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TERM 3 BIOL2292 PATHO 2 > HEMODYNAMICS LECTURE 1: Edema, hyperemia & hemorrhage > Flashcards

HEMODYNAMICS LECTURE 1: Edema, hyperemia & hemorrhage Flashcards

1
Q

What are the 2 circuits of the CVS?

A

Pulmonary circuit, systemic circuit

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2
Q

How do nutrients reach cells?

A

Diffuse from capillaries into interstitial fluid which then transports to cells

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3
Q

What are 3 causes of edema?

A

Vascular permeability, blood pressure, blood osmolarity

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4
Q

What are two terms for excessive blood in vessels?

A

Hyperemia, congestion

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5
Q

What are primary hemodynamic problems?

A

Problem with blood/vessels themselves

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6
Q

What are secondary hemodynamic problems?

A

Due to other problems such as kidney disease, infection

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7
Q

What are the 2 opposing pressures involved in capillary exchange?

A

Blood hydrostatic pressure (BHP) and blood colloid osmotic pressure (BCOP)

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8
Q

How does excess fluid return to blood in healthy individuals?

A

Lymphatic system through thoracic duct

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9
Q

What are 2 reasons liver cirrhosis could cause ascites?

A
  1. Flow obstruction causes portal hypertension and fluid backup
  2. Liver does not produce proteins required for colloid osmosis to occur
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10
Q

What are 2 classifications of edema based on location?

A

Localized, generalized

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11
Q

What are 2 classifications of edema based on origin of fluid?

A

Transudate, exudate

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12
Q

What is an example of systemic edema?

A

Anasarca due to malnutrition

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13
Q

What are 2 causes of transudate?

A

Increased BHP, decreased BCOP

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14
Q

What are 2 causes of exudate?

A

Leaky vessels, vascular damage

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15
Q

Decreased blood pressure causes juxtaglomerular cells of kidneys to produce what?

A

Renin

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16
Q

What is the action of renin?

A

Converts angiotensinogen into angiotensin I

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17
Q

Where is angiotensinogen produced?

A

Liver

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18
Q

What converts angiotensin I into angiotensin II?

A

Angiotensin converting enzyme (ACE)

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19
Q

Where is ACE produced?

A

Lungs

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20
Q

What are 2 actions of angiotensin II?

A
  1. Vasocontriction
  2. Stimulates adrenal cortex to produce aldosterone
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21
Q

What is the action of aldosterone?

A

Increased sodium and water reabsorption in kidneys

22
Q

What else stimulates the adrenal cortex to produce aldosterone?

A

Extracellular potassium

23
Q

What are the 3 outcomes of the renin-angiotensin-aldosterone (RAA) pathway?

A
  1. Increased water and sodium reabsorption
  2. Systemic vasoconstriction
  3. Increased blood volume and pressure
24
Q

What are 2 reasons congestive heart failure leads to increased sodium and water reabsorption?

A
  1. Reduced renal perfusion activate RAA pathway
  2. Reduced liver perfusion reduces aldosterone breakdown
25
Q

What are 2 reasons venous pooling leads to edema?

A
  1. Compensatory mechanisms e.g. increased blood volume means increased blood hydrostatic pressure, so more fluid is forced into tissues
  2. Fluid dilutes blood proteins and decreases blood colloid osmotic pressure, so less fluid is reabsorbed
26
Q

Name 4 consequences of edema

A
  1. Impair wound healing
  2. Increase risk for infection
  3. Compression of vital tissues
  4. Compression of vascular supply
27
Q

What is dependent edema?

A

Dependent on gravity

28
Q

What are 3 kinds of cerebral edema?

A
  1. Vasogenic
  2. Cytotoxic
  3. Interstitial
29
Q

What is the term for cerebral edema caused by increased permeability of vasculature, with fluid accumulating in extracellular spaces?

A

Vasogenic edema

30
Q

What is the term for cerebral edema where neurons swell with fluid?

A

Cytotoxic edema

31
Q

What is the term for cerebral edema where fluid accumulates in brain ventricles, causing a problem with CSF flow?

A

Interstitial edema

32
Q

What physical changes are noted in an edematous brain?

A

Flattened gyri, narrowed sulci

33
Q

What signs and symptoms do patients with cerebral edema exhibit?

A

Nausea, vomiting, disorientation, seizures

34
Q

What is the usually fatal consequence of excessive intracranial pressure?

A

Brainstem is forced downward through foramen magnum

35
Q

Which tissues line internal cavities that do not open to the exterior of the body?

A

Serous membranes

36
Q

What is the structure of serous membranes?

A

2 layers separated by serous fluid

37
Q

What are consequences of pleural effusion?

A

Lung compression and collapse

38
Q

What is the term for compression of cardiac chambers?

A

Cardiac tamponade

39
Q

What is the term for accumulation of lipid-rich lymph fluid in the peritoneal cavity resulting from a blocked thoracic duct?

A

Chylous ascites

40
Q

What kind of hyperemia is a normal response to the body’s needs?

A

Active or physiological hyperemia

41
Q

What kind of hyperemia is due to impaired venous flow?

A

Passive or pathological hyperemia

42
Q

Why do tissues affected by passive hyperemia appear cyanotic?

A

Accumulation of deoxygenated blood in affected vessels

43
Q

What is the term for 1-2 mm hemorrhages in the skin caused by platelet disturbances or infections?

A

Petechiae

44
Q

What is the term for >3mm hemorrhages that can be caused by trauma, vasculitis, or vascular fragility?

A

Purpura

45
Q

What is the term for 1-2cm subcutaneous hematomas that change in colour as blood degrades?

A

Ecchymoses

46
Q

What is the term for pathological hemostasis, or clotting when there is no vascular injury?

A

Thrombosis

47
Q

What 3 key players are involved in hemostasis and thrombosis?

A
  1. Endothelium
  2. Platelets
  3. Coagulation cascade
48
Q

What are 4 steps of hemostasis?

A
  1. Vasoconstriction
  2. Primary hemostasis
  3. Secondary hemostasis
  4. Clot formation
49
Q

What happens in primary homeostasis?

A

Exposed collagen in basement membrane causes platelet adhesion, release of granules, recruitment, and aggregation

50
Q

What happens in secondary hemostasis?

A

Endothelial damage activates coagulation cascade, which activates thrombin, which converts fibrinogen into fibrin

51
Q

What does fibrin do in clot formation?

A

Acts like a mesh to trap more platelets and other blood cells

52
Q

What are tissue plasminogen activator and thrombomodulin, and what are their purpose?

A

Anti-thrombotic mediators that are activated at the same time as hemostasis is occurring, to restrict clot formation

TERM 3 BIOL2292 PATHO 2 (19 decks)

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