Cardiovascular system II Flashcards
Erythropoiesis- Production of RBC- ~15 days
Production and Maturation
Bone marrow»_space;> Blood
Plurpotent hematopoietic > Proerythroblast > Erythoblast > Reticulocyte > Erythocryte
Regulation of Erythropoiesis
Hormonal (Negative Feedback Axis)
Kidney becomes hypoxic (renal arterial oxygen drops) triggering EPO release
What causes Hypoxia?
Haemorrhage or Injury
-Iron deficiency-
-High Altitude or Lung Disease (Pneumonia
O2 sensor protein- Hypoxia-inducible Factor
Low oxygen > to bone marrow to red blood cells
Oxygen levels drop - high demand for oxygen, what happens?
Stimulant for Erythropietin to be released by kidney
High number of Erythropeietin >
High number of Erythrocytes whihc increase O2
Blood becomes…
thicker - harder to flow through the vessels
Whats another word for RBC?
Erythrocytes
Hormone which is release in demand of oxygen:
Erythropoietin (EPO)
What is Erythropoietin made of and where is it secreted?
glycoprotein hormone naturally produced by the peritubular cells of the kidney
Regulation of Erythropoiesis
Hormonal -Ive feedback Axis
Kidney becomes hypoxic (renal arterial oxygen drops) triggering EPO release
Erythropoietin (EPO) stimulate the red bone marrow to produce erythrocytes
Erythrocytes increases O2 transport to the kidney and block EPO release
Why do males have more red blood cells/ more RBC than females per mcL?
More testostrone compared to women
Why does more testostrone means bigger supply of oxygen?
Testosterone enhances EPO production,
(result in higher RBC in Males)
High EPO: Erythrocytes mature faster
Increase haematocrit, dehydration and blood viscosity (clotting, stroke, heart failure)
What is the importance of Iron in blood?
Nutrients
Iron: Dietary
65% in Hb
Bound with protein and stored as ferritin and haemosiderin
How is Iron transferred?
Transported by binding with transferrin
Substrates, like amino acids, lipids and carbohydrates
Folic acid & Vitamin B12 – DNA synthesis/Development of RBC
Life cycle RBC
how many days?
100-120
What happens in the RBC cycle?
Cannot grow, divide and replicate (no nucleus)
-Get older and fragile and degenerate
-trapped/macrophage in spleen- RBC breakdown
-Iron- recycled & stored
Heme
Degraded to bilirubin, yellow pigment-Liver secretes bilirubin in bile (in intestine)-urobilinogen-stercoblin, brown pigment excreted in faeces
Globin
metabolised into aminoacids & recycled
RBC: What could go wrong?
- Anaemia
- Blood loss
- RBC deficiency
- Sickle cell anaemia
- Thalassemia
Anaemia:
Sign of problem and risk
(Low Oxygen- Hypoxia- Growth, Development and Metabolism of several cells)
Symptoms of Anaemia
Fatigue, Pallor, Dyspnoea & chills
Blood Loss:
Haemorrhagic (acute, chronic): Blood loss, replace blood; treat cause
RBC deficiency:
Iron deficiency: RBC turning microcytes lacking Iron-Hb production. Treat or manage with Iron supplements
Renal: lack of EPO; supplement with synthetic EPO
Pernicious: Autoimmune condition-destroy B12 absorption; without B12 RBC cannot divide (or) and they become macrocytes: Treat or manage with either dietary or supplement B12.
Aplastic: Injury to Red Bone Marrow/ Drugs: Chemotherapy, Radiation, chemicals: Transfusion and stem cell transplantations
Sickle cell anaemia (genetic cause):
- Mutation in Hb: one amino acid is wrong in the globin B chain (6th AA- Glutamic acid in normal RBC whereas 6th AA is Valine in sickle RBC)
- Sickle RBC is crescent-shaped
O2 levels are low
Crescent shape block flow in the blood vessels and leads to stroke and other vascular diseases
Symptoms of sickle cell anaemia:
Very fatigue, lots of pain, challenged with work/exercise
(Predominantly in African ethnics)
Thalassemia (genetic cause):
- Globin chain in Hb is absent or malfunction
- RBC become thin, delicate and lack Hb
- Mild to Severe subtypes- Blood transfusions
- Predominantly in Mediterranean ethnics
What is Polycythaemia?
Too many red blood cells in the blood
Bone Marrow Cancer, People living in Highlands
- why is this?
Low O2 in high altitude
Too thick too many cells increase the viscosity
- blood cannot move through the vessels efficiently which can lead to…
- Stroke
- Coronary artery disease
- Renal disease
Haemostasis is key process to stop…
bleeding (Clot)
What are the three stops to blood clotting?
- Vascular spasm
- Platelet Activation - Plug
- Coagulation - Patch
- Vascular spasm
pain reflux, constriction of vascular smooth muscle, trigger clotting chemicals/factors needed & directed to site of injury
- Platelet Activation - Plug
Endothelial Damage
Exposed Collagen
Platelets stick to exposed collagen
Platelets stimulate ADP, Thromboxane A2 and Serotonin
Von Willebrand Factor- Stabilise collagen-platelet adhesion
- Coagulation - Patch
Clotting factors/procoagulants in Liver
Vitamin K, the biosynthesis clotting factors
Plasma proteins I to XIII
Fate of clot and vessel healing
a) Clot retraction concurrent with vessel repair
b) Fibrinolysis
Clot retraction concurrent with vessel repair
The actin and myosin in platelets contract and pulls on fibrin strands
Platelet-derived growth factor (PDGF)
Stimulate smooth muscle and fibroblast division
Vascular endothelial growth factor (VEGF)
Rebuild endothelial lining by multiplying endothelial cells
Fibrinolysis
Plasminogen, plasma protein trapped in clot- converted Plasmin-digest Fibrin
Name Haemostasis disorders
Thromboembolism;
Unregulated Bleeding Disseminated Intravascular Coagulation (DIC)
ADP, Thromboxane A2 and Serotonin are…
Clotting factors - they help to clot the injury site
What is vitamin K’s role in clotting?
Needed to activate the clotting factors = blood will NOT clot otherwise
Where is Vit K secreted
The small intenstine
Pathological Blood Clot
> Thrombosis
Embolism
Thrombosis =
Thrombosis-Blood clotting (Thrombus) in arteries, veins or capillaries
Embolism =
Blood/ clot endogenous materials (Embolus) moving in the blood vessel and obstructing blood flow
Arterial and Venous Thrombi are not the same
There are 2 main types of thrombosis: Venous thrombosis is when the blood clot blocks a vein.
Veins carry blood from the body back into the
heart.
Arterial thrombosis is when the blood clot blocks an artery.
Same two bleeding disorders:
1) Liver dysfunction:
2) Haemophilia
1) Liver dysfunction:
Clotting factors synthesis
Malnutrition of Vitamin
Hepatitis, Cirrhosis
Impaired Bile production- needed for fat and vit.K absorption
2) Haemophilia:
Hereditary (Prolonged bleeding in joint cavities)
CVS compensate the blood loss
> 15<30% loss: Fatigue and Pallor
30% loss: Lethal
**3) Coagulation STEP by STEP
1) Intrinsic (blood) and Extrinsic (tissue) [always together] activates the X-A, Prothrombin Activator
2) Then the X, Prothrombin converts to Thrombin
3) Through dual role Thrombin converts to Fibrinogen (SOLUBLE)
4) Then Fibrinogen converts to Fibrin (INSOLUBLE - which is why a scab appears which is solid) XIII
5) Thrombin also produces a fibrin (mesh to bind everything together ( this is the completion of the dual role)
Does Coagulation happen internally or externally?
Both
ABO - Blood grouping
Antigen A
Antibody B
(IgM)
Antigen B
Antibody A (IgM)
Antigen AB
Antibody (None)
Antigen (No)
Antibody A + Antibody B
Why do people with blood group AB have no antibodies?
Antigen: Immune-responsive sensor of foreign biologicals
- RBC antigens are agglutinogens
- RBC antibodies are agglutinins
With blood type O why do they have antibodies A and B
Antibodies are naturally occurring
Starts at 2 months of age and ends at 8-10 years of age
Antigens AB
35 different blood grouping in human
ABO & Rh factors has the most severe transfusion reactions
Blood Transfusion
Antibody for Rh are not spontaneous formation
For example: Rh- receive Rh+ blood or
Rh- mother carrying Rh+ (First Pregnancy):
No problem but mother develop Rh antibodies 2nd pregnancy will stimulate health complications to baby
