Lecture 15 Flashcards
Arteries/arterioles
Conduct blood to tissues (away from heart) – maintain BP, lack elasticity so they use smooth muscle cells
Capillaries
Thin endothelium lines vessels that deliver nutrients/oxygen and remove waste products from cells
Veins
Return blood to heart under low pressure with assistance of one-way valves
Capillary hydrostatic pressure
Force pushing fluid from capillaries into extracellular space
Capillary permeability
Determines ease of fluid flow through capillary endothelium
Osmotic pressure
Water-attracting property of a solution; exerted by proteins in the blood (colloid osmotic pressure) that attract fluid from interstitial space back into the capillaries
Open lymphatic channels
Collect fluid forced out of the capillaries by the hydrostatic pressure and return fluid into circulation
Venous thrombosis
Normally, blood does not clot within the vascular system but can be precipitated by any number of conditions “Virchow’s triad” (slowing or stasis of blood flow, blood vessel wall damage, and increased coagulability of blood)
Thrombus
An intravascular clot; can occur in any vessel or within the heart
Arterial thrombi
Related to development of atherosclerosis, formation of lipid plaques causing narrowing and hardening of arteries.
Embolus/Embolism
Blood clots becoming detached and block downstream arterial circulation blocking blood flow
Phlebitis
Inflammation of vein (from stretching, or blockage)
Varices or varicosities (Varicose viens) + treatment
Excessive dilation and tortuosity (many twisting turns), Lack of prevention of retrograde blood flow, varicose veins result if saphenous (large subcutaneous, superficial leg) veins become dilated and valves become incompetent
Treatment: Stocking, limb elevation, surgical removal/ligation in serious cases.
Where can Varicose Viens be found?
Leg, lower rectum (hemorrhoids), scrotum (varicocele), esophageal varices
Predisposing factors to clot formation in leg veins…
Prolonged bed rest, extended period of inactivity, Cramped position for an extended period , Varicose veins or any condition preventing normal emptying of veins, Risk of clotting in post-op patients (increased clotting factors), confined to bed (stasis)
Presentation and treatment of Venous Thrombosis
Leg swelling/pain from partial blockage of venous return in leg, Risk of detachment and further injury causing pulmonary embolism, Treat with anticoagulants – fibrinolytics (tpa – tissue plasminogen activator) and elevate leg
Why does Varicose veins happen
Dilated tortuous veins, usually in the leg - resulting from poor blood return, Results from incompetent valves, runs in the family (genetic)
Pulmonary Embolism + symptoms
Embolus found in the pulmonary artery, manifestations depend on the size (larger the embolus the worse the outcome - immediate fatality), blood can find ways around the clot and the clot is dissolved
Symptoms: Cyanosis and shortness of breath due to inadequate oxygenation of blood
Large Pulmonary Emboli
Complete block of pulmonary artery, Pulmonary artery and right side of heart becomes overdistended (swollen) with blood, causing increased pulmonary pressure, Left ventricle unable to pump adequate blood to brain and vital organs, patient may go into shock
Small Pulmonary Emboli
Small emboli may pass through main pulmonary arteries, becoming impacted in peripheral arteries supplying the lower lobes of the lungs, necrosis can occur in the affected area, if no infarct - mild
Pulmonary Infarct symptoms
Dyspnea, chest pain, cough, and expectoration of bloody sputum due to leakage of blood from infarcted lung tissue into bronchi
Pulmonary Embolism Diagnosis
CTPA (most important test), D-dimer test, chest x-ray, ventilation/perfusion scan
Air Embolism
Large amount of air sucked into circulation from lung injury due to a chest wound, prevents filing of heart due to air in the right heart chambers, result: heart is unable to pump blood
Amniotic Fluid Embolism
Complication of pregnancy, Fetal cells, hair, fat, and amniotic debris fluid block maternal pulmonary capillaries, leads to disseminated intravascular coagulation syndrome (DIC)
Foreign Particulate Matter Embolism
Material injected intravenously and is trapped within small pulmonary blood vessels causing severe respiratory distress
Edema
Refers to accumulation of fluid in interstitial tissues, most often noted in ankles and legs from disturbances of extracellular fluid circulation between capillaries and interstitial tissues
Pitting edema
Extreme form of edema where a pit or indentation formed when edematous tissue is compressed with the fingertips
Ascites
Fluid accumulates in peritoneal cavity (common with liver failure)
Hydrothorax
Fluid accumulates in pleural cavity – most commonly from cardiac failure
Pathogenesis of Edema
Increased capillary permeability (increased swelling of tissues with acute inflammation), low plasma proteins (excess protein loss from liver or kidney disease, Inadequate synthesis), Increased hydrostatic pressure (heart failure, blood clot, inferior superior vena cava syndrome), Lymphatic obstruction
Acute Pulmonary Edema
Manifestation of acute heart failure, right heart pumps blood into lungs faster than left heart can deliver blood to peripheral tissues which engorges lungs with blood.
What happens when the lungs are engorged with blood?
Increased pulmonary capillary pressure, Leakage of fluid in alveoli, Shortness of breath from fluid accumulation in alveoli and impaired oxygenation
Circulatory Disturbances - Shock
Blood flow or blood pressure is too low to adequately supply body with blood and circulating blood volume is less than capacity of vascular system - potentially life threatening
Hypovolemic shock
Low blood volume (blood loss, severe burns, diarrhea, dehydration)
Cardiogenic shock
Reduced cardiac output (heart failure)
Septic shock
Excessive vasodilatation secondary to release of microbial toxins and inflammatory mediators
Anaphylactic shock
Excessive vasodilatation from release of inflammatory mediators
Shock prognosis + treatment
Prognosis depends on early recognition and rapid, appropriate treatment
Treatment: Drugs that promote vasoconstriction (Epinephrine), Intravenous fluids or blood to restore volume, treat underlying cause
Arterial Thrombosis
Injury to vessel wall from arteriosclerosis, causing ulceration, roughening of arterial wall with thrombi formation which blocks blood flow causing infarct
Infarct in Coronary artery
Myocardial infarction
Infarct in Major leg artery
Gangrene
Infarct in Cerebral artery
Stroke
Intracardiac Thrombosis
Clot formation within artria, on the surface of damaged heart valves, and wall of left ventricle; may dislodge into systemic circulation and cause infarction of major organs (Spleen, kidneys, brain, lung, etc.)
Thrombosis by Increased Coagulability (when does this happen?)
Rise in coagulation factors following surgery or injury, polycythemia, estrogen in contraceptive pills stimulate synthesis of clotting factors, hereditary gene mutation in clotting factors
Polycythemia
A rare blood cancer in which bone marrow produces too many red blood cells
Hereditary gene mutations in clotting factors
Mutation of gene that codes for factor V results in abnormal factor V (more resistant to inactivation, prolonged activity, increased coagulability) and Mutation of gene regulating prothrombin synthesis (risk for venous thrombosis increases as prothrombin level rises)
Why are cancer patients more susceptible to thrombosis
Increased platelets and coagulation factors due to the release of thromboplastic materials into circulation from tumor (both arterial and venous thromboses; DIC can occur from this)
Arteriosclerosis
Chronic and progressive degenerative disease of large to mid-sized arteries (thickening/ hardening due to aging)
Atherosclerosis
Narrowing of arteries from lipid deposits (buildup of fat / cholesterol) from bloodstream
Atheroma
Necrotic core rich in lipids with fibrous cap containing immune/inflammatory cells, smooth muscle cell and connective tissue
Atheromatous Deposits
Stable plaque surrounded by fibrous tissue which cause permanent narrowing of the vessel
Risk factors for blocked arteries
Elevated blood lipids (most significant), High BP, Smoking, Diabetes, and genetics (largest impact (40-60%))
Neutral fat
Triglyceride (three molecules of fatty acid combined with glycerol) from ingested fat, sugar, and carbohydrates
Trans fat and saturated fat
Atherogenic
Cholesterol
Synthesized in body and from diet
Low-density lipoprotein (LDL) vs. High-density lipoprotein (HDL)
Bad cholesterol and Good cholesterol; protective; increases with regular exercise, smoking cessation, modest alcohol intake
C-Reactive Protein (CRP, associated with inflammation)
Produced in the liver and released in response to inflammation (accumulation of macrophages, lymphocytes, lipids, and products of tissue injury) - High CRP level predicts high cardiovascular disease risk
Homocysteine
Sulfur-containing amino acid formed from methionine that is abundant in animal protein (high levels indicate early onset of severe atherosclerosis and risk of cardiovascular disease)
Diagnosis and Treatment of CAD
Diagnosis (Angiogram – to detect artery obstruction, Echocardiogram – to evaluate blood flow, structural abnormalities, and Stress tests – measure cardiac function (EEG))
Treatment: Lifestyle changes (diet, exercise, stress), Drugs: Anti-anginal drugs (nitroglycerin), anti-arrhythmic, statins (lower blood cholesterol), and Surgical: bypass, angioplasty
Hypertension
Increased sympathetic stimulation can cause excessive vasoconstriction of small arterioles resulting in increased peripheral resistance; increased diastolic blood pressure, Increased force of ventricular contraction, Compensatory increase in systolic pressure
Cardiac effects of hypertension:
Increased peripheral resistance → higher workload → heart enlarges → heart failure
Vascular effects of hypertension:
Increased pressure → premature wearing out of vessels; accelerates atherosclerosis; injury to arterioles → rupture and hemorrhage
Renal effects of hypertension:
Narrowed renal arterioles → decreased blood supply to kidneys → injury and degenerative changes in glomeruli and tubules → renal failure
Secondary hypertension
From a known disease (autoimmunity, chronic kidney disease, pituitary or adrenal tumor, hyperthyroidism)
Treatment for hypertension
Diuretics - to remove salt/water, ACE inhibitors – reduce angiotensin II (potent vasoconstrictor), Calcium channel blockers (inhibit contraction of arteriolar smooth muscle cells)
Isolated systolic hypertension
Mild to moderate rise in systolic pressure, but low or normal diastolic pressure (Increased rigidity of aorta with age,
Aneurysms
Dilatation or outpouching of a weakened portion of the arterial wall caused by arteriosclerosis
Arteriosclerotic aneurysm
Arteriosclerosis causes narrowing, thrombosis, and weakening of vessel wall
Aorta aneurysms
Most common in distal part of aorta; may rupture, leading to massive and fatal hemorrhage (Degenerative changes over time can cause layers of aorta to separate and blood is forced into the aortic wall)
