Disorders of circulation (year 2) Flashcards
1
Q
where is blood at the highest pressure?
A
left ventricle
2
Q
where is blood at the lowest pressure?
A
right atrium
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
4
Q
what is an abnormal accumulation of arterial blood in arterioles/capillary beds known as?
A
active hyperaemia
5
Q
what is an accumulation of blood in veins/venule capillary beds known as?
A
passive hyperaemia (congestion)
6
Q
what is decreased blood supply to an organ/tissue known as?
A
ischeamia
7
Q
what colour does tissue affected by active hyperaemia look?
A
bright red
8
Q
what colour does tissue affected by passive hyperaemia look?
A
dark red/blue
9
Q
what can cause local passive hyperaemia? (3)
A
organ misalignment
venous thrombosis or embolism (mass in vein)
compression
10
Q
what can cause compression leading to local passive hyperaemia? (2)
A
fibrosis
tumour/abscess
11
Q
why are veins more susceptible to compression? (2)
A
lower pressure
thinner walls
12
Q
what are the consequences of local passive hyperaemia? (4)
A
necrosis
atrophy
fibrosis
loss of function
13
Q
what are the types of organ misalignment? (5)
A
intussusception volvulus torsion twist herniation
14
Q
what is intussusception?
A
one part of tubular organ telescopes inside itself
15
Q
what is the intussusceptum?
A
part of the organ that goes inside the intussuscepiens
16
Q
what is volvulus?
A
when an organ twists around its mesenteric root
17
Q
what animals is gastric dilation and volvulus mainly seen in?
A
deep chested dogs
18
Q
what is torsion?
A
rotation around an organs long axis
19
Q
what is a twist?
A
two or more structures wrap around each other
20
Q
what is the main consequence of organ misalignment known as?
A
haemorrhagic infarction
21
Q
how does haemorrhagic infarction occur?
A
venous occlusion
persistent arterial blood supply
increased blood pressure
blood extravasation
22
Q
what is the end result of haemorrhagic infarction?
A
necrosis
23
Q
what is a venous thrombosis/embolism?
A
mass inside lumen of a vein
24
Q
what is ischeamia?
A
inadequate blood supply to an organ/tissue
25
what can cause ischeamia? (3)
heart failure
artery obstruction
venous obstruction
26
what can cause generalised passive hyperaemia? (3)
heart failure
impeded venous return
increased pulmonary resistance
27
what can cause impeded venous return? (3)
caval thrombosis
hydropericardium
exudative pericarditis
28
what can cause increased pulmonary resistance? (3)
thoracic fluid
pulmonary fibrosis
pulmonary emphysema
29
what is haemorrhage?
loss of blood from the vascular system
30
what are the sizes of haemorrhage, in order of smallest to largest? (3)
petechia
purpura
ecchymoses
31
how large is petechia haemorrhage?
1-2mm
32
what is the size of purpura haemorrhage?
>3mm
33
what is the size of ecchymoses haemorrhage?
>1-2cm
34
what is diapedesis?
crossing of the vessel wall by cells
35
what is extravasation?
outside of a blood vessel
36
what is a haematoma?
focal accumulation of blood, usually within a tissue
37
what is another word for rhexis?
rupture
38
what are the possible outcomes of haemorrhage? (4)
haemorrhagic (hypovolaemic) shock
complete recovery
loss of function
iron deficient anaemia
39
what happens to erythrocytes when they are extravascular?
phagocytosed by macrophages
40
what is formed at the different stages of haemoglobin degradation? (4)
haem
biliverdin
bilirubin
haemosiderin
41
what is oedema?
accumulation of fluid in intercellular tissue space or body cavities
42
what type of fluid forms non-inflammatory oedema?
transudate (low cells/protein)
43
what can cause oedema? (5)
```
increased venous hydrostatic pressure
reduced plasma oncotic pressure in veins
lymphatic obstruction
sodium retention
inflammation
```
44
what can lead to reduced oncotic pressure? (3)
malnutrition
reduced hepatic synthesis
nephrotic syndrome
45
what is the difference between the cause of inflammatory and non-inflammatory oedema?
in non-inflammatory the vessel wall permeability isn't changed
46
where do dogs tend to accumulate fluid during generalised oedema?
peritoneal cavity
47
where do cats tend to accumulate fluid during generalised oedema?
thoracic cavity
48
where do sheep tend to accumulate fluid during generalised oedema? (2)
submandibular space
| peritoneum
49
where do horses tend to accumulate fluid during generalised oedema?
limbs
50
where do cattle tend to accumulate fluid during generalised oedema?
brisket
51
what is anasarca?
a generalised oedematous state
52
what can cause pulmonary oedema?
left sided congestive heart failure
irritant gases
inflammation
toxins
53
what is bottle jaw?
sub cutaneous sub-mandibular oedema
54
what is heart failure?
when the heart is unable to pump blood at rate need by tissue
55
what happens to compensate for heart failure? (3)
increase preload
myocardial hypertrophy
neurohormonal system
56
what are the consequences of heart failure? (4)
oedema
tissue hypoxia
RAAS activation
lung/liver congestion
57
what are the functions of angiotensin II? (3)
constrict arteriole walls
increase heartbeat strength
increase sodium reabsorption
58
what is the antagonist of angiotensin?
atrial natriuretic peptide
59
what are the components of normal haemostasis?
vascular wall
platelets
coagulation cascade
60
what does an excess of clotting lead to? (2)
thrombosis
| DIC
61
would could cause bleeding disorders? (4)
thrombocytopenia
defective platelet function
abnormalities in clotting factors
DIC
62
what is the first step of normal haemostasis?
reflex vasoconstriction
63
what is the second step of normal haemostasis?
haemostatic plug forms
64
what is the haemostatic plug made of?
platelets
65
what do platelets adhere to to form the haemostatic plug?
von Willebrand factor
66
what is released at the start of secondary haemostasis?
tissue factor
67
what does the coagulation cascade result in formation of?
fibrin
68
what pathway does tissue factor stimulate?
extrinsic pathway
69
what vitamin is necessary for the coagulation cascade to occur?
vitamin K
70
what are the stages of platelet events in haemostasis? (5)
```
adhere to extracellular matrix
release granules
exposition of phospholipids
stimulate primary plug
fibrin deposition
```
71
what are the possible aetiologies of bleeding disorders? (3)
inherited coagulation factor deficiencies
disorders of platelets
acquire coagulopathies
72
what disorders of platelets could be present causing a bleeding disorder? (2)
defective function
| thrombocytopenia
73
what could cause thrombocytopenia? (3)
increased destruction
decreased production
sequestration
74
what are possible acquired coagulopathies? (3)
poisoning with vitamin K antagonists
hepatic disease
DIC
75
what is thrombosis?
formation of a solid mass (thrombus) in the lumen of a blood vessel or the heart
76
what are thrombosus' usually attaches to?
vessel wall
77
what are the predisposing factors leading to thrombosis? (3)
endothelial injury
abnormal blood flow
hypercoagulability
78
what are the three predisposing factors of thrombosis known as?
virchows triad
79
what is endothelial injury?
exposure of subendothelial collagen
80
what is released during tissue damage?
tissue factor (extrinsic pathway activated)
81
what could cause endothelial damage? (3)
bacterial endotoxins
turbulent blood flow
hypertension
82
what are the types of alterations to blood flow known as? (2)
turbulence
| stasis
83
why does thrombosis occur with stasis? (4)
platelet contact with endothelium
no dilution of activated clotting factors
no inflow of clotting factor inhibitors
promotion of endothelial cell activation
84
what is hypercoagulabilty associated with? (4)
tissue damage
cnacer
DIC
chronic renal disease
85
how do post-mortem clots appear?
red - clotted blood
| white
86
what can happen to a thrombus once it has formed? (4)
propagation
embolisation
dissolution
organisation
87
what is embolism?
intravascular mass carried to a site distant to that of its point of origin
88
what is the outcome of thromboembolism?
infarction
89
what is infarction?
area of ischeamic necrosis caused by a blockage of the arteries or veins
90
what are the types of infarcts?
red infarct
| white infarct
91
what are red infarcts associated with?
venous occlusion
92
what are white infarcts associated with?
arterial occlusion
93
what factors influence the development of an infarct? (4)
nature of vascular supply
rate of development
vulnerability to hypoxia
oxygen content of blood
94
what are some examples of none thromboembolism emboli?
```
bacterial
fat droplet
parasites
bubble of air/nitrogen
tumour fragments
```
95
what does DIC stand for?
disseminated intravascular coagulation
96
what is disseminated intravascular coagulation?
acute, subacute or chronic thrombo-haemorrhagic disorder occurring as a secondary complication in a variety of diseases
97
what are the stages of DIC? (4)
activation of coagulation cascade
formation of micro-thrombi throughout circulation
consumption of platelets, fibrin and coagulation factors
activation of fibronlysis
98
what are the associated clinical signs of DIC? (3)
tissue hypoxia
infarction
haemorrhagic disorder (consumption coagulopathy)
99
what are the major underlying mechanisms of DIC? (2)
release of tissue factor or thromboplastin substances
| widespread endothelial injury
100
what can lead to DIC? (6)
```
sepsis
endothelial injury
immune complex deposition
neoplastic disease
extensive burns/trauma
extensive surgery
```
101
what induces DIC in gram negative sepsis?
bacterial endotoxins
102
what do bacterial endotoxins induce to happen in monocytes?
increased synthesis, membrane exposure and release of tissue factor
103
what do bacterial endotoxins induce activated monocytes to release?
IL1
| TNF
