hemodynamic disorders II

Question 1

infarction

Answer 1

1) area of ischemic necrosis
2) occlusion of vessel
3) embolus or thrombus which occludes it
- necrosis and cell death at the site (infarction)

Question 2

arterial thrombosis

Answer 2

1) most of the infarctions are attributed to it
2) depends on the anatomy of arterial supply, time it develops, and vulnerability of the tissue, and how much blood oxygen content1

Question 3

venous occlusion

Answer 3

1) typically in spongy tissues like lungs
- red / hemorrhagic
2) or pale / white
- dense tissues
3) arterial occlusion and compact tissue
4) depends on the same things

Question 4

dual supply

Answer 4

1) obstruction of pulmonary arteries does not always mean infarction of the lungs bc there is other supply
2) also the liver, which has hepatic artery and the portal vein
3) and the hand and forearm, which has radial and ulnar artery
4) ALLEN tests!!!!

Question 5

allen test

Answer 5

1) should blanch if you occlude the radial and ulnar
2) then when you release one, the hand should flush back
3) if not, it is a negative test
- you should not do an A-line

Question 6

kidney and spleen

Answer 6

1) end arterial circulation
2) obstruction of one is more likely to cause infarction

Question 7

rate of occlusion

Answer 7

1) slowly developing occlusions are less likely to cause infarction

Question 8

tissue vulnerability to ischemia

Answer 8

1) neurons undergo irreversible damage when deprived of blood supply for only 3 to 4 minutes

Question 9

hypoxemia

Answer 9

1) abnormally low blood O2 content increases both the liklihood and extent of infarction

Question 10

white infarcts

Answer 10

1) occlusion is in solid organs with end arteriolar circulation !!!***
2) wedge shaped and clear demarcation
3) lateral margins may be irregular
4) the acute infarctions are indistinct

red and white in lungs

Question 11

ischemic coagulation necrosis

Answer 11

1) liquefactive or coagulative
2) different parts of the body with have either type of necrosis
- brain: ischemia with liquefactive necrosis
3) inflammation along margins => few hours should start being sharply demarcated

Question 12

regeneration of parenchymal tissue

Answer 12

1) can occur at the periphery of the infarct, whether they can regenerate and replace with scar tissue

Question 13

septic infarctions

Answer 13

1 )cardiac valve damaged (vegetation of clot can break and embolize or stay and occlude with necrosis)
2) need dental clearance before they replace their valve

Question 14

shock !!!***

Answer 14

1) pathophysiological state
2) decreased tissue perfusion and hypoxia!!!!
3) three types
- septic, hypovolemic, and cardiogenic
4) massive blood loss, myocardial infarction, sepsis
5) initially reversible, but can lead to irreversible injury (fatal)

Question 15

cardiogenic shock

Answer 15

1) low CO due to heart pump being inadequate
2) MI can also cause it
3) ventricular arrythmia
4) cardiac tymponade
5) outflow obstruction problems

Question 16

hypovolemic shock

Answer 16

1) loss of blood or plasma
2) hemorrhage or burn

Question 17

septic shock

Answer 17

1) arteriolar dilation and venous blood pooling
2) from immune response

Question 18

shock (uncommonly)

Answer 18

1) loss of vascular tone and General anesthesia
2) reversible

Question 19

anaphylactic shock

Answer 19

1) vasodilation and systemic Vasopermeability
2) IgE (type I)

Question 20

treatment for shock

Answer 20

1) IV fluid hydration (except for cardiogenic shock)
2) you’d have to increase the CO
- and give O2

Question 21

septic shock

Answer 21

1) host response to bacteria or fungus
2) endothelial cell activation
- coagulation cascade
3) vasodilation
4) edema
5) DIC
- clotting and bleeding
6) metabolic dearrangment

20% mortality
- decrease in muscle tone and intravascular coagulation

Question 22

pathway for septic shock

Answer 22

1) gram + (most common) and gram - follow it
2) innate and hummoral system
- macrophages and cytokines
3) inflammatory cells
4) vasopermeability
5) complement cascade and anti-coagulation
6) systemic inflammatory response syndrome
- MULTIPLE SYSTEMS

Question 23

inflammatory mediators

Answer 23

1) what cells they’re activating (KNOW THIS)

Question 24

endothelial cell activation and injury

Answer 24

1) thrombosis
2) increased vascular permeability
3) vasodilation

Question 25

in full DIC

Answer 25

1) consumption of clotting factors and platelets
2) CONCOMITANT BLEEDING AND HEMORRHAGE
3) fibrinolytic activity
4) pro-inflammatory activity from sepsis can lead to this!

Question 26

mediators can cause inflammatory cell damage

Answer 26

1) inflammatory mediators like NO
2) can relax vessel wall
- hypotension and worsening tissue perfustion

Question 27

metabolic abnormalities

Answer 27

1 )insulin resistance and hyperglycemia
2) TNF and IL
- stress induced hormones and catecholamines activated => release blood glucose
3) pro-inflammatory cytokines can also cause insulin resistance
4) hyperglycemia can suppress neutrophil function!
5) sepsis is also associated with glucocorticoid production
- adrenal insufficiency due to SIRS and bleeding
- inadequate glucocorticoids

Question 28

immune suppression

Answer 28

1) anti-inflammatory mediators
2) widespread death of lymphocytes in spleen and lymph nodes

Question 29

organ dysfunction of

Answer 29

1) systemic hypotension, vascular permeability, edema, small, vessel thrombosis, and less oxygen
2) respiratory failure (acute respiratory distress syndrome)
3) factors can contribute to many organ failure

Question 30

kidney urine output

Answer 30

1) if it decreases or significantly drops
2) you are in shock
- <20-30 cc per hour

Question 31

stages of shock!!

Answer 31

1) progressive disorder
- sepsis or trauma
- death follows multiorgan failure

2) hypovolemia cariogenic shock
- we know what is causing it

3) septic shock
- if we dont find the microbe and treat it, very fatal

Question 32

initial nongrogressive stage

Answer 32

1) reflec compensatory mechanisms are activated and organ perfusion maintained

Question 33

progressive stage

Answer 33

1) tissue hypoperfusion

Question 34

irreversible stage

Answer 34

1) widespread cell injury and nonreversible
2) myocardial contractile function worsens in part because of increased NO synthesis

Question 35

baroreceptor reflex

Answer 35

1) aortic arch and carotid sinus
- decrease or increase the HR to maintain BP
2) decreased BP => decreased baroreceptor activation, which increases the HR

Question 36

net effect of shock

Answer 36

1) tachycardia, peripheral vasoconstriction and renal fluid conservation, vasoconstriction
2) coolness and pallor

Question 37

cellular and tissue effects of shock are caused by

Answer 37

hypoperfusion and microvascular thrombosis!!!**

Question 38

if underlying cause is not corrected

Answer 38

1) can pass into the next stage
2) metabolic lactic acidosis
- blood pooling in microcirculation and initiating DIC

Question 39

clinical course

Answer 39

1) in hypovolemic and cardiogenic shock, will survive if you manage them 90%
2) biggest factor is if the brain receives oxygen
3) insulin therapy and appropriate antibiotics
- and bring blood pressure up
- steroid doses

Question 40

questions on exam

Answer 40

thrombosis, embolism, DIC, clotting cascade, blood test!, septic shock definition, stages of shock