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PATH3240 > Edema > Flashcards

Edema Flashcards

1
Q

<p>Edema</p>

A

<p>Accumulation of abnormal fluids in the intercellular/interstitial fluid comparment --> swelling of subcutaneous tissues</p>

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2
Q

<p>What mechanisms control edema?</p>

A

<p>1) Starling's forces

2) lymphatic obstruction
3) vascular permeability
4) cardiovascular function
5) overall fluid balance
6) salt retention</p>

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3
Q

<p>Describe Starling's Law</p>

A

<p>The movement of fluid between vessels and tissue is governed by 4 forces!</p>

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4
Q

<p class=”large” style=”text-align:center”;>Describe for 4 Starling forces and their net fluid movement relative to the blood vessel:</p>

A

<p class=”large” style=”text-align:center”;>1) Hydrostatic pressure in vessel (32 arterial to 12 venous) - OUT

2) Oncotic pressure - colloïde osmotic pressure of plasma (reflects the amount of serum protein - albumin) - IN
3) Interstitial fluid pressure (tissue retention) - 3-4 mmHg - IN
4) Interstitial fluid osmotic pressure (very low) - OUT</p>

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5
Q

<p>What are the four main types of edema?</p>

A

<p>Hydrostatic, Oncotic, Inflammatory/Traumatic, and Lymphedema</p>

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6
Q

<p class=”large” style=”text-align:center”;>What causes hydrostatic edema?</p>

A

<p class=”large” style=”text-align:center”;>Increase in intravascular hydrostatic pressure (due to increase venous pressure)</p>

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7
Q

<p>What causes pulmonary/oncotic edema?</p>

A

<p>Decrease in colloid osmotic pressure of plasma due to hypoproteinemia</p>

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8
Q

<p class=”large” style=”text-align:center”;>What causes inflammatory/traumatic edema?</p>

A

<p class=”large” style=”text-align:center”;>The vascular bed becomes leaky following an injury to the endothelium.</p>

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9
Q

<p>What causes lymphedema?</p>

A

<p>Lymphatic obstruction (increases interstitial oncotic pressure)</p>

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10
Q

<p class=”large” style=”text-align:center”;>What are the two types of congestive heart failure?</p>

A

<p class=”large” style=”text-align:center”;>Right side -> peripheral edema
Left side -> lung edema</p>

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11
Q

<p>What diseases are associated with an incrase in intravascular hydrostatic pressure?</p>

A

<p>Congestive heart failure and deep venous thrombosis of lower legs</p>

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12
Q

<p class=”large” style=”text-align:center”;>What diseases are associated with a fall in colloid osmotic pressure?</p>

A

<p class=”large” style=”text-align:center”;>Liver disease (cirrhosis); decreased synthesis of albumin
Renal failure due to loss of albumin
Malnutrition</p>

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13
Q

<p>What diseases are associated with lymphatic obstructions?</p>

A

<p>Cancer, inflammation, post-surgical lyphedema.</p>

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14
Q

<p class=”large” style=”text-align:center”;>What are the diseases associated with sodium retention?</p>

A

<p class=”large” style=”text-align:center”;>Kidney disease.</p>

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15
Q

<p>What are the causes of local edemas?</p>

A

<p>(1) increased hydrostatic pressure due to vascular obstruction and (2) lymphatic obstruction via tumour or inflammation.</p>

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16
Q

<p class=”large” style=”text-align:center”;>What are the causes of generalized edems?</p>

A

<p class=”large” style=”text-align:center”;>(1) increased hydrostatic pressure, (2) decreased colloid osmotic pressure due to loss of albumin, and (3) errors in sodium retention.</p>

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17
Q

<p>What is the difference between a transudate and an exudate?</p>

A

<p>Transudate results form disturbances in starling forces, while exudates result from damage to capillary walls.</p>

18
Q

<p class=”large” style=”text-align:center”;>Hyperaemia</p>

A

<p class=”large” style=”text-align:center”;>Engorgement by blood causes redness (i.e., acute inflammation, exercise)</p>

19
Q

<p>Congestion</p>

A

<p>Impaired venous drainage causes accumulation of deoxygenated blood due to increase in venous hydrostatic pressure.</p>

20
Q

<p class=”large” style=”text-align:center”;>What is thrombosis and what are it’s components?</p>

A

<p class=”large” style=”text-align:center”;>Formation of mass (clotted blood) in the heart or blood vessels. The mass consists of: RBCs, WBCs, Platelets, Fibrin</p>

21
Q

<p>What causes thrombosis?</p>

A

<p>1) Vessel wall damage --> inflammation

2) Changes in blood flow (stasis in lack of activity, or decreased cardiac output, or increase blood viscosity)
3) Changes in blood composition (i.e., increase in [platelets])</p>

22
Q

<p class=”large” style=”text-align:center”;>What is the prognosis of a thrombosis?</p>

A

<p class=”large” style=”text-align:center”;>Obstruction –> breakdown into embolli –> dissolve –> may reorganize</p>

23
Q

<p>Embolism</p>

A

<p>Occlusion of a blood vessels by an embolus transported through the blood stream.</p>

24
Q

<p class=”large” style=”text-align:center”;>Types of emboli (5)</p>

A

<p class=”large” style=”text-align:center”;>Thrombi, gas, fat (in fracture of large bones), tumour, or foreign bodies</p>

25
Q

<p>Infarction</p>

A

<p>Area of necrosis produced by ischemia; is irreversible and healing occurs by fibrosis (scarring)</p>

26
Q

<p class=”large” style=”text-align:center”;>In what cases do you see white infarct?</p>

A

<p class=”large” style=”text-align:center”;>During aterial occlusion, in solid organs (heart, spleen, kidney, brain), and in leg gangrenes.</p>

27
Q

<p>In what cases do you see red infarct?</p>

A

<p>During venous or arterial occlusion, in loose tissues (lung), with dual blood suplies, and in brain/intestines.</p>

28
Q

<p class=”large” style=”text-align:center”;>Hemorrhage</p>

A

<p class=”large” style=”text-align:center”;>Bleeding from vessels into surrounding tissues, body cavity, or exterior of the body</p>

29
Q

<p class=”large” style=”text-align:center”;>Causes of hemorrhages</p>

A

<p class=”large” style=”text-align:center”;>Trauma to blood vessels, infections, weak artery, invasive tumour, hypertension, hemorrhagic diastheses (spontaneous hemorrhaging affecting capillaries)</p>

30
Q

<p>Hematoma</p>

A

<p>Bleeding into soft tissues</p>

31
Q

<p class=”large” style=”text-align:center”;>Purpura</p>

A

<p class=”large” style=”text-align:center”;>diffuse, superficial hemorrhage into the skin</p>

32
Q

<p>Ecchymosis</p>

A

<p>Larger superficial hemorrhage (i.e., black eye)</p>

33
Q

<p class=”large” style=”text-align:center”;>Petechia</p>

A

<p class=”large” style=”text-align:center”;>pinpoint hemorrhage, usually in the skin or mucous/serosal membranes; rupture of capillaries or arterioles</p>

34
Q

<p>Hemothorax</p>

A

<p>Bleeding in pleural cavity</p>

35
Q

<p class=”large” style=”text-align:center”;>Hemopericardium</p>

A

<p class=”large” style=”text-align:center”;>Bleeding in pericardial cavity</p>

36
Q

<p>Hemoperitoneum</p>

A

<p>Bleeding in abdominal cavity</p>

37
Q

<p class=”large” style=”text-align:center”;>Hemoarthrosis</p>

A

<p class=”large” style=”text-align:center”;>Bleeding in a joint</p>

38
Q

<p>Shock</p>

A

<p>Failure of the circulatory system to maintain appropriate blood supply, especially to vital organs</p>

39
Q

<p class=”large” style=”text-align:center”;>Causes of shock</p>

A

<p class=”large” style=”text-align:center”;>Decreased blood volume, decreased cardiac output, redistribution of blood</p>

40
Q

<p>Types of shock</p>

A

<p>1) Hypovolemic (hemorrhage, burns, sweating, diarrhea)

2) Cardiogenic shock (inability to pump, or excessive impairment of cardiac output)
3) Septic shock (bacteremia)
4) Anapyhlactic/Neurogenic (allergic, anaesthesia)</p>

41
Q

<p class=”large” style=”text-align:center”;>Which types of shock cause a decrease in tissue perfusion?</p>

A

<p class=”large” style=”text-align:center”;>Hypovolemic and cardiogenic.</p>

42
Q

<p>Which types of shock cause peripheral vasodilation?</p>

A

<p>Anaphylaxis, neurogenic, and septic shock due to release of factors (cytokines, etc.)</p>

PATH3240 (7 decks)

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