Pathology Flashcards
(211 cards)
1
Q
What is the definition of apoptosis?
A
Programmed cell death
2
Q
Does apoptosis require ATP?
A
Yes
3
Q
Describe how apoptosis occurs.
A
Intrinsic and Extrinsic pathways: both pathways –> activation of cytosolic camases that mediate cellular breakdown.
4
Q
Is there inflammation involved in apoptosis?
A
No. (unlike necrosis)
5
Q
Apoptosis is characterized by deeply _________ cytoplasm.
A
Eosinophilic
6
Q
What is pyknosis?
A
Nuclear shrinkage seen in apoptosis
7
Q
What is karyorrhexis?
A
nuclear fragmentation seen in apoptosis
8
Q
What types of cells increase drastically during apoptosis?
A
basophils
9
Q
Name one sensitive indicator of apoptosis
A
DNA laddering
10
Q
Describe DNA laddering.
A
During karyorhexis, endonucleases cleave at internucleosomal regions, yielding 180-bp fragments.
11
Q
When do we see the intrinsic pathway for apoptosis used?
A
Involved in tissue remodelling in embryogenesis
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Occurs when a regulating factor is withdrawn from a proliferating cell population (e.g IL-2 after a completed immunological reaction –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)
13
Q
Changes in pro-apoptotic factors lead to…
A
increase in mitochondrial permeability and cytochrome c release
14
Q
Name 2 pro-apoptotic proteins.
A
BAX and BAK
15
Q
Name an anti-apoptotic protein.
A
Bcl-2
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.
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.
18
Q
Where are BAX and Bcl-2 found in the cell?
A
mitochondria
19
Q
Where are cytochrome c found in the cell?
A
mitochondria
20
Q
Describe the two pathways of the extrinsic apoptosis
A
- Ligand receptor interactions (FasL binding to Fas [CD95])
2. Immune cell (cytotoxic T-cell release of perforin and granzyme)
21
Q
Fas-FasL interaction if necessary in _______________ selection
A
thymic medullary negative selection
22
Q
What do mutations in Fas do?
A
increase the number of circulating self-reacting lymphocytes due to failure of colonial deletion
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.
24
Q
What does FADD do?
A
FADD binds inactive caspases, activating them.
25
What is the basis for autoimmune disease?
Defective Fas-FasL interaction
26
List the 6 types of necrosis
1. Coagulative
2. Liquefactive
3. Caseous
4. Fatty
5. Fibrinoid
6. Gangrenous
27
Where does coagulative necrosis occur?
Heart, liver, kidney (in tissues supplied by end-arteries)
28
Where does liquifactive necrosis occur?
Barin, bacterial abscess, occurs in CNS due to high fat content
29
How does coagulative necrosis progress?
increased cytoplasmic binding of acidophilic dye. Proteins denature first, followed by enzymatic degradation
30
How does liqifactive necrosis progress?
In contrast to coagulative necrosis, enzymatic degradation due to the release of lysosomal enzymes occurs first
31
What pathogens result in caseous necrosis?
TB, systemic fungi, Nocardia
32
What types of fatty necrosis exist?
Enzymatic - pancreatitis [saponification]
| Non-enzymatic - Breast Trauma
33
What dis-eases lead to fibrinoid necrosis?
Vasculitides (e.g. Henoch-Schonlein purpura, Churg-Strauss syndrome)
Malignant hypertension
34
What types of gangrenous necrosis exist?
Dry (ischemic coagulative)
| Wet (infection)
35
Where are gangrenous necrosis common?
Limbs and GI tract
36
List some processes that cause cell injury that are reversible (O2 is still present)
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
37
List some processes that cause cell injury that are irreversible.
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)
38
What area if susceptible to hypoxia/ischemia and infarction in the brain?
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)
39
What area if susceptible to hypoxia/ischemia and infarction in the Heart?
Subendocardium (LV)
40
What area if susceptible to hypoxia/ischemia and infarction in the Kidney?
Straight segment of proximal tubule (medulla)
| Thick ascending limb (medulla)
41
What area if susceptible to hypoxia/ischemia and infarction in the Liver?
Area around the central vein (zone 3)
42
What area if susceptible to hypoxia/ischemia and infarction in the Colon?
Splenic flexure, rectum
43
What areas of the brain does hypoxic ischemic encephalopathy (HIE) affect?
Pyramidal cells of the hippocampus and Purkinje cells of the cerebellum
44
When/Where do red infarcts arise?
Occur in loose tissue with multiple blood supplies, such as liver, lung, and intestines. Red = reperfusion
45
When/Where do pale infarcts arise?
Occur in solid tissues with a single blood supply, such as heart, kidney, and spleen.
46
What is the first sign of shock?
Tachycardia
47
What types of shock are included under the umber ally term: distributive shock?
Includes: septic, neurogenic and anaphylactic shock
48
What characterizes distributive shock?
High output failure (decreased TPR, increased CO, increased venous return)
Decreased PCWP
Vasodilation (warm skin)
Failure to increase blood pressure with IV fluids
49
What characterizes hypovolemic/cardiogenic shock?
```
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
```
50
What cells mediate acute inflammation?
Neutrophils, eosinophils, antibodies
51
What cells mediate chronic inflammation?
Mononuclear cells and fibroblasts
52
Define Granuloma
nodular collection of epithelioid macrophages and giant cells. Outcomes include scarring and amyloidosis.
53
Define Chromatolysis
Increase in protein synthesis in an effort to repair the damaged axon following axonal injury.
54
What characterizes chromatolysis?
Round cellular swelling
Displacement of the nucleus to the periphery
Dispersion of Nissl substances through cytoplasm
55
What is dystrophic calcification?
Calcium deposition in tissue secondary to necrosis (usually localized).
56
In ______ calcification, patients are generally normocalcemic
In ______ calcification, patients are generally NOT normocalcemic
Dystrophic calcification = normocalcemic
| Metastatic calcification = NOT normocalcemic
57
Define Matastatic Calcification
Widespread deposition of Ca+ in normal tissue secondary to hypercalcemia or higher Ca+/P product
58
What is the interaction between pH levels and Calcium deposition?
```
Increased pH (basic) = higher calcium deposition
Decreased pH (acidic) = less calcium deposition
```
59
Where does leukocyte extraversion predominantly occur?
postcapillary venules
60
What are the 4 steps of Leukocyte extraversion?
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
61
How do free radicals damage cells?
membrane lipid peroxidation
protei modification
DNA breakage
62
How do we end up with free radical injury?
```
Radiation exposure
metabolism of drugs (phase 1)
redox reactions
nitric oxide
transition metals
leukocyte oxidative burst
```
63
How can free radicals be eliminated?
Enzymes, spontaneous decay, antioxidants (Vit. a,c,e)
64
Following an injury to skin, what % of tensile strength can a patient expect to regain and how long will it take
70-80% of pre-injury tensile strength
| in 3 months
65
Describe the differences between hypertrophic scars and keloid scars in terms of collagen synthesis
Collagen synthesis increases in hypertrophic scars but increases MORE in keloids
66
Describe the differences between hypertrophic scars and keloid scars in terms of collagen arrangement
Keloid scars = disorganized collagen
| Hypertrophic scares = parallel scars
67
Describe the differences between hypertrophic scars and keloid scars in terms of extent of scaring
Keloid - extend beyond the borders of the original scar
| Hypertrophic scars - confined to the border of the original wound
68
Describe the differences between hypertrophic scars and keloid scars in terms of recurrence
Keloid - frequently require following resection
| Hypertrophic scars - infrequently recur following resection
69
What is the role of PDGF in wound healing?
secreted by activated platelets and macrophages
Induces vascular remodeling and smooth muscle cell migration
Stimulated fibroblast growth for collagen synthesis
70
What is the role of FGF in wound healing?
Stimulated all aspect of angiogenesis
71
What is the role of EGF in wound healing?
Stimulated cell growth via tyrosine kinases (e.g. EGFR, as expressed by ERBB2)
72
What is the role of TGF-B in wound healing/
Angiogenesis, fibrosis, cell cycle arrest
73
What is the role of metalloproteinases in wound healing?
Tissue remodeling
74
What cells are immediate/inflammatory cell markers of wound healing?
Platelets, neutrophils, macrophages
75
What are the characteristic findings of an area with lots of platelets, neutrophils and macrophages present during wound healing?
clot formation, increased vessel permeability and neutrophil migration into tissue; macrophages clear debris 2 days later
76
What are the characteristic findings of an area with lots of fibroblasts, myofibroblasts, endothelial cells, keratinocytes, macrophages during wound healing?
Depositionof granulation tissue and collagen, angiogenesis, epithelial cell proliferation, dissolution of clot, and wound contraction (mediated by myofibroblasts)
77
What cells are present during the proliferative phase (2-3 days after wound)?
Firboblasts, myofibroblasts, endothelial cells, keratinocytes, macrophages
78
What cells are present in the 3rd and final phase of wound healing - remodelling (1 week after the wound)?
Fibroblasts
79
What are the characteristic finding of an area with lots of fibroblasts present after a wound occurs?
Type 3 collagen replaced by type 1 collagen.
| Increase in tensile strength of tissue.
80
What is it that induces and maintains granuloma formation?
TNF-a
81
List some diseases that are granulomatous
```
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
```
82
Transudate/Exudate - which is thick and which is thin
Exudate - thick
| Transudate - thin
83
Exudate is protein ___
| Transudate is protein ___
Exude - protein rich
| transudate - protein poor
84
Exudate specific gravity _____
| Transudate specific gravity ____
Exudate SG = >1.020
| Transudate SG = <1.020
85
Transudate/Exudate - which is cellular and which is hypocellular
Transudate - hypocellular
| Exudate - cellular
86
When do we see exudates?
Lymphatic obstruction
Inflammation/infection
Malignancy
87
When do we see transudate?
increases in hydrostatic pressure (e.g. CHF)
decreases in oncotic pressure (e.g. cirrhosis)
Na+ retention
88
When do we get an increase in ESR?
```
most anemias
infections
inflammation
cancer
pregnancy
autoimmune disease
```
89
When do we get a decrease in ESR?
sick cell disease
polycythemia
CHF
90
One of the leading causes of fatality from toxicologic agents in children is....
Iron Poisoning
91
What is the mechanism of iron poisoning?
cell death due to per oxidation of membrane lipids
92
What are the symptoms of Iron Poisoning?
Acute - nausea, vomiting, gastric bleeding, lethargy
| Chronic - metabolic acidosis, scarring leading to GI obstruction
93
What is the treatment for Iron Poisoning?
chelation and dialysis
94
Define Amyloidosis.
Abnormal aggregation of proteins (or their fragments) into B-pleated sheet structures --> damage and apoptosis
95
List the 6 types of amyloidosis.
1. AL (primary)
2. AA (secondary)
3. Dialysis-related
4. Heritable
5. Age-related (senile) systemic
6. Organ specific
96
Describe AL type amyloidosis
Deposition of proteins from Ig Light chains
97
Describe AA type amyloidosis
Seen w/ chronic conditions, such as RA, IBD, spondyloarthropathy, protracted infection. Fibrils composed of serum Amyloid A. Often multi systemic like AL amyloidosis.
98
Describe Dialysis-related amyloidosis
Fibrils composed of B2 microglobin in patients with ESRD and/or on long-term dialysis.
99
Which is the amyloidosis types may present with carpal tunnel?
Dialysis-type
100
Describe heritable type amyloidosis
Heterogeneous group of disorders. Example is ATTR neurologic/cardia amyloidosis due to tranthyretin (TTR or prealbumin) gene mutation
101
Describe age-related systemic amyloidosis
Due toe deposition of normal (wild type) TTR in myocardium and other sites. Slower progression of cardiac dysfunction relative to AL amyloidosis
102
Describe organ specific amyloidosis
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
What is lipofuscin?
A yellow/brown "wear and tear" pigment associated with normal aging
104
How is lipofuscin formed?
Formed by oxidation and polymerization of autophagocytosed organellar membranes
105
How does invasive carcinoma manage to invade the basement membrane?
using collagenases and hydrolyses (metalloproteinases)
106
What other name is P-glycoprotein known by?
multi drug resistance protein 1 (MDR1)
107
What does P-glycoprotein (aka MDR1) do?
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
Define Anaplasia
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
Define Neoplasia
A clonal proliferation of cells that is uncontrolled and excessive. Neoplasia may be benign or malignant
110
Define Desmoplasia
Fibrous tissue formation in response to neoplams (e.g. linitis pastica in diffuse stomach cancer).
111
What is the difference between tumour grade and stage?
```
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
Does the grade or stage have more prognostic value?
the stage
113
What is the staging system for tumours called and how does it work?
TNM staging system
T = timor size
N = node involvement
M = metastasis
114
Name the neoplasm associated with this condition: Acanthosis ingrains (hyper pigmentation and epidermal thickening)
Visceral malignancy (esp. stomach)
115
Name the neoplasm associated with this condition: Actinic keratosis
Squamous cell carcinoma of the skin
116
Name the neoplasm associated with this condition: AIDS
Aggressive malignant lymphomas (non Hodgkin) and Kaposi sarcoma
117
Name the neoplasm associated with this condition: Autoimmune disease (e.g Hashimotos thyroiditis, SLE)
Lymphoma
118
Name the neoplasm associated with this condition: Barrett's oesophagus
Esophageal adenocarcinoma
119
Name the neoplasm associated with this condition: Cirrhosis
Hepatocellular carcinoma
120
Name the neoplasm associated with this condition: Cushing syndrome
Small cell lung cancer
121
Name the neoplasm associated with this condition: Dermatocyositis
Lung cancer
122
Name the neoplasm associated with this condition: Down syndrome
ALL, AML
123
Name the neoplasm associated with this condition: Dysplastic nevus
Malignant melanoma
124
Name the neoplasm associated with this condition: Hypercalcemia
Squamous cell lung cancer
125
Name the neoplasm associated with this condition: Immunodeficiency states
Malignant lymphomas
126
Name the neoplasm associated with this condition: Lamber-Eaton myasthenic syndrome
Small cell lung cancer
127
Name the neoplasm associated with this condition: Myasthenia gravis, pure RBC aplasia
Thymoma (tumour of the epithelial cells of the thymus)
128
Name the neoplasm associated with this condition: Paget's disease of bone
secondary osteosarcoma and fibrosarcoma
129
Name the neoplasm associated with this condition: Plummer-Vinson syndrome (decreased iron)
Squamous cell carcinoma of esophagus
130
Name the neoplasm associated with this condition: Polycythemia
Renal cell carcinoma, hepatocellular carcinoma
131
Name the neoplasm associated with this condition: Radiation exposure
Laukemia, sarcoma, papillary thyroid cancer, and breast cancer
132
Name the neoplasm associated with this condition: SIADH (syndrome of inappropriate anti-duiretic hormone secretion)
Small cell lung cancer
133
Name the neoplasm associated with this condition: Tuberous sclerosis (facial angiofibroma, seizures, intellectual disability)
Giant cell astrocytoma, renal angiomyolipoma, and cardiac rhabdomyoma
134
Name the neoplasm associated with this condition: Ulcerative Colitis
Colonic adenocarcinoma
135
Name the neoplasm associated with this condition: Xeroderma pigmentosum, albinism
Melanoma, basal cell carcinoma, and especially squamous cell carcinomas of skin
136
Explain how oncogenes increase cancer risk
Gain of oncogene function --> increased cancer risk.
| Need damage to ONLY 1 allele
137
Explain how tumor suppressor genes increase cancer risk
Loss of function --> increased cancer risk. Both alleles much be lost for expression of disease
138
Name the tumour and gene product associated with the following oncogene: BCR-ABL
CML, ALL
| Tyrosine Kinase
139
Name the tumour and gene product associated with the following oncogene: bcl-2
Follicular and undifferentiated lymphomas
| Anti-apoptotic molecule (inhibits apoptosis)
140
Name the tumour and gene product associated with the following oncogene: BRAF
Melanoma
| Serine/threonine kinase
141
Name the tumour and gene product associated with the following oncogene: c-kit
```
Gastrointestinal stromal tumor (GIST)
Cytokine receptor (for stem cell factor)
```
142
Name the tumour and gene product associated with the following oncogene: c-myc
Burkitt lymphoma
| Transcription factor
143
Name the tumour and gene product associated with the following oncogene: HER2/neu (c-erbB2)
Breast, ovarian, and gastric carcinomas
| Tyrosine Kinase
144
Name the tumour and gene product associated with the following oncogene: L-myc
Lung tumor
| Transcription factor
145
Name the tumour and gene product associated with the following oncogene: N-myc
Neuroblastoma
| Transcription factor
146
Name the tumour and gene product associated with the following oncogene: ras
Colon cancer, lung cancer, pancreatic cancer
| GTPase
147
Name the tumour and gene product associated with the following oncogene: ret
MEN 2A and 2B
| Tyrosine kinase
148
Name the tumour and gene product associated with the following tumour suppressor: APC
```
Colorectal cancer (associated with FAP)
N/A
```
149
Name the tumour and gene product associated with the following tumour suppressor: BRCA1
Breast and Ovarian cancer
| DNA repair protein
150
Name the tumour and gene product associated with the following tumour suppressor: BRCA2
Breast and Ovarian cancer
| DNA repair protein
151
Name the tumour and gene product associated with the following tumour suppressor: CPD4/SMAD4
Pancreatic cancer
| DPC - deleted in pancreatic cancer
152
Name the tumour and gene product associated with the following tumour suppressor: DCC
Colon cancer
| DCC - deleted in colon cancer
153
Name the tumour and gene product associated with the following tumour suppressor: MEN1
MEN type 1
| N/A
154
Name the tumour and gene product associated with the following tumour suppressor: NF1
Neurofibromatosis type 1
| RAS GTPase activating protein (neurofibromin)
155
Name the tumour and gene product associated with the following tumour suppressor: NF2
Neurofibromatosis type 2
| Merlin (schwannomin) protein
156
Name the tumour and gene product associated with the following tumour suppressor: p16
Melanoma
| Cyclin-dependant kinase inhibitor 2A
157
Name the tumour and gene product associated with the following tumour suppressor: p53
Most human cancers, Li-fraumeni syndrome
| Transcription factor for p21, blocks G1 --> S phase
158
Name the tumour and gene product associated with the following tumour suppressor: PTEN
Breast cancer, prostate cancer, endometrial cancer
| N/A
159
Name the tumour and gene product associated with the following tumour suppressor: Rb
Retinoblastoma, osteosarcoma
| Inhibits E2F; blocks G1 --> S phase
160
Name the tumour and gene product associated with the following tumour suppressor: TSC1
Tuberous sclerosis
| Hamartin protein
161
Name the tumour and gene product associated with the following tumour suppressor: TSC2
Tuberous sclerosis
| Tuberin protein
162
Name the tumour and gene product associated with the following tumour suppressor: VHL
von Hippel-Lindau disease
| Inhibitis hypoxia inducible factor 1a
163
Name the tumour and gene product associated with the following tumour suppressor: WT1
```
Wilms Tumour (nephroblastoma)
N/A
```
164
Name the tumour and gene product associated with the following tumour suppressor: WT2
```
Wilms Tumor (nephroblastoma)
N/A
```
165
Can tumour markers be used in cancer diagnosis?
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
What does the presence of the following tumour marker tell us?: Alkaline phosphatase
Metastases to bone, liver, paget disease of bone, seminoma (placental ALP)
167
What does the presence of the following tumour marker tell us?: a-fetoprotein
Normally made by fetus. Hepatocellular carcinoma, hepatoblastoma, yolk sac (endodermal sinus) timor, testicular cancer, mixed germ cell timor (co-secreted with B-hCG)
168
What does the presence of the following tumour marker tell us?: B-hCG
Hydaticorm moles and Choriocarcinomas (Gestational trophoblastic disease), testicular cancer
Commonly associated with pregnancy
169
What does the presence of the following tumour marker tell us?: CA-15-3/CA-27-29
Breast Cancer
170
What does the presence of the following tumour marker tell us?: CA-19-9
Pancreatic adenocarcinoma
171
What does the presence of the following tumour marker tell us?: CA-125
Ovarian cancer
172
What does the presence of the following tumour marker tell us?: CEA
CarcinoEmbryonic Antigen. Very nonspecific but produced by ~70% of colorectal and pancreatic cancers; also produced by gastric, breast, and medullary thyroid cancers
173
What does the presence of the following tumour marker tell us?: PSA
prostate-specific antigen. Used to follow prostate adenocarcinoma. Can also be elected in BPH and prostatitis. Questionable risk/benefit for screening
174
What does the presence of the following tumour marker tell us?: S-100
neural crest origin (e.g. melanomas, neural tumors, schwannomas, Langerhans cell historcytosis)
175
What does the presence of the following tumour marker tell us?: TRAP
Tartate-Resistant Acid Phosphatase (TRAP)
| Hairy cell leukaemia - a B-cell neoplasm
176
What cancer does the following microbe cause?: EBV
Burkitt lymphoma
Hodgkin lymphoma
nasopharyngeal carcinoma
CNS lymphoma (in immonocompromised patients)
177
What cancer does the following microbe cause?: HBV, HCV
Hepatocellular carcinoma
178
What cancer does the following microbe cause?: HHV-8 (Kaposi sarcoma-associated herpesvirus)
Kaposi sarcoma
| body cavity fluid B-cell lymphoma
179
What cancer does the following microbe cause?: HPV
Cervical and penile/anal carcinoma (16,18)
| head and neck or throat cancer
180
What cancer does the following microbe cause?: H. pylori
Gastric adenocarcinoma
| MALT lymphoma
181
What cancer does the following microbe cause?: HTLV-1
adult T-cell leukemia/lymphoma
182
What cancer does the following microbe cause?: Liver fluke (Clonorchis sinensis)
Cholangiocarcinoma
183
What cancer does the following microbe cause?: Schistosoma haematobium
Bladder cancer (squamous cell)
184
What cancer does the following toxin cause?: Aflatoxins (Aspergillus)
Hapatocellular carcinoma (liver)
185
What cancer does the following toxin cause?: Alkalatin agents
Leukemia/lymphoma (blood)
186
What cancer does the following toxin cause?: Aromatic amines (e.g. benzidine, 2-naphthlamine)
Transitional cell carcinoma (bladder)
187
What cancer does the following toxin cause?: Arsenic
Angiosarcoma (Liver)
Lung cancer (Lung)
Squamous cell carcinoma (Skin)
188
What cancer does the following toxin cause?: Asbestos
Bronchogenic carcinoma > mesothelioma (lung)
189
What cancer does the following toxin cause?: Carbon tetrachloride
Centrilobular necrosis, fatty change (liver)
190
What cancer does the following toxin cause?: Cigarette smoke
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
What cancer does the following toxin cause?: ethanol
Haptocellular carcinoma (liver)
192
What cancer does the following toxin cause?: Ionizing radiation
Papillary thyroid carcinoma (thyroid)
193
What cancer does the following toxin cause?: nitrosamines (smoked foods)
gastric cancer (stomach)
194
What cancer does the following toxin cause?: radon
lung cancer (2nd leading cause after cigarette smoke)
195
What cancer does the following toxin cause?: vinyl chloride
angiosarcoma (liver)
196
What effect and associated neoplasm does the following hormone/agent cause?: 1,25-(OH)2 D3 (calcitriol)
Hypercalcemia
| Hodgkin's lymphoma, some non-hodgkin's lymphomas
197
What effect and associated neoplasm does the following hormone/agent cause?: ACTH
Cushings syndrome
| Small cell lung carcinoma
198
What effect and associated neoplasm does the following hormone/agent cause?: ADH
SIADH
| Small cell lung carcinoma and intracranial neoplams
199
What effect and associated neoplasm does the following hormone/agent cause?: Antibodies against presynaptic Ca2+ channels at NMJ
Lambert-Eaton myasthenic syndrome (muscle weakness)
| Renal carcinoma and intracranial neoplasms
200
What effect and associated neoplasm does the following hormone/agent cause?: Erythropoeietin
Polycythemia
| Renal cell carcinoma, thymoma, hemangioblastoma, hepatocellular carcinoma, leiomyoma, pheochromocytoma
201
What effect and associated neoplasm does the following hormone/agent cause?: PTHrP
Hypercalcemia
| Squamous cell lung carcinoma, renal cell carcinoma, breast cancer
202
What is the incidence of prostate cancer in men vs breast cancer in women?
men, prostate, 32%
| women, breast, 32%
203
What is the indigence of lung cancer in men and women?
men - 16%
| women - 13%
204
What is the incidence of colon/rectal cancer in men vs women?
men - 12%
| women - 13%
205
What is the mortality rate of lung cancer in men vs women?
men - 33%
| women - 23%
206
What is the mortality rate of prostate vs breast cancer?
prostate - 13%
| breast - 18%
207
What is the progression of metastasis to the brain?
Lung > breast > genitourinary > osteosarcoma > melanoma > GI
208
What is the progression of metastasis to the Liver?
Colon >>> stomach > pancreas
209
What is the progression of metastasis to the Bone?
Prostate, breast > lung > thyroid
210
What percentage of brain tumours are from metastasis?
50%
211
What are the most common sites of metastasis?
1. regional lymph nodes
| 2. Liver and Lung
