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Pathology > Path I Midterm > Flashcards

Path I Midterm Flashcards

1
Q

Pathology

A

the study of nature and cause of disease which includes changes to structure and function

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2
Q

pathophysiology

A

study of abnormal functioning of diseased organs

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3
Q

etiology

A

cause

every disease has an etiology but, most times, is unknown

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4
Q

idiopathic

A

etiology unknown

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5
Q

ankylosing spondylitis

A

ossification of the all the ligaments of the spine

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6
Q

DISH

A

AKA Forestier’s disease
diffuse idiopathic skeletal hyperostosis
results in ossification of the anterior longitudinal ligament

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7
Q

Congenital etiology

A

genetic information is intact, but other factors interfere with normal embryonic development

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8
Q

Acquired etiology

A

everything that is not genetic or congenital

examples include emphysema, herpes

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9
Q

Genetic etiology

A

damaged or altered genetic material is responsible for some structural or functional defect

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10
Q

symptom

A

subjective feeling

like pain, dizziness, tingling

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11
Q

sign

A

objective finding

ie blood pressure, temperature

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12
Q

syndrome

A

characteristic combination of signs and symptoms associated with a particular disease

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13
Q

raynaud’s syndrome

A

vasoconstriction of peripheral arteries of the fingers, thus no blood flow to fingers
no blood flow into the fingers, followed by no blood flow out of the fingers
fingers are white, then blue, then red

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14
Q

Sjogren’s syndrome

A

autoimmune damage to exocrine glands which results in dryness of mucous membranes which thus weakens the body’s first line of defense
usually a manifestation of rheumatoid arthritis or SLE

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15
Q

acute disease

A

short duration, quick onset, severe symptoms

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16
Q

chronic disease

A

lasts more than 6 weeks

has a more subtle onset

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17
Q

pathogenesis

A

mechanism of development of a particular disease

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18
Q

local disease

A

confined to one region of the body
ie stomach cancer
local diseases can become systemic

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19
Q

focal damage

A

damage is limited to distinct sites within a diseased organ

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20
Q

diffuse damage

A

damage distributed uniformly within the organ

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21
Q

systemic disease

A

considered systemic if it involves other organs and systems

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22
Q

diagnosis

A

identification of a patient’s specific disease

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23
Q

prognosis

A

theory of the outcome of the disease

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24
Q

deficiency

A

lack of substance necessary to the cell

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25
Q

primary nutrient deficiency

A

lack of specific components in the food

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26
Q

pellagra

A

lack of vitamin B3

casel’s necklace rash

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27
Q

scurvy

A

lack of vitamin c

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28
Q

beri beri

A

lack of thiamin (B1)

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29
Q

secondary nutrient deficiency

A

necessary nutrient is present in the diet but cannot be absorbed

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30
Q

pernicious anemia

A

lack of RBC’s in the blood from an inability to absorb vitamin B12 due to a lack of secretion of intrinsic factor by the stomach

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31
Q

intoxication

A

poisoning, toxins, or the presence of a substance that interferes with cell function

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32
Q

exogenous toxins

A

enter the body from outside

can come from infection, chemicals, or an overdose of medication/vitamins

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33
Q

endogenous toxins

A

created within the body

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34
Q

genetic endogenous toxins

A

can occur via accumulation of a normal metabolite or the activation of an alternative pathway

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35
Q

alkaptonuria

A

homogentisic acid is an intermediate of phenylalanine metabolism that builds up in the cartilage
causes onchrosis of the vertebral column
characterized by calcification of the IVD’s
blue ears is another symptom

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36
Q

onchrosis

A

deposition of homogentisic acid in the IVD’s

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37
Q

phenylketonuria

A

activation of an alternate pathway in phenylalanine metabolism
the enzyme that converts phenylalanine to tyrosine is nonfunctional leading to a build up of phenylpyruvic acid in the blood

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38
Q

gout

A

accumulation of metabolic byproducts
uric acid is a byproduct of purine metabilism, hyperuricemia leads to gout
uric acid salts are deposited in the joint capsules as the kidney cannot adequately remove the uric acid from the blood

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39
Q

Cell trauma

A 
loss of structural integrity
can come from :
direct contact
hypo/hyperthermia
mechanical pressure (tumor/high intensity sound)
microorganisms (malaria)
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40
Q

hyrdopic change

A

aka hydropic degeneration
reversible change
cell injury causes a functional inability to produce enough ATP
this causes cell swelling as sodium cannot be actively pumped out

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41
Q

steatosis

A

fatty changes
accumulation of triglycerides in parenchymal cells, pushing cell contents to the periphery and causing lysis in some cases
alcoholism= fatty liver, can also happen in the kidneys, skeletal muscle, and heart

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42
Q

residual bodies

A

fragments of bacteria or cellular organelles found in an injured cell as a result of failure to digest old organelles or bacterial resistance to some lysosomal enzyme
more residual bodies=more cellular disfunction

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43
Q

lipofuscin granules

A

aka lipochrome
complexes of protein and lipid that are derived from free-radical peroxidation of polyunsaturated lipids of subcellular membranes
these complexes are undigestible and are called brown atrophy, a wear and tear (aging) pigment

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44
Q

hemosiderosis

A

associated with deposition of hemosiderin in many organis and tissues in the cases of systemic overload of iron
the pigment of these tissues can be changed, however the function of these tissues is not affected

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45
Q

hemochromatosis

A

can be genetic or congenital
7-8 times the normal amount of iron in the blood leading to damage of the liver and pancreas and can also interfere with DNA (cause neoplasm)
can lead to hemolytic anemia

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46
Q

Wilson’s Disease

A

genetic, mostly seen in males
accumulation of copper ions
copper goes to the liver and is bound to alpha 2 globulin to form ceruloplasmin and would normally be excreted in the bile, but doesn’t like the liver in this case
D penicillamine is used to chelate the copper ions

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47
Q

kayser-fleischer rings

A

copper deposition in the limbus of the cornea

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48
Q

hyalinization

A

accumulation of hyaline (a glass like protein)

considered an irreversible change by our lecturer, but officially classified as reversible

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49
Q

reabsorption droplets

A

intracellular hyaline in the proximal tubules

causes proteinuria

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50
Q

dutcher bodies

A

intranuclear hyaline inclusions

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51
Q

russell bodies

A

intracytoplasmic inclusions of immunoglobulins when a patient has lymphoplasmacytic lymphoma aka waldenstron macroglobulinemia
blood becomes hyperviscous

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52
Q

Mallory bodies

A

aka mallory alcoholic hyaline

intracytoplasmic hyaline inclusions within the hepatocytes of alcoholics

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53
Q

hyaline arteriosclerosis

A

hyalinization in arterioles caused by long term hypertension or diabetes mellitus
makes the arterioles brittle/ may obstruct the lumen and could lead to intracerebral hemorrhagic stroke or ischemic stroke

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54
Q

nephrosclerosis

A

hardening of the kidney as a result of hyaline deposition with chronic hypertension or diabetes mellitus

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55
Q

huntington’s disease

A

genetic etiology
loss of striatal nuclei which control motion
presents around 30-35 years of age

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56
Q

chorea

A

rapid, jerky, involuntary movements of the face and extremities

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57
Q

Down’s Synrome

A

aka trisomy 21
third copy of chromosome 21
chromosomal abnormality resultsing in mental handicap and a characteristic physical appearance

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58
Q

teratogen

A

an agent that causes a physical abnormality in a developing embryo or fetus

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59
Q

Fetal Alcohol Syndrome

A

birth defects resulting from high alcohol consumption by the mother during pregnancy
highest teratogenic effect in the first three days, then the first trimester of pregnancy

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60
Q

thalidomide

A

sleeping medicine prescribed to pregnant women to prevent morning sickness
babies were born with deformed extremities

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61
Q

ionizing radiation

A

could result in the production of free radicals that can destroy cell membranes

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62
Q

Waldenström Macroglobulinemia

A

aka hyperviscosity syndrome or pymphoplamocytic lymphoma
a type of lymphoma due to a monoclonal tumor (cancer of B lymphocytes resulting in overproduction of IgM)
russel bodies and dutcher bodies are commonly seen with this type of cancer

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63
Q

intercellular deposition

A

between or among cells
dangerous, can obstruct the lumen of small vessels
ischemia/ infarction leads to tissue necrosis
increased brittleness of vessels can lead to intracerebral hemorrhagic stroke

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64
Q

amyloid

A

the generic term for a variety of proteinaceious materials that are abnormally deposited in tissue interstitium in a spectrum of clinical disorders

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65
Q

amyloidosis

A

causes death within a year or two
caused by different cells of the body and effects different organs
primary is idiopathic
secondary is the result of another disorder like autoimmune disease (effects liver, brain, kidney, and heart muscle most often)

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66
Q

alternative metabolism

A

use of normal route is impossible due to damage, so the cell uses another pathway
ie using an alternate energy pathway in the absence of oxygen

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67
Q

hypertrophy

A

call/organ enlargement in response to increased demands

ie the heart- increased resistance due to hypertension

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68
Q

atrophy

A

shrinkage due to decreased demands

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69
Q

poliomyelitis

A

contagious (viral)
irreversible, lose anterior horns of spinal cord
muscles atrophy without neuronal stimulation

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70
Q

Hashimoto’s thyroiditis

A 
#1 cause of hypothyroidism in USA
autoimmune, idiopathic
antibodies attack TSH receptors on the thyroid causing a slow loss of thyroid function, atrophy and loss of the gland
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71
Q

Graves Disease

A

autoimmune, idiopathic
occurs 50% more often in females
Antibodies bind to TSH receptors and mimic TSH stimulating excess thyroid hormone production
gland hypertrophies due to increased demand
characterized by toxic goiter and sometimes exopthalmus

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72
Q

blebs

A

out pouching of the cell membrane

1-2 blebs is reversible, but too many becomes an irreversible change

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73
Q

Myelin figures

A

disruption of the cell membrane

a couple is reversible, but too many will overwhelm the cell

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74
Q

karyolysis

A

dissolution of the nucleus

irreversible

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75
Q

pyknosis

A

condensation of the nucleus

irreversible

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76
Q

karyorrhexis

A

fragmentation of the nucleus

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77
Q

necrosis

A

death of cells or tissues through injury or disease, especially in localized areas of the body

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78
Q

coagulative necrosis

A

characterized by denaturation of cytoplasmic proteins, breakdown of cell organelles, and cell swelling
implies preservation of the basic outline of the cells for at least a couple days which allows the body to attempt to heal
fibrosis replaces dead tissue

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79
Q

Necrosis resulting from myocardial infarction

A

ischemia results in coagulative necrosis and the heart undergoes fibrosis to heal the dead tissue

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80
Q

White infarct

A

occurs in tissue with a single blood supply

ie the heart

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81
Q

red infarct

A

occurs in tissue with two or more vessels supplying it

ie lungs or liver

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82
Q

liquefactive necrosis

A

complete digestion of dead cells resulting in the transformation of the tissue into a liquid viscous mass
ie stroke

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83
Q

caseous necrosis

A

“cheese like”

on a microscopic scale: amorphous granular debris seemingly composed of fragmented coagulated cells, enclosed within a distinctive inflammatory border known as a granulomatous reaction

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84
Q

What can cause caseous necrosis?

A

tuberculosis in the lungs- forms cavities, physical disruption of the tissue and vessels
leprosy- chronic bacterial infection causing nerve damage, contagious

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85
Q

gummatous necrosis

A

caused by tertiary syphilis or general paresis

occurs in the CNS

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86
Q

Syphilis

A

aka lues
goes through three stages, can be congenital or an STD
tertiary syphilis- neurosyphilis causes gummatous necrosis in the brain and posterior column of the posterior horn of the spinal cord

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87
Q

General paresis

A

aka general paresis of the insane

occurs in the grey matter of the brain leading to dementia

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88
Q

Zenkers necrosis

A

severe waxy or glassy necrosis of the skeletal muscles in acute infectious diseases like typhoid or cholera

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89
Q

Fat necrosis

A

aka steatonecrosis
necrosis of the adipose tissue, characterized by formation of calcium soaps when fat is hydrolyzed into glycerol and fatty acids

90
Q

pancreatonecrosis

A

fatal
example of steatonecrosis
gall stones obstruct the bile duct after it merges with the pancreatic duct
pancreatic and bile juices stay in the pancreas and lead to necrosis

91
Q

Fibrinoid necrosis

A

occurs in the walls of blood vessels when endothelial or smooth muscle cells are injured or dying
common in immunopathologies

92
Q

aschoff’s nodes

A

seen with rheumatic myocarditis from rheumatic fever

nodes seen in intermuscular connective tissue, surrounding inflammatory cells

93
Q

Gangrenous necrosis

A

aka gangrene

serious, potentially life threatening condition that arises when a considerable mass of body tissue dies

94
Q

dry gangrene

A

a condition when coagulation is sustained

can be caused by ischemia, atherosclerosis and diabetes mellitus

95
Q

systemic sclerosis

A

aka scleroderma

vasospasm and obliteration of small blood vessels leads to dry gangrene (ischemia)

96
Q

diabetic microangiopathy

A

complication of diabetes
seen in the extremities, kidneys, and eyes
cause of dry gangrene

97
Q

Buerger’s disease

A

aka thromboangitis obliterans
seen in smokers
results in development of antibodies that attack endothelial cells
cause of dry gangrene

98
Q

Wet gangrene

A

occurs if the enzymes of invading phagocytic cells break down the necrotic debris and produce some liquefaction
often occurs with blockage of venous flow and in the presence of certain bacteria (clostridium perfringes, bacillus fusiformis)

99
Q

polyarteritis modosa

A

systemic vascularitis of the fingers

naked bones

100
Q

gas gangrene

A

bacterial infection produces gas within the tissues
seen with anaerobic streptococci and clostridium perfringes
strangulation (hernia) of the stomach or intestines can cause this

101
Q

apoptosis

A

pathway of cell death that is induced by a tightly regulated intracellular program in which cells destined to die activate enzymes to degrade their own nuclear DNA, nucleus, and cytoplasmic proteins

102
Q

normal conditions of apoptosis

A

programmed cell death during embryogenesis
menstruation
cell death induced by cytotoxic t cells

103
Q

pathological conditions of apoptosis

A

cell injury in viral diseases

pathologic atrophy in parenchymal organs after duct obstruction

104
Q

anthracosis

A

deposition and accumulation of carbon in the tissues

this term is used to describe a condition, and is not a condition in and of itself

105
Q

coal worker pneumoconiosis

A

lung disease

lung tissues are modified due to reaction of inhalation of particles, leading to connective tissue deposition

106
Q

dystrophic calcification

A

deposition of calcium salts into necrotic or atrophic tissues

107
Q

gohns focus

A

aka primary TB complex
activation of T helper cells leads to a granulomatous reaction
when the body kills the bacteria, it also kills the tissue which then becomes occupied by calcium salts

108
Q

metastatic calcification

A

deposition of calcium into tissues that are not necrotic or atrophic

109
Q

Causes of Metastatic calcification

A 
increased PTH secretion
destruction of bone
excess vitamin D
sarcoidosis
renal failure in secondary hyperparathyroidism
110
Q

Ischemia

A

lack of blood supply to tissue or organ
brain, lung, kidney, splee, heart muscles, are most vulnerable
liver is not vulnerable

111
Q

labile tissue

A

tissue with a high rate of mitosis or cell turnover

112
Q

ionizing radiation

A

labile tissue is most vulnerable

permanent tissue like bone is not vulnerable

113
Q

viral infection

A

intracellular parasites

usually have a site of preference so tissue vulnerability varies by virus

114
Q

Cardinal signs of inflammation

A 
rubor- redness
calor-heat
dolor-pain
tumor- swelling
functio laesa- loss of function
115
Q

two components of inflammation

A

vascular- hyperemia (increased blood flow) and increased permeability in the blood vessels
cellular- blood cells move to the site of inflammation

116
Q

exudate

A

inflammatory fluid at the site of inflammation

protein rich, bloodcells and microorganisms may be present, provides a space for healing the damaged tissue

117
Q

transudate

A

not a protein rich fluid

118
Q

hyperemia

A

vasoconstriction followed immediately by vasodilation
passive enlargement of capillaries to 20-30% larger than normal
increased blood hydrostatic pressure

119
Q

stasis

A

slowing of blood flow so that its movement in capillaries and venules stops

120
Q

increased permeability of vessels

A

constriction of endothelial cells increases the size of the capillary pores
albumin moves into tissue, bringing fluid with it

121
Q

Normal blood protein values

A

albumin 55%
globulins 40-45%
Fibrinogen 5%

122
Q

Benefits of inflammation

A

swelling leads to pain which makes the person stop moving the injured body part
dissolution of toxins
exudate brings antibodies
phagocytic cells ingest pathogens

123
Q

serous inflammation

A

large amount of watery exudate
response to mild injury, only fluid escapes to the interstitial fluid
ie runny nose with common cold or blister

124
Q

fibrinous inflammation

A

fibrinogen in the exudate starts to form fibrin strands
can be dangerous
ie rheumatic pericarditis- can hear friction rubs in the pericardial sac

125
Q

suppurative inflammation

A

characterized by the presence of pus
contains enzymes and cells
pus can be a source of infection and transmit disease to other parts of the body

126
Q

abcess

A

type of suppurative inflammation

localized accumulation of pus that develops at a focus when an agent of injury can’t be quickly neutralized

127
Q

cellulitis

A

suppurative inflammation

diffuse, widespread suppurative inflammation

128
Q

empyema

A

a type of suppurative inflammation that occurs in two cavities: the subarachnoid space and pleura

129
Q

hemorrhagic inflammation

A

accumulation of RBC’s at the site of inflammation

RBC’s do not participate in the inflammatory response

130
Q

Leukocyte emigration

A

active
an outpouring of a large amount of WBC’s from the blood
only occurs in postcapillary venules
WBC’s attach to lumen receptors and move to gap in the endothelial cells and enter the interstitial space

131
Q

axial blood flow

A

normal blood flow

cells move down the center of the lumen in a column with the largest cells in the center

132
Q

margination

A

when WBC’s are positioned at the periphery of the column as a result of the redistribution that occurs when RBC’s move to the center of the column

133
Q

pavementing

A

leukocyte adherence to the endothelial cell surfaces

134
Q

diapedesis

A

a passive process where RBC’s move outside the vessel with or without inflammation

135
Q

Polymorphonuclear cells

A

all are granulocytes

neutrophils, eosinophils, basophils

136
Q

neutrophils

A

normally 55-60% in circulation
first to arrive at site of inflammation
3-4 lobes in nucleus
life span is 8 hours to 3 days

137
Q

eosinophils

A

red granules
2 lobes in the nucleus
normally 2-4% in circulation

138
Q

basophils

A

normally 0.5-1% in circulation
blue granules
2 lobes in the nucleus

139
Q

mononuclear cells

A

all are agranulocytes

lymphocytes and monocytes

140
Q

lymphocytes

A

typically 20-25% in circulation

141
Q

monocytes

A

typically 4-8% in circulation
largest cells in the blood
second to arrive at the site of inflammation
lifespan is for years

142
Q

monocyte life cycle

A

monocytes –> macrophages - APC’s (antigen presenting cells)

143
Q

stages of phagocytosis

A

recognition and attachment- occurs through chemotaxis
engulfing- use of pseudopods and formation of vesicles
ingestion- killing and degradation/fragmentation
exocytosis

144
Q

oxygen independent phagocytosis

A

uses enzymes to digest proteins (lysosomes)

defensin

145
Q

defensin

A

antibody like substance in neutrophils

146
Q

oxygen-dependent phagocytosis

A

uses anions to produce free radicals, found in the granules of phagocytic cells
superoxide, hypochlorite, and hydrogen peroxide are used

147
Q

chronic granulomatous disease

A

rare genetic defect in phagocytes
phagocytic cells are not able to produce free radicals
children die young from chronic infection

148
Q

Chediak-higashi syndrome

A

genetic disease
impairment of phagocytic cell motility
WBC’s cannot degranulate (release contents of granules)

149
Q

Initiators to the Inflammatory response

A 
direct stimulus to mast cells
microbial products
exposure of basement membrane of connective tissue components
complement activation
deposition of antibody/antigen complexes
disruption of vascular integrity
substances released from injured cells
150
Q

Functions of Histamine

A

vasodilation
increased vessel permeability
bronchospasm
increased mucous production

151
Q

Where is histamine released from?

A

Primarily released near the site of inflammation
released from granules in response to physical injury or type I hypersensitivity
from basophils and platelets in circulation
from mast cells (basophils fixed in tissues)

152
Q

Major reservoirs of histamine in the body

A

basophils, past cells, and platelets

153
Q

Serotonin

A

aka the hormone of pleasure
produced by platelets
similar function to histamine

154
Q

Substance P

A

neuropeptide produced by nervous fibers in the CNS and PNS

produced by lungg and GI nervous tissues

155
Q

Functions of substance P

A

promote production o pain
regulate blood pressure
increase blood vessel permeability

156
Q

Nitric oxide

A

aka endothelial-derived releasing hormone

mediator of the sympathetic nervous system

157
Q

Where is nitric oxide produced

A

endothelial cells of blood vessels, macrophages, and brain neurons

158
Q

functions of nitric oxide

A

vasodilator
prevents neutrophil recruitment to site of inflammation
inhibit WBC pavementing
inhibitor to the cellular component of inflammation

159
Q

Eicosanoids

A

arachadonic acid metabolites
from phospholipids in cell membranes
includes prostaglandins, leukotrienes, and lipoxins

160
Q

What are the major producers of eicosanoids?

A

neutrophils and macrophages

161
Q

Prostacyclin

A

PGI2
produced by endothelial cells
inhibits platelet aggregation and causes platelet aggregation

162
Q

Thromboxane A2

A

TXA2
produced by platelets
functions opposite to PGI2
causes vasoconstriction and promotes platelet aggregation

163
Q

What are the functions of PGD2, PGE2, and PGF2

A

vasodilation
potentiate edema
allows for pain perception and fever
produced by macrophages and less by neutrophils

164
Q

Normal physiological function of COX-1

A

Regulate the amount of fluid and salt in the kidneys

protect the GI tract from ulceration and inflammation

165
Q

What two enzymes produce all prostaglandins?

A

cyclooxygenase 1 and 2

166
Q

What inhibits COX-1

A

NSAIDS

167
Q

consequences of inhibiting COX-1

A

can lead to kidney problems and stomach irritation/ulceration
HCl levels rise in its absence

168
Q

Function of COX-2

A

produces extra prostaglandins when needed

169
Q

COX-2 inhibitors

A

Vioxx, celebrex, meloxicam
used to prevent the side effects of NSAIDS
vioxx could result in thrombosis, throboaneurysm, MI (no longer used)

170
Q

Enzyme that produces leukotrienes

A

5-lipoxygenase

171
Q

Function of leukotrienes

A

vasoconstriction (balance out vasodilation)
bronchospasm
increased permeability

172
Q

Enzyme that produces lipoxins

A

12-lipoxygenase

173
Q

Function of lipoxins

A

vasodilation
inhibit neutrophil chemotaxis
stimulate monocyte adhesion

174
Q

What inhibits Eicosanoids?

A

corticosteroids

175
Q

Tumor necrosis factor

A

produced predominantly by activated macrophages

induces acute inflammatory response

176
Q

What inhibits tumor necrosis factor

A

medication for RA, ankylosing spondylitis

may lead to lymphomas

177
Q

what produces IL-3 and IL-6

A

predominantly by helper T cells

178
Q

Function of IL-3 and IL-6

A

Induces acute inflammatory response

179
Q

Acute phase of inflammation response

A 
fever, anorexia, increased sleep
increased c-rp
increased ESR (erythrocyte sedimentation rate)
vasodilation
neutrophilia
180
Q

what protein is increased during the acute phase of inflammation

A

C-RP c-reactive protein

181
Q

Lymphangitis

A

appears as a red line on the skin
inflammation of the lymphatic vessels
injury with infection
will go to the nearest lymph node

182
Q

Lymphadenitis

A

enlarged and painful lymph node due to accumulation of a pathogen
nonpainful lymph nodes- cancer

183
Q

bacteremia

A

infection/bacteria in the blood

very dangerous

184
Q

septicemia

A

accumulation of toxic products of bacterial metabolism in the blood

185
Q

leukocytosis

A

increased leukocytes in the blood due to infection

>9,000 leukocytes per cubic millimeter

186
Q

neutrophilia

A

greater than 60%

187
Q

lymphocytosis

A

indicates a possible viral infection

above 30% blood content

188
Q

Eosinophils

A

normally 2-4%

indicates a type I hypersensitivity reaction or parasitic infection

189
Q

Complement

A

C3a, C4a, and C5a
promotes secretion of histamine from the granules of mast cells
participate in inflammation to a certain degree

190
Q

Hageman factor

A 
aka clotting factor XII
 Hageman factor (clotting factor XII)
191
Q

Functions of prekellikrein

A

vasodilation, promotes the vascular component of inflammation
short-lived (5-10 minutes)

192
Q

monocytosis

A

indicative of a chronic bacterial infection
can increase up to 50% of circulating WBC’s (normally 4-8%)
infectious mononucleosis –> lymphadenopathy of the neck and upper thoracic lymph nodes

193
Q

Juveline RA

A

hands and joints swollen

inflammation can destroy tissue and bone

194
Q

Chronic Inflammation

A

> 6 weeks in duration

usually does not have exudate

195
Q

Cell content of exudate in chronic inflammation

A

When present:

there will be only macrophages, no neutrophils, as they have a shorter lifespan

196
Q

aseptic osteonecrosis

A

compressed blood vessels lead to infarction

dissolution of bone without infection

197
Q

effects of chronic kidney inflammation

A

healthy tissue begins to be replaced by connective tissue

the connective tissue shrinks giving the kidney a granular appearance

198
Q

Agents typically involved with chronic inflammation

A

organic: microorganisms- mycobacterium tuberculosis, m. leprae, listeria, treponema pallidum, brucells
inorganic: asbestos, silica, beryllium, dusts

199
Q

Nonspecific chronic inflammation

A

a diffuse accumulation of macrophages and lymphocytes develops at the site of injury

200
Q

granulomatous inflammation

A

formation of a granuloma

develops in TB

201
Q

Layers of a granuloma from deep to superficial

A 
pathogen
epitheliod cells (derived from macrophages)
lymphocytes
fibroblast
connective tissue
202
Q

Four major components of healing

A

regeneration
repair
revascularization
surface restoration

203
Q

Regeneration

A

tissue is replaced from parenchyma by cell division
new tissue assumes normal function
ideal response to tissue loss

204
Q

Three types of tissue

A

each has different patterns of regeneration

labile, stable, and permanent

205
Q

Labile tissue

A

divides continually to replace cells that are constantly being depleted by normal processes
ie mucous membranes, red bone marrow

206
Q

Stable tissue

A

cells divide, but slowly beyond adolescence when normal development is complete
mitosis rate increases when damaged tissue must be replaced
ie glands, osteoblasts, smooth muscle fibers, and vascular andothelium

207
Q

Permanent tissue

A

loses all mitotic ability after birth
loss of which results in functional loss
cells lost are replaced by scar tissue
ie heart muscle, nervous tissue

208
Q

Repair

A

fibrous scar tissue fills the gaps left by the loss of damaged tissue
restores strength and structural integrity of damaged tissue that cannot regenerate

209
Q

Fibrosis

A

formation of collagen fibers
fibroblasts in stroma secrete procollagen that eventually is activated into collagen
collagen filaments are then bundled together to form fibers

210
Q

revascularization

A

aniogenesis occurs in the loosely gelled, protein-rich exudates that form at the site of damage

211
Q

andiogenesis

A

production of new blood vessels

212
Q

surface restoration

A

restoration of the protective epithelium that covers body and organ surfaces

213
Q

Primary healing

A

healing of an incision or severing wound of the skin

214
Q

secondary healing

A

wound edges are not closely apposed

215
Q

contracture

A

complication of healing

newly formed collagen demonstrates an exaggerated wound contraction response as it matures

216
Q

adhesions

A

complication of healing

joining of serous membranes leads to restriction of movement in structures

217
Q

dehiscence

A

complication of healing

breaking open of a healing wound, possibly due to pressure on the wound

218
Q

keloids

A

complication of healing
irregular masses of scar tissue that protrude from the surface of skin, which results
from the over production of dermal collagen during healing.

219
Q

proud flesh

A

complication of healing

overproduction of granulation tissue

220
Q

suture complications

A

complication of healing

interruption of epithelium

Pathology (4 decks)

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