Test 2- Circulatory Diseases Flashcards Preview

Path > Test 2- Circulatory Diseases > Flashcards

Flashcards in Test 2- Circulatory Diseases Deck (130):
1

Q image thumb

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

 

can see due to bright red color

2


 

Q image thumb

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

3

Q image thumb

Pulmonary hemosiderosis

presence of “heart failure cells).

 

liquid in the cytoplasm

4

Q image thumb

SUBACUTE TO CHRONIC HEPATIC CONGESTION IS USUALLY THE RESULT OF RIGHT-SIDED CHF

Livers are enlarged and exhibit rounded edges

5

Q image thumb

Chronic hepatic congestion: “Nutmeg liver”

6

Q image thumb

Subacute hepatic
Congestion – “Nutmeg Liver

 

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

A image thumb
7

Vascular Endothelium

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

8

Fluid distribution

Total BodyWater:

65% of total body weight  Plasma (5%)
 Interstitial Fluid (15%)
 Intracellular Fluid (40%)

 Transcellular Fluid (5%)

 

YOUNGER INDIVIDAULS HAVE A LARGER WATER CONTENT

9

Homeostasis:

“A tendency to stability in the normal body states”

10

Interstitium

Space between tissue compartments (microcirculation and the cells).

 

Is the medium through which all metabolic products must pass between the microcirculation and the cells.

  Composed of the Extracellular Matrix (ECM) and supporting cells

11

Extracellular Matrix

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

12

Water distribution between plasma & the interstitium is primarily determined by

Water distribution between plasma & the interstitium is primarily determined by the hydrostatic & osmotic pressures differences between the 2 compartments

 

Starling Forces:

In simple terms, the hydrostatic pressure moves fluid out of the vasculature; the osmotic pressure of plasma proteins (oncotic pressure) moves fluid into the vasculature.

 

 

 

 

13

however, if the capacity for lymphatic drainage is exceeded

however, if the capacity for lymphatic drainage is exceeded, tissue edema results

14

Edema

--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).

15

Pathomechanisms of Edema

1. Increased 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)

16

Edema can also be classified as

Edema can also be classified as “inflammatory” or “non-inflammatory” edema.

17

Inflammatory Edema

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.

18

Non-inflammatory Edema

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.

19

Q image thumb

Gross Appearance of Edema:

Wet
 Gelatinous and heavy
 Swollen organs
 Fluid weeps from cut surfaces

 May be yellow

20

Q image thumb

Histological appearance of edema

  Clear or pale eosinophilic staining depending on whether is non-inflammatory or inflammatory edema.( inflammatory is  pink because it has a high protein content)

  Spacesaredistended

  Blood vessels may be filled with

red blood cells

  Lymphaticsaredilated

  Collagenbundlesareseparated

A image thumb
21

Q image thumb

Pitting edema

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

 

- takes a while for the tissue to go back to normal after you press in

22

Q image thumb

Hydrothorax: fluid in the thoracic cavity

 

Heifer, Hydrothorax (idiopathic pulmonary hypertension)

23

Q image thumb

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

 

ass with Vit E/selinum deficiency

24

Q image thumb

Ascites or hydroperitoneum: fluid (transudate) within the peritoneal cavity. Dog with CHF. From McGavin, 2007.

25

Q image thumb

Ascites, horse with CHF, UCVM

26

Q image thumb

Anasarca: Generalized

edema with profuse accumulation of fluid within the subcutaneous tissue

27

Q image thumb

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

 

EDx: homonchus conortus

 

 

A image thumb
28

Q image thumb

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

29

Clinical significance of edema

Dependent upon: extent, location and duration.

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

30

Pulmonary edema

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

31

ARDS

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

permeability: high fatality rate  Followed by pneumonia if animal survives

32

Q image thumb

Pulmonary edema, pig

larger lungs with impressions of the ribs

A image thumb
33

Q image thumb

Pulmonary edema, horse,

A image thumb
34

Q image thumb

pulmonary edema, rat

35

Chronic pulmonary edema

Most commonly associated with cardiac failure

 Alveolar walls become thickened-may lead to fibrosis

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

36

Hyperemia and Congestion

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). INFLAMMATION

  Congestion indicates passive, venous engorgement. Blood is not oxygenated (blue). CONGESTIVE HEART FAILURE, TOURNEQT

37

Physiological Hyperemia:

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.

38

Pathological Hyperemia

Caused by an underlying pathological process – usually

inflammation.

 Arteriolar dilatation occurs secondary to inflammatory stimuli (inflammatory mediators).

  Reddening (“rubor”) is one of the cardinal signs of inflammation (tumor, calor, rubor, pain, loss of function).

  Often associated with edema

39

Q image thumb

Pathological Hyperemia

Gingivitis, dog

40

Q image thumb

Bulbar and palpebral Conjunctivitis, human

 

Pathological Hyperemia

41

Congestion

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 extend: localized (e.g. isolated area of venous obstruction);

generalized: Systemic change like in CHF.

A image thumb
42

Q image thumb

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

 

LOCALIZED CONGESTION

43

Q image thumb

Intestinal volvulus, horse

44

Q image thumb

Colonic torsion, horse

45

Hemorrhage

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

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

46

Causes of Hemorrhage

 Trauma
 Sepsis, viremia, bacteremia or toxic conditions
 Abdominal neoplasia may lead to hemoperitoneum

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

47

Hemorrhage vs hyperemia/ congestion

Hemorrhage- blood is outside the vessel wall

 Hyperemia & congestion blood is within the blood vessels

48

Hemorrhage: Clinical significance

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.

49

Q image thumb

Hemopericardiumleads to fatal cardiac tamponade.

50

Hemorrhage by rhexis:

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

A image thumb
51

Q image thumb

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, Left: pig with Copper deficiency

 

Hemorrhage by rhexis:

52

Q image thumb

Bottom: Male turkey

 

Dissecting aneurysm

 

Hemorrhage by rhexis:

53

In addition to horses, dissecting aneurysms are also reported in the coronary and renal arteries of young male racing greyhounds

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

54

Hemorrhage by diapedesis:

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...)

A image thumb
55

Hemorrhagic diathesis

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

56

Hemothorax

blood in the thoracic cavity

57

Hemoperitoneum

blood in the peritoneal cavity

58

Hemarthrosis

blood within a joint space

59

Hemoptysis

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

60

Epistaxis

Bleeding from the nose.

61

Q image thumb

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

62

Q image thumb

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

63

Q image thumb

A image thumb
64

Q image thumb

Suffusive hemorrhage: larger than ecchymosis and contiguous. Serosal surface of the stomach, dog.

65

Q image thumb

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

66

Hemorrhage - Resolution

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.

67

Resolution of hematoma

  1. hemoglobin, red blue
  2. billirubin, blue green
  3. hemosiderin, yellow, brown

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

68

Step 1 in Resolution of hematoma

Hemoglobin, red-blue

A image thumb
69

Step 2 in Resolution of Hematoma

Bilirubin – blue-green

A image thumb
70

Step 3 in Resolution of  Hematoma

Hemosiderin (yellow-brown)

A image thumb
71

Circulatory Disturbances

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

72

Hemostasis

Hemostasis (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.

73

The pathological form of hemostasis is

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

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

74

General components necessary for normal hemostasis or thrombosis to occur:

1. Vascular wall (mainly the vascular endothelium)

2. Platelets- primary component of the clot/thrombosis
3. Coagulation cascade

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

75

Normal Hemostasis

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.

 

Endothelium gets damaged which exposes the ECM;

A image thumb
76

endothelin

a potent endothelium-derived vasoconstrictor

helps to limit the bleeding

77

Endothelial injury exposes

Endothelial injury exposes highly thrombogenic subendothelial ECM, allowing platelets to adhere (via GpIb (glycoprotein lb) receptors to von Willebrand factor) and become activated

adhere to exposed ECM via the receptors

78

Primary Hemostasis

Activation of platelets results in a dramatic shape change (small rounded → flat platelets 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. This molecules also promote vasoconstriction. Within minutes the secreted products have recruited additional platelets (aggregation) to form a hemostatic plug; this is the process of primary hemostasis- this is the first thing that happens to prevent blood loss!

A image thumb
79

secondary hemostatic plug

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 activated) generation.Thrombin (IIa)cleaves circulating fibrinogen (factor I) 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

A image thumb
80

What happens after the plug has been made?

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.

A image thumb
81

Purpose of Endothelial cells

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 allow the blood to remain in a fluid state, but it can have different functions, such as to cogulate the blood

A image thumb
82

Coagulation Cascade

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

 

At the conclusion of the proteolytic cascade, thrombin converts the soluble plasma protein fibrinogen into fibrin( an insoluble molecule to a soluble molecule)

Coagulation factors are plasma proteins produced mainly by the liver

A image thumb
83

Thrombosis

 

“ Formation or presence of a solid mass (thrombus) within the CV system”

 

Happens when the vessel is normal or when a minor injury is exaserbated

 

when hemostasis goes wrong

84

Thrombus (pl. thrombi):

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.

Thrombus within the pulmonary artery, cow

 

in pic: RBC at top and thrombos in the middle

A image thumb
85

Pathogenesis of Thrombosis

Virchow triad

For thrombosis for occur, you usually need 2/3

1. Endothelial injury

2. Alterations in blood flow

(turbulence or stasis)

3. Hypercoagulability

- ↑in coagulation factors (or ↑sensitivity

to)

- ↓ in coagulation inhibitors

A image thumb
86

Q image thumb

Mural thrombus, left ventricle, Cat

in animals with infection(endothelial damage

Location of thrombi within heart

 

87

Q image thumb

Atrial thrombus, left atrium(left side of the picture), cat with Hypertrophic Cardiomyopathy (HCM)

 

- location of thrombi within Cardiovascular system

due to abnormal blood flow and endothelial damage due to hypoxia

88

Q image thumb

Pulmonary thrombosis, dog( can be caused by heartworms or renal/glomerular disease)

Seen in dogs with severe renal glomerular
disease

protein losing nephropathy

Significant loss of Antithrombin III, a major inhibitor of thrombin

89

Q image thumb

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

friable material attached to the wall

can cause colic

 

A image thumb
90

Q image thumb

Strongylosis – colon, horse, Cornell files

 

venious thrombosis

91

Q image thumb

Saddle thrombosis, cat with Hypertrophic Cardiac Myopathy .Thrombus is located in the trifurcation of the abdominal aorta

 

saddle thrombosis- thrombosis at the trifercation of the terminal aorta;

MOSTLY IN CATS

left sided heart failure

 

92

Outcome of thrombi

Lysis- thrombosis can dissapear
Propagation- thrombosis can become bigger and bigger
Embolization- a piece of the thrombosis breaks off and travels in the blood
Organization/ recanalization- they will be invaded by macrophages, etc and you will have vascularization of new blood vessels and new channels

A image thumb
93

Q image thumb

Recanalization of an occlusive thrombus, cat

 

this became organized and recanalization- new blood vessels

94

embolism

If pieces of a thrombus break off from the original mass and sail downstream to lodge at a distant site, that process is called embolism.

95

embolus

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

 

An embolus is any detached intravascular mass (solid, liquid or gaseous) which is carried by the blood to a site distal to the point of origin; most emboli originate from detached pieces of a thrombus, hence the commonly used term of thromboembolism”

A image thumb
96

Q image thumb

Right: Fibrocartilaginous embolism,
dog – spinal cord- results in spinal cord infarcts(areas of necrosis in the spinal cord)

97

Q image thumb

Fat Embolism

 Could be a complication of long bone fractures

 Right: Bone marrow emboli in pulmonary artery, human –secondary to CPR resuscitation efforts

98

Q image thumb

Infectious causes 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 to inflammation/ abscess Formation(embolicpneumonia).

-friable material attached to the wall

- bacteria from the thrombos can break off  and they can get stuck in the pulmonary vein

A image thumb
99

Q image thumb

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

if you section the brain, you will see sections of necrosis

100

Q image thumb

Fibrin thrombi within glomerular capillaries, PTAH stain - DIC

101

Disseminated Intravascular Coagulation (DIC)

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

“Potentially catastrophic systemic reaction (thrombo-hemorrhagic disorder) in which there is generalized activation of the blood coagulation system”(Not a primary disease because it can be triggered by different things).

Many etiologies including extensive tissue injury, neoplasia, systemic immunologic reactions (e.g. anaphylaxis) and sepsis 

-Can lead to ”consumptive coagulopathy” and hemorrhagic diathesis.

- You will have wide activate of the cogaulation cascade

A image thumb
102

Q image thumb

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 result in backing up and stagnation of blood in the gut.

103

Infarction

Infarction: “Localized area of ischemic or as a result of hypoxic necrosis in a tissue or organ caused by occlusion of either the arterial supply or the venous drainage”

 

Venous infarcts are usually intensely hemorrhagic as blood backs up into the affected tissue behind the obstruction

A image thumb
104

Arterial infarcts

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

105

Q image thumb


Acute pale infarcts, kidney, rabbit. Multiple, pale white to tan pyramidal-shaped infarcts extend from the renal cortex to the medulla.The infarcts bulge above the capsular surface

 

triangular shaped lesions

106

Q image thumb

Indicative of acute cell swelling.The glistening areas on the right are highlights from the photographic lamps

 

triangular shaped section

107

Q image thumb

Renal Infarct, HE

 

again, triangular shape

 

108

Microscopically an infarct is

Microscopically an infarct is a focal area of coagulation necrosis

109

Shock

Shock (Cardiovascular collapse)

-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 hypoperfusion; 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”.

110

systemic hypoperfusion

Regardless of the underlying pathology, shock gives rise to systemic hypoperfusion; 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”.

111

Types of Shock

  1. Cardiogenic Shock

  2. Hypovolemic Shock

  3. Blood Maldistribution

  4.  

112

Cardiogenic Shock

failure of the heart to maintain normal cardiac output

113

Hypovolemic Shock

Fluid loss due to hemorrhage, vomiting, diarrhea

114

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).

115

Septic

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

116

Pathogenesis of Septic Shock

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).

Brain & heart are very susceptible to tissue hypoxia.

117

thrombin

necessary to cleaves fibrinogen into fibrin

118

end result of the clotting cascade

TO MAKE THROMBIN

119

Thrombosis vs post mortem clot

post mortem clot- bright shiny surface smooth

thrombos- mostly platelets and fibrin; surface is dull and granular; will usally be attached to the wall of the blood vessel

120

Q image thumb

horse that came into ross

lesion of veninmous arteritis or parasties in the thrombi

121

vena cava thrombosis

in cattle

ruminal acidosis results from

ruminal acidosis does damage to the rumen; bacteria get into  circulation and result in abysesses that are close to the caudal vena cava and these can rupture or form thrombosis

122

PTAH stain

fibrin thrombin within glomerular capillaries

PTAH satin- DIC

A image thumb
123

What kind of necrosis is associated with isemeic/hypoxia?

Cogulation

124

What are the three layers of tissue in the arteries and veins and which is thicker the wall of an artery or a vein?

tunica intima, tunica media, and tunica externa

 

Walls of Arteries are the thickest!

125

Q image thumb

Iron (Perl‟s) stain – Hemosiderin-laden Macrophages* (“heart failure cells”) within alveoli – UCVM.

 

or siderphages

 

chronic pulmonary edema with LCHF

126

Q image thumb

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

127

Q image thumb

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

128

Q image thumb

Livers of horses with right-sided CHF.
Left: UCVM; Right: Dr. King‟s Show&Tell.
Livers are enlarged and exhibit rounded edges

129

Q image thumb

Chronic hepatic congestion: “Nutmeg liver”

130

Q image thumb

Subacute hepatic
Congestion – “Nutmeg Liver”

 

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