Question | Answer |
Define disseminated Intra-vascular Coagulation (DIC) | multiple thrombi inside vessels, all over the body |
What are the four main things that can cause DIC | Thrombin activating substances enter the circulation Massive tissue necrosis Immune complexes Endothelial damage |
What are some examples causing thrombin activating substances entering the circulation | amniotic fluid embolism snake venom cell necrosis |
What are some examples causing Massive Tissue necrosis | shock obstetric problems acute hepatic necrosis burns cancer |
What are some causes of immune complexes | cancer, infections, vasculitides |
What are some causes of endothelial damage | endotoxic shock, viral infections, Rickettsial infections, other infections |
Define embolus | an abnormal mass of material, that can be solid, a liquid of a gas, present in the circulation that usually ends up lodging in a vessel and producing tissue ischemia or infarction |
What are the six types of embolisms | Thromboembolism Air Embolism Amniotic fluid embolism fat embolism bone marrow embolism miscellaneous |
What is the most common form of embolism? | thromboembolism |
What type of embolus is a thromboembolism | a venous thrombus |
What is the site of origin for a thromboembolism | deep veins of the legs or anywhere where there is inflammation of a vein |
What usually results from a thromboembolism | a pulmonary embolus |
What are the major effects of a thromboembolism | circulatory obstruction if large embolus Flow obstruction to one lung--> exchange problems, death smaller embolus blocks small arteries, breathlessness, chest pain many small lead to pulmonary hypertension |
T/F the pulmonary embolism always leads to pulmonary infarction | F, because the bronchial arteries are still operating |
What is a paradoxical embolus | a venous thrombus that ends up in the systemic arterial circulation; production of a venous thrombus |
How are pulmonary emboli named? | By where they lodge, not where they start |
What are the ways that a paradoxical embolus is formed | Must be due to a genetic defect allowing it to move from R to L side of the heart; atrial/ventricular septal defect,R to L shunt even though the blood flow should be L to R-blood flow switched due to P change |
What is a TIA | Transient ischemic attack, 3-5 minute ischemic attack due to a small embolus, neural function stopped but not killed, temporary. |
What are some associated symptoms of TIA | transient blindness, transient weakness |
Define air embolism | A large bolus above 100mls that can obstruct blood flow through the heart-sudden death |
Define acute decompression sickness | due to nitrogen buubles coming out of solutino when a diver ascends to low pressures |
What are the emboli associated with acute decompression sickness | the bends-emboli in muscles and bones the chokes-in lungs nitrogen emboli-cardiac ischemia,cerebral ischemia |
What is Caisson's disease | chronic problem of air embolism. especially construction workers exposed daily. Ischemic necrosis of the lungs organs and bones |
Amniotic fluid embolism | rare complication of child birth that occurs after placenta detached. amniotic fluid can produce DIC because of fetal skin cells, hair. Can occlude vessels in brain and lungs; abrupt ceo placenti |
Fat embolism | occurs following fracture of long bones in adult. Fat from marrow gets into venous or systemic circulation. |
What happens if a fat embolism obstructs venous circulation | dyspnea and exchange problems |
What happens if a fat embolism obstructs systemic circulation | petechial skin rashes and cerebral dysfunction |
T/F Bone marrow embolisms are harmless | T |
Miscellaneous embolism | usually seen in IV drug abusers who inject various particulate matter with pharmacological agents. |
Define infarction | death of a tissue due to decreased blood supply |
What causes tissue ischemia | arterial and venous obstruction |
Is arterial obstruction local or generalized, or both | usually local due to atherosclerosis or the thrombus that develops on the top of atherosclerosis |
Is venous obstruction local, generalized, or both | both. Local due to venous obstruction, generalized due to cardiac failure |
How are arterial obstruction effects determined | presence of collateral circulation Integrity of collateral circulation Rate of devlp't of obstruction; faster = fatal duration of obstruction tissue susceptibility to ischemia tissue metab rate Pre-existinf state of pt |
Which is more likely to survive, tissue with a low or high metabolic rate | low, because requires less nutrients therefore can handle slower blood flow |
Which organ is most susceptible to ischemia after loss of blood supply | the brain; 5-10 minutes |
What are some of the causes of venous obstruction (generalized) | LVF, RVF |
In LVF in what form is pulmonary edema? | acute |
In LVF in what form is pulmonary congestion | chronic |
In RVF in what form is acute hepatic enlargement | acute |
In RVF in what form is hepatic venous congestion | chronic |
What are the most common causes of chronic RVF | LVF, corporal monoly |
If there is good collateral drainage, what happens in localized obstruction in a venous thrombosis | no effect |
define proptosis | outward bulging of the eyes due to edema |
What are the three different classifications of infarction | pale vs red solid vs liquefied sterile vs septic |
What type of infarctions are pale or anemic | arterial infarctions that occur in solid organs that lack significant collateral circulation |
What type of infarctions are red or hemorrhagic | occur due to venous obstruction or due to arterial obstruction in organs that have a double blood supply or good collaterals |
Where does liquefaction occur | in the CNS in the center of an abscess |
What type of necrosis is in the majority of necrosis cases | coagulative |
T/F most infarctions are not sterile | F, most are sterile unless caused by a septic emboli, tissue contains bacteria, or there's a colonization from the blood |
What is the gross appearance and light microscopy look like of an infarction on day one | minimal changes |
What is the appearance 2-4 days after an infarction (gross, microscope) | coagulative necrosis with rim of acute inflammation, hyperemia neutrophil infiltration and coagulative necrosis |
What is the appearance 4-7 days after an infarction (gross and microscopy) | Granulation tissue appearing around the edges of the infarction and central softening; thrombus in the artery is undergoing organization macrophages and neutrophils are showing active lysis of fibers |
What is the appearance of an infarction after 7-14 days (gross and microscopy) | granulation tissue strongly established; artery starting to recannalize and granulation tissue obvious |
What does an infarction area look like after 2-10 weeks (gross and microscopy) | formation of a fibrous scar; recannalized artery and formation of a fibrous scar |
T/F permanent tissues always get repair | T |
What is the leading cause of mortality and morbidity in the US | the results of abnormal blood flow |
Define shock | inability of the circulation to adequately perfuse the tissues so as to meet their metabolic demands |
T/F you always have a decrease in bp during shock | F, compensation may be able to maintain the bp |
What are the causes of shock | hypovolemic, vascular, cardiogenic, obstructive |
Define bleeding diathesis | abnormal coagulation, can't stop blood flow |
What do you loose a lot of after a burn | plasma, exudates |
What do you loose during neurogenic shock | sympathetic tone to muscles |
What type of shock is type 1 hypersensitivity | anaphylactic |
What is atrial myxoma | a benign tumor of the endothelium |
What two organs are irreversibly affected by shock | heart and brain |
What complications are associated with shock in the lungs | ischemia, hypoxemia, shock lung |
What complications are associated with shock in the kidney | acute tubular necrosis, anuria |
What complications are associated with shock in the heart | myocardial ischemia |
What complications are associated with shock in the brain | ischemia, confusion, coma |
What complications are associated with shock in the liver | centrizonal necrosis, abnormal function |
What complications are associated with shock in the intestines | ischemic necrosis, bacteremia, endotoxemia |
What percentage of young patients with hypovolemic shock survive | 80% |
What is the mortality rate of cardiogenic shock? | 75% |
What other factors determine the prognosis of shock | rapidity of appropriate care, presence/absence of other disease, pre-existing state of the patient |