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Pathology > 1st Exam > Flashcards

1st Exam Flashcards

1
Q

Mediators of vasodilation:

A

Protoglandins, NO, Histamine, and C3a and C5a

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2
Q

mediators of increased vascular permeability:

A

histamine, sreotonin, C3a and C5a, Bradykinin, Leukotrienes C4, D4, E4, PAF, Substance P, prostaglandin

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3
Q

mediators of chemotaxis:

A

C3a and C5a, Cytokines TNF, IL-1, Leukotrienes B4 (LTB4), Bacterial Products, chemokines, IL-8

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4
Q

mediators of fever:

A

prostoglandins, cytokines TNF, IL-1

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5
Q

mediators of pain:

A

prostoglandins, bradykinin, substance P

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6
Q

mediators of tissue damage:

A

NO, Lysosomal enzyes, ROS Chemokines

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7
Q

Effects of prostoglandin:

A

fever, pain, vasodilaiton, increased vascular permeability (at least PGD2 and PGE2)

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8
Q

Effects of NO:

A

Tissue damage, vasodilation

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9
Q

Effects of histamine:

A

Vasodilation, increased vascular permeability

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10
Q

Effects of serotonin:

A

increased vascular permeability, vasod, and vasoc (if injury to bv, primary hemostasis, clotting)

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11
Q

Effectes of C3a, C5a:

A

vasodilation, increased vascular permeability, chemotaxis

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12
Q

Effects of bradykinin:

A

increased vascular permeability, pain, (vasod and bronchial sm contraction?)

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13
Q

Effects of Leukotrienes C4, D4, and E4:

A

Increased vascular permeability

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14
Q

effects of PAF:

A

Increased vascular permeability, aggregate platelets, degranulation (release of pre-formed mediators), bonchoconstriction, vasod (1000 X more than histamine), chemotaxis of inflammatory cells

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15
Q

Effects of Substance P

A

Increased (LL says modulate), vascular permeability, pain, regulate vessel tone, stimulate cytokine P and R

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16
Q

Effects of cytokines TNF, IL-1:

A

chemotaxis, fever

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17
Q

Effects of Leukotrienes B4:

A

chemotaxis:

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18
Q

Effects of Bacterial products:

A

chemotaxis

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19
Q

Effects of lysosomal enzymes:

A

Tissue damage

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20
Q

Effects of ROS:

A

Tissue damage

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21
Q

Effects of chemokines:

A

chemotaxis and tissue damage

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22
Q

Paraneoplastic syndrome(s) assoc w lung small cell anaplastic (oat cell) carcinoma:

A

Cushing Syndrome, Hyponatremia

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23
Q

Paraneoplastic syndrome(s) assoc w various carcinomas:

A

Troussea Syndrome, hypoglycemia

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24
Q

Paraneoplastic syndrome assoc w Lung ssc:

A

hypercalcemia

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25
Q

Paraneoplastic syndrome assoc w renal cell carcinoma:

A

polycythemia (increased concentration of hemoglobin)

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26
Q

Paraneoplastic syndrome assoc w metastatic malignant carcinoid tumors;

A

Carcinoid syndrome

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27
Q

Mechanism of Cushing Syndrome (cortisol levels too high cause CS):

A

ACTH-like substnace

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28
Q

Mechanism of hypercalcemia:

A

PTH-like hormone

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29
Q

Mechanism of hyponatremia:

A

innappropriate ADH secretion

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30
Q

Mechanism of polycythemia:

A

erythropoeitin-lke substance

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31
Q

Mechanism of Trousseau syndrome:

A

hypercoagulable state

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32
Q

Mechanism of hypoglycemia:

A

insulin-like substance

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33
Q

Mechanism of carcinoid syndroe

A

5-hydroxy-indoleacetic acid

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34
Q

15% of ppl w dermatomyositis get:

A

carcinoma of lung, ovary, breast

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35
Q

Tumor assoc w migratory venous thrombosis:

A

pancreatic carcinoma

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36
Q

Tumor assoc w Myasthenia gravis:

A

thymoma, thymus tumor

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37
Q

dermatomyositis:

A

heliotropic (directs toward the sun) rash on malar (cheek) surface of face, ai disease, inflammatory, affects bv, m atrophy

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38
Q

PSA is a marker for:

A

Prostate cancer

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39
Q

AFP is a marker for:

A

Hepatocellular carinoma

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40
Q

CEA is a marker for:

A

colon carcinoma

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41
Q

hCG is a marker for:

A

choriocarcinoma, tumor of uterus, originates from chorion of fetus (human chorionic gonadotropin)

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42
Q

PLAP is a marker for:

A

Seminoma, malignant tumor of testis (balls fFLAP) (from primordial germ cells of sexually undifferentiated embryonic gonad. (I thought -‘oma’ ‘s were benign?)

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43
Q

Health issues that cause chronic inflammation:

A

persistent infections/toxins, ai disorders

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44
Q

4 pw acute inflammation can go down:

A

CHAR: Chronic, Healing, Abscess, Resolution

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45
Q

Histamine is released by:

A

mast, basophils, and platelets

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46
Q

2 main descriptors of inflammatory mediators:

A

pleiotropic and redundant

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47
Q

Why do we need so many mediators with overlapping effects?

A

they are all short lived, leads to amplification

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48
Q

From where are mediator derived?

A

cell or plasma

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49
Q

7 cell derived mediators:

A

VAN PELCC: Vasoactive amines, neuropeptides, prostaglandins, enzymes, leukotrienes, cytokines, chemokines,

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50
Q

3 plasma-derived mediators of inflammation:

A

complement, coagulation, and kinin systems (3 ‘C’ sounds) mp

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51
Q

2 vasoactive amines:

A

histamine and serotonin

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52
Q

Preformed mediators:

A

Vasoactive amines (histamine, serotonin) and leukocyte lysosomal enzyme

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53
Q

3 neutral proteases:

A

elastase, collagenase, cathepsin (endopeptidase found in most cells, autolysis and self-digestion of tissues)

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54
Q

Major sources of newly formed mediators:

A

leukocytes, mast cells, endothelial cells, platelets (LMEndoP)

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55
Q

How are newly formed mediators removed from body?

A

enzymes or spontaneous decay

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56
Q

This liberates AA from the cell if there is cell injury (cell membrane I think):

A

phospholipase

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57
Q

2 pathways for AA metabolism:

A

cyclooxygenase and 5-Lipoxygenase

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58
Q

cyclooxygenase pw to metabolize AA:

A

Thromboxane A2: vasoc, platelet agg/ Prostacyclin: vasod, inhibit platelet agg/ PGD2 and PGE2: vasod, inc perm/ pain and fever

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59
Q

5-Hete:

A

Part of 5-Lipoxygenase pw to breakdown AA, recruits inflammatory cells via chemotaxis

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60
Q

5-Lipoxygenase pw of AA metabolism:

A

5-Hete: recruits inflammatory cells, leukotrienes A4-E4: asthma and increased vascular permeability, Lipoxin A4, B4: inhibits neutrophil adhesion and chemotaxis

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61
Q

Acids besides AA being metabolized via this pw:

A

Omega 3 and 6 fatty acids

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62
Q

Group of natural antiinflammatory mediators:

A

resolvins, natural antagonists to prostaglandins

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63
Q

Why do steroids decerase inflammation?

A

prevent liberation of AA

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64
Q

2 cyclooxygenase inhibitor (Cox-1, Cox-2):

A

aspirin (NSAIDS), indometacin

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65
Q

Newly synthesized mediators of inflammation:

A

AA, PAF, cytokines, chemokines, neuropeptides, ROS, NO (CNNCRAP)

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66
Q

PAG is aka:

A

AGEPC

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67
Q

PAF is derived from:

A

phospholipid

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68
Q

Sources of PAF:

A

platelets, PMN, mast cells, macros, endothelium (PPEMM)

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69
Q

What liberates PAF?

A

activation of phospholipase A2

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70
Q

Families of cytokines:

A

lymphokines, monokines, chemokines, interleukins, interferons (3 kines and 2 I’s)

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71
Q

4 major cytokines in acute inflammation:

A

TNF, IL-1, IL-6, and chemokines

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72
Q

Major cytokines of acute inflammation are produced by (3):

A

macros, mast cells, endo cells

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73
Q

Major cytokines in chronic inflammation:

A

IL-12, INF-gamma

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74
Q

Effect of IL-1 and 6 on liver:

A

production of acute phase proteins

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75
Q

Effect of IL-1 and 6 on brain:

A

fever

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76
Q

Effect of IL-1 and 6 on bone marroe:

A

Wbc production

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77
Q

3 Systemic protective effects of acute inflammation (IL-1 and 6):

A

fever, wbc production, and acute phase protein production (TNF also promotes fever and wbc prod)

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78
Q

5 Pathological systemic effects of TNF:

A

low heart output, hypertension, shock, thrombus formation, insulin resistance of skeletal muscle (IL-1 also causes insulin resistance)

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79
Q

5 Systemic mani of inflammation:

A

fever, leukocytosis, inc acute-phase proteins, decrease apetite, inc sleep (FLAPPAS)

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80
Q

4 Fxn of chemokines:

A

wbc recruitement, cellular organization, active (sic?) leukocytes, regulate cell trafficking

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81
Q

How do chemokines interact with cells?

A

receptors

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82
Q

2 newly synthesized neuropeptides:

A

sub P and calcitonin gene related protein (CGRP)

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83
Q

Neurogenic inflammation occurs when these are activated:

A

neuropeptides (transmit pain)

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84
Q

Effect of CGRP

A

(Calcitonin gene related protein) vasod, pain

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85
Q

Sources of ROS:

A

activated PMN’s and macros

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86
Q

How are ROSs synthesized?

A

NADPH oxidase pw

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87
Q

Effect of low level secretion of ROS:

A

inc chemokine, cytokine, adhesion molecule expression

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88
Q

Effect of high level secretion of ROS:

A

endothelial damage, inc perm, protease activation, antiprotease inactivation

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89
Q

What limits the toxicity of secreted ROS?

A

endogenous antioxidant mechanisms

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90
Q

NO is found in:

A

endo cells, macros

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91
Q

System(s) activated by Hageman factor:

A

Complement, Kinin-Bradykinin, Coagulation (all 3 plasma mediators of inflammation)

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92
Q

Fxn of plasma-protein derived mediators of inflammation:

A

inc perm, vasoactive

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93
Q

This activates fibrinogen:

A

thrombin

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94
Q

2 ways to activate the complement cascade:

A

plasmin or kallikrein (not hageman factor?)

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95
Q

Endogenous antimediators that “stop” inflammation:

A

antioxidnats, lipoxins, protease inhibitors (PAL)

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96
Q

This interleukin inhibtis TNF:

A

IL-10

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97
Q

These interleukins promote repair:

A

IL-2, IL-4

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98
Q

WHat do NSAID’s do?

A

block COX-1 and Cox-2 (from making PG’s)

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99
Q

What do steroids do?

A

prevent AA release by PLA2

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100
Q

What do Etanercept and Infiximab do?

A

block TNF (RA and Crohn’s)

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101
Q

Causes of infection (inflammation?)

A

physical, chemical, infection, immune reaction, ischemia

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102
Q

Type of inflammation depends on:

A

chronology and pathology

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103
Q

Vasoactive mediators that cause gaps due to endothelial contraction:

A

histamine, leukotrienes, etc.

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104
Q

4 mechanisms of inflammation permeability:

A

endothelial gaps, necrosis/apoptosis, leukocyte-dependent injury, transcytosis

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105
Q

Selectins are involved in these cellular events:

A

rolling, activation (P, E, and L selectins_)

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106
Q

Integrins/Immunoglobulins are involved in these cellular events:

A

activation, adhesion

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107
Q

PECAM-1 is involved in this cellular event:

A

transmigration (synonymous with transcytosis?)

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108
Q

List of integrins/Immunoglobulins involved in cellular events:

A

MAC 1, ICAM 1, VCAM-1, LFA 1, VLA-4

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109
Q

These recognize sialylated carbohydrate groups:

A

selectins

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110
Q

This selectin is stored in Weibel–Palade bodies of endothelial cells:

A

P selectin

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111
Q

This selectin is not produced under normal conditions:

A

E selectin

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112
Q

These are the ligands to the homing receptors of lymphocytes and determine which tissues the lymphos will enter next:

A

addressins

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113
Q

Plays a key role in removing aged neutrophils from body:

A

PECAM-1 (involved in transmigration)

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114
Q

4 major groups of adhesion molecules:

A

selectins, addressins, integrins, immunoglobulin superfamily

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115
Q

Mechanism of acute inflammation molecule adhesion:

A

P and E selectin (ELAM-1), then ICAM-1 bind Lewis X (CD15) on WBC’s (check, I think ICAM-1 bonds something else)

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116
Q

What cause P seletins to be expressed on endothelial cell surface?

A

thrombin (or histamine?) act on W-P (Wiebel-Palade) bodies on the bvs, leads to inflammation (vWF is also store in W-P bodies, homeostasis)

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117
Q

Where is L selectin expressed?

A

lymphocyte

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118
Q

Mechanism of chronic adhesion molecules:

A

CD34 (w Lewis X on it) binds L-selectin (on lymphos), ICAM-1 binds CD18 (lyphos and monos), and some acute adhesion molecules

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119
Q

PECAM is involved in:

A

transmigration (diapadesis)

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120
Q

PECAM is aka:

A

CD31, on both endo and lymphos

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121
Q

How does PECAM pierce the basement membrane to allow diapadesis of the WBC?

A

collegenase

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122
Q

How does a cell relocate during chemotaxis?

A

by binding ecm

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123
Q

Chemotactic pw:

A

C5a binds G-protein CR, phospholipase C which activates both phosphatidyl-inositol bisphosphate and inositol 3-phosphate, I3P then increases Ca2+, actin and myosin build and aide in motility, inc number and affinity of adhesion molecules

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124
Q

Bradykinin is broken down via:

A

kininases

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125
Q

Where are the mediators for the cascading enzyme systems synthesized?

A

liver

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126
Q

How is fibrin broken down?

A

plasminogen cascade

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127
Q

How to determine if there is a clot somewhere in he body via blood draw?

A

look for fibrin split products

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128
Q

Activators of Hageman factor(4):

A

platelets, necrosis, collagen, bm

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129
Q

Increased intracellular Ca+ concentration can lead to:

A

Inc expression of endonuclease (DNA), ATPase (energy), protease (protein) , phospholipase (membrane)

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130
Q

Trigger formation of the inflamasome:

A

bacterial endotoxins, necrosis, cytokines

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131
Q

Function of the inflamasome:

A

activate proteases

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132
Q

Function of pyrin:

A

antiinflammatory

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133
Q

Function of corticosteroids:

A

block AA synthesis (blocking inflammation) (and steroid prevent the release from the lipid membrane…?)

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134
Q

4 major groups of antiinflammatory drugs:

A

antihistamines, corticosteroids, NSAIDS, Leukotriene drugs

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135
Q

Function of Leukotriene drugs:

A

5-lipoxygenase inhibitors (zileuton), LT receptor antagonist (Accolate)

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136
Q

Cells of acute and chronic inflammation:

A

acute: polys, chronic: lymphos, macros, and plasma

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137
Q

Sub-acute inflammation is characterised by:

A

polymorphous granulation tissue

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138
Q

Specific causes of granulomatous inflammation:

A

TB, fungus, sutures, syphilis

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139
Q

Contributes to the formation of granulomas:

A

IL-4 (Th2 cells)

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140
Q

water + mucus, nasal discharge:

A

catarrhal

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141
Q

Pus + polys:

A

purulent

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142
Q

pseudomembranous:

A

dead cells + polys

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143
Q

governs the increased production and release of neutrophils from the marrow during inflammation:

A

IL-1 and TNF

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144
Q

Normal WBC count:

A

4,500-11,000 cells/mm^3

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145
Q

Blood test for inflammation or leukocytosis:

A

WBC differential count

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146
Q

Causes of neutrophilic leukocytosis:

A

infection, inflammation, necrosis

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147
Q

Shift to the left:

A

BM cells release immature forms of polys

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148
Q

Lymphocytic leukocytosis:

A

polys aren’t increased, chronic inflammatory process, ie TB, viral diseaese

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149
Q

This type of leukocytosis is common with allergic reactions, parasitic infections:

A

eosinophilic leukocytosis

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150
Q

3 types of leukocytosis:

A

neutrophilic lymphocytic, eosinophilic

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151
Q

4 ex of acute phase reactants:

A

Fibrinogen, globulins, CRP, protein SAA (transport cholesterol to liver for secretion into bile, recruit immune cells to inflammatory sites, induce enzymes that degrade ECM)

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152
Q

How to test for bacterial inflammation:

A

Blood PCT level (procalcitonin)

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153
Q

Is CRP elevated in acute or chronic inflammation?

A

Both

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154
Q

When would blood ESR level be high?

A

Infection and systemic inflammatory disease (erythrocyte sedimentation rate, nonspecific test for inflammation)

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155
Q

ESR results that indicate inflammation:

A

RBC travel further than 20mm

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156
Q

Prime stimulant of CRP:

A

IL-6

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157
Q

CRP is produced here:

A

liver

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158
Q

Elevated blood SAA levels indicate:

A

chronic infammatory disease

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159
Q

Protein SAA is stimulated by:

A

IL-1 and TNF (if these are mediators of acute, do they decrease in numbers once protein SAA identification initiated? I would have thought they would need to be present for continued expression of P SAA)

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160
Q

Protein SAA has a tendency to form:

A

fibrils (amyloidosis), diagnose with congophilic dyes

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161
Q

Calcitonin is made by these cells:

A

C cells of thyroid gland

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162
Q

When does granulation tissue form?

A

as inflammation subsides

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163
Q

Granulation tissue is composed of:

A

proliferating capillaries, fibroblast, and myofibroblasts, amorphous ECM, and macros

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164
Q

Sitmulate angiogenesis:

A

VEGF and betaFGF (made by macros, betafibroblast growth factor)

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165
Q

Activates the transcription of VEGF and B-FGF

A

hypoxia-induced factors (HIF)

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166
Q

These are responsible for wound contraction:

A

myofibroblasts derived from pericytes

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167
Q

Amorphous ECM is made by, and contains lots of:

A

fibroblasts, glucosamines looks acellular

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168
Q

Function of HIF:

A

induce VEGF and BFGF

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169
Q

Effects of VEGF and BFGF:

A

proteolysis of ECM, migration, chemotaxis, proliferation of endo cells, lumen formation, maturation and inhibition of growth, and increased permeability (gaps and transcytosis)

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170
Q

Antagonist of Angiopoietin 1:

A

Angiopoietin 2, tube regression

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171
Q

How does granulation tissue become scar tissue?

A

Organization of fibroblasts and collagen fibrils in tissue

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172
Q

Scars form through:

A

the remodelling of granulation tissue

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173
Q

How is granulation tissue broken down?

A

matrix metalloproteinases

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174
Q

2 inhibitors of angiogenesis:

A

angiopoietin 2 adn angiostatin

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175
Q

Wound contraction starts at day __ and usually ends by day__:

A

3, 30

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176
Q

Granulation tissue starts to form at day __ and usually ends by day__:

A

0.3, 10

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177
Q

How long does it take for inflammation to start?

A

about 0.1 days: 2.4 hrs

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178
Q

Early wound collagen is Type __ and late wound collagen is converted to type __

A

III, I

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179
Q

Which type of collagen is stronger, Type I or Type III?

A

I

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180
Q

dehiscence:

A

Reopening of wound, esp. scar tissue

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181
Q

Stages of skin wound healing:

A

blood clot, dries, scab, polys, macs, granulation tissue, scar (dermis forms),

182
Q

These would be present around a wound 3-7 days after injury:

A

granulation tissue, macs, fibroblasts, new caps

183
Q

How much faster do oral wounds heal than other wounds?

A

2-3 times faster

184
Q

This, found in saliva, speeds mucosal redeneration:

A

histatin

185
Q

Special types of wound healing:

A

fibrosis wo granulation tissue, tumor encapsulation, liver cirrhosis, hyalinized granuloma

186
Q

What is cirrhosis?

A

fibrotic processes bw columns of liver cells

187
Q

Complications of normal wound healing:

A

excessive granulation tissue, excess scar, defective scar, dystrophic calcification

188
Q

Ex of excessive granulation tissue formation:

A

pyogenic granuloma

189
Q

Hypertrophic scar:

A

keloid

190
Q

Stimulus for dystrophic calcification (calcium where you don’t want it)

A

atherosclerosis, aging heart valve, granulomas, tumors

191
Q

Local causes of delayed wound healing:

A

Infection, poor blood supply, foreign material, type/ size/ location of wound

192
Q

Which heals slower, heart or skin?

A

heart

193
Q

Systemic causes of delayed wound healing:

A

age, diabetes, diet (DAD)

194
Q

Antimicrobial, painted on wound, retards bacterial growth:

A

silvadene (silver)

195
Q

bandage with growth factors to stimulate healing:

A

smart dressing

196
Q

Take this from a pt to speed their healing of a wound:

A

PRP (platelet-rich plasma)

197
Q

How can oxygen and pressure be used to speed healing?

A

negative pressure, hyperoxygenated

198
Q

When to order a liver function test:

A

surgical procedures

199
Q

Normal CK levels:

A

38-174 (creatinine kinase)

200
Q

Where in the body is CK present?

A

heart, brain, muscle (run marathon, creatinine kinase elevated)

201
Q

How long does it take for CK levels to peak and return to normal?

A

24h, 5 days

202
Q

Results win __ standard deviations are considered ‘normal.’

A

2 SD’s, 5% will be abnormal (check, I thought 5% would come back as abnormal, despite being normal)

203
Q

TF? Mutations in one gene will always cause the same type of cancer.

A

F. Cancer is gene specific, mutations in one gene can cause many different types of cancer.

204
Q

Most common cancers:

A

breast, uterine, lung, colon (BULC, the bulk of cancers are…)

205
Q

What type of skin cancer is on the highest incidence list?

A

melonama

206
Q

Japan has a high incidence of __ cancer.

A

stomach

207
Q

Cancer is most likely do to:

A

environmental influence, esp. food, no pollutants

208
Q

Fraction of cancer we get that is random and unpredictable:

A

2/3

209
Q

Tobacco is a major player in these cancers:

A

lung, kidney, bladder

210
Q

These food increase risk for bowel, pancreas, breast, and prostate cancers:

A

high fat, low fiber, fried, broiled

211
Q

3 ex of inherited cancers:

A

breast (Brc1, Brc2, prevelant in Ash Jew), colon/ rectal cancer, skin cancer (XP), retinoblastoma (Rb)

212
Q

Diff bw carcinogen and mutagen:

A

Car: anything that causes, mutagen: chemical that causes, so a mutagen is a carcinogen

213
Q

Cancer begins as:

A

a single cell clone, mutation in a specific gene in a specific cell

214
Q

TF? Proto-oncogenes are abnormal genes that will eventually lead to cancer.

A

F. Normal genes

215
Q

Do oncogenes gain or loose activity.

A

Gain (check)

216
Q

Define lose activity:

A

can not supress gene expression

217
Q

This is a test for mutagens:

A

Ames test

218
Q

As long as these are working, you will not get severe cancer:

A

tumor suppressor genes

219
Q

When we first turn on cell growth and cell division we activate

A

cyclin D, activates CDK

220
Q

This stops division if anything is going wrong in G1 phase:

A

p53

221
Q

What occurs during S phase:

A

DNA and histone synthesis

222
Q

The cell cycle is regulated by:

A

cyclins and CDK’s

223
Q

When are cyclins made and destroyed in cell cycle?

A

Destroyed: end of phase they were used in, Made: End of previous phase

224
Q

The longest phase of the cell cycle:

A

G1, protein synthesis/ cell growth

225
Q

Where is the first major checkpoint in the cell cycle?

A

end of G1 phase, if cancerous, tsg would stop the cycle

226
Q

What turns on the cell cycle?

A

D-CDK

227
Q

What turn on the synthesis of DNA?

A

E-CDK

228
Q

TF? Most cells can divide.

A

F.

229
Q

What cells normally do not divide?

A

organ cells: brain, liver, kidney

230
Q

How do pathologist diagnose cancer?

A

less differentiated or undifferentiated

231
Q

How do growth factors stimulate growth?

A

by activating multistep pws

232
Q

What stops cell growth and activate cellular differentiation?

A

differentiation factors

233
Q

Do stem cell precursors normally divide quickly or slowly?

A

slowly

234
Q

Why does the incidence of cancer increase with age?

A

You need many mutations

235
Q

All prokaryotes are:

A

bacteria

236
Q

how do we turn off expression of a gene?

A

tightly wrap it around a nucleosome

237
Q

Nucleosome:

A

octamers of a specific histone that look like beads on a slide

238
Q

Fxn of writers:

A

modify lysines and other residues

239
Q

Readers:

A

proteins that bind to modified lysines (turn gene exp on or off)

240
Q

Levels of this are elevated in metastatic breast and prostate cancer

A

Ez

241
Q

1 type of leukemia is due to:

A

an enzyme that methylates H3K4

242
Q

When are Ez levels markedly increased?

A

worst cases of metastatic breast and prostate cancer

243
Q

Page turners:

A

proteins that loosen DNA around a histone, increasing accessibility

244
Q

Enzymes that remove histone modifications:

A

erasers

245
Q

Trimethylation of __ is very important in gene activation.

A

lysine at position 4 of Histone 3 (H3K4)

246
Q

How do euk’s turn gene expression on and off?

A

wrap or unwrap DNA around a nucleosome, accessibility regulated by a ‘histone’ code

247
Q

How many nucleosomes does it take to wrap around one gene?

A

about 10

248
Q

Enzymes that modify residues:

A

writers

249
Q

Effect of Ez adding 3 methyl groups to H3K27:

A

Turn off adjacent gene

250
Q

Levels of this are increased in the worst types of metastatic breast and prostate cancer:

A

Ez

251
Q

A mutation in an enzyme that methylates H3K4 causes:

A

a type of leukemia

252
Q

A mutation of an enzyme that adds only one methyl groups to H3K4 bound to an enhancer of DNA expression is related to this type of cancer:

A

breast

253
Q

What is Ez?

A

Histone code writer

254
Q

Normal function of Ez

A

adds 3 m groups to H3K27, silencing adjacent genes responsible for early development proteins

255
Q

TF? epigenetics is usually a part of cancer.

A

T

256
Q

Epigenetics:

A

changes passed on from daughter cell to daughter cell

257
Q

How are heterotrimeric G proteins activated?

A

hormone binding

258
Q

What happens when heteromeric G protein is activated?

A

GDP dissociates from G Protein, GTP then binds, a-GTP subunit dissociates and activates an enzyme that makes 2nd msgs, they activate protein kinases that activate hormones

259
Q

How are g proteins turned off?

A

inherent GTpase activity, converting GTP to GDP.

260
Q

How are small G proteins activated?

A

GDP dis and GTP binding

261
Q

How do heteromeric G Protein and small G proteins differ?

A

Small: have GTPase activity for automatic self-inactivation, hetero: can not fully activate GTPase activity wo hormone

262
Q

Quintessential G protein:

A

Ras

263
Q

This G protein is a major player in the pws that either lead to growth or to differentiation (depends on cell type).

A

Ras

264
Q

TF? Ras works through the 2nd msg system.

A

F. directly activates PK’s

265
Q

Inactive, small G proteins are bound to:

A

GDP

266
Q

TF? Small G proteins have GTPase activity.

A

T, for self inactivation

267
Q

What is the multi-hit theory?

A

multiple gene mutations (9-11) are required to initiate cancer

268
Q

TF? Not all cancers affect the cell cycle or decrease TSG function.

A

F.

269
Q

Cancer always involves:

A

cell cycle, TSG, epigenetics, mutant proto-oncogenes

270
Q

How many auxiliary proteins are required to activate and inactivate Ras?

A

3

271
Q

Major players of the growth and differentiation pathways:

A

growth/ differentiation factor, RTK, Small G protein, 3 auxiliary proteins, kinases, phosphatases,

272
Q

What kind of pathways are growth and differentiation pathways:

A

signal transduction pathways

273
Q

All differentiation factors make cells:

A

stop dividing

274
Q

How are growth and differentiation pathways turned off?

A

protein phosphatases

275
Q

What is the first signal in the signal transduction pw of growth and differentiation?

A

a growth factor binding to RTK

276
Q

Fxn of auxiliary proteins:

A

activate and deactivate Ras

277
Q

What happens to the primary signal in signal transduction pwy?

A

transduced to factors that lead to growth

278
Q

What makes the receptor tyrosine kinases come toward each other?

A

growth factor binds the RTK

279
Q

how is the RTK activated

A

auto Phosphorylation

280
Q

How does autophosphorylation of the RTK lead to growth?

A

after A-p, proteins bind to specific sites which leads to growth

281
Q

RTK pw:

A

RTK - auto phosphorylation - GRB2 binds P group - Ras - SOS (binds both) - (GDP off, GTP on) - Raf - Mek - Mapk - in nucleus, P myc, fos, june - activate growth

282
Q

What turns on Ras?

A

SOS, gdp comes off, GTP binds (auxiliary proteins too)

283
Q

What binds bw the 2 receptor tyrosine kinases?

A

growth factor (a protein/ hormone)

284
Q

More than __ tyrosines are normally phopshoylated in the RTK.

A

2

285
Q

TF? Additional, complementary pws are needed for growth to occur besides the RTK pw.

A

T

286
Q

SOS binds:

A

Grb2 and Ras

287
Q

When is GDP released from Ras?

A

when SOS binds Ras

288
Q

Ras recruits Raf to:

A

the membrane

289
Q

a factor that stimulates growth (mitosis)

A

mitogen

290
Q

When does MAPK enter the nucleus?

A

after phosphorylation (by Mek)

291
Q

3 TF’s heavily implicated in cancer:

A

myc, fos, jun (too much of any of these = cancer)

292
Q

TF? Ras has inherent GTPase activity.

A

T, w help from a GTPase Activating Protein (then why do we have audxillary proteins to turn off?)

293
Q

Growth activity of the entire pathway is regulated by:

A

Ras GTPase activity, by inactivation of Ras (w the help of GAP) (not regulated by initial growth hormone binding to RTK?)

294
Q

How is Ras inactivated?

A

Inherently losing its GTPase activity, binds GDP, wo this we would have tons of cancer

295
Q

How can the RTK that EGF binds be permanently turned on (cancer)?

A

mutation/deletion removes part of EC domain, mutated receptors dimerize and activate pw wo growth factor

296
Q

Ras is mutated in _ % of cancers

A

20

297
Q

Mutations in Ras lead to loss of what activity?

A

GTPase to activity, Ras always active, can’t turn itself off anymore

298
Q

This mutation is found in 60% of pt w melanoma:

A

Raf

299
Q

What would a mutation in Myc, Fos, or Jun lead to?

A

cancer

300
Q

What is SARK?

A

a cytoplasmic tyrosine kinase.

301
Q

pw that is initiated by binding phosphotyrosine when a RTK is activated by a growth factor and involved in cancer:

A

Src, causes cancer bc its mitogenic pw is always active

302
Q

How are PI3 kinases acitvated?

A

by many RTK’s (binding Phosphotyrosine on an activated RTK)

303
Q

Fxn of Akt:

A

promote growth and survival, inhibit apoptosis, stimulate mTOR which stimulates protein synthesis

304
Q

What is mTOR?

A

a kinase

305
Q

Most commonly mutated part of the RTK pw:

A

Ras

306
Q

What stops the PI3 pw when needed?

A

PTEN, phosphatase of PI3

307
Q

What would happen if PTEN is mutated?

A

cancer

308
Q

PTEN is a:

A

tumor suppressor, decreases the motor system

309
Q

TF? Certain steps in the pw give you cancer.

A

F. any step that is altered

310
Q

p53, major checkpoint:

A

end of g1

311
Q

3rd checkpoint:

A

G2/M pahse boundary

312
Q

Mitogen:

A

causes mitosis in cell cycle

313
Q

RB protein binds this normally:

A

E2f proteins

314
Q

How to get Rb off of E2f protein?

A

phosphorylation of Rb protein via Myc, enter cell cycle

315
Q

Myc makes

A

d cyclin, then its kinase that p’s the Rb protein, comes off, E2f proteins activated and the cell cycle turns on

316
Q

Ex of a mitogen:

A

Myc,activates cell cycle (anything that promotes growth, cell division)

317
Q

How do mitogens regulate the rate of cell division?

A

by their effects during G1

318
Q

how does normal Myc work?

A

stimulation of gene expression of cyclin D (turns on the cell cycle)

319
Q

What happens if Myc is always active?

A

cancer

320
Q

How to regulate the rate of cell cycle?

A

E2f proteins are bound to genes poised to be expressed but nothing is happening because Rb protein is bound

321
Q

What makes the turning on of the cell cycle so rapid?

A

E2f proteins are there, ready to be actvated to turn on the genes in the cell cycle

322
Q

This can cause cancer of the retina:

A

Mutation in Rb that prevents binding to E2f, retinoblastoma

323
Q

3 ways p53 works:

A

stimulate transcription of p21 protein (can stop cell cycle in G1 or S if there is damage),

324
Q

What happens to p53 if DNA is damaged?

A

it is phosphoryated, preventing its degradation adn the progression to M phase

325
Q

TF? p53 is always active.

A

F. only active when we need it

326
Q

p53 must do this to prevent cancer:

A

bind to DNA

327
Q

oncogenes that lead to a gain of action:

A

mutated Ras or Myc

328
Q

2nd most important ts after p53:

A

p16

329
Q

How is Rb-protein normally phosphorylated?

A

cyclin D-G1 cyclin dependent kinase complex

330
Q

What prevent the formation of the cyclin D complex in stressed or overly-rapidly dividing cells?

A

p16, methylation will silence p16

331
Q

at what stage of cancer ore p16 mutations common?

A

early stages (epigenetic mechanism)

332
Q

Why might drugs that target p53 stop working?

A

if p53 is mutated

333
Q

Does phosphorylation of Rb lead to activation or deactivation?

A

activation

334
Q

Epigenetic change vs. genetic change

A

change in expression (daughter to daughter) vs. change in DNA sequence

335
Q

This can cause gene silencing in cancer cells an prevent the formation of proteins that inhibit growth

A

DNA methylation

336
Q

Methylation of what can lead to permanent gene silencing?

A

H3 and Lys9 (removes ts’s)

337
Q

Is heterochromatin active or inactive?

A

inactive

338
Q

How are developmental genes related to cancer?

A

many of these are turned on AFTER development, causing cancer

339
Q

Ez is active in what cancers?

A

metastatic breast and prostate

340
Q

How does Gleevac work?

A

binds Phile chromo. CML, binds specific mutant protein

341
Q

Marjor factor in whether or not cancer forms

A

how fast stem cells are dividing in a articular organ

342
Q

PAP smears can test for:

A

uterine and cervical

343
Q

Cancer:

A

GROUP of neoplasms, invading tissue

344
Q

Histological groupings of neoplasm:

A

epi, mesnchymal, neuroectoderml, hematopoietic, lymphioid, germ cell

345
Q

Types of epi cancers:

A

squaous or glandular

346
Q

benign growth characteristics:

A

slow, expansile (capable of expansion) gowth, local, encapsulated, push on surrounding structure, small, well differentiated

347
Q

Metastasis:

A

non-adjacent organ

348
Q

Parenchyma:

A

tumor cells

349
Q

supporting cells of tumor:

A

stroma

350
Q

Malignant epi tumor:

A

Carcinoma

351
Q

Malignant mesenchymal tumor:

A

Sarcoma

352
Q

Benign squamous epithelium cancer:

A

squamous papilloma

353
Q

Malignant squamous epithelium:

A

SSC

354
Q

Benign glandular epi:

A

ademoa

355
Q

Malignant glandular epi:

A

adenocarcinoma

356
Q

Benign melanocyte:

A

nevus

357
Q

Malignant melanocyt:

A

malignant melanoma

358
Q

Prefix :adeno”:

A

gland

359
Q

Benign fibrous tumor:

A

fibroma

360
Q

Benign sm tumore:

A

leiomyoma

361
Q

Benign striated muscle tumor:

A

rhabdomyoma

362
Q

Benign cartilage tumor:

A

chndroma

363
Q

exothitic:

A

rising above and growing above the normal epithelium

364
Q

papillary:

A

irregular finger-like growth:

365
Q

scirrhous

A

carcinoma, hard to the touch

366
Q

desmoplastic:

A

Causing fibrosis in the vascular stroma of a neoplasm.

367
Q

What is the mucinous component normally made by?

A

glandular epithelium

368
Q

Ewing’s sarcoma:

A

supporting cell tumor, mostly arises in bone, treated and responds like sarcomas

369
Q

Hodgkin’s disease:

A

Lymphoma, malignant neoplasm of lymphoid cells

370
Q

4 phases of malignant growth:

A

Mutation/ change, growth, invasion, metastasis (not just the ability to invade blood vessels and lymphatics)

371
Q

Are pre-neoplastic morphological changes reversible?

A

some

372
Q

Difference bw hyperplasia and hypertrophy

A

plasia: more cells, trophy: larger cells, same number

373
Q

Ex of when cells atrophy:

A

menophause

374
Q

Dysplasia:

A

proliferation of abnormal cells, disordered development, increased mitosis, varying numbers of cells, tends to disorder in cellular arrangement

375
Q

These can cause metaplasia:

A

toxin, physical stimulus, or gf (change from one epithelium type to another)

376
Q

Ex of metaplasia in smokers:

A

glandular to squamous, don’t secrete mucus

377
Q

loss of normal arrangment of cells:

A

atypia

378
Q

Why do cancerous cells have a darker nuleus?

A

more chromatin

379
Q

Carcinoma in situ is a type of:

A

Intra-epithelial neoplasm

380
Q

Carcinoma in situ is confined to what tissue type?

A

epithelium (full thickness)

381
Q

Invasion :

A

malignant EPI tumor

382
Q

Is carcinoma in situ invasive or non-invasive?

A

non-invasive (pre-malignant)

383
Q

Low-grade dysplasia:

A

confined to lower half of epi, high grade includes outer half

384
Q

When is a cell capable of invasion?

A

When it can express cell surface adhesion molecules

385
Q

epithelial tumors invade:

A

the lymphatics rather than blood vessels

386
Q

sarcomas tend to invade:

A

blood vessels rather than lymphatics

387
Q

osteosarcoma metasizes here:

A

typically to lungs via blood

388
Q

breast cancer metastasizes here:

A

lymphatic, lymph nodes, bone, and lungs

389
Q

How do tumors disrupt the ECM?

A

proteolytic enzymes

390
Q

Tumor cell that lacks differentiation:

A

anaplastic (pleiomorphism, variation in size/shape, abnormal nuclear shape, quickly dividing, numerous mitoses)

391
Q

Tumors are graded by:

A

mitotic activity, nuclear size and shape, presence of nucleoli or architecture

392
Q

Local effects of neoplasms:

A

swelling, irritation, pain, thrombosis, hemorrhage, necrosis, obstruction or perforation of hollow viscera, infection, involvement of adjacent structures

393
Q

Colon might spread to:

A

bladder, pelvic side wall, other loops of bowel

394
Q

Systemic tumor effects:

A

inc or dec hormonal expression, hypercoagulable state, myopathies, neuropathes

395
Q

generalized wasting:

A

cachexia

396
Q

paraneoplastic symptoms:

A

can’t be explained by distant or local tumor growth or indigenous tissue hormones

397
Q

Ex (?) of hypercogulable state;

A

migrating intravascular thrombophlebitis, non bacterial intravascular coagulation, disseminated intravascular coagulation

398
Q

Cancer assoc w inc hemoglobin levels:

A

Renal Cell Carcinoma

399
Q

Cancer assoc w dec Na levels:

A

Lung small cell anaplastic carcinoma

400
Q

Cancer assoc w inc Ca2+ levels:

A

Lung SCC

401
Q

TF? Dermatomyositis is a hormonally related.

A

F. not hormonal, rheumatic or skin disease

402
Q

Serum protein markers are useful for:

A

dx, follow-up

403
Q

Serum protein markers:

A

monoclonal Ab’s against sp antigen produced by tumor cell, not perfect in either specificity or senstivity

404
Q

In what way is staging more reliable than grading?

A

prognosis

405
Q

hidden tumor:

A

occult tumor

406
Q

3 parameters of staging:

A

Size, lymph node metastasis, distant non-lymphoid metastasis

407
Q

Haber’s Law

A

Time/ dose relationship of toxicity, high dose/ brief duration acute disease

408
Q

Threshold dose

A

min dose needed to have an effect, doesn’t apply to all toxins

409
Q

Chloracne

A

acne-like rash, folliculitis, due to PCB exposure

410
Q

iniator;

A

carcinogen makes permanent DAN damage

411
Q

promoter:

A

induce tumors in primed cells (not carcinogens)

412
Q

pnemoconiois

A

lung disease due to dust inhalation: chronic, progressive, dyspnea, cough, disability

413
Q

Basic principles of carcinogenesis:

A

causes: chemicals, radiation, viruses/ nonlethal DNA damage, multistep process, initiators and promoters

414
Q

Farming disease

A

pesticides, herbicides

415
Q

Disease from Lead

A

gingivitis (lead lines on bones and teeth), anemia (rbc stippling), not cancer

416
Q

Disease from Asbestos:

A

Pulmonary cancer: 15-20yrs after exposure, asbestos fibers, highly malignant, Mesothelioma: highly anaplastic, most die in less than a year, in leura and surround the lung parenchyma

417
Q

Most proven human disease is due to:

A

occupation or massive exposure

418
Q

Theshold dosein mainly based on:

A

animal models

419
Q

4 modes of direct toxic effect:

A

tissue vulnerability, mode of action (enz inh), metabolism (procarcinogens), excretion (toxic conc)

420
Q

Rsxns to injury are due to:

A

direct toxic effect, allergic mechs, idiosyncratic factors (genetic or host)

421
Q

formaldehyde causes:

A

throat cancer

422
Q

Sources of formaldehyde:

A

insulation, fixation of tissues

423
Q

Miners are exposed to:

A

arsenic, nickel, asbestos

424
Q

Is DNA damage due to carcinogenesis reversible?

A

No

425
Q

Carcinogenesis causes damage to what types of genes?

A

proto-oncogenes, suppressor genes, genes regulating apoptosis, DNA repair genes

426
Q

Most chemical carcinogens are:

A

indirect acting

427
Q

How do electrophiles react with DNA?

A

covalent bonds

428
Q

What do electrophiles form with DNA?

A

adducts with nucleotides

429
Q

Ex of direct acting carcinogens;

A

alkylating anti-neoplastic drugs

430
Q

Procarciniogens requrie:

A

metabolic conversion, often P-450 dependent mono-oxygenase system in liver

431
Q

3 types of chemical carcinogens:

A

Electrophiles, direct and indirect acting

432
Q

Ex of direct acting carcinogen:

A

alkylating anti-neoplastic drugs

433
Q

benzo(a)pyrene is a:

A

procarcinogen, polycyclic aromatic hydrocarbon

434
Q

benzo(a)pyrene is converted by this and tend to form this:

A

cytochrome P-450 system, epoxides (3 member rings with one O2, active metabolites)

435
Q

What do epoxides react with/

A

covalently bind DNA

436
Q

Determinants of pneumoconiioses:

A

density in air, duration of exposure, particle size (usually les than 2-3um), chemical nature of dust

437
Q

Type of asbestos fiber that is more pathogenic:

A

straight (curved, not very)

438
Q

Asbestos fibers are:

A

hydrated silicates (silica, Fe, Mg, Na)

439
Q

2 examples of curved asbestos fibers:

A

crosidolite, amosite

440
Q

What part of asbestos enters the lung?

A

Amphiboles

441
Q

Number of toxic dump sites in USA:

A

5,000

442
Q

Sources of PCB’s:

A

(polychlorinated biphenyl molecules) insulation, lubricants, caulking, paints, fish, poultry

443
Q

PCB’s:

A

water stable, resist biodegradation, build up in fat tissue, generate free radicals, form xenoestrogens (leads to malignant change in breast epi)

444
Q

PCB exposure can lead to:

A

liver failure, carcinoma of breast

445
Q

Gross morphology of cirrhotic liver:

A

nodular and fibrotic (firm)

446
Q

Pathogenesis of lead poisoning:

A

inhibits ALA dehydrase (heme)

447
Q

Benefit of nano particles in new materials:

A

greater strength and durabiilty, temp resistant, water proof

448
Q

Why are we suspicious of the health effects of nano particles?

A

unusual physical, chemical, biological properties, migrate undetected to various tissues, cancer-causing effects in animal models

449
Q

Cancer-causing effects in animal models from nanoparticle exposure:

A

cross intact membranes, generate free radicals, break DNA strands in mice given water with titanium (tio2)

450
Q

Where is titanium used?

A

coat building windows, sunscreen

451
Q

Shapes of nanoparticles:

A

spherical or fiber-like

Pathology (23 decks)

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