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1
Q

Three characteristics of apoptosis?

A

1) Programmed cell death
2) esinophilis in cytoplasm + cell shrinkage and fragement
3) Cell membrane remains intact without inflammation

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2
Q

What are functions of intrinsic apoptosis (mitochrondrial pathway) ?

A

1) For tissue remodeling in embryogenesis

2) Regulated by Bcl-2 family

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3
Q

What are the pathways for extrinsic cell death?

A

1) Ligand receptor interations (TNF alpha)

2) Immune cell (cytotoxic)

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4
Q

where is coagulative necrosis seen? Histology?

A

1) Ischemia and infarct

2) Histology: Increased cytoplasmic binding of acidophilic dyes

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5
Q

When is liquidefactive necrosis seen? Histology?

A

1) Bacterial abcesses
2) Neutrophils release lysosomal enzymes that digest the tissues
3) Histology: neutrophils and cell debris are seen in bacterial infection

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6
Q

When is caseous necrosis seen?

A

1) TB and fungi
2) Granular debris
3) Fragmented cells and debris surrounded by lymphocytes and macrophages.

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7
Q

When is fat necrosis seen?

A

1) enzymatic (acute pancreatitis), saponification

2) Outline of fat cells with H an E stain

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8
Q

When is fibrinoid necorisis seen?

A

1) Seen in immune reactions, polyartritis nodosa
2) Giant cell temporal arteritis
3) Vessels are think and pink

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9
Q

What are some changes with reversible cell injury?

this is reverisble with oxygen

A

1) Cell swelling (Na K+ pump injury)
2) Membrane blebbing
3) Decrease glycogen, increase fat

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10
Q

What are signs of irreversible cell injury?

A

1) Mitochrondral permeability and vacuoloziation
2) Plasma membrane damage
3) Lysosomal rupture

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11
Q

What are the organs most sensitive to hypoxia?

A

1) Brain (ACA, MCA, PCA bondaries)
2) Heart
3) Kidney
4) Liver
5) Colon

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12
Q

What are the different types of infarcts? Red vs. pale?

A

Red, reperfusion injury, when there are multiple blood supplies (liver, lung, testes)

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13
Q

What are the pale infarcts?

A

1) Single ended arterial supply (heart, kidney, spleen)

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14
Q

What are characteristics of inflammation?

A

1) red, pain, heat, swelling, and loss of function

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15
Q

What is the vascular vs cellular components of inflammation?

A

1) vascular: increased permeability, and vasodilation

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16
Q

What are the cellular componenets (acute) vs chronic?

A

1) Acute is rapid onset, and short duration (can have resolution, abcess)
2) Monocytes, and macrophages, persistent destruction, and repair with blood vessel proliferation
(going to have scarring and amyloidosis)

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17
Q

What is chromatolysis?

A

1) Neuronal cell body, axonal injury (increased protein synthesis)
2) Round cellular swelling
Can have Wallerian degeneration (degeneration of axon distal to site of injury)

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18
Q

What is dystrophic calcification?

A

Calcium deposition secondary to injury or necrosis
(Aortic stenosis)
Tuberculosis in the lungs. Not associated with the level of Ca in the body

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19
Q

What is metastatic calcification?

A

Widespread deposition of Ca in normal tissue
1) Hyperparathyroidism
2) Sarcoidosis
Hyper vitamin D
3) Metastatic calcifications (pneumonitis), patients are NOT normocalcemic

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20
Q

what are the steps of leucocyte extravasation?

A

1) Margination and rolling
2) Tight binding
3) Diapedesis
4) Migration

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21
Q

What is free-radical injury?

A

1) Lipid peroxidation, protein modification, DNA breakage

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22
Q

What are agents that initiate free radical injury?

A

1) Radiation exposure
2) Drug metabolism
3) WBC

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23
Q

What are diseases caused by free-radical injury?

A

1) Retinopathy of prematurity
2) Bronchopulmonary dysplasia
3) Drug/toxicity carbon tetrachloride (heptotoxicity)
4) Metal toxicity (hemochromatosis)

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24
Q

What is are possible causes of inhalation injury?

A

1) Smoke
2) Fire
3) Small particles or irrtiants

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25
What are some examples of inhalation injury?
1) Tracheobronchitis 2) edema 3) Pneumonia 4) ARDS
26
What does bronchoscopy show on inhalation injury?
1) edema 2) congestion 3) soot deposition
27
How long for 80% of tensil strenth to be regained?
3 months
28
What are the differences between the hypertrophic vs keloid ?
Hypertrophic 1) Increased collagen synthesis 2) Confined to borders of original wound 3) Can have regression 4) Infrequent re-occurrence Keloid 1) Increaed collagen ++++ 2) Disorganized 3) Beyond borders 4) Progressive growth
29
Tissue mediator: PDGF?
1) Secreted by actvated platelets and macrophages 2) Induces vascular remodelling 3) Stimulates fibroblasts
30
Tissue mediator FGF?
Stimulates angiogenesis
31
Tissue mediator EGF?
Stimulates cell growth
32
Tissue mediator TFG-B ?
Angiogenesis
33
Metalloproteinases?
Tissue remodelling
34
VEGF?
Stimulates angiogeneis.
35
what are the stages of the wound healing?
1) Inflammatory (3 days after the wound): clot formation, increased vessel permability, and tissue migration 2) Proliferative (day 3 to weeks later) fibroblasts, and myoblasts (deposition of granulation, collagen, and angiogenesis) 3) Remodelling: fibroblasts, and collagen 3 give tensile strength
36
What are examples of granulomatous disease causes?
1) Bacterial (mycobacteria, bartonella, listeria) 2) Fungal (endemic mycoses) 3) Parasites (schistosomiasis) 4) Autoinflammatory (sarcoidosis, Crohns, Primary bilary cirrhosis, Wegners), giant cell, Takayasu. 5) Foreigh matrial: berylloiosis, talcosis
37
What are more common caused of caseating necrosis?
Infectious (TB)
38
How is sarcoidosis diagnosed?
Need to do a biopsy of sarcoidosis. (of the granulomas)
39
Characteristics of exudate vs transudate?
Exudate vs transudate 1) Celluar vs hypocellular 2) Increased protein vs decreased protein and LDF 3) Specific gravity > 1.02 vs
40
What causes the ESR to increase, and to decrease?
``` Increase ESR vs Decrease ESR Anemia vs sickle cell Infections vs polycythemia Inflammation vs Heart failure Cancer vs microcytosis Renal disease vs hypofibrinogenemia ```
41
what is amyloidosis characterized by?
Abnormal segregation of proteins into pleated sheets
42
How is amyloidosis visualized ?
By Congo stain | By Hand E stain
43
What are 6 types of amyloidosis?
1) AL (deposition of light chains) 2) AA (chronic inflammatory conditions sucj as RA, and IBD) 3) Dialysis related ( Fibrils of microglobulin) 4) Heritable: amyloid polyneuropathies 5) Age related: transthyretin deposited in the cardiac chambers 6) Organ specific: amyloidosis to a single organ
44
What is lipofuscin?
Normal wear and tear associated with aging. | In elderly person can be deposited in the heart, colon, or eye
45
what is cellular change, atrophy?
decrease tissue mass due to number of cells (disuse, denervation)
46
What is cellular change hypertrophy?
Increase in size of the cell
47
What is cellular change of hyperplasia?
Increase in number of cells (risk factor for future malignancy)
48
What is cellular change of metaplasia?
Replacement of one cell tyoe by another due to irritant.
49
What is neoplasia?
Clonal proliferation of cells, can be benign or malignant
50
What is dysplasia?
Disrodered, non neoplastic growth (only epithelial cells) severe displasia can lead to neoplasia
51
What is cellular differentiation?
The degree to which the malignant tumor resembles the tissue of origin. Poorly differentiated doesn't look at all like the original tissue
52
What is anaplasia?
Complete lack of differentiation of cells in a malignant neoplasm.
53
What are the stages of neoplastic progression?
Normal cells to dysplasia, to carcinoma insity, to invasive carcinoma (This involves invasion of basement membrane using collagenase and hydrolase) Cell to cell contact lost by inactivation of E-Cadherin
54
What are the seed and soil theory of metastasis?
Seed:tumor embolus Soil: Target the first organ encountered in the capillary bed
55
What is the different between grade and stage of tumor?
Degree of differentiation (low grade means highly differentiated) Stage: Localized or spread
56
What is the TNM staging?
T = tumor size N=Node involvement M=Metastasis
57
What does carcinoma suggest?
Epithilial origin
58
What does sarcoma suggest?
Mesenchymal origin
59
What does benign suggest?
Well differentiated, well demarcated, low mitotic activity no mets
60
What does malignancy suggest?
Poor differentiation, erratic growth, local invasion, mets, decrease apoptosis
61
what are the most common male cancers?
1) Prostate 2) Lung 3) Colon
62
What are most common female cancers?
1) Breast 2) Lung 3) Colon
63
What is the highest mortality for men (cancer)?
1) Lung 2) Prostate 3) Colon
64
what is the highest mortality of woman (cancer)?
1) Lung 2) Breast 3) Colon
65
What are 2 types of paraneoplastic syndromes?
1) Acanthosis nigricans 2) Lser Trelat 3) Hypercalcemia 4) Cushing 5) Hyponatremia 6) Polycythemia 7) Red cell aplasia 8) Good syndrome 9) Trousseacu 10) endocarditis *sterile plaque* 11) Anti-NMDA recepter encephalitis 12) Myoclonus ataxia 13) Paraneoplastic cerebeller degeneration 14) Paraneoplastic encephalomyletis 15) Lambert-Eaton mysanthenic 16) Mysanthia gravis
66
What is acanthosis nigricans consist of?
Hyperpigmented plaques in axilla | Associated with gastric adenocarcinoma (and other viscral malignancies) due to insulin resistance
67
What are the signs of Leser Trelat? And association?
1) Multiple seborrheic keratosis | 2) Associated with GI adenocarcinomas
68
What is the mechanism of hyercalcemia?
1) Increased PTHrP or increased 1.25 OH vitamin D | 2) Squameous cell carcinoma of the lung, head, and neck, renal bladder, breast and ovarian
69
What is the mechanism of Cushing?
1) Increased ACTH | 2) Small cell lung cancer
70
What is the mechanism of Hyponatremia?
1) Increased ADH | 2) Small cell lung cancer
71
What is mechanism of polycythemia?
1) Increased erythropoietin 2) Renal cell carcinoma 3) Hepatocellular carcinoma 4) Hemangioblastoma 5) Pheochromcytoma 6) Leiomyoma
72
Mechanism of pure red aplasia?
1) Anemia with low reticulocytes | 2) Thymoma
73
Mechanism good syndrome?
1) Hypogammaglogulinemia | 2) Thymoma
74
Mechanism Trousseau syndrome?
1) Migratroy superficial thrombophlebitis | 2) Adenocarcinomas (pancreatic)
75
Mechanism nonbacterial endocarditis?
1) Sterile plaque thrombi | 2) Adenocracinomas (pancreatic)
76
Mechanism of Anti-NMDA receptor encephalitis?
1) Psychiatric disturbance, memory deficits, seizures, dyskinesias, autonomic instability, langage dysfunction 2) Ovarian teratoma
77
Mechanism of Opsoclonus, myoclonus ataxia syndrome?
1) Dancing eyes, Dancing feet | 2) Neuroblastoma, small cell cancer
78
Paraneoplastic cerebellar degeneration?
1) Antibodies against Hu, Yo, Tr Antigens in Purkinje cells 2) Small cell cancer 3) Gynecological and breast, Hodgekins
79
Mechanism of paraneoplastic encephalomyelitis?
1) Antibodies against Hu antigens and neurons | 2) Small cell lung cancer
80
what are causes of Lambert-Eaton mysanthenic syndrome?
1) Antibodies against presynaptic (P/Q type) Ca 2+ | 2) Small cell lung cancer
81
What are causes of mysanthia gravis?
1) Antibodies against post synaptic AChR at NMJ | 2) Thymoma
82
Oncogene associated with ALK?
Lung adenocarcinoma
83
Oncogene associated with BCR-ABL?
CML, ALL
84
Oncogene with BCL-2?
Follicular and diffuse large B cell lymphoma
85
Oncogene with BRAF?
Melanona, non hodgkins
86
Oncogene with c-kit?
gastrointestinal stromal tumor (GIST)
87
Oncogene with m-MYC?
Burkitt's lymphoma
88
Oncogene with Her2/neu (c-erbB2)
Breast and gastric carcinoma
89
Oncogene with JAK 2?
Chronic myeloproliferative disorders
90
Oncogene with KRAS?
Colon Lung Pancreatic
91
What is MYCL1?
Lung tumor
92
What is MYCN?
Neuroblastoma
93
What is RET?
Men 2A, and 2B
94
What is APC?
Colorectal cancer
95
What is BRCA1 and BRCA2?
Breast and ovarian cancer
96
What is CDKN2A?
Melanoma and pancreatic cancer
97
What is DCC?
Colon cancer (deleted in colon cancer)
98
What is DPC 4/SMAD4?
Pancreatic cancer
99
What is MEN1?
Menin
100
What is NF1?
Neurofibromatosis type 1
101
What is NF2?
Neurofibormatosis type 2
102
What is PTEN?
Breast cancer Prostate cancer Endometrial cancer
103
What is rb?
Retinoblastoma, osteosarcoma
104
What is TP53?
Most human cancers, Li-Fraumeni syndrome
105
What is TSC1?
Tuberous sclerosis
106
What is TSC2?
Tuberous sclerosis
107
What is VHL?
von Hippel-Lindau disease | Renal cell carcinoma
108
What is WT1/WT2?
Wilms Tumor.
109
Oncogene microbe EBV?
Burkitt lymphoma Hodgekin's lymphoma Nasopharyngeal carcinoma CNS lymphoma
110
Oncogene HBV, HCV?
Hepatocellular carcinoma, lymphoma
111
Oncogene HHV-8?
Karposi sarcoma
112
Oncogene HPV?
Cervical, penile/anal carcinoma (type 16 and type 18)
113
Oncogene H. Pylori?
Gastric Adenocarcinoma | MALT lymphoma
114
Oncogene HTLV-1?
Adult T cell leukemia
115
Oncogene Liver Fluke?
Cholangiocarcinoma
116
Oncogene Schistosoma haematobium?
Bladder cancer (squamous cell)
117
Carconogene: aflatoxins?
Hepatocellular carcinoma
118
Carcinogen: Alkylating agent?
Leukemia/lymphoma
119
Carcinogen aromatic amines?
Bladder: transitional cell carcinoma
120
Carcinogen Arsenic?
Angisarcoma Lung Cancer Squamous cell carcinoma
121
Carcinogenn: Asbestos?
Lung
122
Carcinogen tetrachloride?
Liver | Centrilobular necorisis
123
Carcinogen: Cigarette Smoke?
``` Bladder Cerivix Esophagus Kidney Larynx Lung Pancrease ```
124
Carcinogen: ethanol ?
Esophagus | Liver
125
Carcinogen: ionizing radiation?
Thyroid
126
Carcinogen: niteosamines?
Stomach cancer
127
Carcinogen: Radon?
Lung cancer
128
Carcinogen: Vinyl Chloride?
Liver (angiosarcoma)
129
When are Psammoma bodies seen?
Papillary carcinoma of thyroid Serous papillary cystadenocarcinoma of the ovary Mengingioma Malignent mesothelioma
130
What are serum tumor markers used for?
Cancer diagnosis and screening (however should not be used for number 1, instead, biopsy Can be used for tumor reoccurrence and response to therapy
131
Tumor marker: Alkaline phosphatase?
Mets to bone or liver Paget disease Seminoma ALP
132
Alpha fetoprotein?
Hepatocellular carcinoma Heptoblastoma Yolk Mixed germ cell tumor
133
Tumor marker B-HCG?
Hydratiform moles Choriocarcinomas Testicular cancer Mixed germ cell
134
Tumor marker CA 15-3/CA 27-29?
Breast cancer
135
Tumor marker CA 19-9?
Pancreatic adenocarcinoma
136
Tumor marker CA 125?
Ovarian Cancer
137
Tumor marker: Calcitonin?
Medullary Thyroid carcinoma
138
Tumor marker CEA?
CarcinoEmbyroicAntigen Non specific 70% of pancreatic, gastric, breast
139
Tumor marke PSA?
Prostate specific antigen | Questionable benefit for prostate screening
140
Tumor marker p-glycoprotein?
Adrenal cell carcinoma
141
What hormones cause Cachexia?
TNF IFN-alpha Il-1 Il-6
142
How do sarcomas spread?
Hemtogenously
143
How is carcinoma spread?
Lymphatics
144
What are the most common brain mets?
Lung > Breast> prostate> melanoma> GI
145
What are the most common liver mets?
Colon >> stomach>> pancrease
146
What are the most common bone mets?
Prostate, breast > lung, thyroid, kidney
147
what are the common types of breast mets?
Are usually mixed
148
What are the common types of lung mets?
Mixed
149
What are the types of kidney mets?
Lytic

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