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2420 Pathology > Module 7 Circulation > Flashcards

Module 7 Circulation Flashcards

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
Q

Blood Composition Change Causes

A
  • Increase in platelets
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23
Q

Hypercoagulability

A
  • High blood clotting tendency
  • Alterations in coagulation factors
  • Genetic/acquired
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24
Q

Thrombus Prognosis

A
  • Dissolve/lyzed by fibrinolytic activity
  • Increase in size & obstruct vessels
  • Breakdown & form emboli
  • Organized & may recanalize
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25
Q

Commonly Affected Vessels

A
  • Coronary artery (heart attack)
  • Cerebral artery (stroke)
  • Mesenteric arteries (intestinal infarction)
  • Renal arteries (kidney infarct)
  • Arteries of the leg (gangrene)
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26
Q

Embolism

A
  • Occlusion of blood vessel by mass (embolus)
  • Travels through circulation
  • Becomes lodged in blood stream
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27
Q

Thromboembolus

A
  • Most common type of emboli
  • Formed from a thrombus
  • Thromboemboli arise from thrombi
  • Size range
  • Occur in arteries or veins
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28
Q

Pulmonary Emboli

A
  • Arise from deep veins of the legs
  • Small
  • Clinically silent
  • Undergo organization over time
  • Incorporated into the vascular wall
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29
Q

Arterial Emboli

A
  • Heart
  • Thrombi on heart walls/diseased valves
  • May lodge in brain (stroke/infraction)
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30
Q

Cause of Ischemia

A
  • Due to inadequate blood supply to an area to tissue
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31
Q

Causes of Blood Vessel Obstruction

A
  • Thrombus
  • Embolus
  • Pressure
  • Damage (vessel wall inflammation)
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32
Q

Ischemia Effects

A
  • Infarction (severe & complete)
  • No effects (collateral blood supply)
33
Q

Infarction

A
  • Tissue death
  • Results in necrosis
  • After occlusion of an end artery
33
Q

Infarcts

A
  • Coagulative necrosis
  • Inflammatory response develops along margins
  • Well defined in 1-2 days
  • Majority replaced by scar in repair phase
34
Q

White (Pale) Infarct

A
  • Organs with single blood supply (heart, kidney, spleen)
  • Arterial occlusion/insufficiency
35
Q

Red (Hemorrhagic) Infract

A
  • Organs with dual blood supply (liver, lung, intestine)
  • Venous occlusion/insufficiency
35
Q

Hemorrhage

A
  • Escape of blood from vessels
  • Into surrounding tissue/exterior of body/body cavity
35
Q

Hematoma

A
  • Accumulation of blood in soft tissues
35
Q

Hemorrhage Causes

A
  • Trauma to large blood vessels (surgical/fracture)
  • Weakened artery
  • Infections
  • Invasive tumours
  • Hypertension
  • Hemorrhagic diatheses
36
Q

Petechia

A
  • Pinpoint hemorrhage (1-2mm)
  • In the skin
  • Rupture of capillaries/arterioles
  • Involves mucous membranes & serosal surfaces
36
Q

Purpura

A
  • Superficial hemorrhages in skin (3-5mm)
37
Q

Ecchymosis

A
  • Large superficial hemorrhage
  • Bruise/skin discoloration
  • Heme degradation from hemoglobin in RBCs
37
Q

Hemothorax

A
  • Collection of blood in pleural cavities
  • Trauma/rupture of aorta
37
Q

Hemarthrosis

A
  • Collection of blood in joint
38
Q

Shock

A
  • Diminished cardiac output/reduced circulating blood volume
  • Impairs tissue perfusion
  • Cellular hypoxia
  • Failure of circulatory system to supply blood
39
Q

Shock Causes

A
  • Decreased blood volume
  • Decreased cardiac output
  • Redistribution of blood
39
Q

Hypovolemic Shock

A
  • Hemorrhage
  • Fluid loss
  • Inadequate blood/plasma volume
40
Q

Cardiogenic Shock

A
  • Failure of myocardial pump
  • Intrinsic myocardial damage
  • Extrinsic pressure
  • Obstruction of outflow
41
Q

Neurogenic Shock

A
  • Injury of spinal cord
  • Loss of function of sympathetic NS
41
Q

Consequences of Shock

A
  • Decreased tissue perfusion
  • Hypoxia/anoxic cell injury
  • Decline in cardiac output
41
Q

Septic Shock

A
  • Overwhelming microbial infections
  • Outpouring of inflammatory mediators
  • Innate & adaptive immune cells
  • Arterial vasodilation
  • Vascular leakage
  • Venous blood pooling
42
Q

Anaphylactic Shock

A
  • Allergy condition
  • Systemic vasodilation & increased permeability
  • Triggered by IgE hypersensitivity (type 1)
43
Q

Atria

A
  • Collect blood returned from body/lung
  • Prep ventricles
44
Q

Coronary Arteries

A
  • 2 connect to aorta
  • Supply heart with nutrients & blood
45
Q

Pump Function

A
  • Motor (muscle)
  • Fuel supply from coronary arteries (blood/oxygen)
  • Valves
  • Wiring/control (cardiac conduction)
46
Q

Pulmonary Circulation

A
  • Right ventricle pumps venous blood
  • To lungs for oxygenation
  • Low pressure
47
Q

Systemic Circulation

A
  • Left ventricle pumps oxygenated blood
  • Out to organs
  • High pressure
47
Q

Left Ventricle Wall

A
  • Thicker than right wall
  • Pump blood to body
  • Under high pressure
  • More pathology occurs
48
Q

Atherosclerosis

A
  • Chronic disease
  • Medium & large arteries
  • Initiated on endothelial lining surface
  • Illness results in damage of organ systems
49
Q

Atherosclerosis Pathogenesis

A
  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
50
Q

Chronic Endothelial Injury Examples

A
  • Hypertension
  • Smoking
  • Toxins
  • Virus
  • Immune reactions
  • Homocysteine
  • Hyperlipidemia
51
Q

Endothelial Dysfunction

A
  • Increased permeability
  • Leukocyte adhesion
  • Monocyte adhesion
  • Emigration
51
Q

Atherosclerosis Non-Modifable Risk Factors

A
  • Old age
  • Family history (early onset heart disease)
52
Q

Atherosclerosis Modifiable Risk Factors

A
  • Smoking
  • Hypercholesterolemia
  • Diabetes mellitus
  • Chronic hypertension
53
Q

Coronary Artery Plaques

A
  • Causes stenosis (narrowing)
  • Results in ischemia of supplied organ
54
Q

Ischemic Necrosis

A
  • Severe plaque
  • Tissue death of organ
  • Insufficient blood supply
  • Causes an infarct (dead tissue)
  • Infarction process initiated
55
Q

Endothelial Dysfunction Steps

A
  1. Foam cells
  2. Fatty streak
  3. Intermediate lesion
  4. Fibrous plaque
  5. Complicated lesion/rupture
56
Q

Endothelial Dysfunction Characteristics

A
  • Slow progression
  • Long silent phase
  • Prevention is key
57
Q

Heart Complications of Endothelial Dysfunction

A
  • Angina pectoris
  • Myocardial infarction (dead tissue)
58
Q

Brain Complications of Endothelial Dysfunction

A
  • Transient ischemic attack
  • Stroke
58
Q

Leg Complications of Endothelial Dysfunction

A
  • Intermittent claudication
  • Gangrene
58
Q

Plaque Treatment

A
  • Medications (pain relief)
  • Coronary angioplasty & stent
  • Bypass surgery
59
Q

Acute Coronary Thrombosis

A
  • Blood clot occurs within hours to minutes
  • Emergency (short time period)
  • Tissue damage/death without immediate treatment
59
Q

Thrombolytics

A
  • Medication
  • Dissolve clots (thrombus) in vessel walls
  • Restore blood flow
  • Prevent/limit infarction
  • Does not remove plaques
60
Q

Percutaneous Coronary Intervention (PCI)

A
  • Restore blood flow
  • Expands chronic plaque stenosis
61
Q

Precipitates Acute Myocardial Infarction

A
  • Chronically narrowed coronary artery
  • Occluded by thrombus in lumen
  • Overlying chronic plaque
62
Q

Primary Hypertension

A
  • Vast majority of cases
  • Multifactorial etiology (genetic, lifestyle)
  • Treatable not curable
62
Q

Old/Healed Myocardial Infarct

A
  • Leads to chronic congestive heart failure
  • Scar tissue build up on vessels
62
Q

Secondary Hypertension

A
  • Uncommon
  • Endocrine
  • Drugs/medications
  • Kidney disease
  • Tumours
  • May be curable if cause eliminated
62
Q

Arterial Hypertension Complications

A
  • Risk factor for atherosclerosis
  • Contributes to related diseases
63
Q

Arteriolar Hypertension Complications

A
  • Hyaline arteriolosclerosis in kidney
  • Intraparenchymal brain hemorrhage
  • Chronic renal failure
64
Q

Left Ventricular Hypertrophy

A
  • Increases load due to hypertension
  • Wall thickness increases
  • Heart mass increases
  • Increased demand on coronary blood flow
  • Heart failure/ischemic/arrhythmias

2420 Pathology (13 decks)

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