2420 Pathology > Module 7 Circulation > Flashcards

Module 7 Circulation Flashcards

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1
Q

Body Water Distribution

A
  • 40% intracellular
  • 15% interstitial
  • 5% plasma
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2
Q

Lymphatic System

A
  • Passive drainage
  • Returning excess extravascular fluid to vascular system
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3
Q

Hemostasis

A
  • Blood clotting
  • Prevent excessive bleeding
  • After blood vessel damage
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3
Q

Disrupted Fluid Balance

A
  • Pathological conditions that alter endothelial function
  • Increase vascular hydrostatic pressure
  • Decrease plasma protein content
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3
Q

Inadequate Hemostasis

A
  • Hemorrhage
  • Compromise regional tissue perfusion
  • Hypotension, shock, death
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4
Q

Derangements in Blood Supply/Fluid Balance

A
  • Edema
  • Thrombosis
  • Embolism
  • Ischemia & infraction
  • Altered perfusion (hemorrhage/shock)
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5
Q

Edema

A
  • Accumulation of fluid
  • Interstitial/intercellular tissue
  • Leads to swelling of subcutaneous tissues
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6
Q

Local Edema Factors

A
  • Lymphatic obstruction
  • Vascular permeability
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7
Q

Systemic Edema Factors

A
  • Cardiovascular function
  • Overall fluid balance
  • Salt retention
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8
Q

Sterling Forces (Move Fluid Out)

A
  • Hydrostatic pressure
  • Interstitial fluid osmotic pressure
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9
Q

Sterling Forces (Draw Fluid In)

A
  • Plasma osmotic pressure (colloid)
  • Tissue (interstitial) fluid pressure
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10
Q

Edema Occurrence Conditions

A
  • Increase in intravascular hydrostatic pressure
  • Fall in colloid osmotic pressure/oncotic pressure of plasma
  • Lymphatic obstruction
  • Sodium retention
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11
Q

Localized Edema

A
  • Increased hydrostatic pressure due to local vascular obstruction
  • Lymphatic obstruction compression by tumour/inflammation
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12
Q

Generalized Edema

A
  • Reflects a global disorder of fluid/electrolyte metabolism
  • Increased hydrostatic pressure
  • Decreased colloid osmotic pressure
  • Sodium retention
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13
Q

Decreased Colloid Osmotic Pressure

A
  • Loss of serum albumin proteins in renal failure
  • Decreased synthesis of albumin
  • Loss of serum proteins (malnutrition)
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14
Q

Hydrostatic Edema

A
  • Hydrostatic pressure at venous end elevated
  • Decreases reabsorption
  • If lymphatic capacity exceed edema fluid accumulates
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15
Q

Oncotic Edema

A
  • Decrease in osmotic pressure
  • Loss of albumin
  • Decreases reabsorption
  • Edematous fluid accumulates
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16
Q

Inflammatory/Traumatic Edema

A
  • Vascular bed ‘leaky’ following injury to endothelium
  • Local or systemic
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17
Q

Lymphedema

A
  • Lymphatic obstruction
  • Accumulation of interstitial fluid
  • Insufficient reabsorption
  • Deficient removal of proteins
  • Increasing osmotic pressure in interstitial space
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18
Q

Thrombosis

A
  • Formation of a mass (clotted blood)
  • Within heart or blood vessels
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19
Q

Thrombus Components

A
  • Platelets
  • Fibrin
  • Red & white blood cells
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20
Q

Thrombosis Causes

A
  • Endothelial injury
  • Stasis/turbulent blood flow
  • Hypercoagulability of blood
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21
Q

Endothelial Injury Causes

A
  • Physical injury
  • Inflammation
  • Infectious agents
  • Abnormal blood flow
  • Metabolic abnormalities
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22
Q

Blood Flow Change Causes

A
  • Turbulence
  • Stasis (slow circulation)
  • Decreased cardiac output
  • Increased blood viscosity
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23
Blood Composition Change Causes
- Increase in platelets
23
Hypercoagulability
- High blood clotting tendency - Alterations in coagulation factors - Genetic/acquired
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Thrombus Prognosis
- Dissolve/lyzed by fibrinolytic activity - Increase in size & obstruct vessels - Breakdown & form emboli - Organized & may recanalize
25
Commonly Affected Vessels
- Coronary artery (heart attack) - Cerebral artery (stroke) - Mesenteric arteries (intestinal infarction) - Renal arteries (kidney infarct) - Arteries of the leg (gangrene)
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Embolism
- Occlusion of blood vessel by mass (embolus) - Travels through circulation - Becomes lodged in blood stream
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Thromboembolus
- Most common type of emboli - Formed from a thrombus - Thromboemboli arise from thrombi - Size range - Occur in arteries or veins
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Pulmonary Emboli
- Arise from deep veins of the legs - Small - Clinically silent - Undergo organization over time - Incorporated into the vascular wall
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Arterial Emboli
- Heart - Thrombi on heart walls/diseased valves - May lodge in brain (stroke/infraction)
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Cause of Ischemia
- Due to inadequate blood supply to an area to tissue
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Causes of Blood Vessel Obstruction
- Thrombus - Embolus - Pressure - Damage (vessel wall inflammation)
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Ischemia Effects
- Infarction (severe & complete) - No effects (collateral blood supply)
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Infarction
- Tissue death - Results in necrosis - After occlusion of an end artery
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Infarcts
- Coagulative necrosis - Inflammatory response develops along margins - Well defined in 1-2 days - Majority replaced by scar in repair phase
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White (Pale) Infarct
- Organs with single blood supply (heart, kidney, spleen) - Arterial occlusion/insufficiency
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Red (Hemorrhagic) Infract
- Organs with dual blood supply (liver, lung, intestine) - Venous occlusion/insufficiency
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Hemorrhage
- Escape of blood from vessels - Into surrounding tissue/exterior of body/body cavity
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Hematoma
- Accumulation of blood in soft tissues
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Hemorrhage Causes
- Trauma to large blood vessels (surgical/fracture) - Weakened artery - Infections - Invasive tumours - Hypertension - Hemorrhagic diatheses
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Petechia
- Pinpoint hemorrhage (1-2mm) - In the skin - Rupture of capillaries/arterioles - Involves mucous membranes & serosal surfaces
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Purpura
- Superficial hemorrhages in skin (3-5mm)
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Ecchymosis
- Large superficial hemorrhage - Bruise/skin discoloration - Heme degradation from hemoglobin in RBCs
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Hemothorax
- Collection of blood in pleural cavities - Trauma/rupture of aorta
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Hemarthrosis
- Collection of blood in joint
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Shock
- Diminished cardiac output/reduced circulating blood volume - Impairs tissue perfusion - Cellular hypoxia - Failure of circulatory system to supply blood
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Shock Causes
- Decreased blood volume - Decreased cardiac output - Redistribution of blood
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Hypovolemic Shock
- Hemorrhage - Fluid loss - Inadequate blood/plasma volume
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Cardiogenic Shock
- Failure of myocardial pump - Intrinsic myocardial damage - Extrinsic pressure - Obstruction of outflow
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Neurogenic Shock
- Injury of spinal cord - Loss of function of sympathetic NS
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Consequences of Shock
- Decreased tissue perfusion - Hypoxia/anoxic cell injury - Decline in cardiac output
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Septic Shock
- Overwhelming microbial infections - Outpouring of inflammatory mediators - Innate & adaptive immune cells - Arterial vasodilation - Vascular leakage - Venous blood pooling
42
Anaphylactic Shock
- Allergy condition - Systemic vasodilation & increased permeability - Triggered by IgE hypersensitivity (type 1)
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Atria
- Collect blood returned from body/lung - Prep ventricles
44
Coronary Arteries
- 2 connect to aorta - Supply heart with nutrients & blood
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Pump Function
- Motor (muscle) - Fuel supply from coronary arteries (blood/oxygen) - Valves - Wiring/control (cardiac conduction)
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Pulmonary Circulation
- Right ventricle pumps venous blood - To lungs for oxygenation - Low pressure
47
Systemic Circulation
- Left ventricle pumps oxygenated blood - Out to organs - High pressure
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Left Ventricle Wall
- Thicker than right wall - Pump blood to body - Under high pressure - More pathology occurs
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Atherosclerosis
- Chronic disease - Medium & large arteries - Initiated on endothelial lining surface - Illness results in damage of organ systems
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Atherosclerosis Pathogenesis
1. Chronic endothelial injury 2. Endothelial dysfunction 3. Smooth muscle emigration (macrophage activation) 4. Macrophages & smooth muscle cells engulf lipids 5. Smooth muscle proliferation, collagen & ECM deposition 6. Fatty plaque develops over years
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Chronic Endothelial Injury Examples
- Hypertension - Smoking - Toxins - Virus - Immune reactions - Homocysteine - Hyperlipidemia
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Endothelial Dysfunction
- Increased permeability - Leukocyte adhesion - Monocyte adhesion - Emigration
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Atherosclerosis Non-Modifable Risk Factors
- Old age - Family history (early onset heart disease)
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Atherosclerosis Modifiable Risk Factors
- Smoking - Hypercholesterolemia - Diabetes mellitus - Chronic hypertension
53
Coronary Artery Plaques
- Causes stenosis (narrowing) - Results in ischemia of supplied organ
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Ischemic Necrosis
- Severe plaque - Tissue death of organ - Insufficient blood supply - Causes an infarct (dead tissue) - Infarction process initiated
55
Endothelial Dysfunction Steps
1. Foam cells 2. Fatty streak 3. Intermediate lesion 4. Fibrous plaque 5. Complicated lesion/rupture
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Endothelial Dysfunction Characteristics
- Slow progression - Long silent phase - Prevention is key
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Heart Complications of Endothelial Dysfunction
- Angina pectoris - Myocardial infarction (dead tissue)
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Brain Complications of Endothelial Dysfunction
- Transient ischemic attack - Stroke
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Leg Complications of Endothelial Dysfunction
- Intermittent claudication - Gangrene
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Plaque Treatment
- Medications (pain relief) - Coronary angioplasty & stent - Bypass surgery
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Acute Coronary Thrombosis
- Blood clot occurs within hours to minutes - Emergency (short time period) - Tissue damage/death without immediate treatment
59
Thrombolytics
- Medication - Dissolve clots (thrombus) in vessel walls - Restore blood flow - Prevent/limit infarction - Does not remove plaques
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Percutaneous Coronary Intervention (PCI)
- Restore blood flow - Expands chronic plaque stenosis
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Precipitates Acute Myocardial Infarction
- Chronically narrowed coronary artery - Occluded by thrombus in lumen - Overlying chronic plaque
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Primary Hypertension
- Vast majority of cases - Multifactorial etiology (genetic, lifestyle) - Treatable not curable
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Old/Healed Myocardial Infarct
- Leads to chronic congestive heart failure - Scar tissue build up on vessels
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Secondary Hypertension
- Uncommon - Endocrine - Drugs/medications - Kidney disease - Tumours - May be curable if cause eliminated
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Arterial Hypertension Complications
- Risk factor for atherosclerosis - Contributes to related diseases
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Arteriolar Hypertension Complications
- Hyaline arteriolosclerosis in kidney - Intraparenchymal brain hemorrhage - Chronic renal failure
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Left Ventricular Hypertrophy
- Increases load due to hypertension - Wall thickness increases - Heart mass increases - Increased demand on coronary blood flow - Heart failure/ischemic/arrhythmias
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