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Flashcards in Pathology Deck (251):
1

Pneumatosis intestinalis

gas cysts in the intestine wall

2

Toxic epidermal necrolysis

♣ 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

3

caspases

cytosolic proteases involved in apoptosis

4

apoptosis characteristics

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

5

pyknosis

nuclear shrinkage

6

karyorrhexis

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

7

Indicator of apoptosis

DNA laddering

8

DNA laddering

(fragments in multiples of 180 bp)

9

differentiating feature from apoptosis and necrosis

cell membrane remains intact without significant inflammation

10

Pathway involved in tissue remodeling in embryogenesis

intrinsic (mitochondrial) pathway.

11

When does intrinsic pathway occur?

1) regulating factor is withdrawn from a proliferating cell population (decreased IL-2 after a completed immunologic regulation leading to apoptosis of proliferating effector cells).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).

12

Intrinsic pathway regulation and examples

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

13

Bcl-2 action

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

14

APAF-1 action

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

15

What happens with Bcl-2 over expression?

decreased caspase activation and tumorigenesis.

16

extrinsic (death receptor) pathway

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)

17

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

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

18

What happens with defective Fas-FasL interactions?

Autoimmune lymphoproliferative syndrome.

19

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

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

20

necrosis

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

21

coagulative necrosis cause and location

ischemia/infarcts. Most tissues except brain.

22

What happens with coagulative necrosis

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

23

when does liquefactive necrosis occur?

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

24

liquefactive necrosis pathophys

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

25

liquefactive necrosis histology

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

26

When does caseous necrosis occur?

TB + systemic fungi (histoplasma) + nocardia.

27

What happens with caseous necrosis?

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

28

Histology of caseous necrosis

Fragmented cells and debris surrounded by lymphocytes and macrophages.

29

pathophys of fat necrosis

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

30

Histology of fat necrosis and appearance

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

31

another example of fibrinoid necrosis

GCA

32

Fibrinoid necrosis pathophys

immune complexes combine with fibrin leading to vessel wall damage

33

fibrinoid necrosis pathophys

vessel walls thick and pink.

34

dry vs. wet gangrenous necrosis

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

35

lysosomal rupture -- reversible or irreversible sign of cell injury?

irreverisble

36

membrane blebbing -- reversible or irreversible sign of cell injury?

reversible

37

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

reversible

38

nuclear pyknosis -- reversible or irreversible sign of cell injury?

irreversible

39

karyorrhexis -- reversible or irreversible sign of cell injury?

irreversible

40

karyolysis -- reversible or irreversible sign of cell injury?

irreversible

41

ribosomal/polysomal detachment (decreased protein synthesis)

reversible

42

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

reversible

43

decreased glycogen -- reversible or irreversible sign of cell injury?

reversible

44

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

irreversible

45

mitochondrial permeability/vacuolization

phospholipid-containing amorphous densities within mitochondria

46

plasma membrane damage mitochondrial permeability/vacuolization

irreersible

47

nuerons most vulnerable to hypoxic-ischemic injury

Purkinje cells of cerebellum + pyramidal cells of hippocampus and neocortex

48

area of heart most susceptible to ischemia

subendocardium of LV

49

area of kidney most susceptible to ischemia

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

50

red infarct

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

51

tissues with multiple blood supplies

liver, lung, intestine, testes.

52

What causes reperfusion injury?

damage by free radicals.

53

Pale infarcts

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

54

organs with a single blood supply

heart, kidney, spleen.

55

characteristics of inflammation

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

56

vascular component of inflammation

increased vascular permebaility + vasodilation + endothelial injury

57

Acute inflammation

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

58

Possible outcomes of acute inflammation

Complete resolution + abscess formation OR progression to chronic.

59

What mediates chronic inflammation?

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

60

chronic inflammation histoogy

Blood vessel proliferation, fibrosis.

61

Outcomes of granuloma formation

scarring and amyloidosis.

62

characteristics of chromatolysis

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

63

when does chromatolysis occur?

concurrent with Wallerian degeneration.

64

dystrophic calcification

calcium deposition in abnormal tissues secondary to injury or necrosis

65

dystrophic calcification characteristics

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

66

When does dystrophic calcification occur?

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

67

Is dystrophic calcification related to hypercalcemia?

not directly associated with hypercalcemia (patients usually normocalcemic)

68

calciphylaxis

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

69

metastatic calcification

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

70

metastatic calcification presentation

metastatic calcifications of alveolar walls in acute pneumonitis.

71

Where does calcium deposit in metastatic calcification?

Interstitial tissues of kidney, lung, and gastric mucosa.

72

Why does metastatic calcification occur in these tissues?

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

73

Where does leukocyte extravasation usually occur?

postcapillary venules

74

Steps of leukocyte extravasation

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

75

LAD type 2 defect

defective margination and rolling (decreased Sialyl-Lewis)

76

proteins involved in vasculature stroma of margination and rolling

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

77

leukocyte protein that binds to E and P selectins

sialyl-LewisX

78

Leukocyte protein that binds to GlyCAM-1, CD34

L-selectin

79

which step is defective in LAD type 1?

Tight-binding

80

Proteins involved in tight binding

1) ICAM-1
2) VCAM-1

81

ICAM-1 cell marker

CD54

82

VCAM-1 cell marker

CD106

83

leukocyte protein that binds to ICAM-1?

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

84

leukocyte protein that binds to VCAM-1?

VLA-4 integrin

85

Protein involved in diapedesis

PECAM-1

86

PECAM-1 cell marker

CD31

87

leukocyte protein that binds to PECAM-1?

PECAM-1

88

chemotactic products promoting migration...

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

89

How do free radicals damage cells?

Membrane lipid peroxidation, protein modification, DNA breakage.

90

What initiates free radical damage

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

91

scavenging enzymes and examples

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

92

Other means of eliminating free radicals

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

93

antioxidant vitamins

A, C, and E

94

bronchopulmonary dysplasia

dysplasia due to oxygen toxicity and free radicals

95

Other examples of free radical demage

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

96

Things that can cause inhalational injury

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

97

Inhalational injury presentation

chemical tracheobronchitis + edema + pneumonia + ARDS

98

Bronchoscopy findings in inhalational injury.

Severe edema, congestion of bronchus, and soot deposition

99

soot deposition timeframe

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

100

Scar formation timeline

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

101

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

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

102

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

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

Tissue mediators of wound healing

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

104

PDGF role in wound healing

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

105

FGF role in wound healing

Stimulates angiogenesis.

106

EGF role in wound healing

Stimulates cell growth via tyrosine kinases (EGFR/ErbB1)

107

ErbB1

tyrosine kinase

108

TGF-beta role in wound healing

angiogenesis + fibrosis + cell cycle arrest

109

metalloproteinases role in wound healing

tissue remodeling

110

Phases of wound healing and timeframe

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

111

Effector cells of inflammatory wound response phase

platelets, neutrophils, macrophages

112

Effector cells of proliferative wound response phase

fibroblasts, myofibroblasts, endothelial cells, keratinocytes, macrophages

113

Effector cells of remodeling wound response phase

fibroblasts

114

characteristics of inflammatory wound response phase

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

115

characteristics of proliferative wound response phase

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

116

mediator of wound contraction

myofibroblasts

117

characteristics of remodeling wound response phase

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

118

bacterial causes of granulomatous diseases

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

119

Listeria infection in a newborn disease

granulomatosis infantiseptica

120

parasitic granulomatous disease

schistosomiasis

121

Fungal causes of granulomatous diseases

Fungal: endemic mycosis (histoplasmosis)

122

foreign material causes of granulomatous diseases

1) berylliosis
2) talcosis
3) hypersensitivity pneumonitis

123

autoinflammatory causes of granulomatous diseases

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

124

TNF-alpha function in granuloma formation

INduces and maintains granuloma formation

125

exudate appearance

cellular, cloudy

126

Exudate characteristics

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

127

causes of exudate

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

128

transudate appearance

hypocellular (clear)

129

transudate characteristics

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

130

Causes of transudate

1) increased hydrostatic pressure (eg HF, Na retention
2) decreased oncotic pressure (eg, cirrhosis, nephrotic syndrome)

131

ESR pathophys

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

132

Causes of increased ESR

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

133

Causes of decreased ESR

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

134

H&E staining of amyloidosis

Shows deposits in glomerular mesangial areas and tubular basement membranes

135

amyloidosis pathophys

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

136

AL amyloidiosis (primary) etiology

deposition of proteins from Ig Light chains

137

AA amyloidosis (secondary) substance

fibrils composed of serum AMyloid A

138

Examples of AA amyloidosis

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

139

dialysis amyloidosis

fibrils composed of beta2-microglobulin

140

Heritable amyloidosis

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

141

amyloid deposited in age-related amyoidosis + location + features

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

142

amyloid type in AD

beta-amyloid cleaved from amyloid precursor protein.

143

amyloid type in DM2 + etiology

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

144

Isolated atrial amyloidosis

Due to ANP. Common in normal aging.

145

atrophy

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

146

causes of atrophy

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

147

Is hyperplasia premalignant?

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

148

Is dysplasia reversible?

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

149

Well-differentiated vs. poorly-differentiated

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

150

Anaplasia

complete lack of differentiation of cells in a malignant neoplasm

151

hallmarks of cancer

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

dysplasia

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

153

Carcinoma in situ characteristics

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

154

invasive carcinoma etiology

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

155

Seed and soil theory of metastasis

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

156

Low grade

Well-differentiated

157

high grade

poorly differentiated, undifferentiated, or anaplastic

158

Most important of TNM for staging?

1) Each TNM factor has independent prognostic value.
2) M factor often most impt.

159

carcinoma

epithelial origin

160

sarcoma

mesenchymal origin

161

choristoma

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

162

tumor of connective tissue

fibroma

163

skin cancer epidemiology

basal>squamous>>melanoma

164

Most common cancer

Skin cancer

165

lung cancer epidemiology historically

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

166

Top 3 cancers in men, incidence

1) prostate
2) lung
3) colorectal

167

Top 3 cancers in women, incidence

1) breast
2) lung
3) colorectal

168

Top 3 cancers in men, mortality

1) lung
2) prostate
3) colorectal

169

Top 3 cancers in women, mortality

1) lung
2) breast
3) colorectal

170

Top 2 leading causes of death in US

1) cardiovascular 2) cancer

171

PTHrP/hypercalcemia seen in

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

172

paraneoplastic polycythemia seen in

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

173

Pure red cell aplasia

anemia with low reticulocytes, paraneoplastic syndrome

174

Pure red cell aplasia associated cancer

Thymoma

175

Good syndrome

paraneoplastic hypogammaglobulinemia

176

Good syndrome associated cancer

Thymoma

177

nonbacterial thrombotic (marantic) endocarditis

Deposition of sterile platelet thrombi on heart valves

178

nonbacterial thrombotic (marantic) endocarditis associated with

pancreatic adenocarcinoma

179

Anti-NMDA receptor encephalitis presentation

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

180

Anti-NMDA receptor encephalitis association

ovarian teratoma

181

opsoclonus-myoclonus ataxia syndrome presentation

"dancing eyes, dancing feet"

182

opsoclonus-myoclonus ataxia syndrome association

children --> neuroblastoma
adults --> small cell lung cancer

183

paraneoplastic cerebellar degeneration

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

184

paraneoplastic cerebellar degeneration associations

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

185

paraneopalstic encephalomyelitis etiology

antibodies against HU antigens in neurons

186

paraneopalstic encephalomyelitis etiology

small cell lung cancer

187

ALK gene product

RECEPTOR tyrosine kinase (oncogene)

188

BCR-ABL gene product

NONreceptor tyrosine kinase

189

BCR-ABL association

CML, ALL

190

BRAF gene product

serine/threonine kinase

191

BRAF association

Melanoma + non-Hodgkin lymphoma

192

c-KIT gene product

cytokine receptor

193

HER2/neu (c-erbB2) gene product

tyrosine kinase

194

HER2/neu (c-erbB2) association

breast and gastric carcinomas

195

JAK2 association

chronic myeloproliferative disorders

196

KRAS gene product

GTPase

197

KRAS association

colon cancer, lung cancer, pancreatic cancer

198

MYCL1 gene product

transcription factor

199

RET associated with

MEN 2A,2B + medullary thyroid cancer

200

CDKN2A association

melanoma + pancreatic cancer

201

CDKN2A gene product

p16, blocks G1--> S phase

202

DPC4/SMAD4 association

pancreatic cancer (deleted in pancreatic cancer)

203

MEN1 gene product

Menin

204

NF1 gene product

Ras GTPase activating protein (neurofibromin)

205

NF2 gene product

Merlin (schwannomin) protein

206

PTEN + association

Tumor suppressor gene associated with breast + prostate + endometrial cancer

207

Rb gene product

Inhibits E2F; blocks G1--> S phase

208

TP53 gene product

p53, activates p21, blocks G1-S phase

209

TSC1 gene product

hamartin protein

210

TSC2 gene product

tuberin protein

211

VHL gene product

inhibits hypoxia inducible factor 1a

212

another name for Wilms tumor

nephroblastoma

213

EBV associated cancers

Burkitts
Hogkins
Nasopharyngeal
Primary CNS lymphoma

214

HBV, HCV cancer association

HCC + lymphoma

215

HPV cancer association

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

216

H pylori cancer association

Gastric adenocarcinoma + MALT lymphoma

217

alkylating agents are carcinogenic to...

blood, leukemia/lymphoma

218

benzidine

aromatic amine, bladder carcinogen

219

arsenic carcinogenic to

Angiosarcoma
Lung cancer
squamous cell carcinoma

220

carbon tetrachloride --> 1) organ affected 2) impact

1) liver
2) centrilobular necrosis, fatty change

221

ethanol carcinogenic

esophageal squamous cell carcinoma
HCC

222

2nd leading cause of lung cancer after cigarette smoke

lung cancer

223

psammoma bodies

laminated, concentric spherules with dystrophic calcification

224

psammoma bodies seen in

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

225

Are tumor markers used for diagnosis or screening?

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

ALP as a tumor marker

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

227

alpha-fetoprotein associations

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

228

high levels of alpha-fetoprotein associated with..

NTDs + *abdominal wall defects

229

what produces beta-HCG?

Syncytiotrophoblasts of the placenta

230

Beta-HCG as a tumor morker

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

231

CA 15-3/CA 27-29

breast cancer

232

calcitonin as a tumor marker

Medulary thyroid carcinoma

233

CEA as a tumor marker

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

234

PSA elevated in...

BPH, prostatitis, prostate cancer.

235

PSA useful for screening?

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

236

P-glycoprotein

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

P-glycoprotein cancer associations

Adrenal cell carcinoma classically, but also colon, liver.

238

Cachexia mediators

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

239

General rule of thing about mets

Most sarcomas spread hematogenously; most carcinomas spread via lymphatics.

240

Exceptions to general rule about carcinoma mets

HCC, RCC, follicular thyroid carcinoma, choriocarcinoma.

241

Most common mets to brain

Lung, breast, prostate, melanoma, GI

242

Brain tumors

50% are from mets

243

Most common mets to liver

colon, stomach, pancreas

244

Most common mets to bone

prostate/bresat, lung,thyroid,kidney

245

Most common sites of mets in general

(after regional lymph nodes) liver and lung

246

caveats at bone mets

1) bone mets are a lot more common than primary bcone tumors
2) mets have a predilection for axial skeleton

247

Breast to bone mets pattern

mix of lytic and blastic

248

lung to bone mets pattern

mix of lytic and blastic

249

thyroid to bone mets pattern

lytic

250

kidney to bone mets pattern

lytic

251

prostate to bone mets pattern

blastic