Perfusion

Question 1

What is hyperemia

Answer 1

Vasodilation

Question 2

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

Answer 2

Aortic arch, carotid sinus

Signal medulla to balance SNS/PSNS control of blood pressure

Question 3

Which receptors regulate blood volume and pressue

Answer 3

Left atrial volume receptors
Osmoreceptors in hypothalamus

Signal ADH release/RAA

Question 4

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

Answer 4

Organs that recondition blood:

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

Question 5

Where are B2 receptors most prevalent

Answer 5

Cardiac and skeletal muscle

Question 6

Are alpha receptors present in brain

Answer 6

No!

Question 7

What is congestion

Answer 7

Decreased outflow of blood causing passive engorgement of vascular bed

Question 8

What physiological processes cause hyperemia

Answer 8

Heat dissipation

Increased metabolic activity in GI after meal

Question 9

Whats the main pathological cause of hyperemia

Answer 9

Inflammation (due to prostaglandins, histamine)

Question 10

Where does acute passive venous congestion occur

Answer 10

Liver and lungs —> heart failure

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

Question 11

How would liver appear in acute passive venous congestion

Answer 11

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

Right sided heart failure

Question 12

Pulmonary congestion is caused by

Answer 12

Left sided heart failure

Question 13

Hepatic congestion is caused by

Answer 13

Right sided heart failure

Question 14

What causes chronic passive congestion

Answer 14

Obstruction of venous outflow from:

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

Question 15

The liver appears nutmeg colored. Whats happening

Answer 15

Chronic congestion due to fibrosis

Question 16

Portal hypertension causes

Answer 16

Ascites, hydroperitoneum

Question 17

The liver is dark red. Whats going on

Answer 17

Acute congestion (due to right sided heart failure)

Question 18

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

Answer 18

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

Question 19

Pulmonary hypertension causes

Answer 19

Pleural effusion

Pulmonary edema

Question 20

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

Answer 20

Vessel occlusion resulting in acute infarction

Question 21

What causes venous infarction

Answer 21

Congestion due to volvulus, twisting of organs etc

Question 22

Which organs are most sensitive to oxygen deprivation

Answer 22

Heart and brain

Question 23

Which organs are less susceptible to oxygen deprivation

Answer 23

Lungs
GI
Kidneys
Skin

Question 24

Pathogenesis of reperfusion injury (5)

Answer 24

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.

Question 25

Whats a tan infarct

Answer 25

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

Question 26

Are cellular effects of shock reversible?

Answer 26

Initially Persistent shock leads to irreversible damage to cells and tissues

Question 27

CV collapse leads to

Answer 27

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

Question 28

4 things that hypotension elads to

Answer 28

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

Question 29

Types of shock

Answer 29

Cardiogenic Hypovolemia Blood maldistribution

Question 30

Types of blood maldistribution shock

Answer 30

Anaphylactic shock Neurogenic shcok Septic shock

Question 31

What is blood maldistribution shock

Answer 31

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

Question 32

Pathogenesis of anaphylactic shock

Answer 32

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

Question 33

Pathogenesis of neurogenic shock

Answer 33

Electroshock ---> lightening strike, emotional distress 1) Autonomic discharge, causing vasodilation 2) Venous pooling - ---> hypotension, tissue hypoperfusion

Question 34

Pathogenesis of septic shock

Answer 34

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

Question 35

What is involved in non-progressive shock

Answer 35

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

Question 36

What is progressive shcok

Answer 36

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

Question 37

Mechanism of progressive shock

Answer 37

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

Question 38

Mechanism of irreversible shock

Answer 38

Anerobic metabolism inhibits cellular enzymes for energy Vasodilatory substances accumulate, override compensatory mechanisms Further drop in BP MULTIORGAN FAILURE

Question 39

Morphological changes of shcok

Answer 39

``` 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 ```

Question 40

Morphological changes of shcok

Answer 40

``` 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) ```