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TCM > Exam I > Flashcards

Exam I Flashcards

1
Q

reversible functional and structural changes of cells in response to changes in their environment

A

adaptations

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2
Q

increase in the size of cells

A

hypertrophy

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3
Q

hypertrophy occurs in ___ cells

A

nondividing

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4
Q

physiologic hypertrophy: normal ____ or ____ function

A

organization
enhanced

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5
Q

hypertrophy in response to increased functional demand describes (weight lifter)

A

physiologic hypertrophy

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6
Q

hypertrophy of uterine smooth muscle during pregnancy describes

A

physiologic hypertrophy

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7
Q

in pregnancy, ____ stimulation causes smooth muscle cells to increase in size

A

estrogen

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8
Q

pathologic hypertrophy is seen with up-regulation of (3)

A

fetal genes
fibrosis
dysfunction

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9
Q

hypertension and cardiac valve disease (AORTIC STENOSIS) cause pressure overload which leads to

A

pathologic hypertrophy of cardiac muscle

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10
Q

systolic murmur indicates

A

left ventricular hypertrophy

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11
Q

aortic stenosis causes

A

left ventricular hypertrophy

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12
Q

boxcar nuclei in cardiac muscles indicates

A

left ventricular hypertrophy

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13
Q

increase in the number of cells

A

hyperplasia

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14
Q

hyperplasia is the result of
(2)

A

growth factor driven proliferation of mature cells
OR
decrease in cell death

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15
Q

hyperplasia occurs in ___ cells

A

dividing

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16
Q

physiologic hyperplasia is d/t the action of

A

hormones or growth factors

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17
Q

increased functional demand of lactate glands results in

A

physiologic hyperplasia

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18
Q

low ambient oxygen tension at high altitude results in bone marrow

A

compensatory erythroid hyperplasia (physiologic)

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19
Q

certain viral infections like HPV are cause what characteristic response

A

pathologic hyperplasia

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20
Q

most forms of pathologic hyperplasia are caused by excessive or inappropriate actions of

A

hormones or growth factors on target cells

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21
Q

an enlarged prostate is an example of

A

benign prostatic hyperplasia

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22
Q

endometrial hyperplasia is a response to

A

unopposed estrogen

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23
Q

pathologic hyperplasia elevates the risk of acquiring genetic alterations that drive

A

unregulated proliferation and cancer

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24
Q

pathologic hyperplasia is often associated with increased risk of

A

cancer

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25
Q

stepwise progression from normal to cancer

A

normal
hyperplasia
dysplasia
cancer

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26
Q

reduction in size of an organ or tissue d/t decrease in cell size and/or number

A

atrophy

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27
Q

____ is common during normal development

A

physiologic atrophy

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28
Q

atrophy of the endometrium from premenopausal to postmenopausal is an example of atrophy d/t…

A

loss of hormonal stimultion

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29
Q

disuse atrophy:
immobilized limbs can cause… (3)

A

1 loss of proteoglycans in articular cartilage
2 decreased strength of ligaments
3 osteopenia

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30
Q

loss of innervation can cause

A

denervation atrophy

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31
Q

decreased blood supply, such as renal artery stenosis, can cause

A

atrophy

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32
Q

profound protein calorie malnutrition

A

Marasmus

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33
Q

what is an example of atrophy from pressure

A

Rathke Cleft Cyst causes hypopituitary

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34
Q

atrophy results in decreased _____ and increased ____

A

protein synthesis
protein degradation

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35
Q

what are the two mechanisms of atrophy

A
  1. ubiquitin protease pathway
  2. autophagy
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36
Q

cell eats its own contents

A

autophagy

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37
Q

what molecule does autophagy use

A

LC3

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38
Q

_____ plays a role in cancer, neurodegenerative disorders, infectious diseases, and inflammatory bowel diseases

A

autophagy

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39
Q

adrenal gland atrophy can be caused by

A

exogenous corticosteroids

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40
Q

adrenal gland hyperplasia can be caused by

A

pituitary adenoma

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41
Q

menstrual cycle:
atrophy occurs during

A

menstrual phase

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42
Q

menstrual cycle:
hyperplasia occurs during

A

proliferative phase

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43
Q

menstrual cycle:
hypertrophy occurs during

A

secretory phase

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44
Q

change in which one differentiated cell type is replaced by another cell type

A

metaplasia

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45
Q

metaplasia is the result of

A

reprogramming of normal local tissue stem cells in response to a potentially injurious stimulus

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46
Q

metaplasia can be d/t colonization of differentiated cell populations from

A

adjacent sites

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47
Q

metaplasia is often associated with increased risk of

A

cancer

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48
Q

the cancer is typically the same histologic cell type as the

A

metaplasia

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49
Q

what is the most commonly used example of metaplasia

A

squamous metaplasia

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50
Q

chronic inflammation and vitamin A deficiency can cause

A

squamous metaplasia

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51
Q

most common epithelial metaplasia is _____ and is usually d/t ______

A

columnar to squamous
chronic inflammation

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52
Q

cervical cancer occurs at the ____ which is what cell type

A

transformation zone
squamocolumnar junction

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53
Q

what type of cancer occurs at the transformation zone of the cervix

A

squamous cell carcinoma

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54
Q

____ metaplasia occurs in the esophagus near the esophageal sphincter

A

glandular

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55
Q

what is the cancer risk of glandular metaplasia of the esophagus

A

adenocarcinoma

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56
Q

formation of cartilage, bone, or adipose cells in tissues that normally do not contain these elements

A

connective tissue metaplasia

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57
Q

is connective tissue metaplasia associated with cancer risks?

A

NO!

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58
Q

disordered growth

A

dysplasia

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59
Q

dysplasia is a ____ change

A

premalignant

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60
Q

4 mechanisms lead to intracellular accumulations:
1.
2.
3.
4.

A
  1. inadequate removal of normal substance secondary to abnormal metabolism
  2. accumulation of an endogenous substance secondary to genetic or acquired defects
  3. failure to degrade metabolite secondary to inherited enzyme deficiencies
  4. deposition and accumulation of exogenous substance
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61
Q

abnormal accumulation of triglycerides within parenchymal cells

A

steatosis

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62
Q

steatosis is most commonly seen in

A

liver

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63
Q

in high income nations, steatosis is usually d/t

A

ethanol
nonalcoholic fatty liver disease

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64
Q

intracellular accumulations of cholesterol can cause

A

atherosclerosis

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65
Q

intimal macrophages and intimal smooth muscle cells are filled with lipid vacuoles

A

intracellular cholesterol

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66
Q

multiple small vacuoles

A

foam cells

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67
Q

foam cells

A

atherosclerosis (cholesterol intracellular)

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68
Q

if cells rupture, they spill extracellular cholesterol

A

cholesterol clefts
(long needle shaped crystals)

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69
Q

intracellular accumulation of lipid, usually cholesterol, within macrophages

A

hyperlipidemia

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70
Q

clusters of foam cells in the skin and tendons

A

xanthomas

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71
Q

cholesterol-laden macrophages in the lamina propria of the gallbladder

A

cholesterolosis

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72
Q

strawberry gallbladder

A

cholesterolosis

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73
Q

Niemann-Pick Disease, Type C

A

enzyme mutation that causes cholesterol accumulation in multiple organs

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74
Q

normal secreted protein in excessive amounts

A

Russel Bodies - Plasma Cells

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75
Q

Russel Bodies causes increased synthesis of

A

Immunoglobulins

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76
Q

what normally inhibits neutrophil elastase

A

alpha-1 antitrypsin

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77
Q

alpha 1 antitrypsin deficiency causes misfolded protein to

A

accumulate in hepatocyte cytoplasm and is not secreted

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78
Q

alpha 1 antitrypsin deficiency causes
- lungs:
- liver:

A

lungs: emphysema from lack of PRO enzymatic activity
liver: death from protein accumulation

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79
Q

what should you consider in a young person with liver and lung disease

A

alpha 1 antitrypsin deficiency

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80
Q

eosinophilic cytoplasmic inclusions composed predominantly of cytokeratin intermediate filaments

A

alcoholic hyalin

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81
Q

neurofilaments in Alzheimers disease

A

neurofibrillary tangle

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82
Q

homogeneous, glassy, amorphous, pink appearance on H&E

A

hyaline

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83
Q

increased intracellular glycogen can be seen with abnormality in

A

glucose or glycogen metabolism

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84
Q

positive PAS stain indicates

A

increased glycogen intracellularly

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85
Q

disease involving increased glycogen intracellularly in the heart

A

Pompe Disease
(glycogen storage disease type II)

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86
Q

Von Gierke Disease

A

Liver glycogen storage disease type I

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87
Q

most common exogenous pigment in cells is

A

carbon (coal dust)
(Anthracosis)

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88
Q

purple line on gums, hemolytic anemia, basophilic stippling of RBC

A

Lead Poisoning

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89
Q

golden-brown lipid/protein complexes secondary to lipid peroxidation (WEAR and TEAR pigment)

A

Lipofuscin (in heart)

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90
Q

tumor composed of malanocytes

A

malignant melanoma

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91
Q

hemosiderin

A

iron

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92
Q

hemoglobin derived granular yellow-brown pigment

A

hemosiderin

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93
Q

the two major storage forms of iron

A

ferritin
hemosiderin

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94
Q

incompletely degraded aggregates of ferritin and other subcellular constituents

A

hemosiderin

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95
Q

hemosiderin in the lung indicates

A

left-sided heart failure

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96
Q

what stain confirms iron

A

Prussian Blue

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97
Q

Wilson’s disease

A

endogenous copper in brain, liver, and cornea

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98
Q

rings on the cornea in Wilson’s Disease

A

Kayser-Fleischer rings

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99
Q

bilirubin encephalopathy

A

kernicterus

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100
Q

calcium deposition in damaged tissue or areas of necrosis

A

dystrophic calcification

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101
Q

which calcification tends to be localized and normal serum Ca levels

A

dystrophihc

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102
Q

calcium deposition in normal tissue

A

metastatic calcification

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103
Q

which calcification tends to be widespread or diffuse and has increased serum Ca levels

A

metastatic

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104
Q

where is dystrophic calcification commonly seen

A

arteries (atherosclerosis)
cardiac valves

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105
Q

concentric laminated calcifications seen most frequently in certain ovarian and thyroid cancers and meningiomas

A

Psammoma Bodies

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106
Q

where is metastatic calcification most commonly seen

A

gastric mucosa, lung, kidney (acid-secreting environments)

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107
Q

after a fixed number of divisions, cells become arrested in a terminally nondividing state called

A

replicative senescence

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108
Q

2 mechanisms underlying senescence

A
  1. progressive shortening of telomeres
  2. activation of tumor suppressor genes (p16)
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109
Q

premature aging and increased incidence of malignancies due to defective DNA helicase protein

A

Werner Syndrome

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110
Q

mutation in Lamin A protein leading to premature aging

A

Hutchinson-Guilford Progeria Syndrome

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111
Q

accumulation of misfolded proteins can trigger ____ and contribute to cellular aging

A

apoptosis

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112
Q

___ restriction increases cellular longevity

A

caloric

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113
Q

caloric restriction increases cellular longevity by

A

decreasing IGF-1 and insulin pathway

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114
Q

family of protein deacetylases

A

sirtuins

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115
Q

caloric restriction increases

A

sirtuins

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116
Q

if the limits of adaptive responses are exceeded or if cells are exposed to damaging insults, deprived of nutrients, or compromised by mutations leads to

A

cell injury

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117
Q

is cellular swelling reversible or irreversible

A

reversible

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118
Q

what is the earliest manifestation of all forms of cell injury

A

cellular swelling

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119
Q

is fragmentation of plasma membrane and organelles reversible or irreversible cell injury

A

irreversible

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120
Q

is mitochondrial damage (loss of ATP synthesis) reversible or irreversible cell injury

A

irreversible

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121
Q

are pyknosis, karyorrhexis, and karyolysis reversible or irreversible cell injury

A

irreversible

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122
Q

cellular swelling is d/t dysfunction of

A

plasma membrane sodium transport or Na/K ATPase

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123
Q

ischemia leads to ____

A

ATP depletion and then mitochondrial damage

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124
Q

what is produced in large amounts by leukocytes (neutrophils and macrophages) to kill microbial organisms

A

ROS

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125
Q

what are some antioxidants that inactivate/block free radicals

A

vitamins E and A
ascorbic acid (vit C)
glutathione

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126
Q

what serves as second messengers in signaling pathways

A

Calcium ions

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127
Q

ischemia and some toxins causes increased ____

A

cytosolic Ca and Ca influx across plasma membrane

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128
Q

3 major mechanisms of membrane damage

A

1 hypoxia/ATP depletion
2 ROS
3 increased intracellular Ca

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129
Q

plasma membrane damage causes

A

leakage of intracellular contents into extracellular space (including bloodstream)

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130
Q

elevated LDH indicates

A

cell injury

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131
Q

elevated GGT, AST, and ALT indicate

A

hepatocyte injury

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132
Q

elevated alk phos indicates

A

biliary obstruction

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133
Q

elevated creatine kinase and myoglobin indicates

A

cardiac or skeletal muscle injury

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134
Q

troponin I and T isoenzymes evaluate

A

myocardial cells

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135
Q

lipase and amylase levels evaluate

A

pancreas

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136
Q

hemoglobin levels evaluates

A

RBC hemolysis

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137
Q

deficiency of O2 in blood tissue

A

hypoxia

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138
Q

deficiency of O2 in blood

A

hypoxemia

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139
Q

diminished blood supply to any tissue or organ of the body causing a shortage of oxygen

A

ischemia

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140
Q

describe ischemia-reperfusion injury

A

restoration of blood flow may cause exacerbation of reversible cell injury which may lead to irreversible lethal cell injury

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141
Q

ischemia followed by restoration of blood flow can lead to… (2)

A

recovery
ischemia-reperfusion injury

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142
Q

increased production of ROS, activation of complement, increased cytokines, increased Ca can all cause what injury?

A

Ischemia-Reperfusion Injury

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143
Q

cyanid poisons/attacks…

A

mitochondrial cytochrome oxidase

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144
Q

___ was once widely used in dry cleaning and is converted to a ROS by P-450

A

CCl4

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145
Q

analgesic drug converted to toxic product during detoxification in the liver, leading to cell injury

A

acetaminophen (Tylenol)

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146
Q

what are the two principal types of cell death

A

necrosis
apoptosis

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147
Q

mitochondrial damage, Ca, and membrane damage can lead to

A

necrosis

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148
Q

protein misfolding, DNA damage can lead to

A

apoptosis

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149
Q

necrosis vs. apoptosis:
cell size

A

necrosis: enlarged
apoptosis: reduced (shrinks)

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150
Q

necrosis vs. apoptosis:
plasma membrane

A

necrosis: disrupted
apoptosis: intact

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151
Q

necrosis vs. apoptosis:
adjacent inflammation

A

necrosis: frequent
apoptosis: none

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152
Q

is necrosis pathologic of physiologic

A

pathologic

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153
Q

is apoptosis pathologic or physiologic

A

usually physiologic

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154
Q

what type of necrosis is usually caused by ischemia?

A

coagulative necrosis

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155
Q

describe coagulative necrosis
Cause:
texture:
tissue architecture:
color on H&E:
cell outline:
inflammation?

A

ischemia
firm
preserved architecture
eosinophilic (pink)
preserved cell outline
slight inflammatory infiltrate

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156
Q

loss of ___ is seen in coagulative necrosis

A

nuclei

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157
Q

what is the sequence of nuclear changes in coagulative necrosis?

A

pyknosis
karyorrhexis
karyolysis

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158
Q

nuclei are condensed and dense

A

pyknosis

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159
Q

nuclei break into fragments

A

karyorrhexis

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160
Q

nuclei are dissolved

A

karyolysis

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161
Q

what type of necrosis is seen in MIs

A

coagulative necrosis

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162
Q

what type of necrosis is d/t bacteria/fungi/amoeba infection

A

liquefactive

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163
Q

lung abscess is an example of what kind of necrosis

A

liquefactive

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164
Q

neutrophils + necrotic material =

A

pus

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165
Q

infarction / ischemia of the BRAIN tissue leads to

A

liquefactive necrosis

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166
Q

digestion of dead cells so tissue turns into a viscous liquid describes

A

liquefactive necrosis

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167
Q

necrosis involving a limb

A

gangrenous necrosis

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168
Q

term for tissue necrosis with putrefaction

A

gangrene

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169
Q

necrosis involving the GI tract

A

gangrenous necrosis

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170
Q

ischemic coagulative necrosis of a limb

A

DRY gangrenous necrosis

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171
Q

liquefactive necrosis from superimposed bacterial infection PLUS coagulative necrosis of a limb

A

WET gangrene / gangrenous necrosis

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172
Q

gas gangrene is often caused by

A

anaerobic Clostridia

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173
Q

myonecrosis and gas formation

A

gas gangrene

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174
Q

necrosis resulting in cheese-like debri

A

caseous necrosis

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175
Q

what commonly causes caseous necrosis

A

TB
fungi
Nocardia

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176
Q

describe caseous necrosis:
cell outline:
liquefied?
inflammation?

A

loss of cell outline
not liquefied
GRANULOMATOUS inflammation

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177
Q

granulomatous inflammation = ___ + ____

A

mononuclear cells (lymphs and macrophages)
multinucleated giant cells

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178
Q

acute pancreatitis can cause

A

fat necrosis

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179
Q

what is saponification

A

free fatty acids from fat necrosis combine with Ca to form chalky white areas

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180
Q

is fat necrosis secondary to trauma seen with saponification?

A

no (nonenzymatic)

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181
Q

what type of necrosis is usually seen in blood vessels

A

fibrinoid

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182
Q

the amorphous pink material seen in fibrinoid necrosis resembles

A

fibrin

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183
Q

immune mediated vasculitis (polyarteritis nodosa) can lead to

A

fibrinoid necrosis

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184
Q

what type of necrosis can be seen in aging and severe HTN

A

fibrinoid

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185
Q

programmed cell death

A

apoptosis

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186
Q

what process is used in embryogenesis

A

physiologic apoptosis

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187
Q

death by ___ is a normal phenomenon used to eliminate cells that are no longer needed or maintain a constant # of cell populations in tissues

A

apoptosis

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188
Q

activation of p53 causes

A

cell cycle arrest to repair DNA

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189
Q

if DNA damage is extensive (beyond repair) then p53 initiates

A

apoptosis

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190
Q

describe how viral infections cause apoptosis

A

granzyme enters cell through perforin channel –> apoptosis

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191
Q

activation and cascade of caspase enzymes is central process in apoptosis
- C:
- Asp:

A

cysteine: enzyme activation site
aspartic acid: cleavage site on target pros

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192
Q

____ activation is universal feature of apoptosis

A

caspase

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193
Q

which pathway is responsible for most physiologic and pathologic apoptosis?

A

mitochondrial (Intrinsic) pathway

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194
Q

____ inhibits the intrinsic pathway of apoptosis

A

BCL2

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195
Q

what happens if BCL2 is overexpressed?

A

cells proliferate uncontrolled (BCL2 is anti-apoptotic)

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196
Q

BAX and BAK are (pro or anti)-apoptotic

A

PROapoptotic!

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197
Q

removing apoptotic cells: ____ engulf apoptotic bodies with no significant inflammation

A

macrophages

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198
Q

loss of p53 can lead to

A

cancer

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199
Q

excessive apoptosis can lead to

A

neurodegenerative diseases

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200
Q

insufficient apoptosis can lead to (2)

A

autoimmunity
cancer

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201
Q

hybrid form of cell death with features of both necrosis and apoptosis

A

necroptosis

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202
Q

necroptosis is ___-independent

A

caspase

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203
Q

in necroptosis, ___ is not activated

A

caspase 8

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204
Q

where do we see physiologic necroptosis

A

bone growth plate development

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205
Q

pyroptosis is a form of apoptosis with release of

A

fever inducing cytokine IL-1

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206
Q

programmed cell death accompanied by fever

A

pyroptosis

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207
Q

historically, what is the purpose of inflammation?

A

bring phagocytic cells to the injured area to engulf invading bacteria

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208
Q

what is the inflammation reaction sequence? (5)

A

Recognition
Recruitment
Removal
Regulate
Repair

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209
Q

how are microbial components or substances released from damaged cells recognized

A

DAMPs and PAMPs

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210
Q

PAMPs and DAMPs are recognized by

A

TLRs

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211
Q

cytosol proteins that recognize ATP, dsDNA, PAMPs, and DAMPs

A

NLRs

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212
Q

primary cell of acute inflammation

A

neutrophils

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213
Q

what cells regulates vascular dilation and contraction and mediate leukocyte recruitment?

A

endothelial cells

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214
Q

what cells regulate both acute and chronic inflammation

A

monocyte/macrophage

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215
Q

what are the four cardinal signs of inflammation?

A

pain (dolor)
heat (calor)
redness (rubor)
swelling (tumor)

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216
Q

what are the most common and medically important causes of inflammation

A

infections

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217
Q

infections are recognized via ____ and tissue necrosis is recognized via ____

A

PAMPs
DAMPs

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218
Q

____ on vascular smooth muscle is the earliest manifestation of acute inflammation

A

histamine

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219
Q

what are the 3 major components of acute inflammation

A

1 vasodilation –> increased blood flow
2 increased permeability
3 emigration of leukocytes from microcirculation

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220
Q

histamine on vascular smooth muscle causes

A

vasodilation

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221
Q

the escape of fluid, proteins, and blood cells from the vascular system to the interstitial tissue or body cavities

A

exudation

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222
Q

what is the most common mechanism of vascular leakage

A

contraction of endothelial cells

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223
Q

what mediators increase vascular permeability (3) in acute inflammation

A

histamine
NO
prostaglandins

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224
Q

extravascular fluid that has a high protein concentration and contains cellular debris

A

exudate

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225
Q

exudate implies…

A

existence of an inflammatory process and increased vascular permeability

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226
Q

fluid with low protein content and little/no cellular material

A

transudate

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227
Q

trasudate etiology is not

A

inflammatory

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228
Q

transudate is a result of

A

osmotic or hydrostatic imbalances

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229
Q

CHF leading to b/l pleural effusions is an example of

A

transudate effusions

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230
Q

cirrhosis leading to ascites fluid is an example of

A

transudate effusions

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231
Q

excess of fluid in the interstitial space or body cavity

A

edema

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232
Q

is edema an exudate or tranudate?

A

can be EITHER!

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233
Q

inflammatory exudate rich in leukocytes, dead cell debris, occasionally microbes

A

purulent exudate (pus)

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234
Q

purulent exudate is rich in

A

neutrophils

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235
Q

types of inflammatory exudate:
skin blisters

A

serous

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236
Q

types of inflammatory exudate:
adhesions following surgery

A

fibrinous

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237
Q

types of inflammatory exudate:
cloudy mucus (runny nose)

A

catarrhal

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238
Q

types of inflammatory exudate:
abscesses, boils, cellulitis

A

purulent

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239
Q

types of inflammatory exudate:
hematoma

A

hemorrhagic

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240
Q

inflamed lymph nodes are often enlarged d/t ___ of the lymphoid follicles and increased number of ____ and _____

A

hyperplasia
lymphocytes and macrophages

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241
Q

presence of ____ near a skin wound is a telltale sign of an infection in the wound

A

red streaks

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242
Q

presence of red streaks is diagnostic of ___ and may be accompained by

A

lymphangitis
painful enlargement of the draining lymph nodes (lymphadenitis)

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243
Q

inflammation of lymph vessels

A

lymphangitis

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244
Q

inflammation of lymphh nodes

A

lymphadenitis

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245
Q

what two things assist in leukocyte margination and rolling

A

E-selectin
P-selectin

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246
Q

____ on leukocytes interact with ____ on endothelial cells during leukocyte migration

A

integrins
adhesion molecules

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247
Q

____ are involved in INITIAL leukocyte rolling

A

selectins

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248
Q

____ are involved in firm adhesion of leukocytes

A

integrins

249
Q

migration of leukocytes through intact endothelium

A

transmigration or diapedesis

250
Q

after exiting circulation, leukocytes move in the issues toward the side of injury by a process called

A

chemotaxis

251
Q

what are 3 important chemoattractants for neutrophils and monocytes during acute inflammation?

A

C5a
Leukotriene B4
fMLF

252
Q

in pseudomonas bacterial infections, ___ are CONTINUOUSLY recruited for several days

A

neutrophils

253
Q

in viral infections, ___ may be the first to arrive

A

lymphocytes

254
Q

main cell type of hemlinthic infections and allergic reactions

A

eosinophils

255
Q

leukocytes leaving the vasculature and migrating to the site of bacterial inoculation is mediated by

A

chemokines

256
Q

the two major phagocytes are

A

neutrophils
macrophages

257
Q

killing of microbes by phagocytes is accomplished by

A

ROS
RNS
lysosomal enzymes

258
Q

efficiency of phagocytosis is more efficient when microbes are coated with

A

opsonins

259
Q

inherited deficiencies of components of phagocyte oxidase causes

A

chronic granulomatous disease

260
Q

mutation of lysosomal trafficking regulator protein that leads to decreased phagocytosis

A

Chediak Higashi Syndrome

261
Q

pts with Chediak Higashi Syndrome are at risk of recurrent…

A

pyogenic infections and oculocutaneous albinism

262
Q

inherited defect of phagocytes resulting in impaired microbial killing

A

myeloperoxidase deficiency

263
Q

myeloperoxidase deficiency is asymptomatic unless

A

diabetic
(recurrent severe Candida infections)

264
Q

extracellular fibrillar networks that trap microbes and prevent their spread

A

Neutrophil Extracellular Traps (NETs)

265
Q

in some infections that are difficult to eradicate (TB and some viruses), the prolonged host response contributes more to the pathology than the microbe does itself describes what?

A

leukocyte-mediated tissue injury

266
Q

terminating the acute inflammatory response:
as pathogens are cleared, levels of ____ and ___ markedly decrease –> no triggering of innate immune cells

A

inflammatory cytokines (IL-1)
tumor necrosis factor (TNF)

267
Q

terminating the acute inflammatory response:
increase in anti-inflammatory molecules such as…

A

IL-1 ANTAGonist
TGF-beta
IL-10

268
Q

cell-derived mediators of inflammation are sequestered in

A

intracellular granules

269
Q

plasma-derived mediators of inflammation are produced by ___ and must be ___

A

the liver
activated

270
Q

describe the role of histamine in inflammation

A

vasoactive amine that causes vasodilation and increases permeability of venules by producitng interendothelial gaps in venules

271
Q

histamine is released by

A

mast cell degranulation

272
Q

what increases vascular permeability and causes contraction of smooth muscle, dilation of blood vessels, and pain

A

bradykinin

273
Q

bradykinin is a mediator in some forms of…

A

allergic reaction such as anaphylaxis

274
Q

what is secreted by sensory nerves and various leukocytes and is involved in transmission of pain signals and increasing vascular permeability

A

substance P

275
Q

prostaglandins and leukotrienes are produced from _____ and stimulate…

A

arachidonic acid
vascular and cellular reactions in acute inflammation

276
Q

prostaglandins are generated by the actions of two ____ called…

A

cyclooxgenases
COX-1 and COX-2

277
Q

what are generated from AA and suppress inflammation by inhibiting neutrophil chemotaxis and adhesion to endothelium

A

lipoxins

278
Q

how do lipoxins suppress inflammation?

A

inhibit neutrophihl chemotaxis and adhesion

279
Q

aspirin, ibuprofen, and other NSAIDs are ____

A

cyclooxygenase inhibitors

280
Q

pharmacologic agents that inhibit leukotriene production are useful in tx of

A

asthma

281
Q

leukotriene receptor ANTAGonists are useful in tx of

A

asthma

282
Q

family of proteins that act as chemoattractants for specific types of leukocytes

A

chemokines

283
Q

what do TNF and IL-1 play an important role in?

A

leukocyte recruitment by promoting adhesion and migration

284
Q

TNF alpha acts on the liver leading to production of

A

actue phase proteins (acute phase response)

285
Q

TNF acts on the hypothalamus leading to

A

fever

286
Q

TNF acts on muscle and fat cells leading to

A

increased catabolism
cachexia

287
Q

acute phase response consists of (3)

A

fever
increased acute-phase proteins (CRP and fibrinogen)
leukocytosis

288
Q

what is produced by the liver and is a clinical sign of inflammation

A

C-reactive protein (CRP)

289
Q

what is correlated with TNF and indicates inflammation

A

erythrocyte sedimentation rate (ESR)

290
Q

IL-1 is produced mostly by activated

A

macrophages

291
Q

what is a mediator of acute inflammatory response, specifically playing a major role in induction of fever

A

IL-1

292
Q

IL-1 is a potent ____ cytokine, meaning it suppresses ____

A

anorexic
appetite

293
Q

TNF antagonists have been remarkably effective in the tx of

A

chronic inflammatory diseases (RA, psoriasis, IBD)

294
Q

the critical step in complement activation is the…

A

proteolysis of C3

295
Q

the lectin complement pathway involves mannose-binding lectin binding to carbs on microbes and directly activating

A

C1

296
Q

all three complement pathways lead to formation of

A

active C3 converstase

297
Q

function of active C3 convertase

A

spilts C3 into two functionally distinct fragments (C3a and C3b)

298
Q

what complement cleavage products stimulate histamine release from mast cells leading to vasodilation and increased permeability

A

C3a
C5a

299
Q

C3a and C5a are considered

A

anaphylatoxins

300
Q

4 clinical features of anaphylaxis

A

hypotension
bronchospasm
airway obstruction
hives/urticaria

301
Q

tx for anaphylaxis

A

intramuscular epinephrine (adrenaline)

302
Q

what is the function of C3b

A

acts as opsonins and promotes phagocytosis by neutrophils and macrophages

303
Q

complement proteins form a ring in the plasma membrane of target cell causing cytolysis

A

membrane attack complex (MAC)

304
Q

deposition of MAC results in…

A

increased permeability to water and ions resulting in lysis

305
Q

deficiency of the complement components of MAC predisposes pts to

A

Neisseria infections

306
Q

what is the first complement protein of the classical pathway

A

C1

307
Q

inherited deficiency of C1 inhibitor causes

A

hereditary angioedema

308
Q

DAF prevents…

A

formation of C3 convertases

309
Q

CD59 inhibits…

A

formation of MAC

310
Q

acquired deficiency of enzyme that creates GPI anchors leads to…

A

deficiency of complement regulators and excessive complement activation and lysis of RBC = Paroxysmal Nocturnal Hemoglobinuria (PNH)

311
Q

deficiency of complement regulators and excessive complement activation leads to

A

Paroxysmal Noctural Hemoglobinuria (PNH)

312
Q

____ inflammation is marked by the exudation of cell-poor fluid into body spaces or cavities

A

serous

313
Q

accumulation of fluid into a cavity from the plasma (as a result of increased permeability) or from secretion of mesothelial cells

A

effusion

314
Q

describe fibrinous inflammation

A

with increased vascular permeability, large molecules such has fibrinogen pass out of the blood and fibrin is formed and deposited in the extracellular space

315
Q

a fibrinous exudate is characteristic of inflammation in the

A

lining of body cavities such has meninges, pericardium, and pleura

316
Q

pericardial effusions are often ___ exudates associated with…

A

fibrinous
pericardial murmur– a friction rub sound (PERICARDIAL RUB)

317
Q

____ inflammation is characterized by the production of pus, an exudate consisting of neutrofils, liquefied debris of necrotic cells, and edema fluid

A

purulent

318
Q

___ are localized collections of pus

A

abscesses

319
Q

___ are produced by the shedding of inflamed necrotic tissue

A

ulcers

320
Q

what is “resolution” of acute inflammation?

A

restoration of the site to normal

321
Q

resolution is typically the outcome of acute inflammation when the injury is…

A

limted or short-lived
has had little tissue destruction
damaged parenchymal cells can regenerate

322
Q

what occurs after substantial tissue destruction, injury involves tissues that can’t regenerate, or when there is abundant fibrin exudation that can’t be cleared

A

healing by CT replacement
(scarring, fibrosis)

323
Q

what occurs when the acute inflammatory response cannot be resolved

A

chronic inflammation

324
Q

redness, warmth, and swelling during acute inflammation are caused by

A

increased blood flow and edema

325
Q

what produce histamine, TNF, IL-1, IL-6, and chemokines at the sites of infection of injury

A

Sentinel Cells

326
Q

the products from sentinel cells lead to…
(4)

A

increase vascular permeability
increase adhesion molecules
leukocyte migration
phagocytosis

327
Q

prolonged process in which inflammation, tissue injury, and attempts to repair are all active at once

A

chronic inflammation

328
Q

persistent infections by microbes such as ____ can evoke an immune reaction called _____

A

mycobacteria, viruses, fungi, and parasites
delayed-type hypersensitivity

329
Q

what is a systemic immune mediated chronic inflammatory disease mainly targeting synovial tissue

A

RA

330
Q

RA most commonly causes tissue injury in the

A

hands and wrists

331
Q

in chronic inflammation, attempts at healing by CT replacement of damaged tissue is accomplished by ___ and ___

A

angiogenesis
fibrosis

332
Q

what cells mediate chronic inflammation? (6)

A

monos/macros
lymphocytes
plasma cells
dendritic cells
fibroblasts
eosinophils

333
Q

eosinophils are abundant in… (2)

A

IgE mediated inflammation
parasitic infections

334
Q

the dominant cells in most chronic inflammatory reactions are

A

macrophages

335
Q

macrophages activate other cells, most notably…

A

T lymphocytes

336
Q

macrophages in the liver are called

A

Kupffer cells

337
Q

macrophages in the spleen and lymph nodes are called

A

sinus histiocytes

338
Q

macrophages in the nervous system are called

A

microglial cells

339
Q

macrophages in the lungs are called

A

alveolar macrophages

340
Q

macrophages in the bone are called

A

osteoclasts

341
Q

macrophages in the skin are called

A

Langerhans cells

342
Q

the macrophages throughout the body comprise the

A

mononuclear phagocyte system

343
Q

macrophages display Ag to and recieve signals from ___

A

T lymphocytes

344
Q

what are the two major pathways of macrophage activation?

A

classical
alternative

345
Q

classical macrophage activation may be induced by… (3)

A

microbial products
Th1 cells secreting IFN-gamma
foreign substances including crystals/particulate

346
Q

classically activated macrophages are called

A

M1

347
Q

M1 macrophages produce…
and upregulate…

A

NO and ROS
lysosomal enzymes

348
Q

alternative macrophage activation is induced by… (2) produced by ____

A

IL-4 and IL-13
Th2 cells

349
Q

principal function of M2 macrophages is

A

tissue repair

350
Q

M2 macrophages secrete growth factors that promote… (3)

A

angiogenesis
activate fibroblasts
stimulate collagen synthesis

351
Q

function of IFN-gamma

A

activate macrophage

352
Q

prolonged reactions involving T-cells and macrophages can lead to the formation of

A

granuloma

353
Q

what chemical mediator is most important in granuloma formation

A

IFN-gamma

354
Q

eosinophils have granules that contain ____which is toxic to parasites but also lysis of epithelial cells

A

major basic protein

355
Q

what is the pro and con of eosinophils

A

they control parasitic infections
also cause lysis of mammalian epithelial cells

356
Q

mast cells express FcERI that binds

A

the Fc portion of the IgE Ab

357
Q

in immediate hypersensitivity reactions IgE binds to the Fc receptor leading to…

A

degranulation of histamine and prostaglandins

358
Q

what response occurs during allergic reactions to food, insect venom, or drugs (sometimes anaphylactic shock)

A

mast cell degranulation d/t IgE bindding to Fc receptor

359
Q

basophils are ___ and have receptors for ___ which can trigger release of histamine

A

phagocytic
IgE

360
Q

basophils are the predominant source of

A

IL-4
IL-13

361
Q

in chronic bacterial infection of bone (___), a ___ exudate can persist

A

osteomyelitis
neutropihlic

362
Q

there are no ____ in portal chronic inflammation

A

neutrophils

363
Q

form of chronic inflammation characterized by collections activated macros, T-cells, and sometimes associated with central necrosis

A

Granulomatous inflammation

364
Q

what type of granuloma occurs in the absence of T-cell mediated immune responses

A

foreign body granuloma

365
Q

when FB granulomas form around materials such as TALC (associated with IV drug use), sutures, or other fibers are large enough to

A

preclude phagocytosis by a macrophage and don’t elicit any specific inflammatory response

366
Q

a FB can be identified in the center of the granuloma if viewed with

A

polarized light

367
Q

which type of granuloma is caused by a variety of agents that are capable of inducing a persistent T-cell mediated immune response

A

immune granulomas

368
Q

what kind of granuloma do mycobacteria TB and fungal organisms infections cause?

A

caseating granuloma (necrotizing)

369
Q

what kind of granuloma do sarcoid, Crohn disease, and leprosy cause?

A

Non-caseating granuloma (non-necrotizing)

370
Q

inflammation is associated with cytokine-induced systemic reactions that are collectively called

A

acute-phase response

371
Q

what cytokines are important mediators of the acute-phase reaction

A

TNF
IL-1
IL-6

372
Q

substances that induce fever are called

A

pyrogens

373
Q

increase in body temp is caused by ___ that are produced in the hypothalamus

A

prostaglandins

374
Q

elevated acute-phase proteins are mostly synthesized in the

A

liver

375
Q

three acute-phase proteins are

A

CRP
fibrinogen
serum amyloid A (SAA)

376
Q

CRP and SAA bind to microbial cells walls and act as

A

opsonins and fix complement

377
Q

elevated serum levels of CRP have been preposed as a marker for increased risk of

A

MI in pts with coronary artery disease

378
Q

___ bind to red cells and causes them to form stacks

A

fibrinogen

379
Q

increased inflammation sedimentation rate indicates

A

inflammation!

380
Q

increased thrombopoietin results in

A

thrombocytosis (increased platelet count)

381
Q

most bacterial infections induce

A

neutrophilia

382
Q

viral infections cause

A

lymphocytosis (increase in # of lymphocytes)

383
Q

allergies and parasitic infections cause

A

eosinophilia (increase in # of eosinophils)

384
Q

typhoid fever and infections by some viruses, rickettsiae, and certain protozoa are associated withh

A

leukopenia (decreased circulating white cells)

385
Q

___ and ___ are important in givign the signs and symptoms of infection/inflammation

A

IL-1
TNF

386
Q

the major microscopic abnormalities of Alzheimers are

A

neuritic (senile) plaques
neurofibrillary tangles

387
Q

____ in the brain drives progression from the presence of amyloid plaque and tau tangles to onset of dementia and Alzheimers

A

inflammation

388
Q

chronic hepatitis C infection of the liver is associated with

A

hepatocellular carcinoma

389
Q

chronic H. pylori gastritis is associated with

A

gastric carcinoma

390
Q

inflammatory bowel disease (UC and Crohn’s) are associated with

A

colon carcinoma

391
Q

repair of damaged tissue occurs by two processes:

A

regeneration
scarring

392
Q

restoration of normal cells

A

regeneration

393
Q

deposition of CT

A

scarring

394
Q

what are the 3 tissue groups based on proliferation capacity

A

labile
stable
permanent

395
Q

continuously dividing tissues

A

labile tissues

396
Q

tissues continuously being lost and replaced by maturation from tissue stem cells and by proliferation of mature cells

A

labile tissue

397
Q

surface epithelia and hematopoietic cells in bone marrow are examples of

A

labile cells

398
Q

cells with only minimal proliferative activity normally, however they are capable of dividing in response to loss of tissue mass

A

stable tissues

399
Q

parenchyma of most solid tissue (liver, kidney, and pancreas), endothelial cells, smooth mm. are examples of what cells

A

stable tissues

400
Q

terminally differentiated and nonproliferative cells

A

permanent tissues

401
Q

neurons and cardiac muscle cells are examples of what cell type

A

permanent tissues

402
Q

the most important source of growth factors in cell proliferation are

A

macrophages

403
Q

in cell proliferation, all growth factors activate signaling pathways that stimulate

A

DNA replication and biosynthesis of other cell components

404
Q

which organ has remarkable capacity to regenerate

A

liver

405
Q

liver regeneration occurs by 2 major mechanisms:

A

proliferation of remaining hepatocytes
repopulation from progenitor cells

406
Q

what occurs during the priming phase of liver regeneration?

A

cytokines (IL-6) are produced by Kupffer cells to make liver cells ready to respond to growth factors

407
Q

what happens in the growth factor phase of liver regeneration?

A

growth factors such has HGF and TGF alpha stimulate hepatocyte metabolism and entry of cells into the cell cycle

408
Q

in chronic liver injuries or inflammation, what cells contribute to repopulation?

A

progenitor cells

409
Q

what are the 4 steps of scar formation

A

inflammation
cell proliferation
formation of granulation tissue
deposition of CT

410
Q

in scar formation, endothelial cells and pericytes begin

A

angiogenesis

411
Q

in scar formation, ____ proliferate and lay down collagen fibers

A

fibroblasts

412
Q

what is the growth factor that drives angiogenesis in scar formation and increases vascular permeability

A

VEGF

413
Q

VEGF increasing vascular permeability accounts for ___ in healing wounds

A

edema

414
Q

granulation tissue in scar formation consists of (4)

A

proliferation of fibroblasts
deposition of CT
new formed vessels
leukocytes

415
Q

in scar formation, granulation tissue is progressively replaced by

A

collagen/CT

416
Q

during wound healing, maturation and reorganization of CT produces the

A

stable, fibrous scar

417
Q

the laying down of CT in scar formation occurs in two steps:

A

migration and proliferation of fibroblasts into site of injury
deposition of ECM proteins produced by these cells

418
Q

what is the most important cytokine for the synthesis and deposition of CT during scar formation

A

TGF-beta

419
Q

what stimulates fibroblast migration and proliferation and decreases ECM degradation during scar formation

A

TGF-beta

420
Q

what is involved in fibrosis of lungs, liver, and kidneys. inresponse to chronic inflammation

A

TGF-beta

421
Q

the degradation of collagens and other ECM components is accomplished by a family of

A

matrix metalloproteinases (MMPs)

422
Q

a ___ deficiency leads to delayed wound healing

A

zinc

423
Q

what two deficiencies inhibit collagen synthesis and retards wound healing?

A

protein
vitamin C

424
Q

what drugs cause slow wound healing (4)

A

immunosuppressive agents
corticosteroids
NSAIDs
anticoagulants

425
Q

how do glucocorticoids affects wound healing

A

result in weakness of the scar d/t inhibition of TGF-beta production and diminished fibrosis/collagen synthesis

426
Q

dehisce

A

pulling apart of wounds

427
Q

arteriosclerosis and diabetes and varicose vv. impair healing because of

A

poor perfusion

428
Q

inflammation arising. intissue spaces develops extensive

A

exudates

429
Q

an injury will heal via first intention when…

A

it involves only the epithelial layer

430
Q

first intention:
by day 3, neutrophils are replaced by

A

macrophages

431
Q

first intention:
by day 5, ____ reaches its peak

A

neovascularization

432
Q

first intention:
during the second week, there is continued…

A

collagen accumulation and fibroblast proliferation

433
Q

an injury will heal via second intention when…

A

cell or tissue loss is more extensive (abscesses, ulceration, ischemic necrosis

434
Q

in large wounds, there is a greater volume of ____ and therefore a greater mass of ____

A

granulation tissue
scar tissue

435
Q

second intention healing:
at 2 weeks, provisional matrix is replaced by ____

A

Type I collagen

436
Q

wound ___ is important in healing by secondary union because it decreases the gap between its dermal edges

A

contraction

437
Q

what is the important cell type in wound contraction

A

myofibroblasts

438
Q

sutured wounds have __% of the strength of normal skin

A

70%

439
Q

when sutures are removed, usually at 1 week, wound strength is __% of unwounded skin but increases over the next 4 weeks

A

10%

440
Q

wound strength reaches approximately __-__% of normal by 3 months

A

70-80%

441
Q

defects in wound healing:
venous leg ulcers may develop in elderly people as a result of

A

chronic venous HTN (which may be caused by varicose vv. or CHF)

442
Q

arterial ulcers develop in individuals with h

A

atherosclerosis of peripheral aa. especially associated with diabetes

443
Q

surgical incision reopens internally or externally

A

wound dehiscence

444
Q

wound dehiscence can be precipitated by

A

vomiting
coughing

445
Q

excessive TGF-beta has been associated with

A

keloids
hypertrophic scars

446
Q

scar that extends beyond the borders of original wound

A

keloid

447
Q

keloids are an increase in

A

type I and III collagen

448
Q

scar that is excessive but confined to borders of original wound

A

hypertrophic scar

449
Q

hypertrophic scars are an increase in

A

type III collagen

450
Q

formation of excessive amounts of granulation tissue, which protrudes above the level of the surrounding skin and blocks re-epithelialization

A

exuberant granulation

451
Q

exaggeration of contraction in a wound leads to

A

contracture

452
Q

where are contractures particularly prone

A

palms, wrists, soles, anterior thorax

453
Q

contractures are commonly seen after

A

serious burns

454
Q

function of vascular hydrostatic pressure

A

pushes water and salts into the extracellular space

455
Q

function of plasma colloid oncotic pressure

A

pulls water and salts into intravascular space

456
Q

3 ways that fluid balance is disrupted

A

alteration of vascular endothelium
increased vascular hydrostatic pressure
decreased plasma protein

457
Q

abnormal fluid balance causes

A

edema

458
Q

fluid accumulation in the body cavities

A

effusions

459
Q

fluid accumulation in the tissues

A

edema

460
Q

noninflammatory causes of edema / effusions (4)

A

CHF
liver failure
renal disease
malnutrition

461
Q

why does nephrotic syndrome cause edema?

A

losing protein through the kidneys –>
decreased plasma protein –>
decreased plasma colloid osmotic pressure
–> edema

462
Q

abdominal effusion is called

A

ascites

463
Q

fluid withh low protein content

A

tranudate

464
Q

fluid with high protein content

A

exudate

465
Q

type of effusion in CHF and hypoalbuminemia

A

serous

466
Q

serous fluid plus RBCs

A

serosanguinous

467
Q

type of effusion in hemopericardium (aortic/cardiac rupture)

A

sanguinous

468
Q

type of effusion in infection

A

purulent

469
Q

type of effusion in lymphatic obstruction

A

chylous

470
Q

milky white fluid from lipids

A

chylous

471
Q

type of effusion associated with malignant cells

A

malignant (neoplastic)

472
Q

what two things stem from increased blood volumes within tissues

A

hyperemeia
congestion

473
Q

ACTIVE process where arterial dilation lets more blood into an area

A

hyperemia

474
Q

hyperemia:
increased ____ blood delivery
causes ___

A

oxygenated
erythema

475
Q

PASSIVE process of blockage and reduction of venous outflow

A

congestion

476
Q

congestion-
coloration:
___ hemoglobin

A

cyanotic (blue-red)
deoxygenated

477
Q

one leg larger / more swollen than the other insinuates

A

DVT

478
Q

what is the master regulator of hemostasis

A

endothelial cell

479
Q

6 steps of normal hemostasis

A
  1. endothelial injury and vasoconstriction
  2. primary hemostasis–platelet plug
  3. secondary hemostasis–clot and fibrin deposition
  4. clot stabilization
  5. clot inhibition/cessation
  6. clot dissolution: fibrinolysis
480
Q

Virchow’s Triat

A

hypercoagulability
stasis
endothelial injury

481
Q

immediately after endothelial injury there is reflex ___

A

neurogenic vasoconstriction

482
Q

what substance causes neurogenic vasoconstriction immediately after endothelial injury and who releases it

A

endothelin
injured endothelial cells

483
Q

what is exposed after endothelial injury and what is released

A

collagen
Von Willebrand’s Factor (vWF)

484
Q

vWF on exposed collagen causes

A

platelet ADHESION

485
Q

platelet adhesion is via what protein/receptor

A

PAR G-protein receptor GpIb

486
Q

once the platelets are adhered, what causes platelet activation?

A

ADP

487
Q

activated platelets then…

A

recruit more platelets

488
Q

platelet aggregation occurs d/t what substance

A

thromboxane (TxA2)

489
Q

what platelet receptor attaches to circulating fibrinogen

A

GpIIb/IIIa

490
Q

what leads to irreversible platelet contraction via cytoskeleton changes

A

thrombin

491
Q

the function of secondary hemostasis is to form a

A

clot/thrombus

492
Q

during secondary hemostasis, tissue factor release binds ____ which kickstarts reactions that make

A

thrombin

493
Q

reactions that make thrombin is called the

A

coagulation cascade

494
Q

function of activated thrombin in secondary hemostasis

A

cleaves circulating fibrinogen into insoluble fibrin

495
Q

during the coagulation cascade of secondary hemostasis, which factors are calcium dependent and require vit K as a cofactor?

A

II, VII, IX, X

496
Q

what is special about factors II, VII, IX, and X?

A

Ca dependent
require vit K cofactor

497
Q

in vivo, tissue factor initiates the

A

clotting cascade

498
Q

which pathway does PTT evaluate

A

intrinsic

499
Q

which pathway does PT evaluate

A

extrinsic

500
Q

what is factor II?

A

prothrombin

501
Q

what is factor I?

A

fibrin

502
Q

sequence of Ca-dependent coagulation factors

A

VIIa –> IXa –> Xa –> IIa

503
Q

at which coagulation factor does the common pathway start at

A

X

504
Q

which factors does PT evaluate

A

1, 2, 5, 7, 10

505
Q

what factors does the PTT evaluate?

A

1, 2, 5, 8, 9, 10, 11, 12

506
Q

PTT and PT BOTH evaluate which pathway

A

common pathway

507
Q

what has a positive feedback loop on the clotting cascade?

A

thrombin

508
Q

function of factor IIa

A

(thrombin)
converts fibrinogen into cross linked fibrin

509
Q

what factors does thrombin activate

A

XI, V, VII

510
Q

intrinsic path is activated by factors in the

A

blood

511
Q

extrinsic path is activated by

A

tissue factor

512
Q

clot stabilization:
fibrinogen is converted to

A

fibrin

513
Q

clot stabilization:
what contracts to form the permanent plug

A

fibrin
platelet aggregation

514
Q

clot stabilization:
what is released by nearby healthy (uninjured) endothelial cells to limit the size of a clot

A

plasminogen activator
thrombomodulin

515
Q

what is released by endothelial cells to inhibit platelet function with clot cessation (3)

A

prostacyclin (PGl2)
NO
ADPase

516
Q

function of prostacyclin (PGI2)

A

inhibits platelet aggregation

517
Q

function of NO secreted by endothelial cells

A

inhibits adhesion and aggregation

518
Q

function of ADPase in clot cessation

A

destroy ADP–inhibits aggregation

519
Q

clot inhibition:
what complex activates protein C

A

thrombomodulin, thrombin, and protein C

520
Q

clot inhibition:
activated protein C in the presence of protein S inhibits…

A

factor Va
factor VIIIa

521
Q

what activates antithrombin

A

haparan sulfate proteoglycans

522
Q

antithrombin neutralizes… (3)

A

IIa
IXa
Xa

523
Q

antithrombin’s binding rxn is amplified by

A

heparin

524
Q

how do you measure heparin activity

A

PTT

525
Q

tissue factor pathway inhibitor on the endothelial cell surface (in the presence of protein S) inhibits… (2)

A

VIIa/TF complex
Xa

526
Q

in close dissolution (fibrinolysis), endothelial cells secrete

A

TPA

527
Q

function of TPA

A

converts plasminogen to active plasmin

528
Q

function of plasmin

A

breaks down fibrin

529
Q

what inhibits plasmin

A

alpha2 plasmin inhibitor

530
Q

plasminogen is also converted to plasmin by (besides TPA)

A

factor XII

531
Q

factor XII deficiency causes a ___ state because it activates plasmin

A

hypercoaguable

532
Q

what are 3 clinically administered plasminogen activators?

A

tPA, urokinase, streptokinase

533
Q

a clot that has grown larger than required for its physiologic role as a hemostatic plug

A

thrombus

534
Q

white thrombus

A

arterial thrombus

535
Q

arterial thrombi cause ___ or ____

A

ischemia or infarction

536
Q

red or stasis thrombi

A

venous thrombus

537
Q

venous thrombi cause ____ and ____

A

vascular congestion and edema

538
Q

embolism

A

dislodged thrombus that has traveled to other sites

539
Q

describe Factor V Leiden

A

mutant factor V has decreased to activated protein C and is not deactivated

540
Q

what should you consider in a pt with DVT, or recurrent pregnancy loss

A

Factor V leiden

541
Q

what disease causes increased prothrombin levels and therefore increased thrombin?

A

Prothrombin G20210 A Mutation

542
Q

Protein S Deficiency is a mutation in what gene?

A

PROS1

543
Q

Protein C deficiency can occur with what 6 things?

A

hereditary deficiency
vit K deficiency
pregnancy
liver/renal failure
DIC
Warfarin

544
Q

what can happen when a pt with protein C deficiency is placed on warfarin

A

warfarin skin necrosis

545
Q

Factor XII deficiency causes…

A

decreased plasmin activation and is prothrombotic
(LOW plasmin means less fibrinolysis)

546
Q

what is the etiology of Heparin-Induced Thrombocytopenia Syndrome (HIT) type II

A

heparin induces autoantibodies with Platelet factor 4

547
Q

HIT, type II:
autoantibody-heparin-platelet complexes activate platelets and cause

A

endothelial injury and a prothrombotic state

548
Q

autoimmune disorder characterized by presence of one or more antiphosphlipid (aPL) autoantibodies

A

Antiphospholipid Ab Syndrome (APS)

549
Q

autoimmune disorder characterized by venous or arterial thromboses, pregnancy complications (recurrent miscarriages, unexplained fetal death, premature birth

A

Antiphospholipid Ab Syndrome (APS)

550
Q

how to detect antiphospholipid antibodies clinically (2)

A

lupus anticoagulant detected during a PTT
false + serologic VDRL (syphyllis) test

551
Q

thrombotic fragment that has moved through the venous or arterial system to a different site

A

thromboembolism

552
Q

arterial emboli thhat lodge in systemic capillary beds causing ischemia and necrosis

A

systemic emboli

553
Q

80% of systemic emboli originate from

A

intracardiac mural thrombi (often from L ventricular wall infarcts)

554
Q

embolus from severe skeletal injuries/trauma

A

fat emboli

555
Q

venous emboli lodge in pulmonary capillary bed causing SOB and possibly R sided heart failure

A

pulmonary emboli

556
Q

venous embolism that ends up in systemic circulation causing tissue ischemia

A

paradoxical emboli

557
Q

> 95% of PEs are caused by

A

leg DVTs

558
Q

sudden decreases in atmospheric pressure causes

A

gas embolism–decompression sickness

559
Q

why does decompression sickness occur

A

nitrogen gas is dissolved in the blood and tissues at high pressure
with ascent, nitrogen comes out of solution in the tissues and blood

560
Q

what causes the bends in decompression sickness

A

rapid formation of gas bubbles within skeletal muscles

561
Q

sudden drop in blood flow through the body

A

shock

562
Q

hemorrhagic shock is an example of

A

hypovolemic shock

563
Q

what is the most ocommon cause of septic shock

A

gram + bacteria

564
Q

failure of myocardial pump can cause

A

cardiogenic shock

565
Q

inadequate blood or plasma volume

A

hypovolemic shock

566
Q

activation of cytokine cascades and peripheral vasodilation

A

ditributive shock

567
Q

vitamin K deficiency can cause excessive bleeding because it decreases…

A

factors II, VII, IX, X
proteins C and S

568
Q

Bernard-Soulier Syndrome

A

Gp1b-IX deficiency

569
Q

Glanzmann Thrombasthenia

A

GpIIb/IIIa dysfunction

570
Q

Hemophilia A

A

factor VIII deficiency

571
Q

Hemophilia B

A

factor IX deficiency

572
Q

Hemophilia C

A

factor XI deficiency

573
Q

liver diseases usually causes excessive bleeding d/t decreases in what

A

factors VII, IX, X, proteins C and S

574
Q

umbilical cord stump bleeding

A

afibrinogenemia

575
Q

males, umbilical cord stump bleeding, deep hematomas

A

Factor VIII deficiency

576
Q

poor wound healing, severe scar formation

A

Factor XIII deficiency

577
Q

oculocutaneous albinism, infections, neutrophihl peroxidase in clusions

A

Chediak-Higashi syndrome

578
Q

mucocutaneous bleeding indicates an issue with

A

primary hemostasis / platelet disorder

579
Q

petechiae and purpura indicate

A

platelet disorder

580
Q

how to you dx Bernard-Soulier Syndrome

A

peripheral blood smear

581
Q

no aggregation (flat line) with Ristocetin indicates…

A

Bernard Soulier Syndrome (GpIb deficiency) or vWF deficiency

582
Q

no aggregation with epi, collagen, ADP, and AA indicates…

A

Glanzmann’s Thrombasthenia (GpIIb/IIIa defciency)

583
Q

what are two conditions that are defects in adhesion

A

vWF disease
Bernard-Soulier Syndrome

584
Q

NSAIDs and Aspirin inhibit

A

cyclooxygenase (TxA2 and PGs)

585
Q

effect of NSAIDs and Aspirin

A

stops platelet aggregation

586
Q

occasional spontaneous bleeding occurs with what platelet count

A

10-30,000

587
Q

frequent spontaneous bleeding occurs with what platelet count

A

<10,000

588
Q

describe acute immune idiopathic thrombocytopenic purpura (ITP)

A

childhood disease withhh acute onset 2 weeks post virus
autoantibodies (IgG) against platelet Ags (GpIIb-IIIa or GpIb)

589
Q

describe chronic immune (refractory) idiopathic thrombocytopenic purpura (ITP) of adults >6 months

A

autoantibodies (IgG) against platelet Ags (GpIIb-IIIa or GpIb)

590
Q

what is associated with Shiga-toxin producing E. coli

A

Hemolytic Uremic Syndrome

591
Q

what strain of E. coli is associated with HUS

A

O157:H7

592
Q

HELLP Syndrome

A

hemolysis, elevated liver enzymes, low platelet
(in pregnant women with HTN)

593
Q

majority of people with vWF disease have type __ and it’s MILD

A

I

594
Q

Christmas Disease

A

Hemophilia B (Factor IX deficiency)

595
Q

Warfarin (Coumadin) creates ____ deficiency

A

vitamin K dependent factor deficiency

596
Q

condition initiated by release of tissue factor into circulation–causes all clotting steps to occur simultaneously everywhere

A

DIC

597
Q

what is seen in DIC?
PT:
PTT:
decreased:
release of products from fibrinolysis:

A

prolonged
prolonged
factors V and VIII
d-dimer and fibrin split products

598
Q

microthrombi from DIC in adrenal cortex causes

A

Waterhouse-Friderichsen syndrome

599
Q

microthrombi in pituitary causes what

A

Sheehan postpartum necrosis

600
Q

how to you differntiate between DIC and TTP

A

DIC has prolonged PT and PTT

601
Q

what color tube do you use for electrolytes, proteins, lipids, and drugs

A

red

602
Q

what color tube do you use for CBC, sed rate

A

purple

603
Q

what color tube do you use for PT and PTT, coag studies

A

blue

604
Q

what color tube do you use for blood cultures

A

yellow

605
Q

primary amyloidosis:
associated diseases:
precursor protein:

A

monoclonal plasma cell proliferations
Ig light chains–chiefly gamma

606
Q

secondary amyloidosis:
associated diseases:
precursor protein:

A

chronic inflammatory conditions
SAA

607
Q

hemodialysis-associated amyloidosis:
associated diseases:
precursor protein:

A

chronic renal failure
beta2-microglobulin

608
Q

systemic senile amyloidosis:
associated diseases:
precursor protein:

A

Transthyretin

609
Q

senile cerebral amyloidosis:
associated diseases:
precursor protein:

A

Alzheimers
APP

610
Q

medullary carcinoma of thyroid amyloidosis:
associated diseases:
precursor protein:

A

Calcitonin

611
Q

islets of langerhans amyloidosis:
associated diseases:
precursor protein:

A

T2DM
Islet amyloid peptide

612
Q

anti-DNA topoisomerase I

A

Systemic Sclerosis

613
Q

Anti-Scl-70

A

Systemic Sclerosis

614
Q

Anti-Centromere

A

CREST syndrome (limited scleroderma)

615
Q

Anti-Jo-1

A

Autoimmune Myositis

616
Q

Anti-Ro, Anti-La

A

Sjogren syndrome

617
Q

anti-histone

A

drug induced LE

618
Q

anti-smith, anti-dsDNA, anti-Ro, anti-La

A

SLE

TCM (2 decks)

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