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Human Pathology > Fluid and Hemodynamic Disorders > Flashcards

Fluid and Hemodynamic Disorders Flashcards

1
Q

Body fluid compartments

A

Water = ~60% of body weight
• Changes as you age
• Differences based on sex
Intake = approx. 2.5 L per day (in drink, food, and water of oxidation
Compartments: plasma (4.5%), extracellular (19%), intracellular (35%)
Output = approx 2.5 L per day (in urine, respiration & sweat, and stool)

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2
Q

Fluid compartment exchange

A

Plasma volume can expand and reduce but
only within narrow physiological limits

Dehydration: hemorrhage, sweating,
diarrhea
Overhydration: inadequate renal excretion,
edema
Redistribution: shock
Circulatory disruption: atherosclerosis,
embolism, thrombosis

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3
Q

Edema

A

Excessive fluid in interstitial space & or body cavities

  1. Localized edema:
    • Cerebral edema, pulmonary edema, periorbital (facial) edema
    • Ascites or hydroperitoneum: abdominal cavity
    • hydrothorax: pleural cavity
    • hydropericardium: pericardial cavity
  2. Generalized edema: Anasarca
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4
Q

Types of fluid accumulation

A

Exudate: rich in protein and blood cells, typical of inflammation
Transudate: contains less proteins and fewer cells (ultrafiltrate of plasma fluid)

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5
Q

Pathogenesis of edema

A

• Increased hydrostatic pressure
• Increased permeability
• Decreased oncotic pressure
• Obstruction of lymphatic vessels

Forms of Edema
• Inflammatory
• Hydrostatic
• Oncotic
• Obstructive
• Hypervolemic

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6
Q

Inflammatory edema

A

• Vessel permeability and hyperemia (increase in blood flow)
• Permeable due to mediators of inflammation & increased blood flow (dilation)
• Fluid is initially transudate
• Transforms into exudate hcontaining inflammatory cells

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7
Q

Hydrostatic edema

A

• Increased arterial pressure inside blood vessels (ex. arterial hypertension)
• Increased intravascular pressure promotes transmembranous passage of fluids
• Increased venous backpressure
• Venous stagnation (blood pooling in the veins)

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8
Q
A
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9
Q

Hydrostatic edema from right-sided heart failure

A

Leads to ascites (fluid accumulation in the peritoneal cavity, leading to abdominal swelling), venous congestion, peripheral edema

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10
Q

Hydrostatic edema of left-sided heart failure

A

Leads to pulmonary hypertension, pleural effusion, and chronic congestion of the lungs

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11
Q

Oncotic edema

A

• Reduced oncotic pressure of the plasma
• Albumin = most active oncotic protein

Hypoalbuminemia
• Loss of protein in the urine (proteinurea): nephrotic
syndrome
• Decreased protein synthesis: end stage liver disease
(cirrhosis)
• Usually generalized but prominent in the fac

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12
Q

Obstructive edema

A

Lymphedema
• Obstruction of lymphatic vessels
• Decreased drainage of interstitial fluid
• Rare but caused by tumour cells or chronic inflammation
• Can be caused by worms – filarial nematodes –
“elephantiasis

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13
Q

Hypervolemic edema

A

• Due to retention of Na and H2O in kidneys
• Kidney disease promotes → renin → angiotensin →
adrenal cortex → aldosterone → renal Na retention

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14
Q

Hypervolemic edema

A

• Due to retention of Na and H2O in kidneys
• Kidney disease promotes → renin → angiotensin →
adrenal cortex → aldosterone → renal Na retentio

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15
Q

Hyperemia

A

Accumulation of blood in peripheral circulation
1. Active hyperemia
2. Passive hyperemia
3. Chronic hyperemia

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16
Q

Active hyperemia

A

• Dilation of arterioles and influx of blood
• Blushing, exercise
• Mediated by neural signals to relax arteriolar smooth
muscle
• Acute inflammation (swelling)

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17
Q

Passive hyperemia

A

• Congestion
• Caused by venous backpressure/impaired venous drainage
• Typically due to heart failure (chronic)
• Associated with hydrostatic edema
• Cyanosis: stagnation of deoxygenated blood, bluish
discoloration

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18
Q

Chronic Hyperemia: Passive
Congestion in the Lungs

A
  1. Increased venous pressure → Edema
  2. Leakage of fluid & RBC into alveoli
  3. RBCs fall apart
  4. Macrophages
  5. Hemoglobin is degraded into a brown pigment (hemosiderin)
  6. Accumulates in macrophage
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19
Q

Hemorrhage

A

• Passage of blood outside the cardiovascular system

Clinically it can be:
• Sudden onset (acute)
• Long standing (chronic)
• Recurrent and marked by repeated episodes of blood loss

20
Q

Classification of hemorrhage

A
  1. Cardiac – trauma (gunshot, stab wound), softening of the heart muscle due to myocardial infarct
  2. Aortic – trauma (collisions), aortic wall weakening and dilation (atherosclerosis and hypertension)
  3. Arterial – penetrating wounds (knife, bullet) bone fracture, characterized by bright red pulsating blood (oxygenated)
  4. Capillary – pinpoint droplets
  5. Venous – dark red (deoxygenated), blood flows freely and slow
21
Q

External hemorrhage

A

• Exsanguination and death
• Hypovolemia

22
Q

Internal hemorrhage

A

• Fills body cavities
• Hematomas: blood filled swelling
• Hemorrhages of the skin:
• Petechiae: small <1mm into skin and mucosa
• Purpura: 1mm-1cm
• Ecchymoses: larger blotchy bruises

23
Q

Clinically Important Forms of Hemorrhage

A

Hematemesis: vomiting
Hemoptysis: respiratory bleeding
Metrorrhagia: uterovaginal bleeding
Hematuria: blood in urine
Hematochezia: anorectal bleeding
Melena: black blood in stoo

24
Q

Consequences of hemorrhage

A

• Depends on volume lost, location and duration

  1. Massive acute hemorrhage: increased blood
    loss, hypovolemic shock, exsanguination and
    eventual death
  2. Hematoma: compression of tissues
  3. Intracerebral hemorrhage: stroke
  4. Chronic hemorrhage: slow blood loss, usually
    results in iron deficiency anemia (bleeding
    gastric ulcer
25
Thrombosis
• Transformation of fluid of blood into solid made of blood cells and fibrin → thrombus Pathogenesis: • Thrombi = end product of coagulation • Activated to prevent blood loss in disrupted vessels • Clotting factors and platelets promote thrombosis • Endothelial cells and plasmin counteract thrombosis
26
Coagulation proteins in thrombosis
• Circulate in inactive form • Coagulation factors work to form thrombin • Thrombin = the catalyst promoting polymerization of fibrinogen to fibrin • Mesh of fibrin = framework for the clot, includes blood cells and plasma proteins
27
Endothelial cells in thrombosis
• Secrete substances to prevent coagulation (prostacyclin and nitric oxide) • Injured vessels switch from anticoagulant to procoagulant state – promote thrombus formation • Mediators of inflammation (IL-1, TNF) activate endothelial cells to become initiators of thrombosis
28
Platelets in thrombosis
• Neutralize heparin and other anticoagulation factors • Activated platelets secrete thromboxane → stimulates coagulation process
29
Formation of thrombi
A. Endothelial defect is covered with fibrin and platelets B. Fibrin forms a meshwork that anchors blood cells into the nascent thrombus C. Fully formed thrombus consists of layers of fibrin and blood cells • Normally small and short lived • Degraded by plasmin or washed away
30
Virchows triad of predisposing conditions
1. Endothelial cell injury (severe) 2. Hemodynamic changes (turbulence, slow flow, sedimentation of cells) 3. Hypercoagulability (platelets and coagulation factors)
31
Pathology of thrombi based on location
1. Mural thrombi • Wall of vessel or cardiac chamber 2. Valvular thrombi of heart • Heart valve 3. Arterial thrombi (atherosclerotic aorta, aortic aneurysm) 4. Venous thrombi 5. Microvascular thrombi
32
Gross features of thrombi
1. Red (conglutination) thrombi • tightly intermixed RBC and fibrin • Small vessels 2. Layered (sedimentation) thrombi • distinct layering of fibrin and platelets • lines of Zahn = white layers • Large arteries and veins
33
Fates of thrombi
1. Lysis: resolution & reperfusion 2. Organization: ingrowth of inflammatory cells and vessels, smaller vessel 3. Recanalization: reestablished blood flow, capillary sized channels 4. Thromboemboli: infarct
34
The 3 major consequences of thrombi
1. Occlusion of vascular lumen: arterial occlusion causes ischemia → most common cause of myocardial infarction 2. Narrowing of vascular lumen: reduced blood flow, hypoxia, altered function of organ (chronic heart failure) 3. Embolization: detached thromboemboli carried by blood cause infarcts (pulmonary emboli)
35
Embolism
Freely movable, intravascular mass carried in the blood 1. Thromboemboli: fragments of thrombi 2. Liquid emboli: fat, amniotic fluid 3. Gaseous emboli: air injection, caisson disease 4. Solid particle emboli: cholesterol crystals, bone marrow, tumor embol
36
Venous embolism
• Originate in lower extremities • Typically lodge in pulmonary artery • Pulmonary embolism • Saddle embolism: straddles the pulmonary artery at bifurcation, prevents blood going to lungs and causes acute anoxia • Symptoms (of pulmonary embolism): shortness of breath, hemoptysis, pain, sudden death
37
Arterial thromboemboli
• Originate from cardiac mural or valvular thrombi • Mechanically fragmented by blood flow • Lodge in small to medium vessels (cerebral circulation, organs or extremities) Potential results: Brain infarcts, splenic infarcts, kidney infarcts, intestinal infarcts
38
Infarction
Insufficiency of blood supply, sudden onset, that results in an area of ischemic necrosis Caused by thrombi or emboli
39
White (pale) infarcts
Pale due to arterial occlusion Often rimmed by a thin red zone with extravasated blood Typically found in solid organs
40
Red (hemorrhagic) infarct
Venous obstruction Veins have thin walls, easily compressed Venous congestion, local ischemia, necrosis Intestines (twisting) or testes (torsion)
41
Infarct outcomes
Depends on: anatomic site, types of cells forming the tissue, circulatory status, extent of necrosis Organs with postmitotic cells cannot be repaired (myocardial fibrosis) Organs with mitotic or facultative mitotic cells heal (liver, intestines)
42
Shock
State of hypoperfusion of tissues with blood Three possible mechanisms: 1. Cardiogenic shock: pump heart failure 2. Hypovolemic shock: loss of fluid from circulation 3. Hypotonic shock: loss of peripheral vascular tone, dilation of blood vessels and pooling of blood in dilated peripheral blood vessels
43
1. Compensated shock
1. Tachycardia: increased heart rate 2. Vasoconstriction of arterioles: redistribution of blood, perfusion of vital organs (brain) 3. Reduced urine production: preserve volume of blood No serious signs of vital organ ischemia
44
2. Decompensated reversible shock
1. Hypotension: ↓ Blood pressure and cardiac output 2. Tachypnea, shortness of breath: increased respiratory rate (response to anoxia), pulmonary edema, ARDS 3. Oliguria: constriction of renal cortical vessels reduces glomerular filtration rate, renal fluid output 4. Acidosis: retention of acidic metabolites, ↑anaerobic glycolysis
45
3. Irreversible shock
• End result of decompensated shock • Circulatory collapse • Marked hypoperfusion of vital organs • Loss of vital functions • Cardiorespiratory failure • DEATH
46
Symptoms of shock
• Peripheral pooling of blood • Initial compensation • Vasoconstriction • Acute respiratory distress syndrome • Slow blood flow clotting • Vasoconstriction of renal vessels • Hypoperfusion a low filtration rate • Low urine input → Metabolic acidosis

Human Pathology (9 decks)

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