Vascular disorders part 3 Flashcards

(20 cards)

1
Q

hyperemia

A

vasodilation due to heat or inflammation etc

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2
Q

congestion

A

decreased blood flow
passive engorgement of vascular bed because of decrease in outflow so blood pools
occurs in RIGHT SIDED HEART FAILURE
see blood pooling in the liver. —>hepatic congestion

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3
Q

generalized acute passive venous congestion seen in

A

right sided heart failure with hepatic congestion for instance

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4
Q

chronic passive congestion (more common) can be due to

A

fibrosis from an injury
neoplastic mass
torsion
LEFT SIDED HEART FAILURE OR PULMONARY FIBROSIS (firm lungs that fail to collapse after removal)

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5
Q

With pulmonary fibrosis, where does the yellow come from? and how does the fibrosis even come about?

A

1) Macrophages contain hemosiderin (hemoglobin breakdown pigment – Fe3+Ferritin complex) causes lungs to be yellow-tan
2) Macrophages induce fibroplasia and interstitial fibrosis

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6
Q

Right sided heart failure pathogenesis. Where’s the congestion? What kind of hypertension? Edema seen where? Acute or chronic?

A

Portal vein and hepatic congestion which is passive. Can be acute (red) or chronic (fibrotic nutmeg). Portal hypertension with ascites and hydroperitoneum due to increase in hydraulic pressure.

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7
Q

Left sided heart failure pathogenesis. Where’s the congestion? What kind of hypertension? Edema seen where? Acute or chronic?

A

Pulmonary congestion which is passive. Can be acute or chronic (yellow tan). Pulmonary hypertension with pleural effusion and pulmonary edema due to increase in hydraulic pressure.

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8
Q

Generalized heart failure leads to what kind of edema?

A

generalized

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9
Q

vessel occlusion leads to

A

decreased perfusion and acute infarction. cell swelling.

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10
Q

volvulus compresses venous return causing?

A

venous infarction

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11
Q

Reperfusion is possible if

A

blood is returned to the tissue quickly

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12
Q

if a decrease in perfusion (ISCHEMIA) is prolonged then…

A

1) ATP—>ADENOSINE WHICH CAUSES VASODILATION TO RELIEVE THE ISCHEMIA.
2) BECAUSE ISCHEMIA WAS PROLONGED, ONCE THE BLOOD DOES RETURN IT’LL CAUSE FLUID TO PUSH OUT INTO THE INTERSTITIUM.
3) ALL THE PRESSURE NOW IN THE INTERSTITIUM LEADS TO COMPRESSION OF THE VEINS= HEMORRHAGE
4) CLOTTING FACTORS ACTIVATED. SECONDARY HEMOSTASIS AND THROMBUS FORMED.

5) NOW ATP IS GOING TO BE BROKEN DOWN INTO HYPOXANTHINE ETC= CELL DEATH

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13
Q

What does a progressive infarction look like?

A

tan and pale over time as cells swell, tissue becomes necrotic and RBC lyse.

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14
Q

During shock there is cardiovascular ______?

A

collapse

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15
Q

when there is cardio collapse during shock, what happens?

A

low blood volume
decreased cardiac output
hypotension

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16
Q

what happens during hypotension?

A
  • hypoperfusion
  • Cellular hypoxia
  • Anaerobic metabolism
  • Cellular degeneration/death
17
Q

What are the 5 types of shock?

A

1) cardiogenic
2) hypovolemic due to hemorrhage or fluid loss
3) anaphylactic
4) neurogenic
5) septic most common

the last 3 due to blood maldistribution resulting from decreased vascular resistance due to vasodilation from the hypotension.

18
Q

3 stages of shock

A

non-progressive where the body can right itself by increasing blood volume and cardia output

progressive bc of too much cardiac damage, blood pooling, hypo perfusion etc. –> slow metabolism then anaerobic, hypoxia, waste products, cell death. which then triggers release of cytokines which cause inflammation coagulation etc.

irreversible: *KIDNEY/PANCREAS
Anaerobic metabolism inhibits cellular enzymes for energy production • Vasodilator substances accumulate and override compensatory
mechanisms
• Peripheral vascular resistance/pressure drops • Multiorgan failure
• Lung, liver, intestine, kidney, heart
• Decreased cardiac output ischemia of kidney and pancreas
• Ischemia of kidney electrolyte imbalances that affect the heart (arrhythmias) and ischemic pancreas
• Disseminated intravascular consumption

19
Q

SHOCK clinical signs

A
  • hypotension
  • weak pulse
  • tachycardia
  • hyperventilation with pulmonary rales • reduced urine output
  • hypothermia
20
Q

SHOCK morph changes

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