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Final review for Step 2 Ck > Heme/Onc > Flashcards

Heme/Onc Flashcards

1
Q

What lab does Vit K/ warfarin affect

A

Vit K and warfarin act on 2, 7, 9, 10 C, S and because they have 7 affected the increase PT first followed by PTT (factor 2 and 10)

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2
Q

How is warfarin toxicity reversed

A

reverse warfarin toxicity with FFP

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3
Q

Why is there skin necrosis sometimes with warfarin?

A

Protein C and S and anticoagulants that can be deficient and lead to paradoxical hypercoagulant state because they deplete first and can no longer break down factor VIII and V

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4
Q

What is unique about apixaban and riveroxaban

A

XAaban are Xa direct inhibitors (remember that heparin (-aparins/agrobans) are II a) and do not need lab monitoring, use in poor compliance with Warfarin INR patients

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5
Q

What is used in place of Warfarin with poor INR compliance?

A

Axaban/apixaban 10a direct inhibitors that don’t need PT and PTT monitoring

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6
Q

Diff between thrombolytics (TPA), warfarin, aspirin and IVC filter use?

A

Warfarin is long term anticoagulation (as are Xa axabans) and TPA is for acute thrombolysis. IVC filters are when refractory to medical treatment or haad a recent bleed and aspirin is not sufficient for DVT/afib anticoagulation

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7
Q

When to use IVC filter

A

Use IVC filter with C/I to anticoagulation like a recent bleed or refractory to medical therapy thrombosis

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8
Q

How is warfarin reversed

A

FFP and vitamin K, FFP actutely

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9
Q

What is a classic feature of hemophilia

A

classic feature of hemophilia is repeated hemarthroses, they bump themselves on corners and get huge joint effusions or purpura disproportionate to force

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10
Q

What is increased in hemophilia for coag studies?

A

PTT is increased, PT is fine

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11
Q

FIrst step in suspected hemophilia?

A

DO a mixing study in suspected hemophilia, which will correct it, Then look at specific factors

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12
Q

what is diff between cryoprecipitate and FFP?

A

cryo = VIII and fibrinogen and FFP = vit K derivatives

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13
Q

Hemophilia type A (VIII) tx?

A

DDAVP for VIII release from endothelial cells

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14
Q

Most common inherited bleeding disorder?

A

vWD is AD and most common inherited bleeding disorder

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15
Q

What factor is low in vWF

A

AD, most common bleeding disorder has low VIII and high PTT and low BT due to low vWF aglgutination

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16
Q

Dx of vWD

A

Ristocetein agglutination assay

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17
Q

Tx of vWD

A

DDAVP helps release VIII

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18
Q

What are the causes of hyperhomocysetiein?

A

deficiency in cystathonine B synthase which uses B6 as a cofactor and B12 which makes it methionine

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19
Q

What is tx of hyperhomocysteine?

A

B6 and B12 and anticoagulate

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20
Q

how does HIT present sometimes?

A

HIT may only present with heparin induction then platelet reduction >50% of the normal

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21
Q

What are the two types of HIT

A

HIT 1 happens first and is non immune and occurs 1-4d after and less severe than HIT2 occuring 5-10d after and is due to antibodies of PF4

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22
Q

how is HIT diagnosed?

A

Serotonin release asssay and PF4 ab

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23
Q

How is HIT 1 treated

A

Just due to temporary effect of heparin on plt and they recover just observe

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24
Q

how is HIT2 treated

A

extreme drop on platelets associated with thrombosis stop all heparin containing products

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25
Q

What is done in HIT2

A

STOP ANY HEPARIN PRODUCT and start non-immune derivatives like argotraban

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26
Q

HIT1 tx?

A

Observe, PLT stay above 100K and rebound versus HIT2 when they fall to 50K from platelet consumption and thrombosis

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27
Q

DIC differentiation from liver levels

A

VIII is made in endothelium and not depressed in liver disease, but it used up in DIC which has high PT, PTT, BT and low fibrinogen and high D-dimer with low platelets

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28
Q

What does smear show in DIC

A

in DIC smear shows schistocytes

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29
Q

When are shistocytes seen

A

schistocytes are due to microangiopathic hemolytic anemia from platelet and fribin mesh and are in HUS, TTP and DIC

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30
Q

Does ITP have schitocyte?

A

NO, ITP has normal RBC morphology, but TTP has shistocytes

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31
Q

what is the physiologic difference between ITP and TTP

A

TTP is due to ADAMSTS13 mutation which large multimers of wVF soak up platelets and these deposit all over the body. This causes microthrombi that cause systemic symptoms and then destroy RBC as they go through vasculature. This is why TTP has renal s/s, neuro s/s and fever while ITP does not. ITP is due to igG antibody to platelets and causes megakaryocytes to be large, with a normal RBC morphology because there is no fibrin mesh or deposits anywhere to destroy them, it is just IgG mediated disease. Theese patients are often asyx and need a screen for HIV and HCV as there is a high association

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32
Q

What diseases is ITP associated with

A

ITP is associated with HIV and HCV

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33
Q

How is TTP treated?

A

Treat TTP with plasma exchange to get rid of the vWF multimers and do NOT transfuse platelets as this makes it worse and puts more platelets to be consumed by multimers and worsens disease

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34
Q

what is CI in TTP?

A

In TTP , platelet transfusion is CI, just give plasma transfusion acutely

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35
Q

How is ITP treated

A

Screen for HIV and HCV and then give steroids if plt are below 30K, otherwise not treatment, secdon line is rituximab and splenectomy

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36
Q

Morphology of RBC in ITP?

A

ITP has normal RBC and large megas

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37
Q

RBC in TTP

A

Shcistocytes

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38
Q

Tx of TTP

A

Plasma change and NO plt

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39
Q

Tx of ITP

A

steroids (immune mediated) if below 30K plt

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40
Q

What is high in anemia of chronic disease?

A

Everything in anemia of chronic disease is low except for ferritin which is an acute phase reactant

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41
Q

What are the microcytic (common) anemias?

A

TICS : thal, iron, chronic disease, sideroblastic

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42
Q

What type of anemia is thal

A

thal is microctyic

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43
Q

what type of anemia is chronic disease

A

Anemia of chronic disease is microcytic

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44
Q

What type of anemia is sideroblastic?

A

In sideroblastic anemia, hemoglobins cannot be made so RBCs keep dividing to main concentration, it is microcytic

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45
Q

Why is ferritin normal or high in chronic disease a microcytic anemia

A

ferritin is normal or high in chronic disease because it is an acute phase reactant

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46
Q

What are the levels of ferritin and iron in thalassemia?

A

Ferritin is high and iron is high, it needs to store more, TIBC is inverse of iron because more transferrin is bound and is low

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47
Q

Can alcoholism cause macrocytic sideroblastic anemia?

A

yes, alcohol can cause macrocytic sideroblastic anemia with stippling, even though sideroblastic is usually microcytic

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48
Q

What are two common causes of sideroblastic anemia

A

Alcohol causes basophilic stippling because it is a mitochondrial poison and prevents hemoglobin synthesis

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49
Q

Alcoholic with basophilic stippling, cause?

A

Alcohol is a cause of macrocytic anemia that can cause sideroblasts from mitochondrial poinson

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50
Q

What other deficiency can cause sideroblastic anemia other than too much lead or alcohol

A

B6 deficiency it is cofactor for the first factor in heme synthesis

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51
Q

where does heme synth occur?

A

Mitochondria where alcohol poisons which is why it causes sideroblasts and macrocytic anemia

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52
Q

MCC of iron def anemia?

A

Gi blood loss (get scope) if not on NSAIDS

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53
Q

What is MCHC mean

A

MCHC is if it is hypochromic or not

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54
Q

What lab value represents hypo/hyperchromia?

A

MCHC is chromia

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55
Q

When MCV and MCHC are low first step?

A

MCV and MCHC mean microcytic, hypochromic if both low. The first step for microcytic hypochromic anemia is always iron study and CBC

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56
Q

How is anemia of chronic disease treated?

A

Anemia of chronic disease is treated by treating the underlying disorder – I.e MTX in RA

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57
Q

What is unique about RDW in iron def anemia

A

In iron def anemia RDW is increased

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58
Q

What disease is characteristically hyperchromic

A

HIGH MCHC means hyperchromia = spherocytes = hereditary spheroctyosis

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59
Q

What are the levels of MCV, MCHC, Fe, Transferrin sat, ferritin, TIBC in anemia of chornic disease

A

In anemia of chronic disease, everything is low or normal except ferritin which can be elevated as it is an acute phase reactant and also stores iron in cells which is sequestered

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60
Q

Sideroblastic anemia is microcytic, what is the iron level?

A

Sideroblastic anemia is microcytic because HEMOGLOBIN cannot be made, iron cannot be inserted so iron is high, which means ferritin is high and TIBC is low because iron is high

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61
Q

MCC of sideroblastic anemia?

A

Alcohol is the mCC of sideroblastic anemia

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62
Q

What is the iron level in sideroblastic anemia?

A

Iron is high, ferritin is high, TIBC is low or reduced

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63
Q

Other than liver disease and neuropathy, what else can INH cause

A

INH interferes with all things B6

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64
Q

Common causes sideroblasts

A

Lead, alc (MCC), B6 def

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65
Q

What are two huge, odd key syx for tip off of B12 def for macrocytic anemia

A

Glossitis is associated with b12 deficiency, as is Crohn’s or any gastric resection (stomach = intrinsic factor) ileum = absorption

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66
Q

Who gets B12 def? (diet)

A

Vegans and vegetarians

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67
Q

What is diff in syx / labs betwee folic and b12?

A

Folic def do NOT get the neuro syx

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68
Q

A person who is alcoholic has megaloblastic anemia and is started on folic acid. he then gets neuro syx quickly, what happened?

A

Both folic acid and cobalamin (b12) cause megaloblastic anemia, treating with folic acid when it is due to b12 precipitates neuro syx, once a megaloblastic anemia is diagnosed, MUST figure out which is deficient before starting folate.

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69
Q

What diet gets megalo anemia?

A

Alcoholics and vegetarians/vegas

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70
Q

What other things cause megaloblastic anemia other than vegetarians, alc?

A

Chemotherapeutic agents like MTC and pernicious anemia

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71
Q

Who gest pernicious anemia?

A

Whites with glossitis and neuro syx and other autoimmune disease

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72
Q

Suspect pernicious anemia in who?

A

Autoimmune disease like vitiligo, thryoid and whites with glossitis

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73
Q

What drugs classically HY cause low folate?

A

MTX, TMPSMX and phenytoin

74
Q

Low haptoglobin, high bilirubin, high LDH and schistocytes suggest?

A

hemolytic anemia, especially microangiopathic

75
Q

Why do you wait a month before testing for G6PD def after an episode

A

because the defective cells are hemolysed early and G6PD level will be normal because only normlal cells remain

76
Q

How is G6pD diagnosed?

A

1 month with G6PD levels after hemolytic episode

77
Q

What is seen on smear for G6pD Def

A

Heinz bodies and bite cells

78
Q

When are vaccines given before splenectomy

A

give vaccines for encapsulated several weeks before

79
Q

After spleen out, what is given for 3-5 years?

A

There is a risk of sepsis for 30 years after splenectomy and PCN prophylaxis is needed for 3-5 years after a spleen is taken out

80
Q

How is PNH diagnosed?

A

PNH is diagnosed with flow cytometry

81
Q

what is diagnosed with flow cytometry and CD55/59?

A

PNH is diagnosed by flow cytometry with CD55 and 59

82
Q

How is PNH treated

A

Iron and folate and eclazimub

83
Q

Hemolytic anemia, venous thrombosis and cytopenia, diagnosis how?

A

Suspect PNH due to CD55/9 anchor defect and complement hemolysis causing thrombosis as well get blood cbc studies and diagnose with flow cytometry

84
Q

Hey result in HS on blood smear?

A

MCHC is high (hyperchromic) in HS due to spherocytes

85
Q

Classic s/s of hereditary spherocytosis

A

Hemolysis, splenomegaly and jaundice

86
Q

How is HS treated?

A

Treated with splenectomy as this RBC removal causes syx and gallstones, but the RBC function fine they are just smaller

87
Q

Defect IN HS

A

Spectrin or ankryin

88
Q

How is HS dx?

A

Osmotic fragility test when spherocytes are on smear

89
Q

How is HS inherited?

A

HS is autosomal dominant

90
Q

When should you suspect HS in a family history?

A

HS often has gallstones at a young age from the hemolysis and spilling of bilirubin, it is AD and this will be seen in family members

91
Q

HS labs?

A

Commonly have gallstones, but high MCHC is the key one, along with high RDW (don’t confuse with iron def anemia) and dx with osmotic fragility or esoin 5 malemide test

92
Q

What has spherocytes, high MCHC AND high RDW?

A

HIGH MCHC and RDW = HS (AD disease)

93
Q

What do all SCA patients need?

A

SCA patients commonly get macrocytosis from constant bone marrow turnover due to normocytic hemolytic anemia. They need folate supplementation

94
Q

What anemia is seen in SCA

A

SCA get both normocytic hemolytic (sickling) and macrocytic (constant bone marrow turnover) anemia, so they all need chronic folic acid supplementation due to this chronic folate def from proper bone marrow response

95
Q

How is SCA inhertied?

A

SCA is inherited AR

96
Q

MCC presentation of AR SCA?

A

AR (it is AR because there are CARRIERS) is dactylitis

97
Q

Why do so many people with SCA have nocturia, and is it trait only or full disease?

A

SCA patients, trait and full-disease have nocturia (hypothenuria) because sickling in kidney vasa recta disallows urine concentration

98
Q

What is seen on SCA smear?

A

Sickling is NOT ALWAYS PRESENT, but almost all have Howll-Jowell bodies from splenic autoinfarction

99
Q

Best diagnostic test for SCA?

A

Hg electrophoresis

100
Q

Why is hg electrophoresis best test for SCA?

A

SCA the cells are not always sickling if not hypoxia/stressed/at altitude = do electrophoresis in a family with history of it

101
Q

How is AIHA diagnosed (both types_

A

Both types of AIHA is diagnosed with Coombs testing

102
Q

what are warm IgG AIHA?

A

Dx with coombs and is SLE, CLL and drugs and treat with steroids

103
Q

How is warm IgG AIHA (sle, CLL, drugs) treated?

A

Steroids

104
Q

How is cold IgM (Myco and Mono; M= IgM) treated?

A

Avoid cold and ritixumab if severe

105
Q

What are s/s of aplastic anemia?

A

Aplastic anemia is pancytopenia with pallor, eakness, infection, petechiae, bruising and bleeding

106
Q

How is aplastic anemia diagnosed?

A

CBC then bone marrow biospy with fatty, hypocelluar type

107
Q

How does B thal minor usually prsent?

A

It usually presents as iron def anemia and is confused with it, note RDW and RBCs are different from iron

108
Q

Does B thal minor need tx?

A

NO. just observe

109
Q

What is a common presenting syx of PCV

A

PCV commonly presents as HTN

110
Q

What is noted on labs in PCV

A

High Hct often >60%, but other cell lines are elevated as well

111
Q

What causes PCV

A

JAK2 mutation, hypoxemia (Chronic) or low volume

112
Q

What does a low EPO with high Hct tell you

A

PCV due to Jak2 mutation

113
Q

How is PCV treated?

A

PCV is treated with phlebotomy to hct

114
Q

s/s of tumor lysis syndrome

A

GERD, Histamine, AKI, gout

115
Q

Does PCV need EPO? what causes the overproductio?

A

PCV (if JAK2) is EPO INDEPENDENT due to Jak2 mutation and self proliferation

116
Q

PCV often presents as just HTN, is it reversible?

A

Yes, it is reversible with phlebotomy.

117
Q

What are classic s/s of porphyria

A

Vesicles, hyperpigmentation, abd pain and urine color changes after alc, barbs or OCP

118
Q

what disease is cutanea tarde associated with

A

It is associated with HCV

119
Q

How is porphyria treated in hcv?

A

IFNa if they have HCV

120
Q

How is porphyria treated chronically

A

Hydroxyurea to increase HbF

121
Q

How is porphyria diagnosed

A

CBC and smear followed by urine or palsma porphyrin levels

122
Q

What can provide relief during acute porphyria attack

A

Glucose which prevents more photoprophryin from being made

123
Q

Someone Immediately has issues after blood transfusion, cause?

A

igA def

124
Q

IgA def causes issues with transfusion when

A

IgA causes transfusion issues immediately with wheeze, tachy and increased RR and urticaria

125
Q

How is IgA def transfusion issue treated?

A

IM epi, steroids and histamine block, happens immediately with drip

126
Q

When does febrile hemolytic occur

A

1 hour with flank pain, hemoglobinuria, DIC and renal failure

127
Q

Febrile hemolytic reaction due to

A

ABO mismatch, 1 hour after, flank pain, hemoglobinuira, DIC, renal failure + coombs and pink plasma

128
Q

Nonfebrile hemolytic reaction is d/t and happens when?

A

Cytokines. 1-6 hours, fever and chills only

129
Q

Amanestric blood reaction is d/t and happens when?

A

2-10d after, Rh factors, minor reaction.

130
Q

Anaphylactic shock from PRBC is due to

A

igA autoantibodies in IgA deficient individual = AnAphlActic - IgA deficient

131
Q

When are PRBC given

A

Hg less than 7 (even if active bleed) or Hg

132
Q

RIsks in acute ABO hemolytic reaction

A

Happens within an hour and get AKI and DIC, may bleed from IV site

133
Q

What are the AE of mycophenolate

A

bone mycow suppression

134
Q

AE of azathioprine

A

Azathioprine is a 6mp analog causing leukopenia, dose related diarrhea and hepatotoxicity

135
Q

AE of cyclosporin

A

Most serious is renal toxicity causing HTN and hyperkalemia from renovascular constriction and gum hypertrophy and hirsutism along with neurotoxicity and tremor

136
Q

AE of tacrolimus

A

both cyclosporin and tacrolimus are IL2 calcinuerin inhibitor and cause renal toxicity and hyperkalemia with neurotoxicity and HTN, but only cyclo cause hirsutism and gum hypertrophy

137
Q

AML has risk of what presentation

A

AML causes DIC due to Auer rods

138
Q

What is seen on smear with AML

A

AML has Auer Rods

139
Q

What is the defect in AML

A

AML is due to retinoic Acid receptor rAr and causes degran of auer rods and DIC

140
Q

how is AML treated?

A

Treat AML with retinoic acid all trans

141
Q

Other than rods and DIC and rAr issue (vitamin A) wha tis seen in AML smear

A

Myeloblasts

142
Q

How are the leukemias diagnosed

A

CBC with smear and then flow cytometry/genetic analysis

143
Q

Who gest CLL

A

CLL is OLDER adults

144
Q

What are two markers for CLL

A

smudge cells and CD5

145
Q

what has worse prognosis for CLL

A

thrombotycopenia has worse prognosis

146
Q

How is CLL staged

A

Prognosis based on syx, anemia to thrombotycotpneia is the worse

147
Q

Who has Phila chromosome?

A

CML is Phila crhomosome

148
Q

What is defect d/t Phila Csome?

A

Defect due to Phil Csome is ABR Tyr kinase

149
Q

How is CML treated

A

9;22 ABR tyr Kinase with imatanib

150
Q

CML s/s

A

CML classically has low LAP and basophilia withi granulocytes in all stages

151
Q

Where do you see granulocytes in all stages with ABR Tyr Kinase mutation and 9;22 treated with imitanib and basophilia?

A

CML = basohpils, granulocytes, 9;22 phila, imabitninb, tyr kinase, LAP low is classic

152
Q

How is hairy cell treated?

A

Hairy cell is cladribine and and imitanib is CML and retinoic acid is AML

153
Q

What disease are assoc with NHL

A

NHL is due to HIV and autommine commonly and many nodes non contiguously are invovled

154
Q

What are the s/s of HL

A

HL is a group of contiguous nodes

155
Q

What is asso with HL?

A

HL is assoc with EBC and Reed-sternberg CD15 and 30 cells with owl eye nuclei

156
Q

HL distribution and association

A

EBV for HL vs HIV /autoimmune for NHL

157
Q

When do you see alcohol induced pain and LAD?

A

Alc induced pain is a rare association for HL which is REedSternberg and EBC associatied

158
Q

What is the best first test for suspected MM

A

For suspected MM you get serum protein elctrophoresis

159
Q

What presets with high calcium, renal failure, anemia and bone pain?

A

MM

160
Q

Best test for MM?

A

Initial, Electrophoresis looking for M spike fo IgG then Bone marrow test with >10% plasma cells

161
Q

What is MGUS

A

MGUS is IgG related prolfieration without CRAB findings

162
Q

What are urine s/s of MM and Smear s/s

A

Rouleaux formation and Bence Jones protein

163
Q

What are classic s/s of MM

A

M/m is IgG related and causes CRAB of calcemia, renal, anemia and bone with 10% blasts in bone marrow confirmed after igG M SPike

164
Q

What lesions are seen on MM bone scan

A

MM is an osteoclastic process

165
Q

What is the path diff in MM, MGUS and Waldenstrom

A 
MM = 10% plasma cells and IgG
MGUS = less than 10% plasma cells in marrow and IgG and no CRAB syx
Wald = IgM and hyperviscosity, elderly, enroged eye vessels, organomegaly and pain in arms/legs -- BMP shows Dutcher bodies that are PAS + IgM deposits and Raynaud common
166
Q

MGUS s/s

A

Raynaud, organomegaly, eye engorgement, extremity pain, neuro disorders

167
Q

walden dx

A

IgM - M spike with Dutcher, PAS + IgM bodies

168
Q

When do you IgM M spike with Dutcher PAS + bodies?

A

Waldenstrom

169
Q

What is another way to distinguish MM from MGUS?

A

BONE XRAY shows lytic leasions in MM (cannot do bone scan which only shows blastic lesions)

170
Q

Amyloidosis most commonly affecst

A

Kidney, heart and liver affected by amyloidosis

171
Q

S/s of amyloidosis?

A

Kidney, heart, liver and skin/organomegaly and sometimes neural function. Restrictive cardiomyopathy, waxy skin and big tongue and organs, proteinuria and elevated LFTs with heart dysfunction (Restrictive) normal cavity size

172
Q

How is amyloidosis dx?

A

fat pad biospy

173
Q

Gold standard for HIT testing?

A

Serotonin release assay

174
Q

HOw does HIT II present

A

5-10 with 50% decrease in platelets and DIC/clotting; stop heparin and give argotraban derivative

175
Q

How is warm AIHA treated?

A

Warm AIHA is due to IgG and treated with steroids versus cold IgM AIHA treated with avoiding cold and ritixumab if refractory

176
Q

What inherited anemia has high MHCH (hyperchromic) and high RDW?

A

Hereditary spherocytosis = MCHC high and high RDW with family history/ or early gall stones

177
Q

What does INH interfere with (vitamin)

A

INH / TB tx interferes with B6 = sideroblastic anemia = peripheral neuropathy = hepatotoxic = homocysteine increases

178
Q

CML smear

A

Extreme leukocytosis >100K, lots of granulocytes/barely mature neutrophils and 9;22 CML Phil Csome and treat with imatinib + basophilia

179
Q

Classic cell elevation in CML

A

basophilia

180
Q

TTP smear?

A

TTP smear has schistocytes (TTP, DIC, HUS, microangiopathic)

181
Q

S/s of TTp

A

TTP cause neuro changes, renal failure, thrombocytopenia with shistocytes on peripheral smear and is associated with HIV

Final review for Step 2 Ck (12 decks)

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