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VET375 Pathology > Vascular Disturbances > Flashcards

Vascular Disturbances Flashcards

1
Q

Describe the difference between an Exudate and a Transudate

A
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2
Q
  1. What is Oedema/Effusion
  2. What is the difference beween Oedema and Effusion
A
  1. excess of extracellular fluid
  2. oedema = fluid in tissues, effusion = fluid in body cavaities.
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3
Q

Generalised Oedema is called ?

A

Anasarca

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4
Q

What is pulmonary oedema ?

A

Fluid in the lungs.

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5
Q

What is this ?

A
  1. Pulmonary oedema
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6
Q

What are the primary causes of oedema?

A

increase intravascular pressure

lymphatic obstruction

decreased blood oncotic pressure (aka colloid osmotic pressure)

increased interstitial osmotic pressure

increased vascular permeability

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7
Q

Right sided heart failure, sequale

A

liver congestion causes increased hydrostaticpressure in periacinar regions

leads to fluid into space of disse

leads to fluid into lymphatics, beneath and through the liver capsule, leads fluid into abdo cavity = ascites.

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8
Q

Left sided heart failure sequale

A

Lung congestion leads to increased hydrostatic pressure septal capailiaries.

Fluid is forced ionto the alveoli (soft cough) = pulmonary oedema.

RBC leak into alveoli - phagocytosed.

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9
Q
  1. what is hyperaemia?
  2. Defined the two types of hyperaemia
A
  1. Increased blood within tissue organ vascular bed
  2. passive hyperaemia (reduced venous drainage, cap bed is engorged with blood). Everything is black Active (increased cap supply , cap bed is engorged with blood ) everything is red .
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10
Q

What is ischaemia?

What are the two types ?

A

too little blood in the circulation

Generalised - hypovolameia -blood loss/ dehydration

Generalied - anaemia

Localised - obstruction to blood flow ( intraluminal / extraluminal)

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11
Q

What are the physical responses to hypovolaemia due to blood loss ?

A
  1. Venous return falls
  2. cardiac output is reduced
  3. aterial blood pressure falls
  4. carotid & aortic bodies = stimulate the vasomotor centres = strong sympathetic stimulation.
  5. blood supply to the vital organs only - brain and resp muscles is maintained
  6. tachycardia occurs
  7. adrenalin & noradrenalin are released leading to general vasoconstriction and coronary artery dilation (NAdr)
  8. decrease in blood pressure - renin - angiotensin production (potent vasodilator) & aldosterone production (Na & h20 reabsorption).
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12
Q

Phase 2 - restoration of blood volume

A
  1. blood pressure decreases , despite phase 1
  2. fluid moves from extrvascular spaces into circulation (osmotic forces) to replace lost fluid.
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13
Q

Phase 3 Eryhtropoiesis

A

Number of RBC and the haemoglobin content of the blood is restored to normal

there is enhaced manufacture of plasma proteins within the liver

reticulocytes and metarubicytes will be circulating in the blood , takes abnout 4 days

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14
Q

What is shock ?

A

inadequate perfusion of an organ / microcirculation

inability of the body to compensate through stages 2 & 3

Shock leads to multi organ failure

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15
Q

What are the types of shock

A

Hypovolaemic shock

Cardiogenic shock

Septic Shock

Anaphylactic Shock

Neruogenic - systemic microcirculation prefusion failure

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16
Q

What are the functions of hemostatis ?

What are there failures called ?

A
  1. maintain blood & fluid state =thrombosis
  2. arrest bleeding follow trauma = heamorraghe
  3. remove platlet plug when healing complete = thrombosis
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17
Q

What are the 7 steps in the hemostatic process?

A
  1. Vascular spasm
  2. Primary platlet response
  3. Initiation of thrombin generation
  4. Amplification of thrombin generation
  5. Propogation of thrombin generation
  6. Fibrin formation
  7. Fibrinolysis
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18
Q

What are the consequences of endothelial injury?

A

Vascular spasm

vWF release (from endothelial cells & platelets)

exposure of sub-endothelial matrix proteins ( collagen, fibrinogen etc )

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19
Q

What are the 4 steps of hemostatic processes?

A
  1. Injury
  2. Adhesion (platelets bind to sub-endothelial matrix proteins)
  3. Activation
  4. Aggregation (fibrinogen-platelet plug)
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20
Q

Platelet inhibition and dysfunction is often aquired , due to what ?

A

Administration of NSAIDs - which inhibit thomboxane

21
Q

What is glanzmann thromboasthenia ?

A

Intrinsic platelet disorder in which the fibrinogen receptor (GPIId/IIIa) is absent or reduced in the surface of platelets.

22
Q

What pathway does prothrobin time (PT) relate to ?

What is the other pathway related to ?

A

Extrinsic pathway

Intrinsic pathway - Partial thomboplastin time (PTT)

23
Q

Write the Clotting Casade, including the Extrinsic and Intrinsic pathway

A
24
Q

What pathway is vitamin K dependant ?

A

Extrinsic pathway - prothrombin time

25
Q

Prothrombin time and PIVKA assesses ?

A

Extrinsic and common pathways

26
Q

Activated partial thromboplastin time (aPTT) and activated coagulation time (ACT) assesses ?

A

Intrinsic and common pathways

27
Q

What is the Common Pathway

A
28
Q

If I had a normal platlet count, prolonged PT and aPTT and negative FDP test what would be my interpretation

A

Rodenticide toxicity

29
Q

If you received a coag test result stating :

thrombocytopenia with prolonged aPTT, PT and positive FDP

What would be your interpretation ?

A

Consumption of both platelets and coagulation factors = DIC (disseminated intravascular coagulation)

30
Q

How does thrombus dissolution occur ?

What inhibits the intrinsic pathway ?

A

Fibrinolysis is inhibited immediately upon vessel injury by the cleavage of plasminogen into plasmin.

Protein C inhibits the pathway

31
Q

Name some inhibitors of the secondary hemostatic response ?

Specific

Pathological

Therapuetic

A
  • Tissue factor pathway inhibitor, antithrombin, protein C
  • antibodies, rodenticides, coagulation factor deficiencies, snake envenomation
  • warfarin, heparin, hirudin
32
Q

What is DIC ?

A

Disseminated intravascular coagulation

increased consumption of coagulation factors

Thrombis is both compensated & uncompensated

Hemorrhage is only uncompensated.

33
Q

Define hemorraghe?

Why does it occur?

A

the extravasation of blood into the extravascular space.

abnormal function or integrity of one or more of the hemostatsis protagnoist

endothelium

platelets

coagulation factors

34
Q

What are the 2 classifications of hemorrhage ?

and what do they mean ?

A

Per diapedesis - loss of function continuity of a vessel wall despite maintenance of morphologic continuity , causes: hypoxia, abnormal coag, toxic injury, vasculitis (inflammation of vessel wall) & nutritional deficiency

Per Rhexis - loss of morphologic and functional continuity of a vessel wall

causes; trauma, vessel wall necrosis, vessel wall invasion by neoplasm, primary vascular disease

35
Q

What are the 3 classification based on size of hemorrhage , within a tissue ?

A
  • Petechiae - pinpoint less than 2mm, per diapedesis assoc with minor vascular damage
  • Purpura - up to 3mm , occurs secondary to trauma, vasculitis & increased vascular fragility
  • Ecchmyosis - subcutaneus heamatoma 1-2cm
36
Q

What are the following

  1. Hematamesis
  2. Melena
  3. Haematochezia
  4. Haemoptysis
  5. Haematuria
  6. Epitaxis
A
  1. Blood in vomit
  2. Digested blood in stool, normally black in colour with offensive smell, small intestine or stomach bleed.
  3. blood from colon not digested
  4. blood from the airway
  5. blood from the bladder
  6. blood nose
37
Q

How does heamoglobin get broken down ?

A
38
Q

What would be the consequence of the rapid loss of 20-30% of blood volume?

A

Hypovolemic shock leading to death

39
Q

What is the consequence of chronic haemorrhage?

ie gi ulcers, blood sucking parasites

A

Chronic anemia due to iron deficiency -non regenerative.

40
Q

What is a thrombus ?

What is thromboembolus?

A

solid aggregate of fibrin , platelets and other blood elements (mainly erythrocytes) on the wall of a blood or lymphatic vessel.

inappropriate thrombus formed free within the lumen.

41
Q

Why does a thrombus form ?

A

abnormal blood flow, turbulance or stasis

or

hypercoagulability

or

endothelial injury

(Virchow’s Triad)

42
Q

What is Virchow’s Triad ?

A
43
Q

What are some consequences of thrombus ?

A

Immediate death; occulsion at critical sites

Lysis

Organisation

Embolisation ; thrombus , or portion of thrombus which break loose and enter the circulation.

44
Q

What is an embolism ?

A

It is a detached intravascular solid, liquid or gaseous mass what is carried by the blood to a site distant from its point of origin.

45
Q

What are some consequences of thrombus / embolism ?

A

Passive hyperhaemia (congestion)

Ischemia - decreased oxygenation of tissue

Infarction - necrosis of tissue caused by lack of oxygen.

46
Q

What is the difference between thrombus and a post mortem clot ?

A
47
Q

How much water is within the body?

How much is intracellular vs extracellular?

A

60% of lean body weight = water

2/3 intra and 1/3 extracellular

48
Q

Physical responses to dehydration include ?

Decrease in blood volume and BP & Increase in osmolarity

A
  1. Barorecptors - strong sympathetic stimulation
  2. Renin (kidney) angiotensin formation , leads to vasoconstriction increase HR and force leads to increase in BP
  3. Increased osmolarity leads to ADH release (no aldosterone) leads to renal water re-absorption and increased thirst.
49
Q

What are the 2 types of haemophilia?

A
  • A - functional or quantitative deficiency of factor VIII , common in human, dogs, cats, horses and sheep
  • B - functional or quantitative deficiency of factor IX human, dogs & cats.

VET375 Pathology (6 decks)

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