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First Aid & Firecracker > First Aid: Pathology > Flashcards

First Aid: Pathology Flashcards

1
Q

What are the two mitochondrial pro-apoptotic regulators? Are they part of the intrinsic or extrinsic pathway?

A

BAX & BAK, Intrinsic

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2
Q

What is the mitochondrial anti-apoptotic regulator? Is it part of the intrinsic or extrinsic pathway?

A

Bcl-2, Intrinsic

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3
Q

What protein is released by the mitochondrial that initiates apoptosis? Is it part of the intrinsic or extrinsic pathway?

A

Cytochrome-c, Intrinsic

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4
Q

Which receptor/ligand pair induce the extrinsic apoptosis pathway?

A

FasL & FasR(CD95)

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5
Q

Which cytosolic protein family is responsible for carrying out apoptosis? Are they part of the intrinsic or extrinsic pathway?

A

Caspases, Both

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6
Q

Describe the action of the FasR receptor?

A

When they bind FasL, the receptors aggregate. This coalescence forms a binding site for Death Domain (FADD). FADD activates Caspases.

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7
Q

What are the six types of necrosis? Give a quick example of where/when they occur. (CLCFFG)

A

Coagulative - Heart, Liver & Kidney (end arteries, acidophilic)
Liquefactive - CNS (release of lysosomal enzymes)
Caseous - TB, Fungi, Nocardia
Fatty - Pancreatitis
Fibrinoid - Vasculitides (amorphous pink)
Gangrenous - Dry (ischemic) and Wet (infection)

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8
Q

Area of the heart most susceptible to ischemic injury

A

Subendocardium

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9
Q

Area of the nephron most susceptible to ischemic injury

A

Straight segment of the PCT & TAL

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10
Q

Area of the liver most susceptible to ischemic injury

A

Zone III, closest to central vein

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11
Q

Area of the colon most susceptible to ischemic injury

A

Splenic flexure, Pectinate line

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12
Q

Compare red versus pale infarcts. Where does each occur?

A

Red (= Reperfusion) occurs in soft tissue with double supply: liver, lungs, intestine. Pale occurs in solid tissue with a single supply: spleen, kidney, heart.

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13
Q

What are the two general classifications of shock? Briefly describe each.

A

Distributive versus hypovolemic/cardiogenic. Distributive is due to a decrease in TPR (pathologic vasodilation, warm & dry); CO and HR increase. Hypovolemic/Cardiogenic is due to a decrease in CO; TPR increases and there is responsive vasoconstriction (cold & sweaty).

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14
Q

What does atrophy mean?

A

Decrease in gross size. It does not specify a decrease in cellularity or a decrease in cell size.

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15
Q

What are the FIVE characteristics or inflammation?

A

Rubor, Tumor, Dolor, Calor & Functio laesa

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16
Q

What three “things” (two of which are cells) are involved in acute inflammation?

A

Neutrophils, Eosinophils, and antibodies.

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17
Q

Which two cell types are involved in chronic inflammation?

A

Lymphocytes and fibroblasts.

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18
Q

What are the three possible outcomes of acute inflammation?

A

Resolution, abscess, or chronic inflammation.

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19
Q

What are the two possible outcomes of chronic inflammation?

A

Scarring & amyloidosis.

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20
Q

What is chromatolysis?

A

Round cellular swelling following axonal injury. Nucleus is displaced to periphery.

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21
Q

Describe the difference between dystrophic and metastatic calcification.

A

Dystrophic is 2o to necrosis(ie. heart valves, abscesses, infarcts, thrombi, Psammoma bodies). Metastatic is 2o to hypercalcemia or to high calcium-phosphate product. The Ca deposits in the renal, pulmonary and gastric mucosa interstitial tissue.

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22
Q

Where does extravasation most likely occur? What are the four steps of leukocyte extravasation?

A

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

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23
Q

Which proteins are important for margination and rolling?

A

E- or P- selecting or GlyCAM-1 on the endothelium, Sialyl-Lewis or L-selectin on the leokocyte

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24
Q

Which proteins are important for tight binding?

A

ICAM and VCAM for the endothelium, Integrins for the leokocyte (CD11/18, VLA-4)

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25
Q

Which proteins are important for diapedesis?

A

PECAM-1 for both the endothelium and the leukocyte

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26
Q

What are the most important chemotactants? Think of five.

A

C5a, IL-8, LTB4, Kallikrein and Platelet Activating Factor

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27
Q

What are the three ways free radicals can damage cells?

A

Lipid peroxidation, protein modification and DNA breakage.

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28
Q

What are the three enzymes involved in getting rid of free radical species?

A

Catalase (both bacterial and human), Superoxide Dismutase (Makes superoxide into peroxide), Gluthation Peroxidase (which uses up gluthatione)

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29
Q

What percentage of tensile strength is regained after scaring? How long does it take?

A

Three months to achieve 70 to 80% of strength.

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30
Q

What are the two types of pathologic scarring? Describe each.

A

HYPERTROPHIC SCARS: Slightly increased collagen synthesis arranged in parallel and can be easily resected.
KELOID SCARS: Incredibly increased collagen synthesis with unorganized deposition that extends beyond wound. It happens more in AA in it tends to recur after resection.

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31
Q

What is the role PDGF in wound healing?

A

Secreted by Macrophages and Platelets to stimulate vascular remodeling, smooth muscle migration and fibroblast growth.

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32
Q

What is the role FGF in wound healing?

A

Stimulate angiogenesis

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33
Q

What is the role EGF in wound healing?

A

Stimulate growth via a tyrosine kinase receptor.

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34
Q

What is the role TGF-beta in wound healing?

A

Angiogenesis, fibrosis and cell cycle arrest

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35
Q

What are the three phases of wound healing? Give a timeline and mention some the cells involved.

A

Immediately - Inflammatory - Platelets, neutrophils, macrophages
Days - Proliferative - Fibroblasts, Endothelium, Macrophages, Keratinocytes
One week - Remodeling - Fibroblasts (replace Col3 with Col1)

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36
Q

What signal initiates granuloma formation and what signal maintains it?

A

Th1 secrete gamme-INF and macrophages maintain it with TNF-alpha. (Note: anti-TNF drugs can release TB)

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37
Q

What three things can cause a decreased ESR?

A

Sickle Cell, Polycythemia and CHF

38
Q

What are the symptoms of acute Fe poisoning?

A

All GI. Nausea, vomiting, gastric bleeding, lethargy.

39
Q

What are the symptoms of chronic Fe poisoning?

A

Met Acidosis

40
Q

What are the chelating agents for Fe poisoning?

A

IV deferoxamine or Oral deferasirox. (Defero = no Iron)

41
Q

What is the difference in the etiology of AL versus AA amyloidosis?

A

AL is primary and it is due to Multiple Myeloma or Plasma Cell disorder that causes Ig LLLight chain deposition. AA is secondary and it is seen in chronic inflammation. Fibrils are composed of Amyloid A.

42
Q

What causes dialysis related amyloidosis?

A

Deposition of beta2-microglobulin. Presents as carpal tunnel. (Bonus: can you remember what this protein does?)

43
Q

What is the relation between TTR and amyloidosis?

A

Mutant TTR (ATTR) or WT TTR (in senile patients) can cause amyloid deposits in the heart. Restrictive Cardiomyopathy. TTR is the T4 carrier protein. Pre-albumin can cause similar problems.

44
Q

What is Lipofuscin?

A

Age related deposited pigment of yellow-brown color. Formed by oxidation and polymerization of lipids.

45
Q

What is the difference between hyperplasia and dysplasia?

A

Hyper = Growth, Dys = Growth with loss of features

46
Q

Which two proteins are used by cancerous cells to invade?

A

Collagenases and Hydrolases (Metalloproteinases)

47
Q

What is the difference between metaplasia and dysplasia?

A

Metaplasia is change in differentiation to a different cell type. Dysplasia is a loss of differentiation.

48
Q

What is anaplasia?

A

Irreversible form of dysplasia with primitive cells lineages. Giant cells may be seen.

49
Q

What is neoplasia?

A

Uncontrolled proliferation.

50
Q

What is desmoplasia?

A

Fibrous tissue in response to neoplasm. (ie. Linitis Plastica)

51
Q

What is the TNM System? Explain how it works.

A

TNM Staging is based on Tumor size, Nodal involvement and Metastases.

52
Q

What is the difference between Sarcoma and Carcinoma?

A

Sarcoma = Mesenchymal, Carcinoma = Epithelial

53
Q

What is cachexia? What are the mediators?

A

Weight loss, muscle atrophy, fatigue. TNF-alpha, IFN-gamma, IL-6

54
Q

What tumor is associated with BCR-ABL?

A

Oncogene. CML and ALL

55
Q

What tumor is associated with bcl-2?

A

Oncogene. Lymphoma (Follicular or undiff.) Over-expression caused by with t(14:18).

56
Q

What tumor is associated with BRAF?

A

Oncogene. Melanoma

57
Q

What tumor is associated with c-kit?

A

Oncogene. GIST

58
Q

What tumor is associated with c-myc?

A

Oncogene. Burkitt

59
Q

What tumor is associated with HER2/neu?

A

Oncogene, Breast ovarian and gastric adenoma

60
Q

What tumor is associated with L-myc?

A

Oncogene. Lung

61
Q

What tumor is associated with N-myc?

A

Oncogene. Neuroblastoma

62
Q

What tumor is associated with ras?

A

Oncogene. Colon, lung, pancreatic cancer

63
Q

What tumor is associated with ret?

A

Oncogene. MEN2A and MEN2B

64
Q

What tumor is associated with APC?

A

Tumor supressor. FAP

65
Q

What tumor is associated with BRCA?

A

Tumor supresor. Breast and ovarian.

66
Q

What tumor is associated with CPD4/SMAD4?

A

Tumor supresor. Pancreatic cancer.

67
Q

What tumor is associated with DCC?

A

Tumor supresor. Colon cancer.

68
Q

What tumor is associated with MEN1?

A

Tumor supresor. MEN1

69
Q

What tumor is associated with NF1 and NF2?

A

Tumor supresor. Neurofibroblastoma type 1 and type 2 respectively.

70
Q

What tumor is associated with p16?

A

Tumor supresor. Melanoma.

71
Q

What tumor is associated with p53?

A

Tumor supresor. Everything. Li-Fraumeni syndrome.

72
Q

What tumor is associated with PTEN?

A

Tumor supresor. Breast, prostate and endometrial.

73
Q

What tumor is associated with Rb?

A

Tumor supresor. Retinoblastoma.

74
Q

What tumor is associated with TSC1 and TSC2?

A

Tumor supresor. Tuberous Sclerosis.

75
Q

What tumor is associated with VHL?

A

Tumor supresor. von-Hippel-Lindau

76
Q

What tumor is associated with WT1 & WT2?

A

Tumor supresor. Wilms tumor.

77
Q

Alkaline phosphatase is a tumor marker for…

A

Mets to bone
Liver
Pagets disease of the bone
Seminoma (placental)

78
Q

Alpha-Fetoprotein is a tumor marker for…

A

Hepatocellular, Hepatoblastoma, Yolk Sac, Testicular or mixed germ cell tumors.

79
Q

Beta-hCG is a tumor marker for…

A

Hydatidaform mole, Choriocarcinoma, Testicular cancer

80
Q

CA-15-3/CA-27-29 is a tumor marker for…

A

Breast cancer

81
Q

CA-19-9 is a tumor marker for…

A

Pancreatic adenocarcinoma

82
Q

CA-125 is a tumor marker for…

A

Ovarian cancer

83
Q

Calcitonin is a tumor marker for…

A

Medullary thyroid carcinoma

84
Q

CEA is a tumor marker for…

A

CarcioEmbryogenic Antigen for Colorectal and Pancreatic cancer. (Also gastric, breast, and medullary thyroid carcinomas)

85
Q

PSA is a tumor marker for…

86
Q

S-100 is a tumor marker for…

A

Neuralcrest Origin (melanoma, neural, schwannoma, Langerhans cells histiocytosis)

87
Q

TRAPLangerhans cells histiocytosis

A

TRAP = Tartrate Resistant Acid Phosphatase. Seen in Hairy Cell Leukemia. (TRAP the Hairy Animal)

88
Q

What neoplasms are associated with paraneoplastic hypercalcemia?

A

Calcitrol produced by lymphomas (mostly Hodgkin).

Or PTHrP produced by Squamous Cell Lung Carcinoma, Renal cell carcinoma, or Breast Cancer

89
Q

What neoplasms are associated with paraneoplastic Cushing Syndrome?

A

ACTH produced by Small Cell Lung Carcinoma.

90
Q

What neoplasms are associated with paraneoplastic SIADH?

A

ADH produced by Small Cell Lung Carcinoma or intracranial neoplasms.

91
Q

Which neoplasms are commonly associated with Psammoma bodies?

A 
PSMM
Papillary carcinoma of the thyroid
Serous papillary cystadenocarcinoma of ovary
Meningioma
Malignant mesothelioma

First Aid & Firecracker (7 decks)

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