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Head and Neck Pathology > FINAL EXAM Pathology D2 Fall > Flashcards

FINAL EXAM Pathology D2 Fall Flashcards

1
Q

The etiology of most diseases is ____________

A

multifactorial

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2
Q

Hypertrophy

A

Increase in cell SIZE (we want a BIG “trophy”)

physiologic or pathologic

caused by increased workload (functional demand) or by stimulation of trophic hormones

increased production of cellular proteins

Nondividing cell increased tissue mass

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3
Q

Hyperplasia

A

increase in cell NUMBER

physiologic or pathologic

happens in labile cells (cells that are capable of division)

Physiologic hyperplasia can be hormonal (increase in order to gain function) or compensatory (in order to fix damage)

Pathologic hyperplasia is caused by excess hormones or growth factors– may be at higher risk of malignant transformation (ex. enlargement of the prostate)

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4
Q

Metaplasia

A

Change in cell PHENOTYPE

One differentiated cell type (epithelial or mesenchymal) is replaced by another cell type

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5
Q

Necrosis is always __________, whereas apoptosis can be _________ OR _____________

A

Necrosis is always PATHOLOGIC, whereas apoptosis can be pathologic OR physiologic

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6
Q

Necrosis

A

different types described in other cards

If damage to membranes is severe, lysosomal enzymes enter the cytoplasm and digest the cell, resulting in necrosis
- LYSOSOMAL ENZYME RELEASE IS IRREVERSIBLE

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7
Q

Apoptosis

A

caspases and endonucleases degrade DNA and proteins… cells break into fragments (apoptotic bodies)…
phagocytosis of cell fragments

DNA damage is characteristic of APOPTOSIS but NOT necrosis

apoptosis is NOT a cell adaptation to stress (cell adaptations are reversible.. like hyperplasia)

Characterized by:
- nuclear dissolution
- fragmentation of the cell without complete loss of membrane integrity
- rapid removal of cellular disease

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8
Q

Reversible injury is characterized as cellular ___________ or ________ change

A

Reversible injury: cellular swelling or fatty change

Cellular swelling due to failure of energy-dependent ion pumps, loss of fluid homeostasis

Fatty change– occurs in hypoxic injury or toxic and metabolic injury. Seen in cells dependent on fat metabolism (hepatocytes and myocardial cells)

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9
Q

First manifestation of all forms of injury?

A

cellular swelling

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10
Q

Depletion of ATP

A

ATP depletion caused by reduced oxygen and nutrient supply, mitochondrial damage, and the actions of some toxins.

Decreased ATP causes:

  • failure of energy dependent sodium pump– there is influx of calcium and osmotic gain of water– cell swells
  • increased glycolysis
  • failure of calcium pump
  • ribosomes detach from rEr… decreased protein synthesis
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11
Q

Mitochondrial Damage

A

results in apoptosis OR necrosis

apoptosis occurs through the release of pro-apoptotic proteins (like Cytochrome C)

mitochondrial damage causes:
- decreased ATP
- increased ROS
- apoptosis or necrosis

Necrosis occurs with the formation of the mitochondrial permeability transition pore (depletes ATP)

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12
Q

Influx of Ca and loss of Ca2+ homeostasis

A

usually Ca inside cell is LOW

Ischemia and certain toxins cause Ca inside cell to be released, and later calcium influxes through plasma membrane

Calcium activates enzymes, including phospholipase, proteases, endonucleases, and ATPases

Induces apoptosis by activating cascades or increasing mitochondrial permeability

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13
Q

Accumulation of Oxygen-derived Free Radicals

A

Reactive oxygen species (ROS)– single unpaired electron in outer orbit

  1. lipid peroxidation in membranes– attach double bond of unsaturated fatty acids of cell membrane
  2. oxidative modification of proteins– alters activity
  3. lesions in DNA– free radicals can cause single and double strand breaks in DNA

failure of sodium and calcium pumps does NOT HAPPEN with ROS

ROS inactivated by antioxidants
- intracellular: superoxide dismutase, catalase, glutathione peroxidase
- extracellular: vitamins A, C, and E

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14
Q

Hypoxia

A

Reduced oxygen

Energy production may continue by anaerobic means (hypoxia can continue glycolysis)

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15
Q

Ischemia

A

secondary to reduced blood flow

reversible if oxygen is restored, but irreversible injury and necrosis can occur if ischemia continues

Delivery of substrates for glycolysis is compromised– ATP production STOPPED

Loss of ox phos– sodium pump fails, potassium is lost and water enters cell– cell swelling

loss of surface microvilli and blebs develop on the surface

mitochondria are swollen and ER are dilated

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16
Q

Irreversible Cell Damage… “Which would cause the most damage?”

A
  1. irreversible mitochondrial dysfunction
  2. disturbances in membrane function

leakage of intracellular enzymes and other proteins into the blood may provide an indication of cell death (like in myocardial infarction)

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17
Q

Cellular changes in necrosis

A
  • cell swelling
  • cytoplasm is glass, homogenous, and pink and may have vacuoles
  • nuclear changes (karyolysis, pyknosis, karyorrhexis)
  • cells die and release cytoplasm contents– induce inflammation and repair
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18
Q

Name the 6 types of necrosis

A
  1. coagulative
  2. liquefactive
  3. caseous
  4. fat
  5. fibroid
  6. gangrene (only a description word)
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19
Q

Coagulative necrosis

A

intact cellular membrane with NO NUCLEUS

most commonly associated with ischemic injury (irreversible ischemia)

localized area of coagulative necrosis is called an infarct

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20
Q

Liquefactive necrosis

A

enzymatic digestion until tissue is gone and only pus remains

due to release of lysosomal enzymes

major causes are bacterial infections and cerebral infarcts
- cerebral infarcts present similar to wet gangrene

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21
Q

Caseous necrosis

A

associated with M. tuberculosis (mycobacterial infection)

tissue appears white and “cheesy”

morphologically defined by caseating granulomatous inflammation

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22
Q

Fat necrosis

A

common in trauma to breast or pancreatitis

Adipose has chalky white-yellow appearance

dead adipocytes look like “soap bubbles”

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23
Q

Fibroid necrosis

A

associated with autoimmune disease affecting blood vessels
- ex. Lupus erythematosis

neither fibrous or fibrinous

like fibrin but is NOT fibrin– associated with immunoglobulin deposition and necrotic material within blood vessles

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24
Q

Gangrene

A

CLINICAL TERM (description word, not a technical necrosis type)

black necrotic tissue

Wet gangrene: liquefactive necrosis and bacterial infection

Dry gangrene: ischemia and coagulative necrosis (diabetics)

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25
Q

Anti-Apoptotic Proteins

A

BCL2

prevents apoptosis

BLC2 antagonists inhibit the apoptosis prevention… so pro-apoptotic proteins can destroy the cell

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26
Q

Pro-Apoptotic Proteins

A

BAX and BAK

promote outer mitochondrial membrane proteins

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27
Q

Types of Intracellular Accumulations (4 general… not specific substances)

A
  1. normal endogenous substance produced at a higher rate, but the metabolism isn’t high enough to remove it
  2. abnormal endogenous (usually because of mutated gene) accumulates because the body has no enzymes to degrade it)
  3. normal endogenous when there is an enzyme defect, so body can’t degrade it
  4. abnormal exogenous because the cell doesn’t know how to deal with it
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28
Q

Steatosis

A

Lipid accumulation (fatty change)

Abnormal triglyceride accumulation in parenchymal cells (normal endogenous substance at normal or increased rate, but rate of metabolism is not enough)– increased lipid synthesis and reduced breakdown

liver, heart, muscle, and kidney

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29
Q

Cholesterol Intracellular Accumulation

A

can see accumulations by intracellular vacuoles

Atherosclerosis– smooth muscle and macrophages of large arteries filled with lipid vacuoles (can see cholesterol under microscope)

Xanthomas– collection of lipid-laden macrophages (foamy cells)

Cholesterolosis– cholesterol-laden macrophages in the gallbladder

Neumann-Pick Disease– lysosomal storage disease because there is an enzyme deficit in processing lipids

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30
Q

Hyaline Change

A

only a descriptive term

alteration in cells or extracellular space that gives a homogenous, glassy, pink appearance

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31
Q

Glycogen Accumulation

A

glycogen masses appear as clear vacuoles within the cytoplasm

enzymatic defects cause glycogen storage diseases (problems with glycogen or glucose metabolism)

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32
Q

Pigment Accumulation

A

can be endogenous or exogenous (coal dust and amalgam tattoo would be exogenous)

LIPOFUSCIN– wear and tear pigment, polymer of lipids and phospholipids in complex with proteins (NORMAL CONSEQUENCE OF AGING)
- resists autophagy
- associated with free radical injury

Melanin– protective mechanism

Hemosiderin– hemoglobin derived pigment, major storage forms of iron (breakdown product of blood, plays a role in bruising)

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33
Q

Pathologic Calcification

A

Abnormal deposition of calcium salts with other small amounts of mineral salts

Dystrophic calcification– deposition occurs locally in diseased or dying tissues

Metastatic calcification– occurs in otherwise normal tissues, caused by HYPERCALCEMIA

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34
Q

Does apoptosis have inflammation?

A

NO– apoptosis does not have inflammation (no inflammatory infiltrates with apoptosis)

Necrosis, however, DOES have inflammation

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35
Q

Foreign bodies cause which type of inflammation?

A

Foreign body granulomatous inflammation/foreign body granuloma

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36
Q

TLRs are a “sensor for microbes”, and are located where?

A

TLRs are located in…
- plasma membrane
- endosomes
- cytoplasm

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37
Q

Inflammasomes

A

sense CELL DAMAGE

multiprotein cytoplasmic complex for recognition of products of dead cells

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38
Q

Edema vs. warmth/erythema

A

Edema is caused by leakage of exudate/plasma protein

Warmth/erythema (redness) is caused by increased blood flow due to dilation of microcirculation of the injured area

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39
Q

Vascular changes with Inflammation

A

increased blood flow and vasodilation (after transient vasoconstriction)

increased vascular permeability

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40
Q

Herpes infection is an example of ________ inflammation

A

Serous

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41
Q

Dental abcesses are an example of ___________ inflammation

A

Purulent

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42
Q

Which cell is recruited first during cell injury?

A

Neutrophils

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43
Q

Which proteins help mediate with leukocyte rolling and adhesion?

A

rolling– mediated by selectin family of adhesion molecules

adhesion– mediated by integrins (responsible for cytoskeletal protein interactions with ECM)

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44
Q

Diapedesis

A

extravasation of leukocytes

driven by PECAM-1 (CD31)

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45
Q

PECAM-1

A

cell adhesion molecule that drives DIAPEDESIS

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46
Q

What inflammatory mediators are involved in chemotaxis?

A
  • leukotriene B4
  • TNF
  • C5a
    (cytokines, bacterial products)

Chemotaxis is NOT mediated by kinins

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47
Q

Process of microcirculation events mediated by resident inflammatory cells?

A
  1. transient constriction
  2. dilation
  3. increased permeability
  4. leaving of exudate
  5. increase in blood viscosity and decrease in blood flow (blood viscosity increases because exudate is gone)
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48
Q

What molecule activates macrophages?

A

INF-𝛾

(secreted by helper T cells)

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49
Q

Papillon-Lefevre Syndrome

A

genetic disorder

Mutation in the cathepsin C gene, involved in skin development and inflammatory response

depressed blood neutrophil chemotaxis

gingivitis, loss of attachment and alveolar bone resorption

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50
Q

What cell contributes to the major production of histamine?

A

Mast cells

histamine is stored in mast cell granules

histamine dilates arterioles and increases venule permeability

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51
Q

What is the most important coagulation factor?

A

Thrombin

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52
Q

What do opsonins do?

A

They enhance recognition and attachment of PMNs

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53
Q

Which mediators are in charge of fever?

A

IL-1
TNF
Prostaglandins

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54
Q

What are the principal mediators for increased vascular permeability?

A

Histamine and serotonin
C3a and C5a (mast cells)
Leukotrienes C4, D4, E4

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55
Q

Chronic inflammation is associated with what process/pathway?

A

Fibrosis

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56
Q

Macrophage Types (M1 and M2)

A

M1: classically activated macrophages
- phagocytosis and killing of bacteria and fungi
- inflammation

M2: alternatively activated macrophages
- tissue repair and fibrosis
- anti-inflammatory effects

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57
Q

Examples of diseases demonstrating granulomatous inflammation

A

Tuberculosis
Leprosy
Syphilis
Cat scratch disease
sarcoidosis
Crohn’s disease

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58
Q

Systemic Effects of Inflammation

A
  • increased pulse and BP
  • decreased sweating
  • rigors (shivering)
  • chills (search for warmth)
  • anorexia
  • somnolence
  • malaise
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59
Q

Tissue Regeneration

A

100% recovery of lost or damaged tissue

proliferation of new cells to replace lost structures

ex. hematopoietic system and epithelia of the skin and GI tract renew themselves 24/7

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60
Q

Tissue Repair

A

combination of regeneration and scar formation (fibrosis)

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61
Q

Fibrosis

A

extensive deposition of collagen that occurs during repair (replacing parenchymal tissue with scar tissue)

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62
Q

Labile Tissue Differentiation

A

continuous division throughout life, replacing those that are destroyed

epithelial tissue, hematopoietic cells

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63
Q

Stable Tissue Differentiation

A

quiescent, which a low level of replication

liver, pancreas, kidney, bone, cartilage

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64
Q

2 examples of permanent tissues

A

cardiac muscle and neurons

(these are non-dividing cells)

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65
Q

Which stem cells have the easiest and hardest time differentiating?

A

embryonic stem cells have the greatest capacity to form the 3 tissue layers (easiest)

Adult stem cells have the hardest time differentiating

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66
Q

Integrins role in the cell cycle

A

integrins: interaction between cytoskeletal proteins and the ECM

the ECM then signals the division to happen and cytoskeletal proteins actually carry out the division

integrins from ECM activate transcription factors

integrins are “receptors for proliferation”

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67
Q

Cyclins and CDKs

A

progression through the cell cycle is regulated by cyclins and cyclin dependent kinases (CDK)

CDKs form interactions with cyclins in order to drive the cell cycle… CDK INHIBITORS block these interactions and therefore block the cell cycle

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68
Q

Epidermal growth factor (EGF) and transforming growth factor alpha (TGF⍺)

A

both share common EGFR receptor

mitogenic for epithelium, hepatocytes, and fibroblasts

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69
Q

Transforming growth factor beta (TGF-β)

A

considered FIBROGENIC

growth inhibitor for epithelial cells, strong anti-inflammatory effect

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70
Q

ECM structural proteins (3)

A
  • proteoglycans (like GAGs)– provide lubrication and resilience
  • fibrous structural proteins (collagen)
  • adhesive glycoproteins that connect matrix elements
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71
Q

Collagen development from procollagen is dependent on __________

A

Vitamin C

(so collagen development is affected with a Vit. C deficiency)

Remember tensile strength comes from collagen

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72
Q

What things give tissues expansion and recoil capabilities?

A

Elastin
Fibrillin
Elastic Fibers

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73
Q

Name the four families of cell adhesion molecules (CAMs)

A

immunoglobulin family

cadherins

integrins

selectins

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74
Q

Name some glycosaminoglycans and proteoglycans

A

heparin sulfate, chondroitin/dermatan sulfate, keratin sulfate and hyaluronan

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75
Q

Angiogenesis

A

VEGF is the most important growth factor in adult tissues undergoing angiogenesis

vasodilation is response to NITRIC OXIDE produced by macrophages, endothelial cells, etc.

Proteinases are important in tissue remodeling during endothelial invasion, and they cleave extracellular proteins, releasing growth factors like VEGF and FGF-2

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76
Q

2 types of “intention” for cutaneous wound healing

A

primary intention: cell basement membrane injury are limited and wound edges are approximated by surgical sutures

secondary intention: larger tissue defects such as an abscess or ulceration (results in greater scarring)

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77
Q

Proliferative phase of cutaneous wound healing

A

formation of granulation tissue, proliferation and migration of connective tissue cells

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78
Q

Granulation tissue

A

presence of new small blood vessels and proliferation of fibroblasts

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79
Q

Wound contraction occurs through which type of cell

A

Myofibroblasts

happens during maturation stage of cutaneous wound healing

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80
Q

Dehiscence

A

rupture of a wound

can be caused by inadequate formation of granulation tissue or assembly of a scar

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81
Q

Keloids

A

hypertrophic scars

excessive formation of repair components

more common in African Americans

82
Q

Exuberant Granulation

A

formation of excessive amounts of granulation tissue

83
Q

Desmoids

A

exuberant proliferation of fibroblasts that may rarely occur at the site of incisional scars or traumatic injuries

dense collagenous proliferation at site of surgical scars

84
Q

Contracture

A

exaggeration of the contraction of a wound that results in deformities of the would or surrounding tissues

commonly associated with serious burns

85
Q

Fibrosis

A

excessive deposition of collagen and other ECM components with decreased degradation

most commonly caused by CHRONIC DISEASE

major cytokine involved in fibrosis is TGF-beta

86
Q

Effusion

A

accumulation of fluid in body cavities (serial surface involvement)

87
Q

Inflammatory vs. Noninflammatory Edema and Effusion

A

Inflammatory– protein rich exudates accumulation due to increased vascular permeability

Non-inflammatory: protein poor transudates accumulation

88
Q

Transudate vs Exudate

A

transudate: only water leakage

exudate: protein AND water leakage (due to inflammation)

89
Q

Name some causes of Edema

A
  • venous obstruction
  • lymphatic obstruction
  • hepatic cirrhosis
  • congestive heart failure
  • DVT
  • renal disease/failure

Edema can be indicative of underlying cardiac or renal disease

90
Q

Ascites

A

effusion of the peritoneal cavity

malnutrition produced by severely inadequate amount of protein in the diet

pics of kids in other countries with big bellies (KWASHIORKOR)

91
Q

Hyperemia

A

an ACTIVE process

more blood entering (erythema)

arterial dilation– increased blood flow–erythema of affected tissue

ex. student develops red race from embarrassment

92
Q

Congestion

A

a PASSIVE process

resulting from reduced outflow– edema

cyanosis/hypoxia

Systemic (cardiac failure) or localized (venous obstruction)

93
Q

Chronic Pulmonary Congestion

A

thickening of the septa

heart failure cells: hemosiderin- laden macrophages, found in chronic pulmonary congestion

94
Q

Endothelin

A

transient VASOCONSTRICTOR
- does arteriolar vasoconstriction in hemostasis (blood clot formation)

95
Q

Tissue plasminogen activator (t-pA)

A

Fibrinolysis effect
- counterregulatory to blood clot stabilization and resorption

96
Q

Thromboxane A2 pathway

A

thromboxane A2 (TXA2) leads to platelet aggregation

ASPIRIN inhibits this pathway (so, aspirin can decrease thrombi formation in coronary arteries)

activation by thrombin and ADP

97
Q

Glanzmann thrombasthenia

A
  • deficit of fibrinogen binding to GpIIb-IIIa receptors
  • platelet doesn’t change shape so it doesn’t have a good affinity for fibrinogen
98
Q

Bernard-Soulier Syndrome

A

deficit of GpIb receptors so the platelet cannot adhere to vWF (no vWF means that GpIb has no ligand to trigger platelet adhesion)

99
Q

Prothrombin time (PT) assay

A

Assessing the function of the proteins in EXTRINSIC pathway

(2, 5, 6, 10, fibrinogen

100
Q

Partial thromboplastin time (PTT) assay

A

assessing the function of the proteins in INTRINSIC pathway

(2, 5, 7 ,9, 10, 11, 12, fibrinogen)

101
Q

Fibrinogen into fibrin is caused by….

A

Thrombin

102
Q

What inhibits t-pA?

A

Plasminogen Activator Inhibitor-1 (inhibits fibrinolysis)

t-pA activates fibrinolysis along with urokinase prourokinase

103
Q

What inhibits plasmin?

A

Alpha 2 antiplasmin

104
Q

Plasminogen deficiency

A

formation of excessive fibrin in the lamina propria at mucosal sites

CONJUNCTIVA: ligenous conjunctivitis

GINGIVA: ligneous gingivitis

**note: ligneous means excess fibrin

105
Q

Factors for development of THROMBOSIS (3)

A
  1. endothelial injury
  2. alteration in normal blood flow
  3. hypercoagulability (aka thrombophilia)
106
Q

Altered blood flow (stasis vs. turbulence conditions)

A

TURBULENCE:
- atherosclerotic plaque
- hyperviscosity
- deformed red blood cells

STASIS: aneurysms

107
Q

Most common cause of congenital thrombophilia?

A

Factor V leiden

primary (genetic) point mutation in the factor V gene and prothrombin

Protein C and S deficiencies are RARE causes of thrombophilia

108
Q

Patients with __________ are at a high risk for thrombosis

A

cancer
myocardial infarction
prolonged bed rest

109
Q

Factors putting patients at low risk for thrombosis?

A

oral contraceptive use
smoking
sickle cell anemia

110
Q

Lines of Zahn

A

at site of rapid blood flow that happened before death (ante mortem thrombus)

pale platelet and fibrin alternating with darker red cell-rich layers

111
Q

Ante mortem thrombi

A

dry, friable, mottled and attached to vessel wall in which they are formed

112
Q

Post mortem thrombi

A

not attached, gelatinous and have a dark red dependent portion where red cells have settled by gravity and yellow “chicken fat” upper portion

113
Q

What is the worst possible rate of thrombosis?

A

Embolism

114
Q

What is disseminated intravascular coagulation associated with?

A

SEPTIC SHOCK and DIC

complication of many conditions associated with systemic activation of thrombin–microvascular thrombi formation

115
Q

Most common form of thromboembolic disease?

A

Pulmonary embolism

(originated from DVT), associated with pulmonary hypertension and right ventricular failure

116
Q

Systemic thromboembolism– most come from what?

A

intracardiac mural thrombi

other origins are valvular thrombi, aortic aneurysms, or atherosclerotic plaques

117
Q

Fat and Marrow Embolism

A

embolism in lung after fracture of long bones and liposuction (ex. player fractures femur)

118
Q

Air Embolism

A

decompression sickness

gas bubbles in circulation lead to vascular obstruction

119
Q

Amniotic Fluid Embolism– mortality and morbidity mostly due to what?

A

activation of coagulation factors (DIC) rather than mechanical obstruction of pulmonary vessels

120
Q

Infarction

A

an infarct area is an area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage

result of embolism is infarction

121
Q

Red (Hemorrhagic) Infarcts

A

arterial or venous occlusion under conditions permitting accumulation of blood in damaged tissue

happens in tissues with multiple blood supplies (like the lungs)

122
Q

White Infarct

A

arterial occlusion in solid tissue with a single blood supply

could find white infarct in a coronary artery

123
Q

Shock associated with systemic inflammation

A

activation of cytokine cascade

peripheral vasodilation and pooling of blood

124
Q

Neurogenic shock

A

spinal cord injury and anesthetic complications

loss of sympathetic tone and peripheral pooling of blood

125
Q

Anaphylactic shock

A

generalized IgE mediated hypersensitivity leading to systemic vasodilation and increased vascular permeability

hypotension due to increased vascular bed capacity that cannot be adequately filled

126
Q

Nonprogressive stage of shock

A

initial stage in which reflex compensatory mechanisms (neurohumoral) are activated for maintenance of perfusion of vital organs

127
Q

Which type of T cells are the most important in the immune system?

A

T-helper cells

128
Q

What is the most important APC for initiating T-cell responses?

A

Dendritic cells

129
Q

What do the classic and alternate/lectin complement pathways deal with?

A

Classic pathway:
- ADAPTIVE immunity (antibodies)
- activated by antigen/antibody complex

Alternate/lectin pathway:
- INNATE immunity
- activated by microbes

130
Q

Are cytokines stored in cell vesicles?

A

NO– they are secreted, not stored in vesicles

131
Q

CD8+ recognize antigens on which MHC class?

A

MHC class I

132
Q

X-linked agammaglobulinemia (XLA, Bruton Disease)

A

Failure of pre-B cells to differentiate into B cells

Hereditary defect in Bruton tyrosine kinase (BTK) gene

normal T cell response because only B cells are affected…. treatment by replacement of antibodies

133
Q

DiGeorge Syndrome

A

developmental malformation of the 3rd and 4th pharyngeal arches
- this IS NOT ACQUIRED

absence of thymus and parathyroids, so there is deficient T cell maturation

infants are vulnerable to viral, fungal, and protozoal infections

facial structures will be underdeveloped (common cleft lip and palate)

134
Q

What attachment on HIV is necessary for CD4+ receptors?

A

CD4+ receptors must attach to gp120 on HIV

gp120 must also bind coreceptors CCR5 or CXCR4

p24 is NOT required

135
Q

What cells are able to be infected by HIV? (4)

A

all cells with CD4+ receptors:

microglia
macrophages
dendritic cells
T-helpers

136
Q

Type I hypersensitivity (IgE mediated)

A

mast cells release…
- vasoactive amines
- lipid mediators
- cytokines

ex. anaphylaxis, hay fever, food allergies

137
Q

Type II hypersensitivity (IgG mediated cytotoxic)

A

complement-dependent opsonization

Graves disease and erythroblastosis fettles

138
Q

Type III hypersensitivity (Immune complex-mediated)

A

antigen-antibody complexes are deposited in tissues, causing activation of complement, which attracts neutrophils

systemic lupus erythematosus and rheumatoid arthritis

139
Q

Type IV hypersensitivity (cell-mediated)

A

Th1 cells secrete cytokines that activate macrophages and cytotoxic T cells and can cause macrophage accumulation at the site

TB test results, granuloma, contact dermatitis
- these do NOT involve antibodies

140
Q

Anergy

A

functional inactivation of lymphocytes

type of peripheral self-tolerance

141
Q

Systemic lupus erythematosus

A

can cause RENAL FAILURE

erythematosus rash on face in butterfly pattern (molar regions of face)

sterile endocarditis (Libman-Sacks)… vegetations develop on margins of valve

autoantibodies specific for SLE present (different card)

142
Q

Autoantibodies specific for SLE? (2)

A

if they have either of these, they definitely have SLE

Anti-double stranded DNA

Anti-Sm (smith) antibody

only these are SPECIFIC to SLE.. SLE also has antinuclear antibodies, but they aren’t specific to the disease

143
Q

Sjogren Syndrome

A

autoimmune affecting the salivary and lacrimal glands

40 fold increase in LYMPHOMA

parotid gland enlargement in half of cases

primary sjogrens (sicca syndrome)– sjogrens alone… secondary sjogrens is sjogrens + another autoimmune disorder

treat with DMARDs (hydroxychloroquine, methotrexate)

144
Q

Sjogren Syndrome Antibodies?

A

Anti-SS-A (anti-Ro)– 70% positive

Anti-SS-B (anti-La)– 40% positive

rheumatoid factor and antinuclear antibodies

145
Q

Schirmer test

A

tests the tear production levels. less than 5mm in 5 min indicative of SJOGRENS

(small strip of paper placed on lower eye… tears bleed down the paper)

146
Q

Systemic sclerosis (scleroderma)

A

fibrosis of tissues, autoantibodies, and obliterative vascular disease

esophageal dysmotility (trouble swallowing)

Raynaud phenomenon

widening of PDL seen in panoramic radiograph

calcinosis, sclerodactyly, telangiectasia

Joint stiffness

LUNG FIBROSIS is a serious complication

skin changes noted first (thickening and tightening)

147
Q

Antibodies in systemic sclerosis

A

antinuclear antibodies (ANAs) usually present

target normal proteins in nucleus

systemic sclerosis has antitopoisomerase antibodies… also have anticentromeric antibodies

148
Q

Pemphigus (Pemphigus Vulgaris)

A

uncommon autoimmune blistering disorder

oral signs are most difficult to resolve.. “first to show, last to go”

Type II (antiboy mediated) hypersensitivity reaction
- IgG directed against epithelial desmosome complex (desmoglein 1 and 3)

intraepithelial cleating– loss of intercellular attachment due to IgG attaching epithelial desmosome complex

149
Q

Pemphigus Vulgaris immunofluorescence

A

Positive direct immunofluorescence (“fishnet” pattern)

Positive indirect immunofluorescence

(note: MMP has negative indirect immunofluorescence)

150
Q

Mucous membrane pemphigoid (MMP) (cicatricial)

A

type II hypersensitivity, antibodies attack basement membrane

may see intact BLISTERS intraorally (“4mm translucent vesicle of buccal surface”)

symblepharon– scarring of conjunctival mucosa (adhesions between inner surface of lid and eye)

151
Q

MMP immunofluorescence

A

POSITIVE direct immunofluorescence

NEGATIVE indirect immunofluorescence

(confirm MMP biopsy with DIRECT immunofluorescence)

152
Q

What type of tissue graft is LEAST likely to be rejected?

A

Autograft

153
Q

hyperacute tissue rejection

A

occurs within minutes

type II hypersensitivity

antibodies bind antigens on graft and activate complement and clotting systems– ischemic necrosis of graft

154
Q

How long before acute rejection happens to a transplant organ?

A

Days to weeks after transplant

(note: acute rejection is T-cell and antibody mediated)

155
Q

Chronic rejection of transplanted organ

A

occurs over months-years

T cells react against graft alloantigens presented by graft APCs

refractory to most therapies (NOT preventible with immunosuppressives)

156
Q

Graft-Versus Host Disease (GVHD)

A

associated with hematopoietic transplant (bone marrow transplant)– may show lesions and ulcers

** any time you see bone marrow transplant, it is most likely GVHD

immune cells from GRAFT TISSUE recognize the host as foreign and attack the host

157
Q

Amyloidosis

A

deposition of amyloid into the tissue

results in tissue damage and functional compromise – pathology behind morbidity and mortality of amyloidosis is “physical damage and function dysruption”

extracellular deposition of amorphous eosinophilic material

CONGO RED staining positive

158
Q

Expressivity

A

extent to which the inheritable trait is expressed (how “bad” it is)

some people can be diagnosed but not show disease characteristics (low expressivity)

159
Q

Pleiotropy

A

one gene controls multiple phenotypic characteristics

mutation in a pleiotropic gene may have widespread phenotypic effects (Marfan syndrome)

160
Q

Heterogeneity

A

production of similar phenotypic effects by 2 or more genetic loci… several different mutations may be responsible for the same disease state (breast cancer)

may present with a range of severity

ex. Tay-Sachs Disease

161
Q

Single nucleotide polymorphism (SNPs)

A

substitution of a single nucleotide base

type of point mutation

can be silent, nonsense, or missense

162
Q

How common are mendelian disorders?

A

RARE– only account for 1% of adult hospitalizations and 6-8% pediatric admissions

163
Q

Marfan syndrome

A

autosomal DOMINANT

defective extracellular glycoprotein (fibrillin) encoded by genes FBN1 or FBN2– connective tissue alterations

Abraham Lincoln had this

NOT associated with mental retardation

164
Q

Genetic diseases associated with mental retardation?

A
  • Down syndrome
  • Klinefelter
  • Fragile X
165
Q

Neurofibromatosis Type I (NF1) [Recklinghausen disease]

A

mutation of NF1 gene (tumor suppressor)

autosomal dominant
nearly 100% penetrance
highly variable expressivity

multiple neurofibromas
cafe-au-lait pigmentation
lisch nodules
axillary freckling (Crowe sign)
intellectual disability

**note: NF2 has bilateral acoustic neuromas, but this does NOT apply to NF1

166
Q

Autosomal Recessive Diseases characteristics

A

must be homogenous for trait to be expressed

parents usually not affected, siblings have 25% chance

affected individual likely a product of consanguineous partnering

167
Q

Cystic Fibrosis

A

3 nucleotide deletion in cystic fibrosis transmembran conductance regulator gene (CFTR)– disfunction of chloride ion channels

168
Q

Phenylketonuria (PKU)

A

lack of enzyme phenylalanine hydroxylase (PAH)

normal at birth, but severe intellectual disability evident by 6 months (brain damage occurs if untreated during the first month)

seizures and other neurologic abnormalities

distinct musty body odor

autosomal recessive

patients develop hyperphenylalaninemia and phenylketonuria

dietary restriction of phenylalanine

169
Q

Patients with PKU are on a dietary restriction of _______________________

A

phenylalanine

think of any amino acid uptake as dietary protein intake (ex. meat, eggs, and wheat all have high phenylalanine)

so PKU patients need a LOW PROTEIN DIET

170
Q

X- linked disorders

A

almost all are RECESSIVE and therefore only expressed in males

(ex. woman carrier for color blindness… children are:
1/2 females are carriers
1/2 males are colorblind)

females may show partial expression because of Lyon hypothesis– inactivation of one X chromosome in each cell (Barr body)

examples:
- hemophilia
- red/green colorblindness
- Duchenne muscular dystrophy
- Bruton’s agammaglobulinemia

171
Q

Structural abnormality– Deletions

A

loss of portion of chromosome

Ring chromosome: special form of deletion produced when the break occurs at both ends of a chromosome and the damaged ends fuse into a ring

172
Q

Trisomy 21 (Down syndrome)

A

most common chromosomal disorder

caused by meiotic nondisjunction

parents are genetically normal

10 to 20 fold increase of ACUTE LEUKEMIA (AML or ALL)

neuropathology changes characteristic of Alzheimer disease in patients older than 40

173
Q

Klinefelter syndrome

A

most patients are 47 XXY (at least 2 X chromosomes and one or more Y)

nondisjunction of sex chromosomes during meiosis

małe hypogonadism

gynecomastia
-20x increased incidence of breast cancer

oral manifestations: taurodontism (body of tooth is really big and roots are small… apically altered furcations and pulp chambers)

mild to no intelectual impairment

174
Q

Turner syndrome

A

partial or complete monosomy of short arm of X chromosome

typically 45 X karyotype (entire X chromosome missing)

webbing of the neck (from distended lymph nodes)

lack of secondary sex characteristics

175
Q

Fragile X syndrome is a ______________ _____________ mutation

A

triple repeat

(mutation in the FMR1 gene located on Xq27.3)

176
Q

Mitochondrial genetic diseases

A

MATERNALLY INHERITED ONLY (mutations in mitochondrial genes ONLY passed by the mother)

primarily affects organs dependent on ox phos (brain, skeletal muscle, heart, liver, kidney)

177
Q

Genomic Imprinting Diseases

A

disease arising from inactivation of maternal or paternal genes during gametogenesis (genomic imprinting)

imprinting means inactivation of that parent’s allele

some genes are expressed differently depending on maternal or paternal

178
Q

Prader-Willi syndrome

A

deletion in PATERNALLY derived 15q12 region

179
Q

Angelman syndrome

A

deletion in MATERNALLY derived 15q12 region

180
Q

Malformation

A

primary errors of morphogenesis, usually multifactorial with a genetic basis

181
Q

Disruption

A

secondary destruction of an organ/body region that was previously normal in development

182
Q

Deformation

A

localized or generalized compression of the growing fetus by abnormal biomechanics forces

183
Q

Most transcervical perinatal infections are ______________

A

BACTERIAL (ex. streptococcal infection)

there are a few caused by viruses

these are acquired in utero or during birth

184
Q

Choristoma

A

pediatric neoplasm

microscopically normal cells/tissues in abnormal location

185
Q

Hamartoma

A

excessive, focal overgrowth of cells/tissue native to that organ

186
Q

Benign pediatric neoplasms? (3)

A

nevus flammeus (port wine stain)

hemangioma

lymphangioma

187
Q

Nevus Flammeus

A

aka port wine stain

benign pediatric neoplasm

rarely fades with age

most often on face but may be anywhere on body

188
Q

Hemangioma

A

most common tumor of infancy

rapid enlargement followed by gradual recession (likely to spontaneously regress by age 9)

189
Q

Lymphangioma

A

benign pediatric neoplasm

proliferation of lymphatic channels

50-75% in head and neck

190
Q

Malignant pediatric neoplasms? (3)

A
  • neuroblastoma
    -Wilms tumor (nephroblastoma)
  • retinoblastoma
191
Q

Which neoplasms are more common in CHILDREN?

A

leukemias
CNS tumors
rhabdomyosarcoma
neuroblastoma
retinoblastoma

192
Q

Sustaining proliferative signaling

A

one of the hallmarks of cancer

sulf-sufficiency in growth signal: cells have capacity to proliferate without external stimuli due to oncogene activation

mutation/overexpression of port-oncogenes

193
Q

TP53 gene

A

most common tumor suppressor gene

guardian of the genome, most common target for mutations in human cancers

cell proliferation is NOT a function of p53, because it is a tumor suppressor

p53 slows or inhibits cell cycle progression (senescence.. permanent cell cycle arrest, G1 arrest is temporary)

194
Q

Telomere

A

repeated nucleotides at the end of each chromosome

escape of cancer cells from senescence and mitotic catastrophe caused by telomere shortening (because they reactivate telomerase)

195
Q

Are initiators alone enough to induce tumor growth?

A

NO

initiation = exposure of cells to a sufficient dose of carcinogenic agent, making it POTENTIALLY capable of giving rise to a tumor

196
Q

Viruses that can cause oropharyngeal SCC

A

human papilloma virus (HPV… 16 and 18)

197
Q

These classes of medications would be more effective when designing a drug for OSCC:

A

inhibit VEGF binding to receptors on endothelial cells

inhibit type IV collagenase

inhibit lymphangiogenesis

198
Q

Which are classified as Paraneoplastic syndromes? (4)

A

Disseminated intravascular coagulation (DIC)

Cushing syndrome (endocrinopathies)

paraneoplastic autoimmune multiorgan syndrome (PAMS) (Paraneoplastic pemphigus)

acanthuses nigricans

199
Q

Are tumor markers specific? Can they be used for definitive diagnosis?

A

Tumor markers are NOT SPECIFIC and CANNOT be used for a definite diagnosis

200
Q

Examples of tumor markers?

A

hormones (calcitonin)

oncofetal antigens

specific proteins (prostate specific antigen, PSA)

cell-free DNA markers

201
Q

Cancer prognosis… which is most important– grade, stage, or type

A

type > stage > grade

Head and Neck Pathology (3 decks)

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