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PMP-101 > Cardiovascular system II > Flashcards

Cardiovascular system II Flashcards

1
Q

Erythropoiesis- Production of RBC- ~15 days

A

Production and Maturation

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2
Q

Bone marrow&raquo_space;> Blood

A

Plurpotent hematopoietic > Proerythroblast > Erythoblast > Reticulocyte > Erythocryte

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3
Q

Regulation of Erythropoiesis

A

Hormonal (Negative Feedback Axis)
Kidney becomes hypoxic (renal arterial oxygen drops) triggering EPO release

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4
Q

What causes Hypoxia?

A

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

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5
Q

O2 sensor protein- Hypoxia-inducible Factor

A

Low oxygen > to bone marrow to red blood cells

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6
Q

Oxygen levels drop - high demand for oxygen, what happens?

A

Stimulant for Erythropietin to be released by kidney

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7
Q

High number of Erythropeietin >

A

High number of Erythrocytes whihc increase O2

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8
Q

Blood becomes…

A

thicker - harder to flow through the vessels

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9
Q

Whats another word for RBC?

A

Erythrocytes

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10
Q

Hormone which is release in demand of oxygen:

A

Erythropoietin (EPO)

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11
Q

What is Erythropoietin made of and where is it secreted?

A

glycoprotein hormone naturally produced by the peritubular cells of the kidney

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12
Q

Regulation of Erythropoiesis
Hormonal -Ive feedback Axis

A

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

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13
Q

Why do males have more red blood cells/ more RBC than females per mcL?

A

More testostrone compared to women

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14
Q

Why does more testostrone means bigger supply of oxygen?

A

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)

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15
Q

What is the importance of Iron in blood?

A

Nutrients
Iron: Dietary
65% in Hb
Bound with protein and stored as ferritin and haemosiderin

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16
Q

How is Iron transferred?

A

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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17
Q

Life cycle RBC
how many days?

A

100-120

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18
Q

What happens in the RBC cycle?

A

Cannot grow, divide and replicate (no nucleus)
-Get older and fragile and degenerate
-trapped/macrophage in spleen- RBC breakdown
-Iron- recycled & stored

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19
Q

Heme

A

Degraded to bilirubin, yellow pigment-Liver secretes bilirubin in bile (in intestine)-urobilinogen-stercoblin, brown pigment excreted in faeces

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20
Q

Globin

A

metabolised into aminoacids & recycled

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21
Q

RBC: What could go wrong?

A
  • Anaemia
  • Blood loss
  • RBC deficiency
  • Sickle cell anaemia
  • Thalassemia
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22
Q

Anaemia:

A

Sign of problem and risk
(Low Oxygen- Hypoxia- Growth, Development and Metabolism of several cells)

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23
Q

Symptoms of Anaemia

A

Fatigue, Pallor, Dyspnoea & chills

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24
Q

Blood Loss:

A

Haemorrhagic (acute, chronic): Blood loss, replace blood; treat cause

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25
Q

RBC deficiency:

A

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

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26
Q

Sickle cell anaemia (genetic cause):

A
  • 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
27
Q

Symptoms of sickle cell anaemia:

A

Very fatigue, lots of pain, challenged with work/exercise
(Predominantly in African ethnics)

28
Q

Thalassemia (genetic cause):

A
  • 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
29
Q

What is Polycythaemia?

A

Too many red blood cells in the blood

30
Q

Bone Marrow Cancer, People living in Highlands
- why is this?

A

Low O2 in high altitude

31
Q

Too thick too many cells increase the viscosity
- blood cannot move through the vessels efficiently which can lead to…

A
  • Stroke
  • Coronary artery disease
  • Renal disease
32
Q

Haemostasis is key process to stop…

A

bleeding (Clot)

33
Q

What are the three stops to blood clotting?

A
  1. Vascular spasm
  2. Platelet Activation - Plug
  3. Coagulation - Patch
34
Q
  1. Vascular spasm
A

pain reflux, constriction of vascular smooth muscle, trigger clotting chemicals/factors needed & directed to site of injury

35
Q
  1. Platelet Activation - Plug
A

Endothelial Damage
Exposed Collagen

Platelets stick to exposed collagen

Platelets stimulate ADP, Thromboxane A2 and Serotonin

Von Willebrand Factor- Stabilise collagen-platelet adhesion

36
Q
  1. Coagulation - Patch
A

Clotting factors/procoagulants in Liver
Vitamin K, the biosynthesis clotting factors
Plasma proteins I to XIII

37
Q

Fate of clot and vessel healing

A

a) Clot retraction concurrent with vessel repair

b) Fibrinolysis

38
Q

Clot retraction concurrent with vessel repair

A

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

39
Q

Fibrinolysis

A

Plasminogen, plasma protein trapped in clot- converted Plasmin-digest Fibrin

40
Q

Name Haemostasis disorders

A

Thromboembolism;
Unregulated Bleeding Disseminated Intravascular Coagulation (DIC)

41
Q

ADP, Thromboxane A2 and Serotonin are…

A

Clotting factors - they help to clot the injury site

42
Q

What is vitamin K’s role in clotting?

A

Needed to activate the clotting factors = blood will NOT clot otherwise

43
Q

Where is Vit K secreted

A

The small intenstine

44
Q

Pathological Blood Clot

A

> Thrombosis
Embolism

45
Q

Thrombosis =

A

Thrombosis-Blood clotting (Thrombus) in arteries, veins or capillaries

46
Q

Embolism =

A

Blood/ clot endogenous materials (Embolus) moving in the blood vessel and obstructing blood flow

47
Q

Arterial and Venous Thrombi are not the same

A

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.

48
Q

Same two bleeding disorders:

A

1) Liver dysfunction:
2) Haemophilia

49
Q

1) Liver dysfunction:

A

Clotting factors synthesis

Malnutrition of Vitamin

Hepatitis, Cirrhosis

Impaired Bile production- needed for fat and vit.K absorption

50
Q

2) Haemophilia:

A

Hereditary (Prolonged bleeding in joint cavities)

51
Q

CVS compensate the blood loss

A

> 15<30% loss: Fatigue and Pallor
30% loss: Lethal

52
Q

**3) Coagulation STEP by STEP

A

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)

53
Q

Does Coagulation happen internally or externally?

A

Both

54
Q

ABO - Blood grouping

A
55
Q

Antigen A

A

Antibody B
(IgM)

56
Q

Antigen B

A

Antibody A (IgM)

57
Q

Antigen AB

A

Antibody (None)

58
Q

Antigen (No)

A

Antibody A + Antibody B

59
Q

Why do people with blood group AB have no antibodies?

A

Antigen: Immune-responsive sensor of foreign biologicals
- RBC antigens are agglutinogens
- RBC antibodies are agglutinins

60
Q

With blood type O why do they have antibodies A and B

A

Antibodies are naturally occurring

Starts at 2 months of age and ends at 8-10 years of age

61
Q

Antigens AB

A

35 different blood grouping in human

ABO & Rh factors has the most severe transfusion reactions

62
Q

Blood Transfusion

A

Antibody for Rh are not spontaneous formation

For example: Rh- receive Rh+ blood or

63
Q

Rh- mother carrying Rh+ (First Pregnancy):

A

No problem but mother develop Rh antibodies 2nd pregnancy will stimulate health complications to baby

PMP-101 (53 decks)

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