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Foundations- Block 1 > Pathology > Flashcards

Pathology Flashcards

1
Q

The cause of a disease and some examples.

A

Etiology; toxins, pathogens, infections, immunologic abnormalities, genetic abnormalities, nutritional imbalances, trauma

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2
Q

The biochemical and molecular mechanisms of disease development.

A

Pathogenesis

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3
Q

The structural alterations induced in the cells and organs of the body caused by the disease

A

Morphological, functional, and molecular changes

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4
Q

The functional consequences of the etiology, pathogenesis, and morphological changes

A

Clinical manifestations

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5
Q

A departure in normal function, appearance, or sensation experienced and reported by the patient that is indicative of a disease.

A

Symptom

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6
Q

Any abnormality indicative of disease that is discovered by a clinician via physical exam or tests?

A

Sign

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7
Q

What do stains usually behave as?

A

Acids and bases

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8
Q

What type of molecule would be basophilic?

A

Anions, or molecules with a net negative charge

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9
Q

What molecules are acidophilic?

A

Cations; with a net positive charge

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10
Q

What is hypoxia? Ischemia?

A

Low oxygen; blockage of blood flow

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11
Q

what do immune responses generate that can damage healthy cells and lead to cell death?

A

Inflammation

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12
Q

What constitutes a reversible injury?

A

Where the function of a cell is bad, but can ultimately be reversed to normal function

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13
Q

What two morphologic changes correlate to reversible injury?

A

Fatty changes (appearance of lipid/triglycerides bound in cytoplasm in vacuoles) and cell swelling (incr permeability of cell mem)

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14
Q

What are the most common “points of no return” causing irreversible cell injury?

A

No restoration of mitochondrial function; loss of structure and function of plasma membrane and intercellular membranes; loss of DNA/chromatin structure integrity

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15
Q

What is unregulated cell death (or “accidental”) which is the result of severe cell damage beyond salvage? What may cause this?

A

Necrosis; trauma, ischemia, hypoxia, etc

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16
Q

What is a more organized cell death that is mediated via receptors and regulatory proteins?

A

Apoptosis

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17
Q

What response is a good differentiation between apoptosis and necrosis?

A

Inflammatory response, its more present in necrosis

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18
Q

How can leakage of cellular materials via necrosis be useful clinically?

A

Can be signs of disease or dysfunction (troponin and CK detection = MI; transaminases=hepatitis; alkaline phosphotase= hepatic bile duct epithelium)

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19
Q

What is pyknosis? What event could this be observed during? (What histological markers are evident?)

A

Nuclear shrinkage and basophilia of a cell after necrosis (Condensing DNA into a shrunken, dark mass)

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20
Q

What causes the basophilia of a necrotic nucleus to fade during pyknosis?

A

DNase activity degrading DNA during karyolysis

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21
Q

What is coagulative necrosis? Where can this occur? What are characteristics?

A

Necrosis where underlying tissue is preserved and lasts several days; solid organs as a result of ischemia (NOT CNS); firm texture, lack of access from enzymes to underlying tissue via denaturing them

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22
Q

What immune cells persist and are anucleated in coagulative necrotic tissues? What cells clean up?

A

Eosinophils; macrophages and neutrophils phagocytose cell debris

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23
Q

What necrosis type is a result of rapid accumulation of inflammatory cells from bacteria or fungal infections that digest local tissues and give it a viscous form?

A

Liquefactive necrosis

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24
Q

What is not necessarily a distinctive pattern of cell death that is more prevalent in a clinical setting where a limb loses nutrition/o2 supply via coagulative necrosis and involves multiple tissue layers?

A

Gangrenous necrosis

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25
Q

What necrosis morphology forms lesions called granulomas due to collections of WBC, and is characteristic of tuberculosis?

A

Caseous necrosis

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26
Q

What necrosis usually found in the pancreas (acute pancreatitis) results from active pancreatic lipases that have leaked out of acinar cells to the adipose of the peritoneum? What appearance does this have?

A

Fat necrosis; chalky-white (fat saponification) due to Ca2+ combination

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27
Q

What necrotic morphology can occur due to severe hypertension where antigens and antibodies are deposited in the walls of blood vessels and leak out?

A

Fibrinoid necrosis

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28
Q

What is the main activator of apoptosis?

A

Caspases

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29
Q

What is the most common pathway of apoptosis? What leaks out of this membrane to trigger apoptosis-activating enzyme and subsequent death?

A

Mitochondrial (intrinsic) pathway: cytochrome c when mito cell mem becomes permeable

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30
Q

What protein controls the mitochondrial cell membrane permeability? What proteins, responsible for apoptosis triggering, does this hold back?

A

BCL-2; Bax and Bak

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31
Q

What causes/triggers the intrinsic apoptosis pathway? What sensors pick these events up?

A

Misfolded proteins, growth factor deprivation, damaged DNA; BH3 sensors shift to Bax and Bak

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32
Q

What does Bax and Bak do when triggered?

A

Bore holes into the mitochon membrane and allow for release of cytochrome c

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33
Q

What are the prototypical cell death receptors on the exterior cell membrane?

A

FAS and type 1 TNF

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34
Q

Where is the FAS ligand (FasL) expressed mainly?

A

Cytotoxic T-cells

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35
Q

What cell death mechanisms do the following induce:

hypoxia, oxidative stress, accumulation of misfolded proteins, DNA damage, and inflammation

A 
Necrosis
Necrosis
Apoptosis
Apoptosis
Either (depending)
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36
Q

What is hypertrophe? What is hyperplasia? Are they independent?

A

Increase in cell size resulting in increased organ size (cells w/ limited dividing capacity like muscles); increase in # of cells;

They can happen simultaneously

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37
Q

What is the shrinkage of cell size caused by the loss of cell substance? What can cause this?

A

Atrophe;

Caused by decreased workload, loss of innervation, loss of blood supply, loss of endocrine stim, aging

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38
Q

What is the adaptation where cell types (epithelial or mesenchymal) is replaced by another cell type? Why?

A

Metaplasia; old cell types are exposed to a stress it isnt equipped to handle, so it changes to a cell type that can (cig smoke is a good example)

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39
Q

What is autophagy and when does it occur?

A

Lysosomal digestion of the cell’s own components;

During nutrient deprivation

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40
Q

What are the four main pathways of intracellular accumulations?

A

Inadequate removal of normal substances due to defects in packaging and transport

Accumulation of abnormal endogenous substances resulting from genetic defects in folding

Failure to degrade a metabolite due to enzyme deficiency

Accumulation of exogenous substances where cell does not have enzymes to degrade it or ability to exocytose it

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41
Q

Where are fatty changes most common?

A

Liver (also heart, kidney, skeletal muscle, etc)

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42
Q

Accumulation of partially folded proteins, which aggregate in the _____________, is an example of defective intracellular transport

A

ER of the liver

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43
Q

What can ER stress caused by partially folded proteins induce?

A

Apoptosis

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44
Q

What deficiency is a common source of slow-folding proteins that get locked in partially folded intermediates?

A

Alpha1-antitrypsin deficiency

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45
Q

Deficiency in enzymes that synthesize or break down glycogen result in what?

A

Accumulation and apoptosis

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46
Q

Anthracosis is derived from what?

A

Carbons that are inhaled into the respiratory tract and are phagocytosed by alveolar macrophages. (Black pigment in draining lymph, histologically)

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47
Q

Deposits of calcium under dead or necrotic tissue from normal Ca metabolism

A

Dystrophic calcificationq

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48
Q

Occurs in normal tissues as a side effect of hypercalcemia

A

Metastatic calcification

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49
Q

What is an important cause of aortic stenosis in the elderly?

A

Dystrophic calcification (under aging/damaged aortic valves)

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50
Q

What are main causes of metastatic calcification?

A

Parathyroid hormone increased secretion (usually by malignant tumors)

Accelerated tumor destroying bone (by tumors)

Vitamin-D intoxication and sarcoidosis

Renal failure (phosphate retention-> hyperparathyroidism)

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51
Q

What are the external manifestations of inflammation?

A

Heat, redness, swelling, pain, loss of function

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52
Q

What are the causes of inflammation?

A

Infections, tissue necrosis, foreign bodies, and hypersensitivity of immune responses

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53
Q

What are the characteristics of purulent inflammation?

A

Production of pus, usually secondary to bacterial infection that causes liquefactive tissue necrosis

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54
Q

What is the defect, or excavation, of surface organ tissue produced by the shedding of inflamed necrotic tissue?

A

Ulcer: ID as a big hole between epithelia and a pit in the CT (histology)

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55
Q

What are the results of chronic inflammation?

A

Infiltration of mononucleated cells, cell damage, connective tissue replacement of damaged tissue (scarring)

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56
Q

Chronic inflammation characterized by collections of active macrophages associated with central necrosis. What large, macrophage-fused structure is associated?

A

Granulomatous inflammation; Giant cell

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57
Q

What tissue necrosis is associated with granulomatous inflammation?

A

Caseous necrosis

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58
Q

What decides wether tissue is regenerated or scarred?

A

Level of surface trauma

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59
Q

What cells are best at regenerating? What cells are bad at it and almost always scar?

A

Rapidly dividing cells (epithelium, WBC, liver and GI epithelium)

Cardiac cells, neural cells, CNS

60
Q

What type of tissue (general) is constantly being lost and must regenerate constantly?

A

Labile tissues (GI epi, skin, uterus and fallopian tubes, transitional epithelium, oral cavity, etc)

61
Q

What cells are usually not replicating (in G0 of mitosis), but can replicate in response to injury?

A

Stable cells (parenchymal liver and solid organ, endothelial, fibroblasts, smooth muscle)

62
Q

What tissue type (general) are terminally differentiated and cannot proliferate?

A

Neurons and cardiomyocytes (and cells that undergo hypertrophy)

63
Q

What are the four general steps in scar formation?

A

Inflammation, angiogenesis, granulation tissues, remodeling of CT

64
Q

What macrophage types induce inflammation and cell death via ROS, NO, lysosomal enzymes? What are they stimulated by?

A

M1 macrophages; INF-gamma, TLR-ligands

65
Q

What type of macrophages have anti-inflam effects, wound repair and fibrosis? What is presentation of this stimulated by?

A

M2 macrophages; IL-3,4

66
Q

What cytokine is the most important for synthesis and deposition of connective tissue proteins in the formation of granulation tissue?

A

TGF-beta

67
Q

What factors impair tissue repair?

A

Infection, diabetes, glucocorticoids, mechanical factors, poor perfusion, foreign bodies, and location/type/extent of injury

68
Q

What is a keloid?

A

A scar that goes beyond its prior borders and does not regress

69
Q

What contributes to conditions such as liver cirrhosis, idiopathic pulmonary fibrosis, and end-stage kidney disease?

A

Parenchymal fibrosis that replaces functional cells/tissue with CT

70
Q

What are the two terms for increased blood volume in a tissue?

A

Hyperemia, congestion

71
Q

What differentiates types of incr blood volume in tissues?

A

Hyperemia: active process from arteriolar dilation and increased bloodflow at inflamm sites or exercised skeletal muscle (redness)

Congestion: passive process from impaired outflow of venous blood (blue-ish color)

72
Q

What is a result of longstanding congestion?

A

Tissue cell death (hypoxia) and tissue fibrosis; focal hemorrhages due to intravascular back pressure in capillaries

73
Q

What is the accumulation of interstitial fluid in tissues?

A

Edema

74
Q

What is the term for collections of fluid in body cavities? What is the term for severe, generalized edema in subq and body cavities?

A

Effusions; anasarca

75
Q

What is colloid osmotic pressure produced by? What other force mediates fluid movement between vascular and interstitial space?

A

Plasma proteins; hydrostatic pressure (nearly balanced in homeostasis, but a net outflow into ISF and drained by lymphatics)

76
Q

Where is fluid from lymph returned to the bloodstream?

A

Thoracic duct

77
Q

What are causes of plasma protein loss? What can this lead to?

A

Liver disease and kidney disease; edema

78
Q

What are non-inflammatory causes of edema?

A

Incr hydrostatic pressure; lower plasma osmotic pressure; lymphatic obstruction; sodium retention

79
Q

Where does a DVT cause edema? What factor of water movement is increased/decreased?

A

Causes it in lower extremity distally to the DVT; increases hydrostatic pressure (local incr hstatic pressure)

80
Q

How does congestive heart failure cause edema?

A

By increasing the generalized hydrostatic pressure in the venous system

81
Q

What is the most important cause of low serum albumin levels? What else can cause this?

A

Nephrosis; cirrhosis and protein malnutrition also

82
Q

What does increased sodium retention cause? How?

A

Incr hydrostatic pressure; it draws water into the vessels @ the kidneys (low renal function/ renal failure)

83
Q

What are the main causes of hemorrhage?

A

Trauma, atherosclerosis, inflammatory or neoplastic erosion of vessel wall

84
Q

How are large bleeds in the body cavity named?

A

Location (hemothorax, hemopericardium, hemoarthrosis, etc)q

85
Q

What are minute (1-2mm) hemorrhages into the skin? What causes this?

A

Petechiae; low platelet count, loss of vascular wall support, VitC deficiency;

86
Q

What are small (3-5mm) hemorrhages in the skin?

A

Parpura

87
Q

What is the technical term for a 1-2cm subcutaneous hemorrhage? What cause the various colors?

A

Ecchymoses (bruise); hemoglobin phagocytized, bilirubin, hemosiderin

88
Q

What are the factors of hemorrhages that determine severity?

A

Location of hemo., volume lost, rate of blood loss

89
Q

What is the pathological component of blood clotting?

A

Thrombus

90
Q

What are the four components of healthy clotting?

A

Arteriolar vasoconst., 1* hemostasis (platelet plug), 2* hemostasis (deposition of fibrin, clot stabilization and resorption

91
Q

What vasoconstrictor is released from endothelial cells when an artery is damaged?

A

Endothelin

92
Q

What promotes platelet adherence and activation in a ruptured artery?

A

von Willebrand factor (vWF) and collagen

93
Q

What sets a cascade forming thrombin? What does thrombin do?

A

Exposed tissue factor -> factor VII -> thrombin;

Brings fibrin into a meshwork and adds another layer of platelets onto the platelet plug

94
Q

What cell is the progenitor of platelets?

A

Megakaryocytes

95
Q

What are required to start a coagulation cascade?

A

Enzyme, cofactor, and substrate bound to a phospholipid surface provided by active platelets, and calcium

96
Q

What is the cofactor for coagulation?

A

Vit K

97
Q

What is a coagulation enzyme antagonist commonly used clinically?

A

Meds like coumadin

98
Q

What assay assesses the function of the extrinsic and common coagulation pathways?

A

Prothrombin time (PT)

99
Q

What assay screens the function of the intrinsic coagulation pathway?

A

Partial thromboplastin time (PTT)

100
Q

What enzyme breaks down fibrin and its polymerization?

A

Plasmin

101
Q

Fibrin-derived D-dimers can be used how?

A

Clinical indication of thrombotic states

102
Q

What plasminogen activator is synthesized by the endothelium and most active when bound to fibrin?

A

t-PA

103
Q

What are the three primary factors that lead to intravascular thrombosis?

A

Endothelial injury, stasis/turbulent blood flow, hyper-coagulability of blood

104
Q

Where is hypercoagulability most likely to create thrombosis?

A

Veins

105
Q

What can happen to a thrombus after a thrombotic event?

A

Propagation (enlargement), embolization, dissolution (dissolve by fibrinolytic factors), organization and recanalization

106
Q

What typically causes the majority of infarctions?

A

Arterial thrombosis/embolism

107
Q

Neoplasms enjoy a degree of ________ and tend to ________ in size regardless of their local environment

A

Autonomy; increase

108
Q

What is the prognosis of benign tumors?

A

Survival (v good)

109
Q

What does “malignant tumor” imply?

A

Invasion and destruction of adjacent structures and distant site spread

110
Q

What is the parenchyma of a tumor? Stroma?

A

The transformed neoplastic cells; host cells that supply CT, blood vessels, and host-derived inflammatory cells

111
Q

What portion of the tumor determines its biological behavior?

A

Parenchymalq

112
Q

What part of a tumor is crucial to growth and nutrition of the tumor?

A

Stroma

113
Q

How is a benign tumor named?

A

Celltype-oma

114
Q

Benign epithelial tumor nomenclature? Adenoma, papilloma, polyp

A

Ade- produce glandlike structures AND derived from them

Papilloma- epithelial benign tumors that produce finger-like fronds

Polyp- mass projecting above mucosa to create a macroscopically visible structure

115
Q

Malignant tumor nomenclature: sarcoma

A

Derived from solid tissues (mesenchymal); tissuetype-sarcoma (chondrosarcoma)

116
Q

Blood malignant tumor nomenclature?

A

Leukemias or lymphomas

117
Q

Epithelial malignant neoplasm nomenclature?

A

Carcinomas; (adenocarcinomas are epithelial but show glandular growth patterns)

118
Q

What three factors distinguish benign and malignant neoplasms?

A

Differentiation and anaplasia, local invasion, and metastasis

119
Q

What functional capabilities can a well-differentiated neoplasm have? Anaplastic?

A

Retention of host-parenchymal function; no special function

120
Q

What level of invasion separates malignant neo and benign neo?

A

Malignant: invasive af

121
Q

What kind of cancer invests itself in the surrounding tissue and does not have encapsulated boundaries?

A

Malignant

122
Q

How to malignancies metastasize?

A

Blood vessels, lymph vessels, and penetration into body cavities

123
Q

What kind of malignant neo prefers lymphatic spread? Hematogenous? Is it a one-method only rule?

A

Carcinomas; sarcomas; no, they can use both

124
Q

What are the most frequent secondary sites of hematogenous dissemination of malignancies?

A

Lungs and liver due to pulmonary and portal circulation

125
Q

What are paraneoplastic syndromes?

A

Symptoms not explained by local invasion, metastasis, or elaboration of hormones in the tumor’s native tissue

126
Q

What five groups encompass paraneoplastic syndromes?

A 
Endocrine
Hematologic
Osteoarticular
Cutaneous
Neurologic
127
Q

What locations of malignant neo can produce parathyroid hormone related protein (PTHrP)? What does this do?

A

Breast cancer, non-small cell lung, squamous cell carcinomas of the head and neck, esophagus carcinomas

Induce hypercalcemia

128
Q

Release of ACTH or ACTH-like polypeptides cause what? From what cancer cells?

A

Cushing syndrome; small-cell lung carcinoma

129
Q

What are two important acquired conditions that contribute to cancer?

A

Chronic inflammation and immunodeficiency

130
Q

What are disruptions in epithelial differentiation that are indicative of increased risk of cancer development?

A

Precursor lesions

131
Q

What are the four main functional classes of cancer genes?

A

Oncogenes, tumor suppressor genes, apoptosis-regulating genes, tumor-host cell interaction regulatory genes

132
Q

What are oncogenes? What are proto-oncogenes?

A

Over-expressed versions of normal cell genes; participatory in signaling pathways that drive proliferation

133
Q

How does growth factor synthesis contribute to cancer?

A

By producing the same growth factor that they have a receptor for (autocrine loop)

134
Q

What are some common growth factors associated with cancer?

A

Platelet derived growth factor (PDGF); transforming growth factor (TGF-alpha); ERBB1; HER2 (ERBB2)

135
Q

What are two important signal-transducing proteins associated with signaling downstream growth factors in cancer?

A

RAS and ABL

136
Q

What is the most commonly mutated oncogene in human tumors? What type of DNA mutation causes this? What does it cause?

A

RAS; point mutation; continuous proliferation

137
Q

What is a tyrosine-kinase proto-oncoprotein that is translocated from Chromosome 9 -> 22? What does it fuse with @ chrom 22? What does this induce?

A

ABL; BCR; BCR-ABL hybrid that self associates and unleashes continuous tyrosine-kinase activity

138
Q

Stimulation of RAS and ABL lead to continuous stim of ________, which promotes expression of GF genes.

A

Nuclear transcription factors

139
Q

What are some common nuclear transcription factors that upregulate expression of growth-promoting genes?

A

FOS, MYC, and JUN

140
Q

_______ activates transcription of cyclin-dependent kinases (CDKs) that drive cells into the cell cycle. What else does _______ upregulate?

A

MYC; control pathways that make cell-division building blocks (AA, lipids, nucleotides, etc)

141
Q

What silences CDK and downregulates cell division as a result?

A

CDK inhibitors

142
Q

Defects in what stages of the cell cycle are important in cancer?

A

S/G1

143
Q

What two major categories are involved in CDK-associated cancers?

A

Gain of function mutations of CDK and Loss of Function mutations in CDKI

144
Q

What genes apply brakes to cell proliferation and can halt oncogene expression?

A

Tumor suppressor genes

145
Q

What is a negative regulator of the cell cycle that is either actively or indirectly inactivated in most human cancers? (1st TS gene found)

A

Retinoblastoma gene (RB)

146
Q

What is the most commonly mutated gene in human cancer (>70%)? What does it do?

A

TP-53; prevents neoplasm by: temp cell cycle arrest (quiescence), permanent cell cycle arrest (senescence), or apoptosis triggering

147
Q

What is Li-Fraumeni syndrome? What does this mean for likelihood of developing cancer?

A

TP53 allele mutation (inherited); 25x greater chance of cancer

Foundations- Block 1 (17 decks)

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