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pathology > Final review > Flashcards

Final review Flashcards

1
Q

What does the word lentigo mean?

A

small, pigmented spots on skin with clearly defined edge surrounded my normal appearing skin

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2
Q

what is ment by the word nevus

A

nest, melanocytic nevi are nests of multi layered melanocytes found in moles.

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3
Q

what is a nevocellular nevi?

A

benign tumors of melanocyts that have sharp well defined edges stable in shape size and golor.

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4
Q

what is a dysplastic nevi?

A

Larger tumor of melanocytes that have irregular borders and pigment variation., changing in size, elevated and firm.

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5
Q

dysplastic nevus syndrome?

A

autosomal dominant conditions that give one and increased risk of melanoma

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6
Q

what can acanthosis nigricans be an indication of?

A

hyperinsuleniema associated with obesity or sometimes assiciated with a malignancy

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7
Q

what is seborrheic keratosis

A

stuck on keratin filled epidermal speudocysit

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8
Q

what is is called when you suddenly get a lot of seborrheic kerotosis lesions?

A

signs of leser-trelat, may indicate a underlying malignance

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9
Q

What is the test for Psorisis?

A

Auspits sign, scrape away scale and there is pinpoint bleeding

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10
Q

What is the test for Pemphigus?

A

Nikolskis sign, pressing on blister causes the edges to easily expand and its very breakable.

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11
Q

What causes pemphigus?

A

IgG between epidermal keratinocytes that cause blisters

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12
Q

bullae?

A

blisters

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13
Q

what can be a hallmark feature of pemphigus?

A

intraepidermal acanthosysis

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14
Q

what happens if you use steroids on tenia, fungal infections.

A

it will go away for a bit then come back with a vengance.

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15
Q

why does steroids not work on fungus?

A

because it decreases the immune system so the fungus can get a better foothold.

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16
Q

erythema multiforme?

A

Hypersensitivity to drugs or something, targoid lesions, bullae.

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17
Q

what is the most serious form of erythema multiforme?

A

stevens johnson syndrome, extensive involvement of skin and mucus membranes.

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18
Q

Erythema nodosom?

A

shins, 12-20 year olds, raised erythematous (red) painfull nodules of subcutaneous fat.

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19
Q

what is erythema nodosom sometimes associate with?

A

granulomatous diseases and strep, although most of the time there is no known cause, it goes away on its own eventually.

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20
Q

What layers are involved in Squamous cell carcinoma?

A

Keratinocytes invade down into the dermis, rarely metastasize.

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21
Q

what is indicative of keratocanthoma?

A

rapidly growing dome shaped nodules with a keratin filed center

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22
Q

what ususally will cure SCC?

A

complete excision

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23
Q

what is the most common tumor in the western world?

A

Basal cell carcinoma

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24
Q

how invasives is basal cell carcinoma?

A

locally invasive, arising from basal cells of hair follicles

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25
Q

what does basal cell carcinoma look like

A

pearly borders, papules.

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26
Q

what is the growth pattern of BSC?

A

invasive nests of basaloid cells with a palisading growth pattern

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27
Q

Pathology

A

study of the essential nature and charasteristic of disease, signs, symptoms, complications, patogenesis etc.

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28
Q

disease

A

impairment of the noamal states

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29
Q

homeostasis

A

maitenance of a harmonious environmet within body, cell, etc

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30
Q

comorbidity

A

property of disease that gives it a a specific virulence/sequelae

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31
Q

iatrogenic

A

doctor aquired disease

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32
Q

symptoms

A

subjective from patient view

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33
Q

signs

A

objective from doctors view

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34
Q

death

A

no pulse, heart sound or spontaneous respiration, no nucleus in most cells a cell either

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35
Q

sub-clinical

A

no signs or symptoms of infection because the immune system is keeping the infection down

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36
Q

illness

A

unhealthy condition of the body or mind (sickness/disease)

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37
Q

etiology

A

underlying cause of disease

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38
Q

pathogenesis

A

course that a disease takes from start to finish

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39
Q

Morphology

A

presence/conformation of damaged cells and tissues from the infection

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40
Q

functional disease

A

what happens when we know the disease exists but have not discovered any gross or microscopic morphologic changes yet.

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41
Q

syndrome

A

group of signs and symptoms that occur together and characterize a particular abnormality or condition.

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42
Q

Eosin

A

RED and PINK :stains cytoplasm, RBCs and collagen

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43
Q

Hematoxylin

A

BLUE and PURPLE : unclei, bacteria

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44
Q

what are the common causes of cell injury?

A

hypoxia, infections, immunologic reactions, congenital disorders, chemical injury, physical injory

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45
Q

what is the most common cause of cellular injury

A

hypoxia, inability to synthesize sufficient ATP by aerobic oxidation

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46
Q

How do infections cause injury?

A

direct infection, toxins and inflammatory responses of host

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47
Q

Vit A

A

squamous metaplasia, immune deficiency, night blindness

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48
Q

Cit C

A

scurvy

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49
Q

vit D

A

rickets, osteomalacia

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50
Q

Vit K

A

bleeding diathesis

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51
Q

Vit B12

A

megaloblastic anemia, neuropathy, spinal cord degeneration

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52
Q

Folate, B9

A

megaloblastic anemia, neural tube defects

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53
Q

Niacin, B3

A

pellagra, diarrhea, dermatitis dementia and death

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54
Q

when does cloudy swelling occur?

A

intracellular proteins accumulate in cytoplasm, the leaking is from hypoxia and cellular degeneration.

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55
Q

why does cloudy swelling occur?

A

cell is no longer able to maintain homeostasis of ionic and fluid balance. Lack of ATP shuts down necessary pumps,

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56
Q

where do free radicals come from?

A

oxygen derived, uv light, metabolism, inflammation, smoking, ionizing radiation, air polution

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57
Q

what does the release of cytocrome C causes?

A

triggers apoptosis

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58
Q

what releases cytocrome C and why?

A

Mitochondria when its disfunctional and cant make enough atp it becomes permeable.

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59
Q

what pumps fail in mitochondria causing and influx of Na/ water and efflux of K

A

Na/K ATPase pumps start to fail

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60
Q

pyknosis is what?

A

degeneration and condensation of necular chromatin

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61
Q

Karyorrhexis is what?

A

nuclear fragmentation,

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62
Q

karyolysis is?

A

dissolution of nucleus

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63
Q

what is the significance of anaplasia

A

cells divide rapidly but do not bear any resemblance to the normal cells, whether in structure or function.

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64
Q

What are the two chief findings of anaplasia?

A

brick like or random pattern, with dramatic increase of nuclear:cytoplasmic ratio.

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65
Q

Primay intentions closure

A

wound edges are close enough to meet and close, decreases scarring

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66
Q

Secondary intention closure

A

wound edges are far apart, so fills from bottom up with granulous tissue and fibrin

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67
Q

tertiary intention closure

A

keep would open to prevent infection etc so can close later

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68
Q

hypoplasia

A

defective formation or incomplete development of a part

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69
Q

agenesis iis what?

A

absence or failure of formation entirely

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70
Q

what is another name for primay stem cells?

A

labile

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71
Q

where are labile, primary stem cells found?

A

in epidermis, GI tract, etc, and are continuously dividing

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72
Q

Stable stem cells are what?

A

low replication but can be induced to divide

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73
Q

what stem cell type is found in hepatocytes, renal tubular epithelia, alveoli and pancreatic acini

A

stable stem cells

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74
Q

Where are permanent stem cells found?

A

don’t ever divide, are found in nerve cells, cardiac and skeletal muscles.

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75
Q

what are the three stages of fracture healing?

A

procallous, fibrocartilaginous callous, osseus callous

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76
Q

procallous

A

hematoma to provide anchorage but w/o structureal integrity

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77
Q

fibrocartilaginous callous

A

fibrous ball around fracture

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78
Q

pathologic fractures

A

caused by disease sequale, like osteoporosis etc

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79
Q

traumatic fractures

A

cause by trauma

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80
Q

type of traumatic fractures?

A

transverse, linear, non-displaced, comminutes, greenstick, spiral, compound

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81
Q

communited fracture

A

bone broken into many pieces

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82
Q

Karyotype

A

number and visual appearance of the chromosomes in the cell nuclei of an organism or species

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83
Q

ideogram

A

schematic representation of chromosomes showing the relative size of the chromosomes and their banding patterns

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84
Q

P arm?

A

short arm

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85
Q

Q arm

A

long arm

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86
Q

how many pairs of autosomes

A

22 pairs of autosomes

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87
Q

how many total pairs of chromosomes

A

23 pairs total.

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88
Q

gene once ment what ?

A

only protein coding sequence of DNA

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89
Q

what is a gene now?

A

any functional unit of a chromosome outside medical circles.

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90
Q

what percent of genome is protein coding?

A

only about 5%

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91
Q

what is locus on chromosome?

A

exact physical location of a gene on a chromosome, it the same in all people

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92
Q

alleles?

A

used to describe the two or more possible variations of a gene within a population

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93
Q

genotype

A

combo of alleles, it?s the actual sequence

94
Q

penotype

A

the physical reflection of genotype, presence or absence

95
Q

what is a single nucleotide polymorphism, SNP?

A

DNA sequence variation of single nucleotide between members of a species or paired chromosomes.

96
Q

where does SNPs occur more often

A

in non coding reions

97
Q

Imprinting of X chromosome

A

Naturally occuring in females, X inactivation. Only one of the two X chromosomes will be active in cell.

98
Q

Imprinting in general

A

some genes are only active when transmitted by specific sexed parent, so in the other partent its inactived.

99
Q

when does imprinting of autosomal genes happen?

A

during gametogenesis and its maintained in somatic cells.

100
Q

what are the 5 points of control for gene expression?

A

chromatin, transcriptional, translational, post transcript, translate

101
Q

why would dna wrap around histones

A

DNA is negative and histones are positively charged.

102
Q

where does histone methylation occur

A

at CpG islands, it ususally down regulates transcription

103
Q

what does histone acetylation do?

A

up regulating of transcricption cuz it allow unwinding of DNA from histone.

104
Q

what is promoter region?

A

CpG islands ususally, where the polymerase is told to sit down and get ready to copy

105
Q

transudate

A

edema fluid with low protein content and low specific gravity, produces non pitting edema

106
Q

exudates

A

fluid with high protein content and cells and a higher specific gravity

107
Q

what are the three parts of virchows triad?

A

hypercoagulability, stasis and vascular wall injury

108
Q

What causes hypercoaguability?

A

clotting disorders, oral contraceptives, malignancy, pregnancy sepsis

109
Q

what causes stasis?

A

atrial fibrillation, immobility, venous obstruction, venous insufficency,

110
Q

vascular wall injury?

A

trauma/surgery, venepuncture, heart valve disease, replcement, atherosclerosos, catherters.

111
Q

embolism

A

moving clot in bloodstream that leaves site of orgin and it occludes vessel

112
Q

what is thrombosis?

A

non moving clot in arteries, heart chambers, causings infarct, etc.

113
Q

when do fat emboli happen?

A

bone fractures

114
Q

most common thrombosis?

A

thromboemboli

115
Q

gas emboli

A

decompression sickness

116
Q

amniotic fluid emboli

A

labor complications

117
Q

tumor emboli

A

bacteria, drug use

118
Q

where do most pulmonary emboli arise from

A

deep vein thrombosis, diagnosed by spiral CT

119
Q

what is the most common outcome from pulmonary emboli?

A

nothing, 75% are asymptomatic and go away on their own

120
Q

newspaper test?

A

transeudate fluid is if you can read news paper through test tube of fluid

121
Q

countries with highes HIV?

A

African, South africa, nigeria, kenya Mozambique and india

122
Q

why do 10% of hemopheliacs not progress to AIDS

A

maybe they don’t have CCR5 receptors

123
Q

Acute phase of HIV

A

infection, reduced CD4 with viremia, seroconversion, mono, flulike symptoms

124
Q

lantent phase HIV

A

lymphadenopathy, viral replication. Low virema, oppurtunistic infection, 10 years

125
Q

what are the two neoplasms that are often seen in AIDS

A

hairy leukoplakia and kaposi sarcoma, then non hodgkin lymhoma

126
Q

what labs to monitor HIV infection

A

CD4 count, and HIV1 RNA viral load via PCR

127
Q

what is a mitotic body?

A

they are the dividing cells in a tissue

128
Q

what do mitotic bodies tell you about cancer?

A

if there are more mitotic bodies than their should be for specific tissue then you would know tissue was dividing more rapidly and suspect cancer

129
Q

where do sarcomas arise

A

muscles and connective tissue

130
Q

how do sarcomas spread

A

blood stream

131
Q

where do carcinomas arise?

A

epithelium

132
Q

how do carcinomas spread?

A

lymphatic system

133
Q

what is an adenocarcinoma?

A

glandular cancer

134
Q

what cells are most sensitive to ionizing radiation?

A

cells in mitosis or the G2 phase, the are replicating their genome

135
Q

does oma mean the cancer or not?

A

OMA means swelling or tumor, it doesn’t indicate cancer one way or the other.

136
Q

Ames test

A

detects mutagenic effect on DNA, doesn’t show epigenetic changes

137
Q

what cancer kills most males?

A

hepatocellular carcinoma

138
Q

what cancer kills most females?

A

cervical cancer

139
Q

when does cancer peak in first world?

A

80-84 years

140
Q

MEN I

A

pitutary adenoma, parathyroid hyperplasia and pancreatic tumors.

141
Q

MEN II

A

parathyroid hyperplasia, phenochromocytoma, medullary thyroid carcinoma.

142
Q

MEN IIB

A

mucosal neuromas, marfinaoid body habitis, pheochromocytoma, meullary thyroid carcinoma,

143
Q

what does MEN stand for?

A

multiple endocrine neoplasia, a familiar cancer syndrome

144
Q

paraneoplastic syndrome

A

may serve as signal for neoplastic diagnosis, when neoplasm is causing a change but its something that isn’t directly related to tumor growth, like suddenly you are super tired all the time, it may be hormonal

145
Q

preneoplastic disorders

A

Acquired (hep B) - increase liklyhood of reaching a cancerous stage and corelate directly with cancer, HepB,

146
Q

direct acting Initiatior is what?

A

direct acting chemical carcinogens that modify DNA to cause cancer,

147
Q

Indirect initiatior is what?

A

chemical carcinogen gets altered by our body to become an active carcinogen

148
Q

genotoxic mechanisms

A

employ DNA damage, chromosomal misentegration

149
Q

non-genotoxic mechanisnm

A

Employ chronic irrication, cell death ROS , epigenetic to cause problems.

150
Q

what does a person look for to find promoter region?

A

Promoter region alterations, these alterations have been found in all cancers that have been studies.

151
Q

what type of solar radiation is most carcinogenic?

A

UVB

152
Q

how does UVB cause cancer

A

produces dyrimidine dimers in DNA leading to transcritional errors and mutations of proto-oncogenes and tumor supressor genes.

153
Q

what type of radaions used in hospital

A

ioniing ratiation

154
Q

what is neutron radiation not used?

A

because governments have outlawed it because they don’t want it used against them.

155
Q

what are the three activities are protoonca genes involved in?

A

growth, cellular differentiation, gene regulation

156
Q

gain of function

A

oncogenes, one hit process, create more active protein to stimulate cell cycle

157
Q

loss of function

A

tumor supressors, two hit process, creates no active proteins , inhibits cell cycle

158
Q

how do viruses cause cancer or tumors

A

by carrying in oncogenes or by incerting into a tumor supressor gene and breaking it.

159
Q

why may two of the same cancers at same stage in two people progress different?

A

because at each cell divisions, mutations make each cancer different. They may have starteted the same but will continue to be even more different. So one may be hormone sensitive but the other wont

160
Q

7 thing to make tumor be malignant

A

self sufficent, insufficient inhibitory signals, evade apoptosis, limitless replication, sustained angiogensis, ability to invade, and defects in DNA repair

161
Q

what is the guardian of the genome?

A

P53

162
Q

where does P53 work?

A

prevents cell with damaged DNA from entering the S phase.

163
Q

Li-fraumeni syndrome?

A

germ line rotation of p53, it increases rates of tumors, childhood sarcomas leukemia, breast cancer

164
Q

what two genes regulate apoptosis?

A

P53 promotes apoptosis and BCL-2 inhibits apoptosis

165
Q

what is the limit of fine needle aspiration?

A

Does grading (histology) well, it cant determine staging (size, metastisist)it will show that there are cell changes but cant tell if its moved, can’t determine stage

166
Q

what is an abnormal vein growth

A

non fractal growth pattern, it looks evil and twisted.

167
Q

name two nonoclonal antibodies?

A

CA-125 and CA 19-9

168
Q

CA-125 non clonal antibody for what?

A

ovarian cancer

169
Q

CA-19-9 non clonal antibody for what

A

pancreatic cancer

170
Q

BRCA -1

A

brest cancer

171
Q

tumor grading

A

more histological and not prognosis indicatior

172
Q

tumor staging

A

T is size, N is lympnode spread, M is mestatic.

173
Q

TNM is what?

A

degree of size, lymNode and metastasis, indicator of prognosis

174
Q

grade 4 cancer means?

A

glands are fuses, no intervening stroma

175
Q

Stage 4 cancer means

A

metastasis - spreading, poor prognosis

176
Q

Genetic instability in tumor supression

A

malignant cells are more prone to mutate and accumulate additional defects without dying.

177
Q

what does genetic instability mean for cancer reoccurance

A

there was a selective growth advantage for the new cancer, so will more resistance to treatment etc.

178
Q

seeding

A

spread within the same cavity/chamber

179
Q

transplantation

A

no clean margins, surgical insision could spread by indroducing cell toblood

180
Q

sister mary joseph

A

discovered periumbical nodes correlated to pancreatic cancer

181
Q

what three cancers like to move to brain

A

skin, breast and lung

182
Q

what threee cancers like to move to bone

A

breast lung and prostate then kidney and thyroid

183
Q

what causes osteoblastic lesions

A

prostate cancer - builds bumps on bone

184
Q

What causes osteolytic lesions

A

renal and breast cancers - thins out bone

185
Q

how could you test for metastasis to spine?

A

tuning fork

186
Q

Induction treatment

A

only treatment, used for advanced disease or when no other treatment exhists

187
Q

Neoadjuvant

A

chemo first, followed by another treatment

188
Q

adjuvant

A

combination with other modality, given after other treatments are used.

189
Q

salvage

A

hail mary, for those that fail to respond to initial chemo

190
Q

what tumors are more sensitive to XRT (radiosensitive)

A

seminomas and lymphomas - because their cells have high turnover

191
Q

what tumor cells are radio resistane

A

epithelial and carcomas, because they have a lower cell turnover

192
Q

NCCN?

A

national comprehensive cancer network, shows staging and therapies for it.

193
Q

bitter almonds

A

cyanide

194
Q

friity

A

diabetic

195
Q

garlic

A

organophosphates, arsenic, DMSO

196
Q

mothballs

A

naphthalene, camphor

197
Q

how often do patients with CO poisoning turn red

A

not very often but it does cause blood to be very red even though its not carrying oxygen

198
Q

what poisoning often happens in conjunction with CO poisoning

A

cyanide poising because of the burning furniture in fires.

199
Q

what is ment by heavy metals

A

metals or metalloids of environmental concern, denser than iron

200
Q

Do radioisotopes bioconcentrate

A

yes, they do as they are eaten and move up the food chain.

201
Q

before what date should things not have cesium?

A

before 1924

202
Q

how can you increase toxicity of HG

A

methylate it and it becomes more water soluble and can cross the BBB.

203
Q

what are the two main toxicities of mercury poisoning?

A

neruotoxicity (brain) and nephrotoxicity (kidney

204
Q

is arsinic always poisonous?

A

no it can be in some species genome

205
Q

what does acure arsenic poisoning cause?

A

CAN toxicity and hemorragic gastroenteritis

206
Q

what does chronic arsenic cause

A

malaise, abdominal pain, skin changes, mees lines.

207
Q

mees lines arsenic

A

horixontal white lines on nails

208
Q

what do lead lines look like

A

they are not on nails they are at the gingivodental line

209
Q

why is lead worse for children

A

CNS toxicity,

210
Q

Pica

A

desire to eat dirt or ice, may be genetic condition

211
Q

basophilic stippling?

A

seen with microcytic anemia in lead poisoning. Ribosome are spread showing small dots at periphery

212
Q

why do those who start smoking at 30+ not get COPD

A

because they thart after epithelial transition ends at about 20. this also makes it so that cumulative effects take longer

213
Q

what is the 20 pack year thing.

A

packs per day times years smoking. 20 = cancer in the othd view.

214
Q

what illness can second hand smoke cause in children

A

sids, otitis media and asthma/URI

215
Q

what is photochemical smog?

A

chemical reaction of sun, NO, and VOCs in atmosphere leading to ground level ozones and particles and aldehydes, Nos

216
Q

what was in smog in 1905?

A

soot, and sulfer from burining coal

217
Q

how is ozone formed?

A

in atmosphere when NO is broken by sun, and some os for osone.

218
Q

why is silicosis the most common pneumoconiosis?

A

caused by inhalation of dust or pollutants in smok with silica

219
Q

sillicoderosis

A

inhale dust and sillica, swelling of lungs

220
Q

caplans syndrome

A

pneumoconiosis in combination with multiple pulmonary rheumatoid nodes found in rheumatoid arthritis.

221
Q

silicates

A

adding another atom to silica to make mineral

222
Q

silicon

A

chemical element, but almost always in combo with O2

223
Q

silicone

A

polymer of silicone with C and O. solid liquid or gel

224
Q

Pathogonomic

A

symptom/sign that is character of diesase, that will tell you a specific disease without a doubt

225
Q

what is eggshell calcification

A

indicates silicosis on an xray, it is pathogonomonic

226
Q

why does inhaling particles cause fibrosis?

A

magrophage igestion trigger frbrogenic respons via growth factors, promote collagen deposition

227
Q

where do asbestose fibers localize

A

in septum of alveolus and distal lung.

228
Q

what are asbestosed fibers in lungs cause

A

rod or dumbell shaped

229
Q

cancer of asbestose

A

mesothelioma that involves lower lobes and pleura

230
Q

asbestose exposure increases lung cancer by how much

A

5 times then 55 times if the ysmoke to.

pathology (7 decks)

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