Create an account
What is the primary function of the tonsils and adenoids?
To protect the entry into the respiratory system.
What is the primary functin of the adnexa of the eye?
Accessory structures that provide extrnal protection and allow the eyes to move.
What are the functions of sebaceous glands?
Secrete sebum to lubircate the skin and discourage the growth of bacteria on the skin.
What is the primary function of the adrenal glands?
Regulate electrolyte levels, influence metabolism, respond to stress.
What is the function of the pituitary gland?
Secretes hormones that control the activity of the other endocrine glands.
What is the function of the thyroid gland?
Stimulate metabolism, growth, and activity of the nervous system.
What is metaplasia?
The reversible replacement of one differentiated cell type with another mature differentiated cell type.
What is anaplasia?
A change in the structure of cells and a change in their orientation to each other.
When is cell injury reversible and when is it irreversible?
Reversible- when the abnotmal stress/stimuli persists for a short period of time. Irreversible- when the stress/stimuli persists or is severe.
What type of cells will have damage to the plasma membrane ones with reversible or irreversible damage?
What type of cells will have swelling of the ER ones with reversible or irreversible damage?
Both but irreversible damge has contiunued swelling of ER.
Cells with both reversible and irreversible damage have swollen mitochondria, but what is the difference in cells with irreversible damage?
They have vacuolization which is a Ca 2+ influx.
What happens to the nucleus in cells with reversible or irreversible damage?
Reversible- chromatin clumps. Irreversible- Nuclear condensation, fragmentation and dissolution.
What is the pH like for cells with reversible or irreversible damage?
Reversible has low intracelluar pH. Irreversible- continued low intracellular pH.
What happens to reversible damaged cells when looking at them with light microscope?
They have fatty changes (steatosis).
What is the difference between necrosis and apoptosis?
Necrosis- common after ischemia and chemical injury CELL SWELLING. Apoptosis- is programmed cell death and CELL SHRINKAGE.
What happens to the plasma membrane during necrosis and apoptosis?
Necrosis- it is disrupted. Apoptosis- Intact/altered.
What happens with the cells contents with necrosis and apoptosis?
Necrosis- enzymatically digested. Apoptosis- intact.
What type of adjacent inflammation is present with necrosis and apoptosis?
Necrosis- frequent adjacent inflammation. Apoptosis- no adjacent inflammation.
What causes necrosis and apoptosis?
Necrosis- invariably pathologic. Apoptosis- Often physiological.
Cells get injured due to what 2 types of deprivation?
1. Hypoxia- inadequate oxygenation. 2. Ischemia- loss of blood supply.
Mitochondrial damage that causes cell injury is due to what?
Increased Ca2+, oxidative stress, activated phospholiapase A2.
Glutothione is stored mostly where to do what?
Stored in the retina to protect against all redox reactions.
What is the role of P-450?
Detox. It is enzymes that increase the solubility of compounds and help excrete them.
What is the down side of P-450?
While detoxing it can make some reactive oxygen intermediates which can injure cells.
Free radical injury is induced through what?
membrane lipid peroxidation, protein modification, DNA breakage.
Reperfusion after anoxia (an abnormally low amount of oxygen in the body tissues) induces what?
Free radical production.
What commonly happens after thrombolytic therapy?
Reperfusion after anoxia and often causes injury through free radical production.
Give an example of an Indirect toxin?
CCl4 it is metabolized in the liver to CCl3 and this is more toxic.
What happens to the mitochondria with subcellular injury?
Increased number with cellular hypertrophy and decreased number with cellular atrophy. Also mitochondria may assume extreme large and abnormal shapes.
What is damaged subcellularly that will interfere with organelle and molecular transport, cell architecture, cell-to cell signals, cellular mobility and phagocytosis?
What will HSP (heat shock proteins) respond to?
They respond to a variety of chemical/physical stimuli.
What are the 3 roles of HSP?
1. Protein folding. 2. Disaggregation of protein-protein complexes (unclumping). 3. Protein transport to cell organells.
What is wet gangrene?
Coagulation necrosis with liquifactive action of bacterial infection and attracted leukocytes.
What will fat necrosis look like under microscope?
Foci of shadowy outlines of fat cells with basophilic calcium deposits surrounded by inflammatory reaction.
What will cells undergoing apoptosis look like histologically?
Cellular shrinkage, chromatin condensation, apoptotic bodies.
Give an example of a pathologic pathway that could lead to apoptosis?
Injurious stimuli like radiation or hypoxia.
What will Apoptosis look like when in agarose gel culture cells?
It will look like a ladder pattern of DNA fragment.
What will necrosis or coag. Necrosis look like when in agarose gel culture cells?
It will look like diffuse smearing of DNA.
What happens to apoptotic bodies and how?
They are phagocytosed and they have ligands on them for phagocytic receptors.
What wil execution caspases do?
Once a cell is told to undergo apoptosis from: injury, withdrawal from growth factors, ligand FAS and receptor TNF, or cytotoxic T cells then the execution caspases start the degradation of cytoskeleton and nuclear proteins.
With several FAS death domains in proximity what happens?
Autocatalysis of caspase and this leads to apoptosis.
What are 2 catagories of intracellular accumulations?
1. Exogenous material. 2. Endogenous metabolites.
What is anthracosis?
Accumulation of a pigment that blackens the lings and the involved lymph nodes.
Give 2 examples of endogenous metabolites without using hemosiderin?
1. Lipids. 2. Pigment from tattoos.
What is steatosis?
Abnormal accumulation of triglycerides in parenchynmal cells also it is a fatty change.
Where will steatosis usually happen at?
The liver, but can happen in the heart, muscles, and kidneys.
Steatosis can be caused by what?
Alcohol abuse, toxins, protein malnutrition, Diaetes M., Obesity, and anorexia.
What will alcohol dehydrogenase do with methanol and ethylene glycol?
Methanol- converts it to formaldehyde. Ethylene glycol- converts it to oxalic acid.
Under a microscope what will intracellular accumulations of Cholesterol and cholesterol esters look like?
What is an intracellular accumulation of cholesterol and cholesterol esters in arteries called?
What are russell bodies?
excess secretory protein synthesis which leads to intracellular accumulations of protein that leads to a distended ER with large eosinophilic inculsions.
What are some neuro diagnosis of Intracellular accumulations of protein?
Alzheimer's, Huntington's, parkinsons's, Maybe Diabetes M. Type II.
What is the pattern of hyaline cartilage intracellular accumulation?
There is no specific pattern of accumulation due to the variety of alteration.
What will hyaline cartilage accumulations look like in a microscope?
Homogenous GLASSY pink appearance.
What are some examples of intracelluar hyaline accumulations?
reabsorption droplets, russel bodies, Mallory alcoholic hyalin.
Where will intracellular accumulations of glycogen be found at?
In clear vacoules within the cytoplasm.
What causes intracellular accumulations of glycogen?
Glucose metabolism disorders like Diabetes M., and Genetic disorders that lead to glycogen storage disease.
Glycogen accumulations have Numbers like GSD type I-V and these are associated with an enzyme deficiency and a type of disease for the next five questions give the enzyme deficiency and type of disease for the numbers given.
Hemosiderin is what?
A accumulation of Iron from RBC and it is considered an endogenous intracellular accumulation of a golden-brown pigment.
Dystrophic calcifications happens under what serum levels of calcium?
Under normal serum calcium levels.
Dystrophic calcification effects arteries and hearts how?
Arteries- atherosclerosis, heart- damaged heart valves.
What is blood serum like during metastatic calcification?
The Calcium levels in serum are high it is also high in tissues.
What are the 4 pricipal causes of metastatic calcification?
1. Increased PTH from a primary tumor on the parathyroid glands. 2. Bone destruction. 3. Vitamin D related. 4. Renal failure leading to increased phosphate retention leading to secondary hyperparathyroidism.
Metastatic calcification principally affects what?
Interstitial tissue of the vasculature, kidneys, lungs, gastric mucosa.
What is inflammation?
Reaction of blood vessels leading to accumulation of fluid and leukocytes in the extravascular tissues.
What 3 thing will inflammation do?
1. Eliminate microbes and toxins. 2. Eliminate necrotic cells and tissues. 3. prepare for tissue repair.
What are the components of acute and chronic inflammatory responses?
Circulating cells, portiens, blood vessel cells, and proteins of extracellualr matrix.
With inflammation there are how many more neutrophils than lymphocytes?
there are 2 neutrophils for every lymphocyte.
Neutrophil does what with inflammation and turns into what?
It is the first responder that works on bacterial or fungal infections and deaths turns them into pus.
Monocytes do what are? What are they called in tissues?
They present pathogens parts to T cells, and they are called macrophages in tissue.
What are the 5 signs and symptoms of acute inflammation?
1. Redness. 2. Heat. 3. Swelling. 4. Pain. 5. Loss of function.
What is the net result of fluid flow with acute inflammation?
Net is an excess of extravasated fluid.
What is the action of histamine?
Stimulates retraction of endothelial cells of the venules which increases gaps and increases permeability.
Name the liver (the other would be cellular) derived chemical mediators of inflammation?
kinin system which is bradykinin, coagulation/ fibrionlysis system, anaphylatoxins, membrane attack complex.
The complement system is a group of what?
plasma proteins produced by the liver that circulate in an inactive form.
Activation of the complement system leads to what?
formation of biologically active fragments, intermediate complexes, and terminal membrane attack complexes.
What are the 4 main functions of the activated complement derivatives?
1. Opsonization- facilitated phagocytosis of bacteria. 2. Anaphylaxis- histamine release with increased vessel wall permeability. 3. Chemotaxis- migration of leukocytes. 4. Cell lysis- through the action of MAC.
The functions of the complement system are mediated by breakdown of what?
C3 and other complement proteins, and by membrane attack complex.
Thrombin induces inflammation how?
By binding to protease-activated receptors on platelets, endothelium, smooth muscle, and other cells.
What is leukotrienes?
an arachidonic acid derivative that does chemotaxis, vascular permeability, bronchospasm.
What is lipoxins?
an arachidonic acid derivative that does vasodilation, inhibition of neutrophil chemotaxis, monocyte adhesion.
TNF and IL-1 will do what during acute inflammation?
fever, increased sleep, decreased appatite, increase acute-phase proteins, hemodynamic affects (shock), neutrophilia (increase neutorphils).
TNF and IL-1 do what to endothelial cells?
Increase leukocyte adherence, increase PGI synthesis, Increse procoagulant activity, decrease anticoagulant activity, increase IL-1, Il-8, IL-6,PDGF.
TNF and IL-1 do what to fibroblasts?
Increase proliferation, increase collagen synthesis, increase collagenase, increase protease, increase PGE synthsis.
What will NO (nitric oxide) do in blood vessels and macrophages?
Causes vasodilation and toxic free radicals are produced.
What are the other names of primary and secondary neutrophil granules?
Primary- azurophil, secondary- specific.
When acute inflammation is healed by resolution what happens to the vasculature?
It returns to normal.
How is extra fluid from edema drained when inflammation is healed by resolution?
Into lymphatics or by pinocytosis into macrophages.
What happens to neutrophils when acute inflammation is healed by resolution?
Phagocytois and apoptosis.
What is a fistula?
a narrow passage or duct formed by disease or injury, as one leading from an abscess to a free surface, or from one cavity to another
How are macrophages activated?
by cytokines from immune-activated T cells. Or by nonimmunologic stimuli such as endotoxin.
How can an activated macrophage lead to tissue injury?
from toxic oxygen metabolites, proteases, neutrophil chemotactic factors.
Chronic inflammation of the lungs shows what 3 histological characteristics?
1. Collection of chronic inflammatory cells. 2. Destruction of parenchyma. 3. Replacement by connective tissue.
What is the most important part of having the macrophages accumulate in the tissues?
What increases with chronic inflammation?
increased Lymphocytes and increased neutrophils (less than lymphocytes).
What are granuloma's?
focal accumulation of activated macrophages which often develop into epithelial-like appearance.
What leads to commitment of stem cells to differentiate into specific cells?
Activation of key regulatory proteins by growth factors and cytokines.
What happens when growth factor binds to a tyrosine kinase receptor?
Dimerization and autophosphorylation of tyrosine residue.
With a partial hepatectomy what happens during DNA replication?
incorporation of tritiated thymidine.
What are the 3 stages of activating something to undergo enlargment?
1. Priming. 2. Proliferation. 3. Growth inhibition.
What are the adjuvants (helpers) of the proliferation phase?
Norepinephrine, insulin, thyroid hormone, growth hormone.
What binds ECM components and interacts with the cytoskeleton at focal adhesions complexes?
What are the 4 mechanisms of MMP regulation?
1. regulation of synthesis by growth factors or cytokines. 2. Inhibition of synthsis by corticosteroids or TGF-beta. 3. secreted in inactive form. 4. Blockage of the enzymes by specific tissue inhibitors of metalloproteinase.
What type of scaring occurs with primary and secondary and tertiary intention healing?
Primary- minimal scarring. Secondary- broader scar. Tertiary- wound is purposely left open.
What is allowed to happen to the wound with secondary intention healing?
It is allowed to granulate.
Why can the healing process be slower with secondary intention healing?
Due to the presence of drainage from infection surgeons may pack the wound with gauze or use a drainage system.
Activated macrohages and lymphocytes in chronic inflammation areas lead to what?
Production of growth factors, cytokines.
Activated macrohages and lymphocytes in chronic inflammation do what to MMP's?
They decrease their activity.
What happens in chronic inflammation when MMP's decrease their activities?
IT will decrease the collagen degradation.
When collagen is not degraded or is allowed to be synthesised in chronic inflammation what happens?
What happens with an injury when the stimulus that caused the acute injury is removed?
Parenchymal cell death.
Parenchymal cell death with superficial wounds leads to what?
Regeneration- restitution of normal structure.
Parenchymal cell death with deep wounds leads to what?
Healing- scar formation organizatin of exudate.
What are the 2 clinical classifications of tumors and what are they like?
1. Benign- good. 2. Malignant- BAD.
How will large tumors get new blood supply?
They release chemotaxic factors that induce angiogenesis.
What will the benign and malignant tumors look like microscopically?
Benign- look like normal tissue of origin. Malignant- does not resemble normal tissue of origin.
What will benign and malignant tumor cells look like microscopically?
Benign- well differentiated. Malignant- poorly differentiated.
What will benign and malignant tumor cell nuclei look like microscopically?
Benign- normal size and shape also uniform. Malignant- variable shape (Pleomorphic).
What will tumor cells mitoses be like for benign and malignant tumors?
Benign- few. Malignant- Many and irregular.
What are the 4 main pathways of metastasis?
1. Lymphatics. 2. Blood. 3. Seeding surface of body cavity (transcoelomic spread). 4. Intraepitheilal.
What is the third step in the metastatic cascade?
Proliferation of the clone and invasion of vessel.
What is the biological role of tumor-induced angiogenesis?
TO overcome limitations of nutrient and oxygen delivery.
Seeding surfaces of body cavities is a direct seeding and what is the problem?
There is no plain of resistance to spreading.
What is mesenchyme?
cells of mesodermal origin that are capable of developing into connective tissues, blood, and lymphatic and blood vessels.
Mesenchymal tumors are named how (both benign and malignant?
Benign- use cell of origin + oma. Malignant- cell of origin + sarcoma
Epithelial tumors are named how (both benign and malignant?
Benign- use terms like adenoma and papilloma. Malignant- use terms like carcinoma.
What would a benign and malignant tumor of striated muscle be called?
B- rhadbomyoma. M- Rhabdomyosarcoma.
What would a benign and malignant tumor of cartilage cells be called?
B- Chondroma. M- Condrosacroma.
What would a benign and malignant tumor of squamous skin cells be called?
B- Epithelioma. M- Squamouse cell carcinoma.
What would a benign and malignant tumor of transitional epithelium be called?
B-Transitional cell papiloma. M- transitional cell carcinoma.
What would a benign and malignant tumor of glandular ducts in epithelium be called?
B- adneoma. M- adenocarcinoma.
What would a benign and malignant tumor of neuroendocrine cells be called?
B- carcinoid. M- oat cell carcinoma.
What would a benign and malignant tumor of Liver cells?
B- liver cell adenoma. M- Liver cell carcinoma.
What would a benign and malignant tumor of kidney cells be called?
B- renal cell adenoma. M- renal cell carcinoma.
What would a benign and malignant tumor of neuroblasts be called?
B- ganglioneuroma. M- Neuroblastoma.
What would a benign and malignant tumor of schwann cells be called?
B- Schwannoma. M- Malignant schwannoma.
What would a benign and malignant tumor of embryonic cells be called?
B- teratoma. M- Teratocarcinoma.
What will carcinoma look like microscopically?
Neoplastic cells are surrounded by non-specific stroma.
What type of tumor is a blastoma?
Malignant tumors composed of embryonic cells from embryonic primordia.
What type of a tumor is a teratoma?
They are derived from germ cells and contain mixed tissues from all 3 germ layers and can have any type of tissues like teeth.
Tumor staging is based on what?
Clinical assessment during GROSS examination as to the extent of SPREAD.
Tumor staging using the TNM system will accounts for what?
T- size of the tumor. N- presence of lymph Node metastases. M- Distant metastases.
What will stage II mean?
Cancer is locally advanced and lymph nodes on only one side of the diaphragm have metastisis.
Why will cancer cells contain less Mitocondria, RER, and specialized enzymes?
They are less differentiated and don't complete a normal function and therefore don't need to maximize energy production.
What is fetal protein in adults a marker for and why?
A marker for a tumor because the tumor cell regressed into making a fetal protein.
Where is embryonic glycoproteins made at?
by large intestine adenocarcinoma and normal fetal intestines.
What type of cells are anchoreged dependent?
Normal cells. Cancer cells show a lack of contact inhibition.
What type of cells can be passaged from one flack to another? How often can this happen?
Cancer cells. Indefinitely (immortal).
Name 5 major chemical carcinogens?
polycyclic aromatic hydrocarbons, aromatic amines, nitrosamines, steroid hormones, metals and inorganic compounds.
How can we get cancer from polycyclic aromatic hydrocarbons and what type of cancer will it cause?
Inhalation- Carcinoma of lungs, Skin contact- Skin cancer, Metabolic- Liver cancer.
Where will aromatic amines come from and how will it cause cancer and what type?
From dye and rubber industry, it is excreted in urine and causes bladder cancer.
Where will nitrosamines come from and how will they cause cancer and what type?
From food additives (smoked food), it is a bacrial conversion in the gut and it leads to intestinal cancer.
Where will Steroid hormones come from and how will they cause cancer and what type?
Ovary/adrenal, from stimulation of endometrium, causes endometrial carcinoma.
Where will Metals and organic compounds come from and how will they cause cancer and what type?
Pesticides, from skin contact, skin cancer, AND ore, from inhalation, nasal cancer.
Where will asbestos come from and how will they cause cancer and what type?
Industrial, inhalation, lung.
Where will CCL4 come from and how will they cause cancer and what type?
dry cleaning, solvent, refrigerant, contact, liver cancer.
Where will Vinyle chloride come from and how will they cause cancer and what type?
Many sources, inhalation, Liver.
85% of aniline derivatives are used to make what?
Methylene diphenyl diisocyanate (MDI) which is used to make POLYURETHANE.
What is 3rd hand smoke?
Chemicals will remain on areas that smoke touches like clothes and anything it gets on like houses.
What are the 5 steps that carcinogen undergoes?
1. Initiation. 2. Promotion. 3. Conversion. 4. Progression. 5. Clonal expansion.
What type of carcinogen would UV light, X-rays, radioactive isotopes and atomic bombs be called?
Unrepaired DNA that was damaged by UV light can cause what?
Basal cell carcinoma, squamous cell carcinoma, melanoma.
Speaking of viral carcinogens what is transduction?
acute transforming RNA viruses in the form of cellular oncogenes.
Speaking of viral carcinogens what is insertion?
Slow transforming oncogenic RNA viruses; insert into the genome and activate a latent cellular oncogene, which is then capable of transforming the normal cell into a malignant cell.
Human papilloma virus aka HPV is what and what are the 2 types?
Invasive cervical carcinoma types 16, 18.
What are RNA viruses that are carcinogenic?
Human T-cell leukemia/lymphoma virus (HTLV-1), Adult T cell leukemia which is in HIV group.
A proto-oncogene transformes into an oncogene by going through what 4 steps?
1. point mutation. 2. Gene amplification. 3. Chromosomal rearrangement. 4. Insertion of viral oncogene.
What do tumor suppressor genes do?
They protect genes against activated or newly acquired oncogenes.
What happens when a tumor suppressor gene has lost function?
it is no longer a cancer-inhibiting agent.
What is the generic way of naming Tumor suppressor genes?
D___ C. stands for deleted __name of area___ cancer
Name 5 types of hereditary cancers?
1. Neurofibromatosis type I. 2. Familial adenomatous polyposis coli. 3. Wilms tumor. 4. skin tumors in xeroderma pigmentosum. 5. Chromosomal fragility syndromes.
What should tumor markers be used for?
Not as primary diagnosis, but to confirm a diagnosis and to monitor therapy.
Hypercalcemia is a paraneoplastic syndrome caused by what types of cancers?
squamous cell carcinoma of the lung, breast, renal
What are the 7 warning signals of cancer?
CAUTION= Change on bowel or bladder cancer, A sore that doesn't heal, Unusual bleeding or discharge, Thickening or lump in breast or elsewhere, Indigestion or difficulty swallowing, Obvious change in wart or mole, Nagging cough or hoarseness.
Psammoma bodies are seen with several cancers and appear as what?
Laminated, concentricm calcific spherules.
psammoma bodies are though to arise from what?
infarction and calcification of papillae tips. And calcification of intralymphatic tumor thrombi.
Deaths from lung cancer is on the rise or fall for males and females.
Plateaued in males and is rising for females.
What is the most common sign of uterus cancer and what is the most important risk factor?
Vaginal bleeding, and hormonal imbalance.
What is the most common sign of skin cancer and what is the most important risk factor?
Skin lesion, sun expsoure.
What cancer has the most incidence ( New cases) amoung Males and Females?
Males- 1. Prostate 2. Lung. 3. Colon. Females- 1. Breast. 2. Lung. 3. Colon.
For males and females what cancers have the highest mortality rate?
Males- 1. Lung. 2. Prostatic. 3. Pancrease. Females- 1. Lung. 2. Breast. 3. Pancrease.
List the tumors that metasis to the liver in order of highest to lowest?
colon, stomach, pancrease, breast, lung.
How much fluiid is let out in a day and how?
2.5 liters. 0.1 in stool, 0.9 in respiration/sweat, 1.5 in urine.
Transudate contains less proteins and fewer cells and is typical of what?
Hydrostatic or osmotic pressure pathology.
Name 4 pathogenesis of edema?
1. Increased hydrostatic pressure. 2. Increased wall permeability. 3. decreased oncotic pressure. 4. Lymphatic obstruction.
What is oncotic pressure?
Plasma proteins that are in capillaries want to be diluted and pull fluid back into the capillary.
Transudate edema is due to what?
Increased hydrostatic pressure, incresed oncotic pressure, Na retention.
Hydrostatic pressure causes edema and is caused by what 2 things?
hypertension, heart failure (increased venous backpressure).
Oncotic pressure when low causes edema and is caused by what?
decreased protein synthesis, proteinuria (loss of proteins in urine).
Obstructions that cause edema are usually caused by what?
Tumors or chronic inflammation, also parasites like filaria which causes elephantiasis.
What is hydrothorax, hydropericardium, and hydroperitoneum?
Clincal forms of edema that are in cavities.
Chronic passive congestion of the lungs is accompanied by what?
Anoxia (low oxygen in blood), and pulmonary fibrosis.
With chronic passive congestion of the lungs macrophages take up RBC and degrade hemoglobin and this causes what?
What type of hemorrhage has slower onset subdural or epidural and why?
Subderal because the lower pressure veins bleed more slowly than arteries.
Thrombosis takes place how?
transformation of fluid blood into a solid aggregate encompassin gRBCs and fibrin.
What are the 3 principle components of a intravascular coagulation?
1. Coagulation factors. 2. Platelts. 3. Endothelia cells.
What 2 things will platelets do?
neutralize haparin and other cnticoagulant factors, and secrete thromoxane which stimulates coagulation.
How will endothelia cells help with coagulation if they have antithromboit proterties?
IL-1 and TNF activate them and ehy lose their negative charge and antithrombitic properties.
What is the thrid step in forming a thrombi?
Fully formed thrombi consists of layers of fibrin and RBCs
Deep venous thrombosis is predisposed by Virchow's triad which is what 3 things?
1. Stasis. 2. Hypercoagulability. 3. endothelial damage.
What are lines of zahn?
Distinct layering of cellular elements and fibrin that occur in atrial and venous thrombi.
Name 6 origins for arterial thromboemboli/
brain infarct, kidney, spleen, Intestinal, ventricular, extremity infarct.
The fate of infarcts depends on what?
Their anatomical site, type of cells forming the tissue, circulatory status , extent of necrosis.
What are 3 possible causes of shock/
1. Pump failure of the heart. 2. Loss of fluid from circulation. 3. Loss of peripheral vascular tone.
What are the 3 clinical stages of shock/
1. early or compensated shock. 2. Decompensated but reversible shock. 3. Irreversible shock.
What else happens with compensated shock?
Vasoconstriction of arterioles and reduced urine production.
What happens with decompensated reversible shock?
hypotension, tachypnea and shortness of breath, oliuria, acidosis.
Please allow access to your computer’s microphone to use Voice Recording.
Having trouble? Click here for help.
We can’t access your microphone!
Click the icon above to update your browser permissions and try again
Reload the page to try again!Reload
Press Cmd-0 to reset your zoom
Press Ctrl-0 to reset your zoom
It looks like your browser might be zoomed in or out. Your browser needs to be zoomed to a normal size to record audio.
Please upgrade Flash or install Chrome
to use Voice Recording.
For more help, see our troubleshooting page.
Your microphone is muted
For help fixing this issue, see this FAQ.
Star this term
You can study starred terms together