Fluids and Hemodynamics Flashcards
Exudates
Caused by inflammation (aka inflammatory edema) that results from increased permeability of post-capillary venules (due to separation of endothelial junctions), commonly caused by histamine secretion from mast cells
Transudates
Results from abnormalities involving Starling forces acting at the capillary level (noninflammatory edema)
Elevated capillary hydrostatic pressure, decreased plasma oncotic pressure, and decreased lymphatic drainage - promote transudate formation
What initially offsets factors favoring edema during chronic heart failure?
In CHF, increased lymphatic drainage initially offsets factors favoring edema, temporarily delaying edema development
Causes of lymphatic obstruction
Lymphatic network dysgenesis and malignancy
Can result in nonpitting edema
Congenital lymphedema
Due to lymphatic network dysgenesis - common w/ Turner syndrome
Turner Syndrome - characteristically associated with webbed neck, horeshoe kidney, and nail dyslasia
Where do most pulmonary emobli arise?
DVT of the lower extremities
Where do DVTs typically originate
Calf veins, but PE-causing DVTs are much more likely to originate in the large proximal femoral veins
What is a large thromboembolism called that is lodged in the right pulmonary artery?
Saddle PE
Cause of sudden death
Sonographic findings that suggest thrombus
Noncompressible vein
Visible hyperechoic mass
and/or absent or abnormal venous flow
What is the test of choice for dx’ing DVT?
Compression US
What Pt’s should be evaluated for inherited hypercoagulability?
Pt’s younger than 50 y/o who present with thrombosis and no obvious explanation for an acquired m prothrombotic state
Mutation of coagulation factor V
The Leiden mutation - most common inherited cause of hypercoagulable state
Resistance to degradation by activated protein C
Clinical manifestations of factor V Leiden
DVT (associated with PE)
Cerebral vein thrombosis
Recurrent pregnancy loss
Antiphospholipid syndrome
Secondary hypercoagulable disorder characterized by recurrent venous or arterial thrombi, repeated miscarriages, cardiac valvular vegetations (Libman-Sacks endocarditis), and thrombocytopenia
Characterized by formation of procoagulant antiphospholipid autoantibodies: anti-beta-2-glycoprotein antibodies, anticardiolilpin antibodies, and lupus anticoagulant
Lab findings: prolonged PTT w/ normal serum levels of anithrombin III, protein C, and protein S
Atheroembolic disease
Needle-shaped cholesterol clefts in affected vessels (cholesterol emboli) are diagnostic
Typically occurs after invasive vascular procedure (i.e. coronary angiography/aortic surgery), is most often associated with kidney injury.
Hemorrhagic necrosis of the lungs
Can appear due to PE from DVT
Fat embolism syndrome
Results from long-bone fracture
Acute-onset neurologic abnormalities, respiratory failure, and petechiae in a patient wiht a traumatic bone fracture
Sections of lung would reveal fat microglobules in pulmonary arteries
Amniotic fluid emboli
Are related to the rupture of uterine venous sinuses as a complication of childbirth (fetal squamous epithelial cells would be present in the blood vessels in lung of mom)
Bone marrow embolism
May be incidental finding due to CPR that fractures ribs or it may occur with fat embolism syndrome
White infarcts
Located in solid organs that lack a dual blood supply or collateral circulation such as the heart, spleen, and kidneys
Usually caused by arterial occlusion due to thrombosis or thromboembolism which may be seen with atrial fibrillation
Results in coagulative necrosis
Red infarcts
Hemorrhagic infarcts
Can occur in organs with a dual blood supply - such as the lung, or in organs with extensive collateral circulation (i.e. small intestines and the brain)
Also can occur in organs in which the venous outflow is obstructed (venous occlusion) - such as with torsion of the ovary or testis
Why are liver infarcts rare?
Becuase the liver has a dual blood supply: the portal vein and hepatic artery
Hyperemia
Refers to excess amounts of blood within an organ (grossly a red color)
Active hyperemia- increased arterial supply
Passive hyperemia - impaired venous drainage
Exmples of passive hyperemia
aka congestion - blue-red color grossly
Changes produced by CHF - chronic passive congestion of the lung or the liver
Lung - results from pulmonary hemorrhage (erythrocytes within alveoli) which can lead to hemoptysis and produce intra-alveolar, hemosiderin-ladien macrophages (heart failure cells)
Congestion in the liver is characterized by centrilobular congestion (congestion in acinar zone 3 of liver) which is seen grossly as a nutmeg appearance of the liver
Heart failure cells
intra-alveolar, hemosiderin-laden macrophages, called heart failure cells.
These are macrophages that have phagocytize the intra alveolar erythrocytes (note that the special stain for hemosiderin, which contains iron, is a Prussian blue stain).
Increased capillary hydrostatic pressure
Causes
May result from:
- Arteriolar dilation
- Hypervolemia
- Increased venous pressure
Hypervolemia
Downstream effect and potential cause
Increases hydrostatic pressure
May be caused by sodium retention (seen in renal disease)
What disease states increase venous hydrostatic pressure?
Can be seen in venous thrombosis, CHF (most common), or cirrhosis
Decreased plasma oncotic pressure
Results from decreased plasma albumin
May be caused by loss of albumin in the urine (seen with nephrotic syndrome) or by reduced synthesis (seen with chronic liver disease)
Lymphatic obstruction causes
Caused by:
- Tumors (usually lymphoma)
- Surgery (axillary node dissection after mastectomy)
- Microfilaria infection - Wuchereria bancrofti - parasite that can cause lymphatic filariasis (humans are definitive host - mosquitoes are intermediate host)
Elephantiasis
Caused by Muchereria bancrofti
causes lymphatic filariasis
Adult parasites live in lymphatics where they release microfilariae that enter bloodstreamand can be transferred into a mosquito where they mature into motile larvae. Mosquito bite can transfer these larve back to humans where they migrate to lymph nodes, pimarily in the legs and groin - maturing into adult worms
Obstruction of the lymphatics in these areas leads to massive swelling in the legs and genitals
Hydrothorax
Fluid in the thorax
Anasarca
Refers to extreme generalized edema involving the extracellular space in subcutaneous tissue, visceral organs, and body cavities
Ascites
Refers to clinically apparent accumulation of fluid in the peritoneal cavity (may be due to cirrhosis)
Mural thrombi
Associated with MIs and arrhythmias
Thrombi within the aorta
Associated with atherosclerosis or aneurysmal dilatations
Virchow’s triad
- Endothelial damage
- Abnormal blood flow
- Hypercoagulable states
Used to assess risk of thrombosis
Causes of endothelial damage
Atherosclerosis (and causes of atherosclerosis)
Vasculitis
Elevated levels of homocysteine
Primary hypercoagulable states
- Deficiencies of protein C or protein S
- Ledien mutation
- Deficiency of anithrombin III
Functions of proteins C and S
C - inactivate factor Va
S - inactivate factor VIIIa
Therefore deficiency is associated with overactivity of factors Va and VIIIa - increases thromboses
Warfarin
aka Coumadin
Inhibits the production of vitamin k-dependent coagulation factors and proteins C and S
Therefore initial Tx with warfarin may temporarily make clotting worse or precipitate skin necrosis
What binds and inactivates thrombin and factor X
Antithrombin III (ATIII)
Deficiency of ATIII increases thrombin and factor X - increases risk of thrombosis - PTT does not rise with standard heparin therapy
Anti-beta-2 glycoprotein antibodies
β2 glycoprotein, aka apolipoprotein H (apoH), is complex and includes regulating complement and coagulation.
β2 glycoprotein has both antithrombotic effects (anticoagulant and antiplatelet) and procoagulant effects. The balance between these opposing effects are dependent on
multiple factors.
Anti-β2 glycoprotein antibodies can increase the procoagulant effect of β2 glycoprotein, possibly by inhibiting the activation of protein C.
Note that the confirmatory test for the APS is the presence of these anti-β2 glycoprotein antibodies.
Anticardiolipin antibodies
Cardiolipin in an anionic phospholipid that is similar to platelet factor 4 on platelets. Antibodies against cardiolipin can bind to the surface of platelets and make them sticky, leading to clot formation
Lupus anticoagulant
Misnomer
Can artificially prolong PTT (prolonged PTT indicates a deficiency of one of the components of the intrinsic pathway - such as coagulation factor VIII)
Anti-phospholipid syndrome (APS) most commonly occurs secondary to what?
Lupus erythematosus
Individuals with APS may have false positive lab tests - i.e. a false positive for rapid plasma reagin (syphylis)
The pathogenesis of inflammatory edema (exudate) mainly involves increased permeability of post-capillary venules due to which one of the following?
C) Separation of endothelial junctions
Exudates are caused by inflammation (aka inflammatory edema) that results from increased permeability of post-capillary venules, due to separation of endothelial junctions, commonly caused by histamine secretion from mast cells.
Arterial occlusion in solid organs lacking a dual blood supply or collateral circulation, such as the heart, spleen, and kidneys, is most likely to produce what type of infarct?
C) White infarct
White infarcts are located in solid organs that lack a dual blood supply or collateral circulation, such as the heart, spleen, and kidneys.
