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Veterinary Pathology > Vascular Disorders & Thrombosis - End E1 > Flashcards

Vascular Disorders & Thrombosis - End E1 Flashcards

1
Q

What are characteristics of arteries?

A

large lumen: minimal resistance

thick vessel walls: smooth muscle / elastic fibers

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2
Q

What are characteristics of arterioles?

A

narrow lumen
respond to sympathetic and parasympathetic innervation (constriction & relaxation of vessels)

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3
Q

What is the function of capillaries?

A

site of nutrient and waste exchange

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4
Q

What are the 3 types of capillaries?

A

continuous

fenestrated

discontinuous

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5
Q

What is a continuous capillary? Which organs?

A

endothelial cells have a complete cytoplasm

basal lamina is continuous which, in the lungs, allows for the thin endothelial cell cytoplasm to diffuse gases from the alveolus into the blood and vice versa

lungs, bone, thymus, brain (BBB), muscle

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6
Q

What is a fenestrated capillary? Which organs?

A

endothelial cell has many fenestrae with or without a thin diaphragm - basal lamina is continuous

glomeruli, choroid, ciliary process of eye

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7
Q

What is a discontinuous capillary? Which organs?

A

the gaps in discontinuous capillaries are larger than in fenestrated capillaries; the basal lamina is discontinuous

liver: gaps in venous sinusoids of the liver are wider than the discontinuous capillaries

spleen: endothelial cells are elongated and protrude into the lumen; blood cells can pass readily through the walls of the splenic masses

liver, endothelium in sinusoids has NO BASEMENT MEMBRANE

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8
Q

What are characteristics of veins/venuoles

A

mostly collagen (distention>contraction)

little smooth muscle and elastin

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9
Q

Veins can hold up to ____ of total blood volume

A

65%

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10
Q

What does blood passage depend on regarding veins/venuoles?

A

valves - prevent backflow
contraction of skeletal muscles

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11
Q

What are lymphatics and what are their functions?

A

surround microcirculation - capillaries

begin as blind-ended lymphatic capillaries

overlapping endothelial cells and large inter endothelial gaps - can accommodate large particles

valves and contraction of skeletal muscles to move lymph forward towards the heart

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12
Q

Is this an artery or a vein?

A

vein

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13
Q

What are the microanatomy of blood vessels?

A

tunic intima
tunica media
tunica adventitia: CT

elastin: gives elasticity to vessels

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14
Q

What are the mechanisms of edema i.e. what causes it?

A

increased vascular permeability
increased hydrostatic pressure

decreased oncotic pressure
decreased lymphatic drainage

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15
Q

What is wrong with this heart? What side are we looking at?

A

heart is rounded - cardiomegaly

should have fat down subsinuosal interventricular groove and also has a pink serous color which is serous atrophy of fat

auricular face

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16
Q

What is tracheal froth caused by?

A

increase of hydrostatic pressure
pulmonary edema

is caused by the backup of blood into the pulmonary circulation, leading to increased pressure in the pulmonary capillaries. This pressure forces fluid into the lungs, causing pulmonary edema. When air mixes with this fluid, it creates froth, which can accumulate in the trachea and is a sign of severe pulmonary edema

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17
Q

Which side of the heart deals with trachea froth / pulmonary edema and why?

A

left side

is caused by the backup of blood into the pulmonary circulation, leading to increased pressure in the pulmonary capillaries. This pressure forces fluid into the lungs, causing pulmonary edema. When air mixes with this fluid, it creates froth, which can accumulate in the trachea and is a sign of severe pulmonary edema

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18
Q

What is the arrow pointing to in the picture?

A

fibrin adhesions

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19
Q

What is wrong with this heart in this young golden retriever?

A

has an atrial septal defect

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20
Q

What is ascites?

A

yellow-tinged fluid found in the abdominal cavity

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21
Q

What side of the heart deals with ascites and hepatic congestion?

A

right side

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22
Q

What is wrong with this organ?

A

liver has a “mottled-like” appearance - nutmeg liver - reticular pattern
chronic passive congestion

blood flows from portal area to central vein

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23
Q

Which mechanism of edema is responsible for these gross lesions and why?

A

vascular edema

capillary leak: Inflammation or injury to blood vessels can cause them to become more permeable, allowing proteins and fluids to leak into the surrounding tissue

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24
Q

How does bottle jaw anemia by haemonchus contortus cause edema?

A

worms suck protein out of blood which causes fluid to seep out into interstitium (= increases hydrostatic pressure, decrease oncotic in blood vessel which encourages diffusion out of blood vessel)

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25
Q

How does one get decreased lymphatic draining?

A

decrease lymphatic drainage due to obstruction

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26
Q

T/F: This is an example of ascites

A

TRUE - but has more things going on - fetal congenital edema - anasarca

hydrops fetalis which has abnormal accumulation of fluid in the tissues of the fetus, leading to generalized swelling (edema) - can certainly cause ascites and swelling in places such as the skin, thoracic cavity (hydrothorax), and pericardial cavity (hydropericardium)

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27
Q

What is transudate - a classification of edema?

A

hydrostatic imbalance

clear, odorless

lower protein, low specific gravity, low fibrinogen

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28
Q

T/F: With transudate regarding edema, vascular permeability is affected significantly

A

FALSE - would be yellow-tinged

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29
Q

What is an example of a transudate?

A

pulmonary edema - interlobular septa are expanded, prominent, and firm

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30
Q

A dog drowned recently. Necropsy revealed these characteristics. Describe it.

A

pulmonary edema - aka left-sided heart failure

“The lungs are distended and edematous with emphysema, petechiae, random atelectatic foci, and subpleural hemorrhages. Present tracheal red-tinged froth”

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31
Q

What kind of fluid does ascites normally have?

A

modified transudate - SG and protein values slightly higher than with transudate

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32
Q

How would you describe this image of a chicken’s coelomic cavity?

A

ascites - modified transudate

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33
Q

What is affected with exudate? What are its characteristics?

A

vascular permeability

high SG and protein - fibrinogen

numerous cells, especially leukocytes

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34
Q

The fluid in this image is [transudate/modified transudate/exudate]

A

modified transudate - FIP cat

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35
Q

What are the “players in the game” regarding hemostasis?

A

endothelial cells
coagulation factors
platelets

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36
Q

What are the top 4 goals of hemostasis?

A

primary: constrict and “plug “ the hole - platelet plug

secondary: build a bridge (fibrin meshwork)

pull the plug (fibrinolysis)

fix this mess (tissue repair)

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37
Q

What is the goal of primary hemostasis?

A

vasoconstriction and platelet plug - stop bleeding

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38
Q

What are the players in primary hemostasis?

A

exposed sub endothelial collagen

endothelial cells - vWf (also platelets and sub endothelial collagen)

fibrinogen - inactive precursor of fibrin

platelets - produce pro-inflammatory mediators ADP and TXA2

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39
Q

What are the pro-inflammatory mediators for primary hemostasis?

A

ADP
TXA2

40
Q

What does TXA2 do?

A

platelet aggregation and adhesion - make stronger and more stable

41
Q

What does ADP do?

A

binds fibrinogen to platelets (loose meshwork)

42
Q

What does vWf do?

A

promote platelet aggregation and adhesion

has strength against shearing forces (helps resist shear factor of blood)

43
Q

What is the goal of secondary hemostasis? How is this accomplished?

A

formation of fibrin plug - more stable

coagulation cascade - intrinsic pathway, extrinsic pathway, common pathway

44
Q

What are the vitamin K dependent factors?

A

2, 7, 9, 10

45
Q

What causes endothelial cells to produce tissue factor (3)?

A

endotoxin
TNF
IL-1
TGF-beta
thrombin

46
Q

What is the role of fibrinogen in primary hemostasis?

A

acts like a bridge between platelets

  • it binds to specific receptors on the surface of platelets called Glycoprotein IIb/IIIa receptors. When fibrinogen binds to these receptors on different platelets, it pulls them together, helping them clump and form a platelet plug
47
Q

What does factor X do?

A

II into IIa (thrombin) which turns fibrinogen to fibrin

a meshwork

48
Q

What is the goal of fibrinolysis?

A

contact group of coagulation factors + tPA

= plasminogen —> plasmin - starts cutting up fibrin threads

fibrin turns into fibrin degradation products

49
Q

What are fibrinolysis inhibitors?

A

tPA —> plasminogen —> plasmin —> fibrin —> FdP

PAI-1: plasminogen activator inhibitor (tPA)

Alpha-2 antiplasmin: inhibits plasmin so it can’t break fibrin down into fibrin degradation products

50
Q

What is fibrinolysis inhibitors?

A

inhibit breakdown of a clot

51
Q

What binds to the c protein-S-thrombomodulin system?

A

antithrombin III (ATIII) and tissue factor pathway inhibitor (TFPI)

52
Q

What is antithrombin III?

A

most potent inhibitor of coagulation

53
Q

Where is antithrombin III produced?

A

hepatocytes and endothelium

54
Q

Which factor does antithrombin III NOT clot?

A

VIIa

55
Q

What are the functions of antithrombin III?

A

inhibits fibrinolysis, kinin formation, and complement activation

prevents the breakdown of clots

56
Q

What is the tissue factor pathway inhibitor (TFPI)?

A

inhibitor of extrinsic pathway of coagulation

suppresses thrombin formation

produced by endothelium and smooth muscle cells

does not substantially inhibit extrinsic coagulation path until factor Xa levels increase

57
Q

What is thrombin?

A

procoagulant but can also act as an anticoagulant by destroying factors V and VIII

58
Q

How does thrombin sometimes act as an anticoagulant?

A

destroying factors V and VIII

59
Q

What is hemorrhage?

A

damage or loss of function to:

endothelium
blood vessel
platelets
coagulation factors

60
Q

What are the causes of hemorrhage?

A

trauma
infectious agents
collagen disorders
thrombocytopenia
neoplasia
severe liver disease

61
Q

What is Ehler’s-Danlos syndrome?

A

collagen deficiency - leads to stretchy skin because less structure in connective tissues

62
Q

This is a necropsy of a guttural pouch. What happened here?

A

fungal thromboemboli

pouch is thickened and something is being added - fibrin, blood, inflamed cells

63
Q

What are the general causes of thrombocytopenia?

A

can’t produce enough platelets

increased platelet destruction

increased use of platelets

64
Q

What are reasons the body cannot produce enough platelets?

A

estrogen toxicity
radiation/drugs
viruses

65
Q

What is a reason why there is increased platelet destruction?

A

autoimmune
inherited
uremia
NSAIDS

66
Q

What is a reason for increased use of platelets?

A

DIC - intravascular coagulation, consumption of platelets and coagulation factors (thrombocytopenia and hemorrhage)

67
Q

What is going on here in this ferret?

A

excess cortisol - makes more estrogen which means platelets are not being produced enough

68
Q

Elaborate on reasons for decreased platelet function

A

Inherited: along with coagulation factor-inherited deficiencies

von Willebrand’s disease: aren’t able to form a clot to an extend
> autoantibodies against vWf leads to decreased platelet aggregation

uremia: severe dehydration or kidney disease

NSAIDS: inhibits pro-inflammatory mediators, lowers thromboxane which decreases function (will still have SAME numbers)

69
Q

Contrast petechiae vs ecchymoses

A
70
Q

What are some reasons the kidney can have increased pallor?

A

consider fat, necrosis, edema, perfusion problem ,inflammation

71
Q

What are important factors in thrombosis - Virchow’s triad?

A

endothelial injury

blood stasis (or slowing) / turbulence

hypercoagulability: coagulation factors, fibrinolytic inhibitors (prevent breakdown of fibrin)

72
Q

What are emboli?

A

free-floating components in a blood vessel

basically, a blood clot forms —> piece of clot breaks off <- that’s the emboli

73
Q

What is an infarct?

A

when the emboli gets stuck

74
Q

What are causes of an embolus?

A

thromboemboli
bacterial
parasitic
fat
fibrocartilaginous
neoplastic
air - “the bends”

75
Q

Give an example of an embolism caused by a parasite

A

heartworms

76
Q

What is wrong with this canine heart?

A

heartworm dog - pulmonary artery should be smooth and shiny

77
Q

Explain how strongylus vulgaris causes emboli

A

migrates through vasculature and fragments of worms go through aorta and get lodged —> causes an infarct

damage to endothelial cells stimulate TF factor 3 to clot

78
Q

Explain what is wrong here. Is the red color due to hyperemia, congestion, or hemorrhage?

A

hemorrhage

79
Q

What is hyperemia?

A

active blood flow TO a site - arteries

80
Q

What is congestion?

A

venous congestion (blood pools in veins), pulmonary edema, allergies, hepatic congestion from R side of heart

81
Q

What is hypoxia?

A

depletion of O2 in rbcs —> cellular injury, anaerobic metabolism, necrosis

82
Q

What is ischemia?

A

poor perfusion; deprives cells of oxygen and nutrients

83
Q

What is re-perfusion injury?

A

restoring blood flow can cause additional injury because of the sudden influx of O2 and inflammatory cells —> creates reactive O2 species i.e. free radicals

84
Q

What is an infarct?

A

area of tissue death because of prolonged reduction of blood supply

85
Q

What is a thrombus?

A

blood clot —> comprised of platelets and fibrin

86
Q

What is emboli?

A

detached, traveling intravascular mass

blood vessels too small —> causes embolism —> leads to obstruction of blood flow to downstream tissues —> can result in ischemia and infarction

87
Q

What are the classifications of shock?

A

cardiogenic
circulatory (non-cardiogenic)

88
Q

What is cardiogenic shock?

A

heart unable to pump blood to meet body’s needs - state of circulatory failure due to low oxygen and perfusion; heart attack

89
Q

What are categories of circulatory i.e. non-cardiogenic shock?

A

volvulus, torsion, etc

hypovolemic

blood maldistribution

90
Q

What is volvulus?

A

intestines twist

non-cardiogenic

91
Q

What is torsion?

A

twisting gut along a longitudinal axis

non-cardiogenic

92
Q

What is hypovolemic?

A

reduced circulating volume - blood and fluid, can get with dehydration

non-cardiogenic

93
Q

What is blood maldistribution and its categories?

A

pooling of blood in peripheral tissues

anaphylactic
neurogenic
septic

94
Q

What is blood maldistribution regarding anaphylactic?

A

type I hypersensitivity, blood goes to viral organs

95
Q

What is blood maldistribution regarding neurogenic?

A

trauma, electrocution, fear
- venous pooling

96
Q

What is blood maldistribution regarding septic?

A

bacteria or fungi release vascular and inflammatory mediators. LPS in bacteria – septic shock leads to systemic vasodilation, hypotension, hypoperfusion (proinflammation and procoagulation factors)

  • not just one thing going on

Veterinary Pathology (11 decks)

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