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Flashcards in Module 3 -Path continued Deck (29):

What is the etiology of a nitrogen embolism/ the bends/Caisson's Disease

Deep sea diving without Caisson's chamber or deeper than 10meters


What is the pathogenesis of a nitrogen embolism?

O2, N2 dissolve in high amounts in blood and tissues due to high pressure --> sudden resurfacing releases N2, O2 --> O2 reabsorbed, N2 bubbles out --ruptures tissues and forms emboli in vessels --> platelets adhere to N2 ,form secondary thrombi and aggravate ischemia


In regards to nitrogen emboli, what are the effects if found in the brain, muscles/joints, or lungs

Brain = death
Muscles/Joints = bends
Lungs = edema and hemorrhage (chokes)


What is Caisson's Disease?

Persistent (Chronic) gas emboli in bones --> necrosis in femur, tibia, and humerus


What is the treatment for Caisson's Disease?

Pressure chamber (slow decompression)


What is an air embolism?

150mL of air in venous circulation through neck wounds, thoracentesis, cut jugular vein, hemodialysis, child birth, abortion


What is the pathogenesis for air embolism?

Air bubbles coalesce and obstruct flow of blood in right ventricle, lungs and brain
Frothy mixture in right ventricles --> ineffective ejection --> may occlude large vessels


Where does a white infarct occur?

Solid organs with single blood supply (no dual or collateral circulation)


What is the pathogenesis for a white infarct?

Arterial occlusion --> decreased O2 supply --> white infarct (wedge shaped) --> ischemic coagulative necrosis


In the heart what is the common etiology for a white infarct?

Occlusion of LAD due to atherosclerosidic plaque with superimposed thrombus and this causes an MI and a pale infarct


In the kidney what is the common etiology for a white infarct? And how would you get a white or pale infarct in the kidney?

Unilateral - asymptomatic
Bilateral --> decreased urine output
Hypovolemic show because this leads to acute ischemia


In the spleen what is the common etiology for a white infarct?

Sickle cell disease


Where do Red (hemorrhagic) infarcts occur?

Loose tissues with collateral/dual blood supply (lungs, small bowl, testicles)
Reperfusion injury via TPA ( free radical damage)
Venous obstruction via testicular torsion (testicular veins are torsed)
Coagulative necrosis


If a red infarct occurs in the lungs what is this usually do to?

Usually due to Major pulmonary embolus (from DVT) + compromised bronchial artery --> hemorrhage/congestion -- >red infarct --> coagulative necrosis


In the GI system if there is a red infarct the area is referred to as a watershed area, where is the exact location in the GI tract?

Splenic Flexure (where SMA ends, IMA begins) most vulnerable to hypoxia


In the small intestine a red infarct is caused by what?

Volvulus, obstruction, or intersusception (proximal bowel goes into the distal bowel)


A cerebral infarct is usually do to what?

Atherosclerosis with superimposed thrombus in vertebro-basilar artery
(thrombo-emboli in the internal carotid/MCA are less common)


In regards to a cerebral infarct explain the progression of necrosis that will be seen

12-24 hours: Coagulative necrosis/hemorrhage due to reperfusion
24-48 hours: microglia engulf necrotic material --> Gitter cells
Then you have liquefactive necrosis and gliosis of surrounding area


What are key findings of a Myocardial infarction?

Coronary atherosclerosis with superimposed thrombosis
Left anterior descending is the commonest involved
Coagulation necrosis
Initially blotchy , later pale scar tissue
Cardiac enzymes raise in serum
Presents with severe chest pain


In a white infarct where is the site of occlusion on gross specimen?



What is the most accurate test for an MI?

Troponin I (does not lower until 7-10 days post MI)
however if a patient is admitted to the floor post MI and you think they are experiencing another MI, what test would you order???? CK-MB because trop will most likely still be high (CK-MB has a much shorter window)


In the lab slides the picture on the left shows what kind of morphological changes of an MI ?

Acute MI: 1-3 days because no nucleus in myocardial fibers: coagulative necrosis and this is irreversible and lots of neutrophils


In the lab slides the picture to the right shows what kind of morphological changes of an MI?

Granulation tissues and collagen so this shows up between 10-14 days post MI. Type III collagen and angiogenesis


What is the most common cause of death when a person experiences an MI?

Arrhythmia's due to damage to the purkinje fibers


In the GI system the patient experiences a red infarct, what is the last place that will get blood?

Mucosa (last place to get oxygenated blood)


A red infarct is a surgical emergency why?

because the walls are soo weak they are ready to perforate
perforation -->peritonitis --> gram negative septic shock from e.coli --> DIC


What are findings on exam of a GI red infarct?

abd pain
blood diarrhea
absent/reduced bowl sounds


What diagostic tools would you do an a patient with a GI red infarct?

Exploratory laparotomy


best investigation for a stroke?

First do a CT to rule out hemorrhagic stroke
then do an MRI to look for ischemic stroke