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54 > 2. Physiology > Flashcards

2. Physiology Flashcards

1
Q

Function of blood

A
  • Transportation: respiratory gases O2 and CO2, nutrients & waste, hormones
  • Regulation: body temperature (redistribute heat - blood is warmer (38 degrees) than body temperature for maintenance), pH and ion composition of interstitial fluids
  • Protection: against blood loss (blood clotting), infections (WBCs)
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2
Q

Composition of blood (4 parts)

A
  • Plasma: water, protein (albumin, globulin, fibrinogen), solutes, fibrinogen
  • serum: no fibrinogen
  • Leukocytes/WBC/buffy coat
  • Platelets (broken pieces of megakarocytes)
  • RBC/erythrocytes
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3
Q

what is hematocrit, what happen when hematocrit is low or high

A
  • Hematocrit = % of RBC in whole blood
  • low levels = anemia
  • high levels = polycythemia
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4
Q

which blood cell is complete

A
  • only WBC are complete cells
  • RBC does not have nuclei or organelles and platelets are just cell fragments
  • most blood cells do not divide but are renewed by cells in bone marrow
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5
Q

function of RBC

A
  • respiratory gas transport- contain hemogloblin to transport O2
  • contain carbonic anhydrase to transport CO2- buffer pH in blood
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6
Q

what does RBC contains

A

globin and heme

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7
Q

what is globin and heme

A
  • Globin: 4 folded polypeptide chains 2α and 2ß Hb chains, each chain bind to 1 heme grp
  • Heme: not a protein but a pigment. Each heme grp contains 1 iron (Fe) that binds to 1 O2 molecule each (binding is weak and reversible)
  • each Hb molecule can transport 4 molecules of O2
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8
Q

how does the body transport O2?

A

Most O2 in blood is transported by Hb, a small amount can be transported by water of blood

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9
Q

where does erythropoiesis occur? (for different ages)

A
  • <5 years: all bone marrow
  • 5-20 years: bone marrow in ribs, sternum, vertebrae, proximal ends of long bones
  • > 20 years: bone marrow in ribs, sternum, vertebrae
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10
Q

how is RBC production regulated

A

tissue oxygenation and erythropoietin (hormone that stimulate erythropoiesis)

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11
Q

6 triggers that cause erythropoietin release from kidneys

A
  • hypoxia (due to decreased RBC number/function)
  • decreased oxygen availability
  • increase tissue demand for O2
  • anemia
  • reduce blood flow to kidneys
  • blood donation (decreased blood volume)
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12
Q

when should recombinant erythropoietin be given to pt?

A
  • after surgery
  • chemotherapy for leukemia (affects RBC production and function)
  • dialysis pt (poor renal function = less erythropoietin)
  • doping (increase RBC = better performance
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13
Q

describe process of erythropoiesis

A
  1. Bone marrow sense increase erythropoietin → increase in proerythroblast
  2. ribosome synthesis in early proerythroblast
  3. Hb accumulation in late erythroblast and normoblast
  4. ejection of nucleus from normoblast → formation of reticulocytes (immature RBC)
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14
Q

how long does erythropoiesis take

A

7-8 days

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15
Q

how is erythropoiesis measured? what is the normal range?

A

Reticulocyte count is indicative of erythropoiesis (normal range 0.8 - 1%)

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16
Q

describe process of RBC destruction

A

Hb is broken down to heme and globin

  • Globin → broken down into amino acids → reused
  • Heme → broken down into bilirubin and iron
  • Bilirubin → enters liver → secreted into intestine in bile → metabolised by bacteria → excreted in feces
  • Iron → stored as ferritin or hemosiderin in liver → bound to transferrin and released in blood if needed for erythropoiesis
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17
Q

where does RBC breakdown occur?

A

Aged and damaged RBCs are engulfed by macrophages of liver, spleen and bone marrow

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18
Q

which group are at risk of jaundice

A

in baby (underdeveloped liver) and pt with liver disease → unable to take up bilirubin → jaundice

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19
Q

define anemia

A

anemia is the reduction below normal capacity of the blood to carry oxygen.

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20
Q

causes of anemia

A
  • reduction in RBC number
  • reduction in Hb function
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21
Q

sx of anemia

A

(blood O2 cannot support normal metabolism): pale skin, blue lips, fatigue, weak, cold, SOB

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22
Q

Nutritional anemia

A

deficiency of iron, folic acid, vit B12 that are needed for erythropoiesis

Pernicious anemia: lack of vit B12 or intrinsic factor

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23
Q

Aplastic anemia

A

failure of bone marrow to make adequate numbers of RBCs (eg due to radiation damage or chemotherapy)

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24
Q

Renal anemia

A

due to kidney disease causing lack of erythropoietin

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25
Q

Hemorrhagic anemia

A

significant loss of blood

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26
Q

Malaria causing anemia

A

plasmodium falciparum amplifies in RBC and cause RBC rupture

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27
Q

Sickle cell anemia

A

mutation in ß-globin gene → Hb aggregate in in low O2 conditions → rupture RBC membranes

28
Q

Erythroblastosis fetalis causing anemia

A

Rh+ RBC of fetus are destroyed by anti-Rh antibodies of Rh- mother (usually not in first child)

29
Q

Thalessemia

A

low production of Hb (hereditary) [tx: bone marrow transplant]

30
Q

Polycythemia/ erythremia

A

too much RBC and high hematocrit (high % of RBC in blood)

31
Q

primary and secondary causes of polycythemia

A
  • primary polycythemia: caused by tumor/tumor-like condition in bone marrow → overproduction of RBC
  • secondary polycythemia (other causes): dehydration (elevate hematocrit), high altitude (less O2 body produce more O2)
32
Q

issues with polycythemia

A

cause very viscous blood and plugging of capillaries → insufficient O2 delivery to tissues

33
Q

hematocrit in male and female

A

Hematocrit: male 46%, female 42%

34
Q

Leukopenia, what is the concern?

A

too few leukocytes/ WBC- more selectively: lymphopenia (less lymphocytes), neutropenia (less neutrophils) etc
- often leads to opportunistic infections (eg lymphopenia in HIV pt)

35
Q

Leukocytosis
causes

A

too much WBC
- normal response to bacteria or viral infection
- abnormal: cancer of WBCs → leukemia (cancer located in blood)/ lymphoma (cancer in lymphatic system)

36
Q

what organelles does the platelet contain?

A

lack nuclei, contain contractile proteins (actin and myosin)
- mitochondria (to release ADP)
- ER & Golgi (store Ca2+, synthesis of enzymes)

37
Q

what do platelet contain?

A
  • contain growth factors (PDGF, VEGF)
  • allow endothelial cells to repair and grow
  • contain factor XIII (fibrin stabilising factor)
38
Q

3 phases of blood clotting

A

vasoconstriction (immediate)platelet plug (less stable, within seconds)fibrin clot (more stable, within minutes)

39
Q

how is vasoconstriction initiated?

A

initiated by sympathetic nerves. Mediated by vascular smooth muscle cells

40
Q

purpose of vasoconstriction in blood clotting

A
  • provides time for platelet and coagulation phase-
    endothelial cells of opposite sides may stick tgt
  • reduce blood loss but not sufficient
  • endothelial cells contract → exposing basal lamina
41
Q

describe the process of platelet phase

A
  1. damage to the endothelial wall exposes collagen (normally not exposed)
  2. Von Willebrand’s Factor (vWF) binds to platelets to exposed collagen (vWF mediates platelet adhesion)
  3. adhesion to collagen activates platelets
  4. triggers release of granules (PG, TXA2, ADP)
  5. Fibrinogen (found in plasma) links platelets through glycoprotein receptors (weak linkage)
42
Q

function of ADP and TXA2

A
  • ADP attracts and activates more platelets
  • TXA2 promotes aggregation and further vasoconstriction
43
Q

is the platelet phase a positive or negative feedback cascade?

A

positive feedback cascade

44
Q

how does intact endothelial cells inhibit unintentional platelet activation/aggregation

A

intact endothelial cells release nitric oxide and prostacyclins

45
Q

Effects of thrombin (5)

A
  1. enhances it’s own generation (positive feedback loop)
  2. platelet activation
  3. release of platelet factor 3 (PF3) from platelets - activation of intrinsic pathway
  4. convert fibrinogen to fibrin
  5. activates factor XIII (released by platelets) - for stabilisation of fibrin mesh
46
Q

how is the fibrin mesh formed?

A
  1. fibrinogen (factor I) is activated to fibrin (loose meshwork) by thrombin
  2. factor XIII is activated by thrombin to factor XIIIa which stabilises fibrin network with crosslinking
47
Q

describe extrinsic pathway (which steps need Ca?)

A

3,7->10->2,1
1. Factor III (tissue factor/thromboplastin) activates factor VII to factor VIIa
2. Factor VIIa activates factor X to Xa [need Ca]
3. Factor Xa activates factor II (prothrombin) to IIa (thrombin) [need Ca, factor Va/proaccerlerin]
4. Factor IIa activate factor I (fibrinogen) to Ia (fibrin)
5. Fibrin is stabilised by factor XIIIa (activated by thrombin from XIII to XIIIa)

48
Q

describe intrinsic pathway (which steps need Ca?)

A

12,11 -> 9 → 10 -> 2,1
1. Platelet phospholipids activates factor XII to XIIa
2. Factor XIIa activates XI to XIa
3. Factor XIa activates IX to IXa [need Ca]
4. Factor IXa activates X to Xa [need Ca and factor VIIIa/antihemophilic]
5. Factor Xa activates factor II (prothrombin) to IIa (thrombin) [need Ca, factor Va/proaccerlerin]
6. Factor IIa activate factor I (fibrinogen) to Ia (fibrin)
7. Fibrin is stabilised by factor XIIIa (activated by thrombin from XIII to XIIIa)

49
Q

which step requires factor VIIIa/antihemophilic

A

Factor IXa activates X to Xa of intrinsic pathway

50
Q

which step requires factor Va/proaccerlerin

A

Factor Xa activates factor II (prothrombin) to IIa (thrombin)

51
Q

where are clotting factor produced?

A

liver

52
Q

which clotting factor requires vit K?

A

factor II, VII, IX, X

53
Q

how does nitric oxide and prostaglandins regulate blood clotting?

A

Nitric oxide and prostacyclin (a PG) produced by intact endothelial cells → inhibit platelet activation

54
Q

how does serotonin regulate blood clotting?

A

Serotonin at higher concentrations → inhibit ADP activity (prevents attraction and activation of more platelets)

55
Q

examples of procoagulants

A

Procoagulants: form blood clot
- tissue factor/ factor III (extrinsic pathway)
- collagen, anything which activates factor XII (intrinsic pathway)
- collagen (platelet plug)

56
Q

examples of anticoagulants

A

Anticoagulants: prevent blood clot
- artificial: chelators (citrate, EDTA), vit K antagonists (warfarin, coumarin), DOAC
- endogenous: smoothness of endothelial surface, antithrombin III, heparin, thrombomodulin, tissue plasminogen activator (tPA)

57
Q

describe fibrinolysis process

A
  • plasminogen is trapped inside a clot
  • surrounding tissue and vascular endothelial release tPA to cleave inactive plasminogen to protease plasmin- plasmin digest fibrin → dissolve the clot
  • macrophages remove the remains of the clot
58
Q

why is hemophilia a clotting disorder?

A

(only in men, women are carriers)
- caused by a lack of clotting factors (excessive bleeding after an injury, usually affects intrinsic pathway)

  • hemophilia A: deficiency of factor VIII (inhibit factor IX to X)
  • hemophilia B: deficiency in factor IX
  • hemophilia C: deficiency in factor XI
59
Q

how does liver disease cause clotting disorder?

A
  • unable to synthesise procoagulants and clotting factors- produce bile and to absorb fat and vit K
60
Q

how does vit K deficiency cause clotting disorder?

A
  • half of vit K comes from gut bacteria and half from diet
  • long term abx use may cause vit K deficiency and bleeding disorders
61
Q

thrombocytopenia (sx and causes)

A

low levels of platelets

  • sx: spontaneous, widespread haemorrhage → visible by small purple spots on skin
  • cause: damage/destruction of bone marrow (eg malignancy/ chemotherapy)
62
Q

effects of thrombosis

A

too much clotting
- coronary thrombosis (in heart) → heart attack
- cerebral thrombosis (in brain) → stroke

  • ischemic stroke: blockage of cerebral blood vessels → give anticoagulant
  • hemorrhagic stroke: rupture of blood vessels → dont give anticoagulant
63
Q

tx of thromboembolism

A
  • embolus: a freely floating thrombus → can block arteries in lung, heart, brain
  • Tx: tPA, heparin + warfarin
64
Q

what is the content found in a PTT VS PT blood test tube?

A

PTT/aPTT: citrated plasma (anticoagulated plasma) + Ca + phospholipid + kaolin (clay/ foreign surface)

PT: citrated plasma (anticoagulated plasma) + Ca + tissue factor

65
Q

what does PTT/aPTT measures and the normal range

A

measures efficacy of intrinsic and common pathways (factors 12,11,9,10,2,1)
normal range: 25-39 seconds

66
Q

what does PT measures and the normal range

A

measures efficacy of extrinsic and common pathways (factors 3,7,10,2,1)
normal range: 12-15 seconds

67
Q

what is INR and the normal range

A

ratio of patient PT / normal healthy PT
- normal range: 0.9-1.3
- pt on warfarin therapy: 2-3

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