Blood and Hemodynamic Disorders Flashcards
What are the types of haemodynamic disorders?
- Edema
- Hemorrhage
- Thrombosis
- Embolism
- Ischemia + Infarction
- Shock
- Parasites
- Abnormalities in erythrocytes
- Abnormalities in platelets
- Abnormalities in cell counts
What are the mechanisms of edema?
- Increased vascular permeability
- Increased capillary hydrostatic pressure
- Venous obstructions
- Congestive Heart Failure
- Gravity
- Decreased Osmotic pressure
- Hypoproteinemia
- Lymphatic obstruction
Describe edema in congestive heart failure
- Heartweakens and pumps blood less effectively
- Humoral/neurohumoral mechanisms promote sodium and water reabsorption by the kidneys and expansion of the extracellular fluid
- Abnormal Starling forces
- increased venous capillary pressure
- decreased plasma oncotic pressure
- fluid can slowly build up, creating legedema
- If fluid builds up quickly - fluid in the lungs
Treatment: Diuretics, vasodilators, angiotensin converting enzyme inhibitors
What is hemorrhage and the different types?
Hemorrhage = blood loss:
Clinical manifestation
- Acute hemorrhage of > 20 % blood volume (~ 1 L)
- Chronic blood loss e.g. peptic ulcer, menstrual bleeding
- Brain hemorrhage
External (eg. nosebleed) or Internal:
Hemorrhages in body cavity
- e.g. hemothorax, hemopericardium, hemoperitoneum or hemarthrosis
Hemorrhages in tissue:
- e.g. petechiae, purpura & ecchymoses, hematoma
Describe hemorrhages in body cavities
Hemorrhage in body cavity
= Hemarthrosis
- Bleeding into joint spaces
- Can be caused
- by injury
- Haemophilia A
What are the types of hemorrhage in tissues?
- Petechia
- Purpura
- Ecchymoses
- Hematoma
Describe petechia
- Minute 1-2 mm hemorrhages in the skin or mucous membranes
- Result from minute defects in the capillaries
- Usually caused by abnormalities in the platelets
- Can be caused by bacterial sepsis in the blood stream
Describe purpura
- Hemorrhages in skin or mucous membranes>2mm diameter -> form plaque-like lesions
- Often result from inflammation in small blood vessels = vasculities or abnormalities in the platelets
Henoch-Schonlein Purpura (allergic purpura):
- Hypersensitivity vasculitis and inflammatory response within the blood vessel
- Acute immunoglobulin A (IgA)–mediated disorderfollowing an infection
Describe ecchymoses
- Larger extravasations of blood into tissue >1-2cm in diameter
- A purple/red or blue discoloration occurring from ruptured blood vessels with or without trauma
- bleeding underneath the skin (flat) - Ecchymosis cascade includes:
1. Blood vessels rupture
2. Red blood cells die and release hemoglobin
3. Macrophages degrade hemoglobin via phagocytosis 4. Discoloration of skin changes to gold-brown colour - due to degradation of haemoglobin = hemosiderin
Describe hematomas
- Large leakage from large blood vessels, causing blood to pool
- Solid collections of coagulated blood in tissues due to trauma
- Can raise the level of the skin or the surface of the organ
- Hematomas tend to occur deep inside the body
- May require medical attention (surgical drainage)
What is the process of a blood clot?
Platelet Activation:
- Platelet adherence to endothelial layer & each other
-> Fibrinogen blood clot
Vasoconstriction
:
- Epinephrine/Norepinephrine
- Reduced blood flow
Later: Clot dissolves -> granulation tissue
What is a thrombosis and the different types?
Thrombosis:
- Disrupted blood flow
- Blood clot formation in uninjured vessels, adherent to vascular endothelium
- Pathologic converse to hemostasis
- May develop anywhere in cardiovascular system
Types:
- Arterial thrombosis
- Venous thrombosis (phlebothromobisis)
What is the virchows triad?
Virchow’s Triad = Three mechanisms predisposing to formation of a thrombus:
- Endothelial Injury
- Abnormal/Disrupted blood flow
- Hypercoagulability
Describe how endothelial injury leads to the pathogenesis of thrombosis
- Thrombosis is a blood clot in an artery or vein inside the body
Physical loss of endothelium:
- Exposure to subendothelial extracellular matrix (vWf blood clotting factor) –> activation of clotting cascade
Endothelial dysfunction:
- Can be caused by Atherosclerosis, trauma, surgery, venipuncture, chemical irritation and toxins e.g. cigarette smoke, indwelling catheters, hypertension, hyperlipidemia, vascular inflammation
- altered blood flow
- altered platelet adherence
Describe how abnormal/disrupted blood flow (Virchow’s Triad) leads to the pathogenesis of thrombosis
- Blood flow can be altered through stasis or through turbulence
- Endothelium becomes activated
- Laminar flow disrupted
- Platelets will come in contact with the endothelium -> altered margination
- If blood stasis -> prevents dilution of activated clotting factors by fresh flowing blood
Reduces inflow of clotting factor inhibitors
- Promotes endothelial cell activation
- e.g. Immobility or paralysis, aneurysms, obesity, pregnancy
What are the consequences and fate of a thrombosis?
- Resolution – usually recent thrombus removal by fibrinolytic activity
- Organisation and thrombus incorporation into a thickened vascular wall, ie thrombus organised into a scar
- Recanalisation – synthesis of new capillaries by intimal cells and fusion of the capillaries to form larger vessels - scar and residual thrombus 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
Describe the morphology of a thrombosis
- Size and shape depends on site of origin and cause
- Thrombi are focally attached to the underlying vascular surface
- Arterial or cardiac thrombi begin at sites of turbulence or endothelial injury and grow in retrograde direction
- Venous thrombi occur usually at sites ofstasis and grow in direction of the blood flow and often contain large amounts of red blood cells
Describe arterial (cardiac) thrombosis
- Typically composed of platelet aggregates (white thrombus)
Usually occlusive - concern when they cause downstream tissue infarction at critical sites
- E.g. coronary & cerebral vessels causing MI and stroke
- Can embolize to brain, kidneys and spleen
- 80% intra-cardiac mural thrombi
- Main cause: atherosclerotic plaque
- Other causes: vasculitis, trauma
- formation of platelet-rich “white clots” that form after rupture of atherosclerotic plaques
- Exposure of procoagulant material such as lipid-rich macrophages (foam cells), collagen, tissue factor, and/or endothelial breach, in a high shear environment
Describe venous thrombosis (phlebothromobisis)
- Largely consist of fibrin and red blood cells (red thrombus)
- Mainly associated with immobilization & stasis -> most occur in superficial or deep veins of leg
- Superficial: local congestion, swelling, pain, and tenderness (rarely embolize)
- Deep: risk of embolization to the lungs (pulmonary embolus)
What is embolism and the process of embolism recovery?
Hint: 3 Steps of recovery
Embolism: a blocked artery (thrombus) caused by an embolus
Embolus: blood clot, air bubble, fatty deposit, or other object that travels through the blood stream.
- 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
What is infarction and the different types?
Hint: Red or White
Ischaemia + Infarction:
- Ischaemia – reduction of blood supply to a tissue
Infarction:
- Ischaemic necrosis by occlusion of arterial supply or venous drainage
- Septic or bland
Usually due to thrombosis or embolism
- Red (haemorrhagic) infarction
:
- Generally affecting the lungs
- White (anaemic) infarction
:
- Arterial occlusion in solid organs
(heart, spleen,
kidney) - wedge-shaped
- kidney -> Necrosis or renal tubules
- Arterial occlusion in solid organs
(heart, spleen,
Describe echinocytes (crenated erythrocytes, Burr cells)?
- Histology: numerous surface projections, evenly distributed and of similar size
- Usually represent anin vitroartefact - Dehydration of red blood cells, increased pH, and decreased ATP
- Can result from ageing of the blood (e.g. slow drying)
- Can result from excessive concentrations of EDTA (e.g. when the sample tube is significantly underfilled) - Can occur in snake envenomation, neoplasia or glomerulonephritis
Describe acanthocytes (spur cells)?
- Histology: erythrocytes covered by irregularly shaped unevenly distributed surface projections of different lengths
- Results from alteration in cholesterol or phospholipid concentration in the red blood cell membrane
- Can be associated with severe liver disease
Describe spherocytes
- Histology: deep red staining, spherical cells that lack central pallor
- Can result from loss of cell membrane secondary to antibodies or complement on the surface -> partial phagocytosis by macrophages
- Related to immune mediated hemolytic anemia
- Also reported after blood transfusions, snake envenomation, bee stings, and zinc toxicity
Describe codocytes
- Histology: cells with a bull’s-eye appearance
- Result from increased red blood cell membrane cholesterol
- Can be related to liver disease
Describe Poikilocytosis
- Histology: umbrella term to describe erythrocytes with abnormal shape
- Often related to the presence of multiple red blood cell pathologies simultaneously - Can be related to liver disease, disseminated intravascular coagulation and glomerulonephritis
