Test 2 - Circulatory Disturbances Flashcards

1
Q

What is the microcirculation?

A

The microcirculation consists of arterioles (small arteries proximal to a capillary bed), metarterioles (arterial capillaries), capillaries (thin, semipermeable vessels that connect arterioles and venules), and postcapillary venules (small vessels that merge to form veins after collecting blood from a capillary network). Smooth muscle of the arterioles and metarterioles regulates flow of blood into the capillary bed. There is a dramatic drop in pressure and blood flow rate from the arterial to the venous side of the microcirculation, facilitating interactions between capillary blood and interstitial fluid. Blind-ended lymphatic vessels that originate near capillary beds interact
intimately with the microcirculation.

Microcirculation is so called because its components are only visible with the microscope.

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2
Q

Define hemostasis.

A

Arrest bleeding by the physiological properties of vasoconstriction and coagulation or by surgical means

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3
Q

What are the different functions of the vascular endothelium?

A

Role in hemostasis

  • Anti-thrombotic & pro-fibrinolytic in the normal state
  • Pro-thrombotic and anti-fibrinolytic during injury

Modulates perfusion:

  • NO relaxes and causes vasodilation
  • Endothelin causes vasoconstriction

Role in inflammation:

  • Regulates the traffic of inflammatory cells
  • Produces pro-inflammatory cytokines
  • Control angiogenesis and tissue repair
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4
Q

Describe the fluid distribution of the body.

A

Total Body Water: 65% of total body weight

  • Plasma (5%)
  • Interstitial Fluid (15%)
  • Intracellular Fluid (40%)
  • Transcellular Fluid (5%)
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5
Q

Define interstitium.

What is it composed of?

A
  • Space between tissue compartments (microcirculation and the cells).
  • Composed of the Extracellular Matrix (ECM) and supporting cells
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6
Q

What is the medium through which all metabolic products must pass between the microcirculation and the cells?

A

The interstitium

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7
Q

What is the ECM composed of?

A

Composed of structural molecules (collagen, reticulin, elastic fibers) and ground substance (glycoproteins like fibronectin & laminin, plus glycosaminoglycans, proteoglycans etc..)

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8
Q

What accounts for the water distribution between the two compartments of plasma and interstitium?

A

Hydrostatic and osmotic pressures

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9
Q

Describe how changes in hydrostatic and osmotic forces may lead to tissue edema.

A

“Capillary hydrostatic and osmotic forces are normally balanced so that there is no net loss or gain of fluid across the capillary bed. However, increased hydrostatic pressure or diminished plasma osmotic pressure will cause extravascular fluid to accumulate. Tissue lymphatics remove much of the excess volume, eventually returning it to the circulation via the thoracic duct; however, if the capacity for lymphatic drainage is exceeded, tissue edema results”.

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10
Q

Define edema.

A
  • Abnormal accumulation of excess extracellular water in interstitial spaces or in body cavities
  • Fluid is outside both the vascular fluid compartment and cellular fluid compartment (i.e.: within the interstitium).
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11
Q

What are the pathomechanisms of edema?

A
  1. I_ncreased blood hydrostatic pressure:_ (Generalized: e.g. right-sided congestive heart failure (CHF); Localized: e.g.: tightly bandaged limb resulting in venous occlusion.
  2. Decreased plasma colloidal osmotic (a.k.a. oncotic) pressure: Proteins not absorbed from diet (e.g.: starvation, GI malabsorption), Proteins not produced (e.g.: liver disease), Protein loss (e.g. glomerular disease, Intestinal mucosal damage)
  3. Lymphatic obstruction. Damage/ obstruction of lymphatics (e.g.: surgery, neoplasms, inflammation)
  4. Increased vascular permeability (Inflammation)
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12
Q

What are the two classifications of edema?

A
  • Inflammatory: Increased vascular permeability – refers as an “exudate”. Edema fluid in these cases is “protein rich” –> an exudate (high protein content (>30g/L), specific gravity (>1.025), total nucleated cells (<7x109L) –> less than 7,000 cells per μl.
  • Non-inflammatory (e.g.: edema of CHF; edema of liver failure) – refers to as a “transudate”. Edema fluid in these cases is “protein poor” –> low protein content (<30g/L), low specific gravity (<1.025), low cellularity (<1.5x109L) –> less than 1,500 cells per μl.
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13
Q

Describe the gross appearance of edema.

A
  • Wet
  • Gelatinous and heavy
  • Swollen organs
  • Fluid seeps from cut surfaces
  • May be yellow
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14
Q

Describe this image of the gastric wall of a horse.

A

Edema

  • Wet
  • Gelatinous and heavy
  • Swollen organs
  • Fluid weeps from cut surfaces
  • May be yellow
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15
Q

Describe the histological appearance of edema.

A
  • Clear or pale eosinophilic staining depending on whether is non-inflammatory or inflammatory edema.
  • Spaces are distended
  • Blood vessels may be filled with red blood cells
  • Lymphatics are dilated
  • Collagen bundles are separated
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16
Q

Define pitting edema.

A

When pressure is applied to an area of edema a depression or dent results as excessive interstitial fluid is forced to adjacent areas

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17
Q

Hydrothorax

A

Fluid in the thoracic cavity

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18
Q

Pericardial Effusion

A

“Mulberry heart disease”- (inflammatory edema). Note fibrin strands and cloudy appearance of the pericardial fluid.

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19
Q

Ascites/Hydroperitoneum

A

Fluid (transudate) within the peritoneal cavity

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20
Q

Anasarca

A

Generalized edema with profuse accumulation of fluid within the subcutaneous tissue

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21
Q

Edema is dependent on ________.

A

Extent, location, and duration

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22
Q

How does tissue change after prolonged edema?

A

Tissue may become firm and distorted due to an increase in fibrous connective tissue after prolonged edema

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23
Q

What are the types of pulmonary edema? Describe their mechanisms.

A

Non-inflammatory edema: e.g.: Associated to left-sided congestive heart failure (CHF).

Inflammatory edema: Damage to pulmonary capillary endothelium –> e.g.: pneumonia

ARDS (Acute respiratory distress syndrome) Sudden, diffuse and direct- increase in vascular

permeability: high fatality rate –> Followed by pneumonia if animal survives

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24
Q

What is most associated with chronic pulmonary edema?

Describe the pathophysiology.

A
  • Most commonly associated with cardiac failure
  • Alveolar walls become thickened –> may lead to fibrosis
  • Congestion, micro-hemorrhages –> and accumulation of heart failure cells
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25
Q

What are siderophages?

A

Hemosiderin-laden Macrophages* (“heart failure cells”) within alveoli

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26
Q

Describe the difference between hyperemia and congestion.

A
  • Both terms indicate a local increase in blood volume and flow within the vascular bed.
  • Hyperemia indicates increase of arteriole-mediated engorgement of the vascular bed. Blood is oxygenated (red).
  • Congestion indicates passive, venous engorgement. Blood is not oxygenated (blue).
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27
Q

Pathological hyperemia is caused by an underlying pathological process – usually ______.

A

Inflammation

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28
Q

_________ is one of the cardinal signs of inflammation. What are the other signs?

A

Reddening (rubor)

tumor, calor, rubor, pain, loss of function

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29
Q

Describe the mechanism of congestion.

What are the different ways to classify it?

A

Passive engorgement of vascular beds caused by a decreased outflow of blood

Since the vascular beds are engorged with poorly oxygenated blood tissues are dark red to blue (cyanotic), depending on the degree of stagnation.

Like other lesions it can be classified according to duration (acute or chronic) and its extent:

localized (e.g. isolated area of venous obstruction); generalized: Systemic change like in CHF.

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30
Q

List some examples of physiological hyperemia.

A
  • Digestion: ↑ blood flow to the GI tract during digestion.
  • Exercise: ↑ blood flow to muscles during exercise
  • To dissipate heat: ↑blood flow to the skin to dissipate heat and cool down.
  • Neurovascular: Involuntary ↑in blood flow to the face (facial hyperemia) as a result of embarrassment or emotional distress –> common in people with social anxiety.
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31
Q

What is this?

A

Pitting Edema

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32
Q

What is this?

(Heifer)

A

Hydrothorax (idiopathic pulmonary hypertension)

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33
Q

What is this?

A

Pericardial effusion – “mulberry heart disease”- (inflammatory edema). Note fibrin strands and cloudy appearance of the pericardial fluid.

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34
Q

What is this?

A

Ascites or hydroperitoneum: fluid (transudate) within the peritoneal cavity. Dog with CHF

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35
Q

What is this?

A

Ascites, horse with CHF

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36
Q

What is this?

A

Anasarca: Generalized edema with profuse accumulation of fluid within the subcutaneous tissue

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37
Q

What is this?

A

Submandibular edema (“bottle jaw”), is commonly associated with severe GI parasitism and hypoproteinemia in sheep

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38
Q

What is this?

(Horse)

A

Horse, forelimb. This animal had generalized edema due to protein-losing enteropathy

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39
Q

What is this?

What characteristics make this obvious to you?

(Pig)

A

Pulmonary Edema

How to distinguish pulmonary edema in the lungs:

See enlarged lungs –> when you open the thoracic cavity, normally the lungs will collapse. But when you open it up and there is pulmonary edema you will still see them occupying a large amount.

  • Pleural surface looks moist or wet
  • Will also see impression of the lungs (this is not normal!)
  • If you open the trachea - see frothy fluid - this Is abnormal and suggestive of the presence of pulmonary edema
  • Interlobular connective tissue - gives lobulation of pulmonary parenchyma. See expansion of CT. Gelatinous/yellow appearance.
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40
Q

What is this?

(Horse)

A

Pulmonary Edema

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41
Q

This is the the histological appearance of what disorder?

A

Pulmonary Edema

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42
Q

What is the arrow pointing to?

What is distinct about this cell?

What is this associated with?

A

HE-stain, dark brown pigment within the cytoplasm of alveolar macrophages

These are also known as “heart failure cells” or siderophages.

This is diagnostic of chronic pulmonary edema associated with Left sided congestive heart failure. The brown pigmentation results from the phagocytation of the RBCs and metabolizing iron.

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43
Q

What is this? What type of Hyperemia is it?

(Dog)

A

Gingivitis - this is pathological hyperemia (arterial) associated with edema/inflammation.

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44
Q

What is this? What type of Hyperemia is it?

A

Bulbar and palpebral Conjunctivitis

Pathological Hyperemia (arterial)

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45
Q

What is this? Describe what happens as a result of this condition.

(Dog)

A

Gastric volvulus(torsion) in a dog : Twisting of vessels obstructs gastric veins → severe venous congestion (acute, local, congestion) → ischemia (necrosis) → loss of endothelial integrity → hemorrhage →shock → death

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46
Q

What is this?

(Horse)

A

Intestinal volvulus

47
Q

What is this?

(Horse)

A

Colonic torsion

48
Q

What is this?

What is it typically associated with?

(Dog)

A

[Acute] Pulmonary congestion: Usually the result of heart failure and associated with edema.

49
Q

What is this?

(Dog)

A

Diffuse brownish discoloration of the lungs of a dog with chronic pulmonary edema and congestion secondary to left-sided CHF

50
Q

What is this?

(Horse)

A

Livers of horses with right-sided CHF.

51
Q

This is condition is also known as _______.

What is it associated with?

A

Nutmeg Liver

Chronic hepatic congestion

52
Q

What is this?

Describe how this happens.

A

Nutmeg Liver (RCHF)

Chronically there is low-grade Hypoxia & ↑ pressure of centrolobular hepatocytes leading to atrophy and necrosis

53
Q

9 y/o female rottweiler with a history of tumor on one of its left limb toes. What is this associated with?

A

Local lymphatics are distended (lymphangiectasia) and filed with neoplastic cells.

54
Q

Describe the subsequent cascade of events with chronic left sided congested heart failure.

A

LCHF –> Pulmonary edema –> Pulmonary hypertension (backing up of blood in the lungs) –> [Time] –> increased pulmonary resistance –> Right sided CHF –> Congestion in the venae cavae

55
Q

Define Hemorrhage.

A
  • Is defined as the escape of blood from the blood vessels (extravasation)
  • Can be external or internal (within tissues or body cavities)
56
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)
57
Q

Hemorrhage vs. Hyperemia/ Congestion

A
  • Hemorrhage- blood is outside the vessel wall
  • Hyperemia & congestion blood is within the blood vessels
58
Q

________ leads to fatal cardiac tamponade.

A

Hemopericardium

59
Q

How is the clinical significance of hemorrhage determined?

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.

60
Q

Hemorrhage by Rhexis

A

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

61
Q

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…)

62
Q

Hemorrhagic Diathesis

A

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

63
Q

Hemothorax

A

blood in the thoracic cavity

64
Q

Hemoperitoneum

A

blood in the peritoneal cavity

65
Q

Hemarthrosis

A

blood within a joint space

66
Q

Hemoptysis

A

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

67
Q

Epistaxis

A

Bleedingfromthe nose.

68
Q

What are the different classifications of hemorrhage according to size?

A
  1. Petechia (pl. petechiae): up to 1-2 mm in size. Especially found on skin, mucosal and serosal surfaces
  2. Ecchymosis (pl, ecchymoses): Larger than petechia (up to ~1 or 2 cm). As seen in bruise (contusion) or small hematoma.
69
Q

Agonal Hemorrhages

A

Petechiae and ecchymoses associated with terminal hypoxia

Commonly seen in animals after slaughter.

70
Q

Suffusive hemorrhage

A

Larger than ecchymosis and contiguous.

71
Q

Paint-brush hemorrhage

A

Looks like if red paint was hastily applied with a paint brush. Most common on mucosal and serosal surfaces.

72
Q

Describe the resolution of hemorrhage.

A
  • Small amounts can be reabsorbed
  • Larger amounts require phagocytosis and degradation by macrophages
  • Organizing hematoma: Central mass of fibrin & red blood cells surrounded by supportive vascular connective tissue –> macrophages will eventually phagocytize this lesion.
  • Hemoglobin (dark red blue color) –> enzymatically converted to bilirubin (blue-green color) and eventually into hemosiderin (gold-brown color)
73
Q

The pathological form of hemostasis is ______, in which a clot (_______) forms within a vessel which is not injured or only mildly injured.

How can thrombosis be viewed?

A

Thrombosis

thrombus

Thrombosis can be viewed as an inappropriate activation of the normal hemostatic process

74
Q

What are the general components necessary for normal hemostasis or thrombosis to occur?

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

“ Blood clotting is a physiological necessity whereas thrombosis is a pathological manifestation of blood coagulation”

75
Q

List the steps in hemostasis.

A
  1. Vasoconstriction
  2. Primary Hemostasis
  3. Secondary Hemostasis
  4. Thrombus and Antithrombotic events
76
Q

Describe the vasoconstriction phase in normal hemostasis.

A

After initial injury a brief period of arteriolar vasoconstriction occurs mostly as a result of reflex neurogenic mechanisms and is augmented by the local secretion of factors such as endothelin (a potent endothelium-derived vasoconstrictor). The effect is transient, and bleeding would resume were it not for activation of the platelet and coagulation systems.

77
Q

Describe primary hemostasis.

A
  • Endothelial injury exposes highly thrombogenic subendothelial ECM, allowing platelets to adhere (via GpIb (glycoprotein lb) receptors to von Willebrand factor) and be activated
  • Activation of platelets results in a dramatic shape change (small rounded → flat
    plates with ↑surface area) and release of secretory granules [ADP and TXA2] lead to further platelet aggregation (via binding of fibrinogen to platelet GpIIb-IIIa receptors) to form the primary hemostatic plug. Within minutes the secreted products have recruited additional platelets (aggregation) to form a hemostatic plug; this is the process of primary hemostasis
78
Q

Describe secondary hemostasis.

A

Tissue factor (factor III-thromboplastin) is also exposed at the site of injury.Tissue factor is a membrane-bound procoagulant glycoprotein synthesized by endothelium. It acts in conjunction with factor VII as the major in vivo pathway to activate the coagulation cascade, eventually culminating in thrombin (factor II) generation.Thrombin cleaves circulating fibrinogen into insoluble fibrin, creating a fibrin meshwork deposition (secondary hemostatic plug). Thrombin also induces further platelet recruitment and granule release. This secondary hemostasis sequence lasts longer than the initial platelet plug

79
Q

Describe the thrombus and antithrombotic events that occur during hemostasis.

A

Polymerized fibrin and platelet aggregates form a solid permanent plug to prevent any additional hemorrhage. At this stage counter-regulatory mechanisms [e.g., tissue plasminogen activator, t-PA (fibrinolytic product) and thrombomodulin (interfering with the coagulation cascade)] are set into motion to limit the hemostatic plug to the site of injury.

80
Q

What cells are key players in the regulation of hemostasis?

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”

81
Q

Coagulation factors are plasma proteins produced mainly by _______.

A

the liver

82
Q

What is the coagulation cascade?

A

Amplifying series of enzymatic conversions; each step proteolytically cleaves an inactive proenzyme into an activated enzyme, culminating in thrombin formation

83
Q

What happens at the conclusion of the proteolytic cascade?

A

At the conclusion of the proteolytic cascade, thrombin converts the soluble plasma protein fibrinogen into fibrin

84
Q

Thrombus

A

Aggregate of platelets, fibrin and entrapped blood cells. Can result in occlusion of the vascular lumen and embolism. It is adhered to the vascular wall as opposite to a blood clot.

85
Q

Describe Virchow’s triad.

A
  1. Endothelial injury
  2. Alterations in blood flow (turbulence or stasis)
  3. Hypercoagulability: ↑in coagulation factors (or ↑sensitivity to) OR ↓ in coagulation inhibitors
86
Q

Where can thrombi be located within the CV system?

A

Mural thrombus

Atrial thrombus

pulmonary thrombosis

Verminous thrombosis (crainial mesenteric artery)

Saddle Thrombosis (trifurcation of abdominal aorta)

87
Q

What kind of disease is typically associated with pulmonary thrombosis? Why?

A

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

88
Q

Verminous thrombosis

A

Thrombus formation in the cranial mesenteric artery of horses with Strongylus vulgaris infection

89
Q

Saddle thrombosis

A

Thrombus is located in the trifurcation of the abdominal aorta

90
Q

What are the different possible outcomes of thrombi?

A
  • Lysis
  • Propagation
  • Embolization
  • Organization/ recanalization
91
Q

“If pieces of a thrombus break off from the original mass and sail downstream to lodge at a distant site, that process is called ______. The mass that brakes off is called an ________.”

A

embolism

embolus

92
Q

Fibrocartilaginous embolism in the spinal cord may result in ________.

A

Spinal cord infarcts.

93
Q

Fat embolisms may be a complication of ________.

A

Long bone fractures

94
Q

Disseminated Intravascular Coagulation

A

“Potentially catastrophic systemic reaction (thrombo-hemorrhagic disorder) in which there is generalized activation of the blood coagulation system”(Not a primary disease).

Many etiologies including extensive tissue injury, neoplasia, systemic immunologic reactions (e.g. anaphylaxis) and sepsis –> Can lead to ”consumptive coagulopathy” and hemorrhagic diathesis.

Signs of tissue hypoxia, infarction or/and hemorrhage are seen.

95
Q

Infarction

A

Localized area of ischemic necrosis in a tissue or organ caused by occlusion of either the arterial supply or the venous drainage.

Microscopically an infarct is a focal area of coagulation necrosis.

96
Q

Venous vs Arterial Infarcts

A
  • Venous infarcts are usually intensely hemorrhagic as blood backs up into the affected tissue behind the obstruction
  • Arterial infarcts are often initially hemorrhagic but become pale as the area of coagulation necrosis becomes evident
97
Q

Shock/Cardiovascular Collapse

A
  • Shock is the final common pathway for a number of potentially lethal clinical events, including severe hemorrhage, extensive trauma or burns, large myocardial infarction, massive pulmonary embolism, and microbial sepsis
  • Regardless of the underlying pathology, shock gives rise to _systemic hypoperfusio_n; it can be caused either by reduced cardiac output or by reduced effective circulating blood volume. The end results are hypotension, impaired tissue perfusion, and cellular hypoxia. This may lead to DIC and “multi-organ system failure”.
98
Q

List the different types of shock.

A
  1. Cardiogenic Shock (failure of the heart to maintain normal cardiac output)
  2. Hypovolemic Shock (Fluid loss due to hemorrhage, vomiting, diarrhea)
  3. Blood Maldistribution
  • Anaphylactic (Type 1 hypersensitivity)
  • Neurogenic (neurological injury leading to loss of vascular tone and peripheral pooling of blood)
  • Septic (results from the host innate immune response to infectious organisms that may be blood borne or localized to a particular site).
99
Q

Describe the pathogenesis of septic shock.

A

Most cases of septic shock are caused by endotoxin-producing gram-negative bacilli (endotoxic shock) 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).

100
Q

What tissues are very susceptible to tissue hypoxia?

A

Brain and Heart

101
Q

What is this condition known as? What can it lead to?

A

Hemopericardium–>leads to fatal cardiac tamponade.

102
Q

What is this?

(Pig)

A

Dissecting aneurysm. Pig with Copper deficiency

103
Q

Where are dissecting aneurysms typically seen?

A

In addition to horses, dissecting aneurysms are also reported in the coronary and renal arteries of young male racing greyhounds – can lead to arterial rupture and fatal hemorrhage

104
Q

What is a dissecting aneurysm?

A

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.

105
Q

This condition is known as _______.

A

Hemarthrosis –blood within a joint space

106
Q

What is the term for this kind of hemorrhage?

A

Petechia (pl. petechiae): up to 1-2 mm in size. Especially found on skin, mucosal and serosal surfaces

107
Q

What is the term for this kind of hemorrhage?

A

Ecchymosis (pl, ecchymoses): Larger than petechia (up to ~1 or 2 cm). As seen in bruise (contusion) or small hematoma.

108
Q

What kind of hemorrhage is this?

A

Agonal Hemorrhages: Petechiae and ecchymoses associated with terminal hypoxia

Commonly seen in animals after slaughter.

109
Q

Describe the location of the thrombi in the pictures.

A

Left: mural thrombus, left ventricle

Right: Atrial thrombus

110
Q

What is pictured? What kind of thrombosis is this?

A

Infectious thrombosis

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(embolicpneumonia)

111
Q

What is pictured? What kind of thrombosis is this?

A

Infectious Thrombosis

Thrombotic Meningoencephalitis (TME), steer,

Etiology: Histophilus somni infection – results in vasculitis and thrombosis

112
Q

What is this? Explain the pathophysiology.

(pig)

A

Venous infarction, small intestinal volvulus, pig. Note the intensely congested loops of small intestine undergoing early 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 compressed veins result in backing up and stagnation of blood in the gut.

113
Q

What is this?

(Rabbit)

A

Acute pale infarcts, kidney. Multiple, pale white to tan pyramidal-shaped infarcts extend from the renal cortex to the medulla. The infarcts bulge above the capsular surface (center top), indicative of acute cell swelling.