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General Pathology > Blood flow > Flashcards

Blood flow Flashcards

1
Q

Hyperemia

A

Increased flow can be physiologic or pathologic

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2
Q

Congestion

A

Decreased flow blood still in the vessel passive accumulation that can be generalized or localized

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3
Q

Physiologic hyperemia

A

-heat loss in skin
-Increased GI flow after meal

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4
Q

Pathologic hyperemia

A

-Inflammation

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5
Q

Morphology of hyperemia

A

Bright red and warm

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6
Q

Histologic morphology of hyperemia

A

Blood vessel looks engorged

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7
Q

Causes of localized congestion

A

-Venous thrombi can cause total venous obstruction
-External pressure can occur form inflammation or neoplastic masses, organ displacement or localized fibrosis

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8
Q

Causes of generalized congestion

A

Right or left sided heart failure. Once one side fails the other side will soon follow

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9
Q

Morphology of congestion

A

Vessels dark red and engorged

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10
Q

Pulmonary congestion

A

Edema concurrent due to increased hydrostatic pressure. See RBC pop out and the macrophages eat the RBC and they are left with the iron (heart failure cells)

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11
Q

Hepatic congestion

A

Centrilobular sinusoids are initially affected. Have a nutmeg appearance

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12
Q

Significance of congestion

A

-Hypoxia and ischemia
-Often get edema
-Tissues cool because it is stagnant

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13
Q

Ischemia

A

WHen perfusion becomes inadequate to meet metabolic needs of the tissue

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14
Q

Tissue perfusion

A

Have adequate flow in tissues based on their need

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15
Q

Causes of ischemia

A

-Arterial lumenal blockage
-Prolonged arteriolar vasoconstriction
-Venous intralumenal occlusion or external pressure
-Capillary intralumenal occlulsion or external pressure

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16
Q

What dictates severity of ischemia

A

-Vascular anatomy (collateral circulation)
-Extent of decreased perfusion
-Rate of decreased perfusion (rapid more damaging than slow)
-Tissue type (brain and heart)

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17
Q

Outcome of ischemia

A

-return to normal (usually after brief)
-Reperfusion injury (from prolonged)

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18
Q

Reperfusion injury

A

Affected vessels are leaky and move fluid to interstitial
-Damaged tissue releases tissue factor to activate coagulation
-ATP converted to adenosine and combines with O2 and creates O2 radicals and cause additional damage

19
Q

Infarction

A

Local area of peracute ischemia that undergoes coagulative necrosis or liquefactive in nervous tissue. Usually caused by thrombus

20
Q

Highly susceptible tissues to infarction

A

-Myocardium
-Brain
-Renal tubules
-Epithelium

21
Q

Low susceptibility to infarction

A

CT

22
Q

Influencing factors of infaction

A

-susceptibility of tissue
-Vascular anatomy
-Decreased cardiovascular function
-Anemia

23
Q

Characteristics of infarction

A

-Type and siaze (artery which is immediate vs vein which is slower and causes congestion; large or small vessel)
-Tissue affected (susceptibility, anatomy)
-Duration
-Status of tissue prior to infarct

24
Q

Infarction morphology

A

Depends on vessel occuled and tissue affected
-White (anemic)
-Red (hemorrhagic)

25
Q

Red infarcts

A

Infarct and get hemorrhage into damaged cells. Cells swell and undergo necrosis, once it degrades blood flows back in and looks red

26
Q

White infarts

A

Occurs in solid tissues with minimal anastomosis like the heart. See zone of inflammation around. Because it is solid blood can’t seep back into the tissue

27
Q

Reasons for red infarct

A

-Venous stasis or obstruction
-Arterial obstruction in loose tissues
-Tissues with dual blood supply or anastomoses
-Reperfused necrotic tissues

28
Q

Infarction significane

A

-Vital organs can be fatal and serious
-Non vital organs better tolerated
-Want to know what the cause was though that could be important

29
Q

Shock

A

Circulatory dyshomeostasis where circulating blood volume and volume of circulatory system that needs to be filled are disporportionate. Get widespread tissue hypoxia and altered metabolism

30
Q

Cardiogenic shock

A

BLood flow is reduced due to failure of central pump
-Myocardial infarction or arrhythmias
-Pulmonary embolism
-Cardiomyopathy

31
Q

Hypovolemic shock

A

Not enough blood in circulation. Decrease in vascular pressure see compensatory peripheral vasoconstriction and fluid movement. See porblems when you lose 35-45% loss
-Severe hemorrhage
-Vomiting
-Diarrhea
-Burns

32
Q

Blood maldistribution

A

Systemic vasodilation of periphery and get bleed pooling in peripheral tissues

33
Q

Three categories of blood maldistribution

A

-anaphylactic shock
-neurogenic shock
-septic shock

34
Q

Anaphylactic shock

A

Generalized type I hypersensitivity leading to systemic vasodilation from histamine and get increased permeability, decreased pressure and tissue hypoperfusion. IgE based reaction

35
Q

Neurogenic shock

A

Autonomic nervous discharges resut in peripheral vasodilation

36
Q

Causes of neurogenic shock

A

-Trauma
-Electrocution
-Fear or stress

37
Q

Septic shock

A

Excessive release of vsaoactive and pro inflammatory mediators resulting in vasodilation. Bacteria and fungus are the normal causes

38
Q

LPS and septic shocl

A

Activates endothelium and leukocytes
-Decreases anticoagulant properties
-Activates the complement pathways
-Activate Factor XIIa-related pathways
-enhanced leukocyte adhesions
-TNF and IL- release (procoagulant and proinflammatory)

39
Q

3 stages of shock

A
  1. Compensation
  2. Progressive stage
  3. Irreversible stage
40
Q

Compensation

A

Reflex mechanisms
-Increase heart rate
-Peripheral vasoconstriction
-ADH and ANG II increase blood volume
-Diversion of blood to vital tissues
-If mild can return to normal here

41
Q

Progression

A

Compensatory mechanisms are inadequate and tissue hypoperfusion occurs
-Metabolism shifts to anaerobic
-Acidosis
-Host mediators accumulate
-Peripheral vasoconstriction turns to dilation as hypoxia occurs and get pooling of blood

42
Q

Irreversible stage

A

Hypoperfusion, tissue hypoxia, and hemodynamic dysfunction leads to cell damage
-Cell energy stores depleted, and membranes deteriorate
-Disseminated intravascular coagulation
-organ failure

43
Q

Morphology of shock

A

Depends on stage
-Hemorrhage and edema
-Microthrombosis
-Necrosis
-Multiorgan

44
Q

Significance of shock

A

Life threatening
-Hypotension and weak pulse
- Tachycardia and hyperventilation
-Cool extremities and cyanosis
-Multi organ failure

General Pathology (30 decks)

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