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General Pathology > Circulatory Disturbances - Part 2 > Flashcards

Circulatory Disturbances - Part 2 Flashcards

1
Q

What is hemorrhage?

A

Is defined as the escape of blood from the blood vessels (extravasation)

 Can be external or internal (within tissues or body cavities)

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2
Q

What are the causes of hemorrhage?

A

 Trauma

 Sepsis, viremia, bacteremia or toxic conditions

 Abdominal neoplasia may lead to hemoperitoneum

 Coagulation abnormalities (platelet and coagulation factor defects or deficiencies)

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3
Q

What is the difference between hemorrhage and hyperemia & congestion?

A

Hemorrhage- blood is outside the vessel wall

 Hyperemia & congestion blood is within the blood vessels

  • eg: Photo shows congestion. This will lead to hypoxic damage.
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4
Q

What is occuring in this image?

A

Hemorrhage

• Hemopericardium -> leads to fatal cardiac tamponade ( Blood cannot pump effectively due to pressure build up preventing it from being able to make full contractions. Can happen because rib punctured lung after HBC, ect)

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5
Q

What determines the clinical significance of hemorrhage?

A

Determined by the location and the severity
e.g.: Profuse blood loss is the most common cause of hypovolemic shock; Hemorrhage in the brain or heart can be fatal.

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6
Q

What can occur with boxers after a boxing match?

A

• Hemorrhage post boxing match-> fighter can be fine, then start feeling terrible and collapse. Meningeal arteries can cause alot of bleeding

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7
Q

What can occur with enough bloodloss?

A

• enough blood-loss can cause hypovolemic shock. Hemorrhage in brain can be fatal.

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8
Q

What can occur with Hemangiosarcoma located in the right atrium?

A

• Hemangiosarcoma -> sometimes in the right atrium. This will create cystic lesions filled with blood and can just collapse and die. Death is attributed to rupture of R atrium and blood build up in pericardial sac and then tamponade which lead to death.

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9
Q

What is hemorrhage by rhexis?

A

Due to a substantial rent or tear in the vascular wall (or heart).

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10
Q

What is occuring in this image? What is a potential cause of this in humans? What about in Pigs?

A

In humans: aortic dissection, dissecting hematoma: dissection of blood between and along the laminar planes of the media (blood- filled channel within the aortic wall)-> can result in rupture and fatal hemorrhage
Dissecting aneurysm, pig with Copper deficiency

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11
Q

What is an aneurysm?

A

• aneurysm - focal dilation of a blood vessel - > likely an artery. Usually due to weakening of vessel. Could be secondary, but if located in cerebral artery then rupture can lead to death.

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12
Q

What can copper deficiency cause in young male racing greyhounds?

A

• Copper deficiency can cause dissecting aneurysm. Can occur in coronary/ renal arteries of young male, racing greyhounds leading to arterial rupture and fatal hemorrhage.

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13
Q

What can be ruptured in turkeys by an aneurysm?

A

abdominal aorta

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14
Q

What is hemorrhage by diapedesis?

A

Hemorrhage due to a small defect in the vessel wall or rbc’s passing through the vessel wall in cases of
inflammation or congestion (like in the lungs of animals with left-sided CHF…)

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15
Q

What occurs in patients with hemorrhagic diathesis? In what conditions can you see hemorrhagic diathesis?

A

Increased tendency to hemorrhage from usually insignificant injuries (seen in a wide variety of clotting
disorders).

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16
Q

What would you call “ Blood in the thoracic cavity”?

A

Hemothorax

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17
Q

What is a hemoperitoneum?

A

blood in the peritoneum

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18
Q

What is hemoarthrosis?

A

blood within a joint space

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19
Q

What is occuring in this image?

A

Blood in a joint space

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20
Q

What is hemoptysis?

A

Coughing up of blood or blood-stained sputum from the lungs or airways.

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21
Q

What is occuring in this image?

A

Hemoptysis

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22
Q

What is epistaxis?

A

bleeding from the nose

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23
Q

What are the causes of epistaxis?

A

◦ Causes:
‣ Hypo coagulability (rat poison, anticoagulant)
‣ Trauma
‣ Presence of tumor in nasal cavity
‣ Severe inflammation (rhinitis)
‣ Exercise induced pulmonary hemorrhage in horses, mycotic infection in guttural pouches

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24
Q

What is occuring in this image?

A

Epistaxis

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25
Q

What is petechia?

A

Hemmorhage within tissues that are (pl. petechiae): up to 1-2 mm in size. Especially found on skin, mucosal and serosal surface

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26
Q

What is occuring in this image?

A
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27
Q

What is occuring in this image?

A

Ecchymosis

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28
Q

What is ecchymosis?

A

Hemmorrhage within tissues, larger than petechia (up to ~1 or 2 cm). As seen in bruise (contusion) or small hematoma

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29
Q

What is circled in these images?

A

Agonal Hemorrhages: Petechiae and ecchymoses associated with terminal hypoxia

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30
Q

What is agonal hemorrhage?

A

Terminal hypoxia

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31
Q

When can you see agonal hemorrhage? Why?

A

• You can see this sometimes in slaughterhouses, the animal may be unconscious but heart may be alive for a few minutes.

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32
Q

What is suffusive hemorrhage?

A

Suffusive hemorrhage: larger than ecchymosis and contiguous. Serosal surface

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33
Q

What is occuring in this image?

A

Suffusive hemorrhage

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34
Q

What is occuring in this photo? Where is it most commonly found? What are potential causes for it?

A

Paint-brush hemorrhage: Looks like if red paint was hastily applied with a paint brush. Most common on mucosal and serosal surfaces.
◦ Can occur with inflammation of the rumen.
◦ Peritonitis

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35
Q

What can occur in resolution of hemorrhage?

A
  • Small amounts can be reabsorbed
  • Larger amounts require phagocytosis and degradation by macrophages
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36
Q

What is an organizing hematoma?

A

Central mass of fibrin & red blood cells surrounded by supportive vascular connective tissue ->
macrophages will eventually phagocytize this lesion.

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37
Q

What occurs as the steps of resolution of a hematoma? How does the appearence change along the way?

A

Hemoglobin (dark red blue color) enzymatically converted to bilirubin (blue-green color) and eventually into hemosiderin (gold-brown color)

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38
Q

Which stage of hemorrhage resolution is being depicted here. How do you know?

A

3rd stage -> Hemosiderin (yellow to brown)

39
Q

What stage of hemorrhage resolution is occuring? How do you know?

A

1st stage - Hemoglobin, red-blue

40
Q

What step of hemmorhage resolution is occuring? How do you know?

A

2nd stage- Bilirubin – blue-green

41
Q

What is hemostasis? What is the result?

A

(arrest bleeding by physiological or surgical means). Normal hemostasis is a physiological response to vascular damage -> Provides a mechanism to seal an injured vessel to prevent blood loss. It is the result of a complex and well-regulated process which maintains blood as a flowing fluid within the cardiovascular system.

42
Q

What is a thrombosis? What can it cause?

A
  • Thrombosis -> clot ( forms w/in vessel) which is not injured or mildly injured.
  • Inappropriate activation of the normal hemostatic process.
  • Can cause many clinical issues, I.e embolism, death, severe neuro impairment, pain, ect.
43
Q

What is necessary for normal hemostasis or thrombosis to occur?

A
  1. Vascular wall (mainly the vascular endothelium)
  2. Platelets
  3. Coagulation cascade
44
Q

What occurs in the first stage or Vasoconstrictive phase of normal hemostasis?

A
  • After initial injury, there is a brief period of vasoconstriction ( mostly reflex of neurogenic mechanisms) which is augmented by local secretion factors ( like endothelin which is a potent endothelium- derived vasoconstrictor).
  • Effect is transient, and bleeding would resume if not for activation of platelets/ coag factors.
  • Pre sx clotting profile ideal
  • thrombogenic - attracts platelets in blood
45
Q

What occurs in primary hemostasis? (Step 2 of Normal Hemostasis)

A

• platelets attracted to this area and to the von Willebrand factor. Has change in shape, starts aggregating, becomes flat and starts releasing granules that call more platelets to the area. This will cause hemostatic plug. This will attach to the ECM to stop bleeding.

46
Q

What occurs in secondary hemostasis? (Step 3 of Normal Hemostasis)

A

• Will cause tissue factor 3 to be exposed to site of injury. Tissue factor is membrane bound pro coagulation glycoprotein synthesized by epithelium. It acts with factor 7 as way to activate clotting cascade. Eventually will create thrombin, thrombin will cleave circulating fibrinogen (in fluid state) into insoluble fibrin (solid), creating fibrin meshwork deposition. (Secondary Hemostatic plug) Thrombin will induce further platelet recruitment/ granule release. 2nd sequence lasts longer than initial platelet plug.

47
Q

What occurs in the thrombus and antithrombic events ? (Stage 4 of normal hemostasis?

A
  • goal of coagulation cascade is to convert fibrinogen to fibrin.
  • Fibrin and platelet aggregates form a solid permanent plug to prevent additional hemorrhage. This stage is counter regulatory mechanism ( they will produce substances that reverse process essentially)
48
Q

What are endothelial cells? What is their roles?

A

 Endothelial cells are key players in the regulation of homeostasis, as the balance between the
anti- and prothrombotic activities of endothelium determines whether thrombus formation, propagation, or dissolution occurs
Endothelial cells primary release anticoagulant factors (to keep blood in fluid state), but injury will cause endothelial cells to release procoagulant factors (to repair injury).

49
Q

What is the activities of each of these factors secreted by endothelium?

Factors:

  • Prostacyclin
  • Nitric Oxide
  • Tissue Plasminogen Activator (tPA)
  • Thrombomodulin
  • Thromboplastin
  • Platelt activating factor (PAF)

von Willebrand Factor

A
  • Prostacyclin: Vasodialation, inhibits platelet aggregation, anticoagulant
  • Nitric Oxide: Vasodialation, inhibits platelet adhesion and aggregation, anticoagulant
  • Tissue Plasminogen Activator (tPA): regulates fibrinolysis, anticoagulant
  • Thrombomodulin: anticoagulant activity, anticoagulant
  • Thromboplastin: Promotes blood coagulation, procoagulant
  • Platelt activating factor (PAF): activation of platelets and neutrophils, procoagulant

von Willebrand Factor: promotes platelet adhesison and activation of blood coagulation, procoagulant

50
Q

What is the clotting cascade?

A
  • Amplifying series of enzymatic conversions. Each step cleaves an inactive proenzyme into an activated enzyme, culminating in thrombin formation.
  • Conclusion of cascade, thrombin converts the soluble plasma fibrinogen to fibrin
  • Coag factors are plasma proteins mainly produced by liver.
51
Q

What is a thrombosis? Thrombus?

A

Thrombosis: Formation or presence of a solid mass (thrombus) within the CV system

Thrombus: • Form plugs: platelets, fibrin, and entrapped blood cells.
• Can cause occlusion of vascular lumen and embolism.
• Adhered to vascular wall as opposite to post mortem blood clot.

52
Q

What is occuring in this image?

A

thrombus/ thrombosis

53
Q

What is the pathogenesis of thrombosis in reference to the virchow triad?

A

Pathogenesis of Thrombosis - Virchow triad
• Endothelial injury - even alone can cause thrombosis
• Alterations in blood flow ( turbulence or stasis)
• Hypercoagulability
◦ Increase coagulation factors or increase sensitivity
◦ Decrease in coagulation inhibitors

54
Q

What is the # 1 cause of thrombosis in humans?

A

DVT- Deep vein thrombosis

55
Q

Where can thrombis’ appear?

A
  • Thrombus can appear anywhere in cardiovascular system.
  • HCM can cause spontaneous death in young cats. (usually underlying left sided CHF)
  • Mural thrombosis -attached to wall of heart
56
Q

What kind of thrombus can you see in this image?

A

Mural thrombus, left ventricle -> on the wall of the heart

57
Q

What is occuring in this picture?

A

Atrial thrombus, left atrium, cat with Cat Hypertrophic Cardiomyopathy (HCM).

58
Q

How can you tell if a clot is post mortem vs. antemortem?

A

• antemortem thrombi are usually attached to wall of endothelial cell, more pale in color, and dry/ friable looking

  • Post mortem clots -> jelly clots
59
Q

What kind of thrombosis will dogs with renal failure develop? What other condition may dogs also have this type of thrombosis?

A
  • Dogs with renal failure can develop pulmonary thrombosis ( antithrombin III in plasma can be lost with PLN )
  • Many dogs with HWD can develop pulmonary thrombosis.
60
Q

What is this picure showing? What is the cause of this issue?

A

Seen in dogs with severe renal glomerular disease protein losing nephropathy  Significant loss of Antithrombin III, a major inhibitor of thrombin

61
Q

What is verminous thrombosis? What can cause this?

A

Verminous thrombosis – thrombus formation in the cranial mesenteric artery of horses with Strongylus vulgaris infection

62
Q

What is occuring in this image?

A

Verminous thrombosis

63
Q

What could verminous thrombosis cause in horses? Is this seen very common? Why does it occur?

A
  • Used to be quite common/ cause of colic.
  • More cases being seen with antihelminth resistance.
  • parasite makes it way through blood vessels and get lost and they produce damage in that area. Can be very prominent.
64
Q

Where must you look in a patient to confirm the occurence or absence of verminous necrosis during necropsy?

A

• Always check that artery during necropsy in horses. Can be in main branch of mesenteric artery, or in the branches (colic, cecum, ect)

65
Q

What is occuring in this image?

A

Verminous thrombosis from stongylus vulgaris

66
Q

What can be seen in this image?

A

• Pinpoint lesions are stronglyosis larvae

67
Q

What is occuring in this image?

A

Saddle thrombosis, cat with HCM. Thrombus is located in the trifurcation of the abdominal aorta

68
Q

Who can get saddle thrombus? What clinical signs/ damage may be seen if this is present?

A
  • Saddle thrombus : increased turbulence is present, as well as hypercoagulability, and potential endothelial damage.
  • Happens in 30% of cats with HCM
  • You can see it in dogs with HCM but its more rare

Signs: Extreme pain / panting/ respiratory distress, dragging hind legs in cats

dogs can have partial saddle thrombus and still have use of legs.

69
Q

What is the outcome of thrombi?

A
  • Lysis
  • Propagation (thrombus in there, starting to form and can cause obliteration of lumen)
  • Embolization (fragmentation of thrombus breaks off and can get stuck in other areas)
  • Organization/ recanalization (can become infiltrated by connective tissue/ macrophages and make small canals in the large clogged vessels)
70
Q

What is occuring in this histological section?

A

Recanalization of an occlusive thrombus, cat

71
Q

What is it called if a piece of the thrombus breaks off and begins to be transported by the blood? What is the concern with this ?

A
  • If a piece breaks off then it would be called an embolism

• Can end up in longs and cause pulmonary ischemia/ hypoxia/ infarct.

72
Q

What is the difference between an emboism and an embolus?

A

The size of the thrombus that was broken off.

small piece -> embolism

larger piece -> embolus

73
Q

What is the result of fibrocartilaginous embolisms in dogs spinal cord? What are the signs?

A

Fibrocartilaginous embolism, dog – spinal cord -> results in spinal cord infarcts
• Sometimes they are running around, and fine and then all of a sudden are in pain, have neurologic signs, and paralysis.
• Usually you can see degeneration and necrosis in spinal cord.
• Not very common

74
Q

What is being seen in this histological section that is stained with alcian blue?

A

cartilage embolism

75
Q

What is occuring in this image? What could it be a complication of?

A

Fat Embolism
 Could be a complication of long bone fractures
- Image is of Bone marrow emboli in pulmonary artery, human –secondary to CPR efforts

76
Q

What percent of people with long bone fractures will get fat embolisms? What percentage will show clinical signs. How long would it take to present itself? What signs may you see?

A

• fat embolism is a complication of long bone fractures. 90 % of people with long bone fractures will get fat embolism but only 5 % have clinical signs. Sometime they could have it happen 3 days after injury. This can also cause neurologic disturbance (embolism to brain), difficulty breathing (to lungs), ect.

77
Q

What is occuring in this image?

A

an infectious cause of thrombosis/ thromboembolism.

Bacterial valvular endocarditis in cattle often involve the right AV valve and can give rise to septic emboli that will lodge in the pulmonary arteries inflammation/ abscess Formation (embolic pneumonia)

78
Q

What is occuring in this image? What is it a result of? What is the result of this kind of thrombus ?

A

Thrombotic Meningoencephalitis (TME), steer, Noah’ Arkive Etiology: Histophilus somni infection – results in vasculitis and thrombosis

79
Q

What is DIC? What are the causes? What stain should be used?

A

Disseminated Intravascular Coagulation (DIC). Signs of tissue hypoxia,
infarction or/and hemorrhage are seen.

  • DIC -> catastrophic systemic reaction, general activation of blood coagulation system
  • Caused by extensive tissue injury, neoplasia, systemic immunologic reactions ( anaphylaxis) and sepsis.
  • Can lead to consumptive coagulopathy and hemorrhage diathesis.
  • You will see fibrin thrombi within glomerular capillaries.
  • Stain: PTAH
80
Q

What is occuring in this image?

A

Fibrin thrombi within glomerular capillaries ( Stain used: PTAH stain -> DIC)

81
Q

What is an infarct?

A
  • Infarct: Caused by an area of ischemic necrosis in a tissue or organ caused by occlusion of either the arterial supply or venous drainage.
  • Venous infarct’s are usually intensely hemorrhagic as blood backs up into affected tissue behind the obstruction.
82
Q

What is occuring in this image?

A

Venous infarction, small intestinal volvulus, pig. Note the intensely congested loops of small intestine undergoing venous infarction. The twisting of the mesentery associated with the volvulus has resulted compression of the arteries and veins of the intestine. Because arterial pressure is higher than venous pressure, some blood can get into the gut but the compression of the thin-walled veins results in backing up and stagnation of blood in the gut

83
Q

What occurs as time passes with arterial infarcts?

A

“Arterial infarcts are often initially hemorrhagic but become pale as the area of coagulation necrosis becomes evident”

84
Q

What is an infarct microscopically ?

A

Microscopically an infarct is a focal area of coagulation necrosis

85
Q

What is this an image of?

A

Renal infarct.

• Thrombus will cause obliteration of lumen of that artery and you will have a triangular shaped area of necrosis due to hypoxia.

86
Q

What is shock? What will it cause?

A
  • Shock is common pathway for number of potentially lethal events, including severe hemorrhage, extensive trauma, burns, large myocardial infarction, massive pulmonary embolism, and microbial sepsis.
  • Regardless of reason it will cause systemic hypoperfusion which is caused by either reduced cardiac output or by reduced effective circulating blood volume.
  • End results are hypotension, impaired tissue perfusion and cellular hypoxia. This may lead to DIC/ Multiorgan failure.
87
Q

What is cardiogenic shock?

A

(failure of the heart to maintain normal cardiac output)

88
Q

What is hypovolemic shock?

A

Fluid loss due to hemorrhage, vomiting, diarrhea

89
Q

What is blood maldistribution?

A

Anaphylactic (Type 1 hypersensitivity)
 Neurogenic (neurological injury leading to loss of vascular tone and peripheral pooling of blood)

  • Sepsis
90
Q

What is sepsis?

A

(results from the host innate immune response to infectious organisms that may be blood borne or localized to a particular site).

91
Q

What causes most cases of septic shock?

A

• Most caused by endotoxin producing gram negative bacilli.

92
Q

What are endotoxins? What does LPS and other microbial substances do?

A

Endotoxins are bacterial wall lipopolysaccharides (LPS) consisting of a toxic fatty acid (lipid A) core common to all gram-negative bacteria, and a complex polysaccharide coat (including O antigen) unique for each species. LPS and other microbial substances induce injury & activation of the vascular endothelium plus stimulate (“activate”) WBCs to release cytokines vasodilation & pro-thrombotic diathesis (DIC).

93
Q

What organs are very suceptible to tissue hypoxia?

A

Brain & heart are very susceptible to tissue hypoxia.

94
Q
A

General Pathology (18 decks)

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