Term
| What is oncotic pressure? |
|
Definition
| pressure generated by osmosis |
|
|
Term
| What is hydrostatic pressure? |
|
Definition
| pressure of water, influenced by the pumping of the heart, elasticity of blood vessels & volume of blood within a vessel |
|
|
Term
| What are the values of hydrostatic & oncotic pressure in most normal tisues? |
|
Definition
|
|
Term
| In a normal capillary, which is higher, hydrostatic or oncotic pressure? |
|
Definition
| hydrostatic (pushing fluid out of vessels into tissues) |
|
|
Term
True or False
Hydrostatic & oncotic pressures have a significant effect on fluid exchange within the body |
|
Definition
false
Under normal conditions they should be near zero |
|
|
Term
| Where does fluid move out of the capillary? |
|
Definition
| at pores (junctions between endothelial cells) |
|
|
Term
|
Definition
| -small molecules (water, salts, organic molecules) which are able to pass out of the capillary & into the tissue |
|
|
Term
| How does the ultrafiltrate return to the capillary? |
|
Definition
-most of it is drawn back in by the oncotic pressure of the larger proteins remaining in the capillary
-remaining fluid & small molecules drain via the lymphatic systen into the blood stream |
|
|
Term
|
Definition
|
|
Term
| Is the edema of congestive heart failure localized or generalized? |
|
Definition
generalized
-fluid accumulates in body cavities such as the pleural space, pericardial sac, peritoneal cavity |
|
|
Term
|
Definition
| fluid accumulates in body cavities such as the pleural space, pericardial sac, peritoneal cavity |
|
|
Term
|
Definition
| effusion in the peritoneal cavity |
|
|
Term
|
Definition
| massive edema of the whole body |
|
|
Term
| A dog exhibits swelling in a leg below a joint. The leg is the same temperature as other limbs and extends to a firm mass at its upper limits. Heart & lung sounds are normal. What is going on? |
|
Definition
localized edema of the leg
-the mass is likely putting pressure on the capillary bed, so fluid can leave easily through the arterioles but not return at the venular end |
|
|
Term
| Why is venous drainage more likely to be obstructed by a mass than arterial supply? |
|
Definition
| veins are thinner walled than arteries |
|
|
Term
| Why might you not see much, if any, edema in some cases of venous obstruction? |
|
Definition
| if these is considerable collateral drainage, the fluid will simply find other routes |
|
|
Term
| What has more immediate edematous effects, a venous obstruction or lymphatic obstruction? |
|
Definition
|
|
Term
| Why is lymphatic obstruction slower in causing edema |
|
Definition
-at first only a small amount of fluid remains in the interstitium
-more accumulates over time
-small proteins accumulate over time, increasing colloid oncotic pressure, drawing more fluid into the interstitium |
|
|
Term
| What are the causes of localized edema? |
|
Definition
Venous obstruction
Lymphatic obstruction
Acute inflammation
Acute allergic reactions |
|
|
Term
| Why do acute inflammation & acute allergic reactions cause edema? |
|
Definition
-increase in capillary permeability
-allows fluid & proteins to move into the tissues more easily |
|
|
Term
| Why would a person with congestive heart failure show puffy swelling of the lower limbs? |
|
Definition
-the heart is unable to pump blood forward
-venous blood backs up in the systemic circulatory system
-generalized increase in hydrostatic pressure throughout the body increases fluid accumulation in the interstitium
-gravity pulls the fluid to the lower regions |
|
|
Term
| Where would fluid accumulate if the left ventricle is failing? Why? |
|
Definition
in the pulmonary alveoli (lungs)
-hydrostatic pressure of the pulmonary veins would increase, pushing fluid out |
|
|
Term
| What causes congestive heart failure? |
|
Definition
anything which reduces the contractility of the heart muscle, causes mechanical abnormalities or causes electrical disturbance
-reduces cardiac output |
|
|
Term
| What is difference with pulmonary circulation versus systemic circulation? |
|
Definition
| HP is normally lower than OP rather than the other way around |
|
|
Term
| What are the clinical effects of pulmonary venous congestion? |
|
Definition
Dyspnea (shortness of breath)
Coughing & wheezing |
|
|
Term
| Why does sodium & water retention in the body result from heart failure? |
|
Definition
the left ventricle cannot effectively push blood forward, so less glomerular filtration pressure in the kidney
-renin production increases, which causes aldosterone production, increasing sodium resorption |
|
|
Term
| What effect does aldosterone have on the body? |
|
Definition
-increased retention of salt & water in blood
-increased vascular hydrostatic pressure (greater blood volume)
-decreased vascular oncotic pressure (dilutes blood albumin, a large determinant of oncotic pressure) |
|
|
Term
| What effect does decreased hypoproteinemia have on oncotic/hydrostatic pressure? |
|
Definition
| it decreases plasma osmotic force |
|
|
Term
|
Definition
| low levels of protein in the blood, causing decreased plasma osmotic pressure |
|
|
Term
| Low levels of protein in the blood along with elevated levels of protein in the urine are indicative of... |
|
Definition
| a protein-losing disease resulting in hypoproteinemia |
|
|
Term
| How is fluid movement affected by hypoproteinemia? |
|
Definition
| It will flow out of capillaries normally (hydrostatic pressure is normal) but the plasma osmotic pressure will be too low to draw it back into the vasculature |
|
|
Term
| How is glomerular filtration affected by hypoproteinemia? |
|
Definition
-overall plasma volume will decrease, reducing glomerular filtration
-secretion of renin will increase leading to retention of Na/water by the kidneys |
|
|
Term
| What might cause hypoproteinemia? (3) |
|
Definition
low protein intake
insufficient albumin synthesis in the liver
increased loss of albumin into intestine/urine |
|
|
Term
| What are the characteristics of nephrotic protein-losing syndrome? |
|
Definition
-massive generalized edema
-hypoalbuminemia
-proteinuria
-hypercholesterolemia |
|
|
Term
| What is the major determinant of plasma osmotic pressure? |
|
Definition
|
|
Term
| Where is albumin synthesized? |
|
Definition
|
|
Term
| What are the clinical effects of edema? |
|
Definition
-effusion into body cavities, which can affect organ function (e.g. lungs, heart)
-cerebral edema (headache, herniation of brain, can be fatal) |
|
|
Term
| How would you treat cerebral edema? |
|
Definition
| osmotic agents & high doses of anti-inflammatory steroids to reduce the swelling and reduce brain damage |
|
|
Term
| _____ refers to the fluid part of the blood in which blood cells are suspended |
|
Definition
|
|
Term
| _____ is the fluid which remains after the blood has been allowed to clot in a tube |
|
Definition
|
|
Term
True or False
proteins are found in blood plasma |
|
Definition
|
|
Term
| What are the causes of systemic edema? |
|
Definition
increased hydrostatic pressure
decreased plasma oncotic pressure (hypoproteinemia)
sodium & water retention |
|
|
Term
| What are the causes of localized edema? |
|
Definition
increased hydrostatic pressure (venous obstruction)
lymphatic obstruction
inflammation |
|
|
Term
| What are 4 causes of injury to blood vessels which lead to rupture of the vessel wall? |
|
Definition
trauma
atherosclerosis
inflammation
neoplastic erosion of the vessel wall |
|
|
Term
|
Definition
| pinpoint, focal hemorrhages |
|
|
Term
|
Definition
| multiple oval or irregularly shaped hemorrhages |
|
|
Term
|
Definition
| large areas of hemorrhage e.g. bruises |
|
|
Term
| What is the term for hemorrhage into the eye? |
|
Definition
|
|
Term
| What factors contribute to the clinical significance of hemorrhage? |
|
Definition
volume of blood loss
rate of blood loss
site of hemorrhage
net loss of iron if hemorrhage is recurrent |
|
|
Term
|
Definition
| the arrest of bleeding caused by contraction of smooth muscle in the vessel wall |
|
|
Term
| Describe the sequence of events in normal hemostasis. On what do these processes depend? |
|
Definition
1. Transient arteriolar vasoconstriction
2. Formation of hemostatic plug
3. Secondary hemostasis
4. Formation of a permanent plug
-depend on the vascular wall, platelets & the coagulation cascade |
|
|
Term
| Describe transient arteriolar vasoconstriction |
|
Definition
-due to neurogenic reflex mechanisms
-augmented by endothelin (a vasoconstrictor)
-short lived effects |
|
|
Term
| Describe the process of primary hemostasis |
|
Definition
-platelets adhere to matrix, are activated via interactions with VWF
-secretory granules are released, recruit additional platelets
-hemostatic plug is formed |
|
|
Term
| Describe the process of secondary hemostasis |
|
Definition
-exposed tissue factor interacts with factor VII
-coagulation cascade culminates with thrombin generation
-thrombin cleaves fibrinogen into fibrin forming a mesh
-thrombin induces release of more platelets & granules |
|
|
Term
| Describe the process of forming a permanent plug |
|
Definition
-fibrin polymerizes, platelets form aggregates
-counter regulatory mechanisms limit the plug size to the site of the injury |
|
|
Term
| Describe the 3 antithrombotic properties of the endothelium |
|
Definition
Antiplatelet effects
Anticoagulant properties
Fibrinolytic properties |
|
|
Term
| What are the antiplatelet effects of the endothelium |
|
Definition
-prevents inactivated platelets from adhering to the endothelium
-prostacyclin & nitric oxide prevent activated platelets from adhering to un-injured endothelium |
|
|
Term
| What mediates the anticoagulant properties of the endothelium? |
|
Definition
| membrane associated heparin-like molecules & thrombomodulin |
|
|
Term
| What are the prothrombotic properties of the endothelium? (4) |
|
Definition
-synthesis of Von Willebrand Factor
-cyokines/bacterial endotoxin induce secretion of tissue factor
-can bind to activated coagulation factors to enhance their activities
-secretion of inhibitors of plasminogen activators |
|
|
Term
True Or False
Platelets have a nucleus |
|
Definition
|
|
Term
| What 3 reactions occur after platelets are exposed to the constituents of the extracellular matrix, after the endothelium of a blood vessel is injured? |
|
Definition
1. Platelet adhesion to ECM
2. Secretion/Release of Ca & more platelets
3. Aggregation |
|
|
Term
| What mediates platelet adhesion to the extracellulaar matrix? |
|
Definition
|
|
Term
| What happens during the secretion/release reaction? |
|
Definition
-Ca is released (imp for coagulation cascade)
-ADP mediates platelet aggregation & augments platelet releae
-platelets express a phospholipid complex on the surface (binding site for Ca & coagulation factors) |
|
|
Term
| What happens during aggregation? |
|
Definition
-ADP & thromboxane A stimulate aggregation
-coagulation cascade generates thrombin which binds to platelet surface to increase aggregation
-platelet contracts to form a secondary hemostatic plug |
|
|
Term
| What is the role of fibrinogen in hemostasis? |
|
Definition
| Is convertd to fibrin, which connects platelets together to form large aggregates |
|
|
Term
| What effect do prostaglandins have on platelete function? |
|
Definition
PGI2
-vasodilator, inhibits platelet aggregation
TXA2
-vasoconstrictor, activates platelet aggregation |
|
|
Term
| What are the two main functions of the coagulation cascade? |
|
Definition
Thrombin formation
-converts fibrinogen into fibrin monomers, key enzyme in regulation coagulation
Fibrin production
-monomers polymerize to form a gel which encases platelets in the 2ndary hemostatic plug |
|
|
Term
| What is the coagulation cascade? |
|
Definition
| series of enzymatic conversions converting inactive proenzymes into active ones, which in turn activate the next step |
|
|
Term
| What are the intrinsic & extrinsic pathways of coagulation |
|
Definition
Intrinsic: requires only exposure of Factor XII to a thrombogenic surface
Extrinsic: need an exogenous trigger such as exposure of tissue factor at an injury site |
|
|
Term
| What other factors are required to optimize coagulation? |
|
Definition
Calcium ions
Phospholipid surface
Vitamin K (needed for prothrombin synthesis) |
|
|
Term
| What is the role of plasminogen in clot formation? |
|
Definition
| it is incorporated into the developing clot and will be activated to plasmin (fibrinolysin) which breaks down fibrin & interferes with polymerization |
|
|
Term
True or False
Â
Fibrin breakdown products can act as coagulants |
|
Definition
| False they are weak anticoagulants |
|
|
Term
| Why is fibrinolysis important in clot formation? |
|
Definition
| prevents the clot from becoming overly large & interfering with blood flow |
|
|
Term
| What types of coagulation disorders would interfere with hemostasis? (3) |
|
Definition
Hemophilia A
-deficiency in factor VIII due to poor synthesis of factor VIII subunit
Von Willebrand's Disease
-low levels of von Willebrand factor & complete deficiency of factor VIII
-impairs ability o platelets to function AND adhere to vessel walls
Increased anticoagulant activity |
|
|
Term
| What types of platelet disorders would interfere with hemostasis? |
|
Definition
Thrombocytopenia
-low levels of platelets
-deficient production, abnormal distribution or increased destruction
Abnormalities of platelet function
-platelet counts are normal but signs of plately disorders are still present |
|
|
Term
| How would you detect thrombocytopenia? |
|
Definition
| doing a complete blood count (CBC) |
|
|
Term
| If a patient has a tendency to bleed excessively they're likely have.... |
|
Definition
| a coagulation disorder such as Hemophilia A or Von Willebrand's disease |
|
|
Term
| If a patient has several small bleeds they likely have... |
|
Definition
|
|
Term
|
Definition
|
|
Term
| Describe the morphology of a thrombus |
|
Definition
-can form anywhere in the CV system
-clot attached to the underlying vascular surface
-prone to fragmentation, may propagate towards the heart |
|
|
Term
| What is the difference between arterial thrombi & venous thrombi? |
|
Definition
Arterial
-distinct lines of Zahn
-superimposed on ruptured atherosclerotic plaque
Veneous
-have more meshed RBC because venous system flows slowly
-gray fibrin strands |
|
|
Term
| How can you differentiate a thrombus from a post-mortem clot? |
|
Definition
-thrombi are firm, attached, contain grey sections of fibrin
-post mortem clots are gelatinous, dark red, not attached to the underlying wall |
|
|
Term
|
Definition
The 3 basic causes of thrombosis
-endothelial injury
-stasis/turbulent blood flow
-hypercoagulability |
|
|
Term
|
Definition
-raised lesions consisting of lipid core with a fibrous cap
-typically involves large arteries |
|
|
Term
| Why is atherosclerosis clinically significant? |
|
Definition
-affects arteries supplying heart, brain kidneys & lower extremities
-compromises blood flow in smaller arteries
-can lead to thrombus formation (obstructs blood flow)
-can lead to aneurysm formation
-can lead to embolism |
|
|
Term
|
Definition
| blood in the central column of the vessel moves quickly while blood adjacent to the endothelium moves more slowly |
|
|
Term
| What might alter the laminar flow of blood? |
|
Definition
Turbulence
-fast, erratic flow
Stasis/Sludging
-slower flow due to loss of pressure, downstream obstruction, hyperviscosity etc |
|
|
Term
| Why does turbulence contribute to thrombosis? Where is it more likely to be an issue? |
|
Definition
-creates pockets of stasis
-more common in veins as this system flows slightly more slowly |
|
|
Term
| How do turbulence & stasis favour thrombosis? (4) |
|
Definition
-disrupt laminar flow so platelets contact the endothelium
-less fresh flowing blood to dilute activated clotting factors
-slows incoming clotting factor inhibitors
-promotes endothelial cell acivation |
|
|
Term
| What is polychythemia? What are the two types? |
|
Definition
an increase in RBC numbers (increases viscosity)
Primary: more proliferation of myelin stem cells
Secondary: increased erythropoeitin levels (causes RBC proliferation) |
|
|
Term
True or False
Polychythemia can occur 'appropriately' |
|
Definition
true
-when blood oxygenation is deficient e.g. living at high altitudes |
|
|
Term
| What is hypercoagulability? |
|
Definition
| changes in the balance between clotting & fibrinolytic mechanisms so that thrombosis is favoured |
|
|
Term
| What is most likely to cause thrombosis in arteries? |
|
Definition
|
|
Term
| What genetic factors are likely to cause hypercoagulability? |
|
Definition
| mutations in factor V or prothrombin |
|
|
Term
| What are the 4 possible outcomes to thrombosis? |
|
Definition
Propagation: platelets & fibrin continue to accumulate until the vessel is obstructed
Embolization: fragments/dislodges
Dissolution: fibrinolysis to remove the thrombis
Organization & Recanalization: inflammation & fibrosis will be induced to re-establish some degree of flow or incorporate the thrombus into a thickened vessel wall |
|
|
Term
| What is the difference between ischemia and infarction? |
|
Definition
ischemia: a reduction or failure in blood supply to tissue
infarction: a localized area of necrotic tissue due to ischemia (lack of blood supply)
Ischemia can lead to an infarct |
|
|
Term
| What is another term for an infarct? |
|
Definition
|
|
Term
|
Definition
|
|
Term
| What are some of the effects of ischemia? |
|
Definition
hypoxia
functional changes in tissues
gradual death of specialized cells
pain (especially in skeletal & cardiac muscle)
infarction |
|
|
Term
| Why might ischemia in the brain cause a failure of recent memory? |
|
Definition
| loss of the cortical neurons as a result of restricted blood supply |
|
|
Term
| What is a myocardial infarction? |
|
Definition
| when an area of the myocardium is deprived of blood due to blockage of a coronary artery |
|
|
Term
| What is the 'critical level' in the degree of occlusion of a coronary artery? Why? |
|
Definition
75% narrowing or greater
-the artery cannot meet even slightly increased demands for myocardial oxygen
-myocardial infarction will occur |
|
|
Term
| what causes most acute myocardial infarctions? |
|
Definition
| coronary artery thrombosis |
|
|
Term
| What typically causes the initiating event of coronary artery thrombosis? |
|
Definition
Disruption of a plaque due to
-rupture/fissure/ulceration of plaques, exposing thrombogenic plaque constituents
-hemorrhage into the core of plaques |
|
|
Term
| What factors influence the tissue changes resulting from arterial obstruction? |
|
Definition
1. availability of collateral circulation
2. integrity of collateral arteries
3. tissue susceptibility to ischemia
4. tissue metabolic rate
5. rate of development of the obstruction |
|
|
Term
| What is collateral circulation? |
|
Definition
| the presence/development of alternate pathways of blood flow |
|
|
Term
| What tissues are highly susceptible to ischemia? |
|
Definition
|
|
Term
| Why does the rate of development of the obstruction influence the tissue changes resulting from arterial obstruction? |
|
Definition
| a sudden obstruction produces more severe changes because there is less time for enlargement of potential collateral vessels |
|
|
Term
| How would you describe the heart sounds in an individual affected by heart failure? |
|
Definition
rapid heart rate
irregular 'galloping' beat
muffled sound (due to fluid in chest) |
|
|
Term
| What does idiopathic mean? |
|
Definition
| a disease of unknown cause |
|
|
Term
| What is the most common characterization of feline cardiomyopathy? |
|
Definition
| hypertrophy of left ventricular muscle (thickening of the ventricular wall) |
|
|
Term
| What would be the initial appearance of an arterial infarct in the heart or kidney? |
|
Definition
-these are dense tissues, lack significant collateral circulation
-the blood supply is cut off, but venous drainage is still intact
-the infarct will be pale |
|
|
Term
| What would be the initial appearance of an arterial infarct in the lung or liver? |
|
Definition
-these tissues have a double blood supply or collateral blood supply
-some blood continues to flow
-hemorrhage will occur from necrotic small vessels
-infarct will appear hemorrhagic |
|
|
Term
| Why would a developing tumour be more likely to obstruct a vein than an artery? |
|
Definition
|
|
Term
| What happens in regards to ischemia/infarction due to venous obstruction? |
|
Definition
-hydrostatic pressure increases, causing fluid to remain in interstitium
-congestion of local venous capillary congestion
-hypoxia
-endothelial injury due to hypoxia
-capillary permeability increases
-hemorrhage |
|
|
Term
| Why does hypoxia result from a venous obstruction? |
|
Definition
| the deoxygenated blood cannot leave the area |
|
|
Term
| What is a venous infarct also referred to as? |
|
Definition
| a hemorrhagic or red infarct |
|
|
Term
| What is more likely to cause significant clinical problems, an arterial or venous obstruction? Why? |
|
Definition
arterial
-the venous system has better availability of collateral vessels |
|
|
Term
| What is testicular torsion? |
|
Definition
| twisting of the testicle, obstructing venous drainage, leading to edema & hemorrhagic infarction |
|
|
Term
|
Definition
| abnormally rapid heart rate |
|
|
Term
|
Definition
| abnormally rapid breathing |
|
|
Term
| What is reperfusion injury? |
|
Definition
| exacerbated/accelerated injury resulting from the restoration of blood flow to an ischemic area |
|
|
Term
| What two processes mediate reperfusion injury? |
|
Definition
-increased production of ROS due to mitochondrial damage, leads to accumulation of free radicals, OXIDATIVE STRESS
-INFLAMMATION increasing due to inflow of leukocytes and plasma proteins, activation of some leukocytes and exacerbation of the injury |
|
|
Term
| Why is shock likely to precipitate after restoration of blood flow to an obstructed area? |
|
Definition
-inflammatory mediators & toxic byproduct cannot leave due to lack of venous drainage, so they accumulate
-restoration of blood supply releases these into the blood stream all at once, may cause shock |
|
|
Term
|
Definition
| free floating intravascular mass carried from the site of origin to another area in the body through the bloodstream |
|
|
Term
| What is the most common origin of emboli? |
|
Definition
|
|
Term
| Are emboli more likely to affect arteries or veins, and why? |
|
Definition
arteries, as they narrow as they reach capillary beds
(veins become more broad as you flow downstream) |
|
|
Term
| Where is an embolus originating in a vein likely to become lodged? |
|
Definition
In the pulmonary vasculature
-pulmonary artery
-across the bifurcation
-in smaller branched arterioles |
|
|
Term
Where is an embolus originating from a thrombus on the left AV valvu
e likely to embolize? |
|
Definition
| in the arterial circulation |
|
|
Term
| What are the sources of systemic thromboembolism? |
|
Definition
-thrombi in left AV valve, left ventricle, left atria
-aortic aneurisms
-thrombi on ulcerated atherosclerotic plaques
-fragmentation of valvular vegetations |
|
|
Term
| Give an example of possible situations causing fat embolism, air embolism and amniotic fluid embolism |
|
Definition
Fat embolism: severe mechanical injury (long bones, tissue trauma)
Air embolism: scuba diving (decompression sickness)
Amniotic fluid embolism: labour/postpartum complication due to a tear in placental membranes or uterine vein rupture |
|
|
Term
| What organs have a dual blood supply? |
|
Definition
|
|
Term
| What is disseminated cardiovascular coagulation? |
|
Definition
| a thrombohemorrhagic disorder which arises due to activation of systemic coagulation, leading to widespread thrombosis throughout the body |
|
|
Term
| What are some of the disorders/diseases that can lead to DIC? |
|
Definition
Obstetric complications (septic abortion, toxemia)
Infections (sepsis, malaria)
Neoplasms (carcinoma of pancreas)
Massive tissue injury (burns, extensive surgery) |
|
|
Term
| What are the triggers for DIC? |
|
Definition
-release of tissue factor or other thromboplastic substances into circulation
-widespread injury to endothelial cells |
|
|
Term
| Why is DIC often called a consumption coagulopathy? |
|
Definition
| -clotting leads to consumption of clotting factors & platelets, eventually leading to generalized hemorrhage |
|
|
Term
| What effect of DIC is exacerbated by the fibrinolytic system, and why? |
|
Definition
| bleeding, because products of fibrin breakdown have anticoagulant properties |
|
|
Term
| What are the possible consequences of the obstruction of the microcirculation by microthrombi in DIC? |
|
Definition
-impaired delivery of blood to the tissue
-leads to hypoxia, shock and microinfarction |
|
|
Term
| What changes are looked for in the diagnosis of DIC? |
|
Definition
-damaged RBC's (due to passing through fibrin strands of microthrombi)
-thrombocytopenia
-increased concentration of fibrin breakdown products in plasma
-prolongation of PT & PTT due to depletion of platelets & clotting factors
-petichae or ecchymoses on skin |
|
|
Term
| What consequences does the cycle of thrombus formation and fibrinolysis lead to? |
|
Definition
-widespread fibrin deposition in microcirculation (leads to ischemia and hemolysis)
-bleeding diathesis due to depletion of platelets and clotting factors |
|
|
Term
| What is thrombocytopenia? |
|
Definition
| -spontaneous / prolonged bleeding due to abnormally low number of platelets in the blood |
|
|
Term
| What is the main goal of DIC therapy? |
|
Definition
identify the underlying cause
stop the cycle of thrombosis and fibrinolysis |
|
|
Term
|
Definition
| a physiological state characterized by a reduction in blood flow to tissues, due to either ineffective cardiac output or ineffective circulating blood volume |
|
|
Term
| What are the three causes of shock? |
|
Definition
1. Hypovolemia (decreased blood volume)
2. Peripheral vasodilation
3. Cardiogenic shock |
|
|
Term
|
Definition
shock associated with hemorrhage or fluid loss, leading to decreased plasma volume
e.g. due to vomiting, dehydration |
|
|
Term
| What is peripheral vasodilation? |
|
Definition
shock associated with anaphylaxis, neurogenic & septic shock
due to increased capacity of vascular bed, decreasing the hydrostatic pressure, leading to tissue hypoperfusion |
|
|
Term
| What is cardiogenic shock? |
|
Definition
| -failure of the heart to function effectively as a pump leading to reduction of blood supply to tissues |
|
|
Term
| What mechanisms are active during the nonprogressive phase of shock? |
|
Definition
-increase in hear rate (tachycardia)
-peripheral vasoconstriction to maintain blood pressure in vital organs only
-constriction in renal arteries to decrease glomerular filtration
-fluid retention of the kidneys, reduced urine output (conserve fluid!) |
|
|
Term
| What happens if the mechanisms active during nonprogressive shock are ineffective in maintaining cardiac output and blood pressure? |
|
Definition
| widespread tissue hypoxia develops |
|
|
Term
| Widespread tissue hypoxia leads to: |
|
Definition
excessive production of lactic acid due to a switch to anaerobic metabolism
lactic acidosis! |
|
|
Term
| Lactic acidosis resulting from widespread tissue hypoxia causes: |
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Definition
-reduction in tissue pH
-arteriolar dilation
-pooling of blood in microcirculation |
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Term
| What are the effects of prolonged vasoconstriction? |
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Definition
-worsening myocardial contractile function
-ischemic injury to kidneys
-renal tubular necrosis, renal failure
-edema & hemorrhage in the lung
-ischemic necrosis of the intestine leading to endotoxic shock
-DIC |
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Term
| What is actute respiratory distress syndrome> |
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Definition
| edema & hemorrhage in the lung resulting from hypoxic damage to the lung |
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