Block 2 high yield Flashcards
alpha/beta T cells
bind MHC I and II
gamma/delta T cells
bind dirctly w/o MHC
protect mucosal surfaces
T cell
IFN-y
angry mac’s
Th1
like Th1 but more powerful
Th17
Th’s promote healing
Th2
Th’s
help B-cells activate and class switch
Thf
Th’s
IL-10
Tregs
APC — T cell binding
first signal molecules
APC MHC —- TCR (CD8 or CD4)
APC — T cell co-stim
APC B7 (CD 80/86) —- T cell CD28
APC —- T cell
adhesion
APC ICAM 1/3 —– T cell LFA-1
2 general T cell activators
IL-2
IL-15
Th1 activators
IL-12
INF-y
Th2 activator
IL-4
down regulates Th1’s
IL-10
down regulates Th1’s and 2’s
TGF-B
FAS
target cell receptor inducing caspase –> apoptosis
FAS ligand
T-cell molecule –> binds FAS –> apoptosis of target cell
most abundant Ig
crosses placenta
IgG
first, biggest Ig
IgM
B cell membrane Ig….that’s all
IgD
Ig in secretions
IgA
Ig attaches to Mast cells
IgE
IgE mediated hypersensitivity
Type 1
Automimmune Ig mediated hypersensitivity
Type 2
Immune complex mediates hypersensitivity
Type 3
T-cell mediated hypersensitivity
Type 4
No B-cells
X-linked agammaglobulinemia
failure of Ig class switching
CD40 ligand def
or
Activation induced Cytidine deaminase def
failure to produce Ig’s against certain antigens
common variable immunodeficiency
VDJ recombination failure… no BCR or TCR
Omenn Syndrome
failure to produce mature T-cells
X-linked severe combined immunodeficiency
failure of thymus development
DiGeorge Syndrome
CD8/NKs don’t release granules
Hemophagocytic lymphohistiocytosis
point mutation in B-globin chain
Sickle cell
Howell-Jolly bodies
Sickle cell
Pappenheimer bodies
Sickle cell
Can’t make enough a or B globin
Thalassemia
Morphology of thalassemia
hypochromic
microcytic
Basophilic stippling
thalassemia
Demographic for a-thalassemia
Asians, blacks
Demographic for B-thalassemia
Mediterranean
Asian
Black
Bite cells
G6PD deficiency
Heinz bodies
G6PD deficiency
Schistocytes
microangiopathic hemolytic anemia
**severely deformed cells
Triangulocytes
MAHA
microangiopathic hemolytic anemia
Fe absorption OK
…release of Fe screwed up due to overproduction of…
…HEPCIDIN
can’t get Fe into Hgb
Anemia of Chronic Disease
Three labs to differentiate ACD from IDA:
ACD:
- dec TIBC
- inc ferritin
- inc marrow storage Fe
IDA:
- inc TIBC
- dec ferritin
- dec marrow storage Fe
lack of EPO
ESRD
ECHINOCYTES (spiny RBCs)
Anemia of Renal Disease
Pancytopenia
Empty Marrow
usually idiopathic
Aplastic anemia
C4b2a
C3 convertase
Complement proteins that covalently bind bacteria
C4b
C3b
C4b2a3b
C5 convertase
Complement pathway activated by antigen-antibody complexes:
Classical
Complement pathway activated by polysaccharides on microbes:
Mannose-binding lectin pathway
Complement pathway activated by LPS, foreign surfaces, nucleophiles:
Alternative
C1q, C1r, C1s, C4, C2
Classical pathway
MBL
MASP-1
MASP-2
Mannose binding lectin pathway
C3 H20 Factor B Factor D Properdin
Alternative pathway
C5, C6, C7, C8, C9
Terminal lytic pathway
MAC attack (Neisseria)
Ig’s involved in Classical pathway?
IgG (2)
IgM
Protects human cells from C3b binding:
sialic acid
C3bBb
Alternative pathway’s C3-convertase
Stabilizes C3bBb
Properdin
C3bBbC3b
Alternative pathway’s C5-convertase
CD59
Protectin
inhibits binding of C9
Binds C3bBb floating around and dissociates the Bb
Factor H
Uncontrolled complement activation leading to consumption of C4 and C2:
C1 Inh deficiency
**inhibits C1 esterase which cleaves C4/C2
CD35
CR1
Transport of immune complexes by RBC
Transport of immune complexes by RBC
CR1 (CD35) — binds C3b
binds C3d, C3dg, iC3b
on B cells, activated T cells, epithelial cells
increases humoral immunity
high affinity for EBV
CR2 (CD21)
CR3
CR4
cell adhesion
Rh factor refers to which antigen?
D
In massive hemorrhage, transfuse with:
Whole blood
In low hgb, transfuse with:
Red cells
to reduce alloimmunization and allergic rxns, transfuse with:
Leukocyte-reduced Red-cells
Storage of rare blood types:
Frozen Red Cells
In sepsis and neutropenic patients, transfuse:
Granulocytes
In bleeding due to thrombocytopenia, transfuse with:
Platelets
In bleeding due to multiple factor deficiencies, transfuse with:
Fresh Frozen Plasma
low fibrinogen, vW disease, hemophilia A, factor XIII deficiency, transfuse with:
Cryoprecipitate
hemophilia A, transfuse with:
factor VIII
hemophilia B, transfuse with:
factor IX
hypovolemia, hypoproteinemia, transfuse with:
albumin
disease prophylaxis, AI disease, immune deficiency states, transfuse with:
IvIg
Adding antibodies and then anti-anitbody antibodies to patients red cells:
Forward type
adding reagent red cells to patient serum, then adding AHG:
Reverse type
H+ decrease
P-CO2 decrease
Temp decrease
with regards to hgb-O2 binding.
increases affinity
curve shifts left
H+ increase
P-CO2 increase
temp increase
BPG increase
with regards to hgb-O2 binding.
decreased affinity
curve shifts right
benzocaine
methemoglobin
Acites in cirrhosis due to:
reduced protein
oncotic pressure sends fluid out of vessels
defect in RBC cytoskeleton
hereditary spherocytosis
Prevention for hemolytic disease of the newborn:
Rhogam
Tx for jaundice newborn:
phototherapy
Tx in severe HDN:
exchange transfusion
Causes of mature lymphocytosis:
infectious
Bordetella pertussis
transient stress
causes of reactive lymphocytosis
infectious mono
peds viral infx
viral hepatitis
immune disorders
Basophilia
CML
CML
CML
