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STEP > Pathology > Flashcards

Pathology Flashcards

1
Q

Pneumatosis intestinalis

A

gas cysts in the intestine wall

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2
Q

Toxic epidermal necrolysis

A

♣ Code: walls covered in rotting skin oozing green and grim reapers/toxic epidermal necrolysis. John, Canadian immunology professor/usually older. Skin looks like belwo/more severe version of Steven-Johnson syndrome. Russians drinking vodko/presentation = diffuse erythema + blistering with a positive Nikolsky sign. Lips completely necrotic and blistering/usually presents with involvement of mucous membranes. Pile of piles behind him/usually triggered by use of a new medication.
♣ Character: Room inside of SJS room

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3
Q

caspases

A

cytosolic proteases involved in apoptosis

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4
Q

apoptosis characteristics

A
  • cell shrinkage + chromatin condensation + membrane blebbing + formation of apoptotic bodies, which are then phagocytosed.
  • deeply eosinophilic cytoplasm + basophilic nucleus + pyknosis + karyorrhexis.
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5
Q

pyknosis

A

nuclear shrinkage

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6
Q

karyorrhexis

A

fragmentation of the nucleus caused by endonucleases cleaving at internucleosomal regions.

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7
Q

Indicator of apoptosis

A

DNA laddering

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8
Q

DNA laddering

A

(fragments in multiples of 180 bp)

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9
Q

differentiating feature from apoptosis and necrosis

A

cell membrane remains intact without significant inflammation

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10
Q

Pathway involved in tissue remodeling in embryogenesis

A

intrinsic (mitochondrial) pathway.

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11
Q

When does intrinsic pathway occur?

A

1) regulating factor is withdrawn from a proliferating cell population (decreased IL-2 after a completed immunologic regulation leading to apoptosis of proliferating effector cells).
2) after exposure to injurious stimuli (radiation, toxins, hypoxia).

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12
Q

Intrinsic pathway regulation and examples

A

Bcl-2 family of proteins, such as BAX and BAK (proapoptic) and Bcl-2 (antiapoptotic)

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13
Q

Bcl-2 action

A

Prevents cytochrome c release by binding to and inhibiting APAF-1.

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14
Q

APAF-1 action

A

APAF-1 binds cytochrome c and induces activation of caspase 9, initiating caspase casade.

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15
Q

What happens with Bcl-2 over expression?

A

decreased caspase activation and tumorigenesis.

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16
Q

extrinsic (death receptor) pathway

A

2 pathways:

1) ligand receptor interactions (FasL binding to Fas [CD95] or TNF-alpha binding to TNF)
2) Immune cell (cytotoxic T-cell release of perforin and granzyme B)

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17
Q

When is Fas-FasL interaction necessary? What happens with mutations?

A

Thymic medullary negative selection. Mutations in Fas increase numbers of circulating self-reacting lymphocytes due to failure of clonal deletion.

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18
Q

What happens with defective Fas-FasL interactions?

A

Autoimmune lymphoproliferative syndrome.

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19
Q

Intrinsic pathway with DNA damage/radiation/misfolded proteins/hypoxia etc.

A

DNA damage –> p53 activation –> BAX/BAK activation –> cytochrome C release –> initiator caspases –> executioner caspases

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20
Q

necrosis

A

Enzymatic degradation and protein denaturation of cell due to exogenous injury leading to intracellular components leak. *inflammatory process.

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21
Q

coagulative necrosis cause and location

A

ischemia/infarcts. Most tissues except brain.

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22
Q

What happens with coagulative necrosis

A

proteins denature. enzymes are degraded. cell outlines preserved. increased cytoplasmic binding of acidophilic dyes.

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23
Q

when does liquefactive necrosis occur?

A

bacterial abscesses + brain infarcts (due to icnreased fat content)

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24
Q

liquefactive necrosis pathophys

A

Neutrophils release lysosomal enzymes that digest the tissue; enzymatic degradation first, then proteins denature.

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25
Q

liquefactive necrosis histology

A

Early: cellular debris and macrophages.
Late: cystic spaces and cavitation (brain).
Neutrophils and cell debris seen with bacterial infection.

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26
Q

When does caseous necrosis occur?

A

TB + systemic fungi (histoplasma) + nocardia.

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27
Q

What happens with caseous necrosis?

A

Macrophages wall of infecting microorganism –> leading to granular debris.

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28
Q

Histology of caseous necrosis

A

Fragmented cells and debris surrounded by lymphocytes and macrophages.

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29
Q

pathophys of fat necrosis

A

damaged cells release lipase, which breaks down TGs in fat cels.

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30
Q

Histology of fat necrosis and appearance

A

Outlines of dead fat cells without peripheral nuclei; saponification of fat (combined with ca2+). Appears dark blue on H&E stain.

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31
Q

another example of fibrinoid necrosis

A

GCA

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32
Q

Fibrinoid necrosis pathophys

A

immune complexes combine with fibrin leading to vessel wall damage

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33
Q

fibrinoid necrosis pathophys

A

vessel walls thick and pink.

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34
Q

dry vs. wet gangrenous necrosis

A

Dry occurs with ischemia and presents with coagulative necrosis histologically.
Wet occurs with superinfection and presents with liquefactive superimposed on coagulative.

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35
Q

lysosomal rupture – reversible or irreversible sign of cell injury?

A

irreverisble

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36
Q

membrane blebbing – reversible or irreversible sign of cell injury?

A

reversible

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37
Q

cellular/mitochondrial swelling – – reversible or irreversible sign of cell injury?

A

reversible

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38
Q

nuclear pyknosis – reversible or irreversible sign of cell injury?

A

irreversible

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39
Q

karyorrhexis – reversible or irreversible sign of cell injury?

A

irreversible

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40
Q

karyolysis – reversible or irreversible sign of cell injury?

A

irreversible

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41
Q

ribosomal/polysomal detachment (decreased protein synthesis)

A

reversible

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42
Q

nuclear chromatin clumping – reversible or irreversible sign of cell injury?

A

reversible

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43
Q

decreased glycogen – reversible or irreversible sign of cell injury?

A

reversible

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44
Q

mitochondrial permeability/vacuolization – reversible or irreversible sign of cell injury?

A

irreversible

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45
Q

mitochondrial permeability/vacuolization

A

phospholipid-containing amorphous densities within mitochondria

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46
Q

plasma membrane damage mitochondrial permeability/vacuolization

A

irreersible

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47
Q

nuerons most vulnerable to hypoxic-ischemic injury

A

Purkinje cells of cerebellum + pyramidal cells of hippocampus and neocortex

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48
Q

area of heart most susceptible to ischemia

A

subendocardium of LV

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49
Q

area of kidney most susceptible to ischemia

A

straight segment of proximal tubule (medulla) + thick ascending limb (medulla)

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50
Q

red infarct

A

hemorrhagic infarcts that occur in venous occlusion and tissues with multiple blood supplies and with reperfusion (eg after angioplasty) (Red; reperfusion).

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51
Q

tissues with multiple blood supplies

A

liver, lung, intestine, testes.

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52
Q

What causes reperfusion injury?

A

damage by free radicals.

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53
Q

Pale infarcts

A

(anemic) infarcts. Occur in solid organs with a single (end-arterial) blood supply.

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54
Q

organs with a single blood supply

A

heart, kidney, spleen.

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55
Q

characteristics of inflammation

A

rubor (redness), dolor (pain), calor (heat), tumor (swelling), functio laesa (loss of function)

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56
Q

vascular component of inflammation

A

increased vascular permebaility + vasodilation + endothelial injury

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57
Q

Acute inflammation

A

neutrophil, eosinophil, and antibody mediated. rapid onset and short duration.

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58
Q

Possible outcomes of acute inflammation

A

Complete resolution + abscess formation OR progression to chronic.

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59
Q

What mediates chronic inflammation?

A

Mononuclear cells (monocytes/macrophages, lymphocytes, plasma cells) + fibroblasts.

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60
Q

chronic inflammation histoogy

A

Blood vessel proliferation, fibrosis.

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61
Q

Outcomes of granuloma formation

A

scarring and amyloidosis.

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62
Q

characteristics of chromatolysis

A

round cellular swelling + displacement of nucleus to the periphery + dispersion of nissl substance throughout cytoplasm

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63
Q

when does chromatolysis occur?

A

concurrent with Wallerian degeneration.

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64
Q

dystrophic calcification

A

calcium deposition in abnormal tissues secondary to injury or necrosis

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65
Q

dystrophic calcification characteristics

A

Tends to be localized, small bony tissue, and thick fibrotic wall.

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66
Q

When does dystrophic calcification occur?

A

1) TB (lungs and pericardium)
2) liquefactive necrosis of chronic abscesses
3) fat necrosis
4) infarcts
5) thrombi
6) schisto
7) Monckeberg arteriolosclerosis
8) congenital CMV
9) toxo
10) psammoma bodies

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67
Q

Is dystrophic calcification related to hypercalcemia?

A

not directly associated with hypercalcemia (patients usually normocalcemic)

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68
Q

calciphylaxis

A

rare syndrome of vascular calcification + thrombosis + skin necrosis. Usually seen in patients with stage 5 CKD. Affects 1-4% of all dialysis pts.

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69
Q

metastatic calcification

A

Widespread depositoin of calcium in normal tissue secondary to hypercalcemia. Patients usually hypercalcemic.

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70
Q

metastatic calcification presentation

A

metastatic calcifications of alveolar walls in acute pneumonitis.

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71
Q

Where does calcium deposit in metastatic calcification?

A

Interstitial tissues of kidney, lung, and gastric mucosa.

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72
Q

Why does metastatic calcification occur in these tissues?

A

These tissues lose acid quickly, and increased pH favors calcium deposition.

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73
Q

Where does leukocyte extravasation usually occur?

A

postcapillary venules

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74
Q

Steps of leukocyte extravasation

A

1) margination and rolling
2) tight-binding
3) diapedesis
4) migration

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75
Q

LAD type 2 defect

A

defective margination and rolling (decreased Sialyl-Lewis)

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76
Q

proteins involved in vasculature stroma of margination and rolling

A

1) E-selectins
2) P-selectins
3) GlyCAM-1, CD34

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77
Q

leukocyte protein that binds to E and P selectins

A

sialyl-LewisX

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78
Q

Leukocyte protein that binds to GlyCAM-1, CD34

A

L-selectin

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79
Q

which step is defective in LAD type 1?

A

Tight-binding

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80
Q

Proteins involved in tight binding

A

1) ICAM-1

2) VCAM-1

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81
Q

ICAM-1 cell marker

A

CD54

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82
Q

VCAM-1 cell marker

A

CD106

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83
Q

leukocyte protein that binds to ICAM-1?

A

CD11/18 integrins (LFA-1, Mac-1)

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84
Q

leukocyte protein that binds to VCAM-1?

A

VLA-4 integrin

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85
Q

Protein involved in diapedesis

A

PECAM-1

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86
Q

PECAM-1 cell marker

A

CD31

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87
Q

leukocyte protein that binds to PECAM-1?

A

PECAM-1

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88
Q

chemotactic products promoting migration…

A

C5a, IL-8, LTB4, kallikrein, platelet-activating factor.

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89
Q

How do free radicals damage cells?

A

Membrane lipid peroxidation, protein modification, DNA breakage.

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90
Q

What initiates free radical damage

A

Radiation, Phase 1 drug metabolism, redox reactions, NO, transition metals, WBC oxidative burst.

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91
Q

scavenging enzymes and examples

A

enzymes that eliminate free radicals. catalase, superoxide dismutase, glutathione peroxidase.

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92
Q

Other means of eliminating free radicals

A

1) spontaneous decay
2) antioxidants
3) certain metal carrier proteins (transferrin, ceruloplasmin)

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93
Q

antioxidant vitamins

A

A, C, and E

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94
Q

bronchopulmonary dysplasia

A

dysplasia due to oxygen toxicity and free radicals

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95
Q

Other examples of free radical demage

A

1) carbon tetrachloride
2) acetaminophen overdose
3) hemochromatosis
4) Wilson’s

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96
Q

Things that can cause inhalational injury

A

heart, particulates less than 1 micrometer in diameter, irritants (NH3), CO inhalation, arsenic poisoning.

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97
Q

Inhalational injury presentation

A

chemical tracheobronchitis + edema + pneumonia + ARDS

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98
Q

Bronchoscopy findings in inhalational injury.

A

Severe edema, congestion of bronchus, and soot deposition

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99
Q

soot deposition timeframe

A

18 hours after inhalation injury, resolution at 11 days after injury.

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100
Q

Scar formation timeline

A

70-80% of tensile strength regained at 3 months; little additional tensile strength regaiend afterward.

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101
Q

Hypertrophic scars:

1) collagen synthesis
2) collagen organization
3) extent of scar
4) scar evolution
5) recurrence

A

1) increased
2) parallel
3) confined to borders
4) possible spontaneous regression
5) infrequent

102
Q

keloid scars

1) collagen synthesis
2) collagen organization
3) extent of scar
4) scar evolution
5) recurrence

A

1) increased a lot
2) disorganized
3) extends beyond borders of original wound with “clawlike” projections
4) possible progressive growth
5) frequent
* increased in dark skinned people

103
Q

Tissue mediators of wound healing

A

1) PDGF
2) FGF
3) EGF
4) TGF-beta
5) metalloproteinases
6) VEGFg

104
Q

PDGF role in wound healing

A

Secreted by activated platelets and macrophages.
Indcues vascular remodeling and smooth muscle migration.
Stimulates fibroblast growth for collagen synthesis.

105
Q

FGF role in wound healing

A

Stimulates angiogenesis.

106
Q

EGF role in wound healing

A

Stimulates cell growth via tyrosine kinases (EGFR/ErbB1)

107
Q

ErbB1

A

tyrosine kinase

108
Q

TGF-beta role in wound healing

A

angiogenesis + fibrosis + cell cycle arrest

109
Q

metalloproteinases role in wound healing

A

tissue remodeling

110
Q

Phases of wound healing and timeframe

A

1) inflammatory (up to 3 days after)
2) proliferative (day 3-weeks after wound)
3) remodeling (1 week-6+ months after wound)

111
Q

Effector cells of inflammatory wound response phase

A

platelets, neutrophils, macrophages

112
Q

Effector cells of proliferative wound response phase

A

fibroblasts, myofibroblasts, endothelial cells, keratinocytes, macrophages

113
Q

Effector cells of remodeling wound response phase

A

fibroblasts

114
Q

characteristics of inflammatory wound response phase

A

Clot formation + increased vessel permeability and neutrophil migration into tissue; macrophages clear debris 2 days later.

115
Q

characteristics of proliferative wound response phase

A

Deposition of granulation tissue and type III collagen, angiogenesis, epithelial cell proliferation, dissolution of clot, and wound contraction

116
Q

mediator of wound contraction

A

myofibroblasts

117
Q

characteristics of remodeling wound response phase

A

Type III collagen replaced by Type I collagen, which functions to increase tensile strength of tissue.

118
Q

bacterial causes of granulomatous diseases

A

1) mycobacteria (TB, leprosy)
2) bartonella henselae
3) listeria
4) tertiary syphilis
5)

119
Q

Listeria infection in a newborn disease

A

granulomatosis infantiseptica

120
Q

parasitic granulomatous disease

A

schistosomiasis

121
Q

Fungal causes of granulomatous diseases

A

Fungal: endemic mycosis (histoplasmosis)

122
Q

foreign material causes of granulomatous diseases

A

1) berylliosis
2) talcosis
3) hypersensitivity pneumonitis

123
Q

autoinflammatory causes of granulomatous diseases

A 
Sarcoidosis
Crohn disease
PBC
Subacute (de Quervain/granulomatous) thyroiditis
Wegener
Churg-Strauss
GCA
Takayasu
124
Q

TNF-alpha function in granuloma formation

A

INduces and maintains granuloma formation

125
Q

exudate appearance

A

cellular, cloudy

126
Q

Exudate characteristics

A

1) increased protein
2) increased LDH (vs serum)
3) SG>1.020

127
Q

causes of exudate

A

1) lymphatic obstruction (chylous)
2) inflammation/infection
3) malignancy

128
Q

transudate appearance

A

hypocellular (clear)

129
Q

transudate characteristics

A

1) decreased protein
2) decreased LDH (vs serum)
3) SG ess than 1.012

130
Q

Causes of transudate

A

1) increased hydrostatic pressure (eg HF, Na retention

2) decreased oncotic pressure (eg, cirrhosis, nephrotic syndrome)

131
Q

ESR pathophys

A

products of inflammation (eg fibrinogen) coat RBCs and cause aggregation. Denser RBC aggregates fall at a faster rate in a pipette tube.

132
Q

Causes of increased ESR

A

1) anemias
2) infections
3) inflammation (GCA, polymyalgia rheumatica)
4) cancer
5) renal disease (ESDR or nephrotic syndrome)
6) pregnancy

133
Q

Causes of decreased ESR

A

1) sickle cell anemia (altered shape)
2) polycythemia (increased RBCs dilute aggregation factors)
3) HF
4) microcytosis
5) hypofibrinogenemia

134
Q

H&E staining of amyloidosis

A

Shows deposits in glomerular mesangial areas and tubular basement membranes

135
Q

amyloidosis pathophys

A

Abnormal aggregation of proteins (or fragments) into beta-pleated linear sheets causing damage and apoptosis.

136
Q

AL amyloidiosis (primary) etiology

A

deposition of proteins from Ig Light chains

137
Q

AA amyloidosis (secondary) substance

A

fibrils composed of serum AMyloid A

138
Q

Examples of AA amyloidosis

A

1) RA
2) IBD
3) spondyloarthropathy
4) familial Mediterranean fever
5) protracted infection

139
Q

dialysis amyloidosis

A

fibrils composed of beta2-microglobulin

140
Q

Heritable amyloidosis

A

heterogeneous group of disorders, including familial amyloid polyneuropathies due to transthyretin gene mutation.

141
Q

amyloid deposited in age-related amyoidosis + location + features

A

normal (wild-type) transthyretin (TTR). Cardiac ventricles. Slower progression than primary.

142
Q

amyloid type in AD

A

beta-amyloid cleaved from amyloid precursor protein.

143
Q

amyloid type in DM2 + etiology

A

Islet amyloid polypeptide (IAPP). Caused by deposition of amylin in pancreatic islets.

144
Q

Isolated atrial amyloidosis

A

Due to ANP. Common in normal aging.

145
Q

atrophy

A

decrease in tissue mass due to decrease in size and/or number of cells.

146
Q

causes of atrophy

A

1) disuse
2) denervation
3) loss of blood supply
4) loss of hormonal stimulation
5) poor nutrition

147
Q

Is hyperplasia premalignant?

A

Can be an RF for future malignancy but not considered premalignant.

148
Q

Is dysplasia reversible?

A

Only refers to epithelial cells. Mild dysplasia is usually reversible; severe dysplasia usually progresses to carcinoma in situ.

149
Q

Well-differentiated vs. poorly-differentiated

A

Well-differentiated tumors closely resemble their tissue of origin; poorly differentiated look almost nothing like their tissue of origin.

150
Q

Anaplasia

A

complete lack of differentiation of cells in a malignant neoplasm

151
Q

hallmarks of cancer

A

1) evasion of apoptosis
2) growth signal self-sufficiency
3) anti-growth signal insensitivity
4) sustained angiogenesis
5) limitless replicative potential
6) tissue invasion
7) metastasis

152
Q

dysplasia

A

Proliferation of cells with loss of size, shape, and orientation.

153
Q

Carcinoma in situ characteristics

A

1) no BM invasion
2) increased N/C ratio
3) clumped chromatin
4) neoplastic cells encompass entire thickness.

154
Q

invasive carcinoma etiology

A

1) Cells invade BM using collagenases and hydrolases (metalloproteinases).
2) Cell-cell contacts lost by inactivation of E-cadherin.

155
Q

Seed and soil theory of metastasis

A 
Seed = tumor embolus
Soil = target organ, often first-encountered capillary bed
156
Q

Low grade

A

Well-differentiated

157
Q

high grade

A

poorly differentiated, undifferentiated, or anaplastic

158
Q

Most important of TNM for staging?

A

1) Each TNM factor has independent prognostic value.

2) M factor often most impt.

159
Q

carcinoma

A

epithelial origin

160
Q

sarcoma

A

mesenchymal origin

161
Q

choristoma

A

normal tissue in a foreign location (eg gastric tissue in distal ileum in Meckels).

162
Q

tumor of connective tissue

A

fibroma

163
Q

skin cancer epidemiology

A

basal>squamous»melanoma

164
Q

Most common cancer

A

Skin cancer

165
Q

lung cancer epidemiology historically

A

Incidence has dropped in men, but hasn’t changed significantly in women.

166
Q

Top 3 cancers in men, incidence

A

1) prostate
2) lung
3) colorectal

167
Q

Top 3 cancers in women, incidence

A

1) breast
2) lung
3) colorectal

168
Q

Top 3 cancers in men, mortality

A

1) lung
2) prostate
3) colorectal

169
Q

Top 3 cancers in women, mortality

A

1) lung
2) breast
3) colorectal

170
Q

Top 2 leading causes of death in US

A

1) cardiovascular 2) cancer

171
Q

PTHrP/hypercalcemia seen in

A

1) SCC of lung, head, and neck
2) renal
3) bladder
4) breast
5) ovarian
6) lymphoma

172
Q

paraneoplastic polycythemia seen in

A

1) RCC
2) HCC
3) hemangioblstoma
4) pheochromocytoma
5) leiomyoma

173
Q

Pure red cell aplasia

A

anemia with low reticulocytes, paraneoplastic syndrome

174
Q

Pure red cell aplasia associated cancer

A

Thymoma

175
Q

Good syndrome

A

paraneoplastic hypogammaglobulinemia

176
Q

Good syndrome associated cancer

A

Thymoma

177
Q

nonbacterial thrombotic (marantic) endocarditis

A

Deposition of sterile platelet thrombi on heart valves

178
Q

nonbacterial thrombotic (marantic) endocarditis associated with

A

pancreatic adenocarcinoma

179
Q

Anti-NMDA receptor encephalitis presentation

A

psychatric disturbance + memory deficits + seizures + dyskinesias + ANS instability + language dysfunction

180
Q

Anti-NMDA receptor encephalitis association

A

ovarian teratoma

181
Q

opsoclonus-myoclonus ataxia syndrome presentation

A

“dancing eyes, dancing feet”

182
Q

opsoclonus-myoclonus ataxia syndrome association

A

children –> neuroblastoma

adults –> small cell lung cancer

183
Q

paraneoplastic cerebellar degeneration

A

antibodies against Hu, Yo, and Tr antigens in purkinje cells

184
Q

paraneoplastic cerebellar degeneration associations

A

Small cell lung cancer, gynecologic and breast cancer, Hodgkin lymphoma

185
Q

paraneopalstic encephalomyelitis etiology

A

antibodies against HU antigens in neurons

186
Q

paraneopalstic encephalomyelitis etiology

A

small cell lung cancer

187
Q

ALK gene product

A

RECEPTOR tyrosine kinase (oncogene)

188
Q

BCR-ABL gene product

A

NONreceptor tyrosine kinase

189
Q

BCR-ABL association

A

CML, ALL

190
Q

BRAF gene product

A

serine/threonine kinase

191
Q

BRAF association

A

Melanoma + non-Hodgkin lymphoma

192
Q

c-KIT gene product

A

cytokine receptor

193
Q

HER2/neu (c-erbB2) gene product

A

tyrosine kinase

194
Q

HER2/neu (c-erbB2) association

A

breast and gastric carcinomas

195
Q

JAK2 association

A

chronic myeloproliferative disorders

196
Q

KRAS gene product

A

GTPase

197
Q

KRAS association

A

colon cancer, lung cancer, pancreatic cancer

198
Q

MYCL1 gene product

A

transcription factor

199
Q

RET associated with

A

MEN 2A,2B + medullary thyroid cancer

200
Q

CDKN2A association

A

melanoma + pancreatic cancer

201
Q

CDKN2A gene product

A

p16, blocks G1–> S phase

202
Q

DPC4/SMAD4 association

A

pancreatic cancer (deleted in pancreatic cancer)

203
Q

MEN1 gene product

A

Menin

204
Q

NF1 gene product

A

Ras GTPase activating protein (neurofibromin)

205
Q

NF2 gene product

A

Merlin (schwannomin) protein

206
Q

PTEN + association

A

Tumor suppressor gene associated with breast + prostate + endometrial cancer

207
Q

Rb gene product

A

Inhibits E2F; blocks G1–> S phase

208
Q

TP53 gene product

A

p53, activates p21, blocks G1-S phase

209
Q

TSC1 gene product

A

hamartin protein

210
Q

TSC2 gene product

A

tuberin protein

211
Q

VHL gene product

A

inhibits hypoxia inducible factor 1a

212
Q

another name for Wilms tumor

A

nephroblastoma

213
Q

EBV associated cancers

A

Burkitts
Hogkins
Nasopharyngeal
Primary CNS lymphoma

214
Q

HBV, HCV cancer association

A

HCC + lymphoma

215
Q

HPV cancer association

A

cervical and penile/anal carcinoma, head and neck cancer.

216
Q

H pylori cancer association

A

Gastric adenocarcinoma + MALT lymphoma

217
Q

alkylating agents are carcinogenic to…

A

blood, leukemia/lymphoma

218
Q

benzidine

A

aromatic amine, bladder carcinogen

219
Q

arsenic carcinogenic to

A

Angiosarcoma
Lung cancer
squamous cell carcinoma

220
Q

carbon tetrachloride –> 1) organ affected 2) impact

A

1) liver

2) centrilobular necrosis, fatty change

221
Q

ethanol carcinogenic

A

esophageal squamous cell carcinoma

HCC

222
Q

2nd leading cause of lung cancer after cigarette smoke

A

lung cancer

223
Q

psammoma bodies

A

laminated, concentric spherules with dystrophic calcification

224
Q

psammoma bodies seen in

A

1) papillary carcinoma of thyroid
2) serous papillary cystadenocarcinoma of ovary
3) meningioma
4) malignant mesothelioma

225
Q

Are tumor markers used for diagnosis or screening?

A

Shouldn’t be used as primary tool for diagnosis or screening. May be used to monitor recurrence and resposne to therapy, but need biopsy for definitive diagnosis.

226
Q

ALP as a tumor marker

A

Pagets, seminoma, or *mets to bone or liver.

227
Q

alpha-fetoprotein associations

A

HCC
*hepatoblastoma
yolk sac (endodermal sinus) tumor
*mixed germ cell tumor

228
Q

high levels of alpha-fetoprotein associated with..

A

NTDs + *abdominal wall defects

229
Q

what produces beta-HCG?

A

Syncytiotrophoblasts of the placenta

230
Q

Beta-HCG as a tumor morker

A

1) hydatidiform moles and choriocarcinomas
2) testicular cancer
3) mixed germ cell tumor

231
Q

CA 15-3/CA 27-29

A

breast cancer

232
Q

calcitonin as a tumor marker

A

Medulary thyroid carcinoma

233
Q

CEA as a tumor marker

A

Very nonspecific. Produced by 70% of colorectal and pancreatic cancers; also produced by gastric, breast, and medullary thyroid carcinomas.

234
Q

PSA elevated in…

A

BPH, prostatitis, prostate cancer.

235
Q

PSA useful for screening?

A

Questionable risk/benefit for screening given that it’s elevated in other conditions

236
Q

P-glycoprotein

A

AKA multidrug resistance protein 1 (MDR1). Used to pump out toxins, including chemotherapeutic agents (one mechanism of decreased responsiveness or resistance to chemo over time).

237
Q

P-glycoprotein cancer associations

A

Adrenal cell carcinoma classically, but also colon, liver.

238
Q

Cachexia mediators

A

TNF + IFN-gamma + IL-1 + IL-6

239
Q

General rule of thing about mets

A

Most sarcomas spread hematogenously; most carcinomas spread via lymphatics.

240
Q

Exceptions to general rule about carcinoma mets

A

HCC, RCC, follicular thyroid carcinoma, choriocarcinoma.

241
Q

Most common mets to brain

A

Lung, breast, prostate, melanoma, GI

242
Q

Brain tumors

A

50% are from mets

243
Q

Most common mets to liver

A

colon, stomach, pancreas

244
Q

Most common mets to bone

A

prostate/bresat, lung,thyroid,kidney

245
Q

Most common sites of mets in general

A

(after regional lymph nodes) liver and lung

246
Q

caveats at bone mets

A

1) bone mets are a lot more common than primary bcone tumors

2) mets have a predilection for axial skeleton

247
Q

Breast to bone mets pattern

A

mix of lytic and blastic

248
Q

lung to bone mets pattern

A

mix of lytic and blastic

249
Q

thyroid to bone mets pattern

A

lytic

250
Q

kidney to bone mets pattern

A

lytic

251
Q

prostate to bone mets pattern

A

blastic

STEP (85 decks)

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