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Gen Path > Disorders of blood > Flashcards

Disorders of blood Flashcards

1
Q

Describe the pathogesis of hyperaemia

describe its appearance

A

There is histamine and bradykinin release due to an acute inflammatory response causing arteriolar dilation and increased blood flow to a localized area
-grossly: reddness and warmth
-micro: dilated capillaries and inflammatory mediators
THIS IS AN ACUTE PROCESS

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2
Q

Describe congestion and its appearance

A
  • happens because there is a lack of emptying of vessels or a blockage of forward flow so there is a back flow of blood.
  • may result in dependant tissues being dark red or blue
  • grossly: dark red or blue tissues, heavy, oozing and tissues have edema
  • micro: dilated vessels but no signs of inflammation
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3
Q

what is the significance of prolonged congestion

A

may result in ischemic or hypoxic tissue because there is no blood delivering O2 to tissues past the congestion and there is no blood removing wastes from the tissues

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4
Q

What is a bloat line

A

it is a form of antemortem bloat. It is when there is congestion of the head and neck regions and congestion of cranial half of the esophagus and then half way down the esophagus on the distal end it is white and ischemic (the transition occurs at the thoracic inlet)

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5
Q

What is the result of chronic R sided heart failure

A

chronic passive congestion of the liver and systemic edema.

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6
Q

Describe the pathogenesis of chronic hepatic congestion

A

-at first the CV dilates because of the excess blood but with time you start seeing reverse degradation of hepatocytes, starting in zone 3 (right near the CV) and progressing to zone 1. This degradation results in coagulation necrosis.
-zone 3 becomes hypoxic (brown), zone 2 hepatocytes get fatty degeneration (yellow) and zone 3 hepatocytes are normal.
this results in nutmeg liver!!!!

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7
Q

what is the result of left sided heart failure

A

you start to get congestion of the lungs because blood is not being pumped out of the left side of the heart efficiently so there is a back flow and the blood has a hard time leaving the lungs.
-get congestion of alveolar capillaries then get edema in alveolar septa and spaces because of the increased hydrostatic pressure in the vessels
get golden lungs because there is diapedesis so RBC are engulfed by macrophages and broken down into hemosiderin

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8
Q

What is the long term consequence of left sided heart failure?

A

get alveolar septal fibrosis-> increased resistance of blood going into lung -> increased workload on right side of heart -> get right sided heart failure from left sided heart failure!

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9
Q

What are the 4 methods that result in edema?

A
  1. increased venous hydrostatic pressure
  2. decreased plasma oncotic pressure
  3. lymphatic obstruction
  4. endothelial leakage
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10
Q

define thrombosis:

thromboembolism

A

thrombosis is the attachment and formation of a clot made up of fibrin or platelets to the blood vessel wall or heart
-when the clot detaches and is free within the lumen of the vessel

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11
Q

What are the three components for the formation of a thrombosis

A
  1. endothelial injury: in normal uninjured tissue there is no formation of clots because there are anti-thrombic properties on the endothelium but if the endothelium is damaged then vWF is exposed and platelets attached
  2. Blood flow changes: Normally blood is flowing as a fast enough pace that there is no attachments of platelets but if the blood flow is slowed then the activated clotting factors of blood may be able to attach to the vessel wall
  3. hypercoagulability: disturbance between the amount of pro and anticoagulation results in thumbs formation
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12
Q

what is required to occur in order for an arterial thrombi to form?
once formed, what is its appearance

A
  • NEEDS endothelial damage because normally the blood flow is too fast for the thrombin to stop and settle in one place. Once there is endothelial damage, the formation of the coagulation plug causes turbulence and slows down the blood flow.
  • once formed, the thrombi is a firm, grey-white mixture of platelets, fibrin, leukocytes and a small amount of RBC (why it isn’t red)
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13
Q

describe how an arterial thrombi grows

A

once it is established, there are deposits of firmly attached components, but still only a small amount of RBC. The components that are being added to the thrombi attach down stream of the thrombi and this causes more turbulence, slowing the blood down and allowing more RBC to attach (the end of the thrombi is more red then the attachment site)

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14
Q

Describe a venous thrombi

A

-there is a small site that is grey-white right where the thrombi attaches but since the blood flow is slower, more RBC are able to attach easier so the thrombi is more red. This may appear like a postmortem clot but it is attached to the vessel wall and postmortem clots are not

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15
Q

Describe vegetative valvular endocarditis

A

there is endothelial injury on the cardiac valves, causing inflammation and therefore forms a thrombi that consists of fibrin, neutrophils, platelets and RBC. This makes the valves have a cauliflower appearance and a yellow grey colour. The valves are firm and friable.

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16
Q

What are some possible fates of thrombi?

A
  • resolves and injured tissue is replaced
  • propagation: thrombi isn’t resolved and instead there is an accumulation of fibrin and platelets, which may eventually lead to complete occlusion
  • embolism: the thrombi is dislodged and travels throughout the cardiovascular system, possibly causing a blockage
  • dissolution: fibrolyitic activity removes newer, more recently formed thrombi but older thrombi are more resistant this this so it won’t work on them
  • organization and recanalization: older thrombi get organized, which means there is the ingrowth of angioblasts and fibroblasts within the thrombi with neutrophils and macrophages and the fibrin of the thrombi is replaced by fibrous tissue. –> canalization of occlusive thrombi
17
Q

Describe DIC

A

this is a very serious situation with a fatal outcome. it is when there is a widespread formation of microvascular thrombi (consumptive coagulopathy) and may begin due to septicaemia, immunogenic injury to endothelium. It leads to the initiation of fibriolysis

  • it results in a bleeding disorder because so much of the coagulation factors are being used up in the thrombi.
  • a symptom is petekial hemorrhage
18
Q

What is an embolism?

A

a detatched solid, liquid or gas that is carried within the blood to a location other than its initial one. It may occlude a vessel and cause ischemia

19
Q

What are some examples of embolisms?

A
  • vegetative valvular endocarditis
  • saddle thromboembolism in cats
  • strongylus vulgaris in foals
  • heart worm in dogs
20
Q

What is saddle thromboembolism?

A

happens in cats that have cardiomyopathy or CHF because there is turbulent flow in the blood causing the formation of a thromboembolism that moves to the posterior part of the aorta and occludes it, causing paresis, cold and swollen legs

21
Q

Describe what happens to foals with strongylus vulgaris

A
  • foals ingest this parasite that moves through the GIT and into the large intestine where it penetrates the walls of the intestine and moves into the blood stream causing vascular damage, inflammation and thrombi formation.
  • it is possible to get a thromboemboli that occludes a vessel causing local ischemia, resulting in intermittent colic and possibly infarction of part of the intestine
22
Q

Describe heart worm in dogs

A

when dogs are treated with heart worm medication when they already have heart worm, a worm may detach and move into the pulmonary artery causing nematodal embolism and may cause an occlusion, resulting in a lack of blood flow to the lungs

23
Q

Describe an infarction

A

-it is a process of ischemic necrosis where all tissues that have been affected have under gone necrosis due to an occlusion of arterial or venous drainage

24
Q

What are some determinants of infarctions?

A
  1. nature of blood supple - if an organ has dual blood supply then it is able to resist infarction a lot better
  2. vulnerability to hypoxia - how long a tissue is able to survive without O2 (neurons < cardiac muscle < fibroblasts
  3. Oxygen content of blood - if the blood already has low amount of O2 in it then it is more susceptible to infarction
  4. rate of development of occlusion - the slower the occlusion, the better the tissue is able to resist necrosis because it is able to adapt
25
Q

Describe pale-white infarcts in terms of why they have formed and what it means

A
  • it formed because of an arterial occlusion.
  • initially the infarct is pale because the occlusion causes cells to swell due to necrosis and this increases the local pressure so that no blood from surrounding tissue is able to seep into the infarct. The margins of the infarct are red because there is inflammation forming hyperaemia.
  • over time there is degradation of the neutrophils and enzymes allowing the local pressure to decrease and allowing blood from surrounding tissues to seep in causing the infarct to turn red.
  • With more time, the infarct turns pale again and shrinks because fibrosis
26
Q

List and describe the multiple situations with a red infarct

A
  1. pale infarcts turning red
  2. venous occlusion causing congestion and a red infarct
  3. infarcts in tissue with dial blood supply - one blood supply may be cut off causing the infarct but the second blood supply will continue to bring blood into the infarcted area allowing the blood to seep into the area
  4. infarcts in loose tissue - the tissue doesn’t get too tight when the cells swell so blood from the surrounding areas is able to seep into the infarcted area
  5. reprofusion injury
27
Q

What are 3 examples of infarcts

A
  1. intestinal accidents - torsion or strangulation will obstruct venous flow first and then arterial flow causing the intestines to become dark red from the congestion and a thickened wall from the edema and hemorrhage.
  2. renal infarcts -corticol renal infarcts - left sided vegetative valvular endocarditis may more a thromboembolism which may cause an occlusion to the cortex of the kidneys causing an arterial infarct
    medullary renal infarct - use of NSAIDs will decrease the production of prostaglandin, which is a vasodilator causing schema
  3. infarction of distal extremities - get necrosis of tissue due to septicaemia, frost bite or toxic injury. this causes red tissues
28
Q

What is shock

A

a circulatory disturbance with the net result being hypotension leading to impaired perfusion and hypoxia

29
Q

What are some causes of shock

A
  • heart failure
  • hemorrhage
  • sepsis
  • anaphylasis
  • electrocution
  • severe diarrhea
30
Q

What are the 3 types of shock

A
  1. cardiogenic - when the heart is failing so there is decreased SV and CO
  2. hypovolemic shock - reduces blood volume because of blood loss, fluid loss or hypotension and tissue hypo fusion
  3. blood maldistribution - decreased peripheral hydrostatic pressure and blood pooling
31
Q

what are some mechanisms of blood maldistribution

A
  1. sepsis - peripheral vasodilation because of gram negative bacteria –> LPS of cells wall activates endothelium causing vaodilation
  2. anaphylaxis - IgE on mast cell binds to its receptor causing the release of histamine resulting in vasodilation
  3. neurogenic shock - autonomic discharge results in peripheral vasodilation and hypotension when there is electrocution or fear
32
Q

What are the 3 stages of shock?

A
  1. nonprogressive - baroreceptors try to compensate by maintaining CO and increase the peripheral vascular pressure (vasoconstriction) when there is reduced blood pressure. there is the release of norepinephrine and epinephrine
  2. progressive: can’t compensate so tissue becomes hypo perfused, blood begins to pool and cell injury starts
  3. irreversible: increasing cell metabolism derangements results in accumulation of vasodilating substances. As peripheral vasodilation continues, hypotension worsens and start to see multi oral failure and DIC
33
Q

what are some signs of shock

A 
hypotension
weak pulse
increased heart rate
increased respiratory rate (trying to get more blood oxygenated better)
edema
hemorrhage

Gen Path (10 decks)

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