#5 disorders of circulation Flashcards
Hyperemia
occurs due to dilation of an artery or arteriole and increased blood flow into the capillaries. Caused by sympathetic neurogenic discharge or chemical mediators. examples- acute inflammation, blushing, body’s need to dissipate heat. the skin appears red (oxygenated blood)
congestion
passive hyperemia. occurs due to impaired venous drainage, lack of blood flow. Can be systemic or isolated. examples- congestive heart failure, poor venous drainages (blue/red deoxygenated blood)
edema
accumulation of abnormal amounts of fluid in interstitial spaces or body cavities
non-inflammatory edema
fluid accumulates due to changes in hydrostatic pressure and colloid osmotic pressure. Transudate
inflammatory edema
tissue injury alters blood flow and vascular permeability as a result of increased inter-endothelial space. modulated by chemical mediators. Exudate
hemostasis
maintains blood as a liquid and prevents uncontrolled bleeding
hematoma
hemorrhage that is contained within a tissue
hemathorax
bleeding into the space between the chest wall and the lung (the pleural cavity)
hemopericardium
bleeding into the pericardial sac of the heart
hemoperitoneum
bleeding into the peritoneal cavity. The blood accumulates in the space between the inner lining of the abdominal wall and the internal abdominal organs.
hemarthrosis
bleeding into joint spaces
petechiae
a small red or purple spot caused by bleeding into the skin, mucous membranes or serosal surfaces. Caused by low platelet counts, defective platelet function and low of vascular wall support (vit C deficiency)
purpura
slightly larger than petechiae, result from the same things as petechiae plus trauma, vascular inflammation, and increased vascular fragility
ecchymosis
larger than purpura (1-2 cm) subcutaneous hematomas (bruises). Extravasated red cells are phagocytosed and degraded by macrophages. Color changes due to enzymatic conversion of hemoglobin to bilirubin and hemosiderin.
thrombosis
formation of a blood clot within an uninterrupted vascular system- always pathologic
3 mechanisms for thombrosis
- endothelial injury (inflammation, advanced atherosclerosis)
- Altered blood flow (turbulence vs. stasis) (atrial fibrillation, bed rest)
- hypercoagulable state (protein C deficiency, women on BC and smoking)
embolism
intravascular substance (solid, liquid, gas) which is carried by blood from a point of origin to a distant site
types of embolisms
Fragments of thrombi (thromboembolism)
Atherosclerotic
Amniotic fluid
Air (gas) (can occur during surgery or decompression sickness)
Fat (during trauma fat from bone marrow enters circulation)
Infarction
and area of ischemic necrosis within a tissue or an organ. produced by occlusion of either its arterial supply or venous drainage. usually associated with thromboembolism and involved arterial occlusion.
types of infarct
- white: ischemic usually arterial occlusion
2. red (hemorrhagic), usually venous occlusion
what determines the outcome of a thrombus
- degree of occlusion
- size and location of the blood vessel
- collateral circulation
shock
systematic hypo perfusion of tissue. Caused by either diminished CO or reduced effective circulating blood volume
3 most common types of shock
- cardiogenic - low CO due to myocardial pump failure
- hypovolemic- low CO due to loss of blood or plasma volume
- septic shock - arteriolar vasodilation and venous blood pooling from a systemic immune response to microbial infection
Causes of edema
- Increased hydrostatic pressure (Systemic: Heart failure
Local: impaired venous return post deep venous thrombosis) - Decrease colloid osmotic pressure, due to reduced plasma albumin (Decreased synthesis (liver disease, malnutrition). Increased loss (nephrotic syndrome) )
- Lymphatic obstruction (Neoplasm)
- Increased vascular permeability (Inflammation)
- Sodium Retention (Renal failure)
Virchow’s triad in thrombosis
Balance between endothelial integrity, abnormal blood flow and hypercoaguablity.
Endothelial integrity is the most important factor.
Abnormalities of procoagulants or anticoagulants can tip the balance in favor of
thrombosis. Abnormal blood flow (stasis or turbulence) can lead to hypercoagulability
directly and also indirectly through endothelial dysfunction.
Fate of a Venous Thrombus
- resolution
- embolism to lung
- organized and recanalized (restores some blood flow, may be incorporated into the wall)
- propagation toward the heart
White (pale) infarct
Solid organ with end-arterial circulation
Heart, liver, spleen, kidney
Red infarct
Venous occlusions (Ovarian torsion) Tissues with dual circulations (Lung, small intestine) Loose tissues (Lung) When flow re-established after infarction (S/p angioplasty of arterial obstruction)
