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ZOOL463 > Hematology > Flashcards

Hematology Flashcards

1
Q

What divisions do our fluid compartments have?

A

Intracellular and extracellular and within extracellular there is interstitial fluid, plasma, and some other small compartments

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2
Q

What is interstitial fluid?

A

Fluid occupying the space between cells with the same constituents as plasma EXCEPT for large proteins which are present at a lower concentration

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3
Q

Where does interstitial fluid come from?

A

It’s derived from capillary filtration

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4
Q

What maintains membrane potential?

A

Sodium ATPase (3 Na out 2 K in)

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5
Q

What are the total osmotic pressures of the three important fluid types to each other?

A

Interstitial fluid is hypoosmotic to plasma and interstitial fluid is isosmotic to intracellular fluid

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6
Q

What type of cells have blood capillaries with the greatest permeability? How about the least?

A

Hepatocytes and brain cells.

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7
Q

How do cells that are not small enough to pass through even pores in the capillaries with increased permeability pass through?

A

Through intercellular clefts

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8
Q

How does the molecular weight of a substance relate to its permeability?

A

The larger a substance is the lower its permeability is.

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9
Q

What is colloid osmotic pressure/oncotic pressure?

A

Osmotic pressure caused by the presence of proteins

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10
Q

What is the effect of an increase of oncotic pressure on water movement?

A

It increases water movement, but notably protein concentration increases rarely happen so this does not often happen.

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11
Q

What three major proteins are in the plasma that contribute to colloid osmotic pressure?

A

Albumin, globulin, fibrinogen. Other proteins vital but not related to oncotic pressure.

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12
Q

What are the role of albumins?

A

They are the most abundant plasma proteins and act as nonspecific carrier proteins to prolong half-lives by binding loosely and protecting from enzymes. They also contribute to oncotic pressure.

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13
Q

What are the role of globulins?

A

Proteins with specificity like specific carrier proteins, enzymes, and immunoglobulins

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14
Q

What are the role of fibrinogens?

A

Blood clotting! It polymerizes into long fibrin threads.

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15
Q

What are the Starling forces?

A

Forces that affect fluid movement in and out of capillaries. Outward pressure is capillary pressure + outward pressure, and inward pressure is interstitial fluid pressure and plasma colloid osmotic pressure.

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16
Q

What is the net movement of fluid in the capillaries?

A

0.3 mmHg towards the Interstitial compartment

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17
Q

What is the order of key plasma protein contribution to Starling forces?

A

Albumin, globulins, fibrinogen

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18
Q

What does the interstitial compartment contain?

A

Collagen fibres for structure and proteoglycan (hyaluronic acid and protein) filaments to create a semi permeable gel when trapping interstitial fluid. Also a very small amount of free flowing fluid

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19
Q

How does movement of solutes occur in the interstitial compartment?

A

Molecular diffusion slightly slower than in fluid.

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20
Q

What is edema? What are the two main causes?

A

An edema is an increase in the pocket of free fluid in the interstitial compartment which can be caused by an increase in oncotic pressure. Proteins can flux due to a disruption in protein concentration across a membrane and blocked lymph fluid accumulation.

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21
Q

What does the presence of proteoglycans, collagen fibres, and gel formation in the interstitial compartment ensure?

A

Uniform fluid distribution in the body, maintenance of optimal intracellular distance for diffusion, and mechanical support (adhesion proteins)

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22
Q

How does flow from the capillaries into the lymph system work?

A

Most blood flows directly back to the heart but due to Starling forces some gets pushed into the lymph system, a one-way series of valves. It transports fluids and macromolecules and is a function of interstitial fluid pressure, with increased pressure increasing flow.

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23
Q

What is the role of lymph nodes?

A

They filter lymph and contain phagocytic cells which remove foreign blood contaminants and cancer cells before draining into the veins. This is why infection causes swollen lymph nodes.

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24
Q

What disease causes edema?

A

Elephantiasis caused by worms. Block lymphatic flow.

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25
Q

What are the important small fluid compartments and what do they do?

A

Cerebrospinal fluid: cushioning
Intraocular fluid: eyeball pressure
Fluid compartment of GI tract: space
Fluids compartment of lung: lubrication for slippage of lung
Fluids compartment of pericardial cavity, peritoneal cavity, joint spaces, bone and cartilage etc: lubrication

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26
Q

What is haemopoiesis?

A

The production of blood cells

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27
Q

Fill in the blanks: Pluripotent stem cells can differentiate into two types of cells, _ stem cells and _ stem cells. The former can further differentiate into _, _, and _, while the later can further differentiate into _, _, _, _, _, and _.

A

Lymphoid, myeloid, NK cells, B lymphocytes, T lymphocytes, erythrocytes, platelets, monocytes, neutrophils, eosinophils, basophils.

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28
Q

Where are myeloid stem cells located?

A

Bone marrow

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29
Q

The derivatives of the lymphoid system can be grouped as?

A

lymphocytes

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30
Q

What controls the production of blood cells?

A

Cytokines which control the proliferation and differentiation of blood cells. They are committed progenitor cells past the myeloid/lymphoid state.

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31
Q

What increases the production of all hemopoietic stem cells?

A

Interleukins/stem cell factor

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32
Q

What are some specific differentiation factors?

A

Erythropoietin, thrombopoietin (megakaryocytes), granulocytes-monocytes colony stimulating factors

33
Q

What are the three major groups of blood cells?

A

Erythrocytes, Megakaryocytes/platelets, Leukocytes

34
Q

Which blood cell group has further derivatives and what are they all called? Bonus: are they myeloid or lymphoid derived

A

Neutrophils, Eosinophils, Basophils, Monocytes (myeloid)
Plasma cells and B cells, T lymphocytes, NK cells (lymphoid)

35
Q

What are some characteristics of red blood cells?

A

Unnucleated when mature, biconcave disk (to bend to fit through capillaries), the largest population of blood cells

36
Q

What is hematocrit?

A

A measure of the proportion of volume occupied by erythrocytes. Centrifugation determined.

37
Q

What are the main functions of erythrocytes?

A

Transport hemoglobin (important O2 carrier and acid base buffer (proton donor and acceptor)), has carbonic anhydrase which makes bicarbonate, a CO2 carrier.

38
Q

What bones produce erythrocytes and which ones lose this ability with age?

A

The tibia and femur do early in life but the erythropoietic tissue gets replaced by fat at around 17 and 25 respectively. Vertebrae, sternum, and ribs produce it throughout life.

39
Q

Describe the production of erythrocytes from start to finish.

A

Pluripotential hemopoietic stem cells differentiate into myeloid stem cells which become proerythroblasts which are mitotic which mature into basophil erythroblasts which are mitotic and have Hb which mature into polychromatophil erythroblasts which are mitotic with lots of Hb which mature into orthochromatic erythroblasts with are NOT mitotic and have more Hb with mature into reticulocytes which lack a nucleus and move to the blood whcih mature into erythrocytes with no organelles.

Summary: PHSC -> Myeloid stem cells -> proerythroblasts -> basophil erythroblasts -> polychromatophil erythroblasts -> orthochromatic erythroblasts -> reticulocyte -> erythrocyte

Even more summarized: PHSC -> myeloid -> pro -> basophil -> polychrom -> orthochrom -> reticulocyte -> erythrocyte

40
Q

Describe the synthesis of hemoglobin.

A

In mitochondria, succinyl-CoA -> pyrrole
4 pyrroles ->protoporphyrin
protoporphyrin + iron -> heme
heme + globin -> Hb

Hb has 4 subunits, either alpha, beta, gamma, or delta. 2 alpha 2 beta most common in adult human

41
Q

What is the difference between fetal and adult human hemoglobin and why?

A

Adult human hemoglobin has two alpha and two beta subchains, baby has two alpha two gamma. Baby has greater affinity for O2 and is present in higher concentrations.

42
Q

How many oxygen can a functional hemoglobin bind to?

A

4 oxygen, one for each iron (in heme)

43
Q

Why is carbon monoxide poisoning so bad?

A

It competes for heme binding sites and binds irreversibly, unlike oxygen which binds reversibly

44
Q

What is the affinity of hemoglobin for CO2?

A

Higher when not bound to oxygen, lower when bound to oxygen.

45
Q

What does sickle cell anemia do?

A

The blood cells crystallize at hypoxic conditions and rupture at junctions

46
Q

What affects RBC production?

A

Erythropoietin: differentiation factor, glycoprotein in kidney. Triggered by low O2. Stimulates production of proerythroblasts and RBCs

Vitamin B12/B9 (folic acid): a lack of either results in reduced DNA synthesis, cells can’t divide and get bigger and bigger and rupture. Megaloblastic anemia.

Iron metabolism: Most in hemoglobin, some stored as ferritin in liver. Iron binds to transferrin, this complex binds on erythroblasts in bone marrow and increases iron delivery to mitochondria to synthesize heme. Abnormalities in transferrin cause anemia. Saturation of transferrin limits iron absorption from intestine. Transferrin -> bile -> gut -> increased iron transport

47
Q

What happens to damaged RBC?

A

Phagocytosis by macrophages. Iron binds to transferrin for hemoglobin synth and to ferritin Porphyrin to bilirubin released into blood and bile and excreted by bile into gut.

48
Q

What can increased levels of bilirubin lead to?

A

Jaundice

49
Q

What are platelets?

A

Fragments of megakaryocytes lacking a nucleus from the bone marrow. Have other organelles, live 8-12 days, have membrane receptors.

50
Q

What do platelets do?

A

Mainly recognize damaged tissue/collagen fibres in the extracellular space, important for blood coagulation.

51
Q

How do platelets work?

A

They have a surface glycoprotein, recognizes collagen and damaged endothelial tissue.

52
Q

What do platelets contain?

A

Actin, myosin, thrombosthenin: cause contraction + expansion of platelets
Residuals of ER and golgi: can make some enzymes + store calcium
Mitochondria and enzymes: ATP and ADP synth
Enzyme system: Produce eicosanoids (thromboxane A2)
Platelet cytoplasm also contains fibrin-stabilizizng factor, a growth factor, and other growth factors for injury damaged tissue growth to maintain blood clots

53
Q

What are the steps of haemostasis?

A

Vascular spasm and constriction, formation of platelet plug, blood coagulation, growth of tissue to repair injury

54
Q

How does haemostasis work with microtraumas?

A

Only the first step, vascular spasm and constriction, occurs. Very limited.

55
Q

What causes vascular constriction?

A

A cut or rupture of a blood vessel due to local myogenic spasm (stim by thromboxane A2 from platelets) and nervous reflex from pain receptors

56
Q

What activates platelets?

A

Contact with damaged vascular epithelium or collagen

57
Q

What does platelet activation cause

A

Release of ADP as a messenger, the conversion of phospholipids to arachidonic acid to COX-II to Thromboxane A2 which is important for clotting. Thromboxane A2 and ADP activate other platelet cells.

58
Q

What is thrombosis?

A

Too much clotting

59
Q

What does aspirin and other anti inflammatories do?

A

Inhibit COX-11

60
Q

Describe the production pathway of Thromboxane A2

A

Phospholipid -> arachidonic acid -> COX-II -> Thromboxane A2, prostaglandins and prostocycline
Arachidonic acid also produces lipoxygease -> leukotriene which are also eicosanoids

61
Q

Describe the clotting process.

A
  1. Platelet contact with collagen or damaged endothelial tissue activates membrane receptors
  2. ADP and Thromboxane A2
  3. ADP causes swelling, acts on neighboring platelet cells and causes adhesion (also have ADP binding sites)
  4. Thromboxane A2 activates other platelet cells, forms plug
  5. Activated platelets produce fibrin-stabilizing factor for fibrin meshwork and clotting
62
Q

What does blood vessel trauma cause?

A

The activation of extrinsic and intrinsic pathways which leads to activation of thrombin and blood coagulation

63
Q

What does the conversion of prothrombin to thrombin require?

A

Calcium

64
Q

Describe the synthesis of fibrin threads in blood coagulation.

A

Blood vessel trauma -> extrin + intrin pathways -> release of tissue prothrombin activator

Prothrombin -> thrombin which catalyzes and allows fibrinogen -> fibrin monomers and thrombin activates FSF which allows polymerization of fibrin monomers into a fibrin mesh.

65
Q

How do platelets contribute to forming the fibrin mesh?

A

They reinforce crosslinking and release calcium and fibrin holds the platelets together and adheres to the blood vessel to form the clot and prevent further blood loss.

66
Q

How is thrombin produced?

A

Its a proteolytic product of prothrombin in the liver due to action of Vitamin K. Prothrombin activator cleaves prothrombin into thrombin.

67
Q

Name the two important factors in blood coagulation.

A

Factor III/Tissue Thromboplastin
Factor XII/Hageman Factor

68
Q

What does Tissue thromboplastin/factor III do in blood coagulation?

A

Initiates the extrinsic pathway after being released from tissue following trauma.

69
Q

What does HF/factor XII do in blood coagulation?

A

Initiates intrinsic pathway following blood trauma, it contacts platelets and collagen or a wettable surface which results in a configuration change and activation which activates other factors leading to clotting

70
Q

What do both the extrinsic and intrinsic coagulation pathway lead to?

A

The cleavage of prothrombin to thrombin and the formation of fibrin mesh.

71
Q

Which is the slower of the extrinsic and intrinsic pathways?

A

Intrinsic. It’s also longer. Extrinsic is faster and stronger, it directly activates factor X, thus skipping steps.

72
Q

Where do both the extrinsic and intrinsic pathway converge?

A

At factor X, called the stuart factor.

73
Q

Name the steps of the intrinsic pathway

A

Damaged vessel surface/foreign surface -> activates Factor XII/HF -> activates factor XI/PTA and with calcium (factor IV) -> activates factor IX/PTC and with calcium (factor IV) and factor VIII/antihemophilic factor and PF3-> activates factor X which with calcium and factor V/proaccelerin and PF3-> triggers prothrombin cleavage into thrombin which activates factor XIII/FSF and converts fibrinogen into fibrin monomers and the latter leads to a loose meshwork of fibrin which is stabilized by the former leading to a CLOT.

74
Q

Name the steps of the extrinsic pathway.

A

Tissue damage releases tissue thromboplastin/factor III which with calcium and factor VII/SPCA activates factor X which with calcium and factor V/proaccelerin and PF3-> triggers prothrombin cleavage into thrombin which activates factor XIII/FSF and converts fibrinogen into fibrin monomers and the latter leads to a loose meshwork of fibrin which is stabilized by the former leading to a CLOT.

75
Q

What does the absence of factor VIII/antihemophilic factor cause?

A

Hemophilia A, x-linked recessive

76
Q

What are some anticoagulants in the blood?

A
  1. Glycocalyx: a mucopolysaccharide absorbed to inner surface of endothelium of cells which makes it smooth and repels clotting factors and platelets
  2. Thrombomodulin: a membrane protein on the surface of endothelial cells, it binds with thrombin and prevents coagulation
  3. Heparin: activates other factors that remove thrombin and increased antithrombin-III activity
77
Q

What causes clot dissolution?

A

A cycle between clot formation and dissolution. Hageman factor/Factor XII activated both clot formation and plasmin activation quickly, and plasmin/fibrinolysin breaks down fibrin threads in the clot slowly.

78
Q

What are the phases of clotting?

A
  1. Vascular phase
  2. Platelet phase
  3. Coagulation phase
  4. Clot retraction
  5. Clot destruction
  6. Growth factors heal tissue site

ZOOL463 (7 decks)

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