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first aid > First Aid - Hematology > Flashcards

First Aid - Hematology Flashcards

1
Q

Dense granules of platelets contain..

A

ADP and Calcium

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2
Q

Alpha granules of platelets contain…

A

vWF and fibrinogen

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3
Q

Where is 1/3 of platelet pool stored?

A

spleen

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4
Q

Hypersegmented polys =

A

folate/b12 deficiency

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5
Q

increased band cells means…

A

increased myeloid proliferation (in repsonse to things like bacterial infections or CML)

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6
Q

Which cytokine activates macrophages?

A

IFN-gamma

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7
Q

Important macrophage cell marker

A

CD14

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8
Q

Functions of eosinophils

A

Anti-helminthic
Antigen-antibody opsonin phagocytosis
histaminase and arylsulfatase production to limit mast cell degranulation effects

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9
Q

What do basophils secrete to mediate allergic reactions?

A

heparin, histamin, leukotrieneds

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10
Q

Important B-cell markers

A

CD19, CD20

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11
Q

What are all the cells that act as APCs?

A

Macrophages, Dendritic (langerhan cells, B-lymphocytes

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12
Q

Important T-cell markers

A

CD3, CD4, CD8

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13
Q

What is the costimulatory signal necessary for T-cell activation?

A

CD28

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14
Q

What are the markers for T-cell PRECURSORS

A

CD1a; CD2, 3, 4, 5, 7, 8

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15
Q

Which antibody isotype causes hemolytic disease of hte newborn

A

IgG

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16
Q

Hemolytic disease of the newborn is when…

A

Mom has preformed antibodies against a blood type that her new baby has.

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17
Q

What type of antigens are attacked in hemolytic disease of the newborn

A

Rh+ cells

A,B, AB –> usually only by type O mothers, who form IgG rather other bood type moms, who tend to form IgM

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18
Q

What is the hageman factor?

A

Factor XII in the intrinsic pathway

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19
Q

What does vWF act as a carrier protein for?

A

Factor VIII

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20
Q

What is thrombin time?

A

TT = rate of conversion of fibrinogen to fibrin. Different form PTT and PT

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21
Q

Where is Factor VIII synthesized and stored?

A

synthesized in liver; stored in endothelium

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22
Q

How does Vitamin K play into coagulation factors?

A

Vitamin K must be reduced by epoxide reductase before it can act as the cofactor for maturation of coagulation factors 2, 7, 9, 10, C, S.
(epoxide reductase is the enzyme warfarin inhibits

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23
Q

Factor V leiden mutation does what…?

A

makes factor V that is resistant to cleavage/inactivation by Protein C. = procoagulant state.

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24
Q

What does TXA2 do in coagulation?

A

decreases blood flow by vasoconstriction , increases platelet aggregation

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25
Q

What does ADP do in coagulation?

A

induces GP2b/3a expression on platelet surface

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26
Q

What is seen under a crystal violet stain

A

Heinz bodies

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27
Q

What are howell jolly bodies?

A

remnants of nucleus. found in RBCs
supposed to be removed from RBC by splenic macrophages - so if you’re asplenic… womp womp, no howell jolly body removal for you.

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28
Q

What do you think when you see erythroid precursors in liver or spleen?

A

Extramedullary hematopoiesis

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29
Q

What promotes extramedullary hematopoiesis

A

EPO

hyperplastic marrow cell invasion of extramedullary organs

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30
Q

Plummer-Vinson Syndrome

A

Triad of iron deficiency anemia, esophageal webs, atrophic glossitis

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31
Q

koilonhychia (spoon nails)- where do you see it?

A

IRON DEFICIENCy

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32
Q

alpha-thalassemias - Asians vs Africans

A

Asians are Cis

Africans are trans

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33
Q

Alphat thalassemia - all the gene cominations

A

1-2 deletiosn = no anemia
3 = HbH disease (beta tetramers)
4 gene deletions = HbBarts (gamma tetramers) incompatible with life. hydrops fetalis

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34
Q

What is the genetic abnormality with beta thalassemia?

A

mRNA splice site point mutation = mrNA processing screw up

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35
Q

Why is beta thal asmptomatic at birth?

A

HbF for the next 6 months

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36
Q

What is beta thalassemia intermedia?

A

Its beta thal major that happens to have mild clinical presentation

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37
Q

How do beta thalassemics compensate for their messed up hemoglobin?

A

they make HbF (a2g2 for thal major) and HbA2 (a2d2) for thal minor

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38
Q

Special cells in beta thal major

A

target cells, schistocytes

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39
Q

What genetic mutation is beta thal intermedia associated with?

A

kozak sequence = mutaiton tha tprevents mRNA binding to ribosome

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40
Q

Clinical symptom difference between folate and B12 deficeincy

A

Folate deficienty = NO NEUROLOGIC SYMPTOMS

B12 = subacute combined degeneration leads to posterior column, lateral corticospinal and dementia symptoms)

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41
Q

Why folate deficeincy in alcoholics?

A

poor B9 ABSORPTION

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42
Q

What happens to your CBC when you treat B12 deficeincy?

A

give B12 supplement. Early spike in reticulocyes. older reticulocytes are slow to mature because they had a B12 deficient chidlhood. so you have a big proliferaiton of reticulocytes

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43
Q

Alcoholics and B12 vs Folate defiency

A

usually alcoholics dont’ get B12 , they gete B9 deficeincy

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44
Q

old people and B12 deficeincy

A

old people w/ chornic anemia w/o other identifiable causes

Old people = gatric catrophy = low H+ = low release of B!2 from food.

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45
Q

What is haptoglobin?

A

binds free hemoglobin to prevent renal excretion

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46
Q

What happens to haptoglobin in hemolytic anemias?

A

drops because hemolysis produces so much Hb the haptoglobin can’t handle it.

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47
Q

Explain the blood smear appearance of anemai of chronic disease

A

starts off as normocytic but over time you have less and less iron and you become microcytic and hypochromic.

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48
Q

Aplastic anemia presents as…

A

triad of severe anemia, thrombocytopenia and absent stem cells in marrow

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49
Q

Is there splenomegaly in aplastic anemia?

A

no

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50
Q

Marrow tap for aplastic anemia

A

dry. normal cell morphology but hypocellular marrow with fatty infiltration.
low reticulocyte count

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51
Q

Distinction of aplastic anemia from myeloplastic syndromes?

A

Marrow tap is dry in aplastic anemia.

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52
Q

Where are haptoglobin/Hemoglobin complexes cleared?

A

Liver

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53
Q

What is pure RBC aplasia associated with?

A

No RBC but normal WBC and Plateets associated with 1) Thymoma 2) lymphocytic leukemia. Can result from PArvo B19

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54
Q

General principle of inheritance patterns with protein mutations.

A

Structural protein defects = dominant (ankyrin in spherocytosis)
Enzymatic defects = REcessive (G6PD)

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55
Q

INheritance pattern of Hereditary spherocytosis

A

Autosomal dominant

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56
Q

Defect in hereditary spherocytosis

A

ankyrin, band 3, spectrin mutaitons

defective cytoskeleton = loss of plasma membrane = spherocytosis

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57
Q

Clinical findings of hereditary spherocytosis

A

Splenomegaly. Increased risk of aplastic crisis w/ Parvo B19, pigmented gallstones, jaundice and anemia

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58
Q

Diagnostic testing for hereditary spherocytosis

A

positive osmotic fragility test

Increased MCHC

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59
Q

Treatment of hereditary spherocytosis

A

splenectomy - RBCS work find its jsut he spleen keeps clearing them cuz their ugly.

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60
Q

Inheritance pattern of G6PD

A

X-linked recessive

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61
Q

What triggers hemolysis in G6PD?

A

Oxidant stresses like:
Sulfadrugs = sulfonamids, antimalarials, bactrim
infections
Fava beans

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62
Q

Clinical presentation of G6PD

A

Back pain followed by hemoglobinuria a few days later

Jaundice, or could be asymptomatic

63
Q

Labs and smear for G6PD deficeincy

A

Heinz bodies, bite cells, reticulocytosis

decreased haptoglobin

64
Q

Pyruvate kinase deficeincy inheritance pattern

A

autosomal recessive

65
Q

Pathophysiology of pyruvate kinase deficeincy

A

bad pyruvate kinase = low ATP = dead RBC = splenomegaly due to work hypertrophy

66
Q

Clinical presentation of pyruvate kinase deficeincy

A

hemolytic anemia of hte newborn…. as in anemia from destroying RBC when you’re newly born. not antibody mediated??? check with weinstein

67
Q

Whats HbC defect

A

Same as SCA except mutation = Glu to Lys NOT Glu to Val. milder disease than SCA

68
Q

PNH pathophysiology

A

DAF (CD55) and GPI protect RBC from complement damage. It’s deficeincy in this disease.
RBC lysed by complement = anemia

69
Q

Why is PNH calle dparoxysmal nocturanl hemoglobinuria

A

Sleep = shallow breaht = mild acidosis = increased complement = increased lysis of RBC bec/ RBC can’t defend themselves w/ their mutation = hemolysis = peeing blood in the morning rom the hemolysis

70
Q

CLinical presentaiton of PNH

A

triad of hemolytic anemia, pancytopenia and venous thrombosis (including Budd chiari)

71
Q

Labs for PNH

A

CD55/59 negative RBCS

72
Q

Autosplenectomy - you should think of…

A

Sickle cell anemia. REcurrent ischemia and infarction. Almost all SCA adults have this.

73
Q

What is splenic sequestration?

A

This thing with SCA. vasoocclusion of splenic outflow = pooling of blood in spleen = hypovolemia/splenic rupture = medical emergency.
Rarely seen seen in adults bec/ they have autosplenectomized by then

74
Q

What does the spleen look like with autosplenectomy

A

bronw from hemosiderosis. firm and shrunken

75
Q

Crew cut on skull x-ray - you should think off..

A

1) Sickle cell anemias 2) Thalassemia = Marrow expansion for more erythropoiesis.

76
Q

Most common cause of osteomylitis? What about in people with sickle cell anemia?

A 
Normal = Staph aureus
SCA = Salmonella
77
Q

Major complications of Sickle cell DISEASE

A 
aplastic crisis (Parvo B19)
Autosplenectomy (infected by capsuled bacteria)
SPlenic sequestration
Salmonella osteomyelitis
Vaso-cclusive pain
Renal papillary necrosis
78
Q

What are the presentaiton sof vaso-occlusive pain in Sickle cell anemia?

A

Dactylitis (pain in hands)
Acute chest syndrome
Avascular necrosis (of femoral head?)

79
Q

Therapeutic strategy for sickel cell disease

A

Hydroxyurea = increase HbF
Marrow transplant
Gardos-Channel blockers (Ca-dependent K-efflux channels. Keeps ions in the cell to maintain hydration of cell)

80
Q

What physiology/clinical stuf distinguishes sickle cell TRAIT from DISEASE

A

Trait: no sickling (except in renal papilla), no target cells or sickle cells

81
Q

Asplenics are at risk of what?

A

Infection by encapsulated bacteria:
S. Pneumo; Haemophilus Influenza; Neisseria Menigitis; E. Coli; Salmonella, Klebsiella, GBS
SHiNE SKis
relevant to SCA with autosplenectomy

82
Q

Direct vs Indirect Coombs test

A 
Direct = Is there Ig already bound to the RBC?
Indirect = Do you have anti-RBC Igs in your serum?
83
Q

Agglutination in Immune hemolytic anemias – why is it called warm or cold? whats the difference between the two?

A 
Warm = IgG binds in warm central body. 
Cold = IgM binds in cold extremities of body
84
Q

What causes warm agglutin IHA

A

Warm immune hemolytic anemia = SLE, CLL, Drugs (a-methyl dopa, peniccilins/cephalosporins)

85
Q

What causes cold agglutin IHA?

A

Cold immune hemolytic anemia = Mycoplasma, Mononucleosis

86
Q

What causes microangiopathic anemia

A

DIC, TTP/HUS, SLE and malignant hypertension

87
Q

Lab finding sin microangiopathic anemia

A

whatever results form increased Hb in serum

88
Q

Hepcidin does….what?

A

Master regulator of body e Levels. Made in liver and controls ferroportin activity in enterocytes. (Ferroportin = basolateral iron channel in enterocytes)

89
Q

Coarse basophilic stippling

A

Lead poisoning

90
Q

Brutons Lines

A

Blue lead lines in the gums of the tooth

Lead poisoning

91
Q

Clinical appearance of lead poisonign in adults

A

headache, memory loss, weakness, abdominal pain, constipation

92
Q

Why is there no sideroblastic anemia with lead poisoning, acute intermittent porphyria or porphyria cutanea tarda?

A

Because they dont’ inhibit heme synthesis at a step that occurs in the mitochondria. (except lead poisoning which inhibits a mitochondrial step that’s AFTER a cytoplasmic step - ferrochelatase)

93
Q

Affected enzyme in porphyria cutanea tarda

A

Uroporphyrinogen decarboxylase

94
Q

Blood smear appearance with acute intermittent porphyria

A

NORMAL.

95
Q

Why do RBC lose their heme synthesis ability?

A

no mitochondria

96
Q

difference between liver heme and marrow heme?

A

liver heme for CYP450; marrow heme for hemoglobin

97
Q

why do drugs trigger acute intermitten tporphyria attack

A

use up CYP450 for drug metabolism. Liver heme triggers d-ALAS activity in both liver and marrow = d-ALA accumulates

98
Q

Prolonged bleeding after tooth extraction

A

Hemophilia or Von Willebrand’s Disease

99
Q

Prolonged bleeding from venous puncture sites

A

DIC

100
Q

Inheritance of Hemophilia A and B

A

X-linked recessive

101
Q

CLinical presentaiton of hemophilia

A

Macrohemorrhage (hemarthrosis = bleeding into joints; easy bruising) mucocutaneous bleeding

102
Q

When do you get vitamin K deficiency?

A

First week of birth (don’t get it in utero or breast milk)
malabsorptive disease
Liver disease
Broad spectrum antibiotics that kill colonic bacteria (which make vitamin K)

103
Q 
What are the defects in:
Bernard Soulier
Glanzmann's Thrombasthenia
ITP
TTP
A 
Bernard = defect GP1B = poor adhesion
Glanzmann's = defect GP2b3a = poor aggregation
ITP = anti-Gp2b3a Abs = destroyed platelets
TTP = ADAMST13 mutation in vWF metalloprotease = less vWF degradation = too much platelet aggregation and consumption.
104
Q

Difference in bleeding symptoms for coagulative disorders vs platelet disorders

A 
coagulation = macrohemorrhage in large vessels (bleeding into joints, easy bruising) - Hemophilia, DIC, vWF
Platelet disorders = hemorrhage in superficial vessels (petechiae, mucous membrane pleeding) - glanzmans, bernard, ITP, TTP-HUS
105
Q

Pathophysiology of uremic platelet dysfunction

A

uremia from renal failure = elevates plt inhibitory factors in blood = normally removed by kidney or dialysis = REsults in inability to undergo PRIMARY hemostasis. PT/PTT are unaffected

106
Q

Hemolytic URemic Syndrome - platelet effects

A

Shiga toxin causes activation of platelets BUT NO COAGULATION FACTORs systemically

107
Q

Why does vWF disease lead to increased PTT?

A

vWF carriers/protect factor VIII. vWF deficiency = messed up intrinsic pathway

108
Q

Ristocetin is for… what?

A

activtaes Gp1b on platelets to cause adhesion. no adhesions = vWF disease

109
Q

Treatment of vWF

A

DDAVP (desmopressin) = ADH analogue.

FX: vWF release from endothelium. Diuresis. No vasoconstriction (which ADH does) Does not work in severe disease

110
Q

What causes DIC?

A

STOP Making New Thrombi

Sepsis. Trauma, Ob complications, Pancreatitis. Malignancy. Nephrotic syndrome. Transfusion.

111
Q

How does Ob complication cause DIC?

A

dead fetus = placenta releases tissue factor to cause clotting in response to the necrotic tissue = consumes platelets = DIC

112
Q

Labs and Smear for DIC

A

elevated D-dimer (from fibrinogen cleavage)
Decreased fibrinogen
Decreased Factor V and VII
Schistocytes

113
Q

Most common hypercoagulability defect in WHITES

A

Factor V Leiden.

114
Q

Fresh frozen plasma vs Cryoprecipitate

A 
FFP = coagulation factors
Cryoprecipitate = cold soluble precipitates (fibrinogen, Factor 8, 13, vWF)
115
Q

Electrolyte risk with packed RBCs

A

packed blood comes in citrate, which preserves the blood? but chelates Ca = hypocalcemia with transfusions - Clinically appears as parasthesias

116
Q

What is Fresh frozen plasma for?

A

DIC, Cirrhosis, warfarin overdose

117
Q

how to distinguish leukemoid reaction from CML

A

leukemoid rxn = when WBC proliferate as part of hteir normal reaciton to infection.

Both have elevated WBC with left shift, but CML has decreased leukocyte alkaline phosphate. leukemoid reaction has increased

118
Q

Hodgkin’s Lymphoma - age distribution

A

bimodal (30s and older than 50s)

119
Q

Localization of hodgkins vs non-hodgkins

A 
hodgkins = single gorup of nodes. extranodal is rare
non-hodgkins = peripheral nodes with common extranodal invovlement. usually involves B cells (except if of T-cell origin)
120
Q

starry sky

A

burkitt’s lymphoma

121
Q

hstology of burkitts lymphoma

A

medium sized lymphocytes with high proliferation index - starry sky

122
Q

histology of diffuse large b-cell

A

large sized lymphocytes with huge nuclei

123
Q

histology of follicular lymphoma

A

B-cells in follicle center. MANY follicles aggregating that distort normal lymph node architecture

124
Q

Clinical findings of Multiple Myeloma

A

CRAB = hyeprCalcemia; Renal insufficeincy (from infiltration and amyloid deposits), Anemia; Bone lesions/Back pain

125
Q

Age range for multipel myeloma

A

> 40-50 years old

126
Q

Punched out lesions on x-ray

A

multiple myeloma

127
Q

M-spike on electorphoresis

A

multiple myeloma

128
Q

what pathologic processes are associated with multiple myeloma

A 
Primary amyloidosis (accumulation of igG with apple green birefringence)
Increased susceptibility to infection
129
Q

Age ranges of the leukemias

A

ALL = 60
Hairy Cell = Adults
AML = >65
CML = 30-60

130
Q

Neoplasm of Lymphoblasts

A

ALL

131
Q

T-ALL clinical manifestation

A

MEdiastinal mass = dysphagia, SVC syndrome, respiratory symptoms

132
Q

ALL markers

A

TdT+,

CALLA+(CD10) = good prognosis

133
Q

Most common ALL

A

B-ALL = 80% of ALL

No mediastinal mass so no compression syndromes

134
Q

Downsyndrome and ALL

A

Risk is 10-20x higher after 5 years old

135
Q

Neoplasm of naive mature lymphocytes

A

SLL/CLL = lymphocytic lymphocyma/Leukemia

136
Q

Neoplasm of mature B-cells

A

Hairy cell leukemia

137
Q

Markers for Hairy cEll LEukemia

A

TRAP positive

138
Q

Smudge CEll

A

SLL/CLL

139
Q

Clinical findings of SLL/CLL

A

lymphadenopathy, hepatosplenomegaly, anemia

140
Q

pathologic findings of hairy cell leukemia

A

red pulp expansion leading to splenomegaly. The cells are TRAPped in the spleen (TRAP staining)

141
Q

Neoplasm of myeloid blast cells

A

AML

142
Q

Neoplasm that responds to all-trans retinoic acid (ATRA)

A

Promyelocytic Leukemia = M3 subtype of AML

143
Q

CLinical manifestation fo AML

A

Anemia symptoms, Thrombocytopenia symptoms (bleeding from IV puncture sites), Neutropenia symptoms

144
Q

Increased risk before 5 yo in down syndrome

A

M7 subtype of AML = M4Eo AML

145
Q

Cell lineage and Cell differential of CML

A

increased neutrophils, metamyelocytes and basophils (terminally differentiated)
Acceleration = transformation to AML or ALL

146
Q 
t(9;22)
t(8;14/22/2)
t(11;14)
t(14;18)
t(15;17)
A 
t(9;22) = CML (or ALL acc/to Pathoma)
t(8;14/22/2) = Burkitts (c-myc)
t(11;14) = mantle cell
t(14;18) = follicular lymphoma (Bcl-2)
t(15;17) = PML/M3AML (RAR/PML)
147
Q

Genetics and cell signaling in Chromic myeloproliferative disorders?

A

V617F mutation - Jak/Stat mutation leads to hematopoietic signaling except with CML (which has 9;22)

148
Q

Polycythemia vera

A

primary proliferation of Erythroblast = leads to constiutive activity of JAK2 receptors so that it can proliferate w/o EPO stimulation. differs from other polcythemias that are not primary/vera

149
Q

POlcythemia - Appropriate absolute

A

Physiologically compensating for another disease (lugn disease, CHD, high altitude)

150
Q

POlycythemia - inapporpriate absolute

A

Pathologic erythrocytosis secondayr to ectropic EPO (RCC, wilm’s tmor, HCC, anabolic steroids)

151
Q

Relative Polycythemia

A

Increased RBC councentration because odf dehydration

152
Q

Myelofibrosis

A

fibrotic obliteration of boen marrow. Megakaryocytosis can lead to fibroblast proliferation = myelofibrosis

153
Q

Essential Thrombocytosis

A

Abnormla clone of megakaryocyte precursor leads to overproduction of platelets.

154
Q

Hemolytic Uremia Syndrome - presentation

A

Triad of Thrombocytopenia, microangiopathic anemia and renal failure. most common cause of acute renal failure in children

first aid (6 decks)

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