6.0 Vascular Disease Flashcards

Question 1

Q

Define anaemia:

Answer

A

↓ RBC number (usually measured as ↓ Hb conc. in blood) ↓ oxygen capacity of the blood

Question 2

Q

What is the lifespan of RBCs?

Question 3

Q

Structure of haemoglobin:

Answer

A

Tetramer 2 pairs of polypeptides (each with haem group)

Question 4

Q

What Hb chains are present in fetal Hb?

Question 5

Q

What Hb chains are present in adult Hb (major form)?

Question 6

Q

What Hb chains are present in adult Hb (minor form)?

Question 7

Q

Clinical consequences of anaemia:

Answer

A

1) Ectodermal changes - Thin skin + nails - Pale mucosa 2) Hypoxic damage in viscera - Angina, malaise, fatigue, dim vision, faintness 3) Compensatory changes - ↑ HR + CO - ↑ Breathing rate - Hyperplasia of haemopoietic tissue in bone marrow

Question 8

Q

Why do the cells increase in size in megaloblastic anaemia?

Answer

A

Cause of this anaemia is impaired DNA synthesis This means the cell does not divide but RNA and protein synthesis continue → ↑ size

Question 9

Q

What changes are seen in megaloblastic anaemia?

Answer

A

1. Ineffective haemopoiesis - ↓ RBC, granulocytes and platelets (pancytopenia) 2. Expansion of haemopoietic tissue 3. RBC precursors enlarged (megaloblasts) - May appear in the blood 4. RBC enlarged (macrocytosis) and oval shaped 5. RBC different sizes (anisocytosis) and shapes (poikilocytosis) 6. Iron cannot be utilised normally - Deposited in various organs 7. Effects in other cells and tissues - Neutrophils and megakaryocytes large with hypersegmented nuclei - Enlarged nuclei in gut epithelial cells - etc

Question 10

Q

How long does B12 stay stored in liver for?

Question 11

Q

What two deficiencies cause megaloblastic anaemia?

Answer

A

1) Vit B12 deficiency 2) Folate deficiency

Question 12

Q

What does iron deficiency anaemia cause a defect in?

Answer

A

Haem synthesis

Question 13

Q

What does thalassaemia cause a defect in?

Answer

A

Globin synthesis

Question 14

Q

2 types of haemolytic anaemia:

Answer

A

1) Extravascular (removed by macrophages, mainly in spleen) 2) Intravascular

Question 15

Q

What abnormalities cause haemolytic anaemia?

Answer

A

1) Intrinsic to RBCs (hereditary) - Structural defects (hereditary spherocytosis) - Enzyme defects (pyruvate kinase ↓) - Haemoglobinopathies 2) Extrinsic to RBCs (acquired) - Immune (Haemolysis Dx of newborn) - Physical (valve replacement) - Chemical (lead poisoning) - Infection (malaria)

Question 16

Q

What is the amino acid switch in sickle cell disease?

Answer

A

HbS (α2β2 6 glu ⟶ val)

Question 17

Q

Two types of thalassaemia?

Answer

A

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Question 18

Q

What are platelets formed from?

Answer

A

Megakaryocytes

Question 19

Q

Life span of platelets?

Question 20

Q

What do platelets use to adhere to collagen?

Question 21

Q

What do platelets secrete once activated?

Answer

A

1) Thromboxane A2 2) Vasoactive amines (5-HT) 3) ADP These cause vasoconstriction and platelet aggregation

Question 22

Q

What molecules mediate primary haemostats plug?

Answer

A

1) Integrins (α₁₁bβ₃) 2) Junctional adhesion molecules (JAMs) 3) Endothelial cell-specific adhesion molecules (ESAM) 4) Eph + Ephrin families

Question 23

Q

What factors on normal endothelial cells inhibit haemostasis?

Answer

A

1) NO (↓ platelet activation) 2) PGI2 (prostacyclin) (↓ platelet activation) 3) Antithrombin (on cell surface. Binds to thrombin and inactivates it. Complex is then cleared by liver) 4) Tissue factor pathway inhibitor (TFPI) (blocks factor X) 5) Thrombomodulin (conformational change to thrombin → ↓ fibrin activation and ↑ protein C activation) 6) Protein C (↓ factor V + VIII) 7) Protein S (cofactor for protein C)

Question 24

Q

What are Virchow’s triad?

Answer

A

1) Changes in vessel wall 2) Changes in blood flow 3) Changes in blood constituents

Question 25

Q

Structure of thrombi in arteries/cardiac chambers:

Answer

A

Compact Granular Firm Lines of Zahn

Question 26

Q

Structure of thrombi in veins:

Answer

A

Pale head (fibrin + platelets) Long red tail (enmeshed RBCs)

Question 27

Q

Three layers of vessel?

Answer

A

Tunica intima Tunica media Tunica adventitia

Question 28

Q

Define atherosclerosis:

Answer

A

Disease of intima of large and medium sized arteries Lesions = focal thickenings of intima (plaques) These are deposits of fibrous tissues and lipids

Question 29

Q

Arteriosclerosis

Answer

A

Loss of elasticity and physical hardening of the arterial wall from any cause Often accompanied by calcification of the wall ≠ atheroscleosis

Question 30

Q

Do deficiencies in the following components of lipoprotein pathways cause and increase or decrease in atherosclerotic lesions? 1) apoE 2) LDL receptor 3) SR-A 4) CD36 5) Acyl-cholesterol acyl transferase (ACAT)

Answer

A

1) apoE → ↑ 2) LDL receptor → ↑ 3) SR-A (scavenger protein) → ↓ 4) CD36 (scavenger protein) → ↓ 5) Acyl-cholesterol acyl transferase (ACAT) → ↓

Question 31

Q

What are key changes in the vessel wall that cause atherosclerosis?

Answer

A

Endothelial cell injury/dysfunction 2. Monocyte migration into the plaque and maturation into macrophages 3. Smooth muscle cell activation 4. Lipoprotein infiltration 5. T-lymphocyte migration into the plaque 6. Platelet adherence

Question 32

Q

Where do pale infarcts occur?

Answer

A

Solid tissues (heart, kidney, spleen)

Question 33

Q

Where do red infarcts occur?

Answer

A

1) Arterial occlusion Spongy tissues (lung) Tissues with collateral blood supply (gut) 2) Venous occlusion

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6.0 Vascular Disease Flashcards

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