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USMLE HY notes > Hemato-oncology Finals > Flashcards

Hemato-oncology Finals Flashcards

1
Q

Side effect of Aspirin

A
  1. GI- peptic ulcers, Gastritis
  2. bleeding -1-3%
  3. Allergy bronchospasm
  4. Renal and hepatic toxicity at overdose.
  5. Tinnitus
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2
Q

Which are the P2Y12 inhibitors

and what is the MOA?

A

Thioemopyridines
block irrevesibly the affect of ADP on PLT

TicoliPiDe
CloPiDogrel
Prasugrel

PD like ADP. and ptetzel

Ticagrelor- not DPI family, rether is reversbly inhibit P2Y12. can acuse Dyspnea

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3
Q

Indication for DAPT

Aspirin + P2Y12 inhibitors

and indication for P2y12 inhibitors alone

A
  1. replacement of aspirin after- MI, storke, PAD
  2. combination- after BMS for 4 weeks / after DES for > 12 months
  3. CVA / high risk TIA- 3-4 weeks,only aspirin afterwards
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4
Q

Side effect of P2Y12 inhinbitors

(ticolipide, prasugrel, clopidogrel)

A
  1. bleeding- stop 5-7 prior major surgery
  2. TTP (ADAM13 Ab) - most with Ticolipide
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5
Q

When we will give prasugrel?

in which situations?

A

ACS who are going to PCI

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6
Q

What is the main C/I for Prasugrel?

A

complete C/I
Hx for Cerebelovascular disease

relative C/I:
* Renal failure
* weight < 60 Kg
* Age > 75

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7
Q

Indication for Ticagrelor?

A

Secondary prevention after ACS (better then clopidogrel in high risk pt)

mainly as DAPT for 3-4 weeks after ACS / CVA/ high risk TIA

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8
Q

Main side effect of Ticagrelor?

A

Dyspnea (15% pt)

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9
Q

What is the use of Dipyridamole and MOA?

2 main uses

A

MOA
PDE3 inhibitor = high cAMP levels= inhibit PLT + inhibit adenosis uptake by the cells = vasodilation

indications:
1. secondary prevention with Aspirin for Stroke/ TIA
2. Cardiac Chemical stress test- can cause coronary steal

Side effect- vasodilation = flushing, hypotension, headace

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10
Q

all the following medication are class of:——–
Tirofiban
eptifibatide
Abciximiab

How they are administerd?
Side effects?

A

IIB/IIIA antagonists- Fab who bind the receptor
All IV
Side effect
Bleeding
Thrombocytopenia- must follow and monitor PLT count

Every medication has B and A in their name

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11
Q

Whats the different between LWMH and UF heparin

and how its expressed in the MOA?

A

UF heparin- verabile sized of heparin polymers
LMWH- only small polymers

the meaning of that
UFH- activation of ATIII&raquo_space; inactivation of all intinsic pathway including X + Thrombin
LMWH- only inhibit X

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12
Q

What is the Antidote of UF heparin?

A

Protamine sulfate

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13
Q

Pt under UF-heparin should be monitor and adjust doses by?

and when we will use

A

**PTT
**
use:
1. acute setting- DVT, PE, MI, stroke
2. PPx in hospital for DVT

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14
Q

What is a major severe adverse affect of Heparin?

A

HIT (heparin induce thrombocytopenia)

complexes of PLT Factor IV + Heparin + IgG&raquo_space; can activate PLT&raquo_space; Thrombosis + Thrombocytopenia

IgG Ab against PF4- heparin complex is formed

less common in LMWH

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15
Q

Dx of HIT
Tx for HIT

A

Dx:
timeline- 5-14 days after start heparin
Ab against Heparn- PF4
most specific test- Seratonin release essay

Tx
Stop heparin&raquo_space; start direct Anti-thrombin inhibitors (Bivarlirudin / Lepirudin - IV/ SQ).

can give instead of direct thromin inhibitors DOACS (direct thrombin or factor Xa inhibitors- DTI

vein and artery thrombosis

Xa inhibitors- ApiXaban, RibaroXaban
DTI- irudin suffix (IV/ SQ), Dabigatran (PO)

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16
Q

The dose given with LMWH should be adjust to

A

Kidney function

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17
Q

iIn which 3 types of Pt we will monitor use of LMWH (EnoXaheparin)
and by which test

A

Monitor:
anti factor Xa test- flurosence
3 Pt that should be monitored
1. renal insuff.
2. obesity
3. pregnancy

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18
Q

How to start give Warfarin

A

due to its delay affect- start with UFH / LMWH / Fondaparinux until effect of warfarin seen

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19
Q

What is the Goal INR for mechanical valve under Warfarin?

A

most cases- 2-3
in mehanical valve- 2.5-3.5

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20
Q

main adverse effect of Warfarin

A
  1. bleeding
  2. Skin necrosis- most prone are pt with protein C & S def.

בחסר של 2 החלבונים גם ככה יש יותר קרישיות וורפרין מוריד עוד יותר את הרמות שלהם וזה גורם בעצם לאפקט הפוך- להיות היפר-קרישיות ונקרוזיס של העור

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21
Q

Antidotes for Warfarin

A
  1. Vitamin K
  2. FFP
  3. Protein C concentrate
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22
Q

Should a pregnant women continue the use of warfarin?

A

No- Teratogenic
should use UF heparin during pregnancy

לא עובר בחלב אם

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23
Q

What should be done in the following situations:
1. a-symptomatic with INR 3.5-10
2. a-symptomatic with INR > 10
3. Severe bleeding

A

1.** a-symptomatic with INR 3.5-10**- stop comadin until INR reach 2-3
2. a-symptomatic with INR > 10- vitamin K po (2.5-5 mg) + halt warfarin
3. **Severe bleeding **- vitmain K IV 5-10 mg, give PCC (2, 7, 9, 10)

before high risk procedures- stop 5 days earlier warfarin

PCC- prothrombin concentrate complex

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24
Q

When is the only situation we will give warfarin with out Heparin before?

A

propylaxis for Afib

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25
Q

Doac vs Warfarin
* Major bleeding sites risk?
* efficacy in prevention of stoke in Afib pt?
* clearance site?

A
  • Major bleeding sites risk?
    Warfarin- brain
    DOAC- GI
  • efficacy in prevention of stoke in Afib pt?
    SAME
  • clearance site?
    Warfarin- liver
    DOAC- kidneys (C/I CrCl < 15
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26
Q

all of the following are belong to the group of ——

Dabigatran
RivaroXaban
ApiXaban

A

DOAC

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27
Q

Indication for DOACs

A

1.** Stroke ppx in Afib** (no mechanical valve or reumathic fever- warfarin)
2. **VTE Treatment **- theres not resude in doses if renal failure exist (in contrast to ppx Afib)
3. 2nd ppx after VTE
4. after hip / knee surgery
5. 2nd ppx coronary disease / PAD

Not given as a Tx for APLA
Not for pregnent of breasfeeding mom

VTE = venous thromboembolism

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28
Q

Antidote for the following DOACS
Dabigatran
Factor Xa inhibitors ( RivaroXaban + EpiXaban)

A
  • Dabigatran- Idarucizumab
  • Factor Xa inhibitors ( RivaroXaban + EpiXaban)- AdeXanet
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29
Q

Which Anti-coagulent have the same efficacy with less bleeding event as Enoxaheparin in Tx of STEMI

A

Fondaparinux

inhibit only Xa and not thrombin (like LMWH)

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30
Q

Which type of hemolysis will lead to Hemoglobinurea?

A

Intravascular

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31
Q

Which Major complication can be cause by G6PD ?

A

AKI

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32
Q

Whate are the main medications that can cause G6PD Hemolysis ?

A
  • Dapsones
  • ** Sulfadrugs**
  • **Primaquine **+ quinidine - Anti-malerian
  • Isoniazid- TB
  • Nitropronetoin
  • Rasburicase (TLS- hyperuricemia)
  • Methylene blue
  • Sedoral (Phenazopyramdine)

Definite risk in bold

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33
Q

Heredatiry Spherocytosis

whats the problem?
Extravascular / intra-vascular hemolysis

A

Mutation in Spectrin / Ankyrin- RBC cytoskeleton
mainly extravascular

נושאים חמצן סבבה אבל הממברנה קשיחה

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34
Q

In Heraditery Spherocytosis:
what will elevate or decrease:
RDW
MCHC
MCV

A
  • RDW- high
  • MCHC- high (same volume smaller RBC)
  • MCV- normal or a bit low
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35
Q

Warm AIHA:
Ab? Degree?
Extravascular / intravascular

A

IgG in 37 degree
Extravascular-by macrohages in spleen

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36
Q

Warm AIHA Etiologies?

A
  1. SLE
  2. infections- HIV, HCV, EBV
  3. CLL
  4. Methyl DOPA (HTN) pregnancy
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37
Q

Warm AIHA + Autoimmune Thrombocytopenia

we will think of

A

Evan’s syndrome

autoimmune hemolytic anemia (AIHA) and immune thrombocytopenia (ITP), with or without immune neutropenia

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38
Q

How we diagnose warm AIHA and what is the Tx?

A

Dx- **Direct coombs- IgG **

Tx:
**Blood transfusion ** for acute presentation
first line- prednisone + RTX
if refactory- Splenectomy

Direct- test for Ab bound to RBC
indirect- serum Ab against RBC

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39
Q

Cold AIHA
Ab? Dagree?

A

IgM , low temparture < 30
Intra + extravascular hemolysis

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40
Q

how we diagnose cold AIHA?

What are the etiologies?

A

Dx
Direct coombs test- C3 bound

Etiologies
Mycoplasma
EBV
CMV

mechanism- cold Tm&raquo_space; IgM bind to RBC&raquo_space; C3 also bind&raquo_space; elevate TM&raquo_space; IgM dissolve but C3 still bound

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41
Q

Tx for cold AIHA

A
  1. prevent exposue to cold
  2. RTX

no effectivness for prednisone / splenectomy

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42
Q

What are the 3 Disease we will see MAHA (microangiopathic hemolytic anemia)

A
  1. HUS
  2. PTT
  3. DIC

the only situations we will see schiystocytes

also malignant HTN

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43
Q

Which 2 types or parasites can cause normocytic anemia

A

Maleria
Babesia

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44
Q

PNH?
what is the mutation?
how it can affect blood cells?

A

aqueird mut. in GPI anchor &raquo_space; can’t present CD55-CD59 (Complement inhibitory protiens)&raquo_space; cause destruction by the complement and MAC complex

can cause pancytopenia

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45
Q

Which type of cancer can develop on the basis of PNH?

A

AML

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46
Q

reccurent abdominal pain, Budd-chiari , and pancytopenia with hemoglobiurea can raise suspicion for———–?

A

PNH

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47
Q

PNH
Dx?
Tx?

A

Dx:
Flow cytometry- CD55-59
Tx:
Eculizumab- bind C5 and inhibit MAC comlex formation.
does not improve the extra-vasuclar hemolysis, C3 will still be bound to RBC

Definitve- BM transplent- only if severe PH/ aplastic anemia
Anti-coagulation- only after VTE/ other thrombopylic

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48
Q

How to rull out psuado Thrmbocytopenia?

A

Take another sample in a tube with Sodium-citrate or heprain

cause by clampin of PLT in EDTA tube (blood smear = clamping of PLT)

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49
Q

most common cause of thrombocytopenia?

A

Drug induce

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50
Q

Wet purpura and Retinal bleeding in Thrombocytopenia can indicate of

A

high risk for life-thrething bleeding

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51
Q

ITP
pathophysiology
Tx- for low risk / high risk and when we will treat?

A

pathophysiology
Anti- GPIIb/IIIa Ab&raquo_space; digest by spleen
אבחנה שבשלילה
Tx < 30 K PLT
prednisone / Dexamethasone/ AntiD (only in D+), IVIG
low risk pt- in community wth 1 medication
High risk pt- hospitelization + few medications

Hirg risk- bleeding, PLT < 5K, sighs of dangrous bleeding

other options for Tx: Splenectomy, RTX, TPO agonists (Eltrombopag)

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52
Q

Which medication can be given in Refactory ITP?

how much % of remmision is obtained?

A

RTX
30% remission

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53
Q

Which disease are Thrombotic thrombocutopenic Microangiopathies?

A
  • TTP
  • HUS
    DIC
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54
Q

What is the classic Triad of HUS and the pentade of TTP

A

Triad of HUS
1. Renal insuff.
2. MAHA
3. Thrombocytopenia

Petnade of TTP
HUS + Fever + neurologic symptoms

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55
Q

What is the pathophysioligical condition in TTP

A

Ab against ADAMS13

Congenital TTP (apsho-shulman)- congenital deff. in ADAMS13

ADAMS13- the enzyme who cleaves wVF polymerse and prevent blood vessel occlusions&raquo_space; activate of PLT&raquo_space; thrombosis + MAHA

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56
Q

How we diagnose TTP?

A

ADAMS13 < 10%

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57
Q

Tx for TTP

A

daily plasmaphersis- until PLT are normelizeid and no hemolysis for 2 days.
steroid are usally added

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58
Q

which medication can shorten the lengh of TTP episodes and reduce reccurence?

A

RTX

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59
Q

Which medication for TTP is made against vWF and reduce mortality?

A

Caplacizumab

(risk for reccurence- 40%)

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60
Q

Etiology for HUS?
and Tx

A

Etiology- E.coli 0157:H7 infection, pneumoccoc
Tx:
supportive, 40% will need dialysis

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61
Q

Whats the different between HUS and aHUS?

A

aHUS theres not diarrhea before HUS

Tx- aHUS Eculizumab - C5 inhibitor

Eculizumab- also given in PNH, block formation of MAC complex

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62
Q

which Anti-coagulant component are fiven in:
FFP
PCC
cryoparcipitate

A

FFP- everything
PCC- 2,7,9,10, proteins C+S
cryoparcipitate- fibrinogen, 8, vWF

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63
Q

Hemophilia A + B
what is the inheritence?
which is more common?

A

X-linked
A (VIII) more common

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64
Q

if a pt have hemophilia A and theres no avaliable factor 8, what other Best option can the doctor give?

A

Cryoparcipitate
(Factor 8, vWf, fibrinogen)

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65
Q

How Desmopressin can help a pt with hemophilia A

A

Desmopressin helps realse factor 8 + vWF fromt the Whady pallady bodies&raquo_space; more factor avaliable

desmopressin- bed-wetting, central DI

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66
Q

Which medication can be given in hemophilia a thet is skipping factor 8 and do not need it

A

Emicizumab
bringfactor IX to X (does not need factor 8)

עמיקיזומאב מחבר בין שני צידי העמק

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67
Q

How can we diagnose in Hemophilia that Ab are create to the given factor and acts as an inhibitors?

A

Mixing study does not improve after adding normal plasma

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68
Q

Hemophilia C
Which factor is missing
which decendent is common?
Tx?

A

missing of factor XI (prolong PTT solely)
יהודים אשכנזים ועיראקים
Tx
in severe disease before big procedure- F.XI concentreate or FFP. can add hexacepron in mild bleeding not urogenital bleeding

bleeding are muco-cutaneous- similiar to low PLT but here the bleeding time is normal and PTT prolong

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69
Q

DIC
mortality rates

A

30%-8080%

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70
Q

What are the most common cuases for DIC

A
  • Bacterial sepsis
  • Trauma
  • Obs. compications
  • Adenocarcinoma (prostate, pancrea..)
  • APL (acute promyolacyte leukemia)
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71
Q

What is the most sensetive test in DIC?

A

D-dimer

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72
Q

What the Different between DIC and chronic DIC?

A

Chronic DIC
PT/PTT + fibrongens are normal

גידולי מתסתטיים, המנגיומה ענקית ותסמונת העובר המת, דימומים קלים המוגבלים לעור ולמקוזות

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73
Q

Tx for DIC

A

most important- treat the underlying cause
1. **for hemmoragic symptoms- **PLT infusions when < 20K
2. For fingrinogen levels > 150cryopacipitate (8,13,vWF, fibrinogen) or fibginogen
3. PT < 3 below to ULV- FFT, vitamin K, if bleed hexacapron
4. Thrombotic syndromes- low dose heparin only. not when severe DIC or active Bleeding

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74
Q

Which factors are depent in vitamin K?

A

2,7,9,10, protein C + S

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75
Q

what is the erlieast finding in vitamin K def? and why

A

PT prolongation&raquo_space; factor VII has the shortest half life.

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76
Q

Which coagulation factor is use as indicator for liver failure as the reason for a coagulapthy?

A

Factor V

does not depent on vitamin K.

77
Q

Tx for coagulaphtis secondary to liver failure?

A
  1. Vitamin K IV
  2. 4F-PCC prefer on FFP (less vol.)
  3. PLT infusion- PLT < 10-20K in active bleeding or < 50K before surgery
  4. cryoparcipitate- fibrinogen < 100-150 unless pt is bleeding
78
Q

f Ab development against clotting factors

which type of population are more prone?
which factor is most prone

A

Factor VIII- aquicerd Hemophilia A

Pt:
pregnancy/ post-partum.
mainly age > 60

79
Q

What is bethesda assay use?

A

indentify the specific clotting cator and levels of Ab against it

80
Q

How can we eridicate the Ab against Clotting factor?

A

first line- steroids , cyclophospamid
second lie- IVIG, anti-CD20

81
Q

the present of Celiac can lead to which type of anemia?

A

Microcytic hypochromic anemia- Iron Deff. anemia

82
Q

What is the Tx for anemia of elderly?

symptomatic and irreversible

A

EPO

Blood transfusion- only for certain pt with Hb > 7-8

83
Q

What is Pernicious anemia

A

Ab against perital cells in the gut&raquo_space; no IF is produce&raquo_space; can’t bind B12&raquo_space;Megaloblastic anemia

84
Q

In which place B12 is detach from IF and reabsorb in the body?

A

Terminal ilium - thats why chron pt might present with megalobalstic anemia (terminal ilitis)

85
Q

Severe cases of B12 def. can present with

related to blood cells

A

pancytopenia
neurological deficiet- peripheral neuropathy , ataxia, dementia, depression

86
Q

Tx for B12 for irreversible reasons and what should we watch for

A

B12 IM injections for life

can cause hypokalemia
but does not required Tx most of the time

87
Q

MTX can cause a deff. in which vitamin?

A

B9- Folate

88
Q

What are the resons for microcytic anemia

A

TAILS
* Thalasemmia
* Anemia of chronic disease
* Iron deff.
* Lead poisonnig
* Sideroblast

89
Q

What is Mentzer index?
how to calculate

A

MCV/RBC
help differantiate btw talashemia and iron def.

MCV/ RBC < 13 = thalasemmia
MCV/ RBC > 13 = Iron deff.

90
Q

MDS can cause pancytopenia hypo or hypercellularity of BM?

A

Hypocellularity or Hypercellularity

91
Q

Etiologys for Pancytopenia hyper-cellularity of BM?

A

MDS
PNH
Myelofibrosis
sys.diseases- SLE, B12, folate, HIV, TB…

92
Q

What is the first step when pancytopenia is present?

A

**Emeregent blood smear- ** acute leukemia

BM biopsy-if unexplained pancytopenia &raquo_space; mainly hypoproliferative

93
Q

Aplastic anemia def. ?

A

PAncytopenia + hypocellularity of BM

a lot of Fat with hypocellularity- this is the Dx in BM biopsy

94
Q

What is the Tx options for Aplastic anemia

A

BM transplent- 1st line for youngs with match sibiling

Immunosuppresive Tx- for older pt / pt with no match on BM transplent
ATG (antithymocyte globulin) + Cyclosporin- 1st line

עוד תרופות שמגרות מח עצם כמו
TPO
GM-CSF
לחשוב על כל מה שיכול לגרות BM

ההנחה שהתהליך מתווך מע’ חיסון ולכן אנטי-טימוציט גלובין יכול לעזור

95
Q

What is the benefit in using Eltrombopag (TPO) in aplastic anemia?

A

יכול לאושש את השורות במקרים רפקטורים, ומשפר תגובה ל-ATG
כשניתן ביחד

96
Q

What is Fanconi anemia?

A

Heraditery Aplastic anemia

> 50% with physical deformations

mutation in DNA repair anzyme&raquo_space; Mainly crosslink

wierd thumbs, caffe olea, short sature

97
Q

When I say Pure red cell aplasia
you say

98
Q

Pure red cell aplasia
how we diagnose?

A

Reticolocytopenia < 1%

if unexplain demend BM exmination

in kids- if heraditery = Diamond Blackfan- weird fingers, Black BM, high HbF

99
Q

Which secondary conditions can cause Pure red cell aplasia

A
  1. Thymoma (remember M.G)
  2. Lymp. malignancies (CLL)
  3. Parvo B19- Sickle cells, thalasemia , shperocytosis
100
Q

How to diagnose Multiple Myloma?

A
  1. **> 10% plasma cells in BM or Plasmocytomas **( masses in bones or soft tissue of plasma cells)
  2. one of the following- Organ demege:
    * C- hypcercalcemia > 11
    * R- renal failure - Cr > 2 or CrcL < 40
    * A- anemia- below 10 or >2 below Low limit
    * B- bones lesions- lytic

Markers thet can repalce criteria 2:
* > 60% plasma cells in BM
* light chain ratio > 100
* Focal lesion in MRI (step before lytic lesions) - at least 2 in size > 5 mm

SLiM CARB
S- sixty precent
Li- light cheins
M- MRI

101
Q

Defintion of MGUS?

when we dont need to check BM

A

monoclonl Ab < 10% in BM or less then 3 gram in serum
+
no SLiM- CARB

no BM biopsy- monoclonal IgG < 1.5 (low ) light chain ratio - 0.125-8 no need to check for diagnosis follow up is enough

דורש מעקב ולא טיפול, סיכוי של 1% בשנה להתקדמות

102
Q

Defintion of Smoldering MM?

A

monoclonal Ab in serum > 3 gr/dL or 10-60% plasma cells in BM

no SLiM- CARB

דורש מעקב ולא טיפול, סיכוי של 10% בשנה להתקדמות

103
Q

Which test are benefical and not beneficial for Bone test in MM

A
  1. ALKP- not elevated = no osteoblast activity
  2. מיפוי עצמות- לא מתאים

good test- CT/ MRI / PET-CT

Bone reabsoprion = hypercalcemia

104
Q

Most common reason for renal falilure in MM?

A

**Hypercalcemia **- due to iadequate ability to concentrate the urine&raquo_space; polyurea&raquo_space; low GFR…

105
Q

What is the earliest menefistation of Light chain tubular damage in MM?

A

Fanconi syndrome

Metabolic acidosis with normal AG + hypokalemia + hypophosphatemia

106
Q

MM + nephrotic syndrome will raise a suspicion of

A

Amiloydosis

107
Q

Which 2 parameters asses the dagree risk of MM?

the International Staging Systme- SSI

and what is the Strognest single prognostic factor

A

Albumin
B2-microglobulin

if low albumin + high B2-Mg&raquo_space; high risk

B2-microglobulin- Strongest solely prognostic factor

108
Q

Which medication include in the induction therapy at MM?
and what in Maintanence therapy

A
  1. Lenalidomine- rq aspirin or Anti-coagulation
  2. Brotezonib- proteosome inhibitor
  3. Dexa/ prednisone
  4. DaratuMuMab- anti-CD 38

Maintanance:
1 medication from above at low dose

109
Q

Tx of choice in Hyper-viscosity synd?

A

Plasma-phersis

IgM Ab- Waldenstrom macroglobulinemia

110
Q

What are the the distinct features of Waldenstorm macroglobulinemia VS MM

A

WM
1. IgM (in MM rare)
2. CD20+
3. mut. in MYD88 (90% in WM)
4. no lytic lesions

111
Q

Which type of anemia can happen in hyper IgM (Waldenstrom macroglulinemia)

A

AIHA- cold type. (positive coombs- C3)

warm type - IgG

112
Q

how we Dx Waldenstrom macroglulinemia

A

BM biopsy > 10% Lymp + lots of Mast cells

MYD88 mutation > 90% of pt

113
Q

Tx in Waldenstrom macroglulinemia when:
1. mild disease (like MGUS)
2. phenomenon related to abundane IgM
3. severe disease with hyperviscosity
4. Hyperviscosity menefistations

A
  1. mild disease (like MGUS)- followup
  2. phenomenon related to abundane IgM RTX (anti-CD20)
  3. severe disease with hyperviscosity- R&B protocol (Bendamustin + RTX )
  4. Hyperviscosity menefistations- plasmaphersis (remember visual diturbance)

R&B protocol- also in follicular lymphoma

114
Q

**Acute leukemia **
what is the hallmark

ALL, AML,T-ALL,AMPL

A

hallmark- leukocytosis
Blasts - acute

one of the progenitors (precursors)
RBC- PV
Granolocytes - CML
PLT- ET

mature - chronic

115
Q

what are the 3 main cheracteristics of AML

A
  1. BM depresson
  2. Extra-medullary - gums, skin, CNS
  3. Leukemic blast sequel- DIC, luekostasis, TLS

DIC- more common in AMPL (higher auer rods)

116
Q

TLS
Electrolyte disbalance?
Dgx?
Tx?

A

Electrolyte
Hypercalcemia
Hyperurecemia
hyperphosphatemia
hypocalcemia

Dgx:
labs + 1 of the 3:
1. renal insuff.
2. arrythmias/ Cardiac arrest
3. sezuires

Tx:
hydration + alopurinoll (in high risk pt)
Rasburicase- if TLS occure, reduce uric acid. C/I in G6PD

בדיקת רמת חומצהאורית תחת ראזבוקריאז- מבחנה שטופה עם הפרין. על קרח

117
Q

Dgx criteria for Acute leukemia?

A
  • Blasts > 20% in blood smear / BM
  • Genetic changes (leukemia-defing)
  • Extra medullary disease

one of the follows

118
Q

What is the most importent prognostic factor in Acute leukemia?

A

Cytogenetic of tumor cells (translocation and ect)

119
Q

which leukemia and what the prognosis?

t(15:17)

A

AMPL- good prognosis

PML-RARA (fusion)

The t(15:17)- what causes AML to become APL (AMPL)

120
Q

Tx for APL (AMPL)

A

ATRA = A retinoic acid in combination with ATO ( Arsenic Acid)

if pt. first present with DIC - add vitamin A to the DIC therapy ASAP

121
Q

AML Tx:
induction
consolidation
BM transplent

A

induction: intensive or non intensive:
* intensive (age < 65, low co-morbidites) - 3+7 = 7 days cytarabine + 3 daunorubucin
* non-intensive- semi-paliatve tx

Consolidation
* Chemothrapy - for good prognosis like t(15:17), t(8:21)
* BM transplent- bad prognosis (young pt < 75, FLT3-LTD)

BM transplent- allogeniec (other person)
1. no full remission - 20% chance of healing
2. after full remission

122
Q

What are the biological Tx in AML?

A
  1. TKI against FLT3
  2. monoclonal Ab- Gemtuzumab (cd33)
  3. CPX-351
  4. Ventoclax
123
Q

Why we should not give to APL pt the chemothrapy given in AML (Cysterabin + Antracyclin 7+3)?

A

can cause Severe DIC

124
Q

What is APL differentioation syndrome?

A

secondary to ATRA Tx

התאים הממאירים נצמדים לאנדותל כלי דם ריאתיים- דיספניאה, אגירת נוזלים, כאבים בחזה וכדומה

Tx:
Steroids
in severe cases- temporary stop ATRA

125
Q

What mutation we will see it all of the following:
PV
ET
myelofibrosis

A

JAK2 mutation (Chromosome 9&raquo_space; Tyrosine kinase)

in 95% of pt

הפעלה ביתר של רצפטור EPO

126
Q

which MPD are presented with:
1. red and puffy skin
2. Aquagenic pruritus
3. DVT- mainly budd-chiari

A

Polycytemia vera

Thrombosis- atrieal / veins
hyperviscosity- neurologic symptoms

127
Q

Complications of PV?

A
  1. progress to myelofibrosis ~ 15%
  2. Leukemia- AML
  3. Gout- due to high turnover = hyperurecmia

Hyperurecimia- Treat with alloperinol only if symptomatic/ under chemo
pruritus- Anti-histamins / anti-depressant

128
Q

What is the influence of Polycetemia vera on
1. EPO levels
2. Blood vol
3. RBC mass

A
  1. EPO levels- low
  2. Blood vol- high
  3. RBC mass- high
129
Q

Major cause of death in PV?

A

Thrombocytosis&raquo_space; mainly a/w arytrhocytosis

130
Q

Tx for PV

A

phlabetomy- הקזות דם
goal- HB < 14, HCT < 45%- 42% (M-F)
Hydroxyurea- inhibit DNA synthsis (try to prevent as much as can)

131
Q

Erythromealgia is a/w which of the following?
PV, ET, myelofibrosis

and how we treat

A

PV

Tx- Aspirin

Erythema and burning pain in lower extremites

132
Q

What are the clinical featurs of extra-medullary hematopoasis?

A
  • Splenomegaly
  • Tear-drops RBC (dacrocytes)
  • immature meyaloids
  • anemia (normo-normo) + Thrombocytopenia
  • Hyperuricemia

im primary myelofibrosis- also B symptoms = high metabolism

133
Q

Tx for Primary myelofibrosis

A

BM transplent- only curative Tx
PEG-INF-a- reduce fibrosis in early stages, in late can worsen the BM failure

**Ruxolitinib- ** inhibit JAK2. can improve splenomegaly and symptoms. also survival (not curative). S.E- anemia + low PLT.
Steroids- can improbe anemia and Thrombocytopenia

C/I for splenectomy

134
Q

Essiential Thrombocytosis

major risk factor for thrombosis?

what are the 2 major adverse affect?

A

Major risk- smoking
2 makor adverse affect:
1. thrombosis
2. bleeding

also erythromelaglia

135
Q

What we must do in order to establish a diagnosis of ET?

A

Rule out Reactive Thrombocytosis
* Iron def.
* Hemmorage/ Hemolysis
* Infection
* Cancer

which means we also need to take Acute phase reactent

136
Q

When we decide to treat ET?

and what is the Tx?

A

Based on the symptoms and not the PLT number

  1. Aspirin- CVA/TIA/ Ertyhromelalgia
  2. Anagrelide, PEG-INF-alpha , hysroxyurea- lower PLT count
  3. vWF disease (PLT > 1M)- Hexacapron as necessery and avoid aspirin
137
Q

What is the main factor to consider to detrmine prognosis and therapy selection in MDS?

138
Q

Bad and Good prognosis factors in MDS

A

1, negetive- lots of blasts, genetic mutation on chromosome 7 (not q5/q20)
2. positvie- q5del (related to thrombocytosis) good respond to lenalidomide

139
Q

AA amyloidosis is the most common seen in which reumatologic disease?

A

RA- 40 %
FMF

Demage to kidneys.

140
Q

ATTR amyloidosis
which systems are mainly involve?

A

Heart-Restrictive cardiomyopathy (most senstive by MRI)
peripheral nerves

Diastolic HF

141
Q

Which amyloidosis is seen in dialysis pt?

and what are the 2 main clinical features

A

beta-2 microglobulin (is not removed in dialysis)

main features:
Carpal tunnel syndrome
pain in shoulders (also joints)

142
Q

Which Anti-coagulation factor is related to Raccoon eye phenomenon in amyloidosis?

A

Factor X- פגיעה פבעילות שלו, אכימוזות בעיקר סביב העיניים

143
Q

Macroglossia is pathognemonic for which type of Amyloidosis?

A

Light chain

144
Q

Which kidney involvment is seen in amyloidosis?

A

Nephrotic syndrome with hypoalbuminemia

145
Q

How we Dgx Amyloidosis (systemic)?

A
  1. Abdomial fat pad biopsy&raquo_space; if negetive we will biopse from damage organ
  2. Congo red

if ATTR suspect&raquo_space; DPD מיפוי

146
Q

Restrictive cardiomyopathy due to amyloidosis is C/I to use which kind of Heart drugs?

A

CCB, BB, digoxin

147
Q

Which organ is most prone to Damage in AL amyloidosys?

and 2nd most common

A
  1. Kidneys- 70% of pt
  2. heart- number 1 reason of death
148
Q

Tx for AL amyloidosis?

A

like Active MM
1. Lenalidomine- rq aspirin or Anti-coagulation
2. Brotezonib- proteosome inhibitor
3. Dexa/ prednisone
4. DaratuMuMab- anti-CD 38

Maintanance:
1 medication from above at low dose

149
Q

Which translocation define CML?

and whats the survival rates for 10 years?

A

t(9:22) philadelphia chromosome
BCR-ABL - tyrosine kinase

86% survive in 10 years

150
Q

What is the Tx for CML?

A

TKI - Imatinib

BM transplent- only for those who resistance to TKI
Interferon- only for pregnant women

אימת הטירוזין קינאז

Tinib suffix for TKI

151
Q

How can we rule out Leukomoid reaction vs CML

A

LAP score
Low- CML
High- Luekomoid reaction

LAP- leukocyte alakaline phosphetase- CML is low

152
Q

Whats the only different between SLL to CLL?

A

number of lympocytes.
SLL < 5K
CLL > 5K

153
Q

how to Dgx and Tx CLL?

A

Dgx:
* Smudge cells- blood smear
* Flow Cytometry- CD5 , CD20
* monoclonal B cells > 5000
Tx
most of the time only followup

154
Q

Which 2 menefistation are affect in CLL staging to ctage III/IV?

A

Lymphadenpathy / Heptosplenomegaly / cytopenia secondary to BM involvment

Autommune phenomenas does not effect staging

155
Q

What are the main complications of CLL

A

Pure red cell aplasia (also in tymoma)
BM insuff. - reticulocytopenia < 1%
infectios- leading cause of death
warm AIHA (IgG), ITP - RTX, Steroids, IVIG
Transformation to DLBCL- RCHOP or EPOCH-R

הטיפול הוא סימפטומתי בסיבוכים עצמם וגם נוכחות סיבוכים לא בהכרח מחייבת טיפול

156
Q

Which medication (only if decided) is the Tx of choice in CLL?

A

BCL2 inhibitors with or w/o RTX:
1. Ibrtinib- B for BCL and tinib for TKinhibtor. a lot of side effect with risk of bleeding, HTN, Afib
2. Acalabrutinib- same with less side effect
3. Venetoclax- BCL2 inhibitor = more apoptosis

157
Q

Which symptomatic Tx can help in CLL with Hypogamaglubalinemia + reccurent severe infections

158
Q

What is the test of choice in order to classift the lymphoma type?

A

Excisional biopsy

FNA cannot diagnose lymphoma

159
Q

Which test should always be done prior to Tx with antracyclins?

A
  • Echocardiograpy- asses LVEF
  • fertility
160
Q

How we stage Lymphoma

A

By the involvment of LN:
Stage 1- only 1 site involve
Stage 2- 2 or more sites in same side
stage 3- sites from both sides of diapragm
stage 4- extranodular sites involvment

161
Q

Which type of NHL is the most common?
and whats the Tx?

A

DLBCL

Tx:
1st line- R-CHOP (RTX, Cyclophospamid, Doxorubicin, vincristin, presnisone) ~ 60% curable.

if CHF - no antracyclins

162
Q

Which medication from the R-CHOP is the only one to show increase in survival rates in DLBCL

163
Q

When we will consider Allogenic BM tansplantation in DLBCL?

A

A disease which refacrtory to all lines:
1. R-CHOP
2. ICE protocol (rescue protocol) + autologous Transplent
3. CART-T
4. Bi-specific Ab

164
Q

Whice type of indolent lymphoma is the most common?

A

Follicular lymphoma

B- cell

uncurable , survival 15-20 yrs

165
Q

Which translocation is seen in 85% of follicular lymphoma?

A

t(14:18)
BCL2- anti apoptosis protein

b2- microglobulin- a prognostic marker in indolent lymphoma

166
Q

when we will decide to treat follicular lymphoma

and what is the Tx?

A

עומס מחלה משמעותי - עם מחלה סימפטומתית / פגיעה באברי מטרה

R&B- Bndamustin & RTX

like DLBCL- always use RTX (improve survival rate)

Also Tx for Waldarstom macroglubelinemia

167
Q

folliuclar lymphoma to DLBCL

What is the year rate for transformation?
how many pt will tranform?
how we Dgx?

A

year rate- 3%
pt will trnasform- 40%
dgx- LN biopsy

168
Q

A pt with follicular lymphoma present with lymphadenopathy, night sweat, wight loss and increase LDH

we should suspect?
and how we treat?

A

DLBCL

tx:
not seen antracyclin&raquo_space; R-CHOP
seen antracyclin&raquo_space; rescue (ICE) + autologus BM transplant

169
Q

Burkkit lymphoma
virus associated?
histological apperance
translocation?
Tx?

A

EBV
Starry skies
t(8:14)
Tx- EPOCH-R (same as all aggresive lymphomas)

70-80% curable

170
Q

What is the characteristics of the lymphadenopathy in hodgkin lymphoma

A
  • mainly in upper part of the body
  • below diaphargm in older pt
171
Q

Which electrolyte disbalance is common in hodgkin and what type of rush

A

hyperclacemia
arythema nodosum

172
Q

most stong predictble prognosis factor in hodgkin?

A

Staging = PET-CT
* favourable- less LN involve, normal ESR,
* unfavorable- all the other
* early disease- unilateral (one side of dihaprgm)
* late disease- lateral

173
Q

What is the Tx in hodgkin lymphoma

A

standart protocol- ABVD + radiotherapy

troughout the tx we do some more PET-CT scans and then deciding about the therapy.

Brentuxomab- anti-CD30 Ab (the B in ABVD)

brentu like brend new RTX

174
Q

Which 2 types of lung cancers are most related to smoking

A

SCC + SCLC

175
Q

lung cancer

Which type of tumors are mainly a peripharal finding and which are central?

A

peripharal- ACA, LCC (can be both)
Central- SCC, SCLC

176
Q

which 3 main paran-neoplastic syndroms can be seen wth SCLC?

A

the 3 A’s
* ACTH- excess cortisol&raquo_space; cushing&raquo_space; hyperglycemia
* ADH- SIADH , hyponathremia (confusion)
* **Anti-bodies- **anti pre-synaptic C-channel&raquo_space; no Ach is realse = lambert eaton (like Mystenia gravis),

177
Q

Which para-neoplastic syndrome is related to SCC?

A

**PTHrP **
hypercalcemia = Bones, Stones, Groans and psychatric tones

178
Q

Which test will be made for confirmation of lung cancer (in any type)

A

Sampling of the tissue

179
Q

What are the main reasons for False negetive for metastatic disease in SCLC under PET-CT

A

1.DM
2.nodules < 8 mm
3.slow growing tumors (AdenoCarcinoma, Broncoalve.Ca)

180
Q

What are the main reasons for False positive for metastatic disease in SCLC under PET-CT

A
  1. infections
  2. granulomatotic disease
181
Q

What is the imgaing reccomndation for SCLC?

A
  • PET-CT
  • Brain MRI
182
Q

Tx for Non-SCLC

A

Surgery

  • in every stage if the biology allow it- add biologic therapy, options:
  • EGFR inhibitor - Erlotinib
  • ALK inhibitors- Crizotinib (לאלק הירוק יש קריזות)
183
Q

Non- SCLC
when the tumor is operatable and when it is not?

A

Operatble tumor:
* solitary tumor that allow imputation
* with or w/o involve LN only if inside ipsilateral chest to the tumor

not operatable
* involve critical structures in the chest- large vessels, voice cord, phrenic nerve, < 2 cm from carina
* Stage III- chemo (platimum) + radiotherapy&raquo_space; immunotherapy with Durvalmab
* Stage IV- base on the pt (Chemo/ radio/biology/immuno)

184
Q

What is the prefferd Tx in SCLC?

A

Chemo (platinum) + radiation - combination

185
Q

new noudle in CT

what is the approch in high risk cancer lung tumor?

A

removing the lesion with VATS (frozen section)&raquo_space; if malignant&raquo_space; lobectomy

high risk pt- smoker, > 60, large noudles > 1.5 cm, border are not smooth

186
Q

What is the approch for mild risk for lung cancer in a new nodule found on CT?

A

continue work-up
1. PET if nodule >=1 cm
2. Contrast CT
3. peripheral nodule- FNA
4. air bronchous sign positive (direct bronchous to the lesion) - Bronchoscopia

if low risk < 10% for cancer»High reso CT after- 3,6,9,12,18,24 (like baby clothes)

187
Q

what is histocytes?

A

Connective tissue macrophage

188
Q

What are the congenital disease with risk for venous thrombosis (only)

A
  1. homozygous for Factor V lieden
  2. pro-thrombin mutation / loss of prothrombin
  3. def. in protein C + S

USMLE HY notes (34 decks)

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