Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

IMS > blood > Flashcards

blood Flashcards

(67 cards)

Start Studying
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

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

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

what white blood cells are involved in allergic reactions?

A

eosinophils and basophils

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

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

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

which blood cells come from common myeloid progenitor?

A

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

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

what blood cells come frm common lymphoid progenitor cells?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

which blood cells are found in bone marrow?

A

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

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

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

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

what are the major blood group systems?

A

ABO and Rh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

which blood group is universal donor?

A

O

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

what blood group is a universal recipient?

A

AB

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are the main causes of bleeding?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are the main causes of thrombosis?

A

arterial = damage to arterial wall

ventral = blood pooling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is haemotological malignancy?

A

cancer of the blood cells

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are the main causes of acquired anaemia?

A

erythrocyte loss

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

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

A

larger RBC
formation of macroovalocytes
hypersegmented neutrophils

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

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
what are the causes f acquired haemolytic anaemia
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)
26
what are the causes of inherited haemolytic anaemia?
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
27
what causes sickle cell anaemia
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
what is the cause of a sickle cell crisis?
blockage of microvasculature by sickled red blood cells
29
what is the cause of thalassaemia?
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
why are thallasaemia and sickle cell anaemia releatively common in africa and asia?
when heterosygous they provide protection against malaria so due to natural selection they are mpre abundant here
31
what is primary haemostasis?
refers to platelet aggregation and platelet plug formation (platelet adhesion, platelet activation, platelet plug formation)
32
describe primary haemostasis
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
what is the secondary haemostatic response?
deposition of insoluble fibrin generated by the proteolytic coagulation cascade = insoluble fibrin mesh that is incorporated around the platelet plug
34
what is the trigger for primary haemostasis?
dormant platelets in the blood undergo explosive activation when they encounter vascualr injury when come into contact with collagen and von willebrand factors
35
what stimulates adhesion?
collagen and von willebrand factor
36
what stimulates platelet activation?
collagen thrombin ADP
37
what stimulates platelet agrregation?
fibrinogen
38
what are the main structural characteristics of platelets?
reegular shaped cells flat non-nucleated basophillic granules in its centre formed from megakaryocytes
39
describe platelet activation
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
describe platelet adhesion and aggregation
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
what is proteolysis?
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
describe the 4 main reactions and factors in intation of coagulation
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
describe the reactions and factors involved in consolidation phase of the coagulation response
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
discuss the intrinsic coaulation pathway
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
discuss the extrinsic coagulation pathway
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
what is the difference between major and minor bleeds?
major bleeds require intervention whereas minor bleeds do not (bruises, menorrhagia -menstrual periods, epistaxis (nose bleeds etc)
47
what are the common cuases of major bleeding?
``` 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
how can vitamin K deficiency lead to bleeding?
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
what are the causes of vitamin K deficiency?
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
how does oral anticoagulation with warfarin work?
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
what is the difference between haemophilia A and B
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
what are the 3 main types of von willebrand disease?
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
what is thrombocytopenia
loss or dysfunction of platelets
54
what are the primary causes of thrombocytopenia?
``` leukaemia blood loss DIC drug induced immune thrmbocytopenia purpura (ITP) ```
55
Which types of thrombosis are classfied as venous?
deep vein thrombosis | pulmonary embolism
56
what types of thrombosis are classified as arterial?
myocardial infarction atrial fibrillation peripheral vascular disease stroke
57
how does deep vein thrombosis occur?
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
what are the main risk factors of venous thrombosis?
``` immobilisation surgery cancer - tumour cells release TF pregnancy oral contraceptives genetic risk factors ```
59
how does fibrinolysis work?
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
how does arterial thrombosis develop?
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
what are the main risk factors of arterial thrombosis
``` advanced age smoking diabetes hypertension cholesterol poor diet lack of excersize ethnicity ```
62
give 3 different types of drugs that target venous thrombosis
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
give 2 types of drugs used to target arterial thrombosis
antiplatelets - aspirin (inhibition of COX-1 and thromboxane production) anti aIIbb3 , anti P2Y fibrinolytics tPA/uPA derivatives
64
what hormone is essentiasl for stimulating the production of platelets?
thrombopoeitin
65
what does prasugre block in order to inhibit plateet aggregation?
ADP binding to P2Y receptors
66
what happens at high altitude that affects binding of oxygen to haemaglobin?
at high altitude, BPG in red blood cells increases, decreasing affinity of Hb for oxygen
67
abciximab (reppro) inhbits platelet.....?
aggregation

IMS (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions