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Pathology > Path I Final > Flashcards

Path I Final Flashcards

1
Q

Plasma d-dimer ELISA test is elevated in what condition? Why can’t it be used after surgery?

A

elevated in DIC and PE

already have d-dimer after surgery

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2
Q

Endothelin I is the first step in?

A

coagulation and platelet activation

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3
Q

PT/ Extrinsic - used to monitor what?

A

PT= prothromvin time, tests the extrinsic and common coag paths. extrinsic path activated by tissue factor

monitors coagulation problem

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4
Q

PTT/Intrinsic used to monitor what?

A

PTT= partial thromboplastin time. tests intrinsic and common coag. intrinsic activated by contact factors

monitors people on heparin (anti-coag)

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5
Q

Bleeding time

A

platelet problem if elevated

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6
Q

D-dimer fibrin degradation products PE, DIC, Surgery

A

DIC is always second to another disorder. results in widespread microthrombi, consumption of platelts and clotting factors –> hemorrhage **elevated D-dimer prod

PE often clinically silent. caused by deep vein thrombosis **elevated D-dimer prod

Surgery **elevated D-dimer prod

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7
Q

Which cancers kill most f/m worldwide?

A 
F= cervical
M= hepatocellular
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8
Q

what 3 cancers like to metastasize to the brain?

A

breast
lung
melanoma

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9
Q

5 cancers go to the bone?

A 
lung
breast
thyroid
kidney
prostate
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10
Q

Lentigo

A

flat. small pigmented spot with clear edge, benign hyperplasia of melanocytes

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11
Q

nevus

A

nest. mole, benign tumor of melanocutes

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12
Q

dysplastic nevus

A

large or irregular, vary in pigment

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13
Q

what can acanthosis nigricans be an indication of?

A

hyperpigment in axilla/groun – indicates internal GI malignancy

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14
Q

which melanoma is best to have? worst? most common?

A

Best= lentigo
Worst= nodular
Most common= superficial spreading

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15
Q

tests for psoriasis and pemphigus

A

Auspitz sign for psoriasis = remove scale, is therepinpoint bleeding?

nukolski’s sign for pemphigus = does it rupture?

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16
Q

what is the relationship bw topical steroids and Tenia infection of skin?

A

steroid only masks inflammation, does not kill fungus

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17
Q

what is the difference between erythema nodosum and erythema multiforme?

A 
EN = raised, painful nodules of subcutaneous adipose. on shins
EM= hypersensitivity rxn, TARGETED lesions, can be anywhere (ex. Lyme)
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18
Q

Morbidity

A

rate of injury

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19
Q

Mortality

A

death rate

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20
Q

Pathognomic

A

2 definitions:

  1. s/s specific for this dz only
  2. s/s Always happens in the course of this dz
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21
Q

idiopathic

A

no known etiology

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22
Q

iatrogenic

A

doctor acquired

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23
Q

H&E stain- what is red and what is blue?

A

Eosin stains red = cytoplasm, rbc, collagen

Hematoxylin stains blue = nuclei, bacteria

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24
Q

What is the difference between necrosis and apoptosis?

A 
nec= messy, inflammation and lysis
apop= clean, programmed cell death, no inflamm or lysis, Cytochrome C is released
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25
Q

What are the common caused of cellular injury?

A

hypoxia, ischemia, infection, immunological, congenital, chemical

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26
Q

What dz is caused by vit D deficiency?

A

rickets, osteomalacia

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27
Q

What dz is caused by vit B12 deficiency?

A

pernicious anemia, neuropathy, SC degeneration

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28
Q

What dz is caused by vit B9 deficiency?

A

neural tube defects [folate]

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29
Q

What dz is caused by vit B3 deficiency?

A

pellagra = dementia, diarrhea, dermatitis. [niacin]

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30
Q

when does cloudy swelling occur?

A

cell degeneration causes intracellular protein accumulation in serium, cell swells bc cant maintain ionic fluid homeostasis - dec Na/K pump – Na and H2O accumulat

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31
Q

where do free radicals come from?

A

all detox rxns within the body, and externally =

Smog= UV+O2+NO = O3

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32
Q

pathway beginning with mitochondrial dysfunction and leading to cell swelling

A

decrease oxidative phosphorylation –> dec ATP –> mitochondria becomes permeable –> release of Cyto C –> apoptosis triggered –> Na/K pumps fail, influx of Na/H2O, efflux of K –> cell swells, ER swells, Ca released

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33
Q

What is the significance of anaplasia? 2 chief findings?

A

acquired malignant change, total loss of differentiation

chief findings = hypoplasia and agenesis

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34
Q

what is 1’, 2’, 3’ intention?

A

1’= STITCHES. regeneration, edges approximated with scab, dermal healing via scarring.

2’= poor aposition, necrosis, infxn, inc fibrin and GRANULATION tissue, wound contraction

3’= surgical, bring edges closer

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35
Q

what is hypoplasia? agenesis?

A

Hypoplasia = defective formation or incomplete developemtn of a part

Agenesis= abscence/failure of formation

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36
Q

Types of stem cells and which tissues have each?

A

Labile = continuously divide and regenerate. in epidermis, GI, hematopo

Stable = low level of replication, need stimultion to divide. in hepatocytes, PCT, endo, retinal

Permanent = never divide. neurons and cardiac muscle

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37
Q

3 stages of fracture healing?

A
  1. procallous = anchor, not rigid
  2. fibrocartilous/ callous
  3. osseous callous
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38
Q

Traumatic vs Pathological fracture

A 
Traumatic= caused by injury
Patho= caused by dz that led to weakness of sturcture
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39
Q

Karyotype

A

number and appearanc of chromosome in cell nuclei

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40
Q

ideogram

A

show chromosoem size and bodnign pattern of gene location

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41
Q

parts of a chromosome?

A 
p short (p=petite)
q long
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42
Q

how many pairs of autosomes? sex chrom? in human

A

22 pairs autosomes

1 pair sex

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43
Q

Gene

A

protein coding area of a chromosome

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44
Q

Locus

A

location of gene on a chromosome

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45
Q

Alleles

A

2+ variations of a gene in a population

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46
Q

SNP

A

1 nucleotide differs. usually in noncoding region

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47
Q

what is the difference between imprinting of the X chromosome and imprinting of autosomes?

A 
X = early imprinting
AUto = epigenetic
48
Q

5 points of control for gene expression

A
  1. chromatin stage
  2. transcription
  3. translation
  4. post translational control in cytoplasm
  5. post translational modification
49
Q

why does DNA naturally wrap around histones, and what epigenetic changes can occur to histone tails to encourage/discourage winding/unwinding?

A

charges are opposite (DNA+ hist-)

attach to each other and coil

50
Q

What is the promoter region on a gene, and why are promoter regifons generally not methylated?

A

methylation discourages binding to promoter –> proteins wont be made

51
Q

Exudates vs Transudates- which causes non-pitting edema?

A 
Exudates = hi protein content **NON PITTING*
Trans= lo protein content

[newspaper test]
Protein Poor Pits!!

52
Q

Virchow’s triad and examples of dz contributing to stasis, vascular injury, and hypercoagulability?

A

THROMBOSIS =
1. Stasis = atrial fibrulation, L vetricular dysfuncton, paralysis

  1. v. well injury = trama/surger, venupuncture
  2. hypercoag = malignancy, dehydration, thrombocytopenia
53
Q

Embolism vs thrombus

A

thrombus = pathological formation of intravascular fibirin-platelet plug

embolus= traveling thrombus

54
Q

features of a pulmonary emboli?

A

bedridden pt stands up and collapses

95% from DVTs (does not begin in lungs!)

55
Q

what is the most common outcome of PE?

A

NONE– 75% no sequelae

56
Q

why do 10% of hemophiliacs not progress to aids?

A

mutated CCR5 prevents HIV from binding to target cell

57
Q

2 neoplasms most often seen in AIDS

A

kaposi’s sarcoma and non-hodgkin’s lymphoma

58
Q

diagnostic criteria for aids?

A

HIV+ and CD4

59
Q

in what types of tissues do sarcomas arise? how do they prefer to spread?

A

sarcomas arise in MUSCLE or CT. spread via BLOOD STREAM

60
Q

in what types of tissues do carcinomas arise? how do they prefer to spread?

A

carcimomas arise in EPITHELIUM. spread via LYMPATHIC tissue

61
Q

what are adenocarcinomas?

A

Glandular cancers

62
Q

what tissues are most sensitive to ionizing radiation? Why?

A

GI and bone- most turnover here

63
Q

Ames test. Why might it be misleading?

A

detects mutagenic effects of possible carcinogens on bacterial cell.s the initial screen for drugs, induces frameshift mutations.

Ames does not test for epigentic..

64
Q

First world: age range for cancer incidence peak

A

1-4 kids

80-84 aduls

65
Q

MEN Syndromes

A

Men 1: Parathyroid hyperplasia, pituitary adenoma, pancreatic tumors

2: parathyroid hyperplasia, medullary thyroid carcinoma, pheochromocytoma
3: mucosal neuromas, mtc, pheochromocytoma

66
Q

Preneoplastic disorder vs paraneoplastic syndrome

A

Preneoplastic= disorder comes from benign or malignant neoplasm

Paraneoplastic= neoplasm elaborates a substance that reuslts in an effect that is not directly related to the growth, invasion, metastaiss of the tumor itself. {Cushings}

67
Q

what do geneticistd look for when they are trying to ind promoter regions ong enes, why do you increase the risk of malignancy as you increase the number of methylations at these sites?

A

looking for GC islands

68
Q

what type of solar radiation is most carcinogenic?

A

UVB

69
Q

which fase of mitosis is most sensitive to radiation?

A

G2

70
Q

how does UVB cause cancer?

A

produces pyrimidine dimers in NA leading to transcriptional errors and mutations of proto-oncogenes and tumor suppressor genes

71
Q

radiation that is the hospitol’s friend

A

XRT for treating tumors

gamma for sterilization

72
Q

why is neutron radiation not used?

A

difficult to direct, more harmful to healthy tissue

73
Q

3 essential activities of proto-oncogenes?

A

synthesis of receptors
synthesis of messenger symptoms
nuclear transcription

74
Q

gain of function vs loss of function mutations- how many hits to alleles needed for each?

A

Gain= oncogenes encode proteins. stimulate cell cycle. need ONE copy of allele. CREATE MORE ACTIVE PROTEINS

Loss= tumor suppressors, encode proteins, inhibit cell cycle.need mutaion in BOTH copies of allele. create NO active proteins

75
Q

20% of human cancers come from..

A

VIRUSES

76
Q

how do viruses cause cancer? what is an acutely tranforming retrovirus and how does this process work?

A

receptor synthesis -> messenger system -> nuclear transcription [proto->onco]

retroviruses infect cell and integrate proto-onco, release viral onco, revrse transcriptase and integration

77
Q

2 people with grade II stage IIa adenocarcinoma of the distal esophagus. what about the tumor may still make the prognosis in these 2 individuals different?

A

tumors have different cell types

78
Q

7 fundamental changes in cell physiology needed for the tumor to behave in a malignant fashion?

A
  1. self sufficiency in growth signals
  2. insensitivity t growth-inhibitory signals
  3. evasion of apoptosis
  4. limitless replicative potential
  5. sustained angiogenesis
  6. ability to invade and metastasize
  7. defects in DNA repair
79
Q

Guardian of the genome- what phase does it normally stop the cel from entering if the cell has damaged DNA?

A

p53- S phase

80
Q

which 2 genes regulate apoptosis?

A

p53 promotes apop

bcl2 prevents

81
Q

fine needle aspiration

what doesn’t it give the pathologist?

A

suck out cells from a tumor- cannot give full diagnosis because may not represent entire tumor. just gives grade

82
Q

how can you tell if vessel growth is normal on an angiogram? or if it is caused by a neoplasm?

A

neoplasms stimulate hte growth of host blood vessels- 1-2mm diameter indicates neoplasm, tumor derived vessels are tortuous, leaky, irregularly shaped

83
Q

what do monoclonal Ab specifically target in human cancers?

CA-125, CA-19-9

A

used for SCREENING to monitor reccurence of dz. specific for cell components

NOT USED FOR DIAGNOSIS OF CANCER

Ca125 is for ovarian cancer
19-9 pancreatic

84
Q

tumor grading vs staging

A

Grading= histological estimate of malignancy based on degree of differentiation

Staging= clinical estimte of extent of tumor spread based on tumor side, presence of metastatix dz. specific for each organ

85
Q

Grade4 vs Stage4 cancer

A

Stage 4= MI

Grade 4=anaplastic

86
Q

Genetic instability

A

malignant cells are more prone to mutate and accumulate additional genetic defects
- with chemo, increaed resistancy and increased recurrence

87
Q

Seeding vs transplantation

A

Seeding= get small cancer cells on surface [ovarian carcinoma]

trans= mechanical manipultion- find tumor nlood supply on arterial and venous sides, disect out so as not to dislodge LPS into circulation and contribute to spread

88
Q

Sister Mary Joseph and her principle of metastasis

A

she found the periumbilical node in the pancreas, which then became the sign of pancreatic cancer

89
Q

on xray, what cancers produce osteoblastic vs osteolytic lesions?

A 
osteoblastic= prostastic adenocarcinoms
lytic= renal cell carc, MM, breast
90
Q

test for possible bony metastasis to spine

A

tuning fork- does it hurt?

91
Q

induction

A

chemo/xrt as sole treatment

92
Q

noadjuvant

A

chemo, then 2ndry treatment.

before defining treatment

93
Q

adjuvant

A

combiend with other modality.

chemo.xrt given afte other treatments used

94
Q

salvage

A

surgery for tumor that fails to respond to intiial treatment

95
Q

2 types of tumors very sensitive to XRT? why

A

superficial = sensitive because they grow fastest and are thus most vulnerale

seminomas, lymphomas

96
Q

2 types of tumors very radioresistant to XRT?

A

deep, slow-growing

epithelial, sarcomas

97
Q

odors that suggest a diagnosis

A 
arsenic = garlic
cyanide = bitter almodns
98
Q

what poisoning often accompanies CO in residential fires?

A

Cyanide- from insulation fiber glass

for CO- remove person from source, give 100% oxygen
for cya- give amyl nitrate

99
Q

what are heavy metals?

A

any metal that can be metabolized.

100
Q

bioconcentration

A

toxic substances become increasingly concentrated as they move upthe food chain

101
Q

how can you increase the toxicity of Hg?

A

METHYLATE I

102
Q

2 main toxicities from Hg

A

neurotoxicity
nephrotoxicity

“the mad hatter peeing on himself”

103
Q

why is arsenic oison? is it poison to everythin on earth?

A

replaces P in DNA backbone- breaking it apart.

No- not poisonous to some bacteria

104
Q

Mees lines vs lead lines

A

mees- arsenic, striates across fingers

lead- inc bone density at epi plate in long bones and gums

105
Q

why is lead poisoningso much more distructive in children?

A

they absorb 4-5x more lead

106
Q

PICA? Basophilic stippling?

A

eating non-food– investigate for Fe.

stippling= RBCs have basophilic inclusion bodies from Pb deficiency

107
Q

3 main illnesses in cildren from 2nd hand smoke

A

SIDS, OM, URIs, asthma

**NOT UTIS (this is the test ?)

108
Q

phtochemical smog

A

UV + NO + volatile organic compouns –> airborne particles and ozone

109
Q

why is silicosisthemost common pneuomoconiosis?

A

silica is in sand which is everywhere

110
Q

silicasiderosi

A

mixed dust containign silica and iron

111
Q

Anthracosis

A

black lung

112
Q

Caplans syndrome

A

pneuomoconiosis + RA

113
Q

how do inhaled particled cause fibrosis in th elung?

A

fibers localize in disral lung, stimualte gneration of free radicals

114
Q

where in lung do fibers of asbestos localize?

A

lung periphery –> mesothelioma

115
Q

how many fold does a perosn sk of getting lung vancer increase i they are exposed to asbestos? asbestos + smoke?

A

5x, 55x

Pathology (2 decks)

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