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BMS200 final exam > Week 11 > Flashcards

Week 11 Flashcards

1
Q

what gets exposed when blood vessel is injured

A

collagen and thromboplastin

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2
Q

platelets release 5-hydroxytrptamine ofr

A

muscle contraction + vasoconstriction

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3
Q

extrinsic vs intrinsic pathway; which is first

A

extrinsic first and form early fibrin plug

intrinsic to amplify coagulation and make stable fibrin plug

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4
Q

what activates fibrinogen to fibrin

A

thrombin

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5
Q

antithomrobotic factors (prevent clot formation)

A

prostacyclin, NO, ADPase

heparan sulfate
protein C

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6
Q

where are platelets made

A

megakaryotcytes in bone marrow

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7
Q

what regulates platelet production in the marrow

A

thrombopoietin

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8
Q

what increased platelet production

A

IL6 (inflammation) and decreased platelet numbers

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9
Q

lifespan of platelet

A

7-10 days

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10
Q

where are platelets stored

A

spleen

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11
Q

2 types of granules in platelets (which is most abundant)

A

alpha granules (most abundant) and dense granules

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12
Q

dense granules in platelets contain

A

ADP, Ca2+, serotonin, polyphosphate

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13
Q

alpha granules in platelets contain

A

vWF, FV, fibrinogen, growth factors (FGF, VEGF, PDGF), adhesive glycoproteins

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14
Q

which granule in platelet has adhesive glycoproteins to help bind injury

A

alpha granules

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15
Q

platelet glycoproteins in alpha granules

A

GP Ib/IX binds vWF

GP Ia/IIa binds collagen

these 2 above are for initial signals

GPIIb/IIIa- binds fibrinogen or vWF (only after platelet activates it by plateRR) (stabilize plug- platelet aggregation)

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16
Q

healthy endothelium contains _____ to prevent platelet activation

A

NO, prostacyclin, ADPase

vWF and collagen are hidden

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17
Q

plateRR (release reaction) releases many things to help clot

A

ADP, serotonin, thromboxane A2, coagulation factors, Ca2+, polyphosphate

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18
Q

how to platelets get leukocyte to injury

A

express P selectin

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19
Q

1st step in intrinsic and extrinsic pathway and final common pathway

A

extrinsic: FVIIa and TF (aka TPL or thromboplastin)

intrinsic: HMW kinongen kallikrein with FXIIa to activate

final: FXa + FVa + Ca2+ –> activate thrombin

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20
Q

what factor stabilizes fibrin

A

XIIIa

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21
Q

what does kinin-kvllikrein system release

A

bradykinin (vasodilate, pain, muscle contract, permeability)

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22
Q

FXII in intrinsic pathway causes inflammation via

A

bradykinin release

C3 and C5 cleavage

thrombin and fibrin split products (clot left overs)

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23
Q

decrease clot formation by

A

down regulate platelet activation (prostacyclin, NO, ADPase)

down regulate coagulation cascade

destroy clots (fibrinolysis)

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24
Q

antithrombotic/ anticoagulation mechanisms (stop clotting)

A
  • antithrombin via heparin expression

protein C + protein S = thrombomodulin

tissue factor pathway inhibitor (TFPI) via heparin

plasminogen –> plasmin

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25
Q

fibrinolysis

how does plasminogen become plasmin? how does it degrade fibrin? into what?

A

plasminogen into plasmin via tPA (tissue plasminogen activator) and its degrades fibers into d -dimers

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26
Q

how to stop plasminogen from turning into plasmin and causing fibrinolysis (this is if you want clots)

A

plasminogen activator inhibitors (PAIs) block tPA

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27
Q

prothrombin time (PT) vs activated partial thromboplastin time (aPTT)

  • which is for extrinsic vs intrinsic pathway
A

PT= extrinsic
aPTT= intrinsic

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28
Q

hemophilia A vs B

deficiency in which factors

A

A= FVIII (8)

B=FIX (9)

both are x linked recessive + similar clinical presentation

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29
Q

whats more common, hemophilia A or B

A

A

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30
Q

hemophilia presentation

A

deep bleeds in soft tissue… cant clot

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31
Q

RBCs/ erythrocytes are made in _____ (lifespan of _____) and recycled in _____

A

Red blood cells are produced in the bone marrow and have a lifespan of about 120 days (because no nucleus) before being recycled in the liver and spleen.

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32
Q

hemoglobin binds oxygen with low or high oxygen concentrations?

A
  • Hb binds to oxygen at high oxygen concentrations
  • Oxygen dissociates from Hb at low oxygen
    concentrations
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33
Q

RBCs bind CO2 with what enzyme and converts it into what

A

carbonic anhydrase enzyme and converts it into bicarbonate ions (HCO3-)

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34
Q

what are RBCs derived from

A

myeloid progenitor (pronormoblast)

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35
Q

myeloid progenitor (pronormoblast) divide to become RBC via what

A

GM-CSF and EPO (erythropoietin)

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36
Q

erythropoiesis

A

pronormoblast divide to make 16-32 RBC via EPO

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37
Q

low O2 or high O2 to make EPO

A

low oxygen to make EPO

high oxygen HIF (hypoxia inducible factor) degrades EPO

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38
Q

which energy for RBC to make ATP

A

glycolysis (no mitochondria)

39
Q

what is stored in RBC to protect against free radicals and oxidative stress when high oxygen concentrations

A

glutathione

40
Q

hemoglobin composition

A

2 alpha + 2 other

mostly 2 beta

sometimes delta

fetal is gamma

41
Q

what causes Hb to have a lower affinity for oxygen (less binding)

A

increase temp, increase DPG, increase CO2, decrease pH

42
Q

what has greater affinity for Hb than oxygen

A

CO2

43
Q

where are RBCs eliminated

A

red pulp is spleen

44
Q

Hb metabolism

A

iron sent back to bone marrow for storage

heme elimintated in stool and bile as bilirubin (via biliverdin –> unconjugated bilirubin bound to albumin and carried to liver) (UDG catalyzes conjugation of bilirubin)

globin protein recycled back into a.a. components

45
Q

what catalyzed conjugation of bilirubin when gets to liver

A

add glucoronic acid residues via UDG (uridine diphosphate glucosyntransferase)

46
Q

what forms of iron are better absorbed

A

heme (animal)
Fe2+ (reduced)h

47
Q

how to transport iron

A

divalent metal transporter (DMT)

48
Q

what blocks ferroportin transporter (for iron inside the cell to get extracellular)

A

hepcidin - prevent iron overload

49
Q

what transports iron through bloodstream

A

transferrin (accepts iron from ferroportin)

50
Q

ferritin is

A

from when cells with transferring receptors endocytose it

51
Q

what prevents iron overload

A

hepcidin (block ferroportin)

52
Q

what is the storage form of ferritin in hepatocytes, spleen, bone marrow

A

hemosiderin

53
Q

what stimulates hepcidin production

A

IL6

54
Q

what inhibits hepcidin (something that prevents iron overload)

A

-reduced iron stores
-erythroferrone (released from developing erythroblasts)

55
Q

IDA

A

microcytic + hypochromic (decreased MCHC)

increased RDW, TIBC

decrease HB, RBC count, reticulocytes, ferritin

56
Q

what values are sensitive to early iron store depletion

A

Measurements of marrow iron stores, serum ferritin, and total iron-binding capacity (TIBC) are sensitive to early iron- store depletion

57
Q

absolute iron deficiency vs functional iron deficiency

A

absolute: Reduction of total body iron stores, which may progress to IDA. (i.e. increased demand, decrease intake and absorption, chronic blood loss)

functional: Iron is inadequately mobilized from stores to the circulation and erythropoietic tissue. (I.e. chronic inflammation and elevated hepcidin, increased erythropoiesis)

58
Q

anemias of inflammation differ from IDA

A

▪ Present similarly and have similar findings on CBC ▪ Iron handling is quite different

59
Q

in anemias of inflammation what cytokines suppress erythropoiesis

A

rheumatoid arthritis: IL-1

neoplasm, baterial infection: TNF

60
Q

inflammatory cytokines (IL1 and TNF alpha) do what do erythropoeisis

A

suppress it (EPO)

61
Q

what suppresses RBC precurors in anemais of inflammation

A

IFNs (IFN release is stimulated by TNF and IL1)

62
Q

IL1 and TNF alpha stimulate release of ____ which increases the production of _____

A

IL6 to produce hepcidin (which decreases iron)

63
Q

anemia of chronic kidney disease

A

hypo proliferative anemia (not make enough RBC from bone marrow)

from decreased EPO and poor RBC survival

64
Q

RBCs in chronic kidney disease

A

normocytic and normochromic

65
Q

RBC in anemia of inflammation

A

normochromic and mildly microcytic

decrease reticulocytes (immature RBCs)

66
Q

hereditary spherocytosis

A

anemia from defects in cytoskeletal elements

(make abnormal shaped RBCs- spherocytes; so get destroyed)

67
Q

genetic mutations in hereditary spherocytosis

A

ankryin and anion exchanger 1

68
Q

symptoms in hereditary spherocytosis

A

splenomegaly, jaundice

normoctyic anemia, increase RDW and MCHC

69
Q

G6PD deficiency

how does G6PD play a role in RBC

A

source of NADPH for glutathione reduction

70
Q

when do G6PD deficiency symptoms arise

A

in oxidative stress

bc related to NADPH and glutathione

71
Q

type of anemia in G6PD deficiency

A

Hemolytic anemia precipitated by oxidative insults to RBCs

72
Q

Alpha and beta thalassemia

A

reduce adult haemoglobin synthesis

alpha- deficit in alpha globin chain production (more fatal)

beta- defect in beta globin chain production

defects lead to wrong shape and poor RBC production (ineffective erythroposeis) –> increased RBC destruction (hemolysis)

73
Q

if give blood transfusion to thalassemia

A

can help with anemia but then can cause iron overload (the iron levels are normal its just the hemoglobin that’s low)

74
Q

types of beta thalassemia

A

minor: microcytic anemia

intermedia: need transfusions

major (both alleles): splenomegaly, bone deformities

75
Q

4 missing alpha chains for alpha thalasemia is aka

A

hydros fetalis (fatal)

76
Q

3 missing alpha chains in thalassemia

A

hemoglobin H disease

microytci hypochromic anemia, splenomegaly

77
Q

sickle cell disease

A

replace glutamate with valine at codon 6 of beta-globin gene

for malaria protection

sickling damages RBCs and leads to their removal
and micro infarcts

hypoxia

78
Q

type of anemia in sickle cell

A

hemolytic anemia

79
Q

bug that causes malaria

A

female anopheles mosquitos carrying the p. falciparum parasite

invade the liver then get into blood

80
Q

what does malaria induce RBCs to express on their membrane

A

Malaria induces RBCs to express a parasitic protein on their membrane – PfEMP1

makes them get stuck in vasculature

81
Q

bad malaria effects

A

hypoglycemia, convulsions, renal failure, if cerebral , acidosis,

82
Q

leukemia vs lymphoma

A

leuk- bone marrow

lymphoma- lymphatics (can invade bone marrow)

83
Q

lymphoid neoplasms in which cells most common and which enzymes

A

B cell precursors

(malignancies develop during antibody class switching and recombination events)

Enzymes (AID = activation-induced cytosine deaminase and recombinases/RAGs

84
Q

non-hodkin vs hodgkin lymphoma

A

hod- along lymphs
non- widespread

85
Q

acute lymphoblastic leukemia

A

b and T cell precursors

in kids

block differentiation of immature leukemic blast cells

immature non functional blast cells accumulate

crowd out normal cells and bone marrow fails

86
Q

chronić lymphocytic leukemia

A

Tumour of relatively mature B-cells, expressing CD 19, CD 20, and CD 23

87
Q

acute lymphoblastic leukemia vs chronic lymphocytic leukemia

A

acute-b and T cell precursors

chronic- Tumour of relatively mature B-cells, expressing CD 19, CD 20, and CD 23

88
Q

non Hodgkins lymphoma

A

Cancers of mature B, T, and NK cells. ( B cell most common)

89
Q

mutations in which transcription factors to get B cell type of non-hodgkins lymphoma

A

transcription factors MYC and BCL6, and antiapoptotic protein BCL2.

90
Q

Hopkins lymphoma affects

A

matter B cells

91
Q

2 types of Hodgkins lymphoma

A

classical Hodgkin’s lymphoma (cHL) and nodular lymphocyte-predominant Hodgkin’s lymphoma (NLPHL).

92
Q

association between what a Hodgkin lymphoma

A

Epstein barr virus , HIV too

93
Q

type of cells in Hodgkin lymphoma

A

reed-stern berg cells

(large cells with abdundant cytoplasm and multiple nuclei), express EBV protein

BMS200 final exam (14 decks)

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