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Pathology > Patho First Aid > Flashcards

Patho First Aid Flashcards

0
Q

What is occurring? Activation of cytotoxic caspases that mediate cellular breakdown. Char. by deeply eosinophilic cytoplasm, cell shrinkage, and basophilia. DNA laddering is a sensitive indicator; during karyorrhexis, endonucleases cleave at internucleosomal regions, yielding 180-bp fragments.

A

Apoptosis

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1
Q

This process involves tissue remodeling in embryogenesis. Increase in BAX and a decrease in Bcl triggers this.

A

Intrinsic pathway

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2
Q

This factor prevents cytochrome c release by binding to and inhibiting Apaf-1. If it is over expressed (e.g. follicular lymphoma) then Apaf-1 is overly inhibited leading to decreased caspase activation and tumorgenesis.

A

Bcl-2

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3
Q 
2 pathways: Ligand receptor interactions (FasL binding to Fas [CD95]). 
Immune cell (cytotoxic T-cell release of perforin and granzyme B). After Fas crosslinks with FasL, multiple Fas molecules coalesce, forming a binding site for a death domain-containing adapter protein, FADD (which binds inactive caspases, activating them).
A

Extrinsic pathway.

Defective Fas-FasL interaction is the basis for autoimmune disorders (thymic medullary negative selection).

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4
Q

Enzymatic degradation and protein denaturation of a cell resulting from exogenous injury. Intracellular components leak; inflammatory process. Heart, liver, kidney; occurs in tissues supplied by end-arteries; increase in cytoplasmic binding of acidophilic dye. Proteins denature first, followed by enzymatic degradation.

A

Necrosis- Coagulative

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5
Q

Enzymatic degradation and protein denaturation of a cell resulting from exogenous injury. Intracellular components leak; inflammatory process. Brain, bacterial abscess; occurs in CNS due to high fat content. In this case, enzymatic degradation is due to the release of lysosomal enzymes.

A

Necrosis - Liquefaction

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6
Q

Enzymatic degradation and protein denaturation of a cell resulting from exogenous injury. Intracellular components leak; inflammatory process. TB, systemic fungi, Nocardia.

A

Necrosis - Caseous

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7
Q

Enzymatic degradation and protein denaturation of a cell resulting from exogenous injury. Intracellular components leak; inflammatory process. Enzymatic (pancreatitis [saponification]) and nonenzymatic (e.g. breast trauma); calcium deposits appear dark blue on staining.

A

Necrosis - Fatty

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8
Q

Enzymatic degradation and protein denaturation of a cell resulting from exogenous injury. Intracellular components leak; inflammatory process. Vasculitis (e.g. Henoch-Schönlein purpura, Churg-Strauss syndrome), malignant hypertension; amorphous and pink on H&E.

A

Necrosis- Fibrinoid

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9
Q

Enzymatic degradation and protein denaturation of a cell resulting from exogenous injury. Intracellular components leak; inflammatory process. Dry (ischemic coagulative) and wet (infection); common in limbs and GI tract.

A

Necrosis - Gangrenous

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10
Q

What is occurring? ATP depletion, cellular/mitochondrial swelling (decr. ATP–> decr. activity of Na+/K+ pumps); nuclear chromatin clumping. Decreased glycogen; fatty change. Ribosomal/polysomal detachment (decr. protein synthesis); membrane blebbing.

A

Cell injury that is reversible with O2.

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11
Q

What is occurring? Nuclear pyknosis, karyorrhexis, karyolysis; Plasma membrane damage (degradation of membrane phospholipid). Lysosomal rupture. Mitochondrial permeability/vacuolization; phospholipid-containing amorphous densities within mitochondria (swelling alone is reversible).

A

Cell injury with irreversible damage.

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12
Q

What is the difference between a red and pale infarct?

A

Red infarcts-occurs in tissues that have multiple blood supplies (like the liver, lungs, and intestines), thus having reperfusion readily available.

Pale infarcts - occurs in solid tissues with a single arterial blood supply, such as the heart, kidney, and spleen.

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13
Q

Reduction in the size and/or number of cells. Causes include: Decr. in endogenous hormones (e.g. post-menopausal ovaries), incr. exogenous hormones (e.g. factitious thyrotoxicosis, steroid use), decr. blood flow/nutrients, decr. metabolic demand (paralysis), incr. pressure (nephrolithiasis), occlusion of secretory ducts (cystic fibrosis).

A

Atrophy

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14
Q

What is characterized by: rubor (redness), dolor (pain), calor (heat), tumor (swelling), and functio laesa (loss of function)?

A

Inflammation

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15
Q

What is occurring? Neutrophil, eosinophil, and antibody mediated. Rapid onset (seconds to minutes), lasts minutes to days. Outcomes include complete resolution, abscess formation, and progression to chronic…

A

Acute inflammation

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16
Q

What is occurring? Mononuclear cell and fibroblast mediated; characterized by persistent destruction and repair. Associated with blood vessel proliferation, fibrosis. Granuloma: nodular collections of epitheloid macrophages and giant cells. Outcomes include scarring and amyloidosis.

A

Chronic inflammation

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17
Q

This process involves the cell body following axonal injury. Changes reflect incr. protein synthesis in effort to repair the damaged axon. Characterized by round cellular swelling, displacement of the nucleus to the periphery, dispersion of Nissl substance throughout cytoplasm.

A

Chromatolysis

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18
Q

Calcium deposition in tissues secondary to necrosis. Tends to be localized (e.g. on heart valves). Seen in TB (lungs and pericardium), liquefaction necrosis of chronic abscess, fat necrosis, infarcts, thrombi, schistosomiasis, Mönckberg arteriosclerosis, congenital CMV + toxoplasmosis, psammoma bodies. Not directly assoc. with hypercalcemia (Px are normocalcemic).

A

Dystrophic calcifications

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19
Q

Widespread deposition of calcium in normal tissues secondary to hypercalcemia (e.g. 1*hyperparathyroidism, sarcoidosis, hypervitaminosis D) or high calcium-phosphate product (chronic renal failure, long term dialysis). Calcium deposits predominantly in interstitial tissues of kidney, lungs, and gastric mucosa (these tissues lose acid quickly; incr. pH favors deposition). Px usually not normocalcemic.

A

Metastatic calcification

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20
Q

What process is occurring?

  1. Margination and rolling
  2. Tight-binding.
  3. Diapedesis- leukocyte travels between endothelial cells and exits blood vessels.
  4. Migration- leukocyte travels through interstitium to site of injury or infection guided by chemotactic signals.
A

Leukocyte extravasation

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21
Q

Collagen arrangement: parallel vs. disorganized
Extent: confined to borders of original wound vs. extend beyond borders of original wound.
Recurrence: infrequently recur following resection vs. frequently recur following resection.

A

Scar formation: hypertrophic vs. keloid scars

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22
Q

What describes macrophages with granular yellow-brown “wear and tear” pigment associated with normal aging. Formed by oxidation and polymerization of autophagocytosed organellar membranes. Autopsy of elderly person will reveal deposits in heart, liver, kidney, eye, and other organs.

A

Lipofuscin

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23
Q

Tumor nomenclature that denotes mesenchymal origin and implies malignancy.

A

Sarcoma

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25
Q

Tumor nomenclature that describes epithelial origin. It implies malignancy. Usually it spreads lymphatically and includes renal vein, hepatic vein.

A

Carcinoma

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27
Q

What is the associated neoplasm with this condition: Acanthosis nigricans (Hyperpigmentation and epidermal thickening)?

A

Visceral malignancy (esp. stomach)

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28
Q

What is the associated neoplasm with this condition: Actinic keratosis

A

Squamous cell carcinoma of the skin

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29
Q

What is the associated neoplasm with this condition: AIDS

A

Aggressive malignant lymphomas (non-Hodgkin) and Kaposi sarcoma.

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30
Q

What is the associated neoplasm with this condition: Autoimmune diseases (e.g. Hashimoto thyroiditis, SLE)

A

Lymphoma

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31
Q

What is the associated neoplasm with this condition: Barrett esophagus (chronic GI reflux)

A

Esophageal adenocarcinoma

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32
Q

What is the associated neoplasm with this condition: Chronic strophic gastritis, pernicious anemia, postsurgical gastric remnants.

A

Gastric adenocarcinoma

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33
Q

What is the associated neoplasm with this condition: Cirrhosis

A

Hepatocellular carcinoma

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34
Q

What is the associated neoplasm with this condition: Cushing’s Syndrome

A

Small cell lung cancer

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35
Q

What is the associated neoplasm with this condition: Dermatomyositis

A

Lung cancer

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36
Q

What is the associated neoplasm with this condition: Dysplastic Nevus

A

Malignant melanoma

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37
Q

What is the associated neoplasm with this condition: Hypercalcemia

A

Squamous cell lung cancer

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38
Q

What is the associated neoplasm with this condition: Immunodeficiency states

A

Malignant lymphomas

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39
Q

What is the associated neoplasm with this condition: Lambert-Eaton myasthenic syndrome

A

Small cell lung cancer

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40
Q

What is the associated neoplasm with this condition: Myasthenia Gravis, pure RBC aplasia

A

Thymoma

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41
Q

What is the associated neoplasm with this condition: Paget disease of bone

A

Secondary osteosarcoma and fibrosarcoma

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42
Q

What is the associated neoplasm with this condition: Plummer-Vinson syndrome (decr. iron)

A

Squamous cell carcinoma of the esophagus

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43
Q

What is the associated neoplasm with this condition: Polycythemia

A

Renal cell carcinoma, hepatocellular carcinoma

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44
Q

What is the associated neoplasm with this condition: Radiation exposure

A

Leukemia, sarcoma, papillary thyroid cancer,and breast cancer

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45
Q

What is the associated neoplasm with this condition: SIADH

A

Small cell lung cancer

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46
Q

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

A

Giant cell astrocytoma, renal angiomyolipoma, and cardiac rhabdomyoma.

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47
Q

What is the associated neoplasm with this condition: Ulcerative colitis

A

Colonic adenocarcinoma

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48
Q

What is the associated neoplasm with this condition: Xeroderma pigmentosum, albinism

A

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

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49
Q

Weight loss, muscle atrophy, and fatigue that occur in chronic disease (e.g. cancer, AIDS, heart failure, TB). Mediated by TNF-gamma, and IL-6.

A

Cachexia

50
Q

What describes the condition in where there is the abnormal aggregation of proteins (or their fragments) into beta-pleated sheet structures. –> damage and apoptosis.

A

Amyloidosis

51
Q

Deposition of proteins from Ig light chains. Can occur as a plasma cell disorder or associated with multiple myeloma. Often affects multiple organ systems, including renal (nephrotic syndrome), cardiac (restrictive cardiomyopathy, arrhythmia), hematologic (easy bruising), GI (hepatomegaly), and neurologic (neuropathy).

A

Amyloidosis- AL (primary)

52
Q

Seen with chronic conditions, such as rheumatoid arthritis, IBD, spondyloarthropathy, protracted infection, fibrils composed of serum Amyloid A. Often multisystem like AL amyloidosis.

A

Amyloidosis- AA (secondary)

53
Q

Fibrils composed of B2-microglobulin in Px with ESRD and/or on long-term dialysis. May present as carpal tunnel syndrome.

A

Dialysis related amyloidosis

54
Q

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

A

Age-related (senile) systemic amyloidosis

55
Q

Amyloid deposition localized to a single organ. Most important form is amyloidosis in Alzheimer disease due to deposition of amyloid-beta protein cleaved from amyloid precursor protein (APP). Islet amyloid polypeptide (IAPP) is commonly seen in diabetes mellitus type 2 and is caused by deposition of amylin in pancreatic islets.

A

Organ-specific amyloidosis

56
Q

What is this describing?
Protein-rich, cellular, specific gravity >1.020
Due to: Lymphatic obstruction, inflammation/infection, malignancy. Thick.

A

Exudate

57
Q

What is this describing?
Protein poor, hypo-cellular, specific gravity <1.012
Due to: increased hydrostatic pressure (e.g. CHF), decreased oncotic pressure (e.g. cirrhosis), Na+ retention. Thin.

A

Transudate

58
Q

Reversible–> Abnormal growth with loss of cellular orientation, shape, and size in comparison to normal tissue maturation; commonly preneoplastic.

A

Dysplasia

59
Q

Irreversible–> 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.

A

Anaplasia

62
Q

Type of tumor: benign epithelium

A

Adenoma, papilloma

63
Q

Type of tumor: benign blood vessels

A

Hemangioma

64
Q

Type of tumor: benign Smooth Muscle

A

Leiomyoma

65
Q

Type of tumor: benign Striated Muscle

A

Rhabdomyoma

66
Q

Type of tumor: benign connective tissue

A

Fibroma

67
Q

Type of tumor: benign Bone

A

Osteoma

68
Q

Type of tumor: benign fat

A

Lipoma

69
Q

Type of tumor: malignant epithelium

A

Adenocarcinoma, papillary carcinoma

70
Q

Type of tumor (mesenchymal): malignant blood cells

A

Leukemia, lymphoma

71
Q

Type of tumor (mesenchymal): malignant blood vessels

A

Angiosarcoma

72
Q

Type of tumor (mesenchymal): malignant smooth muscle

A

Leiomyosarcoma

73
Q

Type of tumor (mesenchymal): malignant connective tissue

A

Fibrosarcoma

74
Q

Type of tumor (mesenchymal): malignant Bone

A

Osteosarcoma

75
Q

Type of tumor (mesenchymal): malignant Fat

A

Liposarcoma

76
Q

Oncogenes: Gain of function –> Increased cancer risk. Need damage to only 1 allele. Oncogene: BCR-ABL. Gene product: tyrosine kinase

A

Associated tumor: CML, ALL

77
Q

Oncogenes: Gain of function –> Increased cancer risk. Need damage to only 1 allele. Oncogene: bcl-2
Gene product: anti-apoptotic molecule (inhibits apoptosis).

A

Associated tumor: Follicular and undifferentiated lymphomas

78
Q

Oncogenes: Gain of function –> Increased cancer risk. Need damage to only 1 allele. Oncogene: BRAF. Gene product: serine/threonine kinase

A

Associated tumor: Melanoma

79
Q

Oncogenes: Gain of function –> Increased cancer risk. Need damage to only 1 allele. Oncogene: c-kit
Gene product: cytokine receptor (for stem cell factor)

A

Associated tumor: Gastrointestinal stromal tumor (GIST)

80
Q

Oncogenes: Gain of function –> Increased cancer risk. Need damage to only 1 allele. Oncogene: c-myc
Gene product: Transcription factor

A

Associated tumor: Burkitt lymphoma

81
Q

Oncogenes: Gain of function –> Increased cancer risk. Need damage to only 1 allele. Oncogene: HER2/neu (c-erbB2)
Gene product: Tyrosine kinase

A

Associated tumor: Breast, ovarian, and gastric carcinomas

82
Q

Oncogenes: Gain of function –> Increased cancer risk. Need damage to only 1 allele. Oncogene: L-myc
Gene product: transcription factor

A

Associated tumor: Lung tumor

83
Q

Oncogenes: Gain of function –> Increased cancer risk. Need damage to only 1 allele. Assoc. with overexpression Of ocogene: N-myc
Gene product: transcription factor

A

Associated tumor: Neuroblastoma

84
Q

Oncogenes: Gain of function –> Increased cancer risk. Need damage to only 1 allele. Oncogene: ras
Gene product: GTPase

A

Associated tumor: colon cancer, lung cancer, pancreatic cancer

85
Q

Oncogenes: Gain of function –> Increased cancer risk. Need damage to only 1 allele. Oncogene: ret
Gene product: Tyrosine kinase

A

Associated tumor: MEN 2A and 2B

86
Q

Tumor suppressor genes: Loss of function–> Incr. cancer risk; both alleles must be lost for expression of disease. Gene: APC
Gene product: (none)

A

Associated tumor: colorectal cancer (associated with FAP).

87
Q

Tumor suppressor genes: Loss of function–> Incr. cancer risk; both alleles must be lost for expression of disease. Gene: BRCA1 and BRCA2
Gene product: DNA repair protein

A

Associated tumor: Breast and ovarian cancer

88
Q

Tumor suppressor genes: Loss of function–> Incr. cancer risk; both alleles must be lost for expression of disease. Gene: CPD4/SMAD4
Gene product: DPC deletion

A

Associated tumor: Pancreatic cancer

89
Q

Tumor suppressor genes: Loss of function–> Incr. cancer risk; both alleles must be lost for expression of disease. Gene: DCC
Gene product: DCC deletion

A

Associated tumor: Colon cancer

90
Q

Tumor suppressor genes: Loss of function–> Incr. cancer risk; both alleles must be lost for expression of disease. Gene: MEN1
Gene product: (none)

A

Associated tumor: MEN type 1

91
Q

Tumor suppressor genes: Loss of function–> Incr. cancer risk; both alleles must be lost for expression of disease. Gene: NF1
Gene product: RAS GTPase activating protein (neurofibromin)

A

Neurofibromatosis type 1

92
Q

Tumor suppressor genes: Loss of function–> Incr. cancer risk; both alleles must be lost for expression of disease. Gene: NF2
Gene product: Merlin (schwannomin) protein

A

Associated tumor: Neurofibromatosis type 2

93
Q

Tumor suppressor genes: Loss of function–> Incr. cancer risk; both alleles must be lost for expression of disease. Gene: p16
Gene product: Cyclin-dependent kinase inhibitor 2A

A

Associated tumor: Melanoma

94
Q

Tumor suppressor genes: Loss of function–> Incr. cancer risk; both alleles must be lost for expression of disease. Gene: p53
Gene product: Transcription factor for p21, blocks G1–>S phase

A

Associated tumor: most human cancers, Li-Fraumeni syndrome

95
Q

Tumor suppressor genes: Loss of function–> Incr. cancer risk; both alleles must be lost for expression of disease. Gene: PTEN
Gene product: —

A

Associated tumor: Breast cancer, prostate cancer, endometrial cancer

96
Q

Tumor suppressor genes: Loss of function–> Incr. cancer risk; both alleles must be lost for expression of disease. Gene: Rb
Gene product: Inhibits EF2; blocks G1–> S phase

A

Associated tumor: Retinoblastoma, osteosarcoma

97
Q

Tumor suppressor genes: Loss of function–> Incr. cancer risk; both alleles must be lost for expression of disease. Gene: TSC1
Gene product: Hamartin protein

A

Associated tumor: Tuberous sclerosis

98
Q

Tumor suppressor genes: Loss of function–> Incr. cancer risk; both alleles must be lost for expression of disease. Gene:TSC2
Gene product: Tuberin protein

A

Associated tumor: Tuberous sclerosis

99
Q

Tumor suppressor genes: Loss of function–> Incr. cancer risk; both alleles must be lost for expression of disease. Gene: VHL
Gene product: Inhibits hypoxia inducible factor 1a

A

Associated tumor: Von Hippel-Lindau disease

100
Q

Tumor suppressor genes: Loss of function–> Incr. cancer risk; both alleles must be lost for expression of disease. Gene: WT1 and WT2
Gene product:—

A

Associated tumor: Wilms Tumor (nephroblastoma)

101
Q

Tumor markers- may be used to monitor tumor recurrence and response to therapy, but not for Dx.
–> metastasis to bone, liver, Paget disease of bone, seminoma (placental ALP).

A

Tumor marker: Alkaline phosphatase

102
Q

Tumor markers- may be used to monitor tumor recurrence and response to therapy, but not for Dx.
–> Normally made by fetus. Hepatocellular carcinoma, hepatoblastoma, yolk sac (endodermal sinus) tumor, testicular cancer, mixed germ cell tumor (co-secreted with beta-hCG).

A

Tumor marker: Alpha-fetoprotein

103
Q

Tumor markers- may be used to monitor tumor recurrence and response to therapy, but not for Dx.
–> hydatidiform moles and choriocarcinomas (gestational trophoblastic disease), testicular cancer. Assoc. with pregnancy.

A

Tumor marker: beta-hCG

104
Q

Tumor markers- may be used to monitor tumor recurrence and response to therapy, but not for Dx.
–> breast cancer

A

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

105
Q

Tumor markers- may be used to monitor tumor recurrence and response to therapy, but not for Dx.
–> Pancreatic adenocarcinoma

A

Tumor marker: CA-19-9

106
Q

Tumor markers- may be used to monitor tumor recurrence and response to therapy, but not for Dx.
–> Ovarian cancer

A

Tumor marker: CA-125

107
Q

Tumor markers- may be used to monitor tumor recurrence and response to therapy, but not for Dx.
–> Medullary thyroid carcinoma

A

Tumor marker: Calcitonin

108
Q

Tumor markers- may be used to monitor tumor recurrence and response to therapy, but not for Dx.
–> Very nonspecific but produced by ~70% of colorectal and pancreatic cancers; also produced by gastric, breast, and medullary thyroid carcinomas.

A

Tumor marker: CEA - Carcinoembryonic Antigen.

109
Q

Tumor markers- may be used to monitor tumor recurrence and response to therapy, but not for Dx
–>Used to follow prostate adenocarcinoma. Can also be elevated in BPH and prostatis. Questionable risk/benefit for screening.

A

Tumor marker: PSA - prostate specific antigen

110
Q

Tumor markers- may be used to monitor tumor recurrence and response to therapy, but not for Dx.
–> Neural crest Origen (e.g. melanomas, neural tumors, schwannomas, Langerhans cell histiocytosis).

A

Tumor marker: S-100

111
Q

Tumor markers- may be used to monitor tumor recurrence and response to therapy, but not for Dx.
–>Hairy cell leukemia- a B-cell neoplasm. What is the tumor marker?

A

Tumor marker: Tartrate-Resistant Acid Phosphate (TRAP)

112
Q

Irreversible–> A clonal proliferation of cells that is uncontrolled and excessive. Neoplasms may be benign or malignant. These cells are unresponsive to normal regulation of cell division and continue to grow beyond the normal needs of the organism.

A

Neoplasia

113
Q

Irreversible–> Fibrous tissue formation in response to neoplasm (e.g. Linitis plastica in diffuse stomach cancer).

A

Desmoplasia

114
Q

Reversible –> Increase in the number of cells.

A

Hyperplasia

115
Q

Reversible–> One adult cell type is replaced by another. Often secondary to irritation (e.g. Barrett esophagus) and/or environmental exposure (e.g. Smoking induced tracheal/bronchial squamous change).

A

Metaplasia

116
Q

An EKG that displays a U waves is demonstrating what imbalance?

A

Hypokalemia- seen on V2, V3, and V4

117
Q

Type of collagen required for wound repair? Deficiency in what metal would inhibit collagen reduction.

A

Collagen 3 is used for wound repair. After a couple of months, zinc is required to reduce it to collagen type 1, thus increasing tensile strength.

118
Q

What is occurring: basal cell layer proliferates from both sides to go underneath a clot. Key element is granulation tissue. Fibronectin is a very important proteoglycan, adhesion agent, and chemotactic agent involving fibroblasts.

A

This describes the process of skin healing.

119
Q

What pathology is associated with a defect in fibrilin (an elastic tissue)?

A

Ehlers-Danlos - in addition have poor wound healing.

120
Q

What two AAs are involved in a hydroxylation defect in a Px with scurvy?

A

Proline and lysine via ascorbic acid.

121
Q

What is mechanism is responsible for increasing tensile strength in collagen? What effects would,this have on a patient with scurvy?

A

Crossbridges in the form of a triple helix give tensile strength. These crossbridges anchor to hydroxylated proline and lysine –> thus scurvy patients will have hemorrhaging, hemarthrosis, and poor wound healing.

122
Q

In a chronically draining sinus tract involving a scar, antibiotics don’t seem to work. Ulceration lesion was present at the orifice of this chronically draining tract. What is this?

A

Squamous cell carcinoma due to a lot of turnover; type 3 collagen converted to type 1, and fibroblasts are involved. A lot of cell division is occurring, which predisposes to mutations and cancer.

Pathology (5 decks)

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