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Flashcards in Exam 2 Deck (181):
1

The 3 phases/steps in carcinogenesis

1. initiation- an event (often a carcinogenic agent) that causes the permanent genetic alteration that gives the cell neoplastic potential
2. Promotion- an event that stimulates clonal proliferation of the initiated neoplastic cell*
3. Progression- the process leading to malignant behavior (invasion and spread)

*reversible (step 3 can be reversible or irreversible)

2

abnormal swelling, a lesion that results in atonomous growth of a cell that persists after initiating stimulus has been removed
neoplasm= new growth
clinical side use

tumor

3

process of carcinogensis
a normal cell turning into neoplastic

transformation

4

"CA" ones that invade or metastasized

malignant

5

__% of CA risks is due to environmental agents (vs. inherited)

85%

6

how can you identify environmental risk factors of CA

1. epidemiological studies
2. occupational risks
3. Direct accidental exposure
4. Experimental testing

7

give examples of occupational risks associated with CA

1. Scrotal CA in men who chimney sweeps (linked to polycyclic aromatic hydrocarbons
2. Lung CA in people who smoke
3. Cervical CA in sex-workers (linked to HPV)

8

give examples of direct accidental exposure that resulted in risks associated with CA

1. “Radium Girls” → radiation resulted in bone CA
2. Thorotrast use to be used as a contrast dye→ caused liver CA
3. Radioactive iodine after nuclear explosion concentrated in thryroid→ resulted in thyroid CA in children

9

give examples of experimental testing that lead to risks associated w/ CA

1. Test for mutagenicity in bacterial cultures
2. Test for transforming capabilities in cell culture
3. Monitor tumor incidence in lab animals

Ex. food additives, new drugs, potential environmental pollutants

10

Epideiologic evidence that certain kinds of tumors have a putative carcinogenic agent

1. Heptaocellular Carcinoma- 2 factors involved include mycotoxins and hepatitis viruses B and C
2. Esophageal CA- linked to something in the Linhsien’s food because they fed their scraps to their chickens and most developed esophageal CA even after moving locations
3. Lung CA- cigarette smoke
4. Cervical CA- HPV
5. Bone CA- radiation

11

common examples of carcinogens

1. chemicals
2. Viruses
3. Radiation
4. Exogenous hormones (estrogen--> breast and endometrial CA)
5. Bacteria
6. Fungi and parasites

12

H. pylori is associated with what CA

gastric CA

13

aflatoxins is associated with what CA

liver CA

14

Chemical carcinogen: polycyclic aromatic hydrocarbons is associated w/ what CA

lung and skin CA

15

Chemical carcinogen: Aromati amines is associated w/ what CA

bladder CA

*In rubber and dye workers

16

Chemical carcinogen: Nitrosamines/nitrites is associated w/ what CA

gut CA

*Used in fertilizers and can get into water (Proven in animals)

17

Radiation carcinogen: UV light is associated w/ what CA

skin CA like melanoma

18

ionizing radiation is associated w/ what CA

-leukemia in some of the first radiology workers
-skin cancer for those whose hands regularly exposed to X-ray beams
*radiation in Hiroshima and Nagasaki following atomic bombs in 1945 increased tumor incidence in survivors

19

host factors that can affect ones risk of CA

1. inherited genes (XP= skin CA, BRCA /2= breast and ovarian CA)
2. Race (white= increased risk of skin CA)
3. Gender
4. Age
5. Diet (high dietary fat increases risk of both breast and colon CA)

20

what viruses can cause CA

1. HPV (16 and 18)
2. Hep B and C
3. EBV
4. Human herpesvirus-8
5. Human T-cell lymphotropic virus-1

21

HPV is associated w/ what CA

cervical CA
(common wart- squamous cell papilloma)

22

EBV is associated w/ what CA

Burkitt's lymphoma
Nasopharyngeal CA

23

Hep B and C are associated w/ what CA

Hepatocellular carcioma

24

Human herpesvirus-8 is associated w/ what CA

Kaposi's sarcoma
Pleural effusion lymphoma

*explains association btwn venerally acquired AIDS and Kaposi's sarcoma

25

Human T-cell lymphotropic virus-1 is associated w/ what CA

Adult T-cell leukaemia/lymphoma

26

hallmarks of CA

1. Sustaining proliferative signaling (uncontrolled growth)
2. Evading growth suppressors
3. Activating invasion and metastasis
4. Enabling replicative immortality (prevent telomere shortening)
5. Inducing angiogenesis
6. Resisting cell death (resist apoptosis)

27

Genes that slow down cancer development. Cancer cells have mutations that inactivate the function of these genes

Tumor suppressor genes

-mutation: remove the break

28

Genes that, when hyperactive, promote cancer development (promote CA hallmarks). Cancer cells have mutations that enhance the activity of these genes.

oncogenes

-mutation: step on the gas

29

what type of genes are Her2-neu, Ras, Myc, Src, Htert

Oncogenes

30

what type of genes are P53, Rb, APC

tumor suppressor genes

31

Heritable changes in gene expression without underlying changes in the DNA sequence (what genes are turned on and what are turned off)

epigenetics

32

The time between exposure to an oncogenic event and the presence of an overt tumor

latency

33

the 3 minimum genetic alterations necessary for transformation from normal to neoplastic cells.
*Need all 3 to have progession of CA

1. Telomerase enzyme- extends telomeres so it could immortalize a cell when expressed
2. Tumor suppressors- genes that block cell division or promote cell death need to be lost or inactivated
3. Oncogenes- genes that promote cell division or block cell death need to be activated or enhanced

34

-Are the repetitive sequences on the ends of chromosomes
-shorten with each cell division, so they limit the replicative potential of a cell

telomeres

35

“Two-hit” hypothesis

if you inherit one mutated copy (allele) of a gene (hit #1) you only need one mutation in your normal allele (hit #2) to lose the function of a that gene (tumor suppressor)

36

Are necessary genes for normal cell/tissue growth and differentiation

proto-oncogenes

37

2 categories of tumor suppressor genes

1. Governors- protectors of uncontrolled proliferation
2. Guardians- protectors of DNA integrity

38

what category of tumor suppressor genes?
Rb and other cell cycle inhibitors

governors
*protetors of uncontrolled proliferation

39

what category of tumor suppressor genes?
p53

Guardian
*protector of DNA integrity

40

Controls the G1 to S transition by repressing transcription of critical genes required for S phase entry

Rb
(TSgene/governor)

41

the master sensor of cellular stress and maintains DNA integrity

p53
(TSgene/governor)

42

what is the most commonly mutated gene in CA?

p53
~50% of CA

43

5 categories of oncogenes

1. Growth factors
2. Receptors for growth factors
3. Signal Transducers, tyrosine kinases
4. Regulators of cell survival
5. Nuclear-binding onco-proteins

44

what category of oncogene?
sis gene

Growth factor
*codes for PDGF

45

what category of oncogene?
erbB

receptor for growth factor
*codes for EGFR

46

what category of oncogene?
myc

nuclear-binding oncoprotein

47

what is the most commonly mutated oncogene?

Ras

48

what category of oncogene?
src, abl, Ras-GTP

signal transducers, tyrosine kinases

49

what category of oncogene?
BCL-2

regulators of cell survival

50

how is tumor suppressor activity lost? (5)

1. genetic deletion containing tumor suppressory
2. inactivating missense mutation
3. inactivating insertions or deletions causing frameshift
4. promoter silencing through DNA methylation
5. Overexpression of a targeting miRNA

51

Hypermethylation of promoter region (transcriptional activator complexes cannot bind to methylated DNA)- Promoter silencing through DNA methylation

epigenetic loss
*an ex of how tumor suppressor activity can be lost

52

Karyotypic changes that can lead to loss of tumor suppressor activity

1. deletion of TS gene
2. epigenetic loss

53

____ of DNA and histones causes nucleosomes to pack tightly together. Transcription factors cannot bind the DNA, and genes are not expressed

Methylation
*associated w/ closed chromatid

54

how can oncogenes be misexpressed? (4)

1. activating point mutations- addition of an abnormally functioning gene
2. gene amplification- causing excessive production of protein
3. promoter hyperactivation (possibly through chromosomal translocation) leading to increased transcription
4. loss of targeting miRNA

55

karyotypic changes that lead to a misexpressed oncogene

1. duplication or amplification of a gene
2. translocation of an inactive gene to an active region

56

Hypomethylation can activate proto-oncogenes

epigenetic gain

57

_____ results in loose packing of nucleosomes. Transcription factors can bind the DNA and genes are expressed.

Histones acetylation

*associated w/ opening chromatid

58

the steps from core tumor to distant metastasis
(7)

1. Detachment
2. Invasion
3. Intravasation
4. Survival
5. Adherence
6. Extravasation
7. Colonize

59

describe the steps from core tumor to distant metastasis

1. Detachment of tumor cells from their neighbors/environment
2. Invasion of surrounding tissue to access conduits for metastasis (blood and lymphatics) (aka. travel through the ECM and find a vessel)
3. Intravasation into the lumen of vessels (aka. Get into vessel)
4. Survival in the blood stream/Evasion of host defense mechanisms
5. Adherence to endothelium at remote location
6. Extravasation of cells from vessel lumen into surrounding tissue
7. Colonize now found a home, have the right environment to *produce a tumor*

60

factors that influence tumor cell invasion (4)

1. decreased cell-cell adhesion
2. changes in cell-ECM adhesions
3. Secretions of proteolytic enzymes
4. Abnormal or increased cellular motility

61

What needs to be destroyed in CA

the tissue architecture

62

example of extracellular proteins that can be involved in cell-cell adhension

integrins
selectins
CAM

63

features of ____ are hijacked in CA progression

EMT (epithelial to Mesenchymal transition)

*primarily an embryonic mechanism

64

how do changes of Cell-ECM adhension occur during local invasion

Lose Epithelial to mesenchymal transition (EMT) and gain mesenchymal plasticity, which enables more invasion and motile cells

65

example of proteinases

MMPs (matrix metalloproteinases)
uPA (urokinase plasminogen activator
Cathepsins

66

what secretes proteolytic enzymes during local invasion

tumor cells and stromal cells including fibroblasts and immune cells

67

allow malignant cells to digest basement membrane and surrounding connective tissue

proteinases

*often release bioactive ECM fragments (growth factors, angiogenic factors, chemotactic factors)

68

proteinases are counteracted by what

tissue inhibitors of metalloproteinases (TIMPs)

69

describe the process of tumor cell motility

1. protrusion of the leading edge
2. adhension at the leading edge with deadhesion at the trailing edge
3. movement of the cell body

70

what is the single most important criterion of malignancy

invasion

71

in CT tumors, invasion is harder to recognize, so histological features such as ___ are used for prognostic purposes

miotic activity

72

___ bind CA cells (in blood stream metastasis and inhibit _____

platelets

destruction from immune cells

73

_____ are critical in adherence to endothelial membrane (integrins/selectins/CAMs)

transmembrane cell surface receptors

74

let or force out (a fluid, especially blood) from the vessel that naturally contains it into the surrounding area

extravaste

75

how does a tumor cell know where to extravaste?

1. First capillary bed /lymph node after entering circulation
2. Chemokine receptor expression (CXCL12 and CCL21 in breast cancer)

*Tropism travel of a CA to a specific area (ex. Breast CA metastasizes to lungs, liver, and bone because that it where its attractants (CXCL12) are located)

76

what needs to occur for colonizatino of metastaic secondary site

1. tumor cells must proliferate
2. recuit blood vessels
3. communicate w/ resident stromal cells
4. transition back to epithelial characteristics (MET)

77

fates of CA cells post extravasation

1. tumor domancy
2. micrometastasis
3. macrometastasis
4. ineffecient colonization

78

different metastatic routes

1. hematogenous
2. lymphatic
3. transcoelomic
4. implantation

79

what metastatic route?
accidental spillage of tumor cells during clinical manipulation or surgery

implantation

80

what metastatic route?
spreading to regional lymph nodes
Tumor cells settle and grow in the periphery of the node eventually replacing it

lymphatic

*firmer and larger (tend to mat together)

81

what metastatic route?
-spread to pleural, pericardial and peritoneal cavities where this invariably results in a neoplastic effusion
-Fluid is rich in protein (exudate), neoplastic cells that can be identified by cytological methods, and may contain fibrin

transcoelomic

82

______ interrupt flow causing edema in the territory that they drain

Lymph node mets

83

Peritoneal effusion associated with ___ cancers

Pleural and pericardial effusions common in ___ and ____ carcinomas

ovarian CA

breast and lung

84

what metastatic route?
by the bloodstream, to form secondary tumors in organs perfused by blood that has drained from a tumor

Hematogenous

85

clinical effects of tumors are attributed to their:

location
cell of origin
behavior

86

local effects of neoplasms

1. Compression and displacement of adjacent tissues
2. Benign tumors in the right location can be life-threatening
3. Problems arise when destruction of vital tissue occurs (brain or pulmonary artery)
4. Mucosal surface becomes ulcerated

87

risks associated with the mucosal surface becoming ulcerated (via a local effect)

-Blood can ooze from these lesion and cause anemia
-Ulcerated surfaces expose patients to risk of infections

88

metabolic effects of neoplasms

1. Tumor-type specific-Exemplified by well differentiated endocrine tumors
2. Non-specific metabolic effects

89

Non-specific metabolic effects associated with neoplasms

1. Weight loss
2. Catabolic state known as CACHEXIA (When protein metabolism is effected)
3. Neuropathies and myopathies
4. Venous thrombosis

90

Thyrotoxicosis is associated with what type of CA

thyroid adenoma

91

Cushing’s syndrome is associated w/ what type of CA

adrenocortical adenoma

92

Hyperparathydroidism is associated w/ what type of CA

parathyroid adenoma

93

what are prognostic indicators

tumor grade and tumor stage

94

how the tumor cells look

tumor grade

*Assessment of a tumor’s degree of malignancy or aggressiveness (I, II, III or IV)

95

how much the tumor cells have spread

tumor stage

96

histology that is used to infer tumor grade

-Mitotic activity
-Nuclear size and pleomorphism
-Degree of resemblance to the normal tissue (i.e. differentiation)

97

Determined by histopathological examination of resected tumor and clinical assessment

tumor stage

98

what is the TNM staging system

T = Tumor size (primary) 1-4
N = Lymph node involvement (regional) 0-2
M = Metastases (extent of distant metastases) 0-2

If the parameter is unknown, assigned a value of “ x ”

99

most common CA for males and females

males- prostate
female-breast

100

top 3 CA incidences for females

breast, lung/bronchus, colon/rectum

101

top 3 CA incidences for males

prostate, lung/bronchus, colon/rectum

102

top 3 causes of CA deaths for females

Lung/Bronchus, Breast, Colon/Rectum

103

top 3 causes of CA deaths for males

Lung/Bronchus, Prostate, Colon/Rectum

104

characteristics of benign tumors

i. Well circumscribed
ii. Small (2-3cm)
iii. Mobile
iv. Homogenous by radiology or histology
v. Slow growth

105

characteristics of malignant tumors

i. Irregular shape
ii. Large (4-5cm)
iii. Attached to surrounding tissue
iv. Heterogenous, necrosis and/or hemorrhage
v. Grow quickly
vi. Metastasize

106

four basic classes of malignant tumors

1. Carcinoma: from epithelium (ecto- and endoderm)
2. Sarcoma: from connective tissue (mesoderm)
3. Lymphoma or
4. Leukemia: from hematopoietic cells

107

what class is adenocarcinoma

malignant tumor of glandular tissue

108

name cell origin and clinical behavior:
fibroma

benign tumor of fibrous tissue

109

name cell origin and clinical behavior:
Chondroma

benign tumor of cartilage

110

name cell origin and clinical behavior:
Rhabdomyoma

benign tumor of skeletal muscle

111

name cell origin and clinical behavior:
Leiomyoma

benign tumor of smooth muscle

112

name cell origin and clinical behavior:
teratoma

benign tumor of all 3 germ layers

113

name cell origin and clinical behavior:
Cystadenoma

benign glandular tumor which is cystic

114

name cell origin and clinical behavior:
Chondrosarcoma

malignant tumor of cartilage

115

name cell origin and clinical behavior:
angiosarcoma

malignant tumor of blood vessels

116

name cell origin and clinical behavior:
squamous cell carcinoma

malignant tumor of squamous cells

117

name cell origin and clinical behavior:
urothelial carcinoma

malignant tumor of urothelium cells

118

name cell origin and clinical behavior:
small cell carcinoma

malignant tumor composed of small, neuroendocrine cells

119

name cell origin and clinical behavior:
meningioma

malignant tumor of meninges

120

name cell origin and clinical behavior:
melanoma

skin cancer malignant

121

clinical behavior:
lymphoma

malignant

122

name cell origin and clinical behavior:
seminoma

malignant of testis (germ cells

123

clinical behavior:
mesothelioma

malignant

124

name cell origin and clinical behavior:
Hamartoma

normal, but disorganized cells

125

name cell origin and clinical behavior:
Choristoma

normal, but misplaced tissue

126

Malignant tumors that sound benign

Meningioma
Melanoma
Lymphoma
Seminoma
Mesothelioma

127

is the suffix -oma typically benign or malignant

benign
ex. adenoma, benign tumor of glandular cells

128

histological features of neoplasia

1. Loss of Resemblance to normal tissue structure
2. Cell atypia/pleomorphism
3. Increased N/C ratio
4. Increased Mitotic count

129

Based on features seen during pathological diagnosis

tumor grading

*Low vs. high grade
-Well, moderately, or poorly differentiated
-Grade 1, Grade 2, Grade 3

130

Represents the extend or spread of cancer at time of diagnosis
Based on tumor size, imaging results and other tests

tumor staging

131

what tumor stage?
small tumor confined to organ

stage I

132

what tumor stage?
local spread to lymph nodes or nearby organs

stage II-III

133

what tumor stage?
distant metastatic spread

stage IV

134

what are the main 3 elements of Virchow's triad

1. Endothelial injury
2. Stasis or turbulent blood flow
3. Hypercoagulability

135

Ulcerated atherosclerotic plaques
Aneurysms
Myocardial infarction
Hyperviscosity syndromes
Sickle cell disease

are a result of what?

stasis or turbulent blood flow

136

primary (congenital) factors that promote thrombus formation

Factor V Leiden
Prothrombin 20210 mutation
Deficiency of antithrombin, protein C or S

137

what mutation?
increased prothrombin transcription

Prothrombin 20210 mutation

138

what mutation?
Protein C can not turn off mutant factor V

Factor V Leiden

139

secondary factors that promote thrombus formation

Oral contraceptives, pregnancy
Disseminated cancer
Smoking
Obesity
Old age
Heparin induced thrombocytopenia (HIT)
Antiphospholipid antibody syndrome

140

where does the thrombus come from?
Mural thrombi

heart, aorta

*formed against a wall

141

where does the thrombus come from?
red or stasis thrombi

venous thrombi

*90% lower extremities (due to increase chance of peripheral vascular disease→ causes person to be stationary)

142

phlebothrombosis

venous thrombus in a smaller vein

143

lines of zahn

thrombin deposits in layers

144

small blood clots all over the body that comes and goes and often causes pain

migratory thrombophlebitis
(Trousseau's syndrome)

145

-Widespread thrombosis in the microcirculation
-circulatory insufficiency

disseminated intravascular coagulation
(DIC)

146

is DIC a primary or secondary disorder

secondary to activation of thrombin

147

-Consumption of platelets and clotting factors
-Bleeding and clotting at the same time

disseminated intravascular coagulation
(DIC)

148

an intravascular solid, liquid, or gaseous mass that is carried by blood to a site distant from its point of origin

embolus

*usually a piece of a thrombus that has broken free and passes through blood until it gets caught on a narrowed vessel

149

a solid mass of platelets and/or fibrin that forms in a local vessel, usually forms when clotting mechanism has been activated

thrombus

150

Different sources of emboli

1. thromboemboli (PE or systemic thromboembolism)
2. Fat embolism
3. Bone marrow
4. amniotic fluid embolism
5. Air embolism
6. Atherosclerotic
7. Tumor

151

sequelae of PE

1. Single or multiple (at one time or over time)
2. Hypoxia, right heart failure, hypotension
3. Can lead to pulmonary hemorrhage and infarction
4. Saddle embolus
5. Paradoxical embolism

152

PE at bifurcation of pulmonary arteries

saddle embolus

153

PE that passes through atrial or ventricular septal defects and enters systemic circulation

paradoxical embolism (due to a PE)

154

sequelae of systemic thromboembolism

1. From intracardiac mural thrombi: left ventricular infarcts or dilated left atrium from mitral valve disease
2. Or aortic aneurysms, thrombi overlying atherosclerotic plaques
3. Arterial emboli most often go to lower extremities, but can go anywhere

155

sequelae of Fat embolism/bone marrow

1. From soft fatty tissue crush injury, long bone fractures, rupture of marrow sinusoids
2. May be seen after aggressive CPR
3. Fat embolism syndrome

156

pulmonary insufficiency, neurologic symptoms, anemia, thrombocytopenia, diffuse petechial rash, appears 1-3 days after injury, fatal in 10% of cases

fat embolism syndrome

157

sequelae of amniotic fluid embolism

Sudden sever dyspnea, cyanosis, hypotension, shock, seizures, coma, pulmonary edema (DAD), DIC

158

cause of amniotic fluid embolism

-From uterine vein rupture
-Histologically, fetal squamous cells, plugging vessels

*80% mortality, responsible for 10% of maternal death in the US, 85% of survivors have permanent neurologic deficits

159

cause of air embolism

due to surgery, obstetric procedures, chest wall injury

*Small amounts are not significant, but large amounts can occlude vessels (coronary arteries, cerebral arteries)

160

sequelae of air embolisms

Decompressed sickness (“the bends”)

*with sudden decompression, nitrogen dissolved in blood expands and forms bubbles that block small vessels, esp. in muscles, joints, and lungs

161

the gross morphology of an infarct

-Red (hemorrhagic)
-white (anemic)
-Wedge-shaped with vessel at apex
-Become paler and more sharply defined with time

162

an area of ischemic necrosis caused by occlusion of the vascular supply of the affected tissue

infarct

163

dual circulation or reperfusion after occlusion, hemosiderin turns brown grossly

red hemorrhagic morphology

164

Histology of an infarct

-Ischemic coagulative necrosis
-inflammatory response at margins
-Replaced by scar or liquefactive necrosis (brain)

165

Different causes/categorizations of shock

1. cardiogenic
2. hypovolemic
3. neurogenic
4. anaphylactic
5. Systemic inflammatory response syndrome (SIRS)
6. septic shock

166

what shock?
failure of myocardial pump
-MI, ventricular rupture, arrhythmia, cardiac tamponade, pulmonary embolism

cardiogenic shock

167

what shock?
inadequate blood or plasma volume
-Hemorrhage, vomiting, diarrhea, burns, trauma

hypovolemic shock

168

what shock?
loss of vascular tone from anesthesia or spinal cord injury

neurogenic shock

*less common

169

what shock?
severe allergic reaction, can result in pulmonary edema→ decrease intracellular volume)

anaphylactic shock

170

due to:
-Overwhelming microbial infection (G+, G-, fungus)
-Endotoxic shock
-Sepsis
-Superantigens (Toxic shock syndrome, TSS): polyclonal T-lymphocyte activators leading to rash, vasodilation, hypotension

septic shock

171

septic shock pathogenesis

1. cytokine cascade
2. DIC affecting ardenal gland
3. Organ dysfunction
4. Acure respiratory distress syndrome (ARDS): diffuse alveolar damage

172

Waterhoues-Friderichsen syndrome is due to what

DIC affecting ardenal gland in septic shock

173

Cytokine cascade for septic shock

1. Systemic dilation, tissue hypoperfusion
2. Hypercoagulability
3. Metabolic perturbations that suppress cell and tissue function
4. Systemic activation of macrophages, neutrophils, dendritic cells, endothelial cells

174

-Immune suppression
-Apoptosis of lymphocytes
-Increased vascular permeability (Edema)
-Small vessel thrombosis (Decreased delivery of oxygen and nutrients)

results of organ dysfunction due to septic shock

175

stages of shock

1. Nonprogressive stage
2. progressive stage
3. irreversible stage

176

what stage of shock?
tissue hypoperfusion and onset of worsening circulatory and metabolic derangement (may or may not be reversible)

progressive stage

177

what stage of shock?
-Lactic acidosis from anaerobic glycolysis
-Blunting of vasomotor response
-Vasodilation (arterioles)
-Pooling in microcirculation

progressive stage

178

what stage of shock?
reflex mechanisms initiated to maintain organ perfusion

nonprogressive stage

179

what stage of shock?
-Widespread cell injury
-Lysosomal enzyme leakage
-Worsening myocardial contractile function
-Increased NO synthesis
-Bowel ischemia
-Renal failure

irreversible stage

180

what stage of shock?
cellular and tissue injury is so severe that even if the hemodynamic defects are corrected, survival is not possible

irreversible stage

181

what stage of shock?
- Baroreceptor reflexes, catecholamines, ADH, renin-AT-aldosterone (hold onto water), sympathetic nervous system stimulation
-Tachycardia, peripheral vasoconstriction, renal fluid conservation

nonprogressive shock