

Back 494

Bone more dense; but NOT scar tissue formed

Front 495

What are the two keys to successful bone repair/formation

Back 495

1) Alignment (screws, cast)

2) Good blood supply

Front 496

What are required in order to produce osteoblasts and form new bone

Back 496

Bone morphogenic proteins (BMPs) and Mesenchymal stem cells (MSCs)

Front 497

What other healing processes are nearly identical to that of skin

Back 497

Bone, socket healing

Front 498

What are six complications of wound healing and what causes them

Back 498

1) Alveolar Osteitis/Dry Socket - clot doesn't form

2) Delayed healing - from infection

3) Proud flesh/Pyogenic granuloma - too much granulation tissue

4) Dehiscence/Hernias/Scurby - deficient collagen deposition

5) Keloid/hypertropic scar - excessive collagen deposition (mutation)

6) Contracture - excessive contraction

Front 499

What typically causes dry socket formation

Back 499

Infection or trauma; involves dissolution of blood clot

Front 500

What are four predisposing factors to dry socket formation

Back 500

Oral contraceptives

Site of extraction (mandible more prone than maxilla)

Trauma

Smoking

Front 501

Why does infection typically delay wound healing

Back 501

Healing by second intention with infection - results in more granulation tissue/scar formation

common cause of death from burn injuries

Front 502

What is a proud flesh, how does it occur, and how is it treated

Back 502

a protruding mass of granulation tissue; reason for development unknown; tx by cauterization with silver nitrate or surgical removal

Front 503

What is an exuberant proliferation of granulation tissue that occurs in oral tissues called, how does it occur and how is it treated

Back 503

Pyogenic granuloma (NOT actually a granuloma and NOT purulent); usually due to trauma or irritation

Front 504

What wound healing complication is seen here

Back 504

Proud flesh - protruding mass of granulation tissue

Front 505

What wound healing complication is seen here

Back 505

Pyogenic granuloma - protruding mass of granulation tissue in the oral mucosa

Front 506

Where are pyogenic granulomas located 75% of the time

Back 506

Gingiva

Front 507

What wound healing complications are seen here

Back 507

Dehiscence/Incisional hernia - in abdominal wounds; caused by defect in collagen deposition

Front 508

What is a keloid

Back 508

excessive collagen formation that begins at wound site and then spreads to neighboring tissues; ratio of Type III:Type I collagen is high - "maturation arrest"; high rate of recurrence; common in african-americans and young people, common within families

Front 509

What wound healing complication is seen here

Back 509

Keloid - dark; excessive collagen formation that spread

Front 510

What is the pathogenesis of keloid formation

Back 510

Increased fibroblast proliferation and collagen synthesis due to overexpression of TGF-beta and VEGF

Front 511

What is a hypertrophic scar and how does it differ from a keloid

Back 511

Similar in appearance to a keloid; flatten and regress spontaneously over a period of months-years and do NOT spread beyond site of injury

Front 512

Can you treat keloids/hypertrophic scars

Back 512

Can treat hypertrophic scars but if you try to treat keloids they recur, so no

Front 513

What wound healing complication is seen here

Back 513

Hypertrophic scar - light, confined to one region

Front 514

What causes excessive wound contraction, and where does this typically occur

Back 514

Myofibroblasts; palms, soles, burns of skin, liver (cirrhosis)

Front 515

What must be removed from wounds in order to promote healing

Back 515

1) Necrotic tissue (promote bacterial growth, physical barrier, delays healing)

2) Foreign material (harbor bacteria, promote inflammation)

Front 516

What is a decubitis ulcer and how is it treated

Back 516

Bed sore; Pressure induced ulcer from ischemia (inadequate blood supply) - relieve pressure; use pDGF to initiate healing process

Front 517

What local factor in wound healing produced condition is shown here

Back 517

Decubitis ulcer/Bedsore - from pressure induced ischemia

Front 518

What are some of the local factors in wound healing aside from inadequate blood supply

Back 518

1) Endarteritis obliterans - due to post-irradiation scarring of blood vessels; reduces local blood flow

2) Atherosclerosis - restricts arterial perfusion, particularly in diabetics and elderly

3) Smoking - triggers vasoconstriction and may impair tissue oxygenation; also contributes to development of atherosclerosis

Front 519

What are some of the effects that local irradiation has on wound healing

Back 519

Curtains blood flow to wound

Decreased vascularity limits platelet and leukocyte delivery to site

Cytotoxic effects on fibroblasts and keratinocytes leads to increased fibrosis and thinning epidermis

Dry skin due to damaged sebaceous and sweat glands

Front 520

What direction and location of a wound facilitate better healing

Back 520

Incisions made parallel to crease lines of skin

Front 521

What role does movement play in wound healing

Back 521

Immobilization important for bone fractures; excessive mechanical movement can produce additional trauma to skin wounds and may prolong healing

Front 522

Why do oral mucosa wounds tend to heal faster than skin wounds

Back 522

Moist environment promotes healing

Front 523

What systemic factors have a profound effect on wound healing

Back 523

Malnutrition

Cancer

Diabetes Mellitus

Front 524

What are the six major malnutrition involved systemic factors of wound healing and how do they effect wound healing

Back 524

1) Hypoproteinemia - decreased collagen synthesis

2) Reduced carb and fat intake - protein used as energy source instead

3) Vitamin C deficiency - abnormal collagen synthesis

4) Vitamin A deficiency - defective epithelialization

5) Vitamin D deficiency - defective bone healing

6) Zinc deficiency - decreased cell proliferation and granulation tissue formation

Front 525

Why does diabetes mellitus effect wound healing; how can you treat wounds that result

Back 525

Results in decreased growth factor - improper healing; treat with PDGF, antimicrobial, amputation

Front 526

What inflammatory process can follow wound healing

Back 526

Chronic inflammation - if etiologic agent is not removed

Front 527

When do you experience signs and symptoms of acute inflammation and of chronic inflammation

Back 527

Acute - almost immediately; redness, heat, swelling

Chronic - not until late in process; indurated/hard

Front 528

What cells are involved in the first stages of acute inflammation vs chronic inflammation

Back 528

Acute - mast cells and neutrophils

Chronic - Round cells (macrophages and lymphocytes)

Front 529

What is the biological response of acute inflammation vs chronic inflammation

Back 529

Acute - vascular/exudative

Chronic - proliferative

Front 530

What are some of the main clinical examples of chronic inflammation

Back 530

Periodontal disease

Pulpal/periapical lesion

Alcoholic cirrhosis

Front 531

What is the most significant feature of chronic inflammatory diseases

Back 531

permanent or irreversible tissue/organ destruction

Front 532

What two inflammatory responses are occurring here in the lung tissue

Back 532

1) Acute inflammation - normal alveoli and alveolar septae; blood vessels are dilated; lots of neutrophils

2) Chronic inflammation - empty spaces that used to have fluid replaced by fibrosis; foci of inflammatory "round" cells

Front 533

What two cell types interact in a bidirectional way during chronic inflammation

Back 533

Lymphocytes and Macrophages

- Macrophages display antigens (MHC) to T cells, results in production of cytokines (like IL-12) that stimulate T cell responses

- Activated T lymphocytes then produce cytokines (like IFN-gamma) that activate macrophages

- Result is a cycle of cellular reactions that fuel and sustain chronic inflammation

- Both macrophages and lymphocytes also produce other inflammatory mediators that result in leukocyte recruitment and inflamm

Front 534

What cell type produces plasma "cells"

Back 534

activated B lymphocytes - produce antibodies directed against persistent antigens in inflammatory site or against altered tissue components

Front 535

What cells in chronic inflammation go through almost the exact same process as neutrophil recruitment and transmigration in acute inflammation

Back 535

Monocytes

Front 536

Neutrophils can only survive in the blood for 4-5 hrs and in the tissues for 1-2 hrs; how long do monocytes/macrophages survive in both of these locations

Back 536

Blood - day or more

Tissue - more than a year, VERY long-lived

Front 537

What does the foci of inflammatory cells seen in chronic inflammation consist of

Back 537

Macrophages and T cells

Front 538

In what cases might you see neutrophils present in chronic inflammation

Back 538

non-specific chronic inflammation resulting from presence of persistent microbes or necrotic cells

Front 539

What are the two main types of macrophages seen in chronic inflammation and how do they differ

Back 539

M1 - activated by IFN-gamma; produce ROS, lysosomal enzymes and cytokines that induce inflammation and microbial actions (similar fxn to neutrophils)

M2 - activated by cytokines other than IFN-gamma; NOT microbial; promote angiogenesis and collagen synthesis

Activated sequentially

Front 540

What inflammatory process is referred to as frustrated repair

Back 540

Chronic inflammation; b/c tissue destruction is occurring simultaneously

ex: cirrhosis - fibrous tissue repairs liver tissue but also prevents regeneration of normal hepatic lobules and interferes with normal blood supply to lobules - leads to portal hypertension

Front 541

What does fibrosis in kidney (chronic pyelonephritis) cause

Back 541

Loss of renal function/failure and hypertension

Front 542

What does fibrosis in the intestine during peptic ulceration cause

Back 542

Pyloric stenosis

Front 543

What does fibrosis in joint tissue cause

Back 543

Ankylosis

Front 544

What is most of the tissue destruction in chronic inflammation a consequence of

Back 544

activities and products released from inflammatory cells

Front 545

What are five different ways an etiologic agent is able to resist elimination by the host

Back 545

1) macrophages unable to kill bacteria (e.g. TB and Leprosy - delayed type hypersensitivity, DTH)

2) macrophages unable to degrade bacteria (certain strains of streptococci)

3) viruses and fungi (DTH)

4) cause by particulate or physical agents (uric acid, asbestos, gall stones, silica, talc)

5) immune complexes - deposits keep being dumped in lesion even when removed (e.g. joints, skin, kidney)

Front 546

What is delayed-type hypersensitivity

Back 546

An immune response produced by leukocytes in affected tissues that's incited by persistent infection (e.g. inability to remove TB or leprosy microbes; viral and fungal infection)

Front 547

What type of disease probably has an episodic progression of chronic inflammatory lesions (tissue destruction occurs in bursts)

Back 547

Periodontal disease - has active and inactive periods; loss of attachment and alveolar bone may be cumulative effects of one or more bursts of active disease; in quiescent periods, bacteria and leukocytes exist in harmony

Front 548

What are dysbiotic microbiota

Back 548

bacteria that already exist in the body become active and cause disease

Front 549

What does non-specific chronic inflammation usually result from

Back 549

Acute inflammation

Front 550

What are the four most common outcomes of acute inflammation

Back 550

1) Complete resolution

2) Fibrosis

3) Abscess formation

4) Progress to chronic inflammation

Front 551

Under what circumstances do tissue damage, acute inflammation, granulation tissue formation and fibrous repair occur at the same instead of sequentially

Back 551

when chronic inflammation follows acute inflammation (when the acute response can't be resolved because the injurious agent persists or problems with normal healing process)

Front 552

What are chronic peptic ulcers an example of

Back 552

Non-specific chronic inflammation; localized chronic ulcerations of the stomach or duodenum caused by the damaging effects of gastric acid secretion; reflect dynamic balance between tissue damage and repair

Front 553

What are the two sides that create homeostasis in the normal surface of duodenum (preventing ulceration/injury)

Back 553

1) Damaging forces - gastric acids, peptic enzymes

2) Defensive forces - mucus secretion, bicarbonates, mucosal blood flow, etc

Front 554

What two things can trigger injury in stomach/duodenum, breaking homeostasis, and causing an acute inflammatory response

Back 554

1) Increased damage - NSAID, H. pylori infection, aspirin, cigarettes, etc

2) Impaired defenses - ischemia, shock, etc

Front 555

What is bronchiectasis

Back 555

Chronic inflammation of the bronchi, associated with destruction of the wall and permanent dilation; caused by infection or obstruction by a tumor, cystic fibrosis or pneumonia; coexistance of tissue damage and repair

Front 556

What occurs during rheumatoid arthritis

Back 556

chronic inflammation; destruction of the synovial fluid and replacement by fibrotic tissue

Front 557

What is a pannus

Back 557

a formation of granulation tissue in a rheumatoid joint; includes, macrophages, plasma cells, dendritic cells, lymphocytes; eventually converted to fibrosis - causes loss of bone and cartilage

Front 558

What does the presentation of MHC Class II on microbes do during chronic inflammation processes

Back 558

activates T cells - producing cytokines - which activate B cells and more cytokines - eventually form immune complex

Front 559

What is inflammatory periodontal disease an example of and how and when does it occur

Back 559

Chronic inflammation - the gradual destruction of periodontium; usually before age 20; host response to dental plaque; first stage of disease is gingivitis - gingival tissue becomes inflamed and forms an exudate; involves deepening of the gingival sulcus resulting in development of a periodontal pocket; eventually bacteria products initiate a chronic inflamm response - result in resorbed bone due to osteoclasts

Front 560

What increases osteoclast activity and bone resorption

Back 560

Increased RANKL

Front 561

What type of inflammatory process is periodontal disease, why, and what is the result

Back 561

non-specific chronic inflammation - all phases are occurring at the same time; you get bone resorption

Front 562

What is the name for small, separate clusters of activated and differentiated macrophages

Back 562

granulomas

Front 563

What does the formation of a granuloma do

Back 563

provides a mechanism for dealing with particle materials that are difficult to eliminate (e.g. M. tuberculosis, particulate materials)

Front 564

What are the components of a classic granuloma

Back 564

Organized collection of mononuclear cells (T and B lymphocytes and macrophages) = round cells, and proliferating fibroblasts

Front 565

In what type of infection do granulomas contain eosinophils

Back 565

Chronic parasitic infection

Front 566

All of the cells that participate in non-specific chronic inflammation are present in what particular structure

Back 566

Granuloma

Front 567

What characterizes granulomatous inflammation

Back 567

Distinct pattern of chronic inflammation characterized by the presence of granulomas

Epithelioid cells

Surrounded by a collar of "round cells" and fibroblasts

Front 568

What is the name for an activated macrophage

Back 568

Epithelioid cell

Front 569

What is contained in a granuloma

Back 569

Giant cells and Epithelioid cells in the center; lymphocytes, fibroblasts and fibrosis in the periphery

Front 570

What are giant cells

Back 570

a committee of fused epithelioid cells; different types: Langhans, Foreign body, Schaumann body, Aschoff, Asteroid body; >50 micrometers in diameter; have abundant cytoplasm

Front 571

What characterizes epithelioid cells

Back 571

Pink granular cytoplasm

Indistinct cell boundary

Elongated nucleus

May fuse to form giant cells

Front 572

What types of cells are these

Back 572

Epithelioid cells - lots of pink cytoplasm, indistinct boundaries, elongated nuclei

Front 573

What type of giant cell is this

Back 573

Langhans - nuclei arrange in periphery like a horseshoe; often seen in TB

Front 574

What type of giant cell is this

Back 574

Foreign body - can see suture next to giant cell; nuclei arranged haphazardly like pepperoni on a pizza

Front 575

What type of giant cell is this

Back 575

Aschoff - look like owl eyes; often see in rheumatic fever

Front 576

What type of giant cell is this

Back 576

Schaumann Body - calcified secretion

Front 577

What type of giant cell is this

Back 577

Asteroid body - star shaped

Front 578

When/why does granulomatous inflammation occur

Back 578

when the cellular infiltrate of a tissue that is chronically inflamed is arranged in a distinct pattern (usually it's spread fairly evenly over a large area); creates clusters of granulomas - allows you to deal with particle materials or pathogens that are difficult to eliminate

Front 579

What is pictured here

Back 579

Granuloma - giant cell in the center (Langhans), surrounded by epithelioid cells; collar of lymphocytes/round cells surrounding the granuloma

Front 580

What must you see upon biopsy in order to consider something granulomatous inflammation

Back 580

Granulomas (NOT granulation tissue)

Front 581

Is pyogenic granuloma a granulomatous inflammation or a granulation tissue

Back 581

Granulation tissue - no granulomas seen in biopsy

Front 582

What is tuberculosis

Back 582

Chronic inflammatory disease/granulomatous disease, mostly of the lung, caused by mycobacterium; cant digest mycobacterium so granulomas formed in a miliary pattern; granulomas often caseating (b/c due to infection)

Front 583

What has occurred to this lung tissue

Back 583

Most likely TB - can see granuloma formations close together that appear to be caseating adjacent to normal lung parenchyma

Front 584

What does this lung depict

Back 584

TB - miliary formation of granulomas

Front 585

What is a ghon complex

Back 585

Represents beginning phase of TB in lung - see granulomas forming at site of nucleation and hillar lymph nodes; immune system trying to keep bacteria under control

Front 586

What is shown here to distinguish TB and fungal infection histologically, which is it

Back 586

Acid-fast stain; acid fast bacilli, like that in TB stain red

Front 587

Is Tuberculosis a granulomatous inflammation or granulation tissue

Back 587

Granulomatous inflammation

Front 588

Is Crohn's disease a granulomatous inflammation or granulation tissue

Back 588

Granulomatous inflammation

Front 589

Is a Proud Flesh a granulomatous inflammation or granulation tissue

Back 589

Granulation tissue

Front 590

What chronic granulomatous disease mainly involves the small intestine; transmural inflammation, fissures, lymphoid aggregations and non-caseating epithelioid granuolmas

Back 590

Crohn's Disease

Front 591

What are the signs/symptoms of Crohn's disease in the gut/small intestine and proximal colon

Back 591

Abdominal cramping, diarrhea, nausea

Front 592

In what percent of Crohn's disease cases do you see oral lesions before GI lesions and how do they present

Back 592

~30%; cobblestone buccal mucosa, swelling of lips

Front 593

What is the pathogenesis of Crohn's Disease

Back 593

Loss of autophagy - paneth cells contain granules with lysosomal enzymes and anti-microbial peptides that usually keep bacteria at bay; deletion/mutation of gene for autophagy - lose granular contents - macrophages uncontrolled

Front 594

What are common examples of causes of non-infectious granulomatous inflammation

Back 594

Foreign body particles: breast implant silicone leakage, sutures and restorative dental materials in oral tissues, talc injected by iv drug users

Front 595

What multisystem chronic granulomatous disease has unknown etiology

Back 595

Sarcoidosis; blacks more frequently effected than whites; 90% of cases involve the lung; 25% of cases have cutaneous manifestations (lupus perio lesions); often have red macules on hard palate/lower labial mucosa

Front 596

What types of giant cells are frequently found in patients wtih sarcoidosis

Back 596

Schaumann bodies - calcified secretions

Front 597

What does diagnosis of sarcoidosis usually depend on

Back 597

Radiograph - bilateral hilar lymphaenopathy

OR Pulmonary fibrosis

Biopsy of affected tissue

Positive kveim test (inject sarcoid tissue into someone with suspected sarcoidosis)

Raised serum levels of ACE in active phases

Front 598

What chronic granulomatous disease does this patient most likely have

Back 598

Sarcoidosis - lupus perio (lesions on face)

Front 599

What chronic granulomatous disease does this patient most likely have

Back 599

Sarcoidosis - macules on hard palate

Front 600

What is the typical treatment for sarcoidosis

Back 600

60% of cases resolve within 2 years

Corticosteroids

Methotrexate

TNF-alpha antagonist

Front 601

What is the syndrome that involves unilateral facial paralysis, facial swelling (of one or both lips) and fissured tongue

Back 601

Melkersson-Rosenthal syndrome (type of orofacial granulomatosis) - rare triad of signs

Front 602

What is the syndrome that involves swelling of the lips and chararacteristic microscopical appearances

Back 602

Miescher's syndrome/Chelitis Granulomatosa (type of orofacial granulomatosis) - ONLY lips involved

Front 603

What type of infection can you compare a tooth/pulp infection to, and what are the differences

Back 603

Appendix - both enclosed

- appendix infection due to obstruction

- tooth/pulp infection due to breakdown in dentinal area

- appendix infection can move sideways

- tooth/pulp infection can only spread down

Front 604

What type of pulp infection is virulent/pyogenic

Back 604

Periapical abscess

Front 605

What type of pulp infection is less virulent/non-pyogenic

Back 605

Periapical granuloma

Front 606

What are the three major causes of pulp pathology

Back 606

1) Mechanical - trauma, iatrogenic, attrition, abrasion

2) Thermal/Chemical - dental procedure, acidic materials

3) Bacterial - caries

Front 607

What are the three protective responses against caries (make sure bacteria doesn't get into pulp)

Back 607

1) Decreased permeability of dentin

2) Formation of new dentin

3) inflammatory and immune reactions

Front 608

What is the most common cause of pulp disease

Back 608

Dental caries - localized, progressive destruction of tooth structure

Front 609

How does dental caries cause infection of the pulp

Back 609

Products of bacterial metabolism (organic acids and proteolytic enzymes) cause destruction of enamel and dentin - metabolites diffuse from lesion to the pulp and elicit an inflammatory reaction - eventually have extensive involvement of dentin to cause bacterial infection of pulp

Front 610

What is the most common response to dental caries

Back 610

Dentinal sclerosis - dentinal tubules become partly or completely filled with mineral deposits (either caries crystals or peritubular dentin formation - results from tooth abrasion)

Front 611

What is the primary effect of dentinal sclerosis

Back 611

Decreasing dentin permeability

Front 612

What types of cells must be present/vital in tubules for dentinal sclerosis to occur

Back 612

Odontoblasts

Front 613

What type of dentin forms during tooth development

Back 613

Developmental/Primary

Front 614

What type of dentin forms following the completion of tooth development throughout the life of the tooth

Back 614

Physiological/Secondary

Front 615

What type of dentin forms only in response to a specific stimulus/irritant at the base of dentinal tubules

Back 615

Reparative (Irregular secondary or Tertiary)

Front 616

What is the purpose of reparative dentin

Back 616

Defense mechanism against loss of enamel, dentin or cementum

Front 617

What happens to reparative dentin in response to an aggressive insult

Back 617

Swiss-cheese pattern - laid down very haphazardly, areas of soft tissue become entrapped in developing matrix

Front 618

What two factors determine the quality of reparative dentin

Back 618

1) nature/magnitude of the stimulus/irritant

2) status of the pulp - healthy pulp, better quality

Generally less tubular and less well calcified

Front 619

What two factors determine the severity of pulpal inflammation

Back 619

Depth - of bacterial penetration

Degree - to which dentin permeability has been reduced by dentinal sclerosis/reparative dentin formation

Front 620

What appears clinically at the pulp if a lot of neutrophils accumulate

Back 620

Abscess - pus formed when neutrophils release their lysosomal enzymes and surrounding tissue digested (liquefactive necrosis)

Front 621

Why are abscesses at the pulp often painful

Back 621

the area where tissue digestion is occurring has greater osmotic pressure than the surrounding tissue; the pressure differential increases the sensitivity of sensory nerve endings

Front 622

What are the anatomic features of a tooth that affect pulp inflammation

Back 622

Unyielding calcified walls - limits swelling

Constricted blood source - limits blood supply, subject to strangulation

Tooth surrounded by bone - bone infection common

Front 623

How do you classify pulpitis

Back 623

Reversible or irreversible

Front 624

What type of pulpitis is characterized by a mild/moderate, short duration, easily localized, elicited pain response to cold

Back 624

Reversible

Front 625

What type of pulpitis is characterized by a sharp/severe, long duration, unable to localize, spontaneous response to heat

Back 625

Irreversible

Front 626

What is the response of reversible vs irreversible pulpitis to electric pulp testing (EPT)

Back 626

Reversible - response at low current

Irreversible - response at high current or no response

Front 627

What is the histopathology of reversible pulpitis and how is it treated

Back 627

Hyperemia/Edema

Reparative dentin

Tx by removing irritation

Front 628

What is the histopathology of irreversible pulpitis and how is it treated

Back 628

Congestion of venules/necrosis

Necrotic tissue

Chronic inflammation/fibrosis

Tx with extraction or root canal

Front 629

Which form of pulpitis (reversible or irreversible) has mobility/sensitivity to percussion

Back 629

Neither usually; pulp hasn't spread to underlying bone

Front 630

What other tissues is pulp similar to and why

Back 630

Brain, bone marrow, nail bed; housed within mineralized tissue, so in a low compliance environment - no room to swell with inflammation - can create a marked increased in intrapulpal pressure

Front 631

What does the pulp depend on for its blood supply

Back 631

Arterioles entering the apical foramen (no collateral circulation)

Front 632

What is the most common cause of pulp death

Back 632

Bacterial infection

Front 633

How does the pulp die in presence of pyogenic bacteria

Back 633

Liquefactive necrosis - production of pus/abscess

Front 634

What are the three types of pulpal necrosis

Back 634

Liquefactive - heterolysis of cell components by neutrophils; pus and abscess formation

Coagulative - interference with blood supply, hypoxia; NO infection

Gangrenous - necrosis with saprophytic bacteria; putrefaction - very extensive degradation of pulp; produce nitrogenous products, smelly

Front 635

What type of tissue is the connective tissue of the pulp continuous with and what does this connection do

Back 635

Periodontal ligament tissue adjoining the root apex - connection facilitates spread of disease from pulp to periapical tissues

Front 636

What determines whether a periapical granuloma or an abscess will form from an inflammatory lesion in the periapical tissues

Back 636

Virulence of bacteria in the root canal

Status of host defense system

Cell mediated response - periapical granuloma

pyogenic organisms predominate - periapical abscess

Front 637

What is the clinical term for periapical granuloma formation from increased number and pathogenicity of pyogenic organisms

Back 637

Acute suppurative response

Front 638

What type of pulpitis is characterized by infection, necrotic pulp, pain, swelling, elevation of tooth, sensitivity to percussion, fever, malaise, no response to thermal or EPT, lots of PMNs, liquefactive necrosis, early on thickening of PDL and late diffuse bone loss

Back 638

Periapical abscess

Front 639

What are the characteristics of a periapical abscess that develops as a direct extension of suppurative pulpitis

Back 639

develops rapidly, associated with pain, swelling, elevation of tooth in socket; may not be radiographic evidence of periapical bone loss for a week or more after symptoms first appear

Front 640

If a periapical lesion has been present for a while, what might a radiograph show

Back 640

Diffuse area of bone loss that has a "moth-eaten" appearance

Front 641

What is it called when an acute periapical abscess develops within a preexisting granuloma

Back 641

Phoenix abscess - resembles a granuloma radiographically

Front 642

What has occurred at the root apex with acute exacerabtion or a flare-up

Back 642

results after endo treatment; trauma from instrumentation and introduction of pyogenic bacteria into chronic inflammatory tissue at root apex results in suppuration and pain

Front 643

What is the purpose of abscess drainage and where does it occur

Back 643

pus seeks pressure release; may occur through root canal of affected tooth; more common to have a lateral drainage pathway or sinus tract that's created through adjacent tissues - by penetrating the alveolar process at its thinnest point and allowing infection to spread - progression to chronic stage

Front 644

What is a small sessile nodule on the mucosa adjacent to affected (periapical abscess) tooth

Back 644

parulis (gum boil) - pus flow from abscess to here through sinus tract

Front 645

What happens when a parulis ruptures and pus escapes, the lesion regresses and then swells and ruptures again (cyclical)

Back 645

Ludwig's Angina - bilateral infection in floor of mouth; can also involve submental and sublingual; need to resolve quickly, otherwise difficulty breathing/swallowing

Front 646

What is a periapical granuloma

Back 646

Mass of chronically inflamed granulative tissue at the apex of a non-vital tooth; NOT true granuloma; results in radiolucency visible on radiograph; large number of macrophages; fibroblasts and collagen enclose on periphery in capsular arrangement; usually asymptomatic

Front 647

How do small vs large periapical granulomas appear

Back 647

Small - thickening of PDL

Large - well-circumscribed radiolucency

Front 648

How do you successfully treat a periapical granuloma

Back 648

eliminate microorganisms; root canal filling if tooth restorable; periapical surgery if lesion >2cm or tooth not appropriate for endo; non-restorable teeth must be extracted

Front 649

What is a periapical cyst

Back 649

Formed if pulpal canal of periapical granuloma containing necrotic tissue not treated - transforms in several months to a year; epithelium lined cavity within a tissue; commonly in the jaw; usually no symptoms; appears identical to periapical granuloma radiographically and tx is the same; cysts contain mostly fluid

Front 650

What does a Phoenix abscess appear like radiographically

Back 650

Looks like a periapical granuloma; presents with radiolucency

Front 651

What is osteomyelitis

Back 651

infection of the bone marrow space; uncommon in normal, healthy patients; can be acute or chronic; very serious condition that causes destruction of large amounts of bone; usually from odontogenic infection or jaw fractures; more common in males; mandible more susceptible than maxilla

Front 652

What is bone devoid of osteocytes called

Back 652

Sequestrum - dead bone

Front 653

What is sequestration

Back 653

Dead bone wont be resorbed by osteoclasts, spreads to surface and exfoliated

Front 654

What inflammatory response in the jaw is seen here

Back 654

Acute osteomyelitis - bone has no osteocytes; it's sequestra

Front 655

What are the clinical manifestations of acute osteomyelitis

Back 655

severe pain, swelling, malaise, elevated WBC count; radiographs show an ill-defined radiolucency and sequestration of necrotic bone

Front 656

When is chronic osteomyelitis of the jaws formed

Back 656

if acute osteomyelitis left untreated or in absence of clinically detectable acute phase; inflammation is less intense and clinical symptoms milder than acute; bone appears moth-eaten

Front 657

What inflammatory response in the jaw is seen here

Back 657

Chronic osteomyelitis - foci of chronic inflammatory cells (not seen in acute), fibrosis, sequestra, pockets of abscess

Front 658

Why is chronic osteomyelitis more difficult to treat than acute; how must it be treated

Back 658

Dead bone and microbes are shielded by fibrous tissue; limited blood supply

Surgical intervention mandatory - remove all infected tissues; also high dose, long-term iv antibiotics

Front 659

What is condensing osteitis

Back 659

localized lesion; represents reactive hyperplasia of bone (increase in cell number); considered a mild form of chronic inflammation that develops in response to long-standing, low grade pulp infection; more common in patients under 30; usually develops in mandible, near first molar; tx with endo or extraction

Front 660

What type of inflammatory response in the jaw is seen here

Back 660

Condensing osteitis - appears radiopaque radiographically in periapical region; all other forms of osteitis and periapical lesion appear radiolucent

Front 661

Exophytic

Back 661

Lesion growing above the surface, or presents this way (e.g. bump on the skin)

Front 662

Sessile

Back 662

Mass that you can't really move around; appears as a bump on mucosa that you can feel and see; hard to remove

Front 663

Pedunculated

Back 663

Can move the mass around; attached to the tissue by a stalk (like a leaf attached to the treat by a stem - you can move the leaf around); easy to remove the entire lesion at the stem

Front 664

Biopsy

Back 664

Surgical procedure; almost all physical pathology warrants a biopsy for diagnosis

Front 665

What are the two types of biopsy

Back 665

Excisional - entire lesion/mass surgically removed, circumferentially/at the base

Incisional - take part of the lesion/piece of tissue and leave rest of mass intact

Front 666

What results from excisional vs incisional biopsy

Back 666

Excisional - could be diagnostic or therapeutic; if mass is benign then this is the complete treatment

Incisional - do this when you're not sure what you're dealing with clinically or if lesion too large to completely remove; diagnosis guides treatment (cancer - excise the tissue; benign lesion - localized procedure)

Front 667

What are two different incisional biopsy techniques

Back 667

punch biopsy - use a tool with a circular blade at the end, like a hole puncher - punch out the tissue area and send to the lab for analysis

scalpel - take a piece of the mass, put in 10% formaldehyde, send to lab for analysis, diagnose, determine how to treat patient

Front 668

What is a differential diagnosis

Back 668

process of listing two or more diseases with similar signs and symptoms; initially list 5-7 possible diagnoses then narrow list to no more than three

determines additional tests that you can use to diagnose (e.g. blood test, biopsy, stool sample)

Front 669

What are the three causes of tissue injury

Back 669

Physical

Chemical

Trauma

Front 670

What is linea alba and is it considered physiologic or pathologic

Back 670

chronic friction (between teeth and mucosal tissue) leading to epithelial hyperplasia and hyperkeratosis; asymptomatic unilateral or bilateral white lines on buccal mucosa at level of occlusal plane

technically a pathology because it's not found in all mouths; but not really considered clinical pathology, just a variation of normal tissue

Front 671

What are three examples of factitious trauma

Back 671

Factitious injury - self-induced (deliberate or non-deliberate)

Morsicatio buccarum - cheek

Morsicatio labiorum - lip

Morsicatio linguarum - tongue

Front 672

What can be observed clinically/histologically from morsicatio labiorum

Back 672

lip biting; considered a deliberate injury; clinical pathology, but no significant histological changes, just some acute inflammatory cells, no great tissue change

Front 673

What can be observed clinically/histologically from morsicatio buccarum

Back 673

cheek biting; more chronic in presentation than lip biting injury, may see tissue changes in biopsy

most chronic change is hyperplastic - see more epithelial cells than in normal tissue

Front 674

What are the four categories of bruising attributable to trauma

Back 674

Petechiae - pinpoint

Purpura - slightly larger than petechiae

Ecchymosis - true bruise; more than 2cm in diameter

Hematoma - large swelling, palpable

first three are macular, hematoma is raised (mass filled with blood)

Front 675

What happens if a bruise persists

Back 675

If it's a normal bruise related to trauma it should resolve on its own in a 10-14 days; if pathology lasts for more than a couple weeks, should determine cause, probably underlying systemic disease

Front 676

What are the three differential diagnoses for Petechiae and what tests do you do to determine the cause

Back 676

Trauma - take pt history, learn if it suggests trauma

Systemic - blood testing

Viral - add'l testing to rule out viral infection

Front 677

What are the most common causes and sites of Petechiae

Back 677

Trauma - forceful cough, bulimia, BJs

Systemic - coagulation type disorders (hemophilia, thrombocytopenia)

Viral infections - epstein-barr virus, mononucleosis; measles, HIV

Commonly occur on soft palate in oral petechiae

Front 678

What is a bruise

Back 678

trauma-induced extravasation of blood into surrounding tissues

Front 679

What are purpura, how do they differ from petechiae

Back 679

slightly larger area of subdermal or submucosal hemorrhage; can be induced by trauma, or by systemic disease (e.g. thrombocytopenia)

Front 680

What is an ecchymosis

Back 680

hemorrhagic accumulation of over 2 cm; usually induced by trauma with or without underlying systemic disease (e.g. hemophilia)

Front 681

What is the most common cause of intraoral ulceration

Back 681

Trauma

Front 682

What are non-specific ulcers, how do they occur and when do they usually heal

Back 682

intraoral ulceration caused by trauma; sudden onset, usually induced by a sharp cusp or restoration, fractured appliance, etc; non-specific because they have no distinct histologic features except ulceration of epithelium and acute/chronic inflammation

Front 683

What is an example of an ulcer that may persist for an extended period of time even with treatment

Back 683

Eosinophilic ulcer

Front 684

What is the clinical presentation of an eosinophilic ulcer

Back 684

irregular, solitary ulcer surfaced by a fibrinous membrane an surrounded by a zone of erythema; margins typically raised and indurated; may emanate pus; any mucosal surface may be affected, but tongue = ~60% of cases

Front 685

What can many cases of eosinophilic ulcers and reactive hyperplasias resemble

Back 685

Cancer

Front 686

How do eosinophilic ulcers appear histologically

Back 686

mixed inflammatory reaction - large mononuclear cells, numerous eosinophils, and lymphocytes

Front 687

What types of ulcers should ALWAYS be biopsied and what should the biopsy include

Back 687

Non-healing ulcers; differential diagnosis is trauma, infection, cancer

Biopsy of eroded or ulcerated area should ALWAYS include a portion of adjacent, intact epithelium

Front 688

What is the disease in which a form of eosinophilic ulcer develops in infants and why does this occur

Back 688

Riga-Fede disease; usually occurs on anterior ventral tongue; associated with developing anterior primary teeth and nursing; usually resolved by using a protective shield over damaged tissue

Front 689

What are often given to provide temporary relief/comfort when someone has an eosinophilic ulcer

Back 689

NSAIDs or topical anesthetics, topical corticosteroids with Orabase

Front 690

What are examples of caustic chemicals that dentists frequently use in clinical practice and what do they do

Back 690

Methyl methacrylate - keep component of acrylic (may develop contact dermatitis or contact stomatitis)

Sodium hypochlorite/bleach - used in root canal therapy (chemical burn)

Chemical burn lesions usually resolve without scarring in 10-14 days if patient discontinues use of agent; if necrotic - surgical debridement and antibiotics

Front 691

What is a common example of a thermal burn

Back 691

pizza burn - appears as area of erythema and ulceration with focal necrosis; usually heal within a few days

Front 692

What is an extreme example of a thermal burn and what occurs

Back 692

Electrical burn; Usually when mucosa contacts exposed wire; lips most frequently affected; involves charring of area, marked edema, and eventually necrosis; treatment includes tetanus immunization, antibiotics

Extensive scarring may develop during healing - microstomia (want to prevent this)

Front 693

What is nicotine stomatitis an example of and what occurs

Back 693

reactive hyperplasia; benign, asymptomatic condition of palate in smokers; develops in response to the heat generated by the tobacco product, not to the carcinogens; usually in pipe smokers (more heat); presents as red dots (dilated or obstructed salivary glands) and then gray-white papules (inflamed minor salivary glands); see hyperplastic, hyperkeratotic epithelium over mild, chronically inflamed CT; completely reversible if pt stops smoking, healing within 1-2 weeks

Front 694

What is denture-induced reactive hyperplasia

Back 694

result of ill-fitting dentures, bad denture hygiene or wearing dentures 24 hours a day; associated with Candida albicans; presents as multiple, asymptomatic erythematous papillary or papular projections in epithelium with underlying well-vascularized, very inflamed, fibrous CT; inflammatory response - lymphocytes and plasma cells; tx by denture removal, improved denture hygiene, reline/refabricate denture, topical anti-fungal, surgical excision if serious (don't misdiagnose as cancer!)

Front 695

What type of reactive hyperplasia is associated with Candida albicans

Back 695

Denture-induced

Front 696

What is an epulis fissuratum

Back 696

reactive lesion that develops in response to chronic irritation or trauma; induced by ill-fitting denture; more so in females; presents as asymptomatic, unilateral or bilateral folds of hyperplastic tissue in vestibules; typically clinically diagnostic but should be biopsied because could be carcinoma; dense hyperplastic, fibrous CT with hyperparakeratotic and hyperplastic epithelium; usually treat with surgical excision, also reline/refabricate denture

Front 697

What three lesion types are induced by ill-fitting dentures

Back 697

Denture-induced reactive hyperplasia

Epulis fissuratum

Leaf-like denture fibroma

Front 698

What is a leaf-like denture fibroma

Back 698

reactive lesion in response to ill-fitting denture; typically a flat, pedunculated, serrated mass on hard palate underneath max denture; dense, hyperplastic, fibrous CT with hyperparakeratotic and hyperplastic epithelium; surgical excision, reline/refabricate denture

Front 699

What is a reactive osseous and chondromatous metaplasia

Back 699

cutright lesion; in response to chronic mechanical denture irritation; presents as solitary, painful, tumor-like, exophytic growth, develops on atrophied alveolar ridge (usually posterior mandibular); tx: curative excisional biopsy, recontour/graft alveolar ridge, new denture; see metaplastic cartilage and bone

Front 700

What are some of the etiologic factors that can induce generalized gingival hyperplasia

Back 700

Local factors - plaque, calculus

Hormonal factors - puberty and pregnancy

Medications - phenytoin, cyclosporin, nifedipine (three most common causes of this disorder)

Leukemia

Hereditary factors

Front 701

How does generalized gingival hyperplasia present

Back 701

begins as marginal gingivitis, followed by enlargement of interdental papillae; erythema and edema due to superimposed inflammation; dental plaque and calculus/oral hygiene plays a huge role

tx: gingivectomy, good oral hygiene program, stop meds

Front 702

What are the four main examples of tumor-like reactive growth

Back 702

Irritation fibroma

Pyogenic granuloma

Peripheral ossifying fibroma

Peripheral giant cell granuloma

Front 703

What is the most common intraoral soft tissue growth

Back 703

Fibroma

Front 704

How do most fibromas develop

Back 704

In response to chronic irritation or trauma

Front 705

How does a fibroma usually present

Back 705

As a smooth surfaced, painless, sessile, nodular growth of varying size; similar or lighter color than surrounding mucosa; can become secondarily symptomatic; seen anywhere in oral mucosa; NO malignant potential

Front 706

How do most pyogenic granulomas develop

Back 706

reactive lesion in response to chronic irritation or trauma or altered physiologic condition; more so in females - possible hormonal influence

Front 707

How does a pyogenic granuloma present

Back 707

Polypoid, red, pedunculated mass that bleeds easily when touched; can grow rapidly and achieve large size within a few weeks; overlying mucosa ulcerated; usually see on gingiva, especially in pregnant women; periapical radiograph reveals cupping/pressure resorption of underlying alveolar bone; commonly on fingers and face; granulation tissue histology; recurrence common

Front 708

What is a variant of pyogenic granuloma that develops exclusively on the gingiva

Back 708

Epulis granulomatosum; grow out of recent extraction socket, may represent exuberant tissue response to an irritant

Front 709

What is a peripheral ossifying fibroma

Back 709

reactive lesion in response to chronic irritation or trauma; mainly in young adults/adolescents, more so in females; ONLY in gingiva, usually from interdental papilla

Front 710

How does a peripheral ossifying fibroma present

Back 710

red, sessile or pedunculated mass of varying size; usually present a number of weeks before noticed; usually ulcerated; radiopacity in radiograph; cupping/pressure resorption of underlying alveolar bone; dystrophic calcifications

Front 711

What is a peripheral giant cell granuloma

Back 711

benign, reactive lesion that develops in response to chronic irritating factors - tooth extraction, ill-fitting denture, calculus; usually 40-60 years old; more so in females; usually sessile; ONLY on gingiva/edentulous ridge; can be 2cm; ulceration secondary to trauma; cupping/pressure resorption on underlying alveolar bone

Front 712

How does a peripheral giant cell granuloma present histologically

Back 712

unencapsulated, richly cellular mass - abundant, scattered multinucleated giant cells; atrophic or ulcerated epithelium with significant intersitial hemorrhage; hemosiderin deposits; islands of metaplastic bone