FLuid and Edema
In sepsis , what are 4 ways the secreted TNF-a mediates septic shock
1) directs cytotoxicity 2) enhancing the adherence of PMN leukocytes; 3) stimulation of the release of interleukin I (IL-1), a cytokine that injures endothelial cells 4) promotes the expression of procoagulant tissue factor, thereby leading to thrombosis and local ischemia.
what are the 4 stages of shock
1)Early or compensated shock 2)Impaired tissue perfusion (leading to decompensation): 3)Decompensated but reversible shock 4)Irreversible shock
total body water is what percent of our body weight
50-60% of body weight
what four important factors contribute to the pathogenesis of edema
=> increased Venous pressure => increased Vessel wall permeability => decreased Oncotic pressure of plasma because of low albumin concentration => Obstruction of lymphatics
What 3 potential causes of thrombosis does Virchow's triad consists of
Blood coagulability vessel wall changes stasis
what neoplasia causes DIC
Carcinoma of pancreas, prostate, lung, and stomach Acute promyelocytic leukemia
how does right side heart failure cause edema
Congestion in liver, spleen, and lower limbs . Causes ascites to occur and edema in legs.
what is a consequence of thrombus formation in the heart walls and valves
Consequence of thrombus formation is that some can break away and travel (called embolism).
what is edema
Excess fluid in the interstitial spaces or body cavities.
what is the primary pathogenesis of shock
acute respiratory distress syndrome
what the 7 sites of infarction
brain retina heart spleen kidney small intestine lower leg
what are the 4 sources of arterial emboli that are outside the heart
carotid artery aortic artheroslcerosis aortic aneurysm iliac artery aneurysm
how does a catheter become a source for venous emboli
changes atmosphere in veins allows for emboli to form around cath
describe the irreversible stage of shock
circulatory collapse, marked hypofusion of vital organs, loss of vital functions.
what is Disseminated Intravascular Coagulation (DIC)
condition in which small blood clots develop throughout the bloodstream, blocking small blood vessels. The increased clotting depletes the platelets and clotting factors needed to control bleeding, which leads to excessive bleeding.
What is anasarca?
generalized edema
what bacteria usually causes endotoxic shock
gram -negative bacteria
what 5 infectious agents can cause DIC
gram negative sepsis meningococcemia Rocky Mountain spotted fever histoplasmosis aspergillosis malaria
where is the major place for thrombus formation
heart walls and valves
what 3 things can cause hypoperfusion of tissues
hemorrhage heart failure anaphylaxis
what are heart failure cells
hemosiderin + macrophages
what is the mechanism for oncotic edema
hypoproteinemia increased protein loss
In Virchow's triad , stasis refers to
immobility (more possibility of thrombus getting larger)
In Virchow's triad , blood coagulability refers to
increase in clotting factor
what are the 3 types of local edema
inflammatory obstructive allergic
what are ecchymoses
large hemorrhage (> 1 cm), subcutaneous hematomas
what are the 4 sources of arterial emboli that are within the heart
left atrium mitral valve aortic valve left ventricle
how are hemosiderins produced
left side heart failure causes lung congestion (passive hyperemia) ⬇️ leads to lung tissue changes ⬇️ RBC come out of circulation, breaks apart ⬇️ hemosiderin is released ⬇️ hemosiderin gets picked up by macrophage making a heart failure cell
what is the mechanism for allergic edema
local release of vasoactive substance ( histamine)
In Virchow's triad , changes in vessel wall refers to
loss of natural anti-thrombotic mechanism
what is the mechanism for obstructive edema
lymphatic obstruction venous obstruction
what is purpura? pupuras share pathologies with what else?
medium Hemorrhages (1 mm - 1 cm), similar pathologies as petechiae and trauma
in the hemostasis -coagulative cascade, what inhibits platelet activation and aggregation
prostacyclin is secreted by healthy vessels to inhibit platelet activation/ aggregation
what is the pathogenesis of a thrombus formation
prothrombin => thrombin ⬇️ fibrinogen => fibrin ⬇️ fibrin cover damaged endothelium ⬇️ endothelium activates factor 8 and clot formation occurs
how does general heart failure produce edema
reduced general circulation ⬇️ poor circulation to kidney ⬇️ lower using production ⬇️ activated renin/angiotensisn ⬇️ fluid retention
describe the decompensated but reversible shock stage of shock
reflex peripheral vasoconstriction fails progressive hypotension loss of consciousness
In sepsis caused by gram-negative bacterial, the lysis of the organisms releases what ?
releases endotoxin [LPS] into the circulation where it binds to LPS-binding protein (LBP).
what is the mechanism for hypervolemic edema? what is the cause of this edema?
retention of Na+ and H2O cause: too much aldosterone or kidney disease leading to too much renin released which causes sodium retention
What is petechiae? where are they found?
small hemorrhage (< 1 mm) on the skin, found on mucous membranes, serosal surfaces
as a result of infarction , where specifically is a classic sight for venous block
smooth muscle of intestine
what is shock a result of
systemic hypoperfusion of tissues with blood
formation of a thrombus is due to a defect in where
the endothelium
how do starling forces in the capillaries maintain the prevention of edema
there is pressure at the arterial end of a capillary for fluid to come out of the capillary ⬇️ at venous end , pressure by osmotic force due to proteins for fluid to enter the capillary ⬇️ net pressure will move fluidout into the intersticial fluid at the arterial end and on the venous end ⬇️ net fluid movement into venous end
when endothelial cells are injured what factor do they release and what does this factor do
they release Von Willebrand factor what it does: activates factor VIII and platelet adhesion to collagen
what is deep vein thrombosis
thrombus forms in large leg vein and some breaks off and can lodge in lung.
what is the function of thromboxane? what drug targets thromboxane?
vasoconstriction, promotes platelet aggregation drug: aspirin
what is the mechanism of inflammatory edema
vessel permeability + hyperemia
during drowning or heart failure , what is a typical place in the brain that is affected early due to hypo perfusion
watershed arteries. layers of the cortex start dying.
can liver disease and acute intravascular hemolysis cause DIC
yes
can shock cause DIC
yes
can snakebite cause DIC
yes
can tissue injury cause DIC
yes
What are transudates?
Non-inflammatory, protein poor, ultrafiltrate of plasma
can heat stroke , vasculitis , and aortic aneurysm cause DIC
YES
What is ascites? diseases in which organs can cause ascites
High swelling of the abdominal area is called ascites Ascites can be caused my liver, kidney, or heart disease
what is exudate? from where do they arise
Inflammatory, protein rich, where they arise : increased permeability of blood vessels
describe the impaired tissue perfusion stage of shock
Lactic acidosis cell necrosis, most apparent in the kidney, also shock lung (Adult respiratory distress syndrome -ARDS), liver, intestine leading to decompensation
what is a saddle embolism? what can it lead to ?
Large pulmonary embolism that straddles the bifurcation of the pulmonary trunk, lead to : shortness of breath , pain ,sudden death
how does left side heart failure cause edema
Left ventricle not working leads to pulmonary congestion( fluid backs up into the lungs) => Creates edema and a pleural effusion in lungs.
what 4 obstetric complications causes DIC
Septic abortion Retained dead fetus Toxemia Amniotic fluid embolism
what causes early or compensated shock stage? what are its associated symptoms
Stage 1: Compensatory mechanisms activated by decreased cardiac output: reflex sympathetic stimulation causing tachycardia (rapid thready pulse), vasoconstriction of peripheral arterioles (skin pale, cold and clammy) as blood pressure is maintained in vital organs), reduced urine output (oliguria, prerenal uremia)
in sepsis , The LPS-LBP complex binds to what ? what does this binding lead to
The LPS-LBP complex binds to CD14 on surfaces of monocytes/macrophages leads to : stimulated to secrete tumor necrosis factor a (TNF-a).
how does cirrhosis cause ascites
non-functioning liver can't produce albumin ⬇️ this makes osmotic pressure low. ⬇️ HTN in portal vein ⬇️ causes fluid to leak out into space between perinea.
what are the two types of generalized edema
oncotic hypervolemic
