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Mechanism of Human Disease > Disorders of Circulation > Flashcards

Flashcards in Disorders of Circulation Deck (32)
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1
Q

Define hyperemia. Provide clinical examples.

A
  • dilation of an artery/arteriole leading to increased blood flow in the capillary beds
  • caused by sympathetic neuronal discharge or chemical mediators
  • area appears red due to increased amount of oxygenated blood to the area
  • ex: acute inflammation, body dissipating heat, blushing
2
Q

Define congestion. Provide clinical examples.

A
  • impaired venous drainage due to inability of vessel to dilate => pooling of blood
  • caused by sympathetic neuronal discharge or chemical mediators
  • area appears red-blue due to increased amount of deoxygenated blood
  • can be systemic/local or acute/chronic
  • ex: congestive heart failure, poor venous drainage
3
Q

Active hyperemia is __________. Passive hyperemia is __________.

A
active = hyperemia
passive = congestion
4
Q

What causes chronic passive congestion? What can it lead to?

A
  • right heart failure
  • blood backs up into organs: liver, lungs, spleen
  • leads to ischemia b/c stretched sinusoids push adjacent cells => not getting enough O2
5
Q

Define edema. How does it relate to lymphatics?

A

abnormal accumulation of fluid leakage from blood vessels into interstitial space
- when amount of fluid leaked > lymphatic clearance => edema

6
Q

Describe normal physiology of fluid movement across vessel walls.

A

Forces involved:

  • capillary hydrostatic pressure
  • interstitial hydrostatic pressure
  • capillary plasma colloid pressure (osmotic)
  • interstitial colloid osmotic pressure

These forces remain in near equilibrium so that only slight amounts of fluid leak from vessels. Small amount is removed by lymphatics.

7
Q

Define noninflammatory edema.

A
  • due to changes in hydrostatic or osmotic pressure
  • called transudate
  • protein-poor
8
Q

Define inflammatory edema.

A
  • increased intraendothelial space (between endothelial cells)
  • due to chemical mediators of the inflammatory process => increased vascular permeability and blood flow
  • called exudate
  • rich with proteins and cells
9
Q

Define hemorrhage.

A
  • flow of blood from a ruptured vessel into tissue, body cavity, or external environment
  • caused by mechanical injury (congestion, trauma) or pathology (inflammation releases proteases, neoplasm erodes vessel)
10
Q

Define hemostasis. What 3 factors regulate it?

A
  • balance of fluid leakage and clotting in the body
  • maintains blood in liquid state
  • prevents uncontrolled bleeding
  • if abnormal, can predispose to bleeding

3 factors

  • vascular wall
  • platelets
  • coagulation cascade
11
Q

Define thrombosis.

A
  • formation of a blood clot (thrombus) within the vascular system
12
Q

List the mechanisms of thrombosis formation (Wirchow’s triad)

A
  • endothelial injury: inflammation, atherosclerosis
  • altered blood flow: turbulence (loss of laminar flow) vs. stasis (lazy river)
  • hypercoagulable state: predisposed to easy clot formation (protein C deficiency, birth control + smoking)
13
Q

What are the possible fates of a thrombus?

A
  1. propagation - enlarged thrombus increases odds of occlusion or embolization
  2. dissolution - body uses fibrin to shrink or dissolve thrombus; over time, it becomes resistant
  3. embolization - part or all of thrombus travels elsewhere
  4. organization - smooth muscle cells, endothelial cells, and fibroblasts grown within and around the thrombus (weeks-months)
  5. recanalization - smaller capillaries form to reestablish flow within the lumen (weeks-months)
14
Q

Define petechiae

A
  • minute hemorrhages in skin, mucosal/serous surfaces

- causes: low platelets count, defective platelet, loss of vascular wall support

15
Q

Define purpura.

A
  • medium hemorrhages

- causes: same as petechiae, trauma, inflammation

16
Q

Define ecchymoses.

A
  • large subcutaneous hemorrhages
  • RBCs are phagocytosed
  • breakdown of hemoglobin (red) => bilirubin (blue-green) => hemosidirin (yellow-brown) is characteristic of bruise color changes
17
Q

Define embolism.

A
  • substance in the vascular system carried to another site from the point of origin
18
Q

List types of emboli.

A
  • thromboembolism
  • amniotic fluid: enters placental membrane or uterine vein rupture; serious complication of labor
  • air: develops during surgery, decompression syndrome (scuba diving)
  • fat and marrow: marrow vascular sinusoids release fat globules into circulation; caused by soft tissue crush injury or long bone injury
19
Q

Define fat embolism syndrome.

A
  • fatal
  • systemic
  • classic symptoms: respiratory, neurological, petechial rash, anemia, thrombocytopenia
20
Q

Define infarction.

A
  • area of ischemic necrosis (coagulative) in a tissue or organ
  • due to arterial/venous occlusion
  • majority are arterial thromboemboli associated
21
Q

Define white infarct.

A
  • ischemic
  • arterial occlusion
  • appears pale/white
  • single blood supply
  • appears in heart, spleen, kidney
22
Q

Define red infarct.

A
  • hemorrhagic
  • venule or arterial occlusion
  • appears red
  • dual blood supply
  • appears in lung, small intestine
23
Q

List factors that influence development of an infarction.

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

What factors determine clinical outcome of thrombosis?

A

degree of occlusion

  • smaller occlusion will let enough blood by to keep the tissue alive
  • if it’s larger, it may cause ischemia (unless there is collateral support)

size and location of blood vessel

  • main artery occlusion (carotid) or important arteries (brain) may cause death, stroke
  • smaller arteries with many collaterals may be asymptomatic
25
Q

Define shock.

A
  • systemic hypoperfusion of tissues

- caused by low CO, or low effective circulation BV

26
Q

List the 3 most common forms of shock.

A
  1. cardiogenic: low CO due to pump failure
  2. hypovolemic: low CO due to loss of blood volume
  3. septic: systemic immune response to microbial infection leads to venous pooling and arterial dilation
27
Q

What kind of hemorrhage is normal?

A

menstruation

28
Q

Why could a patient have edema?

A
  • increased hydrostatic pressure: CHF, DVT
  • decreased colloid osmotic pressure: decreased albumin synthesis (liver disease, malnutrition), increased protein loss (nephrotic syndrome)
  • lymphatic obstruction
  • increased vascular permeability: inflammation
  • sodium retention: renal failure
29
Q

Describe how heart failure can lead to systemic edema.

A
  1. increases capillary hydrostatic pressure

2. decreases renal blood flow => activate R-A-A system => Na and H2O retention => increase blood volume

30
Q

Describe how malnutrition, hepatic/nephrotic disorders can lead to systemic edema.

A

decreased plasma albumin => decreased plasma oncotic pressure

31
Q

Describe how renal failure can lead to systemic edema.

A

Na and H2O retention => increased blood volume

32
Q

What causes a hypercoagulable state?

A
  • primary genetic factors

- secondary acquired factors