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PMP101 - Health, Disease and Patient > CVS - blood p2 > Flashcards

CVS - blood p2 Flashcards

1
Q

What is erythropoiesis + stages of it?

A

*process by which red blood cells are produced (15 days long)
*proerythroblast → erythroblast → reticulocyte → erythrocyte

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2
Q

What are the steps of the regulation of erythropoiesis?

A

1:Detection of hypoxia
2:EPO release
3:stimulation of erythropoiesis
4:restoration of oxygen levels
5:negative feedback inhibition

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3
Q

What occurs in detection of hypoxia?

A

*Kidney Becomes Hypoxic: When the oxygen level in the blood decreases (hypoxia), the renal arterial oxygen level drops
*Trigger for EPO Release: The kidneys detect the low oxygen levels through specialised cells in the renal cortex

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4
Q

What occurs in EPO release?

A

*Production: In response to hypoxia, the kidneys release erythropoietin (EPO) into the bloodstream.
*Function: EPO travels through the blood to the red bone marrow

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5
Q

What occurs in the stimulation of Erythropoiesis?

A

*EPO Action: EPO stimulates the red bone marrow to increase the production of erythrocytes (red blood cells) from haematopoietic stem cells

*Erythrocyte Production: The bone marrow responds by producing and releasing more red blood cells into the circulation

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6
Q

What occurs in oxygen restoration?

A

*Increased Oxygen Transport: The newly produced erythrocytes increase the oxygen-carrying capacity of the blood.

*improved oxygen delivery: as oxygen levels in the blood rise, more oxygen is delivered to the tissues, including the kidneys

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7
Q

What happens in the negative feedback inhibition?

A

*Reduced Hypoxia: As the kidneys receive more oxygen, the hypoxic stimulus decreases
*Inhibition of EPO Release: The increased oxygen levels in the renal arteries signal the kidneys to reduce the production and release of EPO
*Balanced Erythropoiesis: This feedback mechanism ensures that erythrocyte production is balanced, preventing excessive or insufficient red blood cell counts

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8
Q

What causes hypoxia?

A

-Haemorrhage or Injury
-Iron deficiency-
-High Altitude or Lung Disease (Pneumonia)

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9
Q

What nutrients are needed in erythropoiesis?

A

*Iron: Dietary
*65% in Hb
*Bound with protein and stored as ferritin and haemosiderin
*Transported by binding with transferrin

*Substrates, like amino acids, lipids and carbohydrates
Folic acid & Vitamin B12 – DNA synthesis/Development of RBC

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10
Q

What effects does testosterone have on EPO?

A

*testosterone enhances EPO production in kidneys = more RBC
*higher RBC = higher haemltocrit levels in males compared to females

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11
Q

What are the impacts of high EPO levels?

A

*Faster Maturation of Erythrocytes: Elevated EPO levels cause erythrocytes to mature more rapidly in the bone marrow
*Increased Haematocrit: Higher RBC production increases the proportion of red blood cells in the blood (haematocrit)

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12
Q

What are the potential risks to higher EPO?

A

*dehydration
*increased blood viscosity

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13
Q

What are the health risks associated with increased EPO and haemocrit?

A

*blood clotting
*stroke
*heart failure

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14
Q

What are the key stages in the life cycle of RBC?

A

100-120 days
-Cannot grow, divide and replicate (no nucleus)
-Get older and fragile and degenerate
-trapped/macrophage in spleen- RBC breakdown

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15
Q

What is recycled of RBC components?

A

Iron- recycled & stored
Heme- Degraded to bilirubin, yellow pigment-Liver secretes bilirubin in bile (in the intestine)-urobilinogen-stercoblin, brown pigment excreted in faeces
Globin- metabolised into aminoacids & recycled

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16
Q

What are the signs and risks of anaemia?

A

*low oxygen (Hypoxia) insufficient oxygen supply to tissues
*impact on growth and development
*metabolic dysfunction

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17
Q

What are the causes and types of anaemia?

A

1: blood loss =haemorrhagic anaemia
- acute blood loss
- chronic blood loss

2: RBC deficiency:
- iron deficiency anaemia

3: renal anaemia

4:pernicious anaemia

5:aplastic anaemia

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18
Q

What is iron deficiency caused + effect by?

A

Cause: Insufficient iron, leading to the production of small, pale RBCs (microcytes) that lack adequate haemoglobin

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19
Q

What is renal anaemia caused by + effect?

A

Cause: Kidney disease results in a lack of erythropoietin (EPO), which is necessary for RBC production

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20
Q

What is pernicious anaemia caused by + effect?

A

Cause: An autoimmune condition that impairs the absorption of vitamin B12, essential for RBC division.
Effect: Without B12, RBCs become large and abnormal (macrocytes).

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21
Q

What is aplastic anaemia caused by + effect?

A

Cause: Damage to the red bone marrow, often due to chemotherapy, radiation, or exposure to toxic chemicals.
Effect: The bone marrow fails to produce sufficient RBCs

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22
Q

What is thalassemia caused by? + effect (alpha and beta)

A

Alpha
Cause: Deficiency or absence of alpha-globin chains.
Effect: RBCs become thin, fragile, and deficient in haemoglobin
Beta:
Cause: Deficiency or absence of beta-globin chains.
Effect: Similar to alpha thalassemia, RBCs are thin, fragile, and lack adequate haemoglobin

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23
Q

What are the symptoms of thalassemia?

A

*tiredness
*shortness of breath
*paleness

24
Q

What are the treatments/ management for thalassanaemia?

A

*blood transfusions
*iron chelation therapy
*bone marrow transplantation
*supportive care

25
Q

What is sickle cell anaemia caused by + effects?

A

Mutant Hb (HbS): In sickle cell anaemia, the 6th amino acid is valine instead of glutamic acid due to a genetic mutation
-o2 levels are low

26
Q

What are the characteristics of sickle cell anaemia?

A

Shape: Sickle RBCs are crescent-shaped or “sickle” shaped.
Oxygen Levels: The abnormal shape is more pronounced when oxygen levels are low
Blockage of Blood Flow: Sickle-shaped RBCs can block blood flow in the blood vessels, leading to complications such as stroke and other vascular diseases

27
Q

What are the symptoms and complications of sickle cell anaemia?

A

*Fatigue: Due to the reduced oxygen-carrying capacity of sickle RBCs.
*Pain: Often referred to as sickle cell crises, these painful episodes are caused by the blockage of blood flow and subsequent tissue damage
*Challenges with Physical Activity: Individuals with sickle cell anaemia often experience severe fatigue and pain, making work and exercise difficult

28
Q

What is plycythaemia?

A

Polycythaemia is a condition characterised by an abnormally high number of red blood cells (RBCs) in the blood = thicker blood

29
Q

What causes polycythaemia?

A

1: bone marrow cancer
- polycythaemia vera
2:high altitude
- secondary polycythaemia

30
Q

What are the effects of increased blood viscosity?

A

*Thicker Blood: The increased number of cells makes the blood thicker and more viscous.
*Impaired Blood Flow: The thicker blood flows more slowly and with more difficulty through blood vessels, which can increase the risk of several conditions

31
Q

What are the health risks associated with polycythaemia?

A

*stroke
*coronary artery disease
*renal disease

32
Q

What is step 1 of haemostasis to clot blood?

A

Vascular spasm (Vasoconstriction)
Immediate Response: When a blood vessel is injured, it constricts to reduce blood flow to the affected area.
Mechanism: The smooth muscle cells in the vessel wall contract, causing vasoconstriction.
Purpose: This immediate response minimises blood loss and creates conditions favourable for subsequent haemostatic processes

33
Q

What is step 2 to haemostasis clotting?

A
  • Platelet activation (platelet plug formation)
    Adhesion: Platelets adhere to the exposed collagen fibres at the site of injury, facilitated by von Willebrand factor (vWF).
    *Activation: Once adhered, platelets become activated and change shape, releasing granules containing adenosine diphosphate (ADP), thromboxane A2, and other chemicals that further promote platelet activation and aggregation.
    *Aggregation: Activated platelets stick together (aggregate) to form a temporary platelet plug that covers the injury site
34
Q

What is the purpose of step 2 of haemostasis?

A

Purpose: The platelet plug temporarily seals the break in the vessel wall and provides a surface for the coagulation cascade to build a more stable clot

35
Q

What is step 3 of haemostasis clotting?

A

Clotting factors/procoagulants (Factors I to XIII) are synthesised in the Liver and Vitamin K is an essential cofactor in the biosynthesis of clotting factors. The formation of a stable blood clot, also known as the coagulation patch.

36
Q

What is the intrinsic pathway initiation and factors involved (step 3 of haemostasis)

A

*Initiation: Triggered by trauma inside the blood vessel.
*Factors Involved: Involves clotting factors XII, XI, IX, and VIII

37
Q

What is the initiation and factors involved in the extrinsic pathway (s3 haemostasis)

A

*Initiation: Triggered by external trauma that causes blood to escape from the vascular system.
*Factors Involved: Involves tissue factor (TF) and Factor VII

38
Q

what happens at the common pathway?

A

*convergence point: both intrinsic and extrinsic pathways converge at factor X
*there are several steps

39
Q

What is factor Xa of common pathway?

A

Prothrombin Activation: Factor Xa, along with cofactor Va, converts prothrombin (Factor II) to thrombin (IIa).

40
Q

What happens in clot retraction with vessel repair? PDGF

A

*Platelet Contraction: The actin and myosin in platelets contract, pulling on fibrin strands. This action helps to tighten and consolidate the clot, making it more stable and secure at the site of vessel injury

41
Q

What is the PDFG step?

A

Stimulation of Cell Division: PDGF stimulates the division of smooth muscle cells and fibroblasts. This promotes the repair and regeneration of the vessel wall by encouraging the proliferation of these essential cells

42
Q

What is the VEGF step?

A

Endothelial Lining Repair: VEGF stimulates the rebuilding of the endothelial lining by multiplying endothelial cells. This helps restore the integrity of the blood vessel, ensuring it is properly lined and functional after injury

43
Q

What are the two steps of fibrinolysis?

A

*plasminogen activation
-plasminogen (plasma protein) converted to plasmin
* fibrin digestion = clot breakdown
- plasmin digests fibrin (fibrin mesh) = removal of the clot allowing normal blood flow to return

44
Q

What are some examples of haemostasis disorders?

A

*thromboembolism
*unregulated bleeding

45
Q

What is thrombosis? + types + causes?

A

Definition: Formation of a blood clot (thrombus) within a blood vessel, obstructing blood flow.
Types: Arterial, venous, capillary thrombosis.
Causes: Hypercoagulability, stasis of blood flow, vessel wall injury

46
Q

What is embolism? + types +common sites?

A

Definition: Movement of a blood clot or other endogenous material (embolus) through the bloodstream, causing obstruction
Types: Thromboembolism, fat embolism, air embolism, amniotic fluid embolism.
Common Sites: Pulmonary embolism, cerebral embolism, peripheral embolism

47
Q

What are the symptoms of embolism?

A

Vary depending on the site, but can include shortness of breath, chest pain, sudden weakness, difficulty speaking, and pain in the limbs.

48
Q

How much/ what effect does the cvs compensating for blood loss?

A

Mild Blood Loss: Up to 15% - The cardiovascular system can generally compensate without significant symptoms.
Moderate Blood Loss: 15-30% - Can lead to fatigue and pallor
Severe Blood Loss: Greater than 30% - Potentially lethal, requiring immediate medical intervention

49
Q

what does liver dysfunction cause?

A

*clotting factors synthesis
*malnutrition of vitamin K
*impaired bile production

50
Q

What is haemophilia?

A
51
Q

What are the types of haemophilia?

A
52
Q

What are the symptoms of haemophilia?

A
53
Q

What are the antigens like on different blood groups?

A

A Antigen: Present on the surface of RBCs in individuals with type A blood.
B Antigen: Present on the surface of RBCs in individuals with type B blood
Both A and B Antigens: Present on the surface of RBCs in individuals with type AB blood.
No A or B Antigens: Individuals with type O blood have no A or B antigens on their RBCs

54
Q

What are antibodies like on different blood groups?

A

Anti-A Antibodies: Present in the plasma of individuals with type B or type O blood.
Anti-B Antibodies: Present in the plasma of individuals with type A or type O blood
No Anti-A or Anti-B Antibodies: Individuals with type AB blood have neither anti-A nor anti-B antibodies in their plasma.
Both Anti-A and Anti-B Antibodies: Present in the plasma of individuals with type O blood

55
Q

What is the Rh positive factor classification?

A

Antigen Present: Individuals have the D antigen on the surface of their RBCs.
Notation: Denoted as RhD+ or simply Rh+.

56
Q

What is the Rh negative factor classification?

A

Antigen Absent: Individuals do not have the D antigen on the surface of their RBCs.
Notation: Denoted as RhD- or simply Rh-

57
Q

What blood groups can donate blood to whO?

A

AB: can get from A,B,AB and O
A: A,O
B: B,O
O: ONLY O (universal donor)

PMP101 - Health, Disease and Patient (20 decks)

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