vasculature Flashcards
Structure of the bone marrow
How red blood cells arise
- Starts with division of stem cell
- ribosomes manufacture red cell proteins, some of which help with intake of iron.
- Iron, transfered by transferin is brought to mitochondria where it binds to protoporphyrin to produce heme.
- alpha and beta globin chain are made and joins with heme
- red cell leave blood marrow, and lose their nucleus as they do so.
- Now called reticulocyte, goes to spleen where it loses everything else.
What are platelets and how they are formed and where they are stored.
‘Fragment of cells’ without a nucleus but with mitochondria and adhesive proteins.
- thrombopoeisis: myeloid stem cells differentiate into promegakaryocytes then megakaryocytes. Initiated by thrombopoeitin hormone.
- cytokine stimulation causes megakaryocytes to lose fragments, called platelets.
- platelets circulate in blood and are stored in spleen
neutrophils function and ability to multiply
differentiated, non multiplying cells, first responders in infection, kill bad cells. Highly motile and move towards chemokines
Eosinophil function and examples of cytotoxic secretions
immune cell that secretes many cytotoxic proteins
Monocyte role and function and structure
Become macrophages in tissue, kidney shaped nucleus. Very phagocytic and motile
Subdivisions of lymphocytes
Then helper/ killer t cells, or plasma or memory b cells
Describe intrinsic and extrinsic clotting cascade, and negative feedback mechanisms that are involved
Also written on paper to help
Describe the three main steps of primary hemostasis
- Vasoconstriction (endothelin, nerve reflex…)
- Platelet adhesion (VW factor bind Ib receptors on platelets to collagen on damaged tissues)
- Platelet aggregation (IIa/IIIb receptor on platelets binds to other platelets)
3 main molecules involved in secondary hemostasis
Calcium ion, fibrin and clotting factor 13 and phospholipid (XIII)
Main differences between arterial and venous thrombosis
Arterial: large platelet component, associated with atherosclerosis, prevented with anti-platelet drugs.
Venous: large fibrin component, occcur after surgery issue, or turbulent blood flow, prevented with anticoagulation drugs.
Mechanism of anti-platelet drug and example
prevent plaetelt aggregation (IIb/IIIa antagonist)
e.g. aspirin
IIa/IIIb receptor antagonist drugs side effect and uses
General issue with anti-platelt drugs
Uses: used to prevent constriction of arteris (restenosis) after they have been opened up (coronary angioplasty) and stop immediate platelet aggregation.
Risks: very potent and may cause low platelet count (thrombocytopenia)
General issue: many pathways to platetlet activation so inhibition of a single one won’t make a huge difference.
What class of drugs heparin is and mechanisms of action (which coagulation factors it inhibits)
Anti-coagulant drug
Inhibits factors 12, 11, 10, 9 and thrombin
What class of drugs warfarin is and mechanisms of action (which coagulation factors it inhibits)
Anti-coagulant drug
Inhibits 9, 10 (intrinsic), 7 (extrinsic) and thrombin
Long term prevention therapy
The following are natural clot formation regulators. State how each inhibit the pathway
Endothelial cell nitric oxide and prostacyclin
Endothelial cell nitric oxide and prostacyclin: stop platelet aggregation and adhesion
Tissue factor pathway inhibitor (TFPI) - inhibits factors 10 and 7
Active protein C (ATC) - inhibits factors 5 and 8
Antithrombin - inactivates thrombin, factor 10.
Changes in blood pressure during orthostatis in the venous and arterial circulation in the food
Arterial liying down: 96
Arterial standing: 186
Venous lying down: 10
Venous standing: 100
Increases by 90 mmHg
Changes in BP in next to the heart when you stand (arterial and venous)
Venous standing: 1
Venous lying down: 4
Arterial standing: 100
Arterial lying down: 100
2 effects orthostatis has on CV system
- Reduced cardiac output: less venous return because it is pooling in the bottom
- loss of plasma volume: fluid in blood is flows into the cells because of oncotic pressure
Response of the CV to orthostatis (in the heart and vessels)
Baro- and volume receptors are activated, causing increase in heart rate (heart) and vasoconstriction (TPR), in order to restore BP. Sympathetic nervous system is activated.
What happens to venous and arterial pressures above the heart and flow on standing?
It falls (from 4 to 0) but not below zero since the veins above the heart collape. Flow slows down because the arterial pressure falls (100-60) so pressure gradient falls.
Cerebral blood flow decreases by 20%
Why veins in the cranium don’t collapse
Because CSF is drawn down by gravity, causing a negative intracranial pressure, so the veins in the cranium don’t collapse
Effect of standing on:
Central blood volume
Central venous pressure
stroke volume
Heart rate
Contractility
Cardiac output
Limp and splanchnic flow
TPR
Cerebral blood flow
What is vasvagal syncope
A sudden fall in TPR and heart rate mediated by the vagus nerve, causing fainting (syncope). Can be cause by a tilt up
Average max conxumption of O2 in intensse exercise
5L of O2 per min
Vascular changes observed in exercise
Increased heart rate and stroke volume (CO)
Vasoconstriction of non essential vessels (splanchic circultation)
Increase sympathetic drive, decrease parasympathetic drive
Changes during exercise (increased O2 consumption) in:
Cardiac output
Stroke volume
Heart rate
Blood pressure
TPR
Blood O2 content (venous and arterial)
Vascular changes in skin blood vessels during exercise
Initial vasoconstriction, then vasodilation, then vasconstriction at maximum exercise.
How isometric exercise differs from isotonic exercise in terms of BP, HR and TPR
BP: systolic and diastolic both increase more than in isotonic exercise (increased TPR)
HR: increases
TPR: stays the same or increases because of the compression of the blood vessels in contracting muscle
What is concealed hemorrage and circulatory shock and effects in the body
Concealed hemorrage: bleeding is obvious but hard to quantify
Circulatory shock: generalised inadequacy of blood flow throughout the body
Classification of heamorrage from minimal to mild to moderate to severe -> %blood loss and risks
Immediate compensations after blood loss to maintain BP and CO, and keep blood volume
Reverse stress relaxation: veins shrink around reduced blood volume to maintain venous return. (starts after 10 min)
Baroreceptor reflex: increased HR, decrease parasympathetic (peripheral vasoconstriction)
Ischaemic response (BP below 50mmHg): powerful peripheral vasoconstriction, reduced perfusion of gut and kidney
Activation of RAAS
Effects of blood loss on BP and pulse pressure
PB stays constant (low CO but high TPR) initially. Then falls
Pulse pressure (diff between systole and diastole) decreases.
Restore of blood volume vs RBC after hemorrage
Blood volume: restored within 3 days thanks to RAAS and fluid reabsorption from the interstitium
Plasma protein: 1 week
Haemoglobin and RBC: 4 weeks and more
Non progressive shock, progressive shock and refractory shock. What they are
Non progressive: gets better without treatement (less than 20% loss)
Progressive shock: more than 30% shock, initially improve then decline unless transfusion is rapidly administered (golden hour)
Refractory shock: too late to do anything, patient will probs die due to cardiac damage.
Cardiac changes with age (the heart and baroreceptor reflex) and causes
Lower max HR, fall in cardiac contractility
Due to decrease B1 sensitivity and loss of cardiomiocyte
Baroreceptor reflex less responsive
Change in BP over age, and vascular changes that explain this (arteriosclerosis)
Diastolic rises and then falls at arount 55, systolic constantly rises (hypertensive by 60)
This is due to arteriosclerosis: reduction in elasticity of large arteries (think and fragemnted elastin layer), increase in stiffness (increased collagen)
Also NO release decreases, less vasodilatation
