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FMS III - Week 2 ( Starred week 3 quiz)- Pathology Abnormal Blood Supply
Terms in this set (74)
What is the normal human body water distribution?
40 liters of water in total
15 sequestered in cells
12 sequestered in interstitial fluid (Edema occurs in the interstitial fluid or within body cavities.
3 sequestered in plasma
What is edema?
The consequence of increased formation of interstitial fluid
Within the capillary bed what determines the movement of fluid between vessels and interstitial tissue?
Hydrostatic and Oncotic Pressure
Arteriolar end of capillary bed
Has higher hydrostatic pressure than the venous end because at the venous end of the capillary bed we recognize that the hydrostatic pressure is opposed by oncotic pressure pulling fluid in. The excess amount of fluid is picked up by lymphatics.
Circumstances where edema will accumulate
1. Hydrostatic pressure increases
2. Oncotic pressure decreases
3. Lymphatic obstruction
4. Increased permeability associated with inflammation
Edema can be classified as
Local or Systemic
I - inflammation
A - allergic reaction
V - venous obstruction
L - lymphatic obstruction
This is caused by increased retention of total body sodium and water. The causes of systemic edema are:
1. Congestive Heart Failure
2. Renal Disease
A. Protein loss in the urine due to kidney disease
B. Decreased synthesis due to liver disease
C. Decreased protein intake due to malnutrition
A key characteristic of generalized edema is
Upright - ankles
Bed ridden - sacral
Severe edema throughout the entire body
Transudate vs Exudate
Transudate is non-inflammatory edema that is caused by an increase in hydrostatic pressure, decreased oncotic pressure, or lymphatic obstruction.
Exudate is a result of an inflammatory response and the increased vascular permeability.
Refers to the inflow of fluid into the tissue.
Active process in which arteriolar vasodilation will lead to an increased blood flow (e.g. inflammation or exercise).
Tissues will appear redder and warmer.
In inflammation, exudate will cause edema. In strenous exercise, the transudate will NOT cause edema unless the lymphatic drainage cannot drain due to the exceeding amount of transudate.
Decreased outflow of fluid from the tissue.
Tissues will appear cyanotic due to an increase in deoxygenated blood in the tissue, which may lead to hypoxia with resultant parenchymal cell necrosis.
Increased hydrostatic pressure may capillary rupture due to the fact that you have exceeding amounts of blood coming in, but cannot push it out.
Two forms of congestion
Acute Pulmonary Edema Characteristics
-Sudden left ventricular failure causes hydrostatic pressure increase, engorgement of capillary beds, transudate formation, capillary rupture.
Transudate will mix with plasma and RBC to produce a PINK edema that may suffocate the patient.
Chronic Pulmonary Edema Characteristics
Chronic is over time and as a result the hydrostatic pressure is less than the hydrostatic pressure of acute pulmonary edema.
Airspaces may contain numerous macrophages full of hemosiderin phagocytes from RBCs, we call these heart failure cells.
Acute Liver Congestion
Liver congestion will be secondary to shock or hepatic vein thrombosis.
Chronic Liver Congestion
Due to right ventricular failure.
Arrest of blood flow that most often refers to the specific process responsible for arresting bleeding or hemorrhange in a vessel.
Thrombosis is the counterpart of hemostasis.
What does hemostasis depend on?
Hemostasis depends upon
1. Endothelial cells that compose the vessel wall
3. Coagulation Factors
Endothelial vessel wall
Constitutively is a anti coagulant surface. However, when the endothelial cells are injured, it becomes a site of procoagulant activity.
Following injury, what are the sequence of events that result in hemostasis
1. Exposure to subendothelial collagen.
2. Platelet activation and binding forms the primary platelet plug.
3. Platelet aggregation.
4. Final two steps of the coagulation cascade involve prothrombin to thrombin, fibrinogen to fibrin. This forms the definitive platelet plug.
Three important pathways of hemostasis
Escape of RBC across intact vessels or vascular rupture. It does not refer to any specific volume of blood loss. If severe enough, may lead to shock or even jaundice due to the breakdown of RBC.
Abnormal localized collection of blood OUTSIDE the blood vessels, usually in liquid form within the tissue.
A bleeding disorder in which there is a problem with the body's blood clotting process.
Coagulopathy - clots too slowly
Thrombosis - clots too quickly
The hardening of arteries.
Response to injury and chronic inflammatory disease.
Tends to occur at vessel bifurcations and branch points where blood flow is more turbulent.
Two main causes of artherogenesis
Atherogenesis Proposed Sequence of Events
1. Endothelial injury to large and medium sized arteries. Tends to occur due to hyperlipidemia and hypertension. Occurs at vessel bifurcations where blood flow is more turbulent.
2. Retention of LDC and endothelial activation. During this stage a normally anti-thrombologic surface becomes more pro-thrombolgoic surface.
3. LDL oxidation.
4. Formation of foam cells and propagation of inflammatory response. Macrophages will internalize the oxidized LDL via scavenger receptors to become foam cells. This inflammatory response will continue throughout the course of this.
5. Endothelial dysfunction due to the persistence of insult and oxidized LDL. This makes the loss of regular homeostatic function. Endothelium can't relax because of decreased NOactivity.
Endothelial is reliant on NO for homeostatic and protective functions. Impairment of NO is Due to the increased of ROS.
Three types of thrombosis
Dysregulation between pro coagulation and anticoagulation mechanisms. Essentially it is equivalent to hemostasis, but in an abnormal location.
A solid mass formed from blood constituents within the vascular system.
Coagulation and Platelet
Attachment to endothelial vascular
Result of just coagulation
Not attached to underlying endothelium
Post Mortem clot
1. Endothelial injury
Principle factor for cardiac and arterial thrombosis. Exposure of highly thrombogenic sub endothelial ECM to the blood will lead to platelet adherence. and aggregation.
Changes in blood flow
Stasis or turbulent will disrupt laminar flow and increase the chance of contact between platelets and underlying the vessel wall. Stasiss is more of a factor in the formation of venous, while turbulence is more important in arterial.
Laminar blood flow
all cells and platelets will flow in the central of the vessel while the plasma will be in the periphery
Arises when any alteration occurs in hemostatic regulation that predisposes to thrombosis.
Patients with the mutation in antithrombin III gene can bleed out because of major inactivator of thrombin.
As a result of endothelial damage and turbulence.
Turbulence is increased as plaques are enlarged and progressive encroach upon lumen, reducing the vessel caliber and reducing blood flow.
Turbuelnce at the bifurcations.
Grows in retrograde motion.
Referred to as pale thrombi.
Cardiac and Aortic Thrombosis
Can result because of MI, left atrial dilation, valvular disease, and atrial fibrilliation.
Lines of Zahn indicates that thrombosis occurred at a site of blood flow SO IT IS NOT A POST MORTEM CLOT
Venous thrombi types
Superficial Venous Thrombi [thorombophlebitis]
Deep Vein Thombi [phelbothrombosis]
Occurs in the greater or lesser saphenous veins of the leg secondary to varicose vein formation as a result of trauma/infection.
Varicose veins are superficial leg veins that are not dependent on the milking action of the muscle.
Gravity dependent, if someone is standing you need more pressure in order to push blood to the heart.
A slight weakness in the venous wall in conjunction with the lack of milking would lead to thrombosis.
SVT does not form embolize because no milking action.
Primary concern in surgical patients due to having surgery and immobility.
Calf pain Homan Sign
Deep veins are milked, if a patient is bedridden the muscles are not active, no milking, and the stagnant blood has a higher chance of coagulating.
Can embolize. Anterograde motion
Usually called red thrombi
Fate of a Thrombi
Accumulation of more fibrin and platelets eventually leading to vessel
Conversion to a vascularized mass
Detachment and transport to a distant site of the vasculature
Develop many micro thrombi followed by hemorrhage. It will never occur as a disease in itself, but arises as a complication to some primary event that triggers generalized bleed clotting. The formation of these micro thrombi will use all the coagulation factors, which will cause the patient to bleed out.
Release of thromboplastin substances into the circulation
Widespread injury to endothelial cells
Anemia is very characteristics of DIC.
DIC is usually acute, but in cancer patients we will see a chronic .fom
Major Mechanisms of Disseminated Intravascular Coagulation
1. Endotoxin in blood causing infection, bacteremia.
2. Obsteric complication
3. Trauma/Necrotizing Tissue
4. Malignant Tumor
Detached solid, liquid, or gaseous mass that enters the circulation at one location and is carried until it causes a vascular occlusion.
Five Sources of Systemic Thromboemboli
1. Left Ventricular Wall * Most common
2. Left Atrial Wall
4. Ulcerated Thromboembolic
5. Aorti Aneurysm
Originate in the venous system, travel to the right side of the heart, but instead of making their way through the heart are carried through atiral or ventricle defect which allows a right to left heart pass.
Common destination of systemic emboli
What is the main cause of pulmonary emboli?
When the emboli is so large that it lodges in the pulmonary artery bifurcation and causes a sudden death.
Long bone fracture
Embolize to the lung
Main target is brain and skin
Necrot, lipid debris an atherosclerotic plaque may become an ambles following plaque rupture.
Happens during surgery of arteries.
Amniotic Fluid EMbolism
Labor because amniotic membrane rupture.
Air may evnter the circulation as a side effect of medical care.
it is important to recognize that there is negative pressure in the veins of the head, neck, and chest during inspiration in the upright position, allow them to draw in air, potentially causing a fatal embolus. Could fill the heart or lungs.
Special Gas Embolism
Divers lungs are pressurized to equalize the surrounding water depth to allow them to breathe. If a diver resurfaces too quickly, a rapid change in atmosphere pressure, the dissolved gasses that have saturated his tissues and blood come out of solution.
Gas bubbles cause endothelial damage and platelet aggregation.
Treatment is prompt recompression in a special chamber while breathing during oxygen .
A clinical state characterized by prolonged systemic hypo perfusion resulting from insufficient cardiac output or reduction in input circulating. The end result of hypo perfusion is tissue hypoxia and cellular dysfunction.
Shock is never a separate disease, but rather the manifestation of a serious underlying disorder.
Sufficiently large reduction of intravascular blood. Can be caused by hemorrhage, vomitting,, diarrhea, fluid loss, or plasma loss (burns)
Heart pump failure resulting in a severe compromise of cardiac output. Most usually associated with massive MI
Can occur because of pulmonary embolism
Generalized Vasodilation Shock
Severe allergic hypersensitive shock
brain, spinal cord
Stages of Shock
Stage of Compensation
Stage of impaired tissue perfusion
Stage of Decompensation
Stage of Compensation
Sympathetic including tachycardia, vasoconstriction, shallow breathing, cold, clammy, diminishing
Stage of Impaired Tissue Perfusion Progressive
Excessive vascoconstriction impairs tissue perfusion, resulting in hypoxia and impaired fluid exchange
Worsening of cardiac output
DIC might be initiated
vasodilation might begin
Stage of Decompensation
Complete loss of reflex vasoconstriction, kindney failure, cardiac output blood pressure drops to critical levels. cerebral hypoxia.