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PATH > Disorders of Circulation > Flashcards

Disorders of Circulation Flashcards

1
Q

Describe the normal circulation of blood.

A

Closed system, flow generated by a pump, maintain by pressure differences, hormonal and neuronal controls.

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2
Q

Describe the differences in pressure which dictate movement of fluids.

A

Tissue vs vessel - colloid osmotic (draws fluid into vessels) vs hydrostatic (draws fluid into interstitium). Arterial vs venous - arteries are under high pressure (pushes fluid (+O2) out of vessel), venous low (draws fluid + metabolites) out of interstitium.
Remember 1mmHg is left over, this is absorbed by lymphatics.

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3
Q

Explain the difference between active and passive hyperaemia.

A

Active - occurs due to arterial dilation eg during exercise, at a meal (GI vessels). Passive - due to poor drainage and accumulation eg agonal

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4
Q

Describe and explain the gross appearance of tissues with active and passive hyperaemia.

A

Active = RED - due to accumulation of oxygenated blood in arteries (+caps). Passive = deep red/ BLUE - due to accumulation of metabolised blood in veins (+ caps)

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5
Q

Name three pathological causes of passive hyperaemia.

A

Organ misalignment, vascular mass, compression.

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6
Q

What are the five ways in which organs can become misaligned?

A

Intussusception, volvulus, torsion, twist, herniation

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7
Q

What are the five ways in which organs can become misaligned? What is the outcome of these pathologies?

A

Intussusception (invagination), volvulus, torsion, twist, herniation. NECROSIS

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8
Q

Organ Invagination

A

Segment of a tubular organ becomes folded in on itself. Think telescope.

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9
Q

Volvulus

A

Twisting of the mesenteric root of an organ - leads to occlusion of the mesenteric vessels with little effect on the tubular organ.

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10
Q

How can a pedunculated lipoma cause volvulus?

A

When the lipoma stalk twists around itself – mesenteric vessel occlusion, colon becomes twisted around lipoma.

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11
Q

Describe the pathological features of GDV.

A

Gastric dilation: stomach rotates its long axis from a transverse left-right orientation to one paralleling the abdomen.
Gastric volvulus: 360 twist = pylorus and terminal duodenum to left of midline across and ventral to oesophagus, compressed between oesophagus and dilated stomach.
Spleen (moves with gastrosplenic ligament) in right-ventral position, between stomach and liver/diaphragm (V shape).
Oesophagus: completely occluded

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12
Q

Torsion

A

Rotation along the long axis

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13
Q

Twist

A

Two or more tubular organs twisting around one another

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14
Q

Herniation with strangulation

A

Tubular organ (eg colon/intestine) displacing into an abnormal or physiological “hole” (eg epiploic foramen)

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15
Q

What are the consequences of organ misalignment?

A

O2 deficite, increased blood pressure, haemorrhage and necrosis

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16
Q

What are the consequences of organ misalignment?

A

O2 deficite, increased blood pressure, haemorrhage and necrosis

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17
Q

Describe the difference between a thrombus and embolus.

A

A thrombus is an accumulation of platelets +/- fibrin whereas an embolus is mass (often a fragment of a thrombus) which is found in the brain.

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18
Q

Passive hyperaemia due to compression can be caused by which structures?

A

Tumour/ abscess

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19
Q

Haemorrhage

A

Loss of circulating blood

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20
Q

What can be the outcomes of haemorrhage in the body?

A

Hypovolemic shock, recovery, loss of function, iron deficient anaemia.

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21
Q

Define: Diapedesis, extravasation, haematoma, rhexis

A

Diapedesis - movement of BC’s through intact capillary walls.
Extravasation - blood escaping from vessels.
Haematoma - swelling containing blood.
Rhexis - rupture

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22
Q

What is the difference between petechial, purpura and ecchymoses?

A

Petechial 1-2mm, purpura >3mm, ecchymoses >1-2cm

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23
Q

Name three aetiologies of haemorrhage.

A

physiological - trauma - parasites - bacteria - viruses - toxic agents - clotting deficiencies - neoplastic disease - agonal

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24
Q

Describe the change in colour of degrading blood.

A

HAEM(red) > biliverdin(green) > bilirubin(yellow) > haemosiderin (orange)

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25
Q

Oedema

A

Accumulation of extravascular fluid (here meaning transudate (low protein and cells))

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26
Q

What are the three main physiological causes of oedema?

A

Hypoproteinemia (reduced oncotic gradient), increased hydrostatic pressure (passive hyperaemia), impaired lymphatic drainage, sodium retention (RAS)

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27
Q

Aetiology of pulmonary oedema.

A

Left sided congestive heart failure – passive hyperaemia, Irritant gases, Inflammation, Toxic e.g. Fog Fever, Agonal changes

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28
Q

Bottle Jaw

A

Submandibular oedema often cause by hypoproteinemia, - parasites or johnne’s (sheep)

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29
Q

Passive hyperaemia can result from which three pathologies?

A

Thrombus/ embolism. Hydropericardium. Exudative pericarditis.

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30
Q

Which two hormones (/systems) work antagonistically during heart failure leading to progression of heart failure?

A

ANP - reduces blood pressure due to volume overload during heart failure.
Renin/ RAAS - increases blood volume due to ANP decrease.
These work in a cycle.

31
Q

Describe the differences between concentric and eccentric hypertrophy.

A 
Concentric = pressure overload - reduced outflow tract (stenosis) reduced ventricular lumen. 
Eccentric = volume overload - dilation of ventricular lumen
32
Q

Explain how congestive heart failure can lead to the formation of a thrombus.

A

Due to backflow of blood there is accumulation of blood in the atria which therefore dilate. Blood tends to “pool” in the extensive atria therefore forming clots. Clots get free and make their way into the ventricle and furthermore the systemic circulation.

33
Q

What is meant by nutmeg liver? How does this occur?

A

Increased pressure in central veins - dilation, haemorrhage & necrosis of hepatocytes around central veins = black accumulations. Degeneration of other hepatocytes + fat accumulation = paler tissue

34
Q

How do the compositions of pulmonary oedma and ascites differ?

A

Pulmonary is often more protein filled due to leaky capillaries

35
Q

Ischemia

A

Inadequate blood supply to an organ or tissue. Causes degeneration (necrosis/ atrophy) of the tissue.

36
Q

Causes of ischemia.

A

Heart failure, vascular obstruction.q

37
Q

Idiopathic cardiac hypertrophy.

A

Diastolic disorder (stiff ventricles) reduced compliance to blood entry. Can lead to thrombus formation.

38
Q

Causes of increased pulmonary resistance.

A

Thoracic fluids, pulmonary fibrosis, pulmonary emphysema.

39
Q

Causes of impeded venous return.

A

Caval thrombosis, hydropericardium, exudative pericarditis.

40
Q

Intravascular clotting

A

Thrombosis

41
Q

Fibrinous vs fibrous.

A

Fibrinous = fibrin, fibrous = collagen

42
Q

Membrane-bound smooth discs with granules.

A

Platelets

43
Q

Five functions of platelets during haemostasis.

A
  1. Adhesion (vWF)
  2. Release of granules = TXA2
  3. Exposes PL complex = coagulation cascade
  4. Primary plug stimulation
    5) Fibrin deposites = secondary plug
44
Q

Three aetiologies of bleeding disorders.

A

1) Inherited coagulation factor deficiencies
2) Disorders of platelets (thrombocytes)
3) Acquired coagulopathie

45
Q

Thrombosis

A

A solid mass forms in the lumen of a blood vessel or heart during life.

46
Q

Predisposing factors to thrombosis.

A

Endothelial injury - exposes collagen and releases TF.
Depleted PGI2 and NO
Altered blood flow (stasis)

47
Q

Which bacteria can cause bacterial valvular endocarditis in animals?

A

Arcanobacterium pyogenes, streps, erysipelothrix rhusiopathiae (+others)

48
Q

Outline the pathogenesis which cause BVE.

A

lesions to occur at lines of apposition of the valve surfaces exposed to the forward flow of blood and necessity of sustained or recurrent bacteraemia (leading to debilitation of endothelial cells?) - Selective adherence of some bacteria to the valvular endothelium

49
Q

Why does blood stasis lead to thrombosis?

A

Platelets are more likely to contact epithelium, no dilution of activated clotting factors as blood comes in, no inflow of inhibitors, endothelial activation promoted.

50
Q

How can you differentiate between a thrombus and post-mortem clot?

A 
T = attached to the vessel wall - coarse fibrin seen
PMC = chicken jelly/fat clots - fine fibrin seen
51
Q

What are the four fates of a thrombus?

A

Propagation (moves towards heart), embolisation (distant location), dissolution, organisation and recanalisation.

52
Q

Consequences of recanalisation of a thrombus?

A

Altered blood flow in a vessel, lumen size decreases but blood can still flow.

53
Q

Embolism

A

A detached solid mass in the blood, carried from its site of creation to a distant point.

54
Q

Infarct

A

Area of ischemic necrosis caused by blockage of arterial supply. venous drainage in a tissue.

55
Q

What is the difference between red and white infarcts?

A 
Red = haemorrhagic infarct ( in loose tissue and dual circulation) - due to venous occlusion.
White = arterial occlusion (no blood in = necrosis)
56
Q

Four risk factors for infarct development.

A

nature of vascular supply - rate of development of occlusion - vulnerability to hypoxia - oxygen content of blood

57
Q

Embolic-metastatic

A

Scattered pattern of emboli around the body - common features = high blood flow and narrow tubular lumen.

58
Q

Tyzzer’s disease

A

Bacterial emboli of cats, due to clostrium

59
Q

Describe six types of embolism that aren’t thrombus in origin.

A

Bacterial, parasite, fat droplets (often due to bone fracture), air/ nitrogen, bone marrow, cartilage, FB, tumour fragements.

60
Q

DIC

A

Disseminated Intravascilar Coagulation

61
Q

Acute, subacute or chronic thrombo-haemorrhagic disorder occurring as a secondary complication in a variety of diseases

A

DIC

62
Q

Outline the pathogenesis of DIC.

A

Activation of coagulation cascaded.
Formation of micro-thrombi throughout the microcirculation.
Consumption of platelets, fibrin and coagulation factors leads to activation of fibriolysis.
Thrombosis leads to ischemic tissue damage

63
Q

What are the underlting mechanisms of DIC?

A

TF or thromboplastic substances released into circulation.

Widespread endothelial injury.

64
Q

Name three situations in which you may see DIC.

A

1) severe systemic infections due to:
a) direct endothelial cell injury
b) via immune complex deposition
2) septic (endotoxic) shock
3) neoplastic diseases
4) extensive trauma or burns
5) following extensive surgery

65
Q

How can gram -ve bacterial infection lead to DIC?

A

Gram -ve bacteria release endotoxins which induce monocytes to - increase sysnthesis, membrane exposure and release of tissue factor.
Activated monocytes release IL1 and TNF.
Endothelial cells increase TF and decrease thrombomodulin.
Increased clotting cascade and inhibition of clotting control.

66
Q

How can gram +ve bacterial infection lead to DIC?

A

Bacterial lysis releases cell wall components = inflammation.
Cytokines produced by monocytes.
Systemic inflammation
Shock occurs due to neutrophil adherence to endothelial cells, release of proteases and O2 radicals, capillary damage and haemorrhage

67
Q

Name two viral infections associated with DIC in the core species.

A
  • pigs: Classical swine fever / hog cholera (pestivirus) - dogs: Infectious canine hepatitis (adenovirus) - rabbits: Rabbit haemorrhagic disease (calicivirus) - sheep: Blue tongue (orbivirus) - minks: Aleutian disease (parvovirus; immune complex formation) - deer: Epizootic haemorrhagic disease of deer (orbivirus)
68
Q

What vascular changes are associated with classical swine fever?

A

capillaries: swelling of endothelial cells, hyalinisation, complete obstruction
arteries: thrombosis, necrosis

69
Q

How can immune complexes cause DIC?

A

Immune complexes deposited in vessel walls - activates complement, endothelial cell damage and therefore coagulation cascade.

70
Q

Systemic hypoperfusion during shock results from:

A

Reduced CO and reduced effective circulating blood volume

71
Q

How is shock classified?

HINT x5

A
  • cardiogenic shock (failure of myocardial pump) - hypovolaemic shock (loss of blood / plasma volume) - septic shock (systemic microbial infection; bacteria, fungi) - neurogenic shock (depression of vasomotor centre) - anaphylactic shock (generalised IgE-mediated hypersensitivity)
72
Q

What are the three stages of shock?

A

Non-progressive, progressive, irreversible (leads to death)

73
Q

How does LPS, produced by g-ve bacteria affect the body at low, moderate and high quantities of LPS?

A

Low - activated monocytes, endothelial cells and complement = circumscribed cascade, enhancing local acute inflammation and bacterial clearance.
Moderate - Cytokine-induced effectors NO and PAF, fever, acute phase reactants, endothelial cell injury (DIC)
High - systemic vasodilation, reduced cardiac contractility, DIC

74
Q

How do cell wall components of g+ve bacteria cause septic shock?

A

Inflammatory response leads to neutrophil adherence to endothelial cells - releases proteases and O2 free radicals, leads to capillary damage and haemorrhage.

PATH (8 decks)

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