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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
Q

What are some examples of inhalation injury?

A

1) Tracheobronchitis
2) edema
3) Pneumonia
4) ARDS

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26
Q

What does bronchoscopy show on inhalation injury?

A

1) edema
2) congestion
3) soot deposition

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27
Q

How long for 80% of tensil strenth to be regained?

A

3 months

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28
Q

What are the differences between the hypertrophic vs keloid ?

A

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

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29
Q

Tissue mediator: PDGF?

A

1) Secreted by actvated platelets and macrophages
2) Induces vascular remodelling
3) Stimulates fibroblasts

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30
Q

Tissue mediator FGF?

A

Stimulates angiogenesis

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31
Q

Tissue mediator EGF?

A

Stimulates cell growth

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32
Q

Tissue mediator TFG-B ?

A

Angiogenesis

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33
Q

Metalloproteinases?

A

Tissue remodelling

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34
Q

VEGF?

A

Stimulates angiogeneis.

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35
Q

what are the stages of the wound healing?

A

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

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36
Q

What are examples of granulomatous disease causes?

A

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

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37
Q

What are more common caused of caseating necrosis?

A

Infectious (TB)

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38
Q

How is sarcoidosis diagnosed?

A

Need to do a biopsy of sarcoidosis. (of the granulomas)

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39
Q

Characteristics of exudate vs transudate?

A

Exudate vs transudate

1) Celluar vs hypocellular
2) Increased protein vs decreased protein and LDF
3) Specific gravity > 1.02 vs

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40
Q

What causes the ESR to increase, and to decrease?

A 
Increase ESR vs Decrease ESR
Anemia  vs sickle cell
Infections vs polycythemia 
Inflammation vs Heart failure
Cancer vs microcytosis
Renal disease vs hypofibrinogenemia
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41
Q

what is amyloidosis characterized by?

A

Abnormal segregation of proteins into pleated sheets

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42
Q

How is amyloidosis visualized ?

A

By Congo stain

By Hand E stain

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43
Q

What are 6 types of amyloidosis?

A

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

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44
Q

What is lipofuscin?

A

Normal wear and tear associated with aging.

In elderly person can be deposited in the heart, colon, or eye

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45
Q

what is cellular change, atrophy?

A

decrease tissue mass due to number of cells (disuse, denervation)

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46
Q

What is cellular change hypertrophy?

A

Increase in size of the cell

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47
Q

What is cellular change of hyperplasia?

A

Increase in number of cells (risk factor for future malignancy)

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48
Q

What is cellular change of metaplasia?

A

Replacement of one cell tyoe by another due to irritant.

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49
Q

What is neoplasia?

A

Clonal proliferation of cells, can be benign or malignant

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50
Q

What is dysplasia?

A

Disrodered, non neoplastic growth (only epithelial cells) severe displasia can lead to neoplasia

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51
Q

What is cellular differentiation?

A

The degree to which the malignant tumor resembles the tissue of origin. Poorly differentiated doesn’t look at all like the original tissue

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52
Q

What is anaplasia?

A

Complete lack of differentiation of cells in a malignant neoplasm.

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53
Q

What are the stages of neoplastic progression?

A

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

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54
Q

What are the seed and soil theory of metastasis?

A

Seed:tumor embolus
Soil: Target the first organ encountered in the capillary bed

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55
Q

What is the different between grade and stage of tumor?

A

Degree of differentiation (low grade means highly differentiated)

Stage: Localized or spread

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56
Q

What is the TNM staging?

A

T = tumor size
N=Node involvement
M=Metastasis

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57
Q

What does carcinoma suggest?

A

Epithilial origin

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58
Q

What does sarcoma suggest?

A

Mesenchymal origin

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59
Q

What does benign suggest?

A

Well differentiated, well demarcated, low mitotic activity no mets

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60
Q

What does malignancy suggest?

A

Poor differentiation, erratic growth, local invasion, mets, decrease apoptosis

61
Q

what are the most common male cancers?

A

1) Prostate
2) Lung
3) Colon

62
Q

What are most common female cancers?

A

1) Breast
2) Lung
3) Colon

63
Q

What is the highest mortality for men (cancer)?

A

1) Lung
2) Prostate
3) Colon

64
Q

what is the highest mortality of woman (cancer)?

A

1) Lung
2) Breast
3) Colon

65
Q

What are 2 types of paraneoplastic syndromes?

A

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
Q

What is acanthosis nigricans consist of?

A

Hyperpigmented plaques in axilla

Associated with gastric adenocarcinoma (and other viscral malignancies) due to insulin resistance

67
Q

What are the signs of Leser Trelat? And association?

A

1) Multiple seborrheic keratosis

2) Associated with GI adenocarcinomas

68
Q

What is the mechanism of hyercalcemia?

A

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
Q

What is the mechanism of Cushing?

A

1) Increased ACTH

2) Small cell lung cancer

70
Q

What is the mechanism of Hyponatremia?

A

1) Increased ADH

2) Small cell lung cancer

71
Q

What is mechanism of polycythemia?

A

1) Increased erythropoietin
2) Renal cell carcinoma
3) Hepatocellular carcinoma
4) Hemangioblastoma
5) Pheochromcytoma
6) Leiomyoma

72
Q

Mechanism of pure red aplasia?

A

1) Anemia with low reticulocytes

2) Thymoma

73
Q

Mechanism good syndrome?

A

1) Hypogammaglogulinemia

2) Thymoma

74
Q

Mechanism Trousseau syndrome?

A

1) Migratroy superficial thrombophlebitis

2) Adenocarcinomas (pancreatic)

75
Q

Mechanism nonbacterial endocarditis?

A

1) Sterile plaque thrombi

2) Adenocracinomas (pancreatic)

76
Q

Mechanism of Anti-NMDA receptor encephalitis?

A

1) Psychiatric disturbance, memory deficits, seizures, dyskinesias, autonomic instability, langage dysfunction
2) Ovarian teratoma

77
Q

Mechanism of Opsoclonus, myoclonus ataxia syndrome?

A

1) Dancing eyes, Dancing feet

2) Neuroblastoma, small cell cancer

78
Q

Paraneoplastic cerebellar degeneration?

A

1) Antibodies against Hu, Yo, Tr Antigens in Purkinje cells
2) Small cell cancer
3) Gynecological and breast, Hodgekins

79
Q

Mechanism of paraneoplastic encephalomyelitis?

A

1) Antibodies against Hu antigens and neurons

2) Small cell lung cancer

80
Q

what are causes of Lambert-Eaton mysanthenic syndrome?

A

1) Antibodies against presynaptic (P/Q type) Ca 2+

2) Small cell lung cancer

81
Q

What are causes of mysanthia gravis?

A

1) Antibodies against post synaptic AChR at NMJ

2) Thymoma

82
Q

Oncogene associated with ALK?

A

Lung adenocarcinoma

83
Q

Oncogene associated with BCR-ABL?

A

CML, ALL

84
Q

Oncogene with BCL-2?

A

Follicular and diffuse large B cell lymphoma

85
Q

Oncogene with BRAF?

A

Melanona, non hodgkins

86
Q

Oncogene with c-kit?

A

gastrointestinal stromal tumor (GIST)

87
Q

Oncogene with m-MYC?

A

Burkitt’s lymphoma

88
Q

Oncogene with Her2/neu (c-erbB2)

A

Breast and gastric carcinoma

89
Q

Oncogene with JAK 2?

A

Chronic myeloproliferative disorders

90
Q

Oncogene with KRAS?

A

Colon
Lung
Pancreatic

91
Q

What is MYCL1?

A

Lung tumor

92
Q

What is MYCN?

A

Neuroblastoma

93
Q

What is RET?

A

Men 2A, and 2B

94
Q

What is APC?

A

Colorectal cancer

95
Q

What is BRCA1 and BRCA2?

A

Breast and ovarian cancer

96
Q

What is CDKN2A?

A

Melanoma and pancreatic cancer

97
Q

What is DCC?

A

Colon cancer (deleted in colon cancer)

98
Q

What is DPC 4/SMAD4?

A

Pancreatic cancer

99
Q

What is MEN1?

A

Menin

100
Q

What is NF1?

A

Neurofibromatosis type 1

101
Q

What is NF2?

A

Neurofibormatosis type 2

102
Q

What is PTEN?

A

Breast cancer
Prostate cancer
Endometrial cancer

103
Q

What is rb?

A

Retinoblastoma, osteosarcoma

104
Q

What is TP53?

A

Most human cancers, Li-Fraumeni syndrome

105
Q

What is TSC1?

A

Tuberous sclerosis

106
Q

What is TSC2?

A

Tuberous sclerosis

107
Q

What is VHL?

A

von Hippel-Lindau disease

Renal cell carcinoma

108
Q

What is WT1/WT2?

A

Wilms Tumor.

109
Q

Oncogene microbe EBV?

A

Burkitt lymphoma
Hodgekin’s lymphoma
Nasopharyngeal carcinoma
CNS lymphoma

110
Q

Oncogene HBV, HCV?

A

Hepatocellular carcinoma, lymphoma

111
Q

Oncogene HHV-8?

A

Karposi sarcoma

112
Q

Oncogene HPV?

A

Cervical, penile/anal carcinoma (type 16 and type 18)

113
Q

Oncogene H. Pylori?

A

Gastric Adenocarcinoma

MALT lymphoma

114
Q

Oncogene HTLV-1?

A

Adult T cell leukemia

115
Q

Oncogene Liver Fluke?

A

Cholangiocarcinoma

116
Q

Oncogene Schistosoma haematobium?

A

Bladder cancer (squamous cell)

117
Q

Carconogene: aflatoxins?

A

Hepatocellular carcinoma

118
Q

Carcinogen: Alkylating agent?

A

Leukemia/lymphoma

119
Q

Carcinogen aromatic amines?

A

Bladder: transitional cell carcinoma

120
Q

Carcinogen Arsenic?

A

Angisarcoma
Lung Cancer
Squamous cell carcinoma

121
Q

Carcinogenn: Asbestos?

A

Lung

122
Q

Carcinogen tetrachloride?

A

Liver

Centrilobular necorisis

123
Q

Carcinogen: Cigarette Smoke?

A 
Bladder
Cerivix
Esophagus
Kidney 
Larynx
Lung
Pancrease
124
Q

Carcinogen: ethanol ?

A

Esophagus

Liver

125
Q

Carcinogen: ionizing radiation?

A

Thyroid

126
Q

Carcinogen: niteosamines?

A

Stomach cancer

127
Q

Carcinogen: Radon?

A

Lung cancer

128
Q

Carcinogen: Vinyl Chloride?

A

Liver (angiosarcoma)

129
Q

When are Psammoma bodies seen?

A

Papillary carcinoma of thyroid
Serous papillary cystadenocarcinoma of the ovary
Mengingioma
Malignent mesothelioma

130
Q

What are serum tumor markers used for?

A

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
Q

Tumor marker: Alkaline phosphatase?

A

Mets to bone or liver
Paget disease
Seminoma ALP

132
Q

Alpha fetoprotein?

A

Hepatocellular carcinoma
Heptoblastoma
Yolk
Mixed germ cell tumor

133
Q

Tumor marker B-HCG?

A

Hydratiform moles
Choriocarcinomas
Testicular cancer
Mixed germ cell

134
Q

Tumor marker CA 15-3/CA 27-29?

A

Breast cancer

135
Q

Tumor marker CA 19-9?

A

Pancreatic adenocarcinoma

136
Q

Tumor marker CA 125?

A

Ovarian Cancer

137
Q

Tumor marker: Calcitonin?

A

Medullary Thyroid carcinoma

138
Q

Tumor marker CEA?

A

CarcinoEmbyroicAntigen
Non specific
70% of pancreatic, gastric, breast

139
Q

Tumor marke PSA?

A

Prostate specific antigen

Questionable benefit for prostate screening

140
Q

Tumor marker p-glycoprotein?

A

Adrenal cell carcinoma

141
Q

What hormones cause Cachexia?

A

TNF
IFN-alpha
Il-1
Il-6

142
Q

How do sarcomas spread?

A

Hemtogenously

143
Q

How is carcinoma spread?

A

Lymphatics

144
Q

What are the most common brain mets?

A

Lung > Breast> prostate> melanoma> GI

145
Q

What are the most common liver mets?

A

Colon&raquo_space; stomach» pancrease

146
Q

What are the most common bone mets?

A

Prostate, breast > lung, thyroid, kidney

147
Q

what are the common types of breast mets?

A

Are usually mixed

148
Q

What are the common types of lung mets?

A

Mixed

149
Q

What are the types of kidney mets?

A

Lytic

US (17 decks)

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