hemodynamic disorders/thromboembolic ds/shock Flashcards
starling forces
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
-Reduced albumin synthesis: severe liver diseases (cirrhosis), protein malnutrition
-Albumin loss: nephrotic syndrome
-Lymphatic obstruction: Trauma, fibrosis, invasive tumors, post-surgery, post-radiation and infectious agents
-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 -> RAAS
-increase hydrostatic/capillary pressure
hepatic ascites
-PORTAL HTN
-HYPOALBUMINEMIA
-decrease colloid osmotic pressure
-anasarca
renal edema
-SODIUM RETENTION
-PROTEIN LOSING GLOMERULOPATHIES (NEPHROTIC SYNDROME)
-sodium retention -> sodium/water retention
-nephrotic syndrome -> decrease colloid osmotic pressure
EDEMA
-Subcutaneous edema: gravity
-pitting edema
-renal dysfunction - loose connective tissue (e.g., eyelids) -> periorbital edema
-pulmonary edema- 2 – 3 X normal weight -> frothy, blood-tinged fluid— mixture of air, edema, and extravasated RBC (heart failure)
-HF
-Cerebral edema: localized or generalized; 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
transudate vs exudate
-Transudate
-results from disturbance of Starling forces
-protein content < 3 g/dl, LDH LOW
-Exudate
-results from damage to the capillary wall
-protein content > 3 g/dl, LDH HIGH
pulmonary edema
-pulmonary capillary pressure exceeds plasma colloid osmotic pressure
-HF
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.
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
summary
-PT and PTT are prolonged in liver failure
disseminated intravascular coagulation
-excessive activation of coagulation and formation of thrombi
-consumptive coagulopathy - platelets and factors are being consumed to make microthrombi
-tissue hypoxia and infarction caused by microthrombi
-hemorrhage- lack of factors and activation of fibrinolytic mechanisms
-2ndary- acquired from different conditions!!!!!
-MC associated with obstetric complications, malignant neoplasms, sepsis, and major trauma
-microangiopathic hemolytic anemia!!!!
-RBCs break up (become schistocytes) and burst when trying to get through all the clots -> anemia, thrombocytopenia
-Prolonged PT / PTT
virchow triad in thrombosis
-Endothelial integrity most important factor
-3 major risk factors for thrombosis: virchows
-1. Endothelial Injury
-Atherosclerosis / Hypercholesterolemia / Inflammation
-HTN / Vasculitis / Diabetes
-Toxins (Cigarette smoke) / Elevated Homocysteine
-2. Abnormal Blood Flow
-Stasis / Turbulence
-3. Hypercoagulable State
-Primary (genetic) or Secondary (acquired) disorders
-pregnancy, abnormal blood flow
hypercoagulability
-venous thrombosis - primary (genetic) and secondary (acquired) disorders
-Primary include:
-Factor V Leiden (common)
-Prothrombin gene mutation (common)
-Classically present with recurrent DVTs or DVT at young age (adolescence or early adulthood)
-Acquired
-Prolonged bed rest or immobilization
-MI
-Afib
-Tissue damage (surgery, fracture, burns)
-Cancer (TROUSSEAU syndrome, i.e., migratory thrombophlebitis)- mucin from some cancers trigger coagulation
-prosethetic cardiac valves
pathology of thrombosis
-antemortem clots- gross and microscopic lines of Zahn -> pale platelet and fibrin deposits alternating with darker red cell–rich layers
-postmortem clots- bland, non-laminated
-Postmortem clots - gelatinous with dark-red dependent portion (red cells settled by gravity) and yellow “chicken fat” upper portion
fate of thrombus
-Propagation- thrombi accumulate additional platelets and fibrin
-Embolization
-Dissolution: fibrinolysis
-Organization and recanalization:
-forms new vessels (holes) in the vessel for blood to flow there
pathology of thrombosis
-Venous thrombi - painful congestion and edema distal to obstruction, may embolize to lungs
-Arterial thrombi - infarctions
-Arterial or cardiac thrombi- occur at sites of turbulence or endothelial injury
-venous thrombi- occur at sites of stasis
-arterial systemic emboli- 80% cardiac origin, 20% aorta
arterial and cardiac thrombosis
-Atherosclerosis: major cause of arterial thromboses due to loss of endothelial integrity and abnormal blood flow
-Myocardial infarction can predispose to cardiac mural thrombi by causing dyskinetic myocardial contraction and endocardial injury
-Both cardiac and aortic mural thrombi prone to embolization to any tissue but especially brain, kidneys, and spleen
pulmonary embolism
-Originate from DVT (95%); MC thromboembolic disease
-go to right heart and “slam” into pulmonary vasculature; depending on embolus size can:
-occlude main pulmonary artery
-straddle pulmonary artery bifurcation (saddle embolus), or
-pass into smaller, branching arteries
-sudden death
-Most pulmonary emboli (60% to 80%) small and clinically silent
-obstruct 60% or more: sudden death, acute right heart failure (cor pulmonale), or cardiovascular collapse
-vascular rupture: pulmonary hemorrhage – NOT pulmonary infarction (2 supply)
-obstruction of small end-arteriolar pulmonary branches: often results in hemorrhage or infarction
-!Multiple emboli over time may cause pulmonary hypertension and right ventricular failure
infarction
-An area of necrosis secondary to decreased blood flow
-HEMORRHAGIC vs. ANEMIC
-RED (hemorrhagic) vs. WHITE (anemic)
-END ARTERIES vs. NO END ARTERIES
-ACUTE -> ORGANIZATION -> FIBROSIS
shock
-systemic tissue hypoperfusion from low CO and/or reduced circulation
-Major types of shock:
-cardiogenic (MI) - myocardial pump failure, ventricular arrhythmias, cardiac tamponade, outflow obstruction (pulmonary embolism)
-hypovolemic (e.g., blood loss)- low CO due to low blood volume (massive hemorrhage or fluid loss from severe burns, severe vomiting or diarrhea)
-septic (e.g., infections)
-gram negative
-Less common
-spinal cord injury ( neurogenic shock ), or an IgE-mediated hypersensitivity reaction (anaphylactic shock)
-acute vasodilation -> pooling -> hypotension -> hypoperfusion
-DIC
-Shock of any form can lead to inadequate tissue perfusion and hypoxic tissue injury; may be fatal
shock: clinical stages: irreversible stage
Irreversible stage: cellular and tissue injury so severe that even if hemodynamic defects are corrected, survival is not possible
-necrosis
-sepsis- giving antibiotics will release bacterial toxins
shock pathology
-MULTIPLE ORGAN FAILURE
-SUBENDOCARDIAL HEMORRHAGE
-ACUTE TUBULAR NECROSIS
-DAD (Diffuse Alveolar Damage, lung)
-GI MUCOSAL HEMORRHAGES
-LIVER NECROSIS
-DIC
