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NPLEX 1 > Pathology > Flashcards

Pathology Flashcards

1
Q

What is the definition of apoptosis?

A

Programmed cell death

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2
Q

Does apoptosis require ATP?

A

Yes

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3
Q

Describe how apoptosis occurs.

A

Intrinsic and Extrinsic pathways: both pathways –> activation of cytosolic camases that mediate cellular breakdown.

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4
Q

Is there inflammation involved in apoptosis?

A

No. (unlike necrosis)

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5
Q

Apoptosis is characterized by deeply _________ cytoplasm.

A

Eosinophilic

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6
Q

What is pyknosis?

A

Nuclear shrinkage seen in apoptosis

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7
Q

What is karyorrhexis?

A

nuclear fragmentation seen in apoptosis

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8
Q

What types of cells increase drastically during apoptosis?

A

basophils

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9
Q

Name one sensitive indicator of apoptosis

A

DNA laddering

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10
Q

Describe DNA laddering.

A

During karyorhexis, endonucleases cleave at internucleosomal regions, yielding 180-bp fragments.

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11
Q

When do we see the intrinsic pathway for apoptosis used?

A

Involved in tissue remodelling in embryogenesis

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12
Q

When does the intrinsic pathways of apoptosis initiate?

A

Occurs when a regulating factor is withdrawn from a proliferating cell population (e.g IL-2 after a completed immunological reaction –> apoptosis of proliferating effector cells).
Also occurs after exposure to injurious stimuli (e.g radiation, toxins, hypoxia)

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13
Q

Changes in pro-apoptotic factors lead to…

A

increase in mitochondrial permeability and cytochrome c release

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14
Q

Name 2 pro-apoptotic proteins.

A

BAX and BAK

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15
Q

Name an anti-apoptotic protein.

A

Bcl-2

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16
Q

How does Bcl-2 prevent apoptosis?

A

Bcl-2 prevents cytochrome c release by binding to and inhibiting Apaf-1. Apaf-1 normally activates capsases.

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17
Q

Bcl-2 is over expressed (e.g. follicular lymphoma) then…

A

…Apaf-1 is overly inhibited, leading to decrease caspase activation and tumorigenesis.

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18
Q

Where are BAX and Bcl-2 found in the cell?

A

mitochondria

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19
Q

Where are cytochrome c found in the cell?

A

mitochondria

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20
Q

Describe the two pathways of the extrinsic apoptosis

A
  1. Ligand receptor interactions (FasL binding to Fas [CD95])

2. Immune cell (cytotoxic T-cell release of perforin and granzyme)

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21
Q

Fas-FasL interaction if necessary in _______________ selection

A

thymic medullary negative selection

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22
Q

What do mutations in Fas do?

A

increase the number of circulating self-reacting lymphocytes due to failure of colonial deletion

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23
Q

After Fas cross links with FasL…

A

multiple Fas molecules coalesce, forming a binding site for a death domain - containing adapter protein, FADD.

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24
Q

What does FADD do?

A

FADD binds inactive caspases, activating them.

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25
Q

What is the basis for autoimmune disease?

A

Defective Fas-FasL interaction

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26
Q

List the 6 types of necrosis

A
  1. Coagulative
  2. Liquefactive
  3. Caseous
  4. Fatty
  5. Fibrinoid
  6. Gangrenous
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27
Q

Where does coagulative necrosis occur?

A

Heart, liver, kidney (in tissues supplied by end-arteries)

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28
Q

Where does liquifactive necrosis occur?

A

Barin, bacterial abscess, occurs in CNS due to high fat content

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29
Q

How does coagulative necrosis progress?

A

increased cytoplasmic binding of acidophilic dye. Proteins denature first, followed by enzymatic degradation

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30
Q

How does liqifactive necrosis progress?

A

In contrast to coagulative necrosis, enzymatic degradation due to the release of lysosomal enzymes occurs first

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31
Q

What pathogens result in caseous necrosis?

A

TB, systemic fungi, Nocardia

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32
Q

What types of fatty necrosis exist?

A

Enzymatic - pancreatitis [saponification]

Non-enzymatic - Breast Trauma

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33
Q

What dis-eases lead to fibrinoid necrosis?

A

Vasculitides (e.g. Henoch-Schonlein purpura, Churg-Strauss syndrome)
Malignant hypertension

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34
Q

What types of gangrenous necrosis exist?

A

Dry (ischemic coagulative)

Wet (infection)

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35
Q

Where are gangrenous necrosis common?

A

Limbs and GI tract

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36
Q

List some processes that cause cell injury that are reversible (O2 is still present)

A

ATP depletion
Cellular mitochondrial swelling (decreased ATP –> decreased activity of Na+/K+ pumps)
Nuclear chromatin clumping
Decreased glycogen
Fatty change
Ribosocomal/polysomal detachment (decreased protein syn)
Membrane blebbing

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37
Q

List some processes that cause cell injury that are irreversible.

A

Nuclear pyknosis
karyorrhexis
karyolysis
Plasma membrane damage (degradation of membrane phospholipid)
Lysosomal rupture
Mitochondrial permeability/vacuolization; phospholipid-containing amorphous densities with mitochondria (swelling along is reversible)

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38
Q

What area if susceptible to hypoxia/ischemia and infarction in the brain?

A

ACA/MCA/PCA boundary area (watershed areas (border zones) receive dual blood supply from most distal branches of 2 arteries, which protects these areas from single-vessel focal blockage. However, these ares are susceptible to schema from systemic hypo perfusion)

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39
Q

What area if susceptible to hypoxia/ischemia and infarction in the Heart?

A

Subendocardium (LV)

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40
Q

What area if susceptible to hypoxia/ischemia and infarction in the Kidney?

A

Straight segment of proximal tubule (medulla)

Thick ascending limb (medulla)

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41
Q

What area if susceptible to hypoxia/ischemia and infarction in the Liver?

A

Area around the central vein (zone 3)

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42
Q

What area if susceptible to hypoxia/ischemia and infarction in the Colon?

A

Splenic flexure, rectum

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43
Q

What areas of the brain does hypoxic ischemic encephalopathy (HIE) affect?

A

Pyramidal cells of the hippocampus and Purkinje cells of the cerebellum

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44
Q

When/Where do red infarcts arise?

A

Occur in loose tissue with multiple blood supplies, such as liver, lung, and intestines. Red = reperfusion

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45
Q

When/Where do pale infarcts arise?

A

Occur in solid tissues with a single blood supply, such as heart, kidney, and spleen.

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46
Q

What is the first sign of shock?

A

Tachycardia

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47
Q

What types of shock are included under the umber ally term: distributive shock?

A

Includes: septic, neurogenic and anaphylactic shock

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48
Q

What characterizes distributive shock?

A

High output failure (decreased TPR, increased CO, increased venous return)
Decreased PCWP
Vasodilation (warm skin)
Failure to increase blood pressure with IV fluids

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49
Q

What characterizes hypovolemic/cardiogenic shock?

A 
Low output failure (increased TPR, decreased CO, increased venous return)
PCWP increases in cardiogenic
PCWP decreases in hypovolemic
Vasoconstriction (cold, clammy patient)
Blood pressure restored with IV fluids
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50
Q

What cells mediate acute inflammation?

A

Neutrophils, eosinophils, antibodies

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51
Q

What cells mediate chronic inflammation?

A

Mononuclear cells and fibroblasts

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52
Q

Define Granuloma

A

nodular collection of epithelioid macrophages and giant cells. Outcomes include scarring and amyloidosis.

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53
Q

Define Chromatolysis

A

Increase in protein synthesis in an effort to repair the damaged axon following axonal injury.

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54
Q

What characterizes chromatolysis?

A

Round cellular swelling
Displacement of the nucleus to the periphery
Dispersion of Nissl substances through cytoplasm

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55
Q

What is dystrophic calcification?

A

Calcium deposition in tissue secondary to necrosis (usually localized).

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56
Q

In ______ calcification, patients are generally normocalcemic
In ______ calcification, patients are generally NOT normocalcemic

A

Dystrophic calcification = normocalcemic

Metastatic calcification = NOT normocalcemic

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57
Q

Define Matastatic Calcification

A

Widespread deposition of Ca+ in normal tissue secondary to hypercalcemia or higher Ca+/P product

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58
Q

What is the interaction between pH levels and Calcium deposition?

A 
Increased pH (basic) = higher calcium deposition
Decreased pH (acidic) = less calcium deposition
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59
Q

Where does leukocyte extraversion predominantly occur?

A

postcapillary venules

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60
Q

What are the 4 steps of Leukocyte extraversion?

A
  1. Margination and rolling
  2. Tight binding
  3. Diapedesis - leukocyte travels between endothelial cells and exits blood vessels
  4. Migration - leukocyte travels throug interstitium to site of injury or infection guided by chemotactic signals
    REVIEW THIS PROCESS - First Aid, Pg. 224
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61
Q

How do free radicals damage cells?

A

membrane lipid peroxidation
protei modification
DNA breakage

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62
Q

How do we end up with free radical injury?

A 
Radiation exposure
metabolism of drugs (phase 1)
redox reactions
nitric oxide
transition metals
leukocyte oxidative burst
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63
Q

How can free radicals be eliminated?

A

Enzymes, spontaneous decay, antioxidants (Vit. a,c,e)

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64
Q

Following an injury to skin, what % of tensile strength can a patient expect to regain and how long will it take

A

70-80% of pre-injury tensile strength

in 3 months

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65
Q

Describe the differences between hypertrophic scars and keloid scars in terms of collagen synthesis

A

Collagen synthesis increases in hypertrophic scars but increases MORE in keloids

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66
Q

Describe the differences between hypertrophic scars and keloid scars in terms of collagen arrangement

A

Keloid scars = disorganized collagen

Hypertrophic scares = parallel scars

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67
Q

Describe the differences between hypertrophic scars and keloid scars in terms of extent of scaring

A

Keloid - extend beyond the borders of the original scar

Hypertrophic scars - confined to the border of the original wound

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68
Q

Describe the differences between hypertrophic scars and keloid scars in terms of recurrence

A

Keloid - frequently require following resection

Hypertrophic scars - infrequently recur following resection

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69
Q

What is the role of PDGF in wound healing?

A

secreted by activated platelets and macrophages
Induces vascular remodeling and smooth muscle cell migration
Stimulated fibroblast growth for collagen synthesis

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70
Q

What is the role of FGF in wound healing?

A

Stimulated all aspect of angiogenesis

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71
Q

What is the role of EGF in wound healing?

A

Stimulated cell growth via tyrosine kinases (e.g. EGFR, as expressed by ERBB2)

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72
Q

What is the role of TGF-B in wound healing/

A

Angiogenesis, fibrosis, cell cycle arrest

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73
Q

What is the role of metalloproteinases in wound healing?

A

Tissue remodeling

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74
Q

What cells are immediate/inflammatory cell markers of wound healing?

A

Platelets, neutrophils, macrophages

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75
Q

What are the characteristic findings of an area with lots of platelets, neutrophils and macrophages present during wound healing?

A

clot formation, increased vessel permeability and neutrophil migration into tissue; macrophages clear debris 2 days later

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76
Q

What are the characteristic findings of an area with lots of fibroblasts, myofibroblasts, endothelial cells, keratinocytes, macrophages during wound healing?

A

Depositionof granulation tissue and collagen, angiogenesis, epithelial cell proliferation, dissolution of clot, and wound contraction (mediated by myofibroblasts)

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77
Q

What cells are present during the proliferative phase (2-3 days after wound)?

A

Firboblasts, myofibroblasts, endothelial cells, keratinocytes, macrophages

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78
Q

What cells are present in the 3rd and final phase of wound healing - remodelling (1 week after the wound)?

A

Fibroblasts

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79
Q

What are the characteristic finding of an area with lots of fibroblasts present after a wound occurs?

A

Type 3 collagen replaced by type 1 collagen.

Increase in tensile strength of tissue.

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80
Q

What is it that induces and maintains granuloma formation?

A

TNF-a

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81
Q

List some diseases that are granulomatous

A 
Bartonella henselae (cat scratch disease)
Berylliosis
Churg-Strauss syndrome
Crohn's
Francisella tularensis
Fingal infections
Granulomatosis w/ polyangiitis (Wegener)
Listeria monocutogenes (granulomatosis infantiseptica)
M. leprae
M. tuberculosis
Treponema pallidum (teritary syph)
Sarcoidosis
Schistosomiasis
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82
Q

Transudate/Exudate - which is thick and which is thin

A

Exudate - thick

Transudate - thin

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83
Q

Exudate is protein ___

Transudate is protein ___

A

Exude - protein rich

transudate - protein poor

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84
Q

Exudate specific gravity _____

Transudate specific gravity ____

A

Exudate SG = >1.020

Transudate SG = <1.020

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85
Q

Transudate/Exudate - which is cellular and which is hypocellular

A

Transudate - hypocellular

Exudate - cellular

86
Q

When do we see exudates?

A

Lymphatic obstruction
Inflammation/infection
Malignancy

87
Q

When do we see transudate?

A

increases in hydrostatic pressure (e.g. CHF)
decreases in oncotic pressure (e.g. cirrhosis)
Na+ retention

88
Q

When do we get an increase in ESR?

A 
most anemias
infections
inflammation
cancer 
pregnancy
autoimmune disease
89
Q

When do we get a decrease in ESR?

A

sick cell disease
polycythemia
CHF

90
Q

One of the leading causes of fatality from toxicologic agents in children is….

A

Iron Poisoning

91
Q

What is the mechanism of iron poisoning?

A

cell death due to per oxidation of membrane lipids

92
Q

What are the symptoms of Iron Poisoning?

A

Acute - nausea, vomiting, gastric bleeding, lethargy

Chronic - metabolic acidosis, scarring leading to GI obstruction

93
Q

What is the treatment for Iron Poisoning?

A

chelation and dialysis

94
Q

Define Amyloidosis.

A

Abnormal aggregation of proteins (or their fragments) into B-pleated sheet structures –> damage and apoptosis

95
Q

List the 6 types of amyloidosis.

A
  1. AL (primary)
  2. AA (secondary)
  3. Dialysis-related
  4. Heritable
  5. Age-related (senile) systemic
  6. Organ specific
96
Q

Describe AL type amyloidosis

A

Deposition of proteins from Ig Light chains

97
Q

Describe AA type amyloidosis

A

Seen w/ chronic conditions, such as RA, IBD, spondyloarthropathy, protracted infection. Fibrils composed of serum Amyloid A. Often multi systemic like AL amyloidosis.

98
Q

Describe Dialysis-related amyloidosis

A

Fibrils composed of B2 microglobin in patients with ESRD and/or on long-term dialysis.

99
Q

Which is the amyloidosis types may present with carpal tunnel?

A

Dialysis-type

100
Q

Describe heritable type amyloidosis

A

Heterogeneous group of disorders. Example is ATTR neurologic/cardia amyloidosis due to tranthyretin (TTR or prealbumin) gene mutation

101
Q

Describe age-related systemic amyloidosis

A

Due toe deposition of normal (wild type) TTR in myocardium and other sites. Slower progression of cardiac dysfunction relative to AL amyloidosis

102
Q

Describe organ specific amyloidosis

A

Amyloid deposition, localized to a single organ. E.g. Alzheimer’s disease and B-amyloid plaques, Isley amyloid polypeptide (IAPP) is commonly seen in diabetes mellitus type 2 and is caused by deposition of amylin in pancreatic islets

103
Q

What is lipofuscin?

A

A yellow/brown “wear and tear” pigment associated with normal aging

104
Q

How is lipofuscin formed?

A

Formed by oxidation and polymerization of autophagocytosed organellar membranes

105
Q

How does invasive carcinoma manage to invade the basement membrane?

A

using collagenases and hydrolyses (metalloproteinases)

106
Q

What other name is P-glycoprotein known by?

A

multi drug resistance protein 1 (MDR1)

107
Q

What does P-glycoprotein (aka MDR1) do?

A

Expressed by come cancer cells (e.g. colon, liver) to pump out toxins, including chemotherapeutic agents (one mechanism of decreasing responsiveness or resistance to chemo over time)

108
Q

Define Anaplasia

A

Loss of structural differentiation and function of cells, resembling primitive cells of same tissue; often equated with undifferentiated malignant neoplasms. May see “giant cells” with single large nucleus or several nuclei.

109
Q

Define Neoplasia

A

A clonal proliferation of cells that is uncontrolled and excessive. Neoplasia may be benign or malignant

110
Q

Define Desmoplasia

A

Fibrous tissue formation in response to neoplams (e.g. linitis pastica in diffuse stomach cancer).

111
Q

What is the difference between tumour grade and stage?

A 
grade = degree of cellular differentiation and mitotic activity on histology. 
Stage = degree of localization/spread based on site and size of primary lesion, spread to regional lymph nodes. presence of metastases. Based on clinical/pathological findings.
112
Q

Does the grade or stage have more prognostic value?

113
Q

What is the staging system for tumours called and how does it work?

A

TNM staging system
T = timor size
N = node involvement
M = metastasis

114
Q

Name the neoplasm associated with this condition: Acanthosis ingrains (hyper pigmentation and epidermal thickening)

A

Visceral malignancy (esp. stomach)

115
Q

Name the neoplasm associated with this condition: Actinic keratosis

A

Squamous cell carcinoma of the skin

116
Q

Name the neoplasm associated with this condition: AIDS

A

Aggressive malignant lymphomas (non Hodgkin) and Kaposi sarcoma

117
Q

Name the neoplasm associated with this condition: Autoimmune disease (e.g Hashimotos thyroiditis, SLE)

118
Q

Name the neoplasm associated with this condition: Barrett’s oesophagus

A

Esophageal adenocarcinoma

119
Q

Name the neoplasm associated with this condition: Cirrhosis

A

Hepatocellular carcinoma

120
Q

Name the neoplasm associated with this condition: Cushing syndrome

A

Small cell lung cancer

121
Q

Name the neoplasm associated with this condition: Dermatocyositis

A

Lung cancer

122
Q

Name the neoplasm associated with this condition: Down syndrome

123
Q

Name the neoplasm associated with this condition: Dysplastic nevus

A

Malignant melanoma

124
Q

Name the neoplasm associated with this condition: Hypercalcemia

A

Squamous cell lung cancer

125
Q

Name the neoplasm associated with this condition: Immunodeficiency states

A

Malignant lymphomas

126
Q

Name the neoplasm associated with this condition: Lamber-Eaton myasthenic syndrome

A

Small cell lung cancer

127
Q

Name the neoplasm associated with this condition: Myasthenia gravis, pure RBC aplasia

A

Thymoma (tumour of the epithelial cells of the thymus)

128
Q

Name the neoplasm associated with this condition: Paget’s disease of bone

A

secondary osteosarcoma and fibrosarcoma

129
Q

Name the neoplasm associated with this condition: Plummer-Vinson syndrome (decreased iron)

A

Squamous cell carcinoma of esophagus

130
Q

Name the neoplasm associated with this condition: Polycythemia

A

Renal cell carcinoma, hepatocellular carcinoma

131
Q

Name the neoplasm associated with this condition: Radiation exposure

A

Laukemia, sarcoma, papillary thyroid cancer, and breast cancer

132
Q

Name the neoplasm associated with this condition: SIADH (syndrome of inappropriate anti-duiretic hormone secretion)

A

Small cell lung cancer

133
Q

Name the neoplasm associated with this condition: Tuberous sclerosis (facial angiofibroma, seizures, intellectual disability)

A

Giant cell astrocytoma, renal angiomyolipoma, and cardiac rhabdomyoma

134
Q

Name the neoplasm associated with this condition: Ulcerative Colitis

A

Colonic adenocarcinoma

135
Q

Name the neoplasm associated with this condition: Xeroderma pigmentosum, albinism

A

Melanoma, basal cell carcinoma, and especially squamous cell carcinomas of skin

136
Q

Explain how oncogenes increase cancer risk

A

Gain of oncogene function –> increased cancer risk.

Need damage to ONLY 1 allele

137
Q

Explain how tumor suppressor genes increase cancer risk

A

Loss of function –> increased cancer risk. Both alleles much be lost for expression of disease

138
Q

Name the tumour and gene product associated with the following oncogene: BCR-ABL

A

CML, ALL

Tyrosine Kinase

139
Q

Name the tumour and gene product associated with the following oncogene: bcl-2

A

Follicular and undifferentiated lymphomas

Anti-apoptotic molecule (inhibits apoptosis)

140
Q

Name the tumour and gene product associated with the following oncogene: BRAF

A

Melanoma

Serine/threonine kinase

141
Q

Name the tumour and gene product associated with the following oncogene: c-kit

A 
Gastrointestinal stromal tumor (GIST)
Cytokine receptor (for stem cell factor)
142
Q

Name the tumour and gene product associated with the following oncogene: c-myc

A

Burkitt lymphoma

Transcription factor

143
Q

Name the tumour and gene product associated with the following oncogene: HER2/neu (c-erbB2)

A

Breast, ovarian, and gastric carcinomas

Tyrosine Kinase

144
Q

Name the tumour and gene product associated with the following oncogene: L-myc

A

Lung tumor

Transcription factor

145
Q

Name the tumour and gene product associated with the following oncogene: N-myc

A

Neuroblastoma

Transcription factor

146
Q

Name the tumour and gene product associated with the following oncogene: ras

A

Colon cancer, lung cancer, pancreatic cancer

GTPase

147
Q

Name the tumour and gene product associated with the following oncogene: ret

A

MEN 2A and 2B

Tyrosine kinase

148
Q

Name the tumour and gene product associated with the following tumour suppressor: APC

A 
Colorectal cancer (associated with FAP)
N/A
149
Q

Name the tumour and gene product associated with the following tumour suppressor: BRCA1

A

Breast and Ovarian cancer

DNA repair protein

150
Q

Name the tumour and gene product associated with the following tumour suppressor: BRCA2

A

Breast and Ovarian cancer

DNA repair protein

151
Q

Name the tumour and gene product associated with the following tumour suppressor: CPD4/SMAD4

A

Pancreatic cancer

DPC - deleted in pancreatic cancer

152
Q

Name the tumour and gene product associated with the following tumour suppressor: DCC

A

Colon cancer

DCC - deleted in colon cancer

153
Q

Name the tumour and gene product associated with the following tumour suppressor: MEN1

A

MEN type 1

N/A

154
Q

Name the tumour and gene product associated with the following tumour suppressor: NF1

A

Neurofibromatosis type 1

RAS GTPase activating protein (neurofibromin)

155
Q

Name the tumour and gene product associated with the following tumour suppressor: NF2

A

Neurofibromatosis type 2

Merlin (schwannomin) protein

156
Q

Name the tumour and gene product associated with the following tumour suppressor: p16

A

Melanoma

Cyclin-dependant kinase inhibitor 2A

157
Q

Name the tumour and gene product associated with the following tumour suppressor: p53

A

Most human cancers, Li-fraumeni syndrome

Transcription factor for p21, blocks G1 –> S phase

158
Q

Name the tumour and gene product associated with the following tumour suppressor: PTEN

A

Breast cancer, prostate cancer, endometrial cancer

N/A

159
Q

Name the tumour and gene product associated with the following tumour suppressor: Rb

A

Retinoblastoma, osteosarcoma

Inhibits E2F; blocks G1 –> S phase

160
Q

Name the tumour and gene product associated with the following tumour suppressor: TSC1

A

Tuberous sclerosis

Hamartin protein

161
Q

Name the tumour and gene product associated with the following tumour suppressor: TSC2

A

Tuberous sclerosis

Tuberin protein

162
Q

Name the tumour and gene product associated with the following tumour suppressor: VHL

A

von Hippel-Lindau disease

Inhibitis hypoxia inducible factor 1a

163
Q

Name the tumour and gene product associated with the following tumour suppressor: WT1

A 
Wilms Tumour (nephroblastoma)
N/A
164
Q

Name the tumour and gene product associated with the following tumour suppressor: WT2

A 
Wilms Tumor (nephroblastoma)
N/A
165
Q

Can tumour markers be used in cancer diagnosis?

A

Tumour markers are NOT to be used as the primary diagnostic tool
They may be used to monitor tumour recurrence and response to therapy, but definitive diagnosis can be made ONLY via biopsy

166
Q

What does the presence of the following tumour marker tell us?: Alkaline phosphatase

A

Metastases to bone, liver, paget disease of bone, seminoma (placental ALP)

167
Q

What does the presence of the following tumour marker tell us?: a-fetoprotein

A

Normally made by fetus. Hepatocellular carcinoma, hepatoblastoma, yolk sac (endodermal sinus) timor, testicular cancer, mixed germ cell timor (co-secreted with B-hCG)

168
Q

What does the presence of the following tumour marker tell us?: B-hCG

A

Hydaticorm moles and Choriocarcinomas (Gestational trophoblastic disease), testicular cancer
Commonly associated with pregnancy

169
Q

What does the presence of the following tumour marker tell us?: CA-15-3/CA-27-29

A

Breast Cancer

170
Q

What does the presence of the following tumour marker tell us?: CA-19-9

A

Pancreatic adenocarcinoma

171
Q

What does the presence of the following tumour marker tell us?: CA-125

A

Ovarian cancer

172
Q

What does the presence of the following tumour marker tell us?: CEA

A

CarcinoEmbryonic Antigen. Very nonspecific but produced by ~70% of colorectal and pancreatic cancers; also produced by gastric, breast, and medullary thyroid cancers

173
Q

What does the presence of the following tumour marker tell us?: PSA

A

prostate-specific antigen. Used to follow prostate adenocarcinoma. Can also be elected in BPH and prostatitis. Questionable risk/benefit for screening

174
Q

What does the presence of the following tumour marker tell us?: S-100

A

neural crest origin (e.g. melanomas, neural tumors, schwannomas, Langerhans cell historcytosis)

175
Q

What does the presence of the following tumour marker tell us?: TRAP

A

Tartate-Resistant Acid Phosphatase (TRAP)

Hairy cell leukaemia - a B-cell neoplasm

176
Q

What cancer does the following microbe cause?: EBV

A

Burkitt lymphoma
Hodgkin lymphoma
nasopharyngeal carcinoma
CNS lymphoma (in immonocompromised patients)

177
Q

What cancer does the following microbe cause?: HBV, HCV

A

Hepatocellular carcinoma

178
Q

What cancer does the following microbe cause?: HHV-8 (Kaposi sarcoma-associated herpesvirus)

A

Kaposi sarcoma

body cavity fluid B-cell lymphoma

179
Q

What cancer does the following microbe cause?: HPV

A

Cervical and penile/anal carcinoma (16,18)

head and neck or throat cancer

180
Q

What cancer does the following microbe cause?: H. pylori

A

Gastric adenocarcinoma

MALT lymphoma

181
Q

What cancer does the following microbe cause?: HTLV-1

A

adult T-cell leukemia/lymphoma

182
Q

What cancer does the following microbe cause?: Liver fluke (Clonorchis sinensis)

A

Cholangiocarcinoma

183
Q

What cancer does the following microbe cause?: Schistosoma haematobium

A

Bladder cancer (squamous cell)

184
Q

What cancer does the following toxin cause?: Aflatoxins (Aspergillus)

A

Hapatocellular carcinoma (liver)

185
Q

What cancer does the following toxin cause?: Alkalatin agents

A

Leukemia/lymphoma (blood)

186
Q

What cancer does the following toxin cause?: Aromatic amines (e.g. benzidine, 2-naphthlamine)

A

Transitional cell carcinoma (bladder)

187
Q

What cancer does the following toxin cause?: Arsenic

A

Angiosarcoma (Liver)
Lung cancer (Lung)
Squamous cell carcinoma (Skin)

188
Q

What cancer does the following toxin cause?: Asbestos

A

Bronchogenic carcinoma > mesothelioma (lung)

189
Q

What cancer does the following toxin cause?: Carbon tetrachloride

A

Centrilobular necrosis, fatty change (liver)

190
Q

What cancer does the following toxin cause?: Cigarette smoke

A

Transitional cell carcinoma (bladder)
Squamous cell carcinoma/adenocarcinoma (esophagus
Renal cell carcinoma (kidney)
Squamous cell carcinoma (Larynx)
Squamous cell and small cell carcinoma (lung)
Pancreatic adenocarcinoma (pancreas)

191
Q

What cancer does the following toxin cause?: ethanol

A

Haptocellular carcinoma (liver)

192
Q

What cancer does the following toxin cause?: Ionizing radiation

A

Papillary thyroid carcinoma (thyroid)

193
Q

What cancer does the following toxin cause?: nitrosamines (smoked foods)

A

gastric cancer (stomach)

194
Q

What cancer does the following toxin cause?: radon

A

lung cancer (2nd leading cause after cigarette smoke)

195
Q

What cancer does the following toxin cause?: vinyl chloride

A

angiosarcoma (liver)

196
Q

What effect and associated neoplasm does the following hormone/agent cause?: 1,25-(OH)2 D3 (calcitriol)

A

Hypercalcemia

Hodgkin’s lymphoma, some non-hodgkin’s lymphomas

197
Q

What effect and associated neoplasm does the following hormone/agent cause?: ACTH

A

Cushings syndrome

Small cell lung carcinoma

198
Q

What effect and associated neoplasm does the following hormone/agent cause?: ADH

A

SIADH

Small cell lung carcinoma and intracranial neoplams

199
Q

What effect and associated neoplasm does the following hormone/agent cause?: Antibodies against presynaptic Ca2+ channels at NMJ

A

Lambert-Eaton myasthenic syndrome (muscle weakness)

Renal carcinoma and intracranial neoplasms

200
Q

What effect and associated neoplasm does the following hormone/agent cause?: Erythropoeietin

A

Polycythemia

Renal cell carcinoma, thymoma, hemangioblastoma, hepatocellular carcinoma, leiomyoma, pheochromocytoma

201
Q

What effect and associated neoplasm does the following hormone/agent cause?: PTHrP

A

Hypercalcemia

Squamous cell lung carcinoma, renal cell carcinoma, breast cancer

202
Q

What is the incidence of prostate cancer in men vs breast cancer in women?

A

men, prostate, 32%

women, breast, 32%

203
Q

What is the indigence of lung cancer in men and women?

A

men - 16%

women - 13%

204
Q

What is the incidence of colon/rectal cancer in men vs women?

A

men - 12%

women - 13%

205
Q

What is the mortality rate of lung cancer in men vs women?

A

men - 33%

women - 23%

206
Q

What is the mortality rate of prostate vs breast cancer?

A

prostate - 13%

breast - 18%

207
Q

What is the progression of metastasis to the brain?

A

Lung > breast > genitourinary > osteosarcoma > melanoma > GI

208
Q

What is the progression of metastasis to the Liver?

A

Colon&raquo_space;> stomach > pancreas

209
Q

What is the progression of metastasis to the Bone?

A

Prostate, breast > lung > thyroid

210
Q

What percentage of brain tumours are from metastasis?

211
Q

What are the most common sites of metastasis?

A
  1. regional lymph nodes

2. Liver and Lung

NPLEX 1 (10 decks)

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