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pathology > final, old exams > Flashcards

final, old exams 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

simultaneous presence of one or more additional disorders that co-occur with primary disease. 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

when a disease is present that impairs bodily process but upon inspection, there are no changes or signs, even microscopically, IBS and migraines, maybe depression

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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

52
Q

Folate, B9

A

megaloblastic anemia, neural tube defects

53
Q

Niacin, B3

A

pellagra, diarrhea, dermatitis dementia and death

54
Q

when does cloudy swelling occur?

A

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

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,

56
Q

where do free radicals come from?

A

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

57
Q

what does the release of cytocrome C causes?

A

triggers apoptosis

58
Q

what releases cytocrome C and why?

A

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

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

60
Q

pyknosis is what?

A

degeneration and condensation of necular chromatin

61
Q

Karyorrhexis is what?

A

nuclear fragmentation,

62
Q

karyolysis is?

A

dissolution of nucleus

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.

64
Q

What are the two chief findings of anaplasia?

A

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

65
Q

Primay intentions closure

A

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

66
Q

Secondary intention closure

A

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

67
Q

tertiary intention closure

A

keep would open to prevent infection etc so can close later

68
Q

hypoplasia

A

defective formation or incomplete development of a part

69
Q

agenesis iis what?

A

absence or failure of formation entirely

70
Q

what is another name for primay stem cells?

A

labile

71
Q

where are labile, primary stem cells found?

A

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

72
Q

Stable stem cells are what?

A

low replication but can be induced to divide

73
Q

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

A

stable stem cells

74
Q

Where are permanent stem cells found?

A

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

75
Q

what are the three stages of fracture healing?

A

procallous, fibrocartilaginous callous, osseus callous

76
Q

procallous

A

hematoma to provide anchorage but w/o structureal integrity

77
Q

fibrocartilaginous callous

A

fibrous ball around fracture

78
Q

pathologic fractures

A

caused by disease sequale, like osteoporosis etc

79
Q

traumatic fractures

A

cause by trauma

80
Q

type of traumatic fractures?

A

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

81
Q

communited fracture

A

bone broken into many pieces

82
Q

Karyotype

A

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

83
Q

ideogram

A

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

84
Q

P arm?

A

short arm

85
Q

Q arm

A

long arm

86
Q

how many pairs of autosomes

A

22 pairs of autosomes

87
Q

how many total pairs of chromosomes

A

23 pairs total.

88
Q

gene once ment what ?

A

only protein coding sequence of DNA

89
Q

what is a gene now?

A

any functional unit of a chromosome outside medical circles.

90
Q

what percent of genome is protein coding?

A

only about 5%

91
Q

what is locus on chromosome?

A

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

92
Q

alleles?

A

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

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

pathology (7 decks)

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