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blood Flashcards

1
Q

describe 5 differences between veins and arteries

A

large diameter v small diameter

thin wall v thick wall

thin tunica media v thick tunica media

low pressure v high pressure

valves v no valves

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2
Q

give 6 functions of the blood

A

hydration of tissues and organs
delivery of oxygen and nutrients to tissues and organs
distribution of endocrine hormones
fight infections - innate and adaptive immune response
regulation of body temperature (hypothalamus) and pH
to prevent its own loss

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3
Q

what white blood cells are involved in allergic reactions?

A

eosinophils and basophils

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4
Q

how is the blood involved in hormone distribution

A

endocrin hormones (paracrine) are secreted by specific endocrine glands into the blood to be circulated to remote target tissues

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5
Q

how are different blood cells produced?

A

all blood cells come from the common progentior cell in the bone marrow. multipotential haematopoietic stem cell

there are 2 lineages - myeloid and lymphoid

these produce 11 different types of blood cell

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6
Q

which blood cells come from common myeloid progenitor?

A

platelets, erythrocyte, mast cells, basophil, neutrophil, eosinophil, macrophages

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7
Q

what blood cells come frm common lymphoid progenitor cells?

A

natural killer cell, T lymphocyte, B lymphocytes, plasma cells

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8
Q

which blood cells are found in bone marrow?

A

haemocytoblast, common lymphoid progenitor, common myeloid progenitor, myeloblast, megakaryocyte

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9
Q

what is the difference between blood plasma and serum?

A

blood plasma contains serum and clotting factors

blood serum contains plasma but no clotting factors

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10
Q

what is the haematocrit?

A

relative colume of blood taken up by cellsa nd plasma - normally around 0.4

blood plasma has 55% volume of the blood

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11
Q

what are the major blood group systems?

A

ABO and Rh

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12
Q

which blood group is universal donor?

A

O

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13
Q

what blood group is a universal recipient?

A

AB

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14
Q

describe why in first pregnancy the newborn will not get haemolytic syndrome but may do in second pregnancy?

A

the rhesus blood group - postive = has Rh agglutinogens
negative = no Rh agglutinogens
during first pregnancy, the baby is protected by placenta-blood barrier and the mother is not exposed to Rh agglutinogens until the time of childbirth due to placental tearing

this causes the generation of anti-Rh agglutinins by the mother.

this means in a second pregnancy, antibodies cross the placental barrier and the baby is born with severe anaemia. need to treat with anti-Rh globulin to mask Rh agglutinogens

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15
Q

what are the main causes of bleeding?

A

trauma, surgery, infection, sepsis, aneurysm rupture, drugs, vitamin K deficiency, inherited

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16
Q

what are the main causes of thrombosis?

A

arterial = damage to arterial wall

ventral = blood pooling

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17
Q

what is haemotological malignancy?

A

cancer of the blood cells

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18
Q

how can haemotological maligancies be classified?

A

classified according to blood lineage - myeloid neoplasm or lymphoid neoplasm.

location - leukaemia=blood, lymphoma=lymph nodes

duration - acute=blasts, chronic=mature cells

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19
Q

what are the main causes of acquired anaemia?

A

erythrocyte loss

decreased response to erythroprotein - iron deficiency, B12 deficiency, folate deficiency,

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20
Q

how can iron deficiency be shown on a blood smaple?

A 
small RBC 
increased central zone of pallor
anisocytosis - variation in size
poikilocytosis - variation in shape 
elongated RBC
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21
Q

how can B12 or folate deficiency been seen in a blood sample?

A

larger RBC
formation of macroovalocytes
hypersegmented neutrophils

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22
Q

what are the main differences between iron deficiency and B12 deficiency

A

iron is involved in haemaglobin whereas B12 is involved in DNA replication

iron leads to decreased haemaglobin production whereas B12 leads to problems with mitosis of proerythroblast

iron leads to microcytic anaemica whereas B12 leads to megaloblastic or macrocytic anaemia

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23
Q

what is the difference between haemolytic anaemia and anaemia affecting the production of RBCs

A

haemolytic anaemia is due to increased RBC destruction, reducing lifespan of RBC and bone marrow is unable to replace suffiecntly

whereas anaemias affecting the production of RBCs

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24
Q

what is the role of erythropoietin in stem cell differentiation

A

erythropoietin is a glycoprotein hormones that stimulates the formation and differentiation of erythroid precursor cells in the bone marrow via the EPO receptor

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25
Q

what are the causes f acquired haemolytic anaemia

A

immune - haemolytic syndorme in newborn who is Rh positive whereas mum is Rh neg. - autantibodies

non immune - durg-induced, snake venom, mechanical (heart valves), infections (malaria and septicaemia)

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26
Q

what are the causes of inherited haemolytic anaemia?

A

RBC cytoskeletal defects cuased by mutations in alpha or beta spectrin = hereditary spherocytosis

RBC enzyme defects - causesd by G6PD deficienct involved in NADPH metabolism

haemoglobin defects - sickle cell disease, thalassaemia

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27
Q

what causes sickle cell anaemia

A

mutation of the HbB globin gene Glu6 to Val
leads to polymerisation of Hb, distorting the RBC and causing sickling of the RBC (particularly homozygous)

haemolytic crisis is due to blockage of microvasculature

28
Q

what is the cause of a sickle cell crisis?

A

blockage of microvasculature by sickled red blood cells

29
Q

what is the cause of thalassaemia?

A

microcytic anaemia caused by defects in either alpha or beta chains of ahemoglobin, leading to ineffective erythropoiesis and haemolysis

alpha thallasaemia and beta thallasaemia

30
Q

why are thallasaemia and sickle cell anaemia releatively common in africa and asia?

A

when heterosygous they provide protection against malaria so due to natural selection they are mpre abundant here

31
Q

what is primary haemostasis?

A

refers to platelet aggregation and platelet plug formation (platelet adhesion, platelet activation, platelet plug formation)

32
Q

describe primary haemostasis

A

platelet adhesion and spreading, the first platelet send out chemical messages so other platelets come and bind close to the area

dense granules - ADP, ATP seratonin and Ca2+ help platelet activation (positive feedback)

alpha granules - platelet factor 4, plasminogen activator inhbitor (pAI-1), chemokines = help coagulation and aid wound healing

33
Q

what is the secondary haemostatic response?

A

deposition of insoluble fibrin generated by the proteolytic coagulation cascade = insoluble fibrin mesh that is incorporated around the platelet plug

34
Q

what is the trigger for primary haemostasis?

A

dormant platelets in the blood undergo explosive activation when they encounter vascualr injury

when come into contact with collagen and von willebrand factors

35
Q

what stimulates adhesion?

A

collagen and von willebrand factor

36
Q

what stimulates platelet activation?

A

collagen

thrombin

ADP

37
Q

what stimulates platelet agrregation?

A

fibrinogen

38
Q

what are the main structural characteristics of platelets?

A

reegular shaped cells

flat

non-nucleated

basophillic granules in its centre

formed from megakaryocytes

39
Q

describe platelet activation

A

when endothelial damage occurs platelets come into contact with exposed collagen and von willebrand factor, activating them - also activated by thrombin and negatively charged surfaces such as glass

40
Q

describe platelet adhesion and aggregation

A

von willebrand mediates the linking of platelets to collagen via a specific receptor in the platelet membrane - cuasing platelets to become dentritic = indicates activation and releases prothrombic ADP

by binding of receptors ADP causes adhesion of platelets and induces aggregation, recruiting more platelets

thromboxane binds to platelets and causes cross linkage

activated latelets trigger coagulation

thrombin stimulates further platelet activation = positive feedback

fibrin forms to stabilise clot

41
Q

what is proteolysis?

A

when protein is incubated with relativelt low cxoncentrations of different proteases, which cut at recognition sites throughout the protein - normally exposed regions such as loops.

in coagulation proteolysis activates the clotting factors

42
Q

describe the 4 main reactions and factors in intation of coagulation

A
  1. after injury FVII binds to TF expressed on membrane of cells surrounding blood vessel
  2. FVII is a peculiar clotting factor as it shows auto activation. activated FVIII proteolytically cleaves and activates FX
  3. FXa converts prothrombin to thrombin
  4. thrombin coverts fibrinogen into fibrin
43
Q

describe the reactions and factors involved in consolidation phase of the coagulation response

A

intial pathway is not enoguh for normal haemostatic response so:

activation of FIX by TF/FVIIa which can convert FX to FIXa

activation of FXI, FVII and FV by thrombin which act as cofactors for FIXa and FXa

44
Q

discuss the intrinsic coaulation pathway

A

triggered by glass, clay particles , platelets

FXII is activated by negatively charged surfaces, FXIIa then activates FXI and so on.

FXII deficiency does not lead to bleeding

45
Q

discuss the extrinsic coagulation pathway

A

the extrinsic pathway is triggered by TF on the cell membrane of perivascular cells

TF/FVIIa, FIXa/FVIIIa and FXa/FVa enzyme complexes are vitamin K-dependent

vitamin K dependent carboxylation of factors VII, IX and X is required for calium binding and formation of active enzyme complexes on the activatied platelet membrane

46
Q

what is the difference between major and minor bleeds?

A

major bleeds require intervention whereas minor bleeds do not (bruises, menorrhagia -menstrual periods, epistaxis (nose bleeds etc)

47
Q

what are the common cuases of major bleeding?

A 
trauma
surgery
sepsis 
intravscular TF exposure
systematic coagulation activation leading to microvascular clots/ cnsumption of clotting factors and platelets leads to bleeding
mulitorgan failure
48
Q

how can vitamin K deficiency lead to bleeding?

A

vitamin k is a cofactor for an enzyme used to form completed forms of clotting factors , vitamin is found in diet and is a fat soluble cofactor

49
Q

what are the causes of vitamin K deficiency?

A

malnutrition
fat malabsorption
liver disease (alcoholic cirrhosis)
may occur in newborns (vitamin K injections/tablets for newborns)
due to vitamin K antagonists (VKA = warfarin, acenocoumarol) overdose

50
Q

how does oral anticoagulation with warfarin work?

A

warfarin is a type of anticoagulant medication that helps prevent clots forming in the blood. warfarin inhibits vitamin K dependent synthesis of clotting factors II, VII, IX and X as well as the regulatory factors protein C, S and Z

51
Q

what is the difference between haemophilia A and B

A

haemophilia is an X kinked recessive disease expressed by males and carried by females
it is due to the insufficient thrombin generation
heamophilia A= FVIII
haemophilia B = FIX

52
Q

what are the 3 main types of von willebrand disease?

A

type 1 - mildest, have reduced level of von willebrand in the blood

type2 von willebrand factor does not work properly - heavier bleeding than type 1

type 3 - most severe and rarest , very low levels of von willbrand factor or non at all

53
Q

what is thrombocytopenia

A

loss or dysfunction of platelets

54
Q

what are the primary causes of thrombocytopenia?

A 
leukaemia
blood loss
DIC
drug induced
immune thrmbocytopenia purpura (ITP)
55
Q

Which types of thrombosis are classfied as venous?

A

deep vein thrombosis

pulmonary embolism

56
Q

what types of thrombosis are classified as arterial?

A

myocardial infarction
atrial fibrillation
peripheral vascular disease
stroke

57
Q

how does deep vein thrombosis occur?

A

DVT is a blood clot that forms in a vein deep in the body, usually in legs below the knee
venous thrombus is fibrin and erythrocyte rich
occurs in areas of low blood flow
involves platelets but driven by excess thrombin inareas around valves

the clot can break free a= embolism and become lodged in blood vessel of the lung = pulmonary embolism

58
Q

what are the main risk factors of venous thrombosis?

A 
immobilisation
surgery
cancer - tumour cells release TF 
pregnancy
oral contraceptives
genetic risk factors
59
Q

how does fibrinolysis work?

A

when fibrin clot is broken down. plasmin cuts the fibrin mesh at various places leading to the production of cirulating fragments that are cleared by proteases or by the kidney and liver

60
Q

how does arterial thrombosis develop?

A

caused by atherosclerosis lipids accumulate in the blood vessel wall and oxidise, with time the plawues rupture and induces thrombotic events

  1. platelets bind to collagen and exposed to oxidised lipids form plaques
  2. activation
  3. release of proaggreotry substances - ADP and TxA2
  4. autocatalytic expansion of thrombus
  5. reduced bioavailability of endothelial NO and production of PGI2
  6. occlusive thrombi
61
Q

what are the main risk factors of arterial thrombosis

A 
advanced age 
smoking
diabetes 
hypertension
cholesterol
poor diet
lack of excersize
ethnicity
62
Q

give 3 different types of drugs that target venous thrombosis

A

immediate onset of anticoagulant effects

  • unfractionated heparin (intraveous - helps antithrombin to inhibit thrombin and FXa)
  • low molecular weight heparin subcutaneous

slow onset
-VKA monitored by INR such as warfarin

direct thrombin inhibitors (diagatran ) promising in clinal trials

63
Q

give 2 types of drugs used to target arterial thrombosis

A

antiplatelets - aspirin (inhibition of COX-1 and thromboxane production)
anti aIIbb3 , anti P2Y

fibrinolytics
tPA/uPA derivatives

64
Q

what hormone is essentiasl for stimulating the production of platelets?

A

thrombopoeitin

65
Q

what does prasugre block in order to inhibit plateet aggregation?

A

ADP binding to P2Y receptors

66
Q

what happens at high altitude that affects binding of oxygen to haemaglobin?

A

at high altitude, BPG in red blood cells increases, decreasing affinity of Hb for oxygen

67
Q

abciximab (reppro) inhbits platelet…..?

A

aggregation

IMS (14 decks)

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