Haemodynamic Disorders Flashcards
1
Q
What is edema and how is it caused
A
- Increased interstitial fluid, local or generalised (anasarca, systemic causes)
- Increased vascular permeability and capillary hydrostatic pressure (venous obstructions, congestive heart failure, gravity)
- Decreased osmotic pressure (hypoproteinemia), lymphatic obstruction
2
Q
What is congestive heart failure (complication of edema)
A
- Heart weakens and pumps blood less effectively
- Humoral / neurohumoral mechanisms promote Na / H2O reabsorption by kidneys and expansion of extracellular fluid
- Abnormal Starling forces, increased venous capillary pressure and decreased plasma oncotic pressure
- Fluid builds up slowly (leg) or quickly (lungs)
- Treatment involves diuretics, vasodilators and angiotensin converting enzyme inhibitors
3
Q
What is a lymphatic obstruction (complication of edema)
A
- Elephantiasis
- Immune / circulatory system (infection / debris)
- Caused by filariasis (wuchereria bancrofti)
4
Q
What is a haemorrhage, location names and the types
A
- Loss of blood from the vessels by flow through ruptured walls (bleeding)
- Locations: Hemothorax (plural cavity), hemoperricardium (heart), hemoperitoneum (peritoneal cavity) or hemarthrosis (joint spaces)
- Types: Petechiae, purpura, ecchymoses and hematoma (classified by size)
- Treatment: Limit blood loss, platelet activation and vasoconstriction
5
Q
What are the different types of haemorrhages
A
- Petechiae: Minute defects in capillaries, abnormalities in platelets / bacterial sepsis, 1-2 mm
- Purpura: Skin or mucous membranes, plaque like lesions, result of vasculitis / abnormalities in platelets, hench-schonlein purpura (inflammation), > 2 mm
- Ecchymoses: Extravasations into tissue, purple / red discolouration, bleeding underneath skin, flat , > 1-2 cm
6
Q
What is a thrombosis
A
- A clot that develops and persists in an unbroken blood vessel
- Disruption of blood flow, clot adheres to vascular endothelium
7
Q
What is the virchow’s triad (pathogenesis for thrombosis)
A
- Endothelial Injury: Physical loss of endothelium (sub-endothelial ECM / clotting cascade) or endothelial dysfunction (atherosclerosis, trauma, surgery, toxins)
- Abnormal BF: Altered through stasis / turbulence, endothelium activated, laminar flow disrupted, altered platelet migration, reduces inflow of clotting inhibitors
- Hyper Coagulability: Alteration in coagulation pathways, primary (genetic, factor V / prothrombin mutation) or secondary (immobilisation, MI, age, obesity, pregnancy)
8
Q
What are the consequences of a thrombosis
A
- Resolution: Removal by fibrinolytic activity
- Organisation: Incorporation into a thickened vascular wall (scar)
- Recanalisation: Synthesis of new capillaries by intimal cells and fusion of capillaries to form larger vessels (scar remains)
- Embolisation: Dislodgement or fragmentation of thrombi and transportation to other sites in the vasculature (blockage and infarction)
- Propagation: Accumulation of additional platelets and fibrin (occlusion)
9
Q
What is an arterial thrombus
A
- Composed of platelet aggregates, begin at site of turbulence / endothelial injury
- Occlusive (cause downstream tissue infarction at critical sites)
- Can affect brain, kidneys and spleen
- 80% are intra-cardiac mural thrombi
- Caused by rupture of atherosclerotic plaque, vasculitis or trauma
- Exposure of procoagulant material such as lipid-rich macrophages (foam cells), collagen, tissue factor or endothelial breach
10
Q
What is a venous thrombus
A
- Composed of fibrin and RBC, associated with immobilisation and stasis (superficial / DVT)
- Superficial: Local congestion, swelling, pain and tenderness (rarely embolise)
- Deep: Risk of embolisation to the lungs (pulmonary embolus)
11
Q
What is an embolism
A
- Obstruction of a BV by an embolus (blood clot, fatty mass, air bubble, debris)
- Moves from sight of origin, detached intravascular mass
- Following occlusion, there is an initial inflammatory response
- Later the thrombus becomes organised by ingrowth of granulation tissue
- Eventually replacement of thrombus by fibrovascular granulation tissue
12
Q
What is ischaemia / infarction and the cause
A
- Ischaemia: Local decrease in blood supply to a tissue
- Infarction: Region of dead, deteriorating tissue resulting from occlusion of arterial supply or venous drainage
- Cause: Thrombosis or embolism, red (haermorrhagic infarction) or white (anaemic infarction - arterial occlusion in solid organs)
13
Q
What is shock and list the types
A
- Condition of profound hemodynamic and metabolic disturbance
- Characterised by failure of CVS to maintain adequate perfusion of vital organs (cardiovascular collapse)
- Life-threatening medical condition
- Types: Cardiogenic, hypovolemic, septic and anaphylactic
14
Q
What is cardiogenic shock
A
- Myocardial pump failure
- Decreased systolic cardiac function
- Caused by MI, ventricular arrhythmia, myocarditis, cardiac tamponade, edema in pericardium or pulmonary embolus
15
Q
What is hypovolemic shock
A
- Results from loss of blood or plasma volume
- Insufficient blood to fill circulatory system
- Caused by haemorrhage, fluid loss (severe burn / trauma)
- Widespread vasodilation / vascular permeability
