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pr3154 ca1 > IC2: Physiology > Flashcards

IC2: Physiology Flashcards

1
Q

What is the pH of blood?

A

7.35-7.45

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2
Q

What are the 3 main functions of blood?

A

Transportation, regulation, protection

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3
Q

What does hematocrit refer to?

A

Relative volume of red blood cells out of the total blood volume

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4
Q

What does each hemoglobin molecule contain?

A

Heme (pigment) containing 1 iron
Globin (4 protein chains)

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4
Q

What does each hemoglobin molecule contain?

A

Heme (pigment) containing 1 iron
Globin (4 protein chains)

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5
Q

Describe the different ages and the respective locations of erythropoiesis

A

Fetus → yolk sac then liver, spleen and lymph nodes

<5yo → all bone marrow (mostly big bones)

5-20yo → bone marrow in ribs, sternum, vertebrae and proximal ends of long bones

> 20 yo → bone marrow in ribs, sternum and vertebrae

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6
Q

Explain the negative feedback loop in erythropoiesis

A

If oxygen delivery to the kidneys is decreased, the cells in the kidneys produce more EPO, increasing the rate of erythropoiesis

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7
Q

In what cases will the kidneys stimulate EPO release? (6)

A
  1. hypoxia due to decreased RBC number or function
  2. decreased O2 availability
  3. increased tissue demand for O2
  4. anemia,
  5. reduced blood flow to kidneys
  6. blood donation
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8
Q

What are the 3 phases of progression of proerythroblasts into erythroblasts

A

Phase 1 → ribosome synthesis in early erythroblasts

Phase 2 → Hb accumulation in late erythroblasts and normoblasts

Phase 3 → ejection of the nucleus from normoblasts and formation of reticulocytes

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9
Q

Where are red blood cells destroyed? (2)

A
  • Tiny vessels of the spleen
  • Macrophages
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10
Q

How are the components of RBCs recycled? (3)

A

Iron - recycled in bone marrow or stored in liver
Globin - metabolised into AA and released into circulation
Heme - degraded into bilirubin, excreted via liver

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11
Q

What does polycythemia refer to?

A

Excess in circulating erythrocytes

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12
Q

Describe primary and secondary polycythemia

A

Primary polycythemia is caused by a tumour or tumour-like condition in the bone marrow

Secondary polycythemia is an EPO-induced adaptive mechanism to improve O2-carrying capacity of blood, for example for people living in high altitudes

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13
Q

What are the 3 phases of hemostasis?

A

Vasoconstriction (immediate)
Platelet plug (within seconds)
Fibrin clot (within minutes)

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14
Q

How is vasoconstriction initiated and mediated

A

initiated by the sympathetic nerves, mediated by vascular smooth muscle cells

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15
Q

What happens to endothelial cells during vasoconstriction? (2)

A

Endothelial cells of opposite sides may stick together to reduce blood loss

Endothelial cells contract and expose the basal lamina

16
Q

Outline the processes that occur during the platelet phase

A

Endothelial wall dmg exposes collagen
Platelets stick and secrete vWF
Positive feedback causes more platelets to stick

17
Q

What molecules do platelets contain and what are their functions? (3)

A

Enzymes (PG and TXA synthesis)
Growth factors (PDGF and VEGF)
Factor XIII (fibrin stabilising factor)

18
Q

Explain how vWF leads to platelet aggregation?

A
  • vWF binds to platelets and exposed collagen via glycoprotein receptors
  • Adhesion activates morphological change in platelets
  • Platelets release granules containing platelet agonists (more platelet aggregation)
19
Q

Explain how the extrinsic pathway works (2)

A

Damaged tissues release tissue factor, that activates VII to VIIa, which activates X to Xa
(7 to 10)

20
Q

Explain how the intrinsic pathway works (4)

A

Exposure to collagen fibres or exposure to foreign surfaces (eg. glass) causes a conformational change that actives XII to XIIa

This then activates XI to IX to X
(12 to 11 to 9 to 10)

21
Q

Explain how the intrinsic and extrinsic pathways combine to induce clot formation (4)

A

X is activated to Xa (in the presence of Ca2+ ions and factor Va)

This activates prothrombin (II) to thrombin (IIa)

Thrombin cleaves fibrinogen (I) to fibrin (Ia) monomers that aggregate to form fibrin strands

Thrombin (IIa) also activates factor XIIIa which forms cross-links between fibrin strands to form a fibrin mesh

21
Q

Explain how the intrinsic and extrinsic pathways combine to induce clot formation (4)

A

X is activated to Xa (in the presence of Ca2+ ions and factor Va)

This activates prothrombin (II) to thrombin (IIa)

Thrombin cleaves fibrinogen (I) to fibrin (Ia) monomers that aggregate to form fibrin strands

Thrombin (IIa) also activates factor XIIIa which forms cross-links between fibrin strands to form a fibrin mesh

22
Q

List the 3 functions of thrombin

A
  1. Cleaves fibrinogen to fibrin
  2. Activates factor XIII for fibrin mesh stabilisation
  3. Causes platelets to release PF3 (activates intrinsic pathway)
23
Q

How does clot repair occur? (2)

A

PDGF stimulates vascular SM to build new vessel walls
VEGF stimulates endothelial cell multiplication and restores the inner endothelial lining

24
Q

Explain the two mechanisms of regulation of blood clotting

A

Prostacyclin inhibits platelet activation and limits clot spreads

Blood clots limit the spread of thrombin and other procoagulants to other locations (localises it at site of injury)

25
Q

Explain the process of fibrinolysis

A

Surrounding tissue and vascular endothelial cells slowly release tissue plasminogen activator (tPA) which cleaves inactive plasminogen to protease plasmin

Plasmin then digests fibrin and dissolves the clot

Macrophages remove the remains of the clot

26
Q

What is hemophilia

A

Excessive bleeding after an injury

27
Q

What are the three types of hemophilia and what factor deficiencies cause them?

A
  • Hemophilia A is caused by deficiency of factor VIII
  • Hemophilia B is caused by deficiency of factor IX
  • Hemophilia C is caused by deficiency of factor XI

(A8, B9, C11)

28
Q

Which 4 factors require vitamin K for production?

A

Factors II, VII, IX and XI

29
Q

Which 5 factors does Prothrombin Time (PT) assess and which pathway?

A

Factors I, II, V, VII and X (VII most important)
Extrinsic pathway

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