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Pathology > Perfusion > Flashcards

Perfusion Flashcards

1
Q

What is hyperemia

A

Vasodilation

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2
Q

Where are the body’s main baroreceptors and what do they do

A

Aortic arch, carotid sinus

Signal medulla to balance SNS/PSNS control of blood pressure

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3
Q

Which receptors regulate blood volume and pressue

A

Left atrial volume receptors
Osmoreceptors in hypothalamus

Signal ADH release/RAA

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4
Q

Which organs receive more blood than neccessary for their metabolic needs and why

A

Organs that recondition blood:

  • Lungs (oxygenate blood)
  • GI (nutrient processing)
  • Kidneys (remove waste, balance electrolytes)
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5
Q

Where are B2 receptors most prevalent

A

Cardiac and skeletal muscle

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6
Q

Are alpha receptors present in brain

A

No!

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7
Q

What is congestion

A

Decreased outflow of blood causing passive engorgement of vascular bed

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8
Q

What physiological processes cause hyperemia

A

Heat dissipation

Increased metabolic activity in GI after meal

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9
Q

Whats the main pathological cause of hyperemia

A

Inflammation (due to prostaglandins, histamine)

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10
Q

Where does acute passive venous congestion occur

A

Liver and lungs —> heart failure

Spleen –> euthanasia (smooth muscle relaxation and dilation of vasculature)

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11
Q

How would liver appear in acute passive venous congestion

A

Dark, engorged. Due to blood being unable to return to heart, so it engorges in liver

Right sided heart failure

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12
Q

Pulmonary congestion is caused by

A

Left sided heart failure

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13
Q

Hepatic congestion is caused by

A

Right sided heart failure

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14
Q

What causes chronic passive congestion

A

Obstruction of venous outflow from:

1) neoplastic mass
2) inflammatory mass
3) organ displacement
4) fibrosis of healed injury

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15
Q

The liver appears nutmeg colored. Whats happening

A

Chronic congestion due to fibrosis

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16
Q

Portal hypertension causes

A

Ascites, hydroperitoneum

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17
Q

The liver is dark red. Whats going on

A

Acute congestion (due to right sided heart failure)

18
Q

The lungs are yellow-brown, firm. Whats going on

A

Chronic congestion. Due to macrophage induce fibroplasia. They contain iron so it makes lungs appear yellow

19
Q

Pulmonary hypertension causes

A

Pleural effusion

Pulmonary edema

20
Q

The kidney appears red, swollen and theres a bulge in the capsule. Whats likely happening

A

Vessel occlusion resulting in acute infarction

21
Q

What causes venous infarction

A

Congestion due to volvulus, twisting of organs etc

22
Q

Which organs are most sensitive to oxygen deprivation

A

Heart and brain

23
Q

Which organs are less susceptible to oxygen deprivation

A

Lungs
GI
Kidneys
Skin

24
Q

Pathogenesis of reperfusion injury (5)

A

1) During prolonged ischemia, ATP is degraded to Adenosine (potent vasodilator)
2) When blood returns, fluid moves into interstitium
3) High pressure leads to compression of veins, inhibiting blood return
4) Blood vessels hemorrahge
5) TF released —> secondary hemostasis

You can ALSO get release of reactive oxygen species from ATP breakdown. These damage cells.

25
Q

Whats a tan infarct

A

More chronic infaction. Cells swell and tissue becoming necrotic – lysing of RBCs

26
Q

Are cellular effects of shock reversible?

A

Initially

Persistent shock leads to irreversible damage to cells and tissues

27
Q

CV collapse leads to

A
  1. Decreased volume
  2. Reduced CO
  3. Hypotension (reduced peripheral resistance)
28
Q

4 things that hypotension elads to

A

1) Hypoperfusion
2) Cellular hyoxia
3) Anaerobic metabolism
4) Cellular degeneration/death

29
Q

Types of shock

A

Cardiogenic
Hypovolemia
Blood maldistribution

30
Q

Types of blood maldistribution shock

A

Anaphylactic shock
Neurogenic shcok
Septic shock

31
Q

What is blood maldistribution shock

A

Pooling of blood in peripheral circulation due to neural or cytokine mediated vasodilation

32
Q

Pathogenesis of anaphylactic shock

A

1) Exposure of antigen to sensitized mast cells

2) Degranulation –> release of histamine and other vasoactive mediators
- ———> vasodilation, pooling of blood, hypotension, hypoperfusion

3) Increased vascular permeability
- —> hypotension, hypoperfusion, leaking of fluid into interstitium or lung alveoli

4) Smooth muscle contraction —> constricts broncioles, difficult breathing

33
Q

Pathogenesis of neurogenic shock

A

Electroshock —> lightening strike, emotional distress

1) Autonomic discharge, causing vasodilation

2) Venous pooling
- —> hypotension, tissue hypoperfusion

34
Q

Pathogenesis of septic shock

A

1) Exposure to infectious pathogens (endotoxin, proteoglycans etc)
2) Leukocytes and endothelium activated

3) Macs release IL-1, TNF
A) activate platelet activating factor
B) activate nitric oxide –> vasodilation
C) neutrophil migration to tissues

4) Endothelium release anti-coagulants
- –> activates contact pathway of coagulation

35
Q

What is involved in non-progressive shock

A

Barorecptors: E/NE release
—> Increased CO, increased BP

Left atrial volume and hypothalamic osmoreceptors RAAS, ADH
—> increased blood volume and CO

Vasoconstriction (endothelin)

Shift of fluid from interstitium to plasma

36
Q

What is progressive shcok

A

Damage to heart results in decreased CO, blood pooling, tissue hypoperfusion

37
Q

Mechanism of progressive shock

A

1) Lack of perfusion, lack of oxygen in tissues
2) Metabolism switches to anerobic
3) Decreased ATP, acidosis
4) Metabolic waste leads to increased osmolality, local hypoxia, increased CO2

5) Cell death, releasse of systemic cytokines
- –> inflammation, coagulation, fibrinolysis

38
Q

Mechanism of irreversible shock

A

Anerobic metabolism inhibits cellular enzymes for energy

Vasodilatory substances accumulate, override compensatory mechanisms

Further drop in BP

MULTIORGAN FAILURE

39
Q

Morphological changes of shcok

A 
o	Generalized congestion, pooling of blood (liver, intestine)
o	Edema (lung)
o	Hemorrhage (petechial and ecchymotic)
o	Microthrombosis
o	Centrilobular hepatic necrosis
o	Renal tubular necrosis
o	Intestinal mucosal necrosis 
o	Myocardial fiber degeneration
40
Q

Morphological changes of shcok

A 
o	Generalized congestion, pooling of blood (liver, intestine)
o	Edema (lung)
o	Hemorrhage (petechial and ecchymotic)
o	Microthrombosis
o	Centrilobular hepatic necrosis
o	Renal tubular necrosis
o	Intestinal mucosal necrosis 
o	Myocardial fiber degeneration
o	Cerebral edema and ischema (necrosis)

Pathology (8 decks)

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