Heme/ONC Flashcards
(222 cards)
1
Q
Hemoglobin levels in iron deficiency anemia and thalassemia
A
decreased in both cases
2
Q
MCV in both IDA and thalassemia
A
decreased in both cases
3
Q
serum iron in both IDA and thalassemia
A
IDA: decreased
thalassemia: normal
4
Q
ferritin in both IDA and thalassemia
A
IDA: decreased
thalassemia: normal
5
Q
Hemoglobin electrophoresis in both IDA and thalassemia
A
IDA: normal
alpha thalassemia: normal
beta thalassemia: increased HbA2 and HbF
6
Q
what happens if we give iron in IDA and thalassemias?
A
IDA: improvement
Thalassemias: no improvement
7
Q
RDW (red cell distribution width) in IDA and thalassemias
A
increased in IDA and decreased/normal in thalassemias
8
Q
blood smear for IDA vs thalasemias
A
IDA: pale RBC (central pallor)
thalassemias: target cells
9
Q
tx for IDA vs thalassemias
A
IDA: oral iron supplementation
thalassemias: transfusions if severe
10
Q
what is a thalassemia
A
abnormal synthesis of either the a or b globin chain and can present 1 of 2 ways on USMLE
microcytic anemia with normal ferritin + iron
OR
microcytic anemia despite iron supplementation
11
Q
IDA is mostly seen in
A
mensturating women despite if they are bleeding heavy or not
12
Q
what 3 drugs cause constipation
A
iron, aluminum, verapamil
13
Q
each RBC transfusion contains
A
iron (chelators can be used to treat- deferoxamine)
14
Q
A thalassemias
A
1 mutation- asymptomatic
2 mutations- similar to IDA with no improvement with iron supplementation
3 mutations (HBH disease)- sick as a kid
4 mutations (barts disease)- fatal in utero)
15
Q
B thalassemias
A
1 mutation- IDA symptoms
2 mutations- sick as a kid
16
Q
b thalassemia has increased what
A
hemoglobin HbA2 (a2/g2) and HbF (a2/y2)
17
Q
chipmunk facies/skull and hepatosplenomegaly are seen in thalassemias because of
A
Extramedullary hematopoiesis
18
Q
Anemia of chronic disease is caused by
A
chronic conditions that no longer respond to iron, iron is trapped in macrophages and cytokines are released suppressing hematopoiesis
19
Q
lab studies for anemia of chronic disease
A
low iron
normal-high ferritin
low TIBC
increased hepcidin
20
Q
what is the most common cause of anemia of chronic disease and why
A
renal failure because there is cytokine mediated erythropoietin deficiency
21
Q
what is multiple myeloma
A
cancer of the plasma cells that increase serum immunoglobulins since plasma cells already secrete immunoglobulins
22
Q
symptoms of multiple myeloma
A
middle aged patient with back pain and hypercalcemia
immunoglobulins will deposit in the heart and kidney
23
Q
why does hypercalcemia occur in multiple myeloma?
A
the proliferating cancerous plasma cells cause lytic lesions of the bone.
this may present with pathological rib fractures or pepper pot skull
24
Q
diagnosis algorithm for multiple myeloma
A
- serum electrophoresis which will show increase IgG kappa or lambda light chains - M spike
- bone marrow biopsy to confirm showing greater than 10% plasma cells
25
urinalysis in multiple myeloma will show?
bence jones proteinuria which is IgG light chains in the urine
26
blood smear in multiple myeloma will show what 2 things
blue plasma cells with clockface chromatin
OR
rouleaux RBC which is from IgG light chain sticking to RBCs causing them to stack
27
why can MCV be high in multiple myeloma
more immunoglobulins are being carried by the RBC and since less there is more plasma cell and less RBC the RBC enlarge to compensate
28
what B vitamin deficiencies can be caused by MM
B9 and B12
29
treatment of MM
IV bisphosphonates
30
monocolonal gammopathy of undetermined significance
bone marrow biopsy showing less than 10% plasma cells with fatigue and or increased MCV but not hypercalcemia or renal dysfunction
31
what is waldenstrom macroglobulinemia ?
this is a plasma-like clonal expansion/ cancer that causes a IgM M-protein spike
32
symptoms of waldenstrom macroglobulinemia
hyper viscosity: headache, blurry vision, tinnitus, Raynaud phenomenon
33
what is polycythemia vera
a JAK 2 mutation that causes proliferation of hematopoietic stem cells
at least 2 cell lines will be increased with RBCs always high (Hb)
34
increased Hb can cause what
hyper-viscosity syndrome
35
basophilia can cause
puritis after a shower
36
increased Hb in polycythemia vera suppresses what
EPO
37
treatment of polycythemia vera
phlebotomy to treat acute hyper viscosity syndrome like headache or blurry vision
serial phlebotomy and hydroxyurea to decrease symptom recurrence
38
what is secondary polycythemia
an isolated increase in RBC due to increased erythropoietin
WBC and platelets ar normal
39
what causes increased EPO production
lung diseases with low O2 in the arteries which is sensed by the kidneys to make EPO
renal cell carcinoma can secrete EPO and PTHrp
exogenous administration of EPO
40
Prothrombin time reflects what pathway
extrinsic
41
activated partial thromboplastin time reflects what pathway
intrinsic
42
normal PT time is
10-15 seconds
43
normal PTT time is
25-40 seconds
44
normal bleeding time is
2-7 minutes
45
bleeding time is related to?
platelets!!!
46
PT and PTT are related to
clotting factors!!!
47
Immune/idiopathic thrombocytopenic purpura
antibodies against glycoproteins IIb/IIIa on platelets that causes a decreased number of platelets and increased bleeding time
no change to PT and PTT because clotting factors are not affected
48
platelets in ITP are usually less than?
100,000
49
ITP is typically preceeded by?
viral infection (type 2 hypersensitivity)
50
treatment of ITP
steroids then IVIG then splenecetomy in this order
51
if a splenectomy is preformed in a patient with ITP, platelets return to normal within 6 months then start to fall what is the cause?
acessory spleen
52
symptoms of ITP
brusing
53
inheritance pattern of vonwilliebrand disease
autosomal dominant
54
what is vonwillibrand disease
typically vWF causes platelet adhesion by binding glycoprotein Ib to vascular endothelium and collagen
a disruption causes decreased platelet adhesion and decreased stabilization of factor 8
55
symptoms of vonwilliebrand disease
increased bleeding time, increased PTT (intrinsic, heparin), normal platelet count
56
platelet problems
petechiae, brusing, epistaxis
57
clotting factor problems
excessive with tooth extraction, heavy menses,
58
what cofactor is abnormal in vWD
ristocetin cofactor
59
treatment of vWD
desmopressin which releases vWB from weieble pallide bodies
60
hemophilia A is a deficiency in ?
factor VIII (8)
61
hemophilia B is a deficiency in?
factor IX (9)
62
blood studies in hemophilias?
isolated increased in PTT (intrinsic pathway)
63
symptoms of hemophilias
hemarthrosis, neonate excessive bleeding with circumcision
64
hemophilia A treatment
desmopressin and factor VIII replacement
65
hemophilia B treatment
factor IX replacement
66
How does vitamin K deficiency effect blood studies
increased PT and PTT
no affect on bleeding time ! (no platelets are affected)
67
vitamin K is a cofactor for what?
gamma-glutamyl carboxylase
68
gamma-glutamyl carboxylase activates what factors
II, VII, IX, X, C and S
69
symptoms of vitamin K deficiency
bleeding from umbilical stump , retinal hemorrhages
70
warfarin inhbits what vitamin functions
vitamin K
71
Disseminated intravascular coagulation
consumption of both platelets and clotting factors leading to an increase in bleeding time, PT, PTT, d-dimer, and plasmin activity
decrease in clotting factors, fibrinogen, and platelets
72
why is fibrinogen decreased in DIC
fibrinogen is converted to fibrin with the increased plasmin activity
73
what is D-dimer high in DIC
more fibrin is broken down and d-dimer is a measure of fibrin breakdown products
74
causes of DIC
trauma, sepsis, amniotic fluid embolism, treatment of AML
75
blood smear of DIC shows
schistocytes
76
hemolytic uremic syndrome triad
thrombocytopenia, hemolytic anemia with schistocytes, and renal insufficiency
77
pathogenesis of HUS
ecoli and shigella secrete toxins that cause inflammation of the renal vasculature and inactivate ADAMTS13 protein which leads to big bulky von willebrand multimers. The aggregates of platelets attached to the big vWF shear rbcs as they pass by leading to schistocytes
78
thrombotic thrombocytopenic purpura is
HUS (hemolytic anemia, thrombocytopenia, renal dysfunction) along with fever and neurological symptoms
79
cause of TTP?
antibodies against ADAMTS13 (can no longer breakdown vWF multimers)
80
treatment of TTP
plasmapheresis
81
sickle cell disease inheritance and mutation
autosomal recessive
a glutamic acid to valine missense mutation on the beta chain
82
why does sickle cell exist?
heterozygous advantage (protective against malaria)
83
sickle cell crisis can present as?
abdominal or chest pain
dactylitis (inflammation of the fingers)
84
sickle cell diagnosis
blood smear followed by electrophoresis to detect HbS
85
sickling occurs when
with dehydration and increased acidity
(hydrophobic interactions)
86
treatment of sickle cell
hydroxyurea to increased hemoglobin F and decrease sickling recurrence
87
myelofibrosis is a mutation in
JAK2 (same as polycythemia vera)
88
symptoms of myelofibrosis
fibrosis of the bone marrow
tear-drop-shaped RBCS/poikilocytes , dry tap on bone marrow aspiration
89
pathogenesis of myelofibrosis
Abnormal proliferation of megakaryocytes and granulocytes releases growth factors and cytokines that stimulate collagen deposition in the bone marrow leading to fibrosis
90
essential thrombocythemia
JAK 2 mutation that causes increased proliferation of platelets
91
symptoms of essential thrombocythemia
hyperviscosity: headache, raynaud phenomenon
platelet count is really really high- higher than 1 million
92
tx of essential thrombocythemia
aspirin and plateletpheresis
93
reactive thrombocytosis
a triggering event stimulates the production of thrombopoietin and increased platelet production
common triggering event is endocarditis
usually an incidental finding- asymptomatic
94
treatment of reactive thrombocytosis
treat underlying infection and give aspirin
95
glanzmann thrombasthenia
deficiency in glycoproteins IIb/IIIA on platelets which leads to defective aggregation ( increased bleeding time)
96
bernard- souiler
deficiency in glycoprotein Ib on platelets and causes defective adhesion
abnormal ristocetin cofactor
97
systemic lupus erythematous most common presenting symptom is
arthritis
98
the malar rash in SLE is what type of hypersensitivity reaction
III
99
what blood cell count is down in SLE
Platelets (thrombocytopenia)
all can be down but this is HY
100
SLE has an increased risk for?
lymphomas
101
what kind of renal dysfunction does SLE cause
diffuse proliferative glomerulonephritis
102
SLE in pregnant women can cause
Congenital heart block in neonates
103
treatment of SLE flares
steroids
104
paroxysmal nocturnal hemoglobinuria is what
increased complement mediated hemolysis
the deficiency of CD55 and CD59 which are GPI anchors can no longer protect RBCs from complement mediated breakdown
complement activity is highest at night--> will present with red urine in the morning
105
hageman factor is factor number?
XII (12)
aka the first clotting factor in the intrinsic pathway
106
what is hageman factor deficiency
a def in factor 12 that does not cause symptoms, it has a high PTT
decreased kallikrein
107
what is factor V leiden mutation
there is activated protein C resistance (resisting the anticoagulant)
clots and DVTS
Va stays activated
108
what is protein C deficiency
the anticoagulant protein C is not working and there are DVTs and clots
there is skin necrosis if the patient recieves warfarin
109
what is the job of Antithrombin III
to inactivate IIa, Xa, and IXa
110
what is antithrombin III deficiency
the inability to inactivate IIa, IXa, and Xa
111
symptoms of antithrombin III deficiency
nephrotic syndrome (antithrombin protein is lost in the urine)
superifical thrombophlemitis, renal vein thrombosis
112
what is antiphospholipid syndrome
antibodies against phospholipids that causes an increase in in vitro PTT and paradoxical thromboses
113
cause of antiphospholipid syndrome
idiopathic or secondary to SLE
114
what antibodies are in anti-phospholipid syndrome
antibodies against B2 microglobulin or cardiolipin
115
antiphospholipid syndrome can present with a false positive for what test
VDRL syphillis test
116
usmle symptoms for neutropenia
mouth ulcers, fever, sore throat
117
what is neutropenic fever
neutropenia with a fever caused by chemo/radiation, viruses
this is a medical emergency: infection but no way to clear it
118
treatment for neutropenic fever?
IV broad spectrum antibodies then G-CSF/filgrastim
119
viral induced neutropenia is caused by
Parvovirus B19 that can infect myeloid precursors and cause neutropenia
other viruses can make antibodies against neutrophils
120
what is cyclic neutropenia?
this is a gene mutation that causes episodes of fever, mouth ulcers in a kid 1-3 years of age
usually occurs every 21 days
121
what is aplastic anemia and what are some causes of it?
all cell lines are down (decreased RBC, WBC, platelets)
caused by ParvoB19, Hepatitis A, HIV, chemotherapy, fanconi anemia
122
what is pure RBC aplasia and what is it caused by?
only RBCs are decreased
caused by Parvo B19, thymoma, MG, diamond-blackfan anemia (triphalangeal thumbs)
123
Spherocytosis inheritance pattern
autosomal dominant
124
hereditary spherocytosis is a mutation in ?
ankyrin, spectrin or band proteins causing a RBC cell membrane defect changing them from biconcave discs to spherical
125
blood smear of hereditary spherocytosis
spherical red blood cells that lack central pallor
126
hereditary spherocytosis causes what kind of anemia
normochromic, normocytic
127
hereditary spherocytosis can cause what kind of stones
pigment stones because the spleen identifies the abnormal RBCs and increases RBC turnover
128
hereditary spherocytosis has what lab increased
mean corpuscular hemoglobin concentration (MCHC)
*decreased hemoglobin (Hb)
129
diagnosis of hereditary spherocytosis is made with?
osmotic fragility testing and eosin-5-malimide
130
hereditary spherocytosis has a postive or negative coombs test
negative
*coombs tests if there are antibodies against RBCs
131
treatment of hereditary spherocytosis
Splenectomy to decrease cell turnover
132
spherocytosis caused by a drug or infection induced hemolytic anemia would have what?
antibodies against RBCs and a positive coombs test
133
what is a leukemoid reaction
an exaggerated response to infection where the WBCs skyrocket and can resemble leukemia.
infection (like UTI) + WBC greater than 30,000 + neutrophils on blood smear + ALP is elevated
neutrophilia on labs (reactive granulocytosis)
134
what is leukemia
a cancer of white blood cells in the blood
135
leukemias are almost always from what cell origin
B cell origin
136
acute lymphoblastic leukemia
increased leukocyte count >60,000 with predominately lymphocytes
increased lymphoblasts
137
what is an important DDX for acute lymphoblastic leukemia
pertusis; will have a reactive lymphocytosis (increased WBC with 90% lymphocytes)
BUT will also have cough , post tussive emesis and or hypoglycemia
138
tumor markers for ALL
CD10 and TdT
139
people with what syndrome have an increased risk for ALL
down syndrome (excess lymphoblasts)
140
what is chronic lymphocytic leukemia
proliferation of mature WBC with 90% lymphocytes will show smudge cells in an old patient
141
diagnosis of CLL
quantitative immunoglobulin assay: will show monoclonal immunoglobulin
142
tumor markers for CLL
CD5 and CD23
143
CLL can be associated with?
warm autoimmune hemolytic anemia (IgG against RBC)
144
what is AML?
Acute myeloblastic lukemia that has an increae in myeloblasts (30% blasts)
acute promyelocytic leukemia is a subtype of AML that has a t(15:17 translocation)
145
what is the translocation for acute promyelocytic leukemia
t(15;17)
146
what is the characteristic blood smear for AML
auer rods that are composed of myeloperoxidase which is a blue green heme pigment
147
what is the treatment for acute promyelocytic leukemia
all trans retinoid acid which is a vitamin A derivative (matures blasts)
148
treatment of AML can cause a leukemic cell crisis where the Auer rods are released into circulation and can precipitate?
DIC
149
what is CML
chronic myelogenous leukemia that is caused by a 9;22 translocation (phildelphia chromosome)
bcr-abl tyrosine kinase fusion protein
low ALP
150
treatment of CML
imatinib (targets bcr/abl tyrosine kinase)
151
leukemia that is characterized by cytoplasmic projections that stains positive for tartrate-resistant acid phosphatase (TRAP)
hairy cell leukemia
152
what is sezary syndrome
a cutaneous T cell lymphoma that extends to the blood as a T cell leukemia
caused by the T-cell lymphotropic virus
cerebriform shaped T cells in the blood stream
153
sezary syndrome classically presents as?
erythroderma (red skin)
154
what is a lymphoma ?
cancer of the lymphatic system that it can start in the lymph nodes but be present in other areas of the lymphatic system like the spleen and the bone marrow
155
lymphomas are almost always of what origin
B cell origin
156
lymphomas are characterized by ?
hodgkins or non hodgkins
157
what increases the risk for lymphomas
EBV, HIV, immunosuppression, autoimmune diseases (SLE)
158
hodgkins lymphoma is characterized by
reed-sternberg cells that are CD15/CD30 positive
owl eye appearance
159
symptoms of hodgkins lymphoma
painless lateral neck mass, lymphadenopathy, hepatomegaly, mediastinal lymphadenopathy, virchow node, B signs- fever, night sweats, weight loss
160
the nodular sclerosing type of hodgkins lymphoma typically affects who
women
161
does leukocyte rich or leukocyte deplete hodgkins lymphoma have a better prognosis? why?
rich has a parallel increase in leukocytes to reed sternberg cells giving it a better prognosis
162
burkitt lymphoma translocation
8:14 translocation of the c-myc gene
163
what is c-myc
a transcription factor
164
presentation of burkitt lymphoma
jaw lesion in an african boy, abdominal lesion
165
histology for burkitt lymphoma
starry sky which is basophilic cells with translucent macrophages (tingible body)
166
what is the tingible body in burkitt lymphoma
the macrophage that eats the lymphamtous B cels undergoing apoptosis
167
follicular lymphoma translocation
t (14;18) translocation of the BCL-2 gene
168
what does the BCL-2 gene code for
an anti-apoptotic molecule
169
presentation of follicular nonhodgkins lymphoma
waxing and waning painless neck mass over 2 years that is indolent in its course
170
what is diffuse large b cell lymphoma
the most aggressive NHL
171
mantle cell lymphoma translocation
t(11;14) translocation that overexpresses cyclin D (no stopping the cell cycle)
172
what is mucoides fugoides
cutaenous T-cell lymphoma that has cerebreform shaped cells
presents as a skin rash
when it goes to the blood it is known as sezary syndrome
173
what is a postitive coombs test
antibodies against RBC
174
what is warm autoimmune hemolytic anemia
IgG antibodies against RBC
agglutination of RBC occurs at warm temperatures
occurs with drugs, infections, SLE, CLL, RA
175
what is cold autoimmune hemolytic anemia
IgM antibodies against RBC
RBC agglutinate at cold temperatures
seen in mycoplasma pneumonia and CMV mononucleosis
176
infectious mononucleosis is caused by
usually EBV but can be CMV
177
EBV invades _ cells and stimulates the immune production of _ cells
B cells
CD8+ T cells (attack B cells)- atypical lymphocytes/reactive
178
symptoms of mono
fever lymphadenopathy, tonsillar exudate, lack of cough
179
if amoxicillin or penicillin is given to treat EBV it can cause?
rash
180
test for mono
monospot test
181
following the primary infection of mono there can be recurrent episodes of?
extreme fatigue that arise at intervals of months to years
182
what is langerhans cell histiocytosis
an overproduction of langerhans aka dendritic cells
these are antigen presenting cells that takes antigen to the lymph nodes and presents it to CD4+ cells
with an overproduction of the dendritic cells in bone it causes lytic lesions most commonly the skull
183
electron microscopy of langerhans histocytosis
birbeck granules (tennis raquet shaped) or rod shaped inclusions in the langerhan cell
184
acanthocytes are seen with what pathology
liver failure due to heat stroke or hepatitis
or abetalipoproteinemia
acanthocytes (spiky red blood cells)
185
what is heat stroke
end organ damage due to hyperthermia (over 104 degrees)
abnormal liver or fenal function tests
186
glucose 6 phosphate dehydrogenase deficiency inheritance
X-linked recessive
(most common cause of hemolysis due to an enzyme deficiency)
187
presentation of G6PD deficiency
a boy who has jaundice after recieving a drug or having a viral infection
188
what agents can precipiate oxidative damage and exacerbate G6PD deficiency
fava beans, primaquine, dapsone, sulfa drugs
189
labs in G6PD
increased unconjugated hyperbillirubinemia and LDH
190
RBCs are packed with
LDH
191
the enzyme G6PD is necessary to produce what
NADPH (protects the RBC from oxidative damage)
192
blood smear findings for G6PD deficiency
bite cells and heinz bodies
193
pyruvate kinase deficiency pathogenesis
decreased ATP production and RBC ATPase pumps, this causes less Na to be pumped out of the RBC, water enters the RBC and causes it to swell and burst
194
B9 and B12 deficiencies cause macrocytosis how
these deficiencies both lead to impaired DNA synthesis causing the RBC to stay in the bone marrow longer and allowing them to grow larger and larger
nuclear lobes are also created in neutrophils causing hypersegmented neutrophils
195
high MCV as a result of impaired DNA synthesis is called?
megaloblastic anemia
196
sideroblastic anemia is a deficiency in?
the first step in the heme pathway
succiny coa--> ala synthase
def in : ALA synthetase
197
sideroblastic anemia is the failure to incorporate _ into heme
iron
198
blood smear of sideroblastic anemia
ringed sideroblasts ( iron forms a ring inside the mitochondria of erythroblasts)
199
lead posioning inihbiits what ( 2 things)
ALA dehydratase and ferrochelatase
200
lead posioning leads to a build up of what?
ALA
201
signs of lead posioning
microcytic anemia, mental decline, wrist drop
202
blood smear of lead poisoning
basophilic stippiling which is rRNA precipitates
203
what is the treatment of lead poisoning
calcium EDTA, dimercaprol or succimer
204
what is acute intermittent porphyria
an autosomal dominant deficiency in prophorbilinogen deaminase and causes a buildup of both prohobilinogen and ALA
205
symptom of acute intermittent porhyria
abdominal pain, port wine colored urine
+/- neurological findings
206
what is the treatment of acute intermittent porhyria
hematin and glucose
207
what is porphyria cutanea tarda
this is a deficiency in uroporhyrinogen decarboxylase that leads to increased urinary uroporhyins
photosensitivity blistering
urine is tea colored/dark
208
intravascular hemolysis
lysis of RBC within the bloodstream
billirubin is released into the blood stream
209
labs in intravascualr hemolysis
hemoglobinuria
low serum haptoglobin is decreased
210
examples of intravascular hemolysis
G6PD def, PNH, HUS, TTP, HELLP, DIC
211
what is extravascular hemolysis
phagocytosis and lysis of RBC in the spleen and liver
no hemoglobinuria or low haptoglobin
212
examples of extravascular hemolysis
hereditary spherocytosis , thalassemias, warm and cold autoimmune hemolytic anemia
213
what type of transfusion reaction is this: donor WBC scome in contact with antibodies in the recipients plasma and cytokines are released from the donor WBCs causing fever and chills?- within 2 hours
coombs test is negative
febrile non-hemolytic transfusion reaction
214
how to prevent febrile non-hemolytic tranfusion reaction
leukoreduction(remove wbc from the blood before transfusion)
215
what is a hemolytic transfusion reaction
host antibodies attack ABO antigens on donor RBC
this causes an intravascular hemolysis with release of hemoglobin into the blood stream
increased LDH, low haptoglobin
216
symptoms of hemolytic tranfusion reaction
fever, chills, flank pain within minutes
impeding sense of doom
get antiglobin /coombs test
217
delayed transfusion reaction
host antibodies against minor antigens on donors RBC like Rh, kell, duffy
coombs is positive
218
symptoms of delayed transfusion reaction
symptoms occur over a course of a week and hemoglobin starts falling
coombs _ and unconjugated bilirubin
219
transfusion associated lung injry (TRALI)
bilateral crackles and low O2 sat less than 6 hours after transfusion
neutrophils react to cytokines in the transfused rpoduct
"noncardiogenic pulmonary edema"
220
transfusion associated circulatory overload
cardiogenic pulmonary edema
ARDS > 6 hrs
ARDS+ cardiac disease <6 hours
greater than 6 hours after transfusion
get CXR
221
acute graph vs host disease mechanism and symptoms
CD8+ T lymphocyte mediated injury
symptoms: within 100 days of hematopietic stem cell transplant
maculopapular rash
profuse watery diarrhea
liver inflammation
222
acute gvhd is diagnoised with and treated how?
diagnosed with colonoscopy + biopsy
tx: glucorticoids
