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Vascular Disturbances Flashcards

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1
Q

Hydrostatic pressure (HS)

A

Force due to fluid pressing on vessel walls
Constant along the capillary
Water moves from high PRESSURE to low PRESSURE

–>Capillary HSP = filtration
–>Interstitial HSP = absorption

Higher HSP along most of the capillaries length = filtration (OUT of capillar)

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2
Q

Osmotic pressure (OS)

A

Pressure on membrane by movement of water down conc gradient
Decreases along the capillary
Water moves from high CONC to low CONC

–> Capillary OSP = absorption
–> Interstitial OSP = filtration

Higher protein within the capillaries = absoprtion (INTO the capillary)

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3
Q

What is oedema?

A

Increased fluid in the interstitial space

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4
Q

Name 5 causes of oedema and how these come about

A
  • Increased capillary HS pressure
    –> venous obstruction
    –> inflammation
  • Decreased plasma protein
    –> colloid osmotic pressure OR blood oncotic pressure
    –> reduced production (eg. malnutrition, liver failure)
    –> increased loss (eg. from GI dx, renal dx (hypoperfusion = aldosterone release = RAAS = Na retention = water retention = increased HS pressure = diluted plasma protein)
  • lymphatic obstruction
    –> neoplasia
    –> fibrosis
    –> parasitism
    –> sx lymph node removal
  • Increased vascular permeability
    –> inflammation
    –> toxin
    –> burns damage
  • Increased tissue osmotic pressure
    –> secondary to protein extravasation in inflammation
    –> hypertonic subcutaneous injections
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5
Q

What is anasarca?

A

Generalized oedema - affecting subcutaneous, tissue, body cavities
Severe oedema impacting the whole body

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6
Q

What is effusion?

A

Increased fluid in an anatomical place

Eg. Pleural effusion (hydrothorax)
Eg. Pericardial effusion (hydropericardium)
Eg. Peritoneal effusion (ascites)

*Can be caused by oedema!

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7
Q

Name the 2 general types of effusion

A

Transudate
- clear
- low cell count, low protein
- can be localized or generalized
Exudate
- high cell count, high protein
- can be localized or extreme
- *Some are non septic

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8
Q

Name 6 types of effusions

A
  • Serous - watery
  • Serosanguinous - serous fluid containing erythrocytes (RBCs) - blood tinged
  • Fibrinous (exudate) - contains fibrin
  • Purulent/Suppurative (exudate) - contains neutrophils
  • Hemorrhagic - blood
  • Chylous - lymphatic
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9
Q

Examples of types of effusions

A
  • Hydrothorax (transudate) - serous effusion
  • Pyothorax (exudate) - purulent effusion
  • Haemothorax (exudate) - hemorrhagic effusion
  • Chylothorax (modified transudate) - chylous effusion
  • *Pneumothorax - NOT an effusion - AIR
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10
Q

What is hyperemia?

A

Increased blood within the vessels of a region

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11
Q

Name the 2 types of hyperemia

A

Active hyperemia
- Increased metabolic rate / increased input (arteriolar dilation
- Results in increased CO2 production and increase O2 consumption
- Can be physiological or pathological
- Region is warm, red, oxygenated

Passive hyperemia
- Reduced blood flow / reduced venous drainage = CONGESTION
- Mainly pathological (vascular compression/obstruction)
- Region can be darker, blue or engorged
- May cause tissue hypoxia

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12
Q

Name some examples of each type of hyperemia

A

Active (Phycological OR pathological)
- Blushing (phys)
- Skeletal muscle during exercise (phys)
- Acutely inflamed skin (path)
- Sunburn (path)

Passive (Mainly pathological)
- Twisted intestine
- Enlarged darked liver in RHS heart failure
- Heavy red lungs in LHS heart failure
- Vascular torsion of testes
- *Lowered vs raised hand (Physiological)

Both
- Erectile tissue - increased blood flow and eventually constriction - decrease venous drainage

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13
Q

What is hypervolemia?
Name some causes
What is released when hypervolemia is detected and some examples of what it
causes

A

Increased total blood volume

Causes
- Transfusion
- IV overload
- Excessive Na intake
- Chronic heart failure

ANPs (atrial natriuretic peptides)

What is causes
- vasodilation
- increased Na secretion
- increased vascular permeability
- increased glomerular filtration rate

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14
Q

What is ischemia?

A

Decreased vascular perfusion

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15
Q

Name the 2 types of ischemia and what usually causes them

A

Generalised
- Hypervolemia
- Poor cardiac outflow / low mean arterial pressure

Localised
Obstruction to blood flow by:
- Intraluminal vascular obstruction
- Vascular contraction / Intramural thickening
- Extramural vascular compression

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16
Q

The consequences of ischemia depend on what?

A

speed of onset
duration
severity
location

–> Organ/Tissue redundancy (eg. cortex of brain yes, medulla of brain no)
–> Tissue tolerance to ischemia (eg. brain is vulnerable)
–> Prescence of end arterial or collateral supply (eg. renal arterial supply - end arterial, whereas parts of GI tract, liver and lungs have dual blood supplies)
–> Nature of the infarct (eg. thrombus may be septic (bacterial) or bland)

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17
Q

What is infarction?

A

Localised tissue death (necrosis) from interrupted blood supply

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18
Q

Name the 3 causes of inadequate oxygenation

A
  1. Ischemia (poor flow)
  2. Hypoxia (poor oxygenation of alveoli)
  3. Anemia (inadequate oxygen carrying capacity of the blood)
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19
Q

Explain the regulation of blood pressure following hypovolemia

A

Detected by baroreceptors (arterial baroreceptors located in the carotid sinus and aortic arch)

  • ↓ MAP
  • ↓ Baroceptor firing
  • ↓ Parasymp supply & ↑ Symp supply
    Effectors:
  • SA node
    ↑ Symp activity = ↑ HR = ↑ CO
  • Myocardial cells
    Symp activity = ↑ myocardial contractility = ↑ SV = ↑ CO
  • Arterioles
    Symp activity = vasocontraction = ↑ TPR (total peripheral resistance)
  • Veins
    Symp activity = vasocontraction = ↑ EDV = ↑ SV = ↑ CO

= ↑ MAP

In summary
Baroreceptors recognize ↓ MAP - causing ↑ sympathetic activity - resulting in changes in SA node, myocardial cells, arterioles and veins which cause a net ↑ in HR, SV and TPR - restoring MAP

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20
Q

Explain the regulation of blood volume following hypovolemia

A

SHORT TERM:
- Contribution from fluid shifting from the extravascular space to the intravascular space (mainly via lymphatics)
- Helps restore blood volume BUT not total body water

LONG TERM:
Recognized by volume receptors in the walls of atria and veins

  • ↓ Blood volume
  • ↓ Volume receptor activity
    Effectors:
  • Heart and vessels
    Effects similar to baroreceptor reflex (via ANS)
  • Kidneys
    ↑ aldosterone production (via renin) = ↑ Na retention = ↑ Water retention
  • Pituitary
    ↑ ADH secretion = ↑ Water retention
  • Hypothalamus
    thirst

= ↑ Blood volume

In summary
Blood volume receptors recognize ↓ Blood volume - causing changes in Heart and vessels, kidneys, pituitary and hypothalamus which cause similar effects to baroreceptors, ↑ water retention and thirst - restoring blood volume

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21
Q

Explain the final step following hypovolemia - cell restoration

A

Increased hemopoiesis (bone marrow hyperplasia) - restoring erythrocyte numbers, blood hemoglobin
Plasma protein synthesis in the liver

= ↑ circulating reticulocytes and metarubricytes (immature RBCs)

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22
Q

When does shock occur?

A

When there is severe acute haemorrhage resulting in a loss of more than 20% of blood volume

Imp notes:
* Low tissue perfusion may not always correlate with low MAP - as vasocontraction may be keeping MAP high
* Endothelial injury and ↑ vascular permeability = further fluid loss & ↓ venous return = ↓ CO
* Poor renal perfusion can = renal acidosis

All = ↓ peripheral perfusion

“Shock is a condition of profound hemodynamic and metabolic disturbance characterized by failure of the circulatory system to maintain an appropriate blood supply to the microcirculation, with consequent inadequate perfusion of vital organs and failure to remove metabolites.”

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23
Q

Name the 5 different types of shock

A
  • Cardiogenic - inability of the heart to pump normal venous return (myocardial infarction, myocarditis, cardiac tamponade, pulmonary embolus)
  • Hypovolemic - ineffective blood volume = ↓venous return (hemorrhage, D+, dehydration, burns)
  • Septic (severe infection)
  • Anaphylactic (type I hypersensitivity)
  • Neurogenic (brain damage, spinal cord injury)

Decreased perfusion commonly results from ↓CO due to inability of the heart to pump normal venous return (cardiogenic) OR ↓ effective blood volume (hypovolemic)
Systemic vasodilation (with or without ↑ vascular permeability) = DISTRIBUTIVE SHOCK (septic, anaphylactic, neurogenic)

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24
Q

Why is shock not synonymous with hypotension (low BP)?

A
  • It is not synonymous but is often part of shock
  • Hypotension is actually a late sign in shock and indicates failure of compensation.
  • At the same time that peripheral blood flow falls below critical levels, extreme vasoconstriction can maintain arterial BP.
  • The distinction between shock and hypotension is important clinically because rapid restoration of systemic blood flow is the primary goal in treating shock.
  • When BP alone is raised with vasopressive drugs, systemic blood flow may actually be dramatically diminished, particularly to the peripheries
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25
What is haemorrhage? Why does it occur?
Extravasation of blood into the extravascular space Occurs bcs of abnormal function or integrity of one or more of the homeostatic protagonists: - Endothelium and blood vessels - Platelets - Coagulation factors
26
Name the 3 different way haemorrhage can be classified
- By degree of vascular injury - By size - By site
27
Explain the classifications of haemorrhage based on degree of vascular injury
Per diapedesis > loss of functional continuity of the vessel wall despite maintenance of morphological continuity > Causes: Hypoxia, abnormal coagulation, toxic injury, inflammation of vessel wall (vasculitis), nutritional deficiency Per rhexis > loss of morphological AND functional continuity of vessel wall --> holes in endothelial cells (much worse!) > Causes: Trauma, vessel wall necrosis, vessel wall invasion by neoplasm
28
Explain the classifications of haemorrhage based on size
Petechiae - Pinpoint <2mm (eg. ↑ vascular pressure, thrombocytopenia) Purpura - 2-3mm (eg. associated with similar dx to petechiae) Ecchymosis - subcutaneous hematoma (>1-2cm) (eg. more extensive vascular trauma) Haemorrhage - massive or submassive haemorrhage
29
Explain the classifications of haemorrhage based on site
INTERNAL Hematemesis - V+ of blood Melena - digested blood in stool, from stomach or sml intestine Hematochezia - from colon (not digested) Hemoptysis - from airway Epistaxis - from nose Hematuria - from bladder EXTERNAL Hemothorax Hemopericardium Hemoperitoneum Hemarthrosis Hyphemia
30
Explain the resolution of tissue damage in terms of what happens to the cell types
- Leucocytes = catabolized - removed by apoptosis & phagocytosis - Platelets = used to stop bleeding - Erythrocytes = erythrocytosis --> recycled for iron! - Plasma (proteins) = released into tissue - fibrinogen --> fibrin, fibroblasts activated, collagen, tissue repair!
31
3 consequences of haemorrhage
1. Rapid loss (acute) of MORE THAN 20-30% of blood volume = hypovolemic shock and death 2. Rapid loss of UP TO 20% of blood volume = maintenance of blood pressure, volume and cell regeneration 3. Chronic haemorrhage = chronic anaemia due to iron deficiency (non-regenerative)
32
What is thrombosis?
The formation of a solid aggregate of fibrin, platelets and other blood elements (mainly erythrocytes) on the wall of a blood or lymphatic vessel Can be: >PHYSIOLOGICAL (part of normal haemostasis --> resolved quickly) >PERSISTANT/INAPPROPRIATE (forms on wall of blood or lymph vessel or heart (mural thrombus) or free in the lumen (thromboembolism))
33
Name the 3 things that need to occur SIMULTANEOUSY for a thrombus to form (Virchow's triad)
1. Abnormal blood flow (heart failure, vascular obstruction and/or turbulence (disruption of laminar flow) 2. Hypercoagulability (increased production of procoagulant molecules AND/OR decreased production of anti-coagulant molecules) 3. Injury to the endothelium (= exposure of blood to tissue factor (TF) and subendothelial components eg. collagen and laminin)
34
Name the consequences of thrombosis
- Immediate death - occlusion at critical sites - Lysis (Small thrombi – removed by fibrinolysis and blood vessels return to normal structure and formation) (Larger thrombi – resolved by (1) removal of thrombotic debris by phagocytes with (2) subsequent granulation (of the surface) to incorporate the affected area into the vessel wall) - Organization - Larger mural or occlusive thrombi CANNOT be removed by thrombolysis. Invasion of fibroblasts and endothelium = recanalization - Embolisation - Thrombus or portions of it can break loose and enter circulation = THROMBOEMOLISM
35
What is embolism?
A detached intravascular solid, liquid or gas mass that is carried by the blood to a size distant from its point of origin
36
Examples of what can form an emboli
- Frequently emboli represent part of a dislodged thrombus = thromboembolism - Fat droplets (from bone marrow following a fracture of a long bone) - Nitrogen bubbles (scuba divers) - Atherosclerotic debris (cholesterol emboli)
37
Consequences of an emboli
Occlusive thrombi block flow either into (occlusive arterial thrombus) OR out of (occlusive venous thrombus) an area result in: - Passive hyperaemia (congestion) - Ischemia - ↓ oxygenation of tissues - Infarction – necrosis of tissue caused by lack of oxygen
38
Name some protagonists of haemostasias (5)
- platelets - fibroblasts - procoagulant molecules - anticoagulant molecules - extracellular matrix
39
Name the anticoagulant endothelial cell mediators of haemostasis (8)
- Nitrous oxide (NO) - Prostacyclin (PGI2) - Adenosine Diphosphatase (ADP) - Protein S - Thrombomodulin: - Tissue factor Pathway Inhibitor (TFPI) - Tissue Plasminogen activator (tPA) - Antithrombin III *Top 3 - share the function to prevent vasoconstriction and inhibit platelet adhesion
40
How does NO act as a anticoagulant endothelial cell mediator of homeostasis?
INHIBITS PLATELET AGGREGATION Acts synergistically with protein C pathway and antithrombin II to suppress thrombin production *With PGIs & ADP - maintains vascular relaxation and inhibits platelet aggregation
41
How does Prostacyclin (PGI2) act as a anticoagulant endothelial cell mediator of homeostasis?
INHIBITS PLATELET AGGREGATION Aim to prevent vasoconstriction and prevent platelet adhesion *With NO & ADP - maintains vascular relaxation and inhibits platelet aggregation
42
How does Protein S act as a anticoagulant endothelial cell mediator of homeostasis?
COFACTOR IN PROTEIN C PATHWAY = INACTIVATION OF Va & VIIIa Cofactor in protein C pathway; independently inhibits activation of factors VIII and X
42
How does Adenosine Diphosphatase (ADP) act as a anticoagulant endothelial cell mediator of homeostasis?
INHIBITS PLATELET AGGREGATION Degradation of ADP to inhibit its adhesion and activation *With NO & PGIs - maintains vascular relaxation and inhibits platelet aggregation
43
How does Thrombomodulin act as a anticoagulant endothelial cell mediator of homeostasis?
ACTIVATES PROTEIN C = INACTIVATION OF Va & VIIIa Membrane protein that binds thrombin to initiate activation of protein C
44
How does Tissue factor pathway inhibitor (TFPI) act as a anticoagulant endothelial cell mediator of homeostasis?
INACTIVATES TF-VIIa COMPLEX A cell surface protein that directly inhibits the factor TF:VIIa complex and factor Xa
45
How does Tissue plasminogen activator (tPA) act as a anticoagulant endothelial cell mediator of homeostasis?
ACTIVATES FIBRINOLYSIS Activated fibrinolysis by stimulating plasminogen (inactive) conversion to plasmin (active)
46
How does Antithrombin III act as a anticoagulant endothelial cell mediator of homeostasis?
INACTIVATES THROMBIN (w the aid of Heparin-like molecules): binds thrombin to neutralise it (Thrombin - one of the most powerful coagulation factors – is able to amplify the coagulation cascade – activates the intrinsic pathway to produce more thrombin)
47
What are the very broad roles of primary and secondary haemostasis
Primary - everything to do with platelets Secondary - everything to do with coagulation factors
48
Pathological haemostasis - PRO-COAGULATION Explain the pathway briefly And name the 2 factors that favour thrombosis
Endothelial damage = adhesion of platelets --> FAVOURING THROMBOSIS For platelet adhesion --> need exposure to vWF and TF - vWF: promotes platelet adhesion - TF: activates secondary haemostasis - activates the extrinsic pathway by activating factor VII that activates the production of thrombin (thrombin activates the in intrinsic pathway = MORE thrombin! = MORE fibrin!)
49
Pathological haemostasis - ANTI-COAGULATION Explain the pathway briefly And name the 5 factors that inhibit thrombosis
As soon as platelets adhere = fibrinolysis --> INHIBITS THROMBOSIS anticoagulation factors include: - Antithrombin III: inhibits thombin = no conversion of fibrinogen to fibrin - Protein C: thrombin = protein C activation = proteolysis of factors Va & VIIIa - NO, PGI2 & ADP: inhibition of platelet aggregation
50
Pathological haemostasis - PROCOAGULATION Name the 3 pro-coagulant ENDOTHELIAL CELL MEDIATORS
- Plasminogen Activator Inhibitor - 1 (PAI-1) --> reduces fibrinolysis by inhibiting tPA & activated protein C (=proteolysis of Va & VIIIa) - Tissue factor (TF) --> produced by cytokines, endotoxin, thrombin etc - Von Willebrand factor (vWF) --> released after exposure of endothelial cells to thrombin, histamine and fibrin etc.
51
Pathological haemostasis - PROCOAGULATION Name the 8 pro-coagulant PLATELET MEDIATIORS
- Thromboxane A2 (TxA2) --> induces vasoconstriction and enhances platelet aggreagtion - ADP --> mediates platelet activation and aggregation - A2 --> inhibition of plasmin - Plasminogen Activator Inhibitor - 1 (PAI-1) --> reduces fibrinolysis by inhibiting tPA & activated protein C (=proteolysis of Va & VIIIa) - Factor V, XI, XII --> involved in coagulation cascade - Tissue factor (TF) --> produced by cytokines, endotoxin, thrombin etc - Von Willebrand factor (vWF) --> released after exposure of endothelial cells to thrombin, histamine and fibrin etc. - Thrombin-Activatable Fibrinolysis Inhibitor (TAFI) --> inhibits plasmin production by reducing binding of plasminogen/tPA to fibrin
52
What are qualitative haemostasis problems?
When the number of cells (platelets) are normal but some of their receptors or molecules are no longer produced Commonly hereditary disorders Eg. extrinsic platelet disorders: platelets are normal but protein necessary for their function is either absent, reduced or dysfunctional Eg. intrinsic platelet disorder: involves platelets directly - abnormalities in platelet granules, membrane glycoproteins etc
53
What are quantitative hemostasis problems?
Not enough or too much anticoagulent or procoagulent molecules (usually platelets) Eg. thrombocytopenia - severe deficiency of platelets (↓ production, ↑ destruction, ↑ consumption) Eg. thrombocytosis - too many platelets Eg. coagulation factor deficiencies
54
Name the 7 steps of the homeostatic process
1. Vascular spasm (vasoconstriction triggered by molecules like adrenalin) 2. PRIMARY HEMOSTASIS: Primary platelet response (recruitment and adhesion of platelets, platelet activation with release of granules and recruit more platelets) 3. SECONDARY HEMOSTASIS: Initiation of thrombin generation (extrinsic pathway produces tiny bit of thrombin) 4. Amplification of thrombin generation (intrinsic pathway) 5. Propagation of thrombin generation 6. Fibrin formation 7. Fibrinolysis
55
Extrinsic pathway - what factor is involves and where does it occur?
Factor VII Happens at the site of endothelial damage or subendothelial matrix
56
Intrinsic pathway - where does it occur?
On top of the activated platelets
57
Name 1 abnormality associated with adhesion and aggregation of platelets
Von Willebrand disease (vWD) - missing vWF/deficiency of vWf Most common INHERITED bleeding disorder in humans and dogs Also reported in cats, horses and pigs Clinical signs: epistaxis (nose bleed), mucosal haemorrhage, post sx bleeding
57
Name 3 abnormalities associated with platelet activation
1. Abnormal synthesis or release of platelet granule content (Simmental cattle, dogs, cats) 2. Chediak-Higashi syndrome - defective platelet storage of ADP (Persian cats, cattle) - VERY RARE! 3. NSAID administration eg. aspirin
58
Name 1 abnormality associated with aggregation of platelets
Glanzmann thromboasthenia - intrinsic platelet disorder - fibrinogen receptor (GPIIb/IIIa) is absent or reduced on the surface of platelets
59
Name inhibitors of the secondary hemostasis response (specific, non-specific protease inhibitors, pathological & therapeutic)
- Specific: tissue factor pathway inhibitor (TFPI), antithrombin (AT), protein C, protein S - Non-specific protease inhibitors: a2 macroglobulin, a1 antitrypsin - Pathological: antibodies, rodenticide, coag factor deficiencies, snake envenomation - Therapeutic: Warfarin, herparin, hirudin
59
Name 4 abnormalities associated with secondary haemostasis
1. Haemophillia (A = functional or quantitative deficiency of factor VIII, B = functional or quantitiative deficiency of factor IX) 2. Severe liver dx - decreased production of coag factors 3. Vit K deficiency/rodenticide toxicity - decreased production of coag factors 4. DIC - increased consumption of coag factors
60
Name 1 abnormality associated with impaired fibrinolysis
Disseminated intravascular coagulation (DIC) - excessive activation of coagulation and the formation of thrombi in the microvasculature of the body - * NOT a spontaneous dx, is a SECONDARY complication of another underlying dx, something must trigger the formation of a thrombus Common triggers: > inflammatory cytokines (mainly TNF) > neoplasia > sepsis > severe organ injury/hypoxia/acidosis/shock
61
Name the factors involved in secondary haemostasis --> Extrinsic pathway
VII, TF
61
Name the 9 antithrombotic control mechanisms of clotting
1. thrombin-thrombomoduiln complex 2. Protein C 3. TFPI-1 4. C1 esterase inhibitor 5. Antithrombin 6. TAFI 7. PAI-1 8. a2 antiplasmin 9. *Transamic acid
61
Name the factors involved in secondary haemostasis --> Intrinsic pathway
VIII, IX, XI, XII
61
Name the factors involved in secondary haemostasis --> Common pathway
I (Fibrinogen/Fibrin), II (Prothrombin/thrombin), V, X

VET375 (9 decks)

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