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General Pathology > Exam # 2 > Flashcards

Exam # 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)

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39
Q

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

A

1st stage - Hemoglobin, red-blue

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40
Q

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

A

2nd stage- Bilirubin – blue-green

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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.

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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.
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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
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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
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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.

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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.

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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)
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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).

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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

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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.
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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.

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52
Q

What is occuring in this image?

A

thrombus/ thrombosis

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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

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54
Q

What is the # 1 cause of thrombosis in humans?

A

DVT- Deep vein thrombosis

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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
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56
Q

What kind of thrombus can you see in this image?

A

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

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57
Q

What is occuring in this picture?

A

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

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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
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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.
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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

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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

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62
Q

What is occuring in this image?

A

Verminous thrombosis

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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.
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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)

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65
Q

What is occuring in this image?

A

Verminous thrombosis from stongylus vulgaris

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66
Q

What can be seen in this image?

A

• Pinpoint lesions are stronglyosis larvae

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67
Q

What is occuring in this image?

A

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

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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.

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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)
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70
Q

What is occuring in this histological section?

A

Recanalization of an occlusive thrombus, cat

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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.

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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

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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

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74
Q

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

A

cartilage embolism

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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

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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.

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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)

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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

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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
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80
Q

What is occuring in this image?

A

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

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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.
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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

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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”

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84
Q

What is an infarct microscopically ?

A

Microscopically an infarct is a focal area of coagulation necrosis

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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.

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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.
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87
Q

What is cardiogenic shock?

A

(failure of the heart to maintain normal cardiac output)

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88
Q

What is hypovolemic shock?

A

Fluid loss due to hemorrhage, vomiting, diarrhea

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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
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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
95
Q

What is pathologic calcification?

A
  • Abnormal deposition of Ca++ salts usually in form of phosphates and carbonates.
96
Q

What is Dystrophic calcification?

A

When the deposition of abnormal calcium salts occur locally in dying tissue.

97
Q

What causes Metastatic calcification?

A

Almost always result of hypercalcemia secondary to some disturbance in calcium metabolism.

98
Q

What is the cause of this kind of calcification? Which is the abnormal lesion A or B?

A

Causes can be vitamin E / Selenium deficiency

There will be areas of normal adipose tissue (labeled A) and abnormal calcification ( usually on left ventricle (labeled b)

99
Q

How can you tell if there is calcification when you make your incision? Where is the calcification in this histology slide?

A

You can tell when making your incision if there are calcium deposits because it will feel gritty in comparison to other areas.

The calcium deposits are the dark red areas in this slide.

100
Q

What is occuring in these images? What is the causes of the lesions? Where can it be seen most commonly?

A

This is Metastatic calcification. Cases of Vitamin D toxicity can cause calcium deposition in organs causing metastatic calcification. You will see it most commonly in the intima of major vessels, and you will see raised, granular mineralization.

104
Q

What can cause vitamin D toxicity?

A

Vitamin D toxicity, access to plants that are carcinogenic, that contains vitamin D analogs which can cause hypercalcemia due to excessive vitamin D.

105
Q

What is occuring in this image?

A

Uremic Gastritis

106
Q

What is occuring in this image? What will you feel when palpating this area?

A

Uremic gastritis leading to gastric mineralization.

In this image you can see the mineralization of the mucosa of the intestines.
• You will feel hard tissue in the intestines, this would be deposition of calcium w/in intestinal lumen.

107
Q

Is Uremic gastritis Dystrophic or metastatic calcification?

A

Metastatic Caclification.

108
Q

What will you see with familial renal disease? What will you see on histology segments?

A

You can see congestion and hemorrhage, and inflammation. When the stain (von Koda) is done you can see increased calcium deposits within the mucosa. Could be dystrophic due to vasculitis and ischemia which leads to necrosis, or it could be metastatic due to secondary hyperparathyroidism.

109
Q

What would a histological slide like the one below be showing?

A

Metastatic calcification

110
Q

What is Uremic gastritis? What are causes of uremic gastritis?

A
  • Renal failure -> Secondary Hyperparathyroidism -> Hypercalcemia.
  • Uremia induces vasculitis -> this causes thrombosis in different tissues, including GI tract. This is called uremic gastritis. Sometimes this is the cause of lesions such as this in patients with renal failure.
  • This accumulation of urea, nitrogen products in blood of individual with renal failure will cause vasculitis in the mucosa of the stomach, mucosa of intestine, can lead to thrombosis/ ischemic damage to the tissue, which will cause degeneration/ necrosis and then dystrophic calcification.
  • Can also develop secondary hyperparathyroidism (which would lead to metastatic calcification.
111
Q

What occurs with renal failure?

A

• Renal Failure:
◦ Retention of phosphates-> increased stimulation of parathyroid gland -> increase in parathyroid hormone -> stimulation of osteoclasts -> increased calcium absorption ( increased calcium level (aka hypercalcemia))

This can lead to dystrophic/ metastatic calcification

113
Q

What is anthracosis? What is its cause? Where can it be found? Is it clinically significant?

A
  • position of carbon particles is called anthrocosis
  • most common in lungs, bronchi, regional lymph nodes, ect.
  • From carbon deposition within these areas. Can be seen in areas with high air pollution. Can be seen on pleural surface.
  • Not clinically significant, but can be an indication of exposure to air pollution.
115
Q

What are tattoos used for in animals and what occurs to them after they are introduced to the body?

A
  • tattoos used to identify animals.
  • these pigments are phagocytized by macrophages while others remain free in the Dermis without eliciting an inflammatory response.
116
Q

When can familial renal disease show signs

A

Familial renal disease can show signs at 2 years old.

117
Q

When the term dust is used, what are the stains that are typically used? What are the concerns with inhaling these substances?

A

This term is usually applied to the inhalation of silica
or asbestos (asbestosis) that may lead to significant
pulmonary fibrosis.

  • Silica crystals are birefringent under
    polarized light. Mild will not show any clinical significance.

You don’t see it often. (Sometimes when there is exposure of volcanic ash.

118
Q

What are carotenoid pigments?

A
  • Fat soluable pigements of plant origin
  • Can be seen by over abundance of certain vitamin A precursors.
  • Can be seen in the adipose tissue. Due to consumption of feed with high level of pigment. Seen in horses and cattle.
119
Q

What pigment can you see in this image?

A

Carotenoid pigments.

122
Q

What is subpleural mineralization and where can this be seen? What is this a consequence of?

A

Y ou can see this sometimes in patients with renal failure,. Their could be areas of subpleurital mineralization. This is considered to be both metastatic/ dystrophic depending on the cause. Can be found on the inside of the ribs

123
Q

What is occuring in this photo?

A

Albinism

124
Q

What is occuring in these photos?

A

Melanosis

125
Q

What are the three categories of pigments and where are they formed?

A

Exogenous (formed outside the body)

Endogenous (formed inside the body)

Hematogenous (blood origin)

126
Q

What are tan/ brown colored areas on this histological slide?

A

Lipofuscin

127
Q

What are examples of exogenous pigments?

A
  • Carbon
  • Tattoos
  • Dusts
  • Carotenoids
  • Tetracyclin
128
Q

Where is the area of melanosis located in this image?

A

The leptomeninges

130
Q

What is the most exogenous pigment and what can it lead to?

A

Carbon is the most exogenous pigment. Portal entry is usually by inhalation and can lead to black lungs. This is common in areas with substantial air polution.

132
Q

What are dusts? What are the conditions associated with it ?

A

Dusts. The condition associated with the inhalation and
retention inorganic dusts within the lungs is known as Pneumoconiosis

133
Q

What is occuring in the box in this image?

A

Ceroid -> associated to vitamin E deficiency and the ingestion of unsaturated fatty acids –brown discoloration of the tunica muscularis.

135
Q

What is hemaglobin? What would you see in the mucus membranes of dogs that have adequate oxygen content? In the dogs who do not?

A

Hemoglobin is the normal red pigment of erythrocytes, responsible got oxygen transport.

  • Normal animal Pink MM
  • Cyanosis: Pale grey- Blue MM -> Decreased O2, CO2 may be carried instead
  • Anemia: Pale pink - White - > Decreased RBC count
138
Q

What is occuring in these images?

A

Hemoglobin pigmentation

139
Q

What can be seen in this image?

A
  • Urinary bladder was filled with red urine ( patient with bovine babesiosis)
  • You can see increased bilirubin and since it is difficult to excrete it will accumulate in the tissues which gives the jaundice characteristic yellow color
140
Q

What is parasite hematin?

A

• Black tracks on surface of the liver, this is exhaust from the trematods you can find cystic lesions with trematode clusters. This is the result of breaking down hemoglobin in the area.

141
Q

What is the concern/ what can occur with tetracycline based antibiotics? When should you avoid the administration of tetracycline?

A

When administered during the period of teeth development they
will be it deposited in the mineralizing dentin, enamel and
cementum, staining the teeth or portions of them yellow or
brown.
 high doses may induce enamel hypoplasia
Avoid the administration during pregnancy!

142
Q

What is occuring in this image?

A

Fluke exhaust. Parasite hematin.

143
Q

What are the endogenous pigments?

A

Melanin

Lipofuscin/ Ceroid.

144
Q

What is occuring in these images? What is causing the lesions?

A

Hemosiderin

  • can also be seen in the lungs of individuals with congestive heart failure.
  • when there is breakdown of erythrocytes, iron containing heme will stain.
145
Q

What is occuring in this image? What stain can be used to find hemosiderin? How will it stain?

A

Chronic pulmonary congestion and edema is occuring in a horse with CHF. Iron (Perl’s) stain can be used to find Hemosiderin-laden macrophages (“heart failure cells” -> siderophages). These cells will stain blue.

146
Q

What is melanin? What produces it? What can cause/ is a response of a general lack of melanin?

A

Pigment normally present in the epidermis,
responsible for skin color and hair color.

 Produced by melanocytes.

 Formed by the oxidation of tyrosine, which requires
tyrosinase (copper-containing enzyme).

 Lack of tyrosinase may lead to a general lack of
melanin, a metabolic inherited defect known as
albinism.

148
Q

What is being indicated by the black arrows?

A

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

149
Q

What is occuring in this image?

A

Chronic pulmonary congestion and edema, horse with congestive heart failure, H&E stained section

151
Q

What is lipofuscin?

A

The aging pigment

153
Q

Where can you see melanosis? What is the clinical implications?

A
  • Sometimes can be seen in young animals such as cattle/ pigs, sheep ect. You can also see it in the intima of the aorta, and in the brain.
  • This is presence of melanin in abnormal places.
  • Their is dark brown discoloration on the tissue. This is just accumulation of melanin outside the skin. No proliferation changes/ clinical significance.
155
Q

What is occuring in this image? What pigment is causing it?

A

This is icterus or jaundice. It is caused by an increase in the bilirubin in plasma.

156
Q
A
157
Q

What is occuring in this image?

A

Congenital Erythropoietic Polyphyria

158
Q

What will occur with urine that contains the pigments of Congenital Erythropoietic Porphyria?

A
  • Pigment is excreted in urine that if allowed to stand in light, develops a port-wine color due to photic activation of porphyrins

 Urine and tissues fluoresce blue-green in UV light

159
Q

Where can lipofuscin be found? What does it look like? What can it do to surrounding tissue?

A
  • can be found in an aging animal. Can be seen in cardiac muscle, cardiac myocytes. Brown yellow granular tissue, that is next to nucleus.
  • Wear and tear pigment.
  • Can cause the destruction of organelles over time. This is usually not concerning. But will indicate age.
160
Q

Other than in cardiac muscle/ age, where can you see lipofuscin?

A

In neuronal tissue, you can see lipofuscin as well.

161
Q

What is ceroid?

A

Ceroid has a similar histochemical features to lipofuscin but is not age-related.
Small intestine a bit brown, this is the presence of ceroids. This can be a sign of vitamin E deficiency.

163
Q

What are hematogenous pigments?

A

Hemoglobin

Parasite Hematin

Hemosiderin

Bilirubin

Porphyrins

165
Q

What is cyanide poisoning? What occurs? What color are the mm? What is a common cause of cyanide poisoning?

A
  • Cyanide binds to cytochrome oxidase, the enzyme responsible for oxidative phosphorylation -> leads to impaired cellular respiration within mitochondria -> tissues are unable to use the oxygen carried by the blood hemoglobin causing rapid death.
  • The arterial and venous blood in the poisoned individual appears brightly red.
  • Smoke inhalation is a common cause of cyanide poisoning during fires.
166
Q

What occurs in intravascular hemolysis? Where may this substance be secreted? What doe the color indicate?

A

In intravascular hemolysis Hb is released from lysed erythrocytes and stains the plasma pink.

 It may be excreted by the kidney staining it dark-red and the urine red (hemoglobinuria)

170
Q

What is the fluke infestation that could leave fluke exhaust?

A

• Fascilodis Minor ( fluke infestation)

172
Q

What is hemosiderin? Where does it develop?

A

Golden-brown granular iron-containing pigment
(intracellular aggregates of ferritin) that originates
from the breakdown of erythrocytes.

 It develops within macrophages, particularly common
in the spleen, liver or within foci of hemorrhage.

175
Q

What occurs in chronic pulmonary congestion?

A

• Blood will back up into the lungs, which will increase the hydrostatic pressure in the pulmonary vasculature. Left sided congestive heart failure patients can have dyspnea (especially at night), chest tightness.

176
Q

What are the consequences of left sided CHF?

A
  • Left sided congestive heart failure, since there is an area with stagnated poorly o2 blood, you end up with hypoxic damage to the alveoli. Their is also little foci of hemorrhage (micro hemorrhage).
  • RBC that go into alveoli will be phagocytized by alveolar macrophages, this will leave behind these brown intracytoplasmic pigment. This is called /hemosiderin.
179
Q

What is bilirubin? Where is it derrived from? What color is it?

A
  • normal major pigment found in bile

 Derived from Hb but contains no iron (end product of
heme degradation)

 Yellow to brownish green pigment

180
Q

Will Iron be in bilirubin?

A

no iron, end product is from eme degradation.

181
Q

Where is bilirubin conjugated? Where is it excreted? Is there normally a high concentration in the plasma?

A

 Low concentrations are normal in plasma as a result of the
breakdown of senescent red blood cells.

 Bilirubin is conjugated in the liver and excreted in the bile

182
Q

What will occur with excessive bilirubin in the plasma?

A

Excessive amount of bilirubin in plasma will lead to
icterus (Jaundice)

yellow staining of tissues.

183
Q

What are the 3 classifications of icterus and examples of when each is found?

A
  • Pre-hepatic: IMHA ( common especially in dogs) Destruction of RBC. Will overwhelm the liver.
  • Hepatic Jaundice: Hepatosis dietetica - vitamin E/ selenium deficiency. In pigs this can be main presentation due to liver lesions. Jaundice is easily seen in the intima of the vessel wall.
  • Posthepatic: Any disease that occurs after the liver and causes impairment of function.
185
Q

What are porphyrins? What is another name for accumulation of this pigment and why?

A

Congenital erythropoietic porphyria of calves, cats and pigs is a rare inherited disorder caused by deficiency of uroporphyrinogen III cosynthetase. It affects RBC precursors and results in anemia. The disease is refer to as “pink tooth” because porphyrins accumulate in dentin and bones resulting in reddish teeth in young animals and dark brown teeth in older ones.

186
Q

What are parts of the circulatory system?

A

Consists of blood, central pump, blood distribution (arterial (O2+ nutrients) and collection (venous (metabolites, products ect)).

187
Q

What are the lymphatics?

A

Lymphatics that parallel the veins contribute to circulation by draining fluid from the extravascular spaces into the blood vascular system.

188
Q

What is the part of the circulatory system with the largest cross sectional area?

A

Capillaries (part of a whole)

189
Q

What part of the circulatory system is the largest vessel?
What has the lowest pressure

A

Aorta
Vena cava

190
Q

What are the thickest areas of veins? Arteries? Capillaries?

A

◦ Vein: tunica externa, veins also have valves.
◦ Artery: tunica media
◦ Capillary would just be basement membrane with endothelial tissue.

191
Q

What is microcirculation? What occurs in this area?

A
  • microcirculation is where metabolic exchange occurs due to slowing down of circulation.
192
Q

In terms of vascular endothelium, What is hemostasis? What is its role in hemostasis?

A
  • Provides anti thrombic and pro fibrinolytic in normal state and pro thrombotic and anti fibrinolytic during injury.
    • Hemostasis is the arrest bleeding by physiologic properties of vasoconstriction and coagulation or by surgical means. Bleeding can be stopped.
193
Q

What state do you want blood in when in normal conditions? What will help with that?

A
  • Liquid state
  • anti thrombic, pro thrombic, anti fibrinolytic, fibrinolytic factors help with keeping the blood in a liquid state.
194
Q

The formation of this substance is very important for the formation of a clot.

A

◦ Formation of fibrin is very important for formation of clot.

195
Q

What will injury cause to repair the vessel?

A

• Injury will cause prothrombotic, and antifibrinolytic which will help to repair the vessel.

196
Q

What will occur if there is a leaking vessel after an injury?

A

• Leaking vessels after an injury, and endothelial cells will produce cytokines so WBC can go and repair the area. This makes the area more more able to absorb nutrients and bring cells to repair the area.

197
Q

What modulates perfusion in vascular endothelium? What causes vasodilation? What causes vasoconstriction.

A

NO ( nitric oxide) relaxes and causes vasodilation.
Endothelin causes vasoconstriction.

198
Q

What is the role in inflammation of vascular endothelium?

A
  • Regulates traffic of inflammatory cells.
  • Produces pro-inflammatory cytokines
  • Control angiogenesis and tissue repair
199
Q

What is the break down the total body water? What is the body percentage referencing water?

A

Total Body Water: 65 % total body weight

  • Plasma 5%
  • Interstitial Fluid 15%
  • Intracellular Fluid 40%
  • Transcellular Fluid 5%
200
Q

What changes total fluid content in the body?

A

Age. Infant have increased water content in their blood. Fluid loss occurs with age, and that is why wrinkles occur.

201
Q

What is the interstitium? What is ECM?

A
  • Interstitium: Space between tissue compartments. It is the medium through which all metabolic products must pass and is made up of ECM and supporting cells.
  • ECM: Collagen, reticulin, elastic fibers) ground substance (glycoproteins, ect)
202
Q

What is the hydrostatic pressure? What is osmotic pressure? What is the role of both of these?

A
  • Hydrostatic: Pressure of fluid within the vasculature
  • Osmotic: Pressure based on presence of solutes, primarily proteins, albumin.
  • These control the amount of fluids that will be within the vasculature vs. in the third space.
203
Q

What does it mean if there is increased hydrostatic pressure and decreased osmotic pressure ? What can occur with fluid backup ?

A

Increased Filtration.
Edema.

204
Q

What occurs on the arteriole side ? what occurs on the venous side? what happens to the remaining fluid.

A

• Arteriole side has increase of hydrostatic pressure( increased in fluid exchange), venous side has increase in oncotic pressure. remaining fluid is drained by lymphatic system
◦ Arteriole: Favors filtration
◦ Veins: Favor absorption.

205
Q

What will cause extravascular fluid to accumulate?

A

• Increased hydrostatic pressure or diminished plasma osmotic pressure within capillaries will cause extravascular fluid to accumulate. If capacity of lymph drainage is exceeded tissue edema will result.

206
Q

What are the categories of circulatory disturbances?

A

Edema
Hyperemia & Congestion
Hemostasis
Hemorrhage
Thrombosis, Embolism, DIC
Infarction
Shock

207
Q

What is edema?

A
  • abnormal accumulation of excess extracellular fluid.
  • Fluid outside vascular compartment.
208
Q

What are the pathomechanisms of edema?

A

• Increased hydrostatic pressure
◦ (Right sided CHF, Tightly bandaged limb)
◦ Impairing venous return will increase hydrostatic pressure.
• Decreased plasma colloidal osmotic pressure aka oncotic pressure ( decreased protein absorption, decreased protein synthesis, increased protein loss)
◦ (proteinuria can indicate protein loss via damage of glomeruli in kidneys. This can lead to generalized edema in an individual
◦ Starvation, hypoproteinemia, PLE, ect.
• Lymphatic obstruction: Damage/ obstruction of lymphatics
◦ Tumor, surgery, inflammation ect.
• Increased vascular permeability
◦ inflammation, cytokines will decrease vascular permeability, and cause localized edema.

209
Q

What is occurring in this image? What is the cause? What other causes can cause similar effects?

A
  • Diffusely swollen leg, this is due to lymphatic obstruction.
  • Some tumors of dogs (i.e melanoma which this dog had), can spread along the lymphatics)
210
Q

What is occuring in this image?

A

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

213
Q

What is occuring in this image?

A

Horse Gastric wall edema

214
Q

What can you see on a histological slide of edematous tissue?

A
  • Clear or pale eosinophilic staining depending on whether it is non-inflammatory or inflammatory edema
  • Spaces are distended
  • Blood vessels may be filled with RBC
  • Lymphatics are dilated
  • Collagen bundles are separated
215
Q

What are the classifications of edema, and what are the associated signs of each?

A

• Edema can be classified as:
◦ Inflammatory: Increased vascular permeability, - Refers to “exudate” -> high protein, high specific gravity, higher cellularity, less than 7,000 cells/uL
◦ Non Inflammatory: Edema of CHF, Edema of Liver failure) Referred to as a “transudate” -> Low protein content, low specific gravity, low cellularity, less than 1500 cells/uL

Inflammatory may indicate peritonitis.

216
Q

What is occurring in the image in the circled part?

A

Pitting edema

217
Q

What is a hydrothorax? When can you see it?

A

• Presence of fluid w/in the thoracic cavity - hydrothorax
◦ Can be seen with chronic pneumonia
◦ Something in the lungs that causes pulmonary hypertension.
◦ Resistance to blood being pumped into the lungs

218
Q

What is the gross appearence of edema in a patient post mortem?

A

Wet

Gelatinous and Heavy

Swollen organs

Fluid weeps from cut surfaces

May be yellow

220
Q

What is occuring in this image?

A

• Mulberry heart disease - related to vitamin E selenium deficiency.
◦ Increased protein in fluid, fibrin strands and cloudy with high cellularity, kind of inflammatory conditions.

221
Q

What is occuring in this image?

A

• Hydroperitoneum/ Ascites: Fluid ( transudate) within peritoneal cavity.

223
Q

What is occuring in this image?

A

Ascites in a horse

224
Q

What is occuring to the puppies in this image? When does this typically occur?

A

Anasarca

This can be seen typically in aborted fetus’ with severe congenital heart malformations .

225
Q

What is pitting edema?

A

When pressure applied to an area depression or dent results as excessive interstitial fluid is forced to adjacent areas.
Takes a few seconds for area to return to normal.

228
Q

What is occuring in this image?

A

Bottle Jaw/ Submandibular edema

229
Q

What other conditions can cause generalized edema?

A

Protein losses (i.e protein loosing enteropathy, protein loosing nephropathy)

230
Q

What can cause resistance of blood being pumped into the lungs?

A

‣ Increase of hydrostatic pressure, increase amount of plasma within those blood vessels and this causes edema.
‣ Left sided CHF will eventually back up into the lungs and cause all of the same issues as you see above.

231
Q

What is pericardial effusion? What is an example of a condition that causes pericardial eddusion from Vitamin E / Selenium deficiency?

A

• Pericardial effusion: yellowish in color, contains a bit of an exudate
• Mulberry heart disease - related to vitamin E selenium deficiency.
◦ Increased protein in fluid, fibrin strands and cloudy with high cellularity, kind of inflammatory conditions.

234
Q

What is hydroperitoneum/ ascites? What can cause more diffuse edema?

A
  • Hydroperitoneum/ Ascites: Fluid ( transudate) within peritoneal cavity.
  • R sided heart-failure can lead to more diffuse edema.
237
Q

What is anasarca?

A

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

238
Q

What is another term for submandibular edema? What can cause it? Why?

A
  • Submandibular edema: bottle jaw is commonly associated with severe GI parasitism and hypoproteinemia in sheep.
  • Specifically can be seen with infestations of Haemonchus contortus (barber pole worm) . Translucent fluid.
  • Decreased oncotic pressure from hypoproteinemia from heavy parasitism.
239
Q

What parasite is more commonly the cause of submandibular edema?

A

Haemonchus contortus (barber pole worm)

240
Q

What is pulmonary edema? What are the types?

A

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

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

241
Q

What is acute respiratory distress syndrome?

A

ARDS (Acute respiratory distress syndrome) Sudden, diffuse and direct- increase in vascular permeability: high fatality rate -> Followed by pneumonia if animal survives

242
Q

What is occuring in this image?

A

• Pulmonary edema
◦ Lungs slightly enlarged, heavier, fluid coming out, you will see frothy material when you open sections of trachea, lungs, ect.
◦ Gelatinous material in the tissues.

244
Q

What is being shown in this image?

A

• Macrophages with hemosiderin are indicators of micro hemorrhage/ pulmonary hemorrhage.
◦ these are considered heart failure cells or siderophages.

245
Q

What is hyperemia?

A

Hyperemia indicates increase of arteriole-mediated engorgement of the vascular bed. Blood is oxygenated (red).
(i.e: exercise, inflammation)

246
Q

What is congestion?

A

Congestion indicates passive, venous engorgement. Blood is not oxygenated (blue).
(i.e local obstruction, congestive heart failure)

247
Q

What is chronic pulmonary edema? How is it seen in histological slides?

A

Most commonly associated with cardiac failure

 Alveolar walls become thickened -> may lead to fibrosis

 Congestion, micro-hemorrhages -> and accumulation of heart failure cells

250
Q

What is occuring in this image? Is it pathologic hyperemia or physiologic?

A

Gingivitis (pathologic hyperemia)

251
Q

What is occuring in this image? Is it pathologic hyperemia or physiologic?

A

Bulbar and palpebral conjunctivitis, human

253
Q

What is occuring in this image? Is this congestion? What is the pathophysiology behind the damage?

A
  • GDV usually includes splenic involvement.
  • signs -> abd pain, distention, ect.
  • Obstruction of gastric veins which will cause hypoxic damage due to the lack of blood-flow. Sepsis can occur, peritonitis, ect.
  • Can happen in swine as well when they get over excited.
  • Necrosis in the walls of vessel will cause blood to leak into abdomen after death.
254
Q

What is occuring in this image?

A

Intestinal volvulus, horse

255
Q

What is occuring in this image?

A

colonic torsion, horse

256
Q

What is occuring in this image? What is the cause of the discoloration?

A
  • L side of heart can cause pulmonary congestion/ edema and this can cause brownish accumulation on lungs.
  • Lungs will be enlarged, brown changes on lungs is deposition of heart failure cells and hypoxic damage (sign chronic pulmonary edema)
  • Lungs also wet looking
257
Q

What are examples of physiologic hyperemia?

A

Digestion: Inc blood to GI
Exercise: Inc blood to muscles
To dissipate heat: Inc blood to skin to cool down
Neurovascular: Involuntary inc blood in face as result of embarrassment/ emotional distress

258
Q

What is occuring in this picture? What is the likely cause? What are the differences from normal pathology?

A

Chronic hepatic congestion - > likely the result of Right sided CHF

Livers are enlarged and exhibit rounded edges

259
Q

What is occuring in this image? What is this an indication of?

A

Chronic hepatic congestion: “Nutmeg liver”

260
Q

What is pathologic hyperemia?

A

Caused by an underlying pathological process – usually inflammation.

 Arteriolar dilatation->secondary to inflammatory stimuli (inflammatory mediators).

 Redness (“rubor”) is one of the 5 cardinal signs of inflammation : tumor (swelling), calor (heat), rubor (redness), dolor (pain) and loss of function.
Swelling/ edema occurs

261
Q

What are the 5 cardinal signs of inflammation?

A

 Redness (“rubor”) is one of the 5 cardinal signs of inflammation : tumor (swelling), calor (heat), rubor (redness), dolor (pain) and loss of function.

264
Q

What is congestion? What are its classifications?

A

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

269
Q

What occurs with pulmonary hypertension and how does it lead to chronic hepatic congestion? What will the livers look like in these instances?

A
  • Pulmonary Hypertension makes it hard for R side of heart to pump blood so R side will also start failure
  • Increase hydrostatic pressure,
  • Backup of poorly O2 blood will back up into liver and can show congestion in there.
  • Liver will be round, and enlarged, and you will see fibrosis/ discoloration due to backup of blood.
272
Q

What is the cause of nutmeg liver?

A

Chronic hepatic congestion -> nutmeg liver
• Poorly O2 blood/ increased around portal vein, and hypoxic damage due to poor oxygenation.

273
Q
A

General Pathology (18 decks)

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