Disorders of Circulation Flashcards

1
Q

hyperemia

A
  • active proces involving arteriolar dilation and increased blood flow which is caused by sympathetic neurogenic discharge or chemical mediators
  • tissue appears redder
  • ex. sites of inflammation or exercising skeletal muscle
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2
Q

congestion

A
  • passive process caused by impaired outflow of venous blood from a tissue
  • systemic process vs isolated process
  • acute vs chronic
  • tissues have abnormal red-blue color
  • ex. congestive heart failure causes hepatic congestion
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3
Q

chronic hepatocyte congestion leads to…

A

-ischemia (blood squeezes hepatocytes) and centrilobular hepatocyte necrosis

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4
Q

hemostasis

A

series of regulated processes that maintain blood in a fluid clot-free state in normal vessels and that rapidly form a localized hemostatic plug at the site of vascular injury

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5
Q

hemorrhage

A
  • flow of blood from a ruptured blood vessel into a tissue, body cavity or outside the body
  • if a fragile vessel is congested, it can rupture and hemorrhage
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6
Q

hemorrhage mechanisms

A
  • bleeding occurs when large or small blood vessels are disrupted by a mechanical force or a pathological process like congestion, inflammation, or neoplastic erosion of vessels
  • abnormal hemostasis can cause a predisposition to bleeding
  • always abnormal except for menstrual cycle
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7
Q

edema

A

-result of movement of fluid from vasculature into the interstitial spaces or body cavities

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8
Q

function of lymphatics in edema

A

-absorb excess fluid until they reach their mac volume

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9
Q

equilibrium of fluid in body by ____ and ___

A

hydrostatic pressure and oncotic pressure

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10
Q

Causes of edema

A
  • incr hydrostatic pressure (ex. heart failure or impaired venous return post deep venous thrombosis)
  • decr colloid osmotic P due to reduced plasma albumin (from decr synthesis - liver disease or malnutrition- or incr loss - nephrotic syndrome)
  • lymphatic obstruction (ex. neoplasm)
  • incr vascular permeability (inflammation)
  • sodium retention (renal failure)
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11
Q

kwashiorkor and edema

A

severe malnutrition causes hypoproteinemia causing full body edema

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12
Q

how does heart failure cause edema by affecting the kidneys?

A

-decr renal blood flow activates the renin-aldosterone-angiotensis system causing you to retain salt and water

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13
Q

thrombosis

A
  • formation of blood clot (thrombus) within intact vessel

- always pathological

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14
Q

three key elements keeping balance between hemorrhage and thrombosis

A
  • vascular wall
  • platelets
  • coagulation cascade
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15
Q

mechanisms of thrombosis

A
  • endothelial injury (ex. inflammation, advanced atherosclerosis)
  • altered blood flow (ex. turbulence from atherosclerosis or stasis from atrial fibrillation (scar tissue in heart isn’t contractile so blood can pool there) or bed rest)
  • hypercoagulable state (ex. protein C deficiency or women who smoke and use oral contraceptives)
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16
Q

Virchow’s triad in thrombosis

A
  1. Endothelial injuyry - most important factor which can also cause abnormal blood flow or hypercoagulability
  2. Abnormal blood flow - can affect endothelial injury and hypercoagulabilty
  3. Hypercoagulability
17
Q

fate of a venous thrombus

A
  • resolution by a firinolytic system that can breakdown the thrombus
  • embolism to the lungs
  • organization and incorporation into a wall
  • organized and recanalized (restore flow)
  • propagation towards the heart
18
Q

embolism

A
  • intravascular substance (solid, liquid, or gas) which is carried by blood from point of origin to distant site
19
Q

types of emboli

A
  • fragments of thrombi
  • atherosclerotic
  • amniotic fluid
  • air
  • fat- severe trauma to bone can cause some of the intra-marrow fat to go into circulation
20
Q

infarct

A
  • area of ischemic necrosis caused by occlusion of vascular supply to the affected tissue
  • majority of infarcts are associated with thromboemobolism and involve arterial occlusions
21
Q

white (pale) infarct

A
  • arterial occlusions

- solid organ with end-arterial circulation like heart, liver, spleen, and kidney

22
Q

red infarct

A
  • venous occlusions- ovarian torsion
  • tissues with dual circulation - lung, small intestine
  • loose tissues- lung
  • when flow is re-established after infarction- ex. angioplasty of arterial obstruction
  • red because of associated bleeding
23
Q

factors that influence infarct development

A
  • nature of vascular supply
  • rate of development of occlusion
  • vulnerability of tissue to hypoxia
  • oxygen content of the blood
24
Q

clinical outcomes of thrombosis

A
  • depends on degree of occlusion of vessel lumen, collaterals, and size of infarct
  • partial occlusion may allow enough blood to flow to vital tissue
  • complete occlusion usually results in infarct unless there is enough collateral circulation
25
Q

shock

A

systemic hypoperfusion of tissues causing cellular hypoxia

26
Q

cardiogenic shock

A
  • low caridac output due to myocardial pump failure

- ex. MI, ventricular rupture, arrhythmia, and cardiac tamponade (=pericardial effusion)

27
Q

hypovolemic shock

A
  • low cardiac output due to loss of blood or plasma volume

- ex. hemorrhage or fluid loss (vomiting, diarrhea, burns, trauma)

28
Q

septic shock

A

-arteriolar vasodialtion and venous blood pooling that stems from systemic immune response to microbial infection