Exam 2 Flashcards
(181 cards)
1
Q
The 3 phases/steps in carcinogenesis
A
- initiation- an event (often a carcinogenic agent) that causes the permanent genetic alteration that gives the cell neoplastic potential
- Promotion- an event that stimulates clonal proliferation of the initiated neoplastic cell*
- Progression- the process leading to malignant behavior (invasion and spread)
*reversible (step 3 can be reversible or irreversible)
2
Q
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
A
tumor
3
Q
process of carcinogensis
a normal cell turning into neoplastic
A
transformation
4
Q
“CA” ones that invade or metastasized
A
malignant
5
Q
__% of CA risks is due to environmental agents (vs. inherited)
A
85%
6
Q
how can you identify environmental risk factors of CA
A
- epidemiological studies
- occupational risks
- Direct accidental exposure
- Experimental testing
7
Q
give examples of occupational risks associated with CA
A
- Scrotal CA in men who chimney sweeps (linked to polycyclic aromatic hydrocarbons
- Lung CA in people who smoke
- Cervical CA in sex-workers (linked to HPV)
8
Q
give examples of direct accidental exposure that resulted in risks associated with CA
A
- “Radium Girls” → radiation resulted in bone CA
- Thorotrast use to be used as a contrast dye→ caused liver CA
- Radioactive iodine after nuclear explosion concentrated in thryroid→ resulted in thyroid CA in children
9
Q
give examples of experimental testing that lead to risks associated w/ CA
A
- Test for mutagenicity in bacterial cultures
- Test for transforming capabilities in cell culture
- Monitor tumor incidence in lab animals
Ex. food additives, new drugs, potential environmental pollutants
10
Q
Epideiologic evidence that certain kinds of tumors have a putative carcinogenic agent
A
- Heptaocellular Carcinoma- 2 factors involved include mycotoxins and hepatitis viruses B and C
- 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
- Lung CA- cigarette smoke
- Cervical CA- HPV
- Bone CA- radiation
11
Q
common examples of carcinogens
A
- chemicals
- Viruses
- Radiation
- Exogenous hormones (estrogen–> breast and endometrial CA)
- Bacteria
- Fungi and parasites
12
Q
H. pylori is associated with what CA
A
gastric CA
13
Q
aflatoxins is associated with what CA
A
liver CA
14
Q
Chemical carcinogen: polycyclic aromatic hydrocarbons is associated w/ what CA
A
lung and skin CA
15
Q
Chemical carcinogen: Aromati amines is associated w/ what CA
A
bladder CA
*In rubber and dye workers
16
Q
Chemical carcinogen: Nitrosamines/nitrites is associated w/ what CA
A
gut CA
*Used in fertilizers and can get into water (Proven in animals)
17
Q
Radiation carcinogen: UV light is associated w/ what CA
A
skin CA like melanoma
18
Q
ionizing radiation is associated w/ what CA
A
- 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
Q
host factors that can affect ones risk of CA
A
- inherited genes (XP= skin CA, BRCA /2= breast and ovarian CA)
- Race (white= increased risk of skin CA)
- Gender
- Age
- Diet (high dietary fat increases risk of both breast and colon CA)
20
Q
what viruses can cause CA
A
- HPV (16 and 18)
- Hep B and C
- EBV
- Human herpesvirus-8
- Human T-cell lymphotropic virus-1
21
Q
HPV is associated w/ what CA
A
cervical CA
common wart- squamous cell papilloma
22
Q
EBV is associated w/ what CA
A
Burkitt’s lymphoma
Nasopharyngeal CA
23
Q
Hep B and C are associated w/ what CA
A
Hepatocellular carcioma
24
Q
Human herpesvirus-8 is associated w/ what CA
A
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
