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Internal Medicine HYHO > Heme/ONC > Flashcards

Heme/ONC Flashcards

1
Q

Hemoglobin levels in iron deficiency anemia and thalassemia

A

decreased in both cases

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2
Q

MCV in both IDA and thalassemia

A

decreased in both cases

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3
Q

serum iron in both IDA and thalassemia

A

IDA: decreased

thalassemia: normal

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4
Q

ferritin in both IDA and thalassemia

A

IDA: decreased

thalassemia: normal

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5
Q

Hemoglobin electrophoresis in both IDA and thalassemia

A

IDA: normal

alpha thalassemia: normal

beta thalassemia: increased HbA2 and HbF

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6
Q

what happens if we give iron in IDA and thalassemias?

A

IDA: improvement

Thalassemias: no improvement

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7
Q

RDW (red cell distribution width) in IDA and thalassemias

A

increased in IDA and decreased/normal in thalassemias

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8
Q

blood smear for IDA vs thalasemias

A

IDA: pale RBC (central pallor)

thalassemias: target cells

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9
Q

tx for IDA vs thalassemias

A

IDA: oral iron supplementation

thalassemias: transfusions if severe

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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

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11
Q

IDA is mostly seen in

A

mensturating women despite if they are bleeding heavy or not

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12
Q

what 3 drugs cause constipation

A

iron, aluminum, verapamil

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13
Q

each RBC transfusion contains

A

iron (chelators can be used to treat- deferoxamine)

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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)

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15
Q

B thalassemias

A

1 mutation- IDA symptoms

2 mutations- sick as a kid

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16
Q

b thalassemia has increased what

A

hemoglobin HbA2 (a2/g2) and HbF (a2/y2)

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17
Q

chipmunk facies/skull and hepatosplenomegaly are seen in thalassemias because of

A

Extramedullary hematopoiesis

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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

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19
Q

lab studies for anemia of chronic disease

A

low iron

normal-high ferritin

low TIBC

increased hepcidin

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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

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21
Q

what is multiple myeloma

A

cancer of the plasma cells that increase serum immunoglobulins since plasma cells already secrete immunoglobulins

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22
Q

symptoms of multiple myeloma

A

middle aged patient with back pain and hypercalcemia

immunoglobulins will deposit in the heart and kidney

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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

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24
Q

diagnosis algorithm for multiple myeloma

A
  1. serum electrophoresis which will show increase IgG kappa or lambda light chains - M spike
  2. bone marrow biopsy to confirm showing greater than 10% plasma cells
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25
Q

urinalysis in multiple myeloma will show?

A

bence jones proteinuria which is IgG light chains in the urine

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26
Q

blood smear in multiple myeloma will show what 2 things

A

blue plasma cells with clockface chromatin

OR

rouleaux RBC which is from IgG light chain sticking to RBCs causing them to stack

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27
Q

why can MCV be high in multiple myeloma

A

more immunoglobulins are being carried by the RBC and since less there is more plasma cell and less RBC the RBC enlarge to compensate

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28
Q

what B vitamin deficiencies can be caused by MM

A

B9 and B12

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29
Q

treatment of MM

A

IV bisphosphonates

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30
Q

monocolonal gammopathy of undetermined significance

A

bone marrow biopsy showing less than 10% plasma cells with fatigue and or increased MCV but not hypercalcemia or renal dysfunction

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31
Q

what is waldenstrom macroglobulinemia ?

A

this is a plasma-like clonal expansion/ cancer that causes a IgM M-protein spike

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32
Q

symptoms of waldenstrom macroglobulinemia

A

hyper viscosity: headache, blurry vision, tinnitus, Raynaud phenomenon

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33
Q

what is polycythemia vera

A

a JAK 2 mutation that causes proliferation of hematopoietic stem cells

at least 2 cell lines will be increased with RBCs always high (Hb)

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34
Q

increased Hb can cause what

A

hyper-viscosity syndrome

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35
Q

basophilia can cause

A

puritis after a shower

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36
Q

increased Hb in polycythemia vera suppresses what

A

EPO

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37
Q

treatment of polycythemia vera

A

phlebotomy to treat acute hyper viscosity syndrome like headache or blurry vision

serial phlebotomy and hydroxyurea to decrease symptom recurrence

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38
Q

what is secondary polycythemia

A

an isolated increase in RBC due to increased erythropoietin

WBC and platelets ar normal

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39
Q

what causes increased EPO production

A

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

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40
Q

Prothrombin time reflects what pathway

A

extrinsic

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41
Q

activated partial thromboplastin time reflects what pathway

A

intrinsic

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42
Q

normal PT time is

A

10-15 seconds

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43
Q

normal PTT time is

A

25-40 seconds

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44
Q

normal bleeding time is

A

2-7 minutes

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45
Q

bleeding time is related to?

A

platelets!!!

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46
Q

PT and PTT are related to

A

clotting factors!!!

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47
Q

Immune/idiopathic thrombocytopenic purpura

A

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

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48
Q

platelets in ITP are usually less than?

A

100,000

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49
Q

ITP is typically preceeded by?

A

viral infection (type 2 hypersensitivity)

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50
Q

treatment of ITP

A

steroids then IVIG then splenecetomy in this order

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51
Q

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?

A

acessory spleen

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52
Q

symptoms of ITP

A

brusing

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53
Q

inheritance pattern of vonwilliebrand disease

A

autosomal dominant

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54
Q

what is vonwillibrand disease

A

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

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55
Q

symptoms of vonwilliebrand disease

A

increased bleeding time, increased PTT (intrinsic, heparin), normal platelet count

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56
Q

platelet problems

A

petechiae, brusing, epistaxis

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57
Q

clotting factor problems

A

excessive with tooth extraction, heavy menses,

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58
Q

what cofactor is abnormal in vWD

A

ristocetin cofactor

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59
Q

treatment of vWD

A

desmopressin which releases vWB from weieble pallide bodies

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60
Q

hemophilia A is a deficiency in ?

A

factor VIII (8)

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61
Q

hemophilia B is a deficiency in?

A

factor IX (9)

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62
Q

blood studies in hemophilias?

A

isolated increased in PTT (intrinsic pathway)

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63
Q

symptoms of hemophilias

A

hemarthrosis, neonate excessive bleeding with circumcision

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64
Q

hemophilia A treatment

A

desmopressin and factor VIII replacement

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65
Q

hemophilia B treatment

A

factor IX replacement

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66
Q

How does vitamin K deficiency effect blood studies

A

increased PT and PTT

no affect on bleeding time ! (no platelets are affected)

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67
Q

vitamin K is a cofactor for what?

A

gamma-glutamyl carboxylase

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68
Q

gamma-glutamyl carboxylase activates what factors

A

II, VII, IX, X, C and S

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69
Q

symptoms of vitamin K deficiency

A

bleeding from umbilical stump , retinal hemorrhages

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70
Q

warfarin inhbits what vitamin functions

A

vitamin K

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71
Q

Disseminated intravascular coagulation

A

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

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72
Q

why is fibrinogen decreased in DIC

A

fibrinogen is converted to fibrin with the increased plasmin activity

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73
Q

what is D-dimer high in DIC

A

more fibrin is broken down and d-dimer is a measure of fibrin breakdown products

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74
Q

causes of DIC

A

trauma, sepsis, amniotic fluid embolism, treatment of AML

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75
Q

blood smear of DIC shows

A

schistocytes

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76
Q

hemolytic uremic syndrome triad

A

thrombocytopenia, hemolytic anemia with schistocytes, and renal insufficiency

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77
Q

pathogenesis of HUS

A

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

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78
Q

thrombotic thrombocytopenic purpura is

A

HUS (hemolytic anemia, thrombocytopenia, renal dysfunction) along with fever and neurological symptoms

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79
Q

cause of TTP?

A

antibodies against ADAMTS13 (can no longer breakdown vWF multimers)

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80
Q

treatment of TTP

A

plasmapheresis

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81
Q

sickle cell disease inheritance and mutation

A

autosomal recessive

a glutamic acid to valine missense mutation on the beta chain

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82
Q

why does sickle cell exist?

A

heterozygous advantage (protective against malaria)

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83
Q

sickle cell crisis can present as?

A

abdominal or chest pain

dactylitis (inflammation of the fingers)

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84
Q

sickle cell diagnosis

A

blood smear followed by electrophoresis to detect HbS

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85
Q

sickling occurs when

A

with dehydration and increased acidity

(hydrophobic interactions)

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86
Q

treatment of sickle cell

A

hydroxyurea to increased hemoglobin F and decrease sickling recurrence

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87
Q

myelofibrosis is a mutation in

A

JAK2 (same as polycythemia vera)

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88
Q

symptoms of myelofibrosis

A

fibrosis of the bone marrow

tear-drop-shaped RBCS/poikilocytes , dry tap on bone marrow aspiration

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89
Q

pathogenesis of myelofibrosis

A

Abnormal proliferation of megakaryocytes and granulocytes releases growth factors and cytokines that stimulate collagen deposition in the bone marrow leading to fibrosis

90
Q

essential thrombocythemia

A

JAK 2 mutation that causes increased proliferation of platelets

91
Q

symptoms of essential thrombocythemia

A

hyperviscosity: headache, raynaud phenomenon

platelet count is really really high- higher than 1 million

92
Q

tx of essential thrombocythemia

A

aspirin and plateletpheresis

93
Q

reactive thrombocytosis

A

a triggering event stimulates the production of thrombopoietin and increased platelet production

common triggering event is endocarditis

usually an incidental finding- asymptomatic

94
Q

treatment of reactive thrombocytosis

A

treat underlying infection and give aspirin

95
Q

glanzmann thrombasthenia

A

deficiency in glycoproteins IIb/IIIA on platelets which leads to defective aggregation ( increased bleeding time)

96
Q

bernard- souiler

A

deficiency in glycoprotein Ib on platelets and causes defective adhesion

abnormal ristocetin cofactor

97
Q

systemic lupus erythematous most common presenting symptom is

A

arthritis

98
Q

the malar rash in SLE is what type of hypersensitivity reaction

A

III

99
Q

what blood cell count is down in SLE

A

Platelets (thrombocytopenia)

all can be down but this is HY

100
Q

SLE has an increased risk for?

A

lymphomas

101
Q

what kind of renal dysfunction does SLE cause

A

diffuse proliferative glomerulonephritis

102
Q

SLE in pregnant women can cause

A

Congenital heart block in neonates

103
Q

treatment of SLE flares

A

steroids

104
Q

paroxysmal nocturnal hemoglobinuria is what

A

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
Q

hageman factor is factor number?

A

XII (12)

aka the first clotting factor in the intrinsic pathway

106
Q

what is hageman factor deficiency

A

a def in factor 12 that does not cause symptoms, it has a high PTT

decreased kallikrein

107
Q

what is factor V leiden mutation

A

there is activated protein C resistance (resisting the anticoagulant)

clots and DVTS

Va stays activated

108
Q

what is protein C deficiency

A

the anticoagulant protein C is not working and there are DVTs and clots

there is skin necrosis if the patient recieves warfarin

109
Q

what is the job of Antithrombin III

A

to inactivate IIa, Xa, and IXa

110
Q

what is antithrombin III deficiency

A

the inability to inactivate IIa, IXa, and Xa

111
Q

symptoms of antithrombin III deficiency

A

nephrotic syndrome (antithrombin protein is lost in the urine)

superifical thrombophlemitis, renal vein thrombosis

112
Q

what is antiphospholipid syndrome

A

antibodies against phospholipids that causes an increase in in vitro PTT and paradoxical thromboses

113
Q

cause of antiphospholipid syndrome

A

idiopathic or secondary to SLE

114
Q

what antibodies are in anti-phospholipid syndrome

A

antibodies against B2 microglobulin or cardiolipin

115
Q

antiphospholipid syndrome can present with a false positive for what test

A

VDRL syphillis test

116
Q

usmle symptoms for neutropenia

A

mouth ulcers, fever, sore throat

117
Q

what is neutropenic fever

A

neutropenia with a fever caused by chemo/radiation, viruses

this is a medical emergency: infection but no way to clear it

118
Q

treatment for neutropenic fever?

A

IV broad spectrum antibodies then G-CSF/filgrastim

119
Q

viral induced neutropenia is caused by

A

Parvovirus B19 that can infect myeloid precursors and cause neutropenia

other viruses can make antibodies against neutrophils

120
Q

what is cyclic neutropenia?

A

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
Q

what is aplastic anemia and what are some causes of it?

A

all cell lines are down (decreased RBC, WBC, platelets)

caused by ParvoB19, Hepatitis A, HIV, chemotherapy, fanconi anemia

122
Q

what is pure RBC aplasia and what is it caused by?

A

only RBCs are decreased

caused by Parvo B19, thymoma, MG, diamond-blackfan anemia (triphalangeal thumbs)

123
Q

Spherocytosis inheritance pattern

A

autosomal dominant

124
Q

hereditary spherocytosis is a mutation in ?

A

ankyrin, spectrin or band proteins causing a RBC cell membrane defect changing them from biconcave discs to spherical

125
Q

blood smear of hereditary spherocytosis

A

spherical red blood cells that lack central pallor

126
Q

hereditary spherocytosis causes what kind of anemia

A

normochromic, normocytic

127
Q

hereditary spherocytosis can cause what kind of stones

A

pigment stones because the spleen identifies the abnormal RBCs and increases RBC turnover

128
Q

hereditary spherocytosis has what lab increased

A

mean corpuscular hemoglobin concentration (MCHC)

*decreased hemoglobin (Hb)

129
Q

diagnosis of hereditary spherocytosis is made with?

A

osmotic fragility testing and eosin-5-malimide

130
Q

hereditary spherocytosis has a postive or negative coombs test

A

negative

*coombs tests if there are antibodies against RBCs

131
Q

treatment of hereditary spherocytosis

A

Splenectomy to decrease cell turnover

132
Q

spherocytosis caused by a drug or infection induced hemolytic anemia would have what?

A

antibodies against RBCs and a positive coombs test

133
Q

what is a leukemoid reaction

A

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
Q

what is leukemia

A

a cancer of white blood cells in the blood

135
Q

leukemias are almost always from what cell origin

A

B cell origin

136
Q

acute lymphoblastic leukemia

A

increased leukocyte count >60,000 with predominately lymphocytes

increased lymphoblasts

137
Q

what is an important DDX for acute lymphoblastic leukemia

A

pertusis; will have a reactive lymphocytosis (increased WBC with 90% lymphocytes)

BUT will also have cough , post tussive emesis and or hypoglycemia

138
Q

tumor markers for ALL

A

CD10 and TdT

139
Q

people with what syndrome have an increased risk for ALL

A

down syndrome (excess lymphoblasts)

140
Q

what is chronic lymphocytic leukemia

A

proliferation of mature WBC with 90% lymphocytes will show smudge cells in an old patient

141
Q

diagnosis of CLL

A

quantitative immunoglobulin assay: will show monoclonal immunoglobulin

142
Q

tumor markers for CLL

A

CD5 and CD23

143
Q

CLL can be associated with?

A

warm autoimmune hemolytic anemia (IgG against RBC)

144
Q

what is AML?

A

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
Q

what is the translocation for acute promyelocytic leukemia

A

t(15;17)

146
Q

what is the characteristic blood smear for AML

A

auer rods that are composed of myeloperoxidase which is a blue green heme pigment

147
Q

what is the treatment for acute promyelocytic leukemia

A

all trans retinoid acid which is a vitamin A derivative (matures blasts)

148
Q

treatment of AML can cause a leukemic cell crisis where the Auer rods are released into circulation and can precipitate?

A

DIC

149
Q

what is CML

A

chronic myelogenous leukemia that is caused by a 9;22 translocation (phildelphia chromosome)

bcr-abl tyrosine kinase fusion protein

low ALP

150
Q

treatment of CML

A

imatinib (targets bcr/abl tyrosine kinase)

151
Q

leukemia that is characterized by cytoplasmic projections that stains positive for tartrate-resistant acid phosphatase (TRAP)

A

hairy cell leukemia

152
Q

what is sezary syndrome

A

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
Q

sezary syndrome classically presents as?

A

erythroderma (red skin)

154
Q

what is a lymphoma ?

A

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
Q

lymphomas are almost always of what origin

A

B cell origin

156
Q

lymphomas are characterized by ?

A

hodgkins or non hodgkins

157
Q

what increases the risk for lymphomas

A

EBV, HIV, immunosuppression, autoimmune diseases (SLE)

158
Q

hodgkins lymphoma is characterized by

A

reed-sternberg cells that are CD15/CD30 positive

owl eye appearance

159
Q

symptoms of hodgkins lymphoma

A

painless lateral neck mass, lymphadenopathy, hepatomegaly, mediastinal lymphadenopathy, virchow node, B signs- fever, night sweats, weight loss

160
Q

the nodular sclerosing type of hodgkins lymphoma typically affects who

A

women

161
Q

does leukocyte rich or leukocyte deplete hodgkins lymphoma have a better prognosis? why?

A

rich has a parallel increase in leukocytes to reed sternberg cells giving it a better prognosis

162
Q

burkitt lymphoma translocation

A

8:14 translocation of the c-myc gene

163
Q

what is c-myc

A

a transcription factor

164
Q

presentation of burkitt lymphoma

A

jaw lesion in an african boy, abdominal lesion

165
Q

histology for burkitt lymphoma

A

starry sky which is basophilic cells with translucent macrophages (tingible body)

166
Q

what is the tingible body in burkitt lymphoma

A

the macrophage that eats the lymphamtous B cels undergoing apoptosis

167
Q

follicular lymphoma translocation

A

t (14;18) translocation of the BCL-2 gene

168
Q

what does the BCL-2 gene code for

A

an anti-apoptotic molecule

169
Q

presentation of follicular nonhodgkins lymphoma

A

waxing and waning painless neck mass over 2 years that is indolent in its course

170
Q

what is diffuse large b cell lymphoma

A

the most aggressive NHL

171
Q

mantle cell lymphoma translocation

A

t(11;14) translocation that overexpresses cyclin D (no stopping the cell cycle)

172
Q

what is mucoides fugoides

A

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
Q

what is a postitive coombs test

A

antibodies against RBC

174
Q

what is warm autoimmune hemolytic anemia

A

IgG antibodies against RBC

agglutination of RBC occurs at warm temperatures

occurs with drugs, infections, SLE, CLL, RA

175
Q

what is cold autoimmune hemolytic anemia

A

IgM antibodies against RBC

RBC agglutinate at cold temperatures

seen in mycoplasma pneumonia and CMV mononucleosis

176
Q

infectious mononucleosis is caused by

A

usually EBV but can be CMV

177
Q

EBV invades _ cells and stimulates the immune production of _ cells

A

B cells

CD8+ T cells (attack B cells)- atypical lymphocytes/reactive

178
Q

symptoms of mono

A

fever lymphadenopathy, tonsillar exudate, lack of cough

179
Q

if amoxicillin or penicillin is given to treat EBV it can cause?

A

rash

180
Q

test for mono

A

monospot test

181
Q

following the primary infection of mono there can be recurrent episodes of?

A

extreme fatigue that arise at intervals of months to years

182
Q

what is langerhans cell histiocytosis

A

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
Q

electron microscopy of langerhans histocytosis

A

birbeck granules (tennis raquet shaped) or rod shaped inclusions in the langerhan cell

184
Q

acanthocytes are seen with what pathology

A

liver failure due to heat stroke or hepatitis
or abetalipoproteinemia

acanthocytes (spiky red blood cells)

185
Q

what is heat stroke

A

end organ damage due to hyperthermia (over 104 degrees)

abnormal liver or fenal function tests

186
Q

glucose 6 phosphate dehydrogenase deficiency inheritance

A

X-linked recessive

(most common cause of hemolysis due to an enzyme deficiency)

187
Q

presentation of G6PD deficiency

A

a boy who has jaundice after recieving a drug or having a viral infection

188
Q

what agents can precipiate oxidative damage and exacerbate G6PD deficiency

A

fava beans, primaquine, dapsone, sulfa drugs

189
Q

labs in G6PD

A

increased unconjugated hyperbillirubinemia and LDH

190
Q

RBCs are packed with

A

LDH

191
Q

the enzyme G6PD is necessary to produce what

A

NADPH (protects the RBC from oxidative damage)

192
Q

blood smear findings for G6PD deficiency

A

bite cells and heinz bodies

193
Q

pyruvate kinase deficiency pathogenesis

A

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
Q

B9 and B12 deficiencies cause macrocytosis how

A

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
Q

high MCV as a result of impaired DNA synthesis is called?

A

megaloblastic anemia

196
Q

sideroblastic anemia is a deficiency in?

A

the first step in the heme pathway

succiny coa–> ala synthase

def in : ALA synthetase

197
Q

sideroblastic anemia is the failure to incorporate _ into heme

A

iron

198
Q

blood smear of sideroblastic anemia

A

ringed sideroblasts ( iron forms a ring inside the mitochondria of erythroblasts)

199
Q

lead posioning inihbiits what ( 2 things)

A

ALA dehydratase and ferrochelatase

200
Q

lead posioning leads to a build up of what?

A

ALA

201
Q

signs of lead posioning

A

microcytic anemia, mental decline, wrist drop

202
Q

blood smear of lead poisoning

A

basophilic stippiling which is rRNA precipitates

203
Q

what is the treatment of lead poisoning

A

calcium EDTA, dimercaprol or succimer

204
Q

what is acute intermittent porphyria

A

an autosomal dominant deficiency in prophorbilinogen deaminase and causes a buildup of both prohobilinogen and ALA

205
Q

symptom of acute intermittent porhyria

A

abdominal pain, port wine colored urine

+/- neurological findings

206
Q

what is the treatment of acute intermittent porhyria

A

hematin and glucose

207
Q

what is porphyria cutanea tarda

A

this is a deficiency in uroporhyrinogen decarboxylase that leads to increased urinary uroporhyins

photosensitivity blistering

urine is tea colored/dark

208
Q

intravascular hemolysis

A

lysis of RBC within the bloodstream

billirubin is released into the blood stream

209
Q

labs in intravascualr hemolysis

A

hemoglobinuria

low serum haptoglobin is decreased

210
Q

examples of intravascular hemolysis

A

G6PD def, PNH, HUS, TTP, HELLP, DIC

211
Q

what is extravascular hemolysis

A

phagocytosis and lysis of RBC in the spleen and liver

no hemoglobinuria or low haptoglobin

212
Q

examples of extravascular hemolysis

A

hereditary spherocytosis , thalassemias, warm and cold autoimmune hemolytic anemia

213
Q

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

A

febrile non-hemolytic transfusion reaction

214
Q

how to prevent febrile non-hemolytic tranfusion reaction

A

leukoreduction(remove wbc from the blood before transfusion)

215
Q

what is a hemolytic transfusion reaction

A

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
Q

symptoms of hemolytic tranfusion reaction

A

fever, chills, flank pain within minutes

impeding sense of doom

get antiglobin /coombs test

217
Q

delayed transfusion reaction

A

host antibodies against minor antigens on donors RBC like Rh, kell, duffy

coombs is positive

218
Q

symptoms of delayed transfusion reaction

A

symptoms occur over a course of a week and hemoglobin starts falling

coombs _ and unconjugated bilirubin

219
Q

transfusion associated lung injry (TRALI)

A

bilateral crackles and low O2 sat less than 6 hours after transfusion

neutrophils react to cytokines in the transfused rpoduct

“noncardiogenic pulmonary edema”

220
Q

transfusion associated circulatory overload

A

cardiogenic pulmonary edema

ARDS > 6 hrs

ARDS+ cardiac disease <6 hours

greater than 6 hours after transfusion

get CXR

221
Q

acute graph vs host disease mechanism and symptoms

A

CD8+ T lymphocyte mediated injury

symptoms: within 100 days of hematopietic stem cell transplant

maculopapular rash
profuse watery diarrhea

liver inflammation

222
Q

acute gvhd is diagnoised with and treated how?

A

diagnosed with colonoscopy + biopsy

tx: glucorticoids

Internal Medicine HYHO (3 decks)

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