Module 3 -Path continued Flashcards

1
Q

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

A

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

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2
Q

What is the pathogenesis of a nitrogen embolism?

A

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

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3
Q

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

A
Brain = death 
Muscles/Joints = bends 
Lungs = edema and hemorrhage (chokes)
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4
Q

What is Caisson’s Disease?

A

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

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5
Q

What is the treatment for Caisson’s Disease?

A

Pressure chamber (slow decompression)

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6
Q

What is an air embolism?

A

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

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7
Q

What is the pathogenesis for air embolism?

A

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

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8
Q

Where does a white infarct occur?

A

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

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9
Q

What is the pathogenesis for a white infarct?

A

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

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10
Q

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

A

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

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11
Q

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?

A

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

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12
Q

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

A

Sickle cell disease

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13
Q

Where do Red (hemorrhagic) infarcts occur?

A

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

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14
Q

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

A

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

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15
Q

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?

A

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

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16
Q

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

A

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

17
Q

A cerebral infarct is usually do to what?

A

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

18
Q

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

A

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

19
Q

What are key findings of a Myocardial infarction?

A

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

20
Q

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

A

Apex!

21
Q

What is the most accurate test for an MI?

A
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)
22
Q

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

A

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

23
Q

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

A

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

24
Q

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

A

Arrhythmia’s due to damage to the purkinje fibers

25
Q

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

A

Mucosa (last place to get oxygenated blood)

26
Q

A red infarct is a surgical emergency why?

A

because the walls are soo weak they are ready to perforate

perforation –>peritonitis –> gram negative septic shock from e.coli –> DIC

27
Q

What are findings on exam of a GI red infarct?

A

abd pain
blood diarrhea
fever
absent/reduced bowl sounds

28
Q

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

A

Exploratory laparotomy

Angiogram

29
Q

best investigation for a stroke?

A

First do a CT to rule out hemorrhagic stroke

then do an MRI to look for ischemic stroke