hemodynamics Flashcards
edema/effusions
-Normal: hydrostatic pressure pushes water and salts out of capillaries into interstitial space; nearly balanced by tendency of plasma colloid osmotic pressure to pull water and salts back into vessels
-!!!!Elevated hydrostatic pressure or diminished colloid osmotic pressure disrupts balance, resulting in increased movement of fluid out of vessels!
-If net rate of fluid movement > rate of lymphatic drainage, fluid accumulates!
-Within tissues result is edema!
-If a serosal surface is involved, fluid may accumulate within the adjacent body cavity as an effusion!
pathophysiologic categories of edema
-Increased hydrostatic pressure
-Impaired venous return (e.g., ascites (cirrhosis), congestive heart failure)
-Arteriolar dilation (e.g., heat)
-Reduced plasma osmotic pressure (hypoproteinemia): caused by decreased synthesis or increased loss of albumin from circulation
-Reduced albumin synthesis: severe liver diseases (cirrhosis), protein malnutrition
-Albumin loss: nephrotic syndrome - albumin leaks into urine through abnormally permeable glomerular capillaries
-Lymphatic obstruction: Trauma, fibrosis, invasive tumors, post-surgery, post-radiation and infectious agents - disrupt lymphatic vessels/impair clearance of interstitial fluid: resulting in lymphedema
-Sodium retention – Increased salt retention—with retention of associated water—causes both increased hydrostatic pressure (due to intravascular fluid volume expansion) and diminished vascular colloid osmotic pressure (due to dilution
-e.g., excessive salt intake with renal insufficiency, increased tubular reabsorption of sodium, renal hypoperfusion, increased renin-angiotensin-aldosterone secretion
-Inflammation
congestive HF
-INCREASED VENOUS PRESSURE DUE TO HEART FAILURE
-Decreased renal perfusion results in activation of renin-angiotensin-aldosterone axis (sodium retention)
-Early: beneficial (retention of sodium and water and other adaptations, including increased vascular tone and elevated levels of antidiuretic hormone): improve cardiac output and restores normal renal perfusion
-As heart failure worsens and cardiac output diminishes, retained fluid increases hydrostatic pressure, leading to edema and effusions
hepatic ascites
-PORTAL HTN
-HYPOALBUMINEMIA
-portal htn causes edema of organs and tissues within portal circulation- splenomegaly, hepatomegaly
-hypoalbuminemia may cause systemic edema
renal edema
-SODIUM RETENTION
-PROTEIN LOSING GLOMERULOPATHIES (NEPHROTIC SYNDROME)
EDEMA
-Subcutaneous edema: distribution influenced by gravity (e.g., appears in legs when standing and sacrum when recumbent), aka, dependent edema
-Finger pressure over markedly edematous subcutaneous tissue displaces interstitial fluid and leaves a depression, aka pitting edema
-Edema resulting from renal dysfunction often appears initially in parts of the body containing loose connective tissue (e.g., eyelids); periorbital edema is characteristic finding in severe renal disease
-With pulmonary edema, lungs often 2 – 3 X their normal weight; sectioning yields frothy, blood-tinged fluid— mixture of air, edema, and extravasated red cells (heart failure)
-Cerebral edema: localized or generalized; swollen brain shows narrowed sulci and distended gyri, compressed by skull – herniation may occur
-ANASARCA - general swelling of the whole body, can occur when tissues of the body retain too much fluid
brain herniation
1) Falx
2) Hippocampal cingulate gyrus
3) Cerebellar tonsillar
-dont need to know
effusions
-Effusions may involve:
-pleural cavity (hydrothorax)
-pericardial cavity (hydropericardium)
-peritoneal cavity ( hydroperitoneum or ascites)
-Transudative effusions: typically protein-poor, translucent, and straw colored
-Exudative effusions: protein-rich and often cloudy due to the presence of white cells
transudate vs exudate
-Transudate
-results from disturbance of Starling forces
-specific gravity < 1.012
-protein content < 3 g/dl, LDH LOW
-Exudate
-results from damage to the capillary wall
-specific gravity > 1.012
-protein content > 3 g/dl, LDH HIGH
edema review
-Edema: result of movement of fluid from vasculature into interstitial spaces; the fluid may be protein-poor (transudate) or protein-rich (exudate)
-Edema may be caused by:
-Increased hydrostatic pressure (e.g., heart failure)
-Decreased colloid osmotic pressure caused by reduced plasma albumin, either due to decreased synthesis (e.g., liver disease, protein malnutrition) or to increased loss (e.g., nephrotic syndrome)
-Increased vascular permeability (e.g., inflammation)
-Lymphatic obstruction (e.g., infection or neoplasia)
-Sodium and water retention (e.g., renal failure)
hyperemia vs congestion
-Hyperemia: active process - arteriolar dilation (e.g., at sites of inflammation or in skeletal muscle during exercise) leads to increased blood flow; affected tissues turn red (erythema) because of increased delivery of oxygenated blood
-Congestion: passive process - reduced venous outflow of blood from a tissue; may be systemic (e.g., cardiac failure), or localized
-Congested tissues: abnormal blue-red color (cyanosis) from accumulation of deoxygenated hemoglobin in affected area
-As a result of increased hydrostatic pressures, congestion commonly leads to edema
pulmonary edema
-pulmonary capillary pressure exceeds plasma colloid osmotic pressure
-Vessel borders become progressively hazier because of increasing extravasation of fluid into the interstitium.
heart failure
-Heart failure cells are hemosiderin laden macrophages (broken down blood)
-in the lungs
-Blood escapes into the alveolar space because chronic congestion causes the thin walled alveolar capillaries to burst.
acute/chronic passive congestion: liver
-nutmeg liver
-aka “NUTMEG” liver - associated with necrosis in the CENTRAL part of the hepatic lobule.
hemostasis
Physiologic blood clot at sites of vascular injury
-1. Arteriolar Vasoconstriction
-2. Primary Hemostasis (Platelet Plug) - adhesion, shape change, secretion of granules to induce aggregation, recruitment, aggregation
-3. Secondary Hemostasis (Coagulation Cascade)
-4. Clot Stabilization and Anti-Thrombotic Events
-Following a vascular injury:
-platelets adhere and aggregate to form primary hemostatic plug
-also promote key reactions in the coagulation cascade that lead to secondary hemostasis and formation of a fibrin clot
thrombosis
Pathologic blood !clot within blood vessels or within! chambers of the heart
hemorrhage
Excessive bleeding when hemostatic mechanisms are blunted, insufficient or defective
-EXTRAVASATION beyond vessel
-HEMATOMA (implies MASS effect)
-PETECHIAE (1-2 mm) (PLATELETS)
-PURPURA <1cm
-ECCHYMOSES >1cm (BRUISE)
-HEMO-: -thorax, -pericardium, -peritoneum, -arthrosis
petechiae vs purpura vs ecchymossi
-Petechiae: 1-2 mm minute hemorrhage (1°) -> platelets
-Purpura: ≥3mm hemorrhage
-Ecchymosis or bruise: ≥1cm hemorrhage (2°)
-bigger- worry about coagulation factors
-dont memorize size
hemostasis process: primary
-Involves platelets, clotting factors, and endothelium - at site of vascular injury; results in formation of a blood clot, to prevent/limit extent of bleeding
-Arteriolar vasoconstriction occurs immediately, greatly reduces blood flow to injured area - mediated by reflex neurogenic mechanisms; TRANSIENT
-Primary hemostasis: formation of the platelet plug
-!!Disruption of endothelium exposes subendothelial von Willebrand factor (vWF) and collagen, which promote platelet adherence and activation
-!!Activation of platelets results in dramatic shape change and release of secretory granules
-Within few minutes, secreted products recruit additional platelets that undergo aggregation to form a primary hemostatic plug !
hemostasis: secondary
-Secondary hemostasis: deposition of fibrin; consolidates/stabilize initial platelet plug
-Vascular injury exposes tissue factor at site of injury
-What is tissue factor? membrane-bound procoagulant glycoprotein
-!!Tissue factor binds and activates factor VII resulting in coagulation cascade leading to thrombin generation
-Thrombin cleaves circulating fibrinogen into insoluble fibrin, creating a fibrin meshwork;
-Clot stabilization and resorption: Polymerized fibrin and platelet aggregates undergo contraction: form a solid, permanent plug that prevents further hemorrhage
-To limit clotting to injury site and eventual clot resorption: counterregulatory mechanisms(e.g., tissue plasminogen activator [t-PA]
endothelium
-NORMALLY:
-ANTIPLETELET PROPERTIES
-ANTICOAGULANT PROPERTIES
-FIBRINOLYTIC PROPERTIES
-IN INJURY:
-PRO-COAGULANT PROPERTIES
-ACTIVATED by:
-Trauma
-INFECTIOUS AGENTS
-Hemodynamic forces
-Pro-inflammatory mediators
platelets
-After traumatic vascular injury, platelets encounter parts of the subendothelial connective tissue, such as vWF and collagen
-On contact with these proteins, platelets undergo sequence of reactions that end in the formation of a platelet plug
-you can have enough platelets but have quality of platelet issues
different disease (dont need to know)
-Gplb- no adhesion
-bernard soulier syndrome- no aggregation
platelets: sequence: platelet adhesion (she barely went over this)
-Platelet adhesion: mediated by interactions between platelet surface receptor glycoprotein Ib (GpIb) and vWF in the subendothelial matrix;
-!!!!!!!Genetic deficiencies of vWF (von Willebrand disease) or GpIb (Bernard-Soulier syndrome) result in bleeding disorders (dont need to know this until we learn about this disease)
-Platelets rapidly change shape after adhesion - from smooth discs to spiky cells with increased surface area
-Secretion (release reaction) of granule contents occurs with changes in shape; (together referred to as platelet activation)
