Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

M1 > Brandon Ong's M1 Anki Deck__3. Physiology__A. Blood > Flashcards

Brandon Ong's M1 Anki Deck__3. Physiology__A. Blood Flashcards

1
Q

Where does erythropoiesis occur?

A

Fetus: yolk sac then liver/spleen/lymph nodes
Infant: all bone marrow
Adult: bone marrow of ribs, sternum, vertebrae, proximal ends of long bones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the steps and requirements of erythropoiesis?

A
  1. Proerythroblasts from haematopoietic stem cells
  2. Early erythroblasts: ribosome synthesis
  3. Late erythroblasts: Hb accumulation; ejection of nucleus
  4. Reticulocytes: complete Hb synthesis, leave bone marrow by diapedesis and mature in blood

Requires:
- Vitamin B9 (folic acid) & B12 (cobalamin)
- Iron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How is erythropoiesis regulated?

A
  1. Hypoxia
  2. Secretion of erythropoietin by kidneys and liver
  3. EPO stimulates haematopoietic stem cells to form proerythroblasts and increases proliferation rate of proerythroblasts and erythroblasts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Where does leukopoiesis occur?

A

Bone marrow
T-lymphocytes migrate to thymus where they mature
B-lymphocytes complete maturation in bone marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How is leukopoiesis regulated?

A

Cytokines
1. Interleukin-2: stimulate differentiation of myeloid stem cell
2. Granulocyte-Macrophage Colony Stimulating Factor (GM-CSF): stimulate differentiation of progenitor cells
3. Granulocyte Colony Stimulating Factor (G-CSF): stimulate differentiation of myeloblast
4. Macrophage Colony Stimulating Factor (M-CSF): stimulate differentiation of monoblast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What does haemostasis consist of?

A

Haemostasis = prevention of blood loss
1. Vasoconstriction
2. Platelet plug (Primary Haemostasis)
3. Blood clotting (Secondary Haemostasis)
4. Repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the measurements used for disorders of blood clotting?

A
  1. Prothrombin Time (PT): extrinsic pathway and common pathway
  2. activated Partial Thromboplastin Time (aPTT): intrinsic pathway and common pathway
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What causes Hemophilia A?

A

Factor VIII deficiency resulting in excessive bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What causes Hemophilia B?

A

Factor IX deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is thrombocytopenia?

A

Insufficient platelets with bone marrow destruction (spontaneous, widespread hemorrhage)
Associated w chemotherapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the thrombotic disorders of blood clotting?

A
  1. Factor V Leiden: mutated factor V cannot be deactivated (excessive thrombin formation)
  2. Activated Protein C (APC) resistance: poor anticoagulant response to activated protein C (normal protein C cannot result in anticoagulation)
  3. Deep vein thrombosis: immobility (post-op or air travel) and clot travels to pulmonary arteries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the mechanism of heparin?

A

Combines with anti-thrombin III to bind thrombin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the mechanism of coumarins eg. warfarin?

A
  • Vitamin K antagonist, prevent activation of factors II,VII,IX,X and protein C & S
  • Requires rundown of Vitamin K stores first (pregnancy is contraindication)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the characteristics of von Willebrand’s Factor (vWF)?

A
  1. Bound to Factor VIII while FVIII is inactive in circulation to increase its half-life; only released by the action of thrombin
  2. Binds to collagen beneath endothelial cells when it is exposed due to damage of blood vessel (endothelium also releases vWF which forms additional links between platelets’ gpIb/IX/V and collagen fibrils)
  3. Mediates platelet adhesion in face of high shear stress
  4. Produced and stored in alpha granules of platelets
  5. Cleaved by a metalloprotease (ADAMTS13)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the primary haemostasis mechanism (platelet plug)?

A
  1. Platelet adhesion: gpIa/IIa, gpVI&raquo_space; collagen
  2. Platelet adhesion under shear stress: vWF & gpIb/V/IX&raquo_space; collagen
  3. Platelet aggregation: gpIIb/IIIa, fibrinogen
  4. Alpha granules release: factor V, factor IX, vWF, fibrinogen, platelet derived growth factor, vascular endothelial growth factor
  5. Dense granules release: ADP (increase platelet stickiness), histamine, serotonin
  6. Link to coagulation: thrombin
  7. Thromboxane A2 released: aids in platelet aggregation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the secondary haemostasis mechanism (blood clotting)?

A

<img></img>

17
Q

What is the importance of post-translational modification by vitamin K?

A
  • Vitamin K dependent gla residues that are inhibited by warfarin
  • Required for Factors II, VII, IX, X
  • Required for Protein C and S
18
Q

What is anti-thrombin III activity?

A
  • Inhibits serine protease activity
  • Inhibits thrombin, Factor 9a, 10a, 11a, 12a
  • Potentiated by heparin
19
Q

What is the Protein C anticoagulant pathway?

A

Thrombin binds to thrombomodulin which activates Protein C with cofactor Protein S
Activated Protein C inactivates Factor 5a and 8a (which is required for coagulation pathway)

20
Q

What is the fibrinolytic pathway?

A
  1. Endothelial cells express thrombomodulin which binds to thrombin to activate protein C (stops coagulation cascade)
  2. Injured tissues slowly release tissue-plasminogen activator (t-PA) that converts plasminogen to plasmin to convert fibrin to fibrin degradation products
  3. Small quantities of heparin continually secreted by mast cells and basophils which bind to anti-thrombin III to remove thrombin
21
Q

What is the Direct Coombs Test used for?

A

Detects and shows the effect of antibodies causing RBC destruction i.e. autoimmune hemolytic anaemia

22
Q

What is the purpose of mixing studies?

A
  • Performed on blood plasma of patients or test subjects to distinguish factor deficiencies from factor inhibitors, such as lupus anticoagulant, or specific factor inhibitors, such as antibodies directed against factor VIII
  • If factor inhibitors, the timing for mixing studies will increase
23
Q

What does Thrombin Clotting Time test for?

A

Fibrinogen abnormalities; common pathway

24
Q

What does bleeding time test for?

A

Tests for platelet function and number (duration of time for clot to form)

25
Q

What is the tourniquet test for?

A

Capillary fragility (thrombocytopenia) i.e. common result of chemotherapy

26
Q

What are some of the main genetic bleeding disorders?

A
  • Haemophilia A (Factor 8 deficiency)
  • Haemophilia B (Factor 9 deficiency)
  • vWF deficiency (most common)
  • Platelet disorders
  • Factor V Leiden
27
Q

What are the different types of anaemia and their causes?

A

Microcytic (small mean corpuscular volume): Fe deficiency
Normocytic (normal RBC, just low numbers): acute hemorrhage, chronic renal failure
Macrocytic: vitamin B9 (folate) and/or B12 (cobalamin) deficiency
Haemolytic (changed shape/structure of RBC causing it to be more easily destroyed): sickle cell anaemia, beta-thalassemia, malaria, G6PD deficiency

28
Q

What is the significance of high D-dimer levels?

A
  • Clot has formed (released after clot has been broken down).
  • Factor 13 causes cross-linking of D-dimers in fibrin mesh
  • Breakdown of clots will increase D-dimer levels in blood
29
Q

What are the relevant anticoagulant drugs that could be given to a patient with pulmonary embolism?

A

Drugs that dissolve clot: streptokinase (more effective than urokinase), tissue-plasminogen activator
Drugs that prevent further clots from forming: heparin (immediate) and warfarin (long-term)

30
Q

What is the difference between plasma and serum?

A

Serum is plasma after the removal of coagulation factors

31
Q

What is cross matching?

A
  1. Mixing of donor’s RBC with recipient’s serum
  2. Check for agglutination of antigens from donor’s RBC and antibodies from recipient’s serum
    - Minimises danger of transfusion reaction
32
Q

What are the characteristics of an acute (1 day) vs delayed (7+ days) transfusion reaction?

A

Acute reaction: pre-formed major antibodies reacting with major antigens
Delayed reaction: memory B cells produced antibodies for minor antigens

33
Q

What is the most common heme synthesis genetic defect?

A

Porphyria cutanea tarda

34
Q

What are the types of blood cells?

A
  • Erythrocytes: RBCs
  • Reticulocytes: young RBCs
  • Leukocytes: WBCs
  • Granulocytes: neutrophils, basophils, eosinophils
  • Myelocytes: young granulocytes
  • Monocytes: give rise to macrophages
  • Lymphocytes: T cells, B cells, NK cells
35
Q

What is the composition of the body by weight?

A
  • 40%: solid
  • 60%: water
  • 40%: ICF
  • 20%: ECF
  • 15%: interstitial fluid
  • 5%: plasma

M1 (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions