Vascular disturbances 1 Flashcards
What’s the word given when there are a small number of red blood cells leak into extra vascular tissue.
Not a true haemorrhage.
Diapedesis
You watch the Blood vessels leak out and you say
Di ape die
What is hyperaemia.
What are the 2 types of hyperaemia and give an ex of how can each occur
An increased amount of blood in a part of the vascular system.
- Active hyperaemia- increased blood present coz of increased supply through arteries/arterioles, which actively dilate.
- well oxygenated blood- bright red
- can be normal physiological process
- pathological process eg inflammation- requires increased nutrients, O2, and defence mechanisms to over come causative agent. - Passive hyperaemia = congestion
- decreased drainage
- poorly oxygenated blood- dull red
What happens when there is blood volume expansion and why does it happen?
Increase in atrial stretch/pressure (high salt diet etc)
- stimulates cardiomyocytes to release natriuretic peptides
- this has potent vasodilatory effect and natriuretic (excrete bulk salt in the urine)
How do the natriuretic peptides cause a reduction in extra cellular fluid volume and blood pressure?
Stimulates:
- vasodilation
- increased glomerular filtration rate
- increased sodium excretion
- inhibits renin-angiotensin-aldosterone system (system causes blood vessels to constrict and increases reabsorption of sodium- all aim to increase blood pressure and volume)
- inhibit endothelial release
- increase vascular permeability
- inhibit vascular smooth muscle, endothelial cell and cardiac myocyte proliferation
Slide 11
Imagine: you take a natriuretic pill, you swell up (vasodilate), then do a massive poo made of salt (⬆Na+ excretion) ange and ranin comes along, smells it and runs away (⬇renin-angiotensin-aldosterone system)
-then all that swelling just starts seeping through your skin (⬆vascular permeability)
-all the fluid that falls out of you goes through this glomerular processer (⬆ glomerular filtration rate)
What is ischemia and what can it be due to?
What’s it called if this happens rapidly and tissues die?
What will the affected organs look like?
Too little blood within a circulatory bed.
May be due to:
1. Too little blood (anaemia)
2. Intra luminal obstruction to blood flow eg clot (thrombus), tumor etc
3.extraluminal obstruction to blood flow eg compression due to a growing tumor, torsion, herniation
Ischemic necrosis
Affected organs will appear pale and area will be cool
What is a haemorrhage?
What are the 3 main elements that stop a haemorrhage?
What are some causes of a haemorrhage?
A haemorrhage is defined as escape of blood from a damaged blood vessel.
The arrest can be achieved by 3 main elements:
1. Coagulation factors
2. Platelets
3. Blood vessel wall
Imagine: blood starts gushing from a vessel- how to stop it➡ you start shooting plates out of a gun to try and fill up the hole. You then watch the vessel wall trying to engulf the hole and stop loss. Last➡ coagulation cascade duh
A disease affecting one or all of these will result in a huge haemorrhage or a thrombosis= excessive clotting
Endothelial cell damage causes purpuric tendency (small haemorrhages on the skin) or
Tiny pinpoint haemorrhages into mucus membranes on skin are called petechia. What could cause this? Pg 8
Imajine: your pet has walked all over you leaving red pin pricks Everywere.
Causes?
A) mechanical trauma eg bruise
B) vessel wall weakness eg arteriosclerosis, bit C deficiency
C) toxic damage to endothelium
D) disorders of clotting mechanisms: haemophilia, vit K deficiency
Reasons for haemorrhage: before the blood vessel wall burst open what happens? ➡ You want it to burst open so you throw rocks at it (mechanical trauma), you then proceed to suck all the Vit C and vit K out of the walls leaving the wall as an un elastic arteriosclerotic mess. It still doesn’t work so you get toxic waste (all the vitamins in concentrate and spray the endothelium, giving the blood vessel many disorders eg haemophilia, vit K deficiency etc.
What are the physiological events subsequent to a sudden significant but non-fatal haemorrhage
Pg 15-19 info and written down it bum fart notes
Phase 1- redistribution of remaining blood
1. Venous return falls
2. Cardiac output is reduced
3. Arterial blood pressure falls
4. Carotid and aortic bodies ➡stimulate the vase motor centres➡ strong sympathetic stimulation
5. Blood supply to vital organs -brain and respiratory muscles maintained
6. Tachycardia occurs
7. Adrenalin and noradrenaline are released➡ general vasoconstriction + coronary artery dilation
8. ⬇ Blood pressure ➡renin➡ angiotensin production (potent vasoconstriction) and aldosterone production (Na and H20 reabsorption)
Phase 2: restoration of blood volume
- Blood pressure ⬇ despite phase 1
- Fluid moves from extra vascular spaces into circulation (osmotic forces) to replace lost fluid.
Phase 3:
- this phase is one if erythropoiesis in which the number of RB s and the haemoglobin content of the blood is restored to normal.
- there is enhanced manufacture of plasma proteins in the liver.
- reticulocytes and metarubricytes will be circulating in the blood, this takes about 4 days
Imagine: VR, CO and BP All drop
-carotid and aortic bodies sense this and give strong sympathetic stimulation to constrict ➡
What is shock characterised by?
Characterised by failure of the circulatory system to maintain an appropriate blood supply to an organs micro circulation.
Can lead to multi-organ failure
What is a thrombus?
What is it called when this system functions normally/ inappropriately?
What are the major predisposing causes for thrombosis?
A compact mass if aggregated platelets and fibrin that build up in the flowing blood stream of a living animal. It represents the end result of blood coagulation
- formed by interaction between blood vessel walls, platelets and clotting factors
- it forms a plug to decrease blood flow and initiates healing.
Functioning normally in appropriate situation= heamatostasis
Excessive haemostasis is called a thrombosis
Major causes:
1) damage to endothelial surface
2) sluggish or abnormally turbulent blood flow
3) hypercoagubility of the blood
What are the anti thrombotic properties of endothelial cells?
Antithrombotic properties of endothelial cells
Antiplatelet factors
1) physical presence- this prevents contact between platelets and au endothelial collagen
2) production of Prostacyclin
-acts as a vasodilator and inhibits platelet aggregation by a direct effect on thromboxane A
3) Nitric Oxide
-this is a smooth muscle relaxant causing vasodilation and also inhibits platelet aggregation both PGI2 and nitric oxide
4) Adenosine Disphosphatase:
This degrades ADP and so inhibits platelet aggregation
Anticoagulant factors
Fibrinolytic factors
1. t-PA- promotes fibrinolytic activity to clear fibrin deposits from endothelial surfaces
What are the Prothrombotic properties of endothelial cells?
- Vin Willebrand Factor (vWF)- this is a cofactor for Factor VIII and assists in platelet adhesion to collagen
- Tissue factor- this is produced in response to endotoxins, tumor necrosis factor and activates the extrinsic clotting cascade
- Inhibitors of Plasminogen Activators- these suppress fibrinolysis.
Platelets in haemostasis. What is their function how do they do it?
Platelets are the cellular components of blood. When an area of endothelium is damaged, an initial platelet plug is Formed to minimise loss. Involves following steps
1) platelet adhesion- vascular damage exposed sub endothelial collagen and decreased prostacyclin production, which encourages platelets to stick to the exposed extra cellular matrix
2) platelet secretion: step one triggers synthesis and secretion of a number of substances to platelet adhesion and development of platelet aggregation
Coagulation cascade
Extrinsic pathway
Extrinsic Pathway:
1) tissue injury activating both extrinsic and intrinsic pathways
2) tissue factor is released from endothelial cells
3) this activates factor 7
4) which then triggers a cascade which activates factor 10
5) common pathway: thrombin gets activated to factors 5,8,11 and 13
6) then fibrin released and glues platelets together and covers hole in blood vessel to glue damaged tissue together.
7) activates fibroblasts and inflammatory response
Coagulation cascade: lNtrinisc cascade
Activated by not just tissue damage but also exposure of collagen fibres.
1) when collagen comes in contact with blood activates Factor 12
2) once collagen comes in contact with factor 12 triggers cascade
3) factors 11, 9 and 8 are activated sequentially
4) resulting in activation of factor 10
Then common pathway.
What is pathology?
The study of structural and functional abnormalities in cells, tissues, organs and body systems. These abnormalities are known as disease.
