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Animal Health & Disease > Lecture #6: Edema & Thormbosis > Flashcards

Lecture #6: Edema & Thormbosis Flashcards

1
Q

what is edema?

A

excess of fluid (usually a clear fluid or transudate) in interstitial space or body cavities (outside of cellular or vascular fluid compartments)

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2
Q

what is ascites?

A

accumulation of fluid in cavities (edema in cavities)

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3
Q

what is hydroperitoneum?

A

edema of the peritoneal cavity

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4
Q

what is hydrothorax?

A

edema of the pleural cavity- thorax

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5
Q

what is hydropericardium?

A

edema of the pericardial sac- thorax

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6
Q

what is hydrometra?

A

edema in the uterus

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7
Q

what is anasarca?

A

a severe and generalized edema with profound subcutaneous tissue swelling (swelling of different tissues and organs)

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8
Q

what is interstitium?

A

the space between tissue compartments (leftover after removing vessels, nerves and parenchymal cells)

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9
Q

what are some characterisitcs of the Extracellular Matrix or ECM

A

-consists primarily of fibrous proteins embedded in a hydrated gel-like substance
-fibers: collagens, elastin
-glycosaminoglycans (GAGs) or mucopolysaccharides
-proteoglycans= GAGs + proteins
-glycoproteins: fibronectin (connective tissue)
and Laminin (basement membranes)

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10
Q

what is Starling Equilibrium?

A

How we calculate the role of hydrostatic and oncotic forces in the movement of fluid across capillary membranes= balance of filtration pressure and absorption pressure

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11
Q

How is filtration pressure calculated?

A

the difference between hydrostatic and colloidal osmotic pressure in the arterial end of the capillary vascular bed :
(plasma hydrostatic pressure- tissue hydrostatic pressure) - (plasma colloidal-osmotic pressure- tissue colloidal-osmotic pressure)

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12
Q

how is absorption pressure calculated?

A

the difference between the hydrostatic and colloidal osmotic pressure in the venous end of the capillary vascular bed :
(PHP-THP)-(PCOP-TCOP)

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13
Q

what are the main factors affecting fluid balance across capillary walls?

A
  • intact circulatory system
  • normal lymphatic system
  • albumin (protein) concentration
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14
Q

what is the pathophysiology of edema (what happens to the body)?

A
  • decreased plasma colloidal-osmotic pressure (decrease of proteins)
  • increased blood hydrostatic pressure
  • lymphatic obstruction
  • increased vascular permeability
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15
Q

what is the most important group of colloid in the body fluids?

A

proteins

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16
Q

what exerts the main osmotic pressure to oppose the hydrostatic pressure in the capillary bed ?

A
  • proteins: albumin most important

- globulins (25% of albumin effect)

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17
Q

what is a cause for edema?

A

Hypoalbuminemia (reduced amount of proteins-albumin) (also called hypoproteinemia)

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18
Q

hypoalbuminemia is caused by two things:

A
  • insufficient synthesis of proteins (caused by starvation or liver disease)
    OR
  • excessive loss of proteins (renal- glomerylonephritis, gastrointestinal- enteritis, parasites)
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19
Q

what is submandibular edema?

A

also known as “bottle jaw”

- swollen jaw area caused by starvation or infection with parasites

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20
Q

what happens if the venous pressure increases?

A

the fluid filtered at the arterial end fails to return to the circulation leading to edema

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21
Q

what are the most common causes of increased blood hydrostatic pressure (venous pressure)

A
  • local: obstruction of the venous flow (thrombus, abscess, tumors, torsions)
  • generalized: cardiac failure
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22
Q

lymphatic obstruction can also cause edema, what are the causes of this?

A
  • lesions that impede normal lymph flow or absorption
  • inflammation in lymph nodes or neoplastic diseases (parasites)
  • trauma, surgeries, elephantiasis
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23
Q

what is obstructive edema?

A

also called lymphatic filariasis (Elephantiasis)

  • caused by helminthic parasite Wuchereria bancrofti
  • blockage of lymphs drainage
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24
Q

another cause of edema is increased vascular permeability- what is the cause of this?

A

endothelial integrity is compromised by :

  • toxins: E. coli enterotoxin in pigs, bee stings
  • inflammatory reaction: inter-endothelial gaps, passage of leukocytes and proteins
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25
Q

what causes edema disease in pigs?

A

the proliferation of enterotoxigenic E.coli in the intestines (E.coli enterotoxemia; SLTIIe toxin or verotoxin 2e)

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26
Q

what are the symptoms of edema disease in pigs?

A
  • peracute death
  • ataxia
  • paralysis
  • recumbency
  • affects submucosa of the stomach, messentary, the subcutaneous tissues of the forehead and eyelids, the larynx and the brain
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27
Q

what can cause edema disease in pigs? (not the toxin- but underlying causes)

A
  • stresses of mixing pigs
  • changes in diet
  • loss of milk antibodies
  • affects primarily healthy, rapidly growing nursery pigs
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28
Q

when does edema disease usually occur?

A

1-2 weeks after weaning and typically involves the healthiest animals in a group

29
Q

what is hydrallantois?

A

accumulation of fluid in the fetal membrane causing a distended abdomen

30
Q

what are the characteristics of hydrallantois?

A
  • observed in last trimester of pregnancy
  • caused by placental or uterine dysfunctions
  • placentomes frequently altered (lower # and hypertrophied)
  • more frequent in cows with multiple fetuses
  • electrolytes (Na, Cl, K) concentration increased in fluid
31
Q

what are the characteristics of hydraminios?

A
  • observed during the last trimester of pregnancy
  • associated with fetal problems (prevent swallowing or intestinal transport of amniotic fluids)
  • fluid is more viscous and syrupy in consistency
32
Q

which is more common hydrallantois or hydraminios?

A

hydrallantois

33
Q

what is a placentome?

A

placentome= cotyledon(placenta) + caruncle (uterus)

34
Q

what are some symptoms of hydrallantois and hydramnios?

A
  • progressive distension of the abdomen (last 4-6 weeks of pregnancy)
  • decreased appetite and difficulty moving and rising
  • tachycardia, anxiety, dehydration, recumbency
  • metabolic problems, abdominal muscle herniation
35
Q

what are the diagnosis and treatment of hydrallantois or hydramnios?

A

diagnosis: rectal palpation and/or ultrasound to confirm
treatment: induce parturition, abortion, cesarean section, immediate slaughter

36
Q

what are some characteristics of udder edema?

A
  • more common in heifers than older cows
  • more frequent in winter (less exercise)
  • higher in pimiparous cows giving birth to male calves
  • high potassium and sodium and low magnesium intake during dry period (diet)
37
Q

what is a thrombus?

A

a solid mass formed within the blood vessels or heart from the constituents of blood (blood clot) can be a physiological necessity (hemostatic plug) or a pathological manifestation (pathological blood clot)

38
Q

what are the three primary conditions (Virchow’s triad) predisposing thrombus formation?

A
  • endothelial injury- integrity of endothelial cells
  • stasis or turbulence of blood flow- how fast the blood flow is
  • blood hypercoagulability- blood coagulation factors
39
Q

what occurs in normal primary hemostasis (immediate platelet plug)?

A
  1. platelet adherence and activation vWF (von Willebrand factor)
  2. shape change
  3. granule release (ADP, TXA2-thromboxane A2)
  4. recruitment
  5. aggregation (hemostatic plug)
40
Q

what occurs in normal secondary hemostasis?

A
  1. tissue factor
  2. activation of coagulation cascade
  3. thrombin activation
  4. fibrin polymerization
41
Q

what is the function of endothelin ?

A

it is a hormone to reduce the amount of blood to the site of infection- so we don’t bleed out

42
Q

what is the final role or the coagulation cascade?

A

to activate thrombin which cleaves fibrinogen to fibrin and forms a mesh of proteins forming the secondary hemostatic plug

43
Q

what gets rid of fibrin?

A

plasmin degrades fibrin

44
Q

what causes platelet attachment?

A

induced by exposure to subendothelial proteins like von Willebrand factor

45
Q

list the main parts of the general sequence of events in hemostasis at the site of vascular injury.

A
  1. brief period of arteriolar vasoconstriction caused by secretion of enothelin
  2. platelets adhere and become activated by exposed thrombogenic subendothelial ECM and change shape and release secretory granules
  3. recruitment of additional platelets (aggregation) to form hemostatic plug
  4. tissue factor (procoagulant factor synthesized by endothelium) acts with secreted platelet factors to activate coagulation cascade
  5. activation of thrombin which converts fibrinogen to fibrin causing local fibrin deposition
  6. polymerized fibrin and platelet aggregates form solid permanent plug
46
Q

what is the job of antiplatelets and what are the main ones?

A

block platelet adhesion and aggregation

  • platelets adhesion is inhibited by endothelial prostacyclin (PGI2) and nitric oxide
  • endothelial cells also express adenosine diphosphatase which degrades ADP, inhibiting platelet aggregation
47
Q

what is the job of anticoagulant and what are the main ones?

A

interfere with the coagulation cascade

- heparin-like molecules and thrombomodulin

48
Q

what is the job of fibrinolytic factors what are the main ones?

A

lyses of blood clots

- tissue-type plasminogen activator (t-PA) helps to clear fibrin deposits from endothelial surfaces

49
Q

what are main prothrombotic properties of endothelial cells?

A
  • platelet effects: adhesion of platelets facilitated by von Willebrand factor (vWF)
  • pro-coagulant proteins: tissue factor (thromboplastin) activates extrinsic clotting cascade (factors IXa and Xa)
  • antifibrinolytic system: inhibitors of plasminogen activator (PAIs) which depress fibrinolysis
50
Q

what two things are essential in various reactions in the coagulation cascade?

A

phospholipid complexes and Calcium ions

51
Q

what are the roles of thrombin?

A
  • generates fibrin
  • platelet aggregation and secretion
  • activates endothelium
  • leukocyte adhesion
  • secretion
  • activates inflammatory cells
52
Q

what are the fates of thrombi?

A

dissolution: most are removed by finbrinolytic activity (thrombolysis-plasmin)
- propagation: accumulate more platelets and fibrin (eventually causing vessels obstruction)
- organization and recanalization (thickened vascular wall)
- embolus formation: thrombi can dislodge and travel to other sites

53
Q

what is an embolus?

A

a detached (movable) intravascular mass that is carried by the blood

54
Q

what occurs in an embolism?

A

emboli lodged and occlude vessels causing ischemic necrosis (infarction)

55
Q

what are the 4 main types of embolism?

A

1) thromboembolism: dislodged thrombus
2) gaseous emboli
3) solid particle emboli
4) amniotic fluid embolism: rupture of uterine veins

56
Q

what is gaseous emboli?

A

accidental injection of air into vessels, decompression sickness in divers, chest wall injury

57
Q

what is solid particle emboli?

A

fat (fracture of long bones), atherosclerotic debris (cholesterol emboli) tumor cell clumps, aggregate of bacteria or parasites

58
Q

what are red infarcts?

A

venous occlusion - blood cannot leave

59
Q

what are white infarcts?

A

arterial occlusions- blood cannot get in

60
Q

what are septic infarcts?

A

emboli with bacteria, the infarct is converted into an abscess

61
Q

what can cause shock (cardiovascular collapse)?

A
  • severe hemorrhage
  • extensive trauma or burns
  • large myocardial infarction
  • massive pulmonary embolism
  • microbial sepsis
62
Q

what can shock give rise to?

A

systemic hypoperfusion caused by reduction either in cardiac output or in the effective circulating blood volume- not enough blood getting to organs

63
Q

what are the consequences of cardiovascular collapse?

A
  • hypotension
  • cellular hypoxia
  • multiple organ failure
  • unconsciousness & death
64
Q

what are the 4 types of shock?

A

1) Cardiogenic shock
2) Hypovolemic shock
3) Septic shock
4) Anaphylactic shock

65
Q

what are the consequences of cardiogenic shock?

A
  • myocardial damage (infarction)
  • ventricular arrhythmias
  • cardiac compression
  • outflow obstruction (pulmonary embolism)
66
Q

what happens in hypovolemic shock?

A

-hemorrhage, fluid loss from severe burns or trauma

67
Q

what is septic shock?

A

systemic microbial infection, most commonly cause by gram-negative infections (endotoxic shock)

68
Q

what happens in anaphylactic shock?

A

IgE-mediated hypersensitivity response (hypersensitivity type I)
antibodies on basophils, release of granules
blood vessels contract and effects respiratory tract

Animal Health & Disease (7 decks)

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