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biology of disease I > Exam 1 > Flashcards

Exam 1 Flashcards

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1
Q

Pathology

A

study of disease which includes the study of abnormal form and function, important to understand the mechanisms of injury and to diagnose, prevent, mitigate, prognosticate, and institute specific therapy for a disease

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2
Q

disease

A

the cumulative abnormalities at the molecular, cellular and tissue level which lead to clinically apparent dysfunction (illness)

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3
Q

pathogenesis

A

the sequence of events and abnormalities that leads to disease

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4
Q

lesion

A

physical and/or physical tissue abnormality

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5
Q

pathobiology

A

study of mechanisms by which abnormal structure and function cause disease in the context of the whole animal

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6
Q

pathophysiology

A

abnormal function resulting from the cumulative abnormalities leading to illness

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7
Q

what are some factors leading to disease

A

host factors, environmental factors, characteristics specific to injurious agent

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8
Q

Etiology

A

the cause of the disease

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9
Q

Dermatitis

A

inflammation of the skin (generic)
specific site can be modified (foot- pododermatitis or scrotum- scrotum dermatitis)

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10
Q

pyoderma

A

suppurative inflammation of the skin

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11
Q

Mastitis

A

inflammation of the mammary gland

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12
Q

Thelitis

A

inflammation of the nipple

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13
Q

laminitis

A

inflammation of the hoof corium

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14
Q

Palpebritis

A

inflammation of the eyelid

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15
Q

Onychitis

A

inflammation of the nailbed and claw

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16
Q

Osteoarthritis

A

inflammation of the joint and bone

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17
Q

Gonitis

A

inflammation of the stifle joint

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18
Q

Spondylitis

A

inflammation of the vertebra

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19
Q

Discospondylitis

A

inflammation of the intervertebral disc

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20
Q

Rhinitis

A

inflammation of the nasal cavity

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21
Q

Maxillary sinusitis

A

inflammation of the maxillary sinus

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22
Q

Valvular endocarditis

A

inflammation of a heart valve

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23
Q

Phlebitis

A

inflammation of a vein

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24
Q

lymphadenitis

A

inflammation of a lymph node

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25
Q

lymphangitis

A

inflammation of a lymphatic channel

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26
Q

pyometra

A

inflammation of the uterus, pus filled

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27
Q

Pyelitis

A

inflammation of the kidney pelvis

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28
Q

Chelitis

A

inflammation of the cheek

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29
Q

Stomatitis

A

inflammation of the mouth or oral cavity

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30
Q

Sialoadenitis

A

inflammation of the salivary gland

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31
Q

Typhlitis

A

inflammation of the cecum

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32
Q

cholecystitis

A

inflammation of the gall bladder

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33
Q

sclerosing

A

scarring

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34
Q

peracute

A

very acute, rapid onset, last hours, exudative, few cells (ex: anaphylaxis)

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35
Q

acute

A

symptoms or signs that worsen quickly often, a few days, primarily neutrophils

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36
Q

subacute

A

symptoms or signs that persist for a week or two, not quite chronic, exudative changes diminished, cell infiltrate evolves from neutrophilic to mononuclear

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37
Q

chronic

A

onset is days to weeks following injury, can last years, mononuclear infiltration, tissue regeneration, new vessel and connective tissue growth neovascularization and fibrosis

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38
Q

focal

A

there is only one lesion

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39
Q

multifocal

A

there are multiple lesions with normal tissue in between

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40
Q

regionally extensive

A

a lesion that involves a large portion of the body

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41
Q

diffuse

A

a lesion where all of the parenchyma is involved

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42
Q

disseminated

A

the same disease process is present in multiple organs.

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43
Q

multifocal coalescing

A

multiple lesions that join together

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44
Q

severe

A

there is substantial tissue destruction, significant resolution cannot occur

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45
Q

chronic-active

A

recurrent bouts of active inflammation super-imposed on chronic inflammation

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46
Q

etiologic diagnosis

A

a diagnosis denoting cause. two elements the cause and tissue process. Ex: streptococcal pneumonia

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47
Q

immunohistohemistry

A

use of an antibody to identify a specific epitope with colorimetric identification of bound antibody

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48
Q

trichrome

A

a special stain used to stain collagen, important for fibrosis

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49
Q

Necrosis

A

a passive degradative process, where the cell doesn’t partake in its own demise but it is induced
2 concurrent processes: protein denaturation and enzymatic digestion

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50
Q

gangrene

A

not the form of necrosis but describes the fate of dead tissue after it dies, it can be dried out or colonized by organisms from the environment

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51
Q

coagulative necrosis

A

tissue architecture is maintained by cytologic detail is fundamentally lost. (cell detail lost but you can still tell tissue organization)
Histologically a hypereosinophilic cytoplasm with nuclear features of necrosis

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52
Q

What are some causes of coagulative necrosis?

A

ischemia, burns, and caustic injury
additionally this is commonly observed in tissues that have few proteases so the tissue doesnt degrade readily, thus maintaining tissue architecture of coagulative necrosis

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53
Q

Liquefactive necrosis

A

necrosis where at gross appearance the tissue is liquified
common in tissues with little stroma (collagen) and is usually bacterial
tissue is cavitated, may be bordered by profilerating fibrovascular (granulation) tissue containing many neutrophils

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54
Q

What kind of necrosis is common in the brain?

A

liquefactive necrosis is common as there is little to no connective tissue in the brain

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55
Q

Caseous necrosis

A

a form of necrosis that has a gross appearance of chunky cheese
sheets of macrophages (granulomatous) surrounding a central focus of amorphous debris that did not liquify
caused by a specific immuno-pathologic phenomenon seen with corynebacterium and mycobacterium

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56
Q

fat necrosis

A

a form of necrosis that has a gross appearance of white chalky fat
histologically it is lightly basophilic, smudgy saponified material, sometimes with granulomatous inflammation
caused by ischemia, toxins, lipases (especially pancreatitis in small animals)

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57
Q

What are some causes of fat necrosis

A

ischemia, toxins, lipases

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58
Q

dry gangrene

A

coagulated tissues that dries out

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59
Q

wet gangrene

A

tissue that is digested and liquified by opportunistic environmental flora

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60
Q

autolysis

A

enzymatic degradation and protein denaturation by microbial and host enzymes
what happens to body after death

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61
Q

How does necrosis differ from autolysis

A

necrosis is where adjacent tissue is unaffected, RBC intact, and an inflammatory response is present while autolysis- all of the tissue is affected, RBC lysed, no inflammation, and bacterial overgrowth and gas formation

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62
Q

rigor mortis

A

the muscular contraction following death (2-4 hours) but regresses in 24-48 hours. affects all muscle tissue and progresses from the jaw to trunk to limbs

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63
Q

What factors might influence rigor mortis?

A

delayed progression in well fed and rested animals
slight
rapid and intense in those dying following exertion or exsanguination
temperature, glycogen stores, pH of muscle

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64
Q

How does rigor mortis take place

A

since muscle contraction is a very energy dependent process, glycogen stores are used to maintain ATP stores after death. As ATP falls, Ca2+ enters the cytoplasm initiating muscle contraction
rigor ceases as myofibers autolyze

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65
Q

ischemia

A

a cause of cell injury through there being no blood flow to the cells, thus leading to oxygen deprivation and infarction if serious

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66
Q

hypoxia

A

a cause of cell injury through there being no oxygen to cells, thus leading in oxygen deprivation and infarction if serious

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67
Q

physical causes of cell injury

A

trauma, heart, cold, ionizing radiation

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68
Q

What are some methods where ATP might be depleted thus resulting in cell injury

A

membrane transport, protein synthesis, lipogenesis, phospholipid turnover, metabolism

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69
Q

How might an increase cytoplasmic calcium concentration lead to cell injury?

A

this increases expression of enzymes and leading changes: ATPase (decreased ATP), phospholipase (decreased phospholipids), protease (disruption of membrane and cytoskeletal proteins), and endonuclease (nuclear chromatin damage)

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70
Q

How might changes in membrane permeability lead to cell injury

A

This leads to ATP depletion, calcium activated phospholipases, and direct damage to bacterial toxins, viral proteins, complement, perforins, chemican and physical agents, and oxidative damage

71
Q

How might changes in membrane permeability lead to cell injury

A

from ATP depletion, calcium activated phospholipases, and direct damage to bacterial toxins, viral proteins, complement, perforins, chemican and physical agents, and oxidative damage

72
Q

How might mitochondrial damage lead to cell injury

A

mitochondrial damage can be induced by increased cytosolic calcium, oxidative stress, or phospholipid breakdown
this results in mitochondrial permeability transition, cytochrome C leakage, and loss of membrane potential

73
Q

How might reactive oxygen species lead to cell injury?

A

they are derived from normal cellular metabolism and inflammatory cells cause damage to membranes, proteins, and nucleic acids

74
Q

How does hypoxia lead to reversible cell injury

A

ATP depletion- increases in phosphate promote anaerobic glycolysis which depletes glycogen stores and decreases pH, Na/K/ATPase pumps in the cell membrane are shut down
intracellular NA increases and intracellular K decreases as cells cant maintain pumps. higher Na+ in the cell and cells accumulates water via osmotic mechanisms. intracellular calcium also increased with Ca-ATPases shut down. Increased water draw cause ribosomes to detach so the cell cant make protein. Cytoskeleton disperses, surface blebs, and myelin figures appear

75
Q

hydropic change

A

cell swelling that is reversible.

76
Q

hydropic degeneration

A

cell swelling that is irreversible

77
Q

How does cell swelling present histologically?

A

it appears enlarged, pale staining glassy or cloudy cytoplasm, less intense staining

78
Q

when is ischemic injury irreversible?

A

when there is severe mitochondrial swelling, massive calcium influx, increased membrane permeability, lysosomes leak acid hydrolases as well as other enzymes leak in extra-cellular space

79
Q

Pyknosis

A

a sign of irreversible or dead cellular injury where there is a shrinkage and clumping of nuclear chromatin,
calcium deposits begin to form in mitochondria as the cell’s ability to deal with cytoplasmic calcium becomes overwhelmed
visualized a dark staining circle of condensed nuclear chromatin

80
Q

Karyorrhexis

A

a sign of irreversible or dead cellular injury where nuclear material is in clumps,

81
Q

Karyolysis

A

a sign of irreversible or dead cellular injury where protein and nuclic acids are lysed contributing to mitochondrial mineralization and dissolution as well as dissolution of endoplasmic reticulum and plasma membrane. Appears light staining and pale in color

82
Q

ischemia reperfusion injury

A

continued cell death following reperfusion
either caused by cells being structurally intact but have lethal functional changes and new injuring processes are initiated; including elaboration of ROS

83
Q

How can reperfusion generate reactive oxygen species for damage?

A

As ATP is depleted, hypoxanthine enzyme substrate increases as well as elevated intracellular calcium promotes the conversion of oxidase from dehydrogenase
However, upon reperfusion, xanthine oxidase converts the accumulated hypoxanthine to urates and superoxide radicals

84
Q

Fenton reaction

A

a reaction that promotes the generation of reactive oxygen species through iron and copper being catalyzed

85
Q

Superoxide dismutase

A

a specific antioxidant that activates superoxide with there being two forms Mg SOD (mitochondria) and Cu Zn SOD (cytosol) into hydrogen peroxide

86
Q

Haber-Weiss Reaction

A

a reaction where a superoxide and hydrogen peroxide interacts in a reaction to generate oxidative damage

87
Q

Catalase

A

a specific antioxidant that inactivates hydrogen peroxide into oxygen and water

88
Q

Glutathione peroxidase

A

a specific antioxidant that inactivates hydrogen peroxide or a hydroxyl radical by use of glutathione

89
Q

What are some specific cellular antioxidant defenses?

A

Vitamin A, E, and C
Caeruloplasmin (binds Cu and prevents the fenton reaction)
Ferritin (binds Fe and prevents the fenton reaction)
Transferring, Lactoferrin,

90
Q

Fatty Change/Degeneration

A

The second most common type of cell injury after hydropic
Occurs in cells which handle large amounts of lipids (ex:liver), detected as excess accumulation of intracellular lipid “depostion injury”
change is reversible while degeneration is not

91
Q

What might be some gross signs that a tissue has undergone fatty change

A

the liver is enlarged, friabe, greasy with rounded margins, yellow to orange in color, and floats in formaldehyde

92
Q

What are some microscopic changes that a tissue has undergone fatty change?

A

vacuoles are few and large or many in small (ex: oil in water)
cells are well demarcated, perfectly round, appear empty because lipids are removed in the tissue fixation process

93
Q

Acute interstitial pneumonia

A

a pneumonia seen in cattle, also described as fog fever. In the spring the new green grass i rich in tryptophan and the ecology of the rumen changes with the generation of 3-Methyleneindolenine (3-MEIN) in the lung and this pulmonary oxidant damages the epithelial lining of the lung

94
Q

Is there inflammation with apoptosis?

A

No there is not

95
Q

Apoptosis

A

active genetically programmed cell death that is triggered by many physiologic and pathogenic settings, cell deletion with little to no inflammation and tissue remodeling

96
Q

Where might apoptosis occur?

A

in tissues that undergo physiologic or post-pathologic atrophy
for example post-lactational mammary gland or postpartum uterus, resolution of hyperplasia, post-barbiturate hepatocytes (liver returning to normal size), exocrine glands following duct occlusion or embryonic tissues that dissolve

97
Q

After birth, the uterus involutes over time with no inflammation, is it likely that this reduction in cell mass is accredited to necrosis or apoptosis

A

apoptosis

98
Q

The destruction of self-reactive T-lymphocytes is an example of what mechanism of cell death?

A

Apoptosis

99
Q

Cells with DNA damage and cells injured by hypoxia, irradiation, hyperthermia, toxins, and drugs are eliminated through what process?

A

apoptosis

100
Q

Is karyolysis present in apoptosis?

A

NO

101
Q

How might apoptosis present histologically?

A

pynkosis and karyorrhexis (no karyolysis)
increased cytoplasmic eosinophilia
formation of apoptotic bodies

102
Q

Is apoptosis an active or passive process?

A

active, programmed process of autonomous cellular dismantling that avoids eliciting inflammation

103
Q

is necrosis an active or passive process?

A

passive, accidental cell death resulting from environmental perturbations with uncontrolled release of inflammatory cellular contents

104
Q

Do mitochondrial and endoplasmic reticulum changes occur in apoptosis, like they do in necrosis?

A

NO

105
Q

apoptosis process

A

the enzyme cascade resulting in protein cleavage by activated caspases, protein crosslinking, DNA cleavage by endonucleases- DNA cut at regular intervals
Phagocytic recognition; phophatidylserine and thrombospondin

106
Q

Pyroptosis

A

a process distinct from apoptosis that is a Caspase-1 dependent cell death
It results in swelling and lysis of the cell
Cytokine release causing inflammation is present

107
Q

Oncosis

A

a capase independent form of programmed cell death where there is increased membrane permeability, cell swelling, and rupture
can be induced by conditions with high cell infection burdens
Inflammation is present

108
Q

Pyronecrosis

A

capase independent form of programmed cell death,
resulting in inflammation

109
Q

Autophagy

A

programed cell death process useful for removing damaged or redundant organelles, activate in cells with high pathogen burden
Double membrane lysosomal digestion of cell components - vacuolization, degradation of cell components, and lack of chromatin condensation
Neighboring cells phagocytose (non-inflammatory)

110
Q

Neoplasia

A

a disorder associated with decreased apoptosis
over expression of anti-apoptotic proteins and down regulation of pro-apoptotic proteins, damage to p53, and diminished response to death receptor

111
Q

autoimmune disease

A

can be a disorder of decreased apoptosis of autoreactive cells, not destroying themselves

112
Q

Disorders with increased apoptosis

A

neurodegenerative disorders, exacerbation of damge in ischemic injury, virus-induced lymphocyte depletion in acquired immune deficiency syndromes

113
Q

venetoclax

A

a cancer therapy targeting apoptosis where it blocks Bcl-2, which is overexpressed in lymphoid cancer to prevent apoptosis, therefore leads to cell death of these cancer cells

114
Q

hemorrhage

A

loss of blood from within vasculature caused by either trauma, hypoxia (endothelial cell death), or degenerative conditions. factors that influence hemorrhage are anticoagulants, or neoplastic or infectious diseases

115
Q

petechia

A

pinpoint hemorrhages, up to 1mm in diameter

116
Q

ecchymosis

A

larger hemorrhages, up to a few centimeters in diameter

117
Q

purpura

A

petechiae and ecchymoses on the mucus membrane

118
Q

hematoma

A

a focal hemorrhage which produces a mass-like lesion collection of blood
common in the ears and induced by stress of capillaries

119
Q

What happens to blood in internal hemorrhages

A

blood components are largely recovered

120
Q

What are the secondary effects of hemorrhage?

A

1) fluid can be resabsorbed into the circulation
2) erythrocytes lysed and phagocytosed
3) fibrinolysis
4) potential scarring if too much or cant be brokendown in time

121
Q

Hyperemia

A

increased amount of blood in the vasculature in an organ or part of the body. can be passive or active

122
Q

Physiologic active hyperemia

A

the passive process of increased blood to a part of the body. Ex: after a move blood flow is increased to your GI muscosa

123
Q

Pathological active hyperemia

A

increased blood flow with injury- an active process

124
Q

Passive hyperemia

A

always pathologic as a result of a disease condition.
For example, when blood cannot move out of an organ (Left side heart failure there is pulmonary backup) or the mechanical occlusion of channels

125
Q

What are the effects of passive congestion?

A

1) With hyperemia, the blood progressively gets deoxygenated
2) Edema
3) Hemorrhage
4) Thrombosis
5) Fibrosis

126
Q

Acute passive congestion

A

pathological. the sudden occlusion of vessels leading to congestion with or without severe anoxia ex: ovarian torsion or limb strangulation

127
Q

Chronic passive congestion

A

long standing interference which does not cause complete ischemia
For example: heart failure leading to relative hypoxia but not complete ischemia

128
Q

What will be impacted with right heart failure?

A

the liver as there is backflow into the systemic circulation can also be associated with valvular insufficiency or stenosis, lung blood flow obstruction or obstruction of the posterior vena cava

129
Q

What will be impacted with left heart failure?

A

the heart as there is back flow in the pulmonary circulation

130
Q

Nutmeg liver

A

caused by chronic passive hepatic congestion of the liver as there is backup of blood into the sinusoids leading to hepatic cell death through necrosis and fibrosis

131
Q

Congested lung

A

interference with blood flow through the left heart due to valvular insufficiency or stenosis
leads to pumonary edema; if long-standing there may be pulmonary fibrosis with hemosiderosis (heart faulure cells)
leading to pleura effusion

132
Q

Congested spleen

A

common incidental finding after barbiturate euthanasia

133
Q

Hypostatic congestion

A

the ante- or post-mortem gravitational settling of blood in the tissues, can occur in recumbent animals animals (surgery or debilitated animals)

134
Q

Edema

A

the accumulation of watery fluid in extravascular spaces, tissues are swollen and pit when pushed
excess fluid separates tissue planes
gelatinous tissue appearance

135
Q

Effusion

A

a type edema where fluid accumulates in the body cavity

136
Q

transudate

A

a type of edema with not many cells or protein in the fluid, clear fluid

137
Q

exudate

A

a type of edema with inflammation and wbc cells and blood present if necrosus

138
Q

cardiac edema

A

venous congestion with sodium and water retention resulting in increased blood volume and increased hydrostatic pressure (renin-aldosterone activation)
a cause of edema

139
Q

What are some causes of edema

A

-cardiac dema through increased hydrostatic pressure from renin-aldosterone activation
-renal failure: urinary protein loss leads to a decreased oncotic pressure, thus drawing fluid out
-hepatic failure or malnutrition: leading to decreased plasma oncotic pressure (parasites hypoproteinemia)

140
Q

heart failure cells

A

alveolar macrophages that contain hemosiderin pigment. stain very darkly

141
Q

glycogen

A

steroid hepatopathy
can be iatrogenic or endogenous hyperadrenocortism (tumor of adrenal or pituitary)
results in hepatic glycogen storage with hepatocellular hydropic degeneration

142
Q

What are some causes of why you might have elevated cortisol

A

adrenocortical adenoma, adrenocortical hyperplasia, pituitary tumor, or iatrogenic treatment of glucocorticoids

143
Q

Hypertrophy of cellular organelles

A

can be caused term anti-convulsant therapy with barbiturates, leads to the hypertrophy of smooth endoplasmic reticulum in hepatocytes- microvacuolar change change that may enlarge the liver

144
Q

lysosomal storage diseases

A

congenital: lipidoses, glycogenoses, sphingolipidoses, mucopolysaccharidoses, mucolipidoses, carbohydratoses cause the cell to enlarge because of decreases in enzymes that degrade cellular product.

145
Q

locoism

A

an acquired lysosomal storage disease that causes cytoplasmic vacuolization of neurons and lymphocytes from eating a certain wildflower

146
Q

Hyaline

A

a descriptor that implies an homogeneous glassy appearance- a result from protein deposition in the cell can be intracellular or extracellular protein

147
Q

Amyloid

A

an extracellular protein deposit composed of protein fibrils that are insoluble and indigestible, significance depends on the site
stained w Congo red or Thioflavine

148
Q

AA amyloid

A

from serum amyloid A (SAA) an acute phase reactant, associated with inflammatioj

149
Q

AL amyloid

A

amyloid from immunoglobulin light chains associated with lymphoid follicles and plasma cell tumors

150
Q

AF amyloid

A

amyloid type, usually prealbumin named for its presence in human familial amyloidoses

151
Q

Endocrine amyloid

A

formed from a variety of hormone and hormone-like proteins example Type II diabetic cats will build up endocrine amyloid

152
Q

Lipofuscin

A

a lipid breakdown product within lysosomes, increases with aging often incidental finding
granular bolden brown

153
Q

lipfuscinosis

A

brown dog gut- subcinical; linked to deficient vitamin E
from when dogs on a strictly fish diet

154
Q

Anthracosis

A

when carbon is present in the lung from environmental and incidental inhalation

155
Q

Melanosis

A

incidental pigmentation of tissues in pigmented animals; pleura and meninges most commonly affected.

156
Q

reactive melanosis

A

also called hyperpigmentation, seen in damaged skin
seen commonly in dogs with flea bite allergy

157
Q

pseudomelanosis

A

a postmortem production of hydrogen sulfide by bacteria with subsequent reaction with iron in hemoglobin to form insoluble iron sulfide

158
Q

Hemosiderin

A

a lighter brown granular pigment that represents accumulations of iron and apoferritin

159
Q

Hematoidin

A

a yellow pigment that occurs during wound resolution as iron is removed from hemosiderin by macrophages

160
Q

Bilirubin

A

a greenish brown pigment usually not granular accumulated from breaking down old red blood cells
seen within hepatocytes, bile canaliculi, and renal tubular epithelium
may be bright yellow and stain all tissues in hemolytic anemia- Jaundice

161
Q

Mineralization

A

synonymous with calcification
granular basophilic material often smudged and fragmented in section

162
Q

Dystrophic mineralization

A

the calcification of dead or dying cells/tissues
membrane vesicles form as cell membranes break down and these serve a nidus for mineral deposition
common of fungal diseases, absesses, tuberculosis

163
Q

metastatic calcification

A

excess calcium and phosphorus in the blood precipitate according to the law of mass action
most common in the gastric mucosa, blood vessels and basement membranes in the lung and kidney

164
Q

How do you treat metastatic calcification from rat poison ingestion?

A

Since rat poison is a vitamin D analog high dose it leads to elevated blood calcium mineralizes their tissues and kills them- treat with calcitonin (decrease calcium concentration)

165
Q

What are some causes metastatic calcification?

A

hypervitaminosis D (rotenticides, iatrogenic dietary excess)
renal disease (hypercalcemia-causes problems in the lungs)
primary hyperparathyroidism
tumor cells produce parathyroid hormone like activity peptides (lymphosarcoma, anal sac apocrine gland neoplasms)

166
Q

hemostasis

A

the termination of blood loss from vasculature. normal hemostasis is due to balance of pro and anti-coagulant mechanism- loss of control leads to thrombosis and or hemorrhage

167
Q

How is hemostasis achieved?

A

vasoconstriction- transient neurogenic reflex
platelet plug- platelets adhere to damaged endothelial cells or collagen and adhere to one another (aggregation)
coagulation- enzyme cascade involving pre-formed clotting factors in blood
fibrinolysis and healing

168
Q

How does the intrinsic factor differ from the extrinsic factor pathway?

A

the extrinsic factor is initiated by tissue damage (Tissue like factor) while the intrinsic factor is initiated by intrinsic cues like surface contact (collagen, platelets, prekallikrein)

169
Q

Thrombin

A

production of this promotes further aggregation and polymerizes fibrin producing the definitive hemostatic plug

170
Q

Thromboxane A2

A

along with ADP, promotes aggregation producing the temporary or primary hemostatic plug

171
Q

Pro-coagulant factors

A

endothelial pro-coagulant factors include von Willebrands factor, tissue factor, binding sites for activated clotting factors, platelet activating factor, inhibit fibrinolysis through plasminogen activator inhibitor

172
Q

How is clotting controlled?

A

locally controlled through antithrombins, protein C&S, and the plasminogen-plasmin system (plasminogen activator)
and inhibit platelet aggregation through NO and PGI2
Blood proteins:Antithrombins, protein C&S

173
Q

Disseminated Intravascular Coagulation

A

thrombo-hemorrhagic disorder characterized by widespread activation of clotting mechanisms, consumption of platelets and clotting factors, activation of fibrinolysis and widespread hemorrhage

biology of disease I (3 decks)

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