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pathology > Pathology I, Exam I review for brain scape > Flashcards

Pathology I, Exam I review for brain scape Flashcards

1
Q

Pathology is what?

A

the study of the nature and characteristic of disease including signs/symptoms etc.

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2
Q

Disease?

A

impairment of the normal state of the living animal or pland body. It normally has distinguishing signs and symptoms

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3
Q

Homeostasis

A

ability of organism to seek and maintain conditon of equilibrium and stability within its internal environment even with external changes

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4
Q

Morbidity

A

diseased state or symptom

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5
Q

comorbidity

A

simultaneous presence of two chronic diseases or conditons in a patient

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6
Q

mortality

A

the state or conditon of being subject to death

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7
Q

iatrogenic

A

doctor caused disease

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8
Q

idiopathic

A

disease or conditon whos cause is unknown or arrives spontaneously

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9
Q

signs

A

objective, things the doctor can see

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10
Q

symptoms

A

subjective, what the patient says they are experiencing

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11
Q

self-limiting disease

A

disease process that resolves spontaneously with or without specifict treatment.

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12
Q

death

A

not living

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13
Q

illness

A

an unhealthy condition or body or mind, sickness or disease

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14
Q

etiology

A

cause of diesase, genetic or aquired

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15
Q

pathogenesis

A

temporal sequence and patterns of cellular injury that lead to disease

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16
Q

morphology

A

gross and microscopic changes of diseased tissue

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17
Q

functional derangements

A

morphologic changes, cellular adaptations

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18
Q

syndrome

A

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

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19
Q

clinical significance

A

signs and symptoms, progression, prognosis

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20
Q

What three things does eosin turn RED or pink?

A

cytoplasm, RBC, Collagen

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21
Q

What 2 things does hematoxylin stain blue to puple?

A

nuclei and bacteria,

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22
Q

What is and H and E stain?

A

Gold standard of microscopic examination of tissue using hematoxylin and Eosin

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23
Q

How can normal pink stained protein be differientated from amyloid that is found in disease?

A

Use the congo red stain that turns amyloid green under polarized light

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24
Q

In what 6 disease would you find amyloidosis?

A

B cell proliferations, chronic inflamation and renal failure, alzheimers, Type II diabeetes and prion disease

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25
Q

What is amyloidosis?

A

Idopatic (cause unknown) disease that has extracellular accumulation of amyloid in tissues,

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26
Q

What is amyloid?

A

pathologic protein found in lots of clinical conditions, mostly idiopathic, cause unknown.

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27
Q

southern blot

A

Used to identify specific gene sequences.check for specific gene exhists for disease

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28
Q

northern blot

A

Used to detect specific sequence of RNA

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29
Q

western blot

A

Used for lime disease, used to identify specific amino acid sequences

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30
Q

necrosis

A

Cell death cause by irreversable cell injury

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31
Q

Apoptosis

A

programed cell death, it does not cause inflammation

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32
Q

Most common causes of cellular injury?

A

Hypoxia, lack of acequate oxygen that is caused by ischemia is the most common cause of cell injury

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33
Q

What is hypoxia?

A

lack of adequate oxygen to tissues

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34
Q

What is ischemia?

A

lack of adequate blood to tissues caused by cardiopulmonary failure, or anemia, decreased oxygen carrying capacity

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35
Q

Marasmus

A

lack of total caloric intake

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36
Q

Kwashiorkor

A

lack of total protein intake

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37
Q

What are 7 causes of cells injury?

A

lack of oxygen, infections, trauma, chemical, immune reactions, congenital disorders, nutritional imbalances

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38
Q

Vit A defidiency causes?

A

squamous metaplasia, immune defiency, night blindness

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39
Q

Vit C

A

scurvy

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40
Q

Vit D

A

rickets and osteomalacia

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41
Q

Vit K

A

bleeding and diathesis

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42
Q

Vit B12

A

megaloblastic anemia, neuropathy, spinal cord degeneration

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43
Q

Folate

A

megaloblastic anemia and neural tube defects

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44
Q

niacin

A

ellagra - ddd diarrhea, dermatitis dementia and death

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45
Q

When would cloudy swelling occur?

A

whenever cells are incapable of maintaining ionic and fluid homeostasis

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46
Q

What are 6 places that free radicals come from?

A

UV, ionizing radiation, smoking, polution, inflammation, metabolism (mitochondria)

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47
Q

How does cell go from mitochondrial function that leads to swelling, 8 steps

A
  1. mito disfunction, 2. decrease in oxadative phosphorylation, 3. release of cytochrome C to trigger apoptosis, 4. NaK ATPase fail, 5. influx of Na and H20 that follows, 6. cellular welling, 7. ER swelling
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48
Q

What is the most common form of necrosis?

A

Coagulative necrosis

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49
Q

Characteristics of coagulative necrosis?

A

denature and coagulation of proteins in cytoplasm

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50
Q

Three places coagulative necrosis is most common?

A

liver, heart and kidney

51
Q

Liquafaction necrosis character

A

cell destruction by hydrolytic enzymes due to autolysis

52
Q

Where is liquafaction necrosis found?

A

abcesses, brain infarcts and pancratic necrosis

53
Q

Caseous necrosis characteristics

A

combo of coagulation and liquafaction necrosis, ie denature/coaguation of proteins with cell destruction by hydrolytic enzymes

54
Q

Where would casuous necrosis be found?

A

granulomatous disease like TB with a soft friable cottage chese like appearance

55
Q

What is more dangerous, dry or wet gangrene?

A

Wet gangrene is more dangerous because it almost always involves infection and it can spread quicky.

56
Q

What category is gas gangrene in?

A

it is a wet gangrene cause by clostridium perfringens

57
Q

THe difference between the look of dry and wet gangrene?

A

Dry gangreen looks like cuagulative necrosis while wet looks like liquefactive necrosis

58
Q

How does gene reguation of apoptosis work?

A

One gene inhibits, bcl-2 and one gene stimulates, p-53

59
Q

bcl2 does what

A

inhibits apoptosis by preventing release of cytocrome C and binding proteases that would otherwise cause apoptosis

60
Q

p-53 does what?

A

stimulates apoptosis, and arrests the cell cycle

61
Q

two paths to apoptosis?

A

incrinsic with mitochondria and Extrinic with receptor initiated cell death FAS and TNF

62
Q

What mediates the execution of apoptosis

A

cascade of caspases that activeate endonucleases and then digest nuclear and cytoskeletal proteins

63
Q

Why are caspases importaint?

A

embryogenesis, menstration, thymus selective death of lymphocytes

64
Q

Why would the appearance of lipofuscin be importaint?

A

Its not pathological, liver spots, indigestable material accumulating in the lysosomes most common in heart and liver

65
Q

What is hemosiderosis?

A

Iron overload disorder, hemosiderin collects in skin and is slowly removed after bruising, heme that leaks is phagocytosed by macrophages that recovers iron,

66
Q

Metastatic calcification is what?

A

occurs when there is elevates derum calcium or phosphate like durining bone destruction, milk, antacid abuse, and parathyroid adenoma

67
Q

Distrophic calcification is what?

A

local calcification of non-viable tissues, atheroma, TP, on damaged heart valves

68
Q

atrophy

A

decrease in cell or organ size and functional ability

69
Q

hypertrophy

A

increase in cell size and functional ability due to increased synthesis of intracellular components

70
Q

hyperplasia

A

increase in number o cells in a tissue or organ

71
Q

metaplasia

A

reversible change in one cell type to another often in response to irritation

72
Q

displasia

A

abnormal proliferation of cells that is characterized by changes in size, shape and loss of organization

73
Q

anaplasia

A

total loss of differentiation as might be seen in malignant neoplasms,

74
Q

what is physiologic cause of hypertrophy?

A

lifting weights to increase muscle size, puberty, lactating breast

75
Q

What is pathologic cause of hypertrophy?

A

cardiac muscle working to hard cus of hypertension

76
Q

What are this heart walls a sign of?

A

diastolic failure, can fit enough blood in

77
Q

What are thin heart walls a sign of, systolic failure

A

walls are not strong enough to pump the blood

78
Q

What is signifigant in anaplasia?

A

total loss of differentiation, increased nucleus to cytoplasm ratio, nucleus will be strange shapes with corners rather than round

79
Q

Primary intentions wound healing

A

primary union - approximate edges, epidermal aproximation under scab, ROUTINE SCARRING

80
Q

Secondary intention or union

A

fail of first intention, huge hole, edges arent close together, more fibrin and granulation tissue is used, wound contracts

81
Q

tertiary intention

A

surgical, need sutures to help approximate tissue so it will heal more like primary DELAYED CLOSURE- leave open to make sure its not infected

82
Q

in what intervention is granulation tissue used?

A

secondary inention filling of hole

83
Q

agenesis is what?

A

complete absence of organ, like a missing kidney

84
Q

Hypoplasis

A

underdevelopment of organ etc

85
Q

Totipotent stem cell

A

can form every type of body cell, this is the first one.

86
Q

multipotentet

A

can develop into more than one cell but are limited

87
Q

example of multipotent stem cells?

A

adutl stem cells or cord blood stem cells

88
Q

Labile cells-

A

Primary stem cells, contiuously dividing like in the epidermis and epithelium

89
Q

Stable cells

A

low level of replication like in liver or pancreatic acini

90
Q

Penmanent cells

A

never divide like nerve cardiac myocytes and skeletal mm

91
Q

Tissues with Labile cells?

A

surface epithelial, mucosal lining, hematopoietic cells, stem cells

92
Q

Tissues with stable cells?

A

hepatocytes, proximal tubule cells, endothelium

93
Q

Three stages of fracture healing?

A

Procallus, fibrocartilagenous and ossous

94
Q

Procallus

A

provide anchorage but no ridigity, this happens first

95
Q

Fibrocartilagenous stage

A

second stage with calous

96
Q

Osseous stage

A

callous

97
Q

What is the difference between traumatic and pathologic fracture?

A

Traumatic is from trauma, pathologic is from a disease, or dificiency like osteoporosis or bone cancer

98
Q

Why are desmosomes importain in skin pathology?

A

because this is what should hold skin together and its often damaged

99
Q

differnece between vitiligo and melasma?

A

vitalago is the absence of melanocytes forever, melasma is hormonally induced often temporay hyperpigmentation in the face.

100
Q

what is the main difference between freckles and lintigo?

A

freckels have normal number of melanocytes that are producing extra melanin, lintigo is proliferation of melanocytes

101
Q

lentigo

A

localized proliferation of melanocytes

102
Q

characteristic of a congenital birthmark?

A

are present at birth

103
Q

what does nevus mean?

A

Nest, like in a mole nevocellular nevus it?s a nest of melanocytes

104
Q

what would indicate a dysplastic nevus?

A

larger, irregular edges, pigment variation, chaning in shape in size

105
Q

What melanoma has the best and worst prognosis?

A

Best prognosis is lentigo maligna melanoma, worst is nodular melanoma

106
Q

what is the most common type of melanoma

A

superficial spreading melanoma

107
Q

Malignant potential of melanoma is measured how?

A

by the depth of invasion, clarks or breslows

108
Q

Acanthos nigracans is what?

A

looks like ring a round the collar, can indicant sugar regulatory problems or internal malignancies

109
Q

What is the sign of leser trelat?

A

a bunch or seborrehic keratosis showing up all at once, it could indicate a malignancy

110
Q

Basic pathology of psorisis

A

autoimmune, increased proliferation and turnover of epidermal keratinocytes, causing well demarcated red plaque with silvery scale.

111
Q

What sign is used to detect psorisis

A

Auspits sign, scale removal causing pinpoint bleeding.

112
Q

Basic pathophysiology of phemphigus?

A

the basment membran is separated from underlying tissue or the tissue immediately above basement membrane separates causing a bilister. This is cause by antibodies to desmosome. IgG A cantholysis

113
Q

What test would be used to test for phemphigus?

A

Testing for antibodies for desmoglein 3 part of desmosome using floresence

114
Q

What immunoglogulin is involved in pathologenis of dermatitus herpetiformis?

A

Dermal papillae, IgA against gliadin

115
Q

What disease is dermatitis herpetiformis linked to?

A

celiac sprue

116
Q

what is the difference between xeres and exzema?

A

Xerosis is dry skin or membranes and ezema inflammatiory skin disease is characterized by an eurathematous (red) rash with puritus (iching)

117
Q

what is the basis for the lupis rash?

A

DNA anti DNA immune complexes in the basement membrane of epidermis causeing epidermal atrophy

118
Q

Is pityriasis rosea dangerous?

A

Ichy rash in tre shape following upper respiratory infection, it resolves on its own

119
Q

Difference between erythema nodosum and erythema multiforme?

A

Erythema nodosum is on the shins and its inflammation of adipocyts and the cause is usually unknown, erythema multifoma is a hypersensitivity reaction caused by a reaction to a drug or bug bite and has a target shaped red marks.

120
Q

What is signifigant in acitinic kerratosis?

A

old lady hands, its concidered precanderous pre SCC, induced by sun displasia or keratinocytes

121
Q

what layers of skin is involved in SCC?

A

Keratinocites, the outer layers

122
Q

What layer of skin in involved in BCC

A

Basment layer, stratum basalie

123
Q

What skin layer for melanoma?

A

Stratum basale with melanocytes

pathology (7 decks)

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