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Human Organs and Tissues > Blood/lymphatics > Flashcards

Blood/lymphatics Flashcards

1
Q

Functions of blood

A 
oxygen delivery via RBCs
CO2 removal via RBCs/HCO3
distribute nutrients to the body 
distrbuution of hormones
hemostasis (clotting)
buffer body fluids/ osmotic balance 
regulation of body temp
removal of metabolic waste
immune cell circulation
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2
Q

plasma composition

A

see table

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3
Q

cellular blood components

A 
red cells 
platelets
white cells:
neutrophils
lymphocytes
monocytes
eosinophils
basophils
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4
Q

normal red cell morphology

A

anucleate
biconcave shape - helps them fit through capillaries
central pallor (dent) should be less than 1/2 the diameter of the cell

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5
Q

red cell function

A

oxygen delivery to tissues
removal of CO2 from tissues

both of these processes are mediated by hemoglobin in RBCS

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6
Q

Hemoglobin structure

A

two alpha and two beta chains

hemoglobin cannot be made without iron

each chain has a heme group

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7
Q

myoglobin

A

stores oxygen in tissues

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8
Q

iron deficiency anemia

A

hemoglobin cannot be made without iron -

red cells with very little hemoglobin appear pale and small

patients feel tired and shortness of breath, possibly heart palpitations

treatment = provide them with iron

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9
Q

hereditary spherocytosis

A

red cells look like perfect spheres, slightly smaller than normal RBCs and no biconcave shape

occurs due to mutations in the cytoskeleton or on membrane surface

  • this causes them to have reduced SA but same volume - causes splenic trapping
  • oxygen goes down and pH changes = hemolysis by WBCs

patients are anemic and present with symptoms of iron deficiency

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10
Q

sickle cell anemia

A

red blood cells take on sickle shape

at the nucleation phase the process is reversible - this stage can also be prolonged

when explosive growth of polymers occurs - red cells cant fit through capillaries - stick to vessel walls - clog blood vessels = sickle cell crisis - dangerous and painful

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11
Q

what is a platelet

A

cytoplasmic fragments of cells called megakaryocytes

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12
Q

platelet structure

A

electron dense granules: mainly nucleotides (ADP) and Ca2+

specific alpha granules:
fibrinogen, factor V, vWF

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13
Q

platelet receptors

A

GP1bIX receptor - mediates attachment to vWF, leads to platelet activation

GPIIbIIIa receptor - mediates attachment to fibrin (final step in clotting) - seals the clot+activates the platelet

ADP receptors (P2Y12) - self activation mechanism

thrombin receptors (PAR1/2) -0 major part in coagulation cascade - also activation of platelet

thromboxane A2 receptor = activation

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14
Q

hemophilia

A 
X linked recessive disorder
hemophilia A = F8 deficiency
hemophilia B = F9 deficiency
clinically identical 
strong association between factor level and severity of disorder
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15
Q

hemophilia spectrum of disease

A

factor level is less than 1%:
severe disease, frequent spontaneous bleeding; joint deformity and crippling

factor level 1-5%:
moderate disease, post traumatic bleeding, occasional spontaneous bleeding

factor level 5-20%:
mild disease
post traumatic bleeding

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16
Q

neutrophils

A

polymorphonuclear neutrophil or segmented neutrophil
generally first to arrive to site of infection

primary function is phagocytosis of bacteria, fungi, and debris

kill ingested bacteria via oxygen dependent or independent methods

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17
Q

reactive oxygen and nitrogen intermediates that neutrophils use to kill bacteria

A

reactive oxygen intermediates:
superoxide anion-phagocyte NADPH oxidase

hyperchlorite anion - myeloperoxidase

reactive nitrogen intermediates:
nitric oxide - NO synthetase

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18
Q

chronic granulomatous disease (CGD)

A

caused by deficiency of phagocyte NADPH oxidase (cant make superoxide anions)

leads to dysfunctional killing of bacterial and fungal organisms by neutrophils

patients present with recurrent bacterial and fungal infections

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19
Q

leukocyte adhesion deficiency (LAD)

A

caused by deficiency of LFA-1 integrin

leads to inability of neutrophils to migrate from blood to tissues

most patients with LAD die before 1 year of life from bacterial infections

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20
Q

eosinophil function

A

anti-parasitic function - anti parasitic protein called eosinophil cationic protein (ECP)
involved in allergic reactions
have enzymes that can generate lysosomal and oxygen radicals

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21
Q

basophil function

A

support mast cell responses during inflammation

involved in allergic reactions

have histamines

make prostaglandins and leukotrienes

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22
Q

granulocytes

A

basophils
eosinophils
neutrophils

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23
Q

monocytes

A

migrate into tissues and differentiate into tissue macrophages

have horse shoe nucleus

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24
Q

monocyte/macrophage function

A

phagocytosis of microorganisms and then killing via oxygen independent or dependent

macs only:

  • secrete cytokines and chemokines to recruit immune cells to site fo inflammation
  • present antigen to CD4+ t cells via MHC 2
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25
Q

changes involved in monocyte differentiation into macrophages

A

increase in size
increased number+complexity of organelles
increased phagocytic activity
increased amount of hydrolytic enzymes

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26
Q

complement cascade

A

series of enzymatic reactions where inactive precursors are converted to their active forms

cascades can be activated by antibody-antigen complexes or microbial cell wall components

results in generation of:

  • anaphylotoxins
  • opsonin (C3b): facilitates phagocytosis of microbes
  • membrane attack complex
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27
Q

how are host cells spared from the complement cascade?

A

host cell receptors inactivate complement activation/effector function

decay accelerating factor inhibits formation of C3 convertase

membrane inhibitor of reactive lysis (MIRL/CD59) inhibits MAC assembly

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28
Q

lymphocytes

A

T cells =70-80%
- CD4:CD8 = 2:1 ratio

B cells = 10-20%

NK cells = 5-10%

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29
Q

T cells

A

formed in bone marrow - mature in thymus

CD4+ helper T cells = generals of immune response, help activate or silent other immune cells

CD8+ cytotoxic t cells = kill virally infected cells

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30
Q

B cells

A

produced and mature in bone marrow

produce and secrete antibodies

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31
Q

NK cells

A

formed and mature in bone marrow

kill virally infected cells and cancer cells

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32
Q

lymphocyte function

A

circulate between blood and secondary lymphoid tissues to facilitate the encounter with specific antigen

when it encounters its specific antigen in the lymph node it undergoes clonal expansion

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33
Q

severe combined immunodeficiency (SCID)

A

genetic disorder where t and b cells are deficient or dysfunctional
- usually defect in RAG1/2 or IL-2y receptor subunit

usually die within first year of life

treatment = bone marrow transplant

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34
Q

bone marrow function

A

origin, maturation, development of all peripheral blood cells

classified as primary lymphoid tissue

blood cell formation is called hematopoiesis

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35
Q

sites of hematorpoiesis

A

fetus:
0-2 months = yolk sac
2-7 months = liver + spleen
5-9 months = bone marrow

infants:
bone marrow in practically all bones

adults:
vertebrae, ribs, sternum, skull, sacrum, pelvis, end of femurs
- progressive fatty replacement of bone marrow

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36
Q

components of the bone marrow

A

stem cells

bone marrow microenvironment

hematopoietic factors

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37
Q

stem cells

A

arise from yolk sac

self renewal

multi lineage differentiation potential

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38
Q

bone marrow microenvironment

A

extracellular matrix

stromal cells

notes have more details

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39
Q

hematopoietic growth factors

A

see notes

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40
Q

marrow sinusoids - egress of blood cells

A

blood vessels are lnes by endothelial cels but there are gaps

WBCs and RBCs can pass through

megakaryocytes - have protrusions that reach through the gaps - little buds break off of these and become platelets

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41
Q

bone marrow exam

A

extract bone barrow then take tissue chunk for biopsy

these are complementary to each other and therefore you need both to confirm the diagnosis

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42
Q

erythropoiesis

A

produces mature rbcs

cytoplasm changes from blue to orange due a decrease in NRA and increase in hemoglobin

nucleus becomes smaller as the chromatin becomes more compact - nucleus eventually expelled from cells - macs eat the nuclei

1 progenitor = 16 RBCs (circulate for 120 days)

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43
Q

control of erythropoiesis

A

kidney senses that O2 is low

the peritubular interstitial cells of outer cortex produce and secrete erythropoietin - promotes erythropoiesis = circulating red blood cells

patients with renal failure do not produce enough erythropoietin and become anemic -treatment = recombinant erythropoietin

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44
Q

thrombopoiesis

A

thrombopoietin is the major driving factor - made in the liver

megakaryocytes are large because they undergo nuclear divisions but not cytoplasmic divisions -make a lot of mRNA and package them into granules

platelets are small plasma cells with granules inside of them

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45
Q

thrombocytopenia in liver failure

A

liver produces thrombopoietin

patients with liver failure often have decreased platelet count (thrombocytopenia) and are at risk for bleeding

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46
Q

granulopoiesis

A

negative feedback inhibition by mature forms

segmented nucleus indicates maturation

eosinophil and basophil maturation are similar

key factor = G-CSF

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47
Q

monocytopoiesis

A

same progenitor cell as for segmented neutrophil

key factor = M-CSF

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48
Q

acute myeloid leukemia

A

mutations that preserve the self renewing properties of stem cells by interfere with maturation lead to continuous proliferation of immature daughter cells

these cells eventually take over the bone marrow and lead to acute myeloid leukemia

see notes for mechanism

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49
Q

lymphopoiesis

A

T cells, B cells, NK cells arise from the same stem cell

stages of maturation defined by surface antigen expression

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50
Q

antibody (immunoglobulin) structure

A

antibodies have 4 polypeptide chains: 2 heavy and 2 light

each b cell produces antibodies with a single specificity that is different from those produced by other b cells

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51
Q

immunoglobulin heavy chain rearrangement (VDJ)

A

RAG-1 and RAG-2 are involved

similar gene rearrangement occurs within the light chain gene

produces 10^10 antibody repertoire

52
Q

outcomes of b cell maturation

A

see notes

53
Q

Burkitts lymphoma

A

b cell lymphoma
grows rapidly
cells appear large and nuclear chromatin are open
stary sky pattern bc macs are trying to phagocytose dying malignant cells

caused by:

  • C-myc is an oncogene normally on chromosome 8
  • the gene is rearranged and placed on chromosome 14 in front of b cell heavy chain promoter - therefore starts making a bunch of the c-myc gene causing uncontrolled cell proliferation
54
Q

folicular lymphoma

A

b cell lymphoma

usually in older patients

uncontrolled growth in lymph nodes

caused by:

  • translocation involving BCL-2 which is a tumor surpressor gene
  • bcl-2 gets translocated to promoter , doesn’t let cells die because it stops apoptosis
55
Q

cellular composition of the thymus

A 
thymocytes (immature t cells)
dendritic cells
macrophages
cortical epithelial 
epithelio-reticular cells
56
Q

thymocytes

A

immature t cell precursors

migrate to thymus from bone marrow using CD44 and alpha integrin 4 homing

rearrange TCR genes in the thymus

selected to die via apoptosis or mature into T cells based on TCR specificity

57
Q

t cell maturation/development

A

see notes

58
Q

cortical epithelial cells

A

interact with double positive thymocytes in the cortex to mediate positive selection

59
Q

dendritic cells

A

located in thymic medulla

interact with single positive thymocytes and mediate negative selection

60
Q

epithelio-reticular cells

A

form a continuous cellular layer that lines the capsule and around the blood vessels called the blood-thymus layer

barrier prevents exposrue of te immature thymocytes to blood borne antigens

61
Q

Hassall’s Corpuscles

A

appear early in life and are of unknown function

made of epithelial cells that had undergone degeneration and organize themselves into concentric eosinophilic whorls of material called thymic corpuscles

62
Q

self tolerance: regulatory t cell model

A

t regs prevent autoimmunity

immune suppressors

63
Q

thymic involution

A

as we age functional parenchyma of the thymus is replaced with fat and connective tissue - organ diminishes in size

thymus is not nonfunctional:

  • with age, more lymphocytes get trained, don’t need as many new ones (still need some)
  • parenchyma never completely disappears - retains some function
64
Q

primary and secondary lymphoid tissues

A

primary:
bone marrow
thymus

secondary:
spleen
lymph nodes
tonsils, adenoids
payers patches
65
Q

circulatory/lymphatic system interaction

A

at the capillary beds - interstitial fluids + cells/cell products/pathogens/debris enter lymphatic capillaries

afferent lymph vessel carries lymph fluid to lymph node (acts as a filter)

filtered lymph exits node via efferent vessels

drains into the thoracic and returned to the heart

66
Q

lymphatic vessels

A

have valves to make sure fluid flow is unidirectional

afferent vessels bring lymph to the lymph node

efferent vessels take lymph fluid away from node via thoracic duct and back in circulation

67
Q

blind-ended lymphatic capillaries

A

lined by endothelial cells - the gaps are where the interstitial fluid will get through into the lymph vessels

68
Q

tissue fluid management depends on:

A 
capillary hydrostatic pressure 
capillary permeability 
effective oncotic pressure (difference between plasma and interstitium)
lymphatic drainage
tissue tension
69
Q

lymphedema

A

net accumulation of interstitial fluid due to impaired lymph drainage

blockage or damage of lymphatic vessels - causes impaired lymphatic drainage

secondary lowering of colloid osmotic pressure differential due to reduced removal of protein from interstitium

examples: radiation treatment, post-mastectomy, filariasis

70
Q

contents of afferent lymphatic vessel

A

contains DCs carying antigen, particulate antigen, few lymphocytes

71
Q

function of lymph nodes

A

generation of t and cell immune responses

location where lymphocytes can interact with APCs and particulate antigen

particulate matter and microorganisms that enter lymph are phagocytosed to prevent them from entering blood

allows for lymphocyte activation and is a barrier for blood infections

72
Q

lymph node structure

A 
capsule 
sinuses
afferent and efferent lymphatics 
blood vessels
parenchyma: cortex, paracortex, medulla
73
Q

lymphocyte compartments in lymph node

A

cortex:

  • primary follicles - naïve b cells
  • secondary follicles - activated b cells in germinal centres

paracortex:
- t cell areas

medulla:

  • plasma cells secreting antibody
  • few activated/memory t cells and b cells transiting into efferent lymph
74
Q

high endothelial venules (HEV)

A

specialized post capillary venous swellings characterized by plump endothelial cells

allow lymphocytes that are circulating in the blood to directly enter a lymph node (crossing HEV)

75
Q

follicular dendritic cell (FDC)

A

located in the germinal centers of primary and secondary follicles

present antigen to b cells but do not digest and present on MHC
- instead they bind particulate in antigens and present that to the b cells

76
Q

medulla of lymph node

A

medullary cords contain plasma cells which secrete antibodies into medullary sinuses

medullary sinuses empty into efferent vessels
- sinuses contain macrophages which phagocytose particulate matter/microorganisms, preventing their entry to blood

77
Q

T and B cell activation in the lymph node

A

DCs from afferent vessel meet with lymphocytes from HEV (paracrotex)
migrate back to cortex and start to proliferate - some will access medullary sinus and become blood borne

78
Q

what does the efferent lymphatic vessel carry?

A

antibodies from plasma cells

activated/memory t and b cells into thoracic duct - empties into venous circulation

facilitates distribution of antibodies and effector cells throughout the body

79
Q

function of spleen white pulp

A

generation of t and b cell responses (antibodies) against blood borne pathogens

main protection against streptococcus pneumoniae and niseria menigitidis

80
Q

function of spleen red pulp

A

macrophages in splenic cords phagocytose blood borne pathogens

grooming of RBCs and phagocytosis of old ones - gets rid of RBCs with defects

81
Q

splenic sinusoids

A

removes damaged or aged RBCs from circulation

also allows the migration of leukocytes from the cords into the circulation

they are lined with DCs so if pathogens or antigens pass through they will be phagocytosed

82
Q

post splenectomy

A

patients are susceptible to blood borne infections:
meinigitis and pneumonia

these infections would be fatal in asplenic patients

patients must be immunized against these and treated quickly if infected

red cell grooming is absent therefore red cells contain characteristic inclusions:

  • howell jolly bodies (sm. nuclear remnants)
  • pappenherimer bodies are abnormal granules of iron
83
Q

ABO blood antigen system

A

ABO antigens= carb antigens expressed on surface of RBCs, platelets, endothelial cells

inherit one allele from each parent

co-dominant expression

four possible phenotypes: A,B,AB,O

84
Q

genetic basis of ABO blood antigen system

A

fucosyl transferase 1 (FUT1) gene: makes the O or H antigen backbone (chromosome 19)

Glycosyltransferase A (GTA or A gene): adds N-acetylgalactosamine, A antigen (chromosome 9)

glocosyltransferase B (GTB, B gene): adds galactose (B antigen) (chromosome 9)

O blood group is due to lack of GTA an GTB

85
Q

hyperacute rejection mechanism

A

see notes

86
Q

acute hemolytic transfusion reaction

A

see notes

87
Q

Rh blood group system

A

glycoprotein antigens expressed on red cells

coding genes on chromosome 1

RHD gene: RHD protein present = D antigen, lacking = d

Rh+ = D
Rh- = d
88
Q

hemolytic disease of the newborn

A

result of incompatibility between maternal and fetal blood antigens (most common with RhD incompatibility)

mother is Rh- and fetus is Rh+

fetal Rh+ RBCs cross placenta and enter maternal circulation from:

  • miscarriage
  • bleeding
  • delivery

mother then develops anti-Rh antibody

antibody crosses placenta and results in hemolysis in fetus

first born is usually not affected bc antibody formation takes time

consequences for fetus:
develops anemia 
death due to heart failure
jaundice/anemia (cant clear bilirubin)
seizures and brain damage (high bilibrubin)
89
Q

how to prevent hemolytic disease of the newborn

A

all mothers are tested for Rh early in pregnancy

if mom is Rh -:

  • rhig/rhogam (anti-RhD immunoglobulin) is given at 28 weeks of gestation - at the time of delivery and any trauma or significant bleeding
  • this antibodies masks D antigen on fetal red cells and prevents maternal sensitization
90
Q

treatment of hemolytic disease of the newborn

A

fetal blood transfusion through umbilical vein

group O, Rh- donor red cells are given

91
Q

indications for transfusion

A

RBCs:
- anemia ( hemoglobin is 70-80 when it should be 120-170)

Platelets:
- thrombocytopenia (normal 150-450x10^9)

Plasma:

  • acute bleeding due to trauma or surgery)
  • warfarin therapy related intracranial hemorrhage
  • patient on warfarin needing urgent surgery
92
Q

complications of transfusion

A

see notes

93
Q

ensuring safety in blood supply

A

health screen: questionnaire, interview + physical exam

diversion pouch (rid of skin pathogens)

universal leukoreduction

testing

selective donor use

investigation of transfusion reactions

donors notify of changes in their health

94
Q

donor testing

A

ABORh: fwd and rev

matched blood transfused

clinically significant blood group antigens in select cases

infectious disease

95
Q

most common bad reactions to blood transfusions

A

febrile non-hemolytic reaction

minor allergic

TACO

96
Q

transfusion complications with highest mortality

A

TRALI is the most fatal but less common

TACO causes most deaths bc it is more common and is deadly

97
Q

compatibility for platelet transfusion

A

try to match with the abo blood type because could have a hemolytic reaction due to antibodies in donor plasma or could have donor platelet destruction

98
Q

compatibility for RBC transfusion

A

notes

99
Q

compatibility for plasma transfusion

A

notes

100
Q

ABORh typing: forward vs reverse typing

A

Forward: have three tubes: one with anti-A, one with anti-B and one with anti-D
put patients red cells into the tube and centrifuge-positive =cells stay higher in tube

reverse: have two tubes: one with cells that a antigen and the other has cells with b antigen
- add patient serum to determine if they have antibodies for that antigen

101
Q

screen - indirect antiglobulin test (IAT)

A

goal: to see if the patient has antibodies against the antigens on the allogenic (donor) red blood cells

method:
screening red cells will be selected to have all clincially significant antigens on them

if a we get a positive reaction then we must determine the specific antigen

102
Q

antibody identification (following positive screen)

A

similar method to IAT but have a panel with more cells

potential targets are ruled in or out based on reactivity with panel

103
Q

crossmatch IAT

A

final check for compatibility
- ABO is checked and antibody reactivity against antigens not represented in the screen cells

method:
IAT method is performed with donor red cells instead of screening cells + patient serum
- positive reaction = pellet stays higher up in tube and does not migrate

104
Q

electronic cross match

A

computer tells us if a red cell unit is compatible with the patient

this is done instead of phsyical cross match if:
- patient has no history of positive screen
-patient has no history of an antibody
patients ABO blood type is unknown

105
Q

delayed hemolytic transfusion reactions

A

primary antibody response to a red cell alloantigen on recently transfused RBC

secondary antibody response to a blood group antigen that was previously encountered during pregnancy or transfusion

most commonly against RHD

usually extravascular hemolysis
- RBCs are opsonized and then phagocytosed in spleen by macs

milder presentation of anemia, low grade fever

106
Q

direct antiglobulin test (DAT)

A

check for antibody bound to red cells in a patient

use a poly-specific anti-human globulin reagent ( can have specific ones is initial test is positive)

do this to investigate anemia and hemolysis

107
Q

types of transplantation

A

solid organ transplantation

tissue transplantation

hematopioetic stem cells transplantation

108
Q

types of grafts

A

homograft - genetically identical twins (no rejection)

allograft - within same species but not genetically identical (susceptible to rejection)

xenograft - between species (very susceptible to rejection)

109
Q

types of donors

A

deceased donors: any solid organ or tissue can be taken

living donors: liver and kidneys

110
Q

types of graft rejection

A

hyperacute- minutes to hours (caused by preformed antibody)

acute - days to months (preformed antibody is the cause but immunosuppression should stop this)

chronic - years ( not sure why this happens)

111
Q

what causes hyperacute rejectoin

A

pre-existing antibodies to:

ABO blood group antigens on endothelium (mainly IgM)

HLA antigens: usually IgG against MHC1
- acquired through previous alloimmunizaton (transfusions, transplants, pregnancy)

112
Q

MHC in humans

A

human leukocyte antigen =HLA

class 1 = A, B, C
class 2 = DR, DQ, DP
class 3 = complement proteins, TNF, heat shock proteins

polymorphism:
500 genes that most of us have
can’t match outside of ethnic groups
inherited on chromosomes - get a copy from mom and dad

113
Q

HLA inheritance

A

follows typical medelian inheritance

1/4 chance that a sibling will be identical to you and a 50% chance that they would share half of the HLA genes, 1/4 chance of no match

114
Q

HLA class 1 and 2 antigens

A

class 1:
monomer (alpha subunits) associated non-covalently with B2 microglobulin subunit
presents antigenic peptides to CD8+ t cells
expressed by all nucleated cels including endothelium

class2:
heterodimer
presents antigen peptides to CD4+ t cells
restricted expression to APCs or can be induced on endothelium/epithelium

115
Q

functional relevance of HLA

A

required to initiate t cell mediated immune responses against pathogens:

  • polygenic = survival advantage to individual
  • polymorphic = survival advantage to species

transplantations- causes sensitization and can lead to transplant rejections

116
Q

direct allorecognition

A

self T cell recognizes HLA of donor presenting on graft that is presenting donor self antigen

this results in transplant reactions which are more robust compared to pathogen detection

117
Q

lymphocyte crossmatch

A

complement dependent cytotoxicity (CDC) cross match

flow cytometry crossmatch (more sensitive)

both are ways to avoid/minimize HLA antibody mediated rejection

118
Q

virtual crossmatch

A

HLA typing/HLA antibody ID

similar to blood banking

typing for HLA-A,B,C,DRB,DQB,DQA,DPB

Methods:
serological
molecular techniques (sequence specific priming, sequence specific oligonucleotide probe)

119
Q

HLA ID by luminex (solid phase) assay

A

latex bead coated with recombinant HLA

each bead has slightly different fluorescence emission

tells you exactly what the patient has

120
Q

acute rejection

A

types: cellular, antibody mediated, mixed

dependent on t cell stimulation and co-stimulation

first step in allorecognition/activation

second step is effector mechanisms

121
Q

How to minimize acute rejection

A

immunosuppressive agents:

  • T cell depleting agents
  • calcinerurin inhibitors
  • MTOR inhibitors
  • anti-proliferatives
  • corticosteroids
122
Q

typical immunosuppressive therapy for rejection prophlyaxis

A

induction with basiliximab (IL-2 receptor antagonist), if high risk induction with t cell depleting agents, mainly ATG

FK506 (or cyclosporin A for low risk patients)

mycophenolate mofetil (MMF) or myfortic - may switch to rapamycin if rejection occurs

predenisone - taper over time

123
Q

treatment of acute cellular rejection

A

steroids

switch immunosuppressives:
cyclosporin to FK506
MMF/myfortic to rapamycin

ATG

124
Q

acute antibody mediated rejection

A

difficult to treat

treatment options:

  • plasmapheresis
  • intravenous immunoglobulin (IVIG)
  • rituximab - anti-CD20 mAB that depletes B cells but no activity against plasma cells)
  • bortezomib: proteozome inhibitor with activity against plasma cells (still experimental)
125
Q

problems with immunosuppression

A

opportunistic infection
increased risk of neoplasm
nephrotoxicity
tacrolimus - increased incidence of diabetes

Human Organs and Tissues (3 decks)

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