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Pathology > Disorders of circulation (year 2) > Flashcards

Disorders of circulation (year 2) Flashcards

1
Q

where is blood at the highest pressure?

A

left ventricle

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2
Q

where is blood at the lowest pressure?

A

right atrium

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3
Q

what are the types of redistribution of blood? (2)

A

local increased volume to a particular tissue

reduced blood supply to organ/tissue

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4
Q

what is an abnormal accumulation of arterial blood in arterioles/capillary beds known as?

A

active hyperaemia

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5
Q

what is an accumulation of blood in veins/venule capillary beds known as?

A

passive hyperaemia (congestion)

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6
Q

what is decreased blood supply to an organ/tissue known as?

A

ischeamia

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7
Q

what colour does tissue affected by active hyperaemia look?

A

bright red

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8
Q

what colour does tissue affected by passive hyperaemia look?

A

dark red/blue

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9
Q

what can cause local passive hyperaemia? (3)

A

organ misalignment
venous thrombosis or embolism (mass in vein)
compression

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10
Q

what can cause compression leading to local passive hyperaemia? (2)

A

fibrosis

tumour/abscess

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11
Q

why are veins more susceptible to compression? (2)

A

lower pressure

thinner walls

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12
Q

what are the consequences of local passive hyperaemia? (4)

A

necrosis
atrophy
fibrosis
loss of function

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13
Q

what are the types of organ misalignment? (5)

A 
intussusception
volvulus
torsion
twist
herniation
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14
Q

what is intussusception?

A

one part of tubular organ telescopes inside itself

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15
Q

what is the intussusceptum?

A

part of the organ that goes inside the intussuscepiens

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16
Q

what is volvulus?

A

when an organ twists around its mesenteric root

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17
Q

what animals is gastric dilation and volvulus mainly seen in?

A

deep chested dogs

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18
Q

what is torsion?

A

rotation around an organs long axis

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19
Q

what is a twist?

A

two or more structures wrap around each other

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20
Q

what is the main consequence of organ misalignment known as?

A

haemorrhagic infarction

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21
Q

how does haemorrhagic infarction occur?

A

venous occlusion
persistent arterial blood supply
increased blood pressure
blood extravasation

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22
Q

what is the end result of haemorrhagic infarction?

A

necrosis

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23
Q

what is a venous thrombosis/embolism?

A

mass inside lumen of a vein

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24
Q

what is ischeamia?

A

inadequate blood supply to an organ/tissue

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25
Q

what can cause ischeamia? (3)

A

heart failure
artery obstruction
venous obstruction

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26
Q

what can cause generalised passive hyperaemia? (3)

A

heart failure
impeded venous return
increased pulmonary resistance

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27
Q

what can cause impeded venous return? (3)

A

caval thrombosis
hydropericardium
exudative pericarditis

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28
Q

what can cause increased pulmonary resistance? (3)

A

thoracic fluid
pulmonary fibrosis
pulmonary emphysema

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29
Q

what is haemorrhage?

A

loss of blood from the vascular system

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30
Q

what are the sizes of haemorrhage, in order of smallest to largest? (3)

A

petechia
purpura
ecchymoses

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31
Q

how large is petechia haemorrhage?

A

1-2mm

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32
Q

what is the size of purpura haemorrhage?

A

> 3mm

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33
Q

what is the size of ecchymoses haemorrhage?

A

> 1-2cm

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34
Q

what is diapedesis?

A

crossing of the vessel wall by cells

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35
Q

what is extravasation?

A

outside of a blood vessel

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36
Q

what is a haematoma?

A

focal accumulation of blood, usually within a tissue

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37
Q

what is another word for rhexis?

A

rupture

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38
Q

what are the possible outcomes of haemorrhage? (4)

A

haemorrhagic (hypovolaemic) shock
complete recovery
loss of function
iron deficient anaemia

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39
Q

what happens to erythrocytes when they are extravascular?

A

phagocytosed by macrophages

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40
Q

what is formed at the different stages of haemoglobin degradation? (4)

A

haem
biliverdin
bilirubin
haemosiderin

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41
Q

what is oedema?

A

accumulation of fluid in intercellular tissue space or body cavities

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42
Q

what type of fluid forms non-inflammatory oedema?

A

transudate (low cells/protein)

43
Q

what can cause oedema? (5)

A 
increased venous hydrostatic pressure 
reduced plasma oncotic pressure in veins
lymphatic obstruction
sodium retention
inflammation
44
Q

what can lead to reduced oncotic pressure? (3)

A

malnutrition
reduced hepatic synthesis
nephrotic syndrome

45
Q

what is the difference between the cause of inflammatory and non-inflammatory oedema?

A

in non-inflammatory the vessel wall permeability isn’t changed

46
Q

where do dogs tend to accumulate fluid during generalised oedema?

A

peritoneal cavity

47
Q

where do cats tend to accumulate fluid during generalised oedema?

A

thoracic cavity

48
Q

where do sheep tend to accumulate fluid during generalised oedema? (2)

A

submandibular space

peritoneum

49
Q

where do horses tend to accumulate fluid during generalised oedema?

50
Q

where do cattle tend to accumulate fluid during generalised oedema?

51
Q

what is anasarca?

A

a generalised oedematous state

52
Q

what can cause pulmonary oedema?

A

left sided congestive heart failure
irritant gases
inflammation
toxins

53
Q

what is bottle jaw?

A

sub cutaneous sub-mandibular oedema

54
Q

what is heart failure?

A

when the heart is unable to pump blood at rate need by tissue

55
Q

what happens to compensate for heart failure? (3)

A

increase preload
myocardial hypertrophy
neurohormonal system

56
Q

what are the consequences of heart failure? (4)

A

oedema
tissue hypoxia
RAAS activation
lung/liver congestion

57
Q

what are the functions of angiotensin II? (3)

A

constrict arteriole walls
increase heartbeat strength
increase sodium reabsorption

58
Q

what is the antagonist of angiotensin?

A

atrial natriuretic peptide

59
Q

what are the components of normal haemostasis?

A

vascular wall
platelets
coagulation cascade

60
Q

what does an excess of clotting lead to? (2)

A

thrombosis

DIC

61
Q

would could cause bleeding disorders? (4)

A

thrombocytopenia
defective platelet function
abnormalities in clotting factors
DIC

62
Q

what is the first step of normal haemostasis?

A

reflex vasoconstriction

63
Q

what is the second step of normal haemostasis?

A

haemostatic plug forms

64
Q

what is the haemostatic plug made of?

65
Q

what do platelets adhere to to form the haemostatic plug?

A

von Willebrand factor

66
Q

what is released at the start of secondary haemostasis?

A

tissue factor

67
Q

what does the coagulation cascade result in formation of?

68
Q

what pathway does tissue factor stimulate?

A

extrinsic pathway

69
Q

what vitamin is necessary for the coagulation cascade to occur?

70
Q

what are the stages of platelet events in haemostasis? (5)

A 
adhere to extracellular matrix
release granules
exposition of phospholipids
stimulate primary plug
fibrin deposition
71
Q

what are the possible aetiologies of bleeding disorders? (3)

A

inherited coagulation factor deficiencies
disorders of platelets
acquire coagulopathies

72
Q

what disorders of platelets could be present causing a bleeding disorder? (2)

A

defective function

thrombocytopenia

73
Q

what could cause thrombocytopenia? (3)

A

increased destruction
decreased production
sequestration

74
Q

what are possible acquired coagulopathies? (3)

A

poisoning with vitamin K antagonists
hepatic disease
DIC

75
Q

what is thrombosis?

A

formation of a solid mass (thrombus) in the lumen of a blood vessel or the heart

76
Q

what are thrombosus’ usually attaches to?

A

vessel wall

77
Q

what are the predisposing factors leading to thrombosis? (3)

A

endothelial injury
abnormal blood flow
hypercoagulability

78
Q

what are the three predisposing factors of thrombosis known as?

A

virchows triad

79
Q

what is endothelial injury?

A

exposure of subendothelial collagen

80
Q

what is released during tissue damage?

A

tissue factor (extrinsic pathway activated)

81
Q

what could cause endothelial damage? (3)

A

bacterial endotoxins
turbulent blood flow
hypertension

82
Q

what are the types of alterations to blood flow known as? (2)

A

turbulence

stasis

83
Q

why does thrombosis occur with stasis? (4)

A

platelet contact with endothelium
no dilution of activated clotting factors
no inflow of clotting factor inhibitors
promotion of endothelial cell activation

84
Q

what is hypercoagulabilty associated with? (4)

A

tissue damage
cnacer
DIC
chronic renal disease

85
Q

how do post-mortem clots appear?

A

red - clotted blood

white

86
Q

what can happen to a thrombus once it has formed? (4)

A

propagation
embolisation
dissolution
organisation

87
Q

what is embolism?

A

intravascular mass carried to a site distant to that of its point of origin

88
Q

what is the outcome of thromboembolism?

A

infarction

89
Q

what is infarction?

A

area of ischeamic necrosis caused by a blockage of the arteries or veins

90
Q

what are the types of infarcts?

A

red infarct

white infarct

91
Q

what are red infarcts associated with?

A

venous occlusion

92
Q

what are white infarcts associated with?

A

arterial occlusion

93
Q

what factors influence the development of an infarct? (4)

A

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

94
Q

what are some examples of none thromboembolism emboli?

A 
bacterial
fat droplet
parasites
bubble of air/nitrogen
tumour fragments
95
Q

what does DIC stand for?

A

disseminated intravascular coagulation

96
Q

what is disseminated intravascular coagulation?

A

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

97
Q

what are the stages of DIC? (4)

A

activation of coagulation cascade
formation of micro-thrombi throughout circulation
consumption of platelets, fibrin and coagulation factors
activation of fibronlysis

98
Q

what are the associated clinical signs of DIC? (3)

A

tissue hypoxia
infarction
haemorrhagic disorder (consumption coagulopathy)

99
Q

what are the major underlying mechanisms of DIC? (2)

A

release of tissue factor or thromboplastin substances

widespread endothelial injury

100
Q

what can lead to DIC? (6)

A 
sepsis
endothelial injury
immune complex deposition
neoplastic disease
extensive burns/trauma
extensive surgery
101
Q

what induces DIC in gram negative sepsis?

A

bacterial endotoxins

102
Q

what do bacterial endotoxins induce to happen in monocytes?

A

increased synthesis, membrane exposure and release of tissue factor

103
Q

what do bacterial endotoxins induce activated monocytes to release?

Pathology (17 decks)

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