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Clinical Pathology > Quiz 2 part 1 > Flashcards

Quiz 2 part 1 Flashcards

0
Q

Define Thromboemboli

A

Fragments of thrombi carried by venous or arterial blood

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1
Q

What type of embolism accounts for most of the emboli in clinical practice

A

Thromboemboli

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2
Q

How are thromboemboli classified?

A

Classified on the basis of the vessels through which they are carried

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3
Q

2 examples of liquid emboli

A
  1. Fat emboli that occur after bone fracture

2. Amniotic fluid emboli caused by the entry of amniotic fluid into the uterine veins during delivery

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4
Q

2 ways an air embolism can be produced

A
  1. injecting air into the veins

2. Air that is liberated under pressure, as in decompression sickness is yet another form

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5
Q

Describe a few examples of solid particle emboli

A
  1. Cholesterol crystals can detach from atherosclerotic plaques as well as from tumor cells, bone marrow emboli or bullets
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6
Q

Describe the venous emboli. What can they cause?

A

Originate in veins and typically lodge in the pulmonary artery and its pulmonary branches causing pulmonary embolism

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7
Q

What is a paradoxical emboli

A

Venous emboli that reach the arterial circulation through the foramen ovale or an interventricular septal defect that can cause symptoms similar to those of arterial emboli

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8
Q

Where do arterial emboli originate? Describe arterial emboli in general

A

Originate in the left atrium or ventricle, aorta, and major arteries
- Carried by arterial blood, important cause of infarction resulting from occlusion of peripheral arteries

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9
Q

What is a true bone marrow emboli? When do you normally see them?

A

One complete with hematopoietic cells and fat are often seen in the lungs at autopsy.
- Usually encountered after cardiac resuscitation in which fractures of the bones of the sternum, thorax and ribs are common. No symptoms related to this event.

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10
Q

What are the 3 types of shock?

A
  1. Cardiogenic Shock
  2. Hypovolemic shock
  3. Septic Shock
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11
Q

Describe Cardiogenic shock

A

Results from pump failure of the heart

  • Most often secondary to an infarction that destroys a large part of the functioning myocardium
  • THe loss of contractile elements decreases the ability of the heart to pump blood, leading to arrythmia
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12
Q

Describe Hypovolemic shock

A

Results from a loss of circulatory volume, attributed to massive hemorrhage or to water loss related to massive burn, vomiting, or diarrhea

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13
Q

Describe Septic Shock

A

Severe G- endotoxin bacteremia –> shock resulting from the spread of bacteria from a severe localized infection into the bloodstream (ie. abscesses, pneumonia, or peritonitis)

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14
Q

T or F, Septic shock only occurs with endotoxin-producing G- bacteria

A

False, It can also occur with G+ and fungal infections

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16
Q

What is the most common cause of death in ICU’s

A

Septic shock (>100,000/year)

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17
Q

Describe the components of a thrombus

A

Transformation of the fluid blood into a solid aggregate encompassing:

  • blood cells
  • fibrin (thin filaments binding together cellular elements of blood)
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18
Q

What is fibrin made up of?

A

Fibrin is polymerized fibrinogen and forms a meshwork of thin filaments that bind together the cellular elements of the blood forming a thrombus or clot

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19
Q

Describe the first step of the fate of a thromus

A

Initially, the attachment of the larger thrombi is mediated by the actions of adhesion molecules such as fibrin

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20
Q

Describe the organization process of thrombi

A

With time after attachment, the thrombus stimulates the in growth of inflammatory cells and vessels, producing granulation tissue. This tissue provides firmer anchorage.

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21
Q

What do the inflammatory cells of the granulation tissue do to a thrombus during or immediately after the “organization” process

A

The inflammatory cells of the granulation tissue dissolve the thrombus, while the thrombus is replaced by collagen from the granulation tissue.

22
Q

What are the 4 fates of the thrombi

A
  1. Lysis and resolution
  2. Organization
  3. Recanalization (Occlusive thrombi recanalizes)
  4. Embolism (if cannot attach it breaks off)
23
Q

What is a heart failure cell

A

Are alveolar “hemosiderin-laden” macrophages.

- These MO take up disintegrated RBC’s that were let into the alveoli of the lungs as a result of Hyperemia.

24
Q

What is the component of the heart failure cells

A

RBCs found in alveoli
Hemoglobin of RBC (Hemosiderin)
- this accumulates in lysosomes of these macrophages

25
Q

Where do venous emboli originate? where do they end up?

A

in veins and typically lodge in the pulmonary artery and its pulmonary branches causing pulmonary embolism

26
Q

Where does a pulmonary embolism originate?

A

typically originate in the deep veins of the lower extremities and are carried by venous blood to the vena cava, through the right atrium and ventricle and then into the pulmonary artery

27
Q

Define saddle embolus

A

An embolus that straddles the branching of an artery blocking both branches (specifically pulmonary artery from heart)

28
Q

How lethal are saddle emboli and why?

A

Often lethal because they prevent the entry of blood into the lungs and cause acute anoxia.

29
Q

What two other things may block pulmonary circulation other than pulmonary embolism

A

Amniotic fluid and Air emboli

30
Q

What is the end result of a paradoxical emboli?

A

Can cause symptoms similar to those of arterial emboli which are common causes of ischemia in various organs (including infarction)

31
Q

Where do arterial emboli originate?

A

Most originate from the endocardium or from valvular thrombi

32
Q

Arterial emboli usually flow in the blood stream in what shape? Why?

A

They are fragmented inside the vessels because blood flows fast and disrupts them
- They tend to lodge in medium-sized and smaller arteries

33
Q

Which is the greatest risk of arterial emboli

A

The greatest risk is associated with emboli of the cerebral circulation, which typically lodge in the middle cerebral artery and causes infarcts of the basal ganglia

34
Q

Describe a fat embolism

A

Describes the release of emboli of fatty marrow into damaged blood vessels following trauma to fat-containing tissue, particularly with bone fractures.

35
Q

How quickly does fat embolism syndrome appear

A

1-3 days after the injury

36
Q

What characterizes fat embolism syndrome in its most severe form? What other things may characterize it?

A 
Respiratory failure (ARDS)
- It is also characterized by mental changes, thrombocytopenia, and widespread petechiae.
37
Q

What organs are generally involved in fat embolism syndrome

A

Lungs - Exhibit changes of ARDS and microscopically show numerous fat globules within the microvasculature

Brain - Lesion here include cerebral edema, red petechiae and microinfarcts, with fat globules also seen in microvasculature.

38
Q

Fat embolism is usually considered a direct result of what?

A

Trauma, with fat entering ruptured capillaries at the site of the fracture.

39
Q

what causes thrombocytopenia in fat embolism

A

Platelets adhere to the fat globules, causing thrombocytopenia

40
Q

T or F, Fat emboli are usually clinically inapparent

A

True, Fat embolism occurs in about 90% of patients with severe skeletal injuries, but less than 10% of such patients have clinical findings

41
Q

What are the 4 most common end-locations for arterial emboli

A

Cerebral
Spleen
Renal
Intestine

42
Q

What are the clinical expressions of the 4 most common end-locations for arterial emboli?

A

Cerebral - Lodge in the middle cerebral artery and causes infarcts of the basal ganglia
Spleen - Sharp subcostal pain
Renal - Hematuria
Intestine - Results
from embolus that lodges in one of the major intestinal arteries, causing gangrene and necrosis of the bowel

43
Q

What is LPS and how it functions

A

LPS- found in bacterial cell wall of G- bacteria

- Complex binds to receptors on white blood cells and tissue cells, causing release of inflammatory mediators.

44
Q

How is septic shock and LPS related

A

Septic shock is caused by endotoxin-producing G- bacteria

45
Q

What is Waterhouse-Freidrichsen syndrome

A

Bilateral adrenal hemorrhage

- Shock due to massive adrenal hemorrhage (possible due to G- bacteria Nesseira mengitidis and E. coli

46
Q

How is Waterhouse-Freidrichsen syndrome associated with shock?

A

It has to do with septic shock

47
Q

Describe Red Infarcts

A

Are typical of venous obstruction involving the intestines or testes. The venous circulation may be interrupted as a result of twisting of the organ around its supporting structure.

48
Q

Other than intestines or testes, red infarcts are also typical of what organs

A

Those that have dual blood supply. Such as liver or lungs

49
Q

Describe White (pale) infarcts

A

Typical of arterial occlusion in solid organs such as heart or kidney

50
Q

T or F, the area of ischemic necrosis caused by the arterial obstruction is typically darker than the surrounding tissue when speaking of white infarcts

A

False, They are typically paler than surrounding tissue.

51
Q

T or F, Ischemic necrosis due to infarction in organs like the heart cannot be repaired except by replacement of damaged cells with fibrous tissue, resulting in myocardial fibrosis and scarring

A

True

52
Q

Can necrotic brain cells be replaced?

A

They cannot be replaced by regeneration either but fibrous scars do not form

Clinical Pathology (7 decks)

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