2nd lecture clinical cases of cell death Flashcards

1
Q

Renal infraction (anemic, coagulative necrosis) description

A

Thrombosis: in one of the vessels = triangular necrosis in cortex and medulla. Related to atherosclerotic plaque, superimposed with the coagulative blood
Embolus: fragments of blood clots. The source of the emboli 90% come from the heart; atrium and ventricle.

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2
Q

what causes the embolus to come from the atria of the heart?

A

In atria due to: arrhythmia absoluta, the oscillating of atria (not contracting) the stasis of the blood predisposes it to coagulation.

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3
Q

what causes the embolus to come from the ventricle of heart?

A

after myocardial infraction. It can also come from an atherosclerotic plaque from large vessels such as the aorta. 90% from heart, 10% from the aorta.

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4
Q

The process of healing in the kidney after Renal infraction?

A

1st day = pale area of in the shape of wedge
LATER = hyperemic rim around the tissue due to the ingrow of vessels and fibroblasts to heal tissue, macrophages eat up tissue to replace it with fibrotic tissue which contracts and make depression in the organ, as they pull the 2 sides of the organ together.
MOSTLY clinically silent: no problems as long as its not too big of an infraction.

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5
Q

Spleen infraction (coagulative anemic)

A

Very similar to Renal infraction but 100% related to emboli. Scar tissue healing and depression is seen. Silent clinical effects.

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6
Q

Acute myocardial infraction description?

related to ischemia of tissue (disruption of supply and demand of cells)

A
  • coronary disease due to atherosclerosis (narrowing of lumen) the atherosclerosis plaque development take 10-20 years to develop, but the infraction is very sudden.
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7
Q

what is the Fixed coronary?

A

fixed coronary = arteriosclerosis narrowing of lumen of coronary vessel in heart.

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8
Q

critical stenosis?

A

Lumen is occluded more then 70-75%, at any moment the patient may have myocardial infraction.

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9
Q

what is needed in a fixed coronary atherosclerotic artery.

A

it needs dynamic changes such as: 2 methods.

  • vasospasm (emotional stress event), the atherosclerotic plaque ruptures, which releases cell debris causing activation of clotting in artery
  • plaque lipid core extends and grows into the vasa-vasorum rupturing them causing blood to go into the plaque and increasing its size as a result rupture occurs.
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10
Q

Myocardial infraction results in 3 types of changes, name them?

A

biochemical = drop in O2 supply = acidity of myocardium do to lactic acid.
functional = loss of contraction ability
morphological changes = wave front theory

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11
Q

what is the WAVE front theory?

A

the infraction starts in the subendocardial layer to progress to transmural. withing 30 minutes the subendocardium is effected, it takes 3-6 hours

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12
Q

why does the infraction start in the subendocardium 1st?

A
  • The pressure is higher in the subendocardium area, the high pressure may compress the arteries.
  • The heart contraction occurs in a more of a spiral. Thus the subenocardium works harder and is more sensitive to O2 deprivation. (hypoxia, ischemia)
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13
Q

what is the therapeutic window?

A

the window of times that you have to re-establish blood flow in an occluded coronary artery to save as much tissue as possible as the wave front progresses.
3-6 hours is the therapeutic window.

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14
Q

occlusion of Left coronary interventicular descending blood?

A

myocardial infarction of anterior wall and the 1st part of septum and apex.

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15
Q

occlusion of left coronary circumflex?

A

Marginal myocardial infraction.

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16
Q

obstruction of right coronary?

A

posterior wall and posterior 2/3 septum

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17
Q

morphological alteration of myocardial infraction at less then 30 minutes?

A

less then 30 minutes: reversible damage, no micro/macroscopic changes.
Electron microscopy changes: small dilated mitochondria, more relaxed myocardium. (stunned myocardium)

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18
Q

what is “stunned myocardium”

A

non-functional myocardium but still alive. (dilated mitochondria, relaxed myocardium.

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19
Q

morphological alteration of myocardial infraction at 30min to 4 hours.

A

1st steps of irreversible necrosis. Nothing is visible via micro/macroscopy.
diaphorase substrate of DI-hydrogenase enzyme which are needed for living cells, so adding the substrate shows a brown coloration. No hydrogenase enzyme results in a pale area.

20
Q

4-12 hours infraction of heart.

A

complete anemic infraction, pale, not contraction, disorganization of organelles, karyorexis, karyolysis.

21
Q

day 1 to day 2 infraction of heart.

A

healing procedure starts in the damaged heart tissue, heal necrotic part.
a hypanemic rim around necrotic tissue do to polymorphonucleis, macrophages, monocytes, migrate to the area to remove cell debris, by releasing digestive enzymes.

22
Q

day 2 to day 5 of heart infraction

A

yellow area of ischemic area do breakdown of cells, and digesting of tissue.
This is the most dangerous time for the patient due to the thin wall that may rupture.

23
Q

day 5 to day 30 of heart infraction.

A

necrotic tissue is replaced by white scar, fibrous tissue.

24
Q

what are the morphological changes during reperfusion of heart muscle?

A

hypercontractile, dark morphological change. The actin myosin take up and bind to Calcium.
if the reperfusion is past 3-6 hours (therapeutic window) will causes hemorrhagic acute myocardial infraction.

25
Q

forms of performing reperfusion?

A
  1. use certain infusion of digestive enzymes (thrombolitic enzymes) like streptase.
  2. balloon catheter that they push through the thrombus and insert a metal net tube (stent)
  3. coronary by-pass
26
Q

every disease that is covered in Pathology has to cover 5 things, name them

A
  1. pathogenesis (fixed coronary, dynamic changes)
  2. how does the morphology macroscopy look like (anemic, hyperanemic border)
  3. how does the microscopy look like? (coagulative necrosis)
  4. what are the consequences of the disease?
  5. what is the clinical aspect (symptoms and treatment)
27
Q

clinical aspects of myocardial infraction (symptoms, treatment)

A
  1. CLINICAL SYMPTOMS Angina (heavy pressure of pressure/shrinking pressure) radiating to the arm. Atypical angina (abdominal pain) characteristic of posterior infraction of heart.
  2. ECG, ST elevation is typical for myocardial infraction
  3. there is a leakage of necrotic enzymes into the circulation. (lab test for; toponin I and toponin T, Creatin kinase specific to myocardium)
    NOTE: some myocardial infraction are silent.
28
Q

Consequences of infraction of the heart?

A
  1. Cardiac failure (damage is so great that the heart can no longer pump) thus pulmonary edema develops do to stasis of the blood as a result of backpressure
  2. arrhythmia; if the myocardial infraction affects the conduction system of the heart.
  3. myocardial fracture (characteristic at 3-6 days do to the weakened wall of the heart)
  4. Aneurysm: (dilation of blood containing tubes)
  5. Cardiac failure (chronic ischemic heart disease)
  6. pericarditis (inflammation of the heart pericardium)
  7. Reinfraction another thrombosis of coronary vessels.
29
Q

Describe the consequences of rupture of the heart?

A

at around 3-6 days the weakened area of the heart is most vulnerable to rupture since at this point it is the weakest.
blood from the left ventricle goes into the pericardium filling it up (hemopericardium). the pressure of the left ventricle is about 120mmHg while in the right ventricle it is about 40mmHg. The high pressure form the left ventricle presses on the right ventricle. (cardiac tamponade)

30
Q

what is cardiac tamponade?

A

fluid in the pericardium compresses the heart preventing adequate filling. If the left ventricle ruptures the higher pressure causes right cardiac failure.

31
Q

describe what causes aneurysm after myocardial infraction?

A

the necrotic area is unable to contract anymore, so during systole only the normal muscle tissue that is still intact will dilate while the areas that could not withstand the pressure (necrotic areas) dilate. (paradox palsation)
when healing occurs the fibrosis will fix the dilated necrotic tissue in its dilated position forming an aneurysm.
the flow in all areas is laminar but in the aneurysm is static thus potentially forming a mural thrombosis which may fragment forming an embolism.

32
Q

define paradox pulsation?

A

when the heart contracts, the necrotic area of the heart dilates.

33
Q

describe chronic ischemic heart disease. (cardiac failure)

A

one atherosclerotic plaque may also have an effect on other areas of the coronary circulation. The heart has to adapt when an area of tissue dies off, hypertrophy of the heart occurs, thus there will be discrepancy of blood supply in the remaining healthy area of the heart.

34
Q

pericarditis (inflammation of the pericardium)

A

In the necrotic area of the heart there will be a healing area. Which will result in the leakage of enzymes from polymorphonucleocytes, monocytes, macrophages, inflammatory cells. The leakage of digestive enzymes may act on the pericardium as well causing inflammation.

35
Q

Pulmonary infarction (coagulative hemorrhagic necrosis)

A

emboli in the pulmonary artery, mostly coming from the lower leg artery (femoral or poplateal artery) due to DEEP VEIN THROMBOSIS

36
Q

Deep vein thrombosis

A

the circulate the blood in the lower extremities, the skeletal muscle is required. Anything that minimizes movement may increase the chance of a deep vein thrombosis. Bed rest after operation, (heparin has to be administered to prevent this). Cast on a broken bone.

37
Q

under what conditions does the thrombosis in the lung have no effect?

A

Healthy heart with good circulation. An embolism in the lungs will have no effect do to the dual circulation of the lungs;

  • artery pulmonary
  • artery bronchialis
38
Q

consequences of the left side heart failure?

A

the pumping power of the left side of the heart is reduced. thus have low oxygen saturation of bronchial artery, not enough to prevent necrosis of tissue and thus hemorrhage will occur from the bronchial artery due to the destruction of the tissue that did not get enough oxygen.

39
Q

hemmorhagic intestine infraction (coagulative hemorrhaic necrosis) description

A

the superior and inferior mesenteric artery connected via the riolan anastomosis (arch of riolan).
Thrombosis: usually occurs at the orifices
emboli: mostly comes from the heart
- superior mesenteric artery is occluded will result necrosis of tissue after it, but the blood coming from the inferior mesenteric resulting in hemorrhage. (95% lethal)
- if the inferior mesenteric artery is occluded nothing happens because its the smaller one, and can be compensated by the superior mesenteric.

40
Q

what happens if a thrombosis occurs in the portal vein?

A

blood will flow in but not out of the intestine causing necrosis of the whole intestine.

41
Q

why is occlusion of the superior mesenteric artery 95% lethal.

A

something about the lymph nodes??
the intestine is very soft.
the large intestine necrosis bacteria can cross the necrotic tissue. (heavy abdominal pain)

42
Q

cerebral infraction (liquefactive anemic)

A

the brain makes liquefactive necrosis, no preservation of the outline. Thrombus of cerebral artery, the emboli will come from the heart.

43
Q

encephalomalacia alba (cerebral infraction) description?

A

white in the beginning of the cerebral infraction

44
Q

encephalomalacia flava (cerebral infraction) description?

A

Yellow appearance due to breakdown of myelin, breakdown of neurons and ingrowth of arteries.

45
Q

cysta-post-encephalomalacia

A

macrophages eat up cell debris leaving a cyst.

46
Q

Hemorrhagic cerebral infraction (liquefactive hemorrhagic)

A
  1. obstruction of cerebral vessel —-> ischemia of tissue —–> the emboli is allowed to advance farther down the necrotic vessel causing re-perfusion causing bleeding.
  2. obstruction of the sinuses via thrombosis, and the drain of the brain is blocked and thus will be hemorrhagic.