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MBBS > 201 HI - Physiology > Flashcards

201 HI - Physiology Flashcards

1
Q

Hematocrit

A

Packed cell volume (PCV)
Volume occupied by RBCs after centrifugation of blood

Normal: ~45%

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2
Q

What is in the buffy coat of hematocrit?

A

Platelets & WBCs

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3
Q

Mean corpuscular (cell) volume (MCV)

A

Average volume of each RBC

MCV = PCV/RBC count × 10

Normal: 80-100 fL

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4
Q

Mean corpuscular (cell) haemoglobin (MCH)

A

Average amount of haemoglobin in each RBC

MCH = (haemoglobin conc)/(RBC count) × 10

Normal range: 28-32 pg

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5
Q

Mean corpuscular (cell) haemoglobin concentration (MCHC)

A

% of the RBC volume occupied by Hb

MCHC = (haemoglobin conc)/PCV × 100

Normal: 33-34%

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6
Q

Normal red cell distribution width (RDW)

A

11 - 15%

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7
Q

Anisocytosis

A

Increased RDW - high variation size

Seen in iron deficiency & B12 deficiency

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8
Q

Anaemia

A

Decrease in RBC count or Hb conc below lower limit of normal for a particular age or sex
- Decreases oxygen carrying capacity of blood

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9
Q

Etiological classification of anaemia

A

Nutritional - Iron deficiency, B12 or folic acid deficiency
Aplastic - Decreased production of bone marrow
Haemorrhagic - acute (trauma) & chronic (ulcers)
Haemolytic - sickle cell anaemia

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10
Q

Morphological classification of anaemia

A

Microcytic hypochromic

  • iron-deficiency anaemia
  • thalassemia
  • chronic blood loss
  • anemia of chronic disease

Normocytic normochromic

  • aplastic anemia
  • acute hemorrhage
  • chronic renal failure - lack erythropoietin

Macrocytic

  • B12 & folic acid deficiency
  • Alcoholism
  • Liver disease
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11
Q

What happens to blood flow during anemia?

A

Circulation becomes quicker - due to decrease viscosity in blood

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12
Q

Polycythemia

A

High RBC, high Hb conc

Primary - polycythemia vera
Secondary - hypoxia
Relative - dehydration

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13
Q

4 mechanisms of hemostasis

A
  1. Vasoconstriction
  2. Platelet plug formation
  3. Formation of blood clot
  4. Fibrosis – growth of fibrous tissue to seal the defect
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14
Q

Platelet plug formation (5)

A
  1. Platelets attach to exposed collagen – von Willebrand factor (vWF) on injured endothelium
  2. Platelet activation – swell up and throw multiple pseudopodia
  3. Release ADP & thromboxane A2
  4. More platelets aggregate → temporary plug
  5. Clotting → more permanent plug
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15
Q

Platelet adhesion

A

GP1b proteins on platelets attach to von Willebrand factor (vWF) in subendothelial collagen

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16
Q

Bernard Soulier syndrome

A

Absence of GP1b → platelets cannot stick to subendothelial collagen

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17
Q

Platelet activation

A

Platelet activated after binding to vWF → release ADP & thromboxane A2

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18
Q

Platelet aggregation

A

ADP & thromboxane A2 cause platelet to aggregate

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19
Q

Clopidogrel

platelet plug formation

A

blocks ADP receptor – prevents platelet aggregation

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20
Q

Aspirin

platelet plug formation

A

Inhibits cyclooxygenase enzyme that forms thromboxane A2 – prevents platelet aggregation

21
Q

Abciximab

platelet plug formation

A

Antagonist of GPIIb/IIIa - absence of platelet aggregation – Glanzmann’s thrombasthenia 血小板無力症

22
Q

GP1b

A

Binding between platelet & vWF

23
Q

GPIIb/IIIa

A

Binding between fibrinogen & platelet

24
Q

The final common pathway of clotting

A
  1. Prothrombin (II) → (by prothrombin activator) Thrombin (IIa)
  2. FIbrinogen (I) → (by thrombin) Fibrin (Ia)

II → I

25
Q

The extrinsic pathway of clotting

A
  1. TF released from injured tissue → activates VII
  2. VII activates X – along w calcium & tissue factor
  3. Xa + calcium, phospholids & Va → prothrombin activator
  4. → common pathway

VII → X

26
Q

The intrinsic pathway of clotting

A
  1. XII activated on contact with collagen
  2. XIIa activates XI
  3. XIa activates IX
  4. IXa + VIIIa + calcium & phospholipids → activate X
  5. → common pathway

XII → XI → IX → X

27
Q

Anticoagulant mechanisms of endothelial surface

A
  1. Smoothness of the endothelial cell surface - prevents contact activation of the intrinsic clotting system
  2. A layer of glycocalyx on the endothelium - repels clotting factors and platelets - preventing activation of clotting
  3. Normal endothelium produced NO & prostacyclin (PGI2) – prevents platelet adhesion & aggregation
  4. Thrombomodulin - binds thrombin
  5. Antithrombin III inactivates thrombin
28
Q

Clinically used plasminogen activators

A

Alteplase - tissue plasminogen activator – stroke

Streptokinase - MI

29
Q

Tranexemic acid

A

Prevent bleeding by inhibiting the fibrinolytic pathway

  • Inhibits plasminogen activation and thus prevents fibrinolysis
30
Q

What may cause bleeding disorders? (2)

A

Liver disease – cirrhosis, hepatitis etc can lead to decreased production of clotting factors

Vitamin K deficiency – vitamin K is needed for the addition of carboxyl group to glutamic acid of factors II, VII, IX and X in liver

31
Q

Haemophilia A

A

Factor VIII deficiency

- X linked recessive disease

32
Q

Haemophilia B

A

Factor IX deficiency

- X linked recessive disease

33
Q

Haemophilia C

A

Factor XI deficiency

- Autosomal recessive inheritance

34
Q

Features of Haemophilia

A

Bleeding w minor trauma – tooth extraction
Bleeding following surgery
Haemarthrosis 關節炎 – bleeding into joints

35
Q

Clot retraction

A

Compacts the clot and bring the torn edges together

- Due to actin, myosin, thrombosthenin of platelets

36
Q

Left side emboli vs right side emboli

A

Left side can block anywhere in blood

Right side only lung

37
Q

Which test tests for extrinsic + common pathway?

A

Prothrombin test (PT)

38
Q

Which test tests for intrinsic + common pathway?

A

Activated partial thromboplastin time (aPTT)

39
Q

Test of haemostasis - bleeding time

A

Time taken for standardized wound to stop bleeding

Normal: 1-6 min
Prolonged in platelet & vWF deficiency

40
Q

Test of haemostasis - clotting time

A
  1. Blood collected in capillary tube
  2. Time taken for clot formation assessed
    Normal: 1-6 min

Prolonged in clotting factor deficiency

41
Q

Test of haemostasis - Activated partial thromboplastin time (aPTT)

A
  1. Anticoagulated blood
  2. Excess calcium & phospholipid added → stimulate clotting
  3. Kaolin or silica then added to activate intrinsic pathway

Tests intrinsic & common pathway

42
Q

Test of haemostasis - Prothrombin time (PT)

A

Prothrombin time (PT)

  1. Blood collected with anticoagulant
  2. Excess calcium & TF added to activate extrinsic pathway
  3. Time for clotting noted

Normal value: 0.9 – 1.3

  • High – increased risk of bleeding
  • Low – increased risk for clot formation

Test extrinsic & common pathway

43
Q

Test of haemostasis - thrombin time

A

Used to estimate fibrinogen levels

  1. Anticoagulated blood
  2. Excess calcium & thrombin added
  3. Time taken to clot noted

Prolonged in afibrinogenemia

44
Q

Which condition has high MCHC?

A

Hereditary spherocytosis

遺傳性球囊病

45
Q

Bleeding time & clotting time are both prolonged in which disease?

A

vonWillebrand disease

46
Q

Why does hemolytic anemia cause splenomegaly?

A

Spleen is over-functioned, as it cannot remove the abnormal RBCs as quick as they are generated

47
Q

β thalassemias

A

β chain defect

Minor - ↑ HbA2 (α2δ2) - 1 β chain problem
Major - ↑ HbF (α2γ2) - 2 β chain problem

48
Q

α thalassemia

A

α chain defect

HbH disease - ↑ HbH (β4)

49
Q

3 things that cause vasoconstriction

A
  1. Myogenic – injury to sm of blood vessel
  2. Neurogenic – stimulation of pain fibres
  3. Chemicals – released from platelets (thromboxane A2 & serotonin) & endothelium (endothelin)

MBBS (28 decks)

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