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מבואות > המטולוגיה > Flashcards

המטולוגיה Flashcards

1
Q

Pseodo pelger form in blood smear?

A

גרנולוציטיים דיספלסטיים בצורת משקפיים

מאפיין MDS

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2
Q

macrocytic anemia DD?

A

חסר B12 חסר חומצה פולית
MDS
אנמיה אפלסטית
אנמיה המוליטית

תרופות
היפותירואידיזם
אלכוהול

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3
Q

Polychromasia

A

reticulocytosis

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4
Q

Hemolytic Anemia lab tests

A

LDH (up)

Bilirubin (uncon, up)

Haptoglobin (down)

Free plasma hemoglobin (up)

Reticulocytes (up, except in Megaloblastic anemia and Thalassemia)

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5
Q

כיצד נוכיח/נשלול אנמיה המוליטית?

A

increased LDH and reduced haptoglobin-
90% specific for diagnosis of hemolysis

normal LDH and haptoglobin>25mg/dL -
92% sensitive for ruling out hemolysis

blood smear- diagnostic

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6
Q

סוגי אנמיה המוליטית?

A

מפגם בתוך התא האדום: (מולדות)
המוגלובינופתיה- טלסמיה וחרמשית
אנזימופתיה-
חסר G6PD

פגם בקרום התא:
congenital (most)- ספרוציטוזיס, אליפטוציטוזיס
acquired - Acanthocytosis, PNH

פגם מחוץ לתא:
מכאני- קרישים, מסתם טוטב
אימוני (הרוב) - אנמיה המוליטית אוטואימונית - נוגדן עצמי, תרופות
היפר-ספלניזם -הרס מוגבר של תאים בתוך הטחול
רעילות

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7
Q

microcytic anemia DD (tails)?

A 
חסר ברזל מתקדם
מחלה דלקתית
תלסמיה
עופרת 
אנמיה סידרובלאסטית
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8
Q

normocytic anemia DD?

A

חסר ברזל כרוני

טלסמיה מינור

אנמיה סידרובלסטית (דפקט בסינטזת heme)

אנמיה כרונית/ דלקתית

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9
Q

low MCV and low reticulocytes anemia DD?

A

חסר ברזל בינוני או בתחילתו
אנמיה כרונית/ דלקתית

כימו
כשל כלייתי

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10
Q

high MCV and low reticulocytes anemia DD?

A

אנמיה מגלובלסטית
MDS
אנמיה אפלסטית

תרופות
היפוטיירודיזם
אלכוהוליזם

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11
Q

DD אנמיה עם רטיקולוציטים גבוהים?

A

MCV נורמאלי/נמוך:

תלסמיה מג’ור
ספרוציטוזיס

MCV גבוה:

אנמיה חרמשית
G6PD
IHA
מלריה

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12
Q

DD של אנמיה עם לויקופניה ו/או טרמבוציטופניה

A

רטיקולוציטים נמוכים:

אנמיה אפלסטית
MDS
כימוטרפיה 
אלכוהוליזם
אנמיה מגלובלסטית

רטיקולוציטים גבוהים:

TTP/DIC
היפרספלניזם
אימוני

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13
Q

מה נבדוק אם רואים סכיסטוציטים (שברי תאים) במשטח עם חשד לאנמיה המוליטית?

A

פרוטזה- לא?
נבדוק תפקודי קרישה לDIC- לא?
TTP/HUS

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14
Q

מה נבדוק אם לא רואים סכיסטוציטים (שברי תאים) במשטח עם חשד לאנמיה המוליטית?

A

coombs (IgG/M)
positive? thus diagmosis
negative? cytometry for PNH

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15
Q

באיזו אנמיה נראה-

רמות EPO גבוהות

הפטוספלנומגליה, הרחבת מח עצם, המטופואיזה חוץ- מדולרית, כולליטיאזיס

A

תלסמיה מייג’ור

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16
Q

Soluble transferrin receptor (sTfR).

מהו ומה רמתו בחסר ברזל?

A

circulating protein derived from cleavage of the membrane transferrin receptor on erythroid precursor cells in the bone marrow

iron deficiency- TfR density increases on cell membranes, and truncated sTfR increases in the serum.

ACD/AI- cytokines suppress expression of sTf

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17
Q

סיבוכים של עירויים

A

עודפי ברזל

התפתחות נוגדנים

זיהומים- HCV

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18
Q

איברי מטרה לעודפי ברזל

A

עור

לב- אי ספיקה, הפרעות קצב (שקיעה במערכת ההולכה)

כבד- carcinoma

מערכת אנדוקריני

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19
Q

Deferoxamime (Desferal)

A

תרופה לפינוי ברזל- עושה כלציה בזרם הדם. מתן בזריקה ופינוי ברזל בשתן.

ת”ל- הפרעות ראייה ושמיעה.

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20
Q

Deferasirox (Exjade)

A

תרופה לסילוק ברזל דרך המעי.
POx1xD

ת”ל: GIT, kidney, liver

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21
Q

(Deferiprone (L1, ferriprox)

A

תרופה לסילוק ברזל דרך המעי.
POx3xD
ת”ל: arthralgia, agranulocytosis, GIT

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22
Q

Luspatercept

A

תרופות המשפרות הבשלת התאים האדומים במח העצם

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23
Q

מהי ההמלצה לגבי שילוב תרופות פומיות וזריקות לסילוק ברזל?

A

שילוב של זריקות ומתן פומי

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24
Q

לאילו מחלות ניתן תרופות שעושות אינדוקצייה של המוגלובין F?

A

תלסמיה- בעיקר אינטרמדיה ואנמיה חרמשית

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25
Q

RBC - Storage Limitations

A

PH (down)

plasma K (up)

plasma LDH (up)

plasma HB (up)

(down) 2,3-BPG

ATP (down)

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26
Q

PLT collection characteristics

A

seperation from blood:
unit volume: 50 ml
dose for transfusion: 4-6 units

apheresis:
unit volume: 200 ml
dose for transfusion: 1 unit

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27
Q

Indications for Granulocytes Transfusion

A

Neutropenia and fever

bacterial or fungal sepsis

No response to appropriate antibiotic treatment

Bone marrow hypoplasia

Reasonable chance for BM recovery

Basic disease with favorable prognosis

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28
Q

Indications for FFP transfusion

A

Vitamin K deficiency (II, VII, IX, X)

Coumadin overdose

Liver disease

Dilutional coagulopathy (massive transfusion)

DIC

Congenital (when no factor concentrate available)

Plasmapheresis for TTP

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29
Q

Cryoprecipitate Characteristics

A

von Willebrand factor

factor VIII

factor XIII

fibrinogen

fibronectin

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30
Q

blood typing unexpected results

A
  1. Direct typing: no antigens present (O)
    reverse typing: only anti-B present (A)

The reason: weak A

  1. Direct typing: only A antigen present (A)
    reverse typing: anti-A and anti-B antibodies (O)

The reason: mutated A (A2) 15% of type A patients

  1. Mother: B (exome 7 mute) , father: O (exome 6 mute); child: A

שחלוף של אקסום 6 בין שני האללים של האמא.
כעת יש אלל אחד שנושא את שתי המוטציות - הופך אותו ‘או’, ואלל שני חסר מוטציות כלל- הופך ל’איי’- הנ”ל עבר לילד.

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31
Q

how to Type and Match bloods?

A
  1. AB and D (direct and reverse)
  2. Antibody screening

If (2) is negative - cross matching

If (2) is positive - identification of antibody (11 cells) and cross matching with a unit lacking the relevant antigen(s)

  1. If auto-antibody is suspected - direct anti

globulin (Coombs) test

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32
Q

how does Antibody Screening performed?

A

Patients serum is mixed with 3 samples of commercially available red cells with known blood groups (indirect coombs)

For some reagents, subsequent direct anti-globulin test

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33
Q

Antibody Screening pan agglutination reasons?

A

Auto-antibody (most cases, constant domain of the Rh molecule)

Antibodies to a high-frequency antigen

Antibodies to a large number of antigens

(usually - different strength of reaction)

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34
Q

Transfusion Reactions

A

immunological:

hemolytic (rbc)
Febrile non-hemolytic reactions (wbc, plt)
Allergic reactions (plasma proteins)- most common
GVHD
TRALI

non- immunological

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35
Q

Transfusion hemolytic Reactions mechanism

A

immidiate: ABO, IgM
renal failure, bronchospasm, anaphylaxis and DIC

delayed: Rh (D, C, c, E, e), Kell, Kidd, S/s
fever, rash, jaundice

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36
Q

Transfusion immediate hemolytic Reactions treatment

A

stop the transfusion;
fluids, oxygen, anti-histamines, vasopressors;

DIC- give FFP;

ventilatory support

send the unit back to the blood bank for repeated testing

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37
Q

Transfusion delayed hemolytic Reactions treatment

A

fluids, steroids
anti-histamines and anti-pyretics;

send a new sample of recipient’s serum to the blood bank

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38
Q

Transfusion Febrile Non-Hemolytic Reaction mechanism

A

immediate/delayed

Antibodies to granulocytes in recipient’s plasma

Cytokine accumulation by WBCs in stored blood components

fever, usually with chills
‘impending doom’

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39
Q

Transfusion Febrile Non-Hemolytic Reaction treatment

A

stop the transfusion;

supportive: steroids, anti-histamines, Morphine

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40
Q

Transfusion Febrile Non-Hemolytic Reaction prevention

A

Leukoreduction

FNHTR <5x10^8

CMV <5x10^7

alloimmunization to HLA <5x10^6

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41
Q

transfusion allergic reaction mechanism

A

most frequent (1%)

Antibodies to transfused plasma proteins

more common in IgA deficient patients

pruritus, urticaria, Anaphylaxis

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42
Q

transfusion allergic reaction prevention

A

wash cellular blood products

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43
Q

TRALI (transfusion related acute lung injury)

A

Transfused anti-HLA antibodies react with recipient’s granulocytes and cause their agglutination in pulmonary blood vessels

usually within 6h of blood transfusion

pulmonary edema, fever, hypotension, shock

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44
Q

TRALI (transfusion related acute lung injury) treatment

A

treat with o2 or ventilation (self limited)

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45
Q

TRALI (transfusion related acute lung injury) prevention

A

wash cellular blood products

Disqualification of multiparous female donors

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46
Q

transfusion GVHD mechanism

A

Inability of recipient to reject donor’s lymphocytes: immunocompromised recipients (not HIV)

transfusion from a close relative (homozygote vs heterozygote)

  • Fever, characteristic skin eruption
  • LFT abnormalities
  • BM aplasia
  • Death (95% within 3 weeks)
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47
Q

transfusion GVHD prevention

A

irradiation of blood products

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48
Q

transfusion Non-Immunological Reactions

A

Volume overload

Metabolic (hypothermia, hypocalcemia, hyperkalemia)

Infections:
- Bacterial (PLT transfusion)
Gram negative < Gram positive
- Viral

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49
Q

Weibel-Palade bodies

A

sub endothelial vesicles of vWF multimers

stress brings a release to blood

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50
Q

Von Willebrand Disease

A

chromosome 12

Type 1 VWD - Partial deficiency of VWF

Type 2 VWD - Qualitative defects of VWF

Type 3 [AR] - Complete deficiency of VWF

51
Q

Type 2 VWD sub classes

A

Type 2A - D2, CK sections
selective deficiency of large VWF multimers (15% of patients) intracellular assembly or ADAMTS13 mutations

Type 2B - A1 section
increased affinity to platelets GPIb, thrombocytopenia ( 5%)

Type 2M - A1/3 sections
reduced binding of VWF to platelets GPIb normal VWF multimers

Type 2N [AR] - DD3 section
Decreased affinity to F8- hemophilia like

52
Q

in which VWD types is there a reduction in F8 lvls?

A

2N thus soft tissue and joint bleadings

3 bleed all around

53
Q

WVD treatment?

A

type 1:

  • Desmopressin (DDAVP)- weible bodies release (Contraindicated in type 2B)
  • Antifibrinolytic agent : Tranexamic Acid

type 2-3: F8/VWF concentrate

type 3: rF7a (antibodies to vWF)

54
Q

Acquired VWD etiology?

A

immune:

  • VWF-binding antibodies
  • Lymphoproliferative and autoimmune diseases
  • MGUS, MM

non-immune:

aortic stenosis

  • angiodysplasia of the GI tract (?)
  • Myeloproliferative diseases (ET)- inverse relationship between PLT count and vWF multimers.
55
Q

Aggregometry test conduction

A
  1. Ristocetin (antibiotic) induced activation of platelets in FFP through vWF.
  2. aggregation and plug sinking.
  3. measuring transmittance of light beam percentage.
56
Q

Aggregometry in VWD?

A

2a- no rising in transmittance due initial lack of large multimers

2b- too early rising in transmittance due increased affinity to platelets GPIb

57
Q

Western Blotting in VWD?

A

1- semi reduction in all proteins

2a+b- no large multimers (heavier- first lines)

3- complete disappearance of all VW proteins

58
Q

Glanzmann’s thrombasthenia

A

chromosome 17 [AR]

Type 1 : GPIIb-IIIa receptor is not expressed

Type 2 : Non functional GPIIb-IIIa

59
Q

most common Bleeding symptoms in GT?

A

Menorrhagia 98%

Easy bruising 86%

60
Q

laboratory finding of GT?

A

Platelet count - normal

PT, PTT, fibrinogen - normal

FACS- GPIIb-IIIa expression (CD41, CD61) - reduced /absent

61
Q

aggregometry in glazmann’s?

A

no response to ADP, EPI and Collagen

normal response to Ristocetin
opposite to VWD and Bernard-soulier

62
Q

Treatment of GT

A

platelet transfusion- hard cases

Screening for inhibitor (type 1)- rF7a

Iron and blood replacement when needed

Anti fibrinolytics (Tranexamic acid)

Local adhesive if needed (fibrin sealants)

Menorrhagia-
Anti fibrinolytics, contraceptives, hormonal IUD

Hematopoietic stem cell transplantation

63
Q

Hemophilia A and B inheritance

A

X linked (more men)

30% sporadic

A- F8 gene inversion (intron 22)

64
Q

Hemophilia A and B Bleeding symptoms

A

hemarthrosis- originates from the synovial vessels

internal organs

3-5% develop significant subgaleal or ICH in the perinatal period

65
Q

Hemophilia A and B Classification

A

severe : < 1% factor activity (spontaneous bleeding)

Moderate : 1-5% activity (mostly traumatic Bleeding)

mild : 5-20% activity (only traumatic Bleeding)

Coinheritance of the factor V Leiden - fewer bleedings and a later onset of first bleed

66
Q

Moderate aplastic anemiaCRITERIA?

A

Bone marrow cellularity <30 percent

Absence of severe pancytopenia

Depression of at least 2 OF 3 blood elements below normal

67
Q

Severe aplastic anemia (SAA) criteria?

A

A bone marrow biopsy showing <25 percent of normal cellularity,

Two or three of the following in the peripheral blood:
absolute reticulocyte count <40,000/microL
absolute neutrophil count (ANC) <500/microL
platelet count <20,000/microL.

68
Q

Very severe aplastic anemia criteria?

A

Severe aplastic anemia (SAA) criteria met
+
ANC is <200/microL

69
Q

Moderate AA treatment?

A

close follow up

rarely blood products

70
Q

SAA and VSAA treatment?

A

Hematopoietic Stem cell transplantation (HCT)
<50y with ready donor 🡪 1st line
mutations of DNMT3 or ASXL1

Immuno-suppression (IST) 🡪 Doesnt cancel HCT in future
>50y
ATG + CsA or ATG alone
IST + Eltrombopag
Single agent Eltrombopag or Cyclosporine A

  1. ATG:
  2. CSA - cyclosphorin A ==calcineurin inhibitor
    3.Eltrombopag - An oral thrombopoietin mimetic
    that binds to c-MPL promotes megakaryocytopoiesis
    and the release of platelets from mature megakaryocytes
71
Q

MPN associated thrombosis?

A

unprovoked VTE? 🡪check for MPN (JAK2-V617F) mute

72
Q

NOAC antidotes?

A

idarucizuman- dabigatran

Andexanet alfa- Xabans

73
Q

ITP (immune thrombocytopenia)- Treatment?

A

“Watch and wait” policy- 30% spontaneous remmission

First line:
Steroids
IVIG
Anti D (only for Rh+ 🡪 competition for Fc receptor 🡪 mild hemolysis 🡪 macrophages occupied 🡪 less PLT phagocytosis)

Second line- 
anti CD20
splenectomy (less in young) 
CsA
ChemoRx
thrombomimetics
74
Q

Wiskott-Aldrich syndrome triad?

A

thrombocytopenia
immune def.
eczemaD

75
Q

Tumor Lysis Syndrome treatment?

A

Hydration 3000ml/24h
Allopurinol 300mg/day- prevent uric acid formation

Phosphate binders if needed
Rasburicase in severe cases- degrades uric acid in blood

76
Q

Neutropenic Fever treatment?

A

Broad Spectrum AB

77
Q

High suspicion for Leukostasis treatment?

A

Leukophersis
Hydroxyurea
Hydration

78
Q

AML induction therapy?

A

7 days of continuous Cytarabine
3 days of Daunorubicin
D14 Assessment
Repeat BM on D28

79
Q

AML consolidation therapy?

A 
Allogeneic BMT (graft vs leukemia risks) 
NOT AUTOLLOUGUS!

chemotherapy-based consolidation:
High dose Ara-c and BM check alternation

80
Q

non-chemo based AML therapy (elders?)?

A

Induction:

Combination of Vidaza- Venetoclax

81
Q

ALL: HIGH RISK PATIENTS- MRD BASED?

A

ההנחה: תאי הדגימה ממח העצם מייצגים את מספר התאים הממאירים במחלה, אי לכך כמותם מהווה עדות או פרוגנוזה או תגובה טיפולית
pcr identification

82
Q

ALL therapy agents?

A

B cell ALL [t(12.21) -1%]:

Blinantumumab - chimeric CD 19/ CD 3 antigen, brings T cell to malignant B cells,
fast clearance: 28d constant IV

if chemo+ steroids resistant:
T-CARS- modify T cells to have CD19-type-TCR to makethe, attack malignant B cells

t(9;22)/ BCR-ABL like?
give TKI like imatinib or glivec

83
Q

leukocytosis inducing drugs?

A

BM immobilization and production?
ATRA
G-CSF

84
Q

most common cause of leukocytosis in adults?

A

smoking:
WBC up by 25%
ANC doubled after 2 years

85
Q

LEUKEMOID REACTION etiology?

A

CDT
TB
Pertussis
Visceral lava migrans

תרופות
Asplenia
ממאירות לא המטלוגית

86
Q

LEUKOSTASIS?

A

עליה בצמיגות הדם =>חסימה של כלי דם קטנים => היפוקסיה מקומית => דימומים

פגיעה ריאתית
היפוקסיה, קוצר נשימה
פגיעה נוירולוגית
הפרעות ראייה
סחרחורות, חוסר יציבות
בלבול, שקיעה במצב ההכרה
87
Q

LEUKOSTASIS treatment?

A

לויקופרזיס

88
Q

PV criteria?

A

need 3 major or 2 moajor with 1 minor:

Major Criteria:

Hemoglobin > 16.5 g/dL in men or >16 in women; or hematocrit >49% in men or >48% in women

Bone marrow tri-lineage proliferation with Pleomorphic mature megakaryocytes

Presence of JAK2 mutation

Minor criterion
Subnormal serum erythropoietin level

89
Q

most common cause of thrombocytosis?

A

Iron deficiency anemia

in hospitalized: infection!

90
Q

reactive thrombocytosis pathogenesis?

A

IL-6 stimulates TPO and CRP production in the liver

91
Q

ET criteria?

A

4 major or 1 major + 1 minor:

Major criteria:

Platelets>450X109/L
Bone marrow megakaryocyte proliferation and loose clusters
Not meeting WHO criteria for other myeloid neoplasms
JAK2/CALR/MPL mutation

Minor Criterion
Other clonal marker present or no evidence of reactive thrombocytosis

92
Q

anti emetic drugs?

A

5-HTR antagonist
glucocorticoids
aprepitant
olanzapine (anti psychotics with anti emetic effects)

93
Q

MCV in children between 2-10 years?

A

lower limit 70fl + age (years)

upper limit 84fl + age x 0.6

94
Q

decreased red cell production etiology?

A
  1. Diamond-Blackfan anemia (congenital red cell pure aplasia)
  2. Transient erythroblastopenia of childhood;
  3. Aplastic crisis caused by parvovirus B19 (in patients with chronic hemolytic anemia);
  4. Marrow replacement (by malignant cells or myelofibrosis/osteopetrosis);
  5. Aplastic anemia;
  6. PNH (Paroxysmal nocturnal hemoglobinuria)

Impaired Erythropoietin production:

  1. Anemia of chronic disease in renal failure;
  2. Chronic inflammatory diseases;
  3. Hypothyroidism;
  4. Severe malnutrition;
95
Q

most common Acute blood loss etiology in children?

A

older children: GI tract is the most common

Menstruating girls: blood loss due to dysmenorrhea

neonates: through placenta, abruption, fetomaternal transfusion (vWd)?

premature new born- iatrogenic (many blood samples)

96
Q

Clinical diagnosis of Fanconi anemia?

A

Phenotypic features:
digital and facial dysmorphism
short stature

Progressive thrombocytopenia
Progressive macrocytic anemia
Progressive neutropenia
Increased chromosomal fragility

97
Q

Diamond Blackfan Syndrome (pure red cell aplasia)?

A 
[AR] OR [AD]
intrinsic defect in RBC, early apoptosis
anemia
High MCV
 low reticulocyte rate
decreased erythroid precursosrs in BM
elevated ADA in RBC
98
Q

MM prognosis criteria?

A

ISS:
serum Albumin >3.5 gr/dl (higher- better)
serum b2 microglbulin >3.5 /3.5-5.5/ >5.5 mg/L (lower the better)

R-ISS:
ABOVE
+elevated LDH+
+FISH – t4:14, t14:16, 17p (P53)

SixtyLIM CRAB 🡪 80% Myeloma in 2y
BM PCs > 60%
light chain: FLC Ratio >100
MRI lesions> 0.5cm

99
Q

MM treatment (multiple myeloma)?

A

if able to go through autologous BM transplant- 1st line
can even do TANDEM- transplant X2
if not: (3 combined is better than 2)

Immune Modulators (IMiDs)
Thalidomide
Lenalidomide (Revlimid)
Pomalidomide

Antibodies:
daratumumab- anti CD38
elotuzumab- slmaF7

Proteasome Inhibitors:
Bortezomib (velcade)
Carfilzomib
Ixazomib

bisphosphonates or denosumab

100
Q

ROULEAUX FORMATION?

A

characteristic of MM

protein in blood elevated thus masking RBS negative charge, allowing them to rouleaux

101
Q

pre-engraftment (phase 1) bacterial complications?

A 
gram negative bacilli 
gram positive
GI streptococci species 
reactivation of herpes simples virus
respiratory and enteric viruses
candidiasis
later, aspergillus (the longer the neutropenia)
102
Q

Acute Graft Versus Host Disease?

A

most common reason of death in first 100d post transplantation

pathogenesis:
destruction of BM 🡪 HOST APC activation 🡪 HOST t cell activation 🡪 cytokines and inflammation mediators

103
Q

Acute Graft Versus Host Disease risk factors?

A 
HLA disparity 
age
female to male tranplantation 
strong pre-engraftment treatment (eradication)
peripheral blood graft
104
Q

clinical manifistation of acute GVHD?

A

Erythematous maculopapular rash, often involving the palms and soles
May- entire body surface
May be pruritic and/or painful
In severe cases, bulla may form leading to desquamation

Cholestasis with or without jaundice
Cholestatic enzymes comparatively more deranged than transaminases

Anorexia, nausea and vomiting
Diarrhea, typically green and watery
In severe cases diarrhea contains fresh blood and mucosa and is accompanied by abdominal pain and on occasions followed by paralytic ileus

105
Q

acute GVHD treatment?

A

steroids

immunosuppressants

106
Q

post-engraftment (phase 2) bacterial complications?

A

impaired cellular and humoral immunity:
correlates with GVHD and immunosuppressants intensity
CMV (herpes family):
seropositive host and seronegative donor (haven’t had)
seronegative host and seropositive donor (have had)
pneumocystis
aspergillus

107
Q

CMV In BM transplant treatment?

A

do PCR every weak to detect CMV at beginning
if serum positive than :
ganciclovir

108
Q

Chronic Graft Versus Host Disease?

A

main cause of death after 100d post transplant

109
Q

Chronic Graft Versus Host Disease risk factors?

A 
age
aGVHD
HLA disparity
female to male transplantation 
peripheral blood graft
110
Q

Chronic Graft Versus Host Disease clinical features?

A

40% Matched Siblings, related MM-50%, MUD-70%

Lichen planus , hypo/hyper pigmentation, scleroderma, sweat impairment

nails- Dystrophy, splitting

Alopecia, premature grey hair

Lichen planus, xerostomia

Dry eyes, keratoconjuctivitis, photophobia, blepharitis

strictures or stenosis of esophagus, exocrine pancreatic insufficiency

Fasceitis, joint stiffness (scleroderma)

oral>skin>GI>liver>eyes

111
Q

latephase graft complications?

A

CMV, VZV
Encapsulated bacteria
aspergillus
pneumocystis

112
Q

Bisphosphonates kinds?

A

Clodronate
Non-nitrogen-containing BP
– low potency

Pamidronte, Alendronte
Linear nitrogen-containing BP
– moderate potency

Zoledronic acid, Risedronate
Ring nitrogen-containing BP
– high potency

113
Q

Medication-related osteonecrosis of the jaws cretiria?

A

All the 3 following should be positive:
1. exposed maxillofacial bone or fistula for at least 8 wks
2. current/previous treatment with anti-resorptive and/or anti- angiogenic medications
3. no history of radiation therapy or obvious metastatic
malignancy to the jaw

114
Q

Oral mucositis secondary to cancer therapy Causing agents?

A

Radiotherapy (90-100%) (only in non keratinized mucosa)
> 30 Gy
> 50 Gy → severe mucositis

Chemotherapy (conventional= 20% to 40%< strong =80%), (in keratinized and non keratinized mucosa):

cisplatin, fluorouracil (5-FU), melphalan, doxorubicin, methotrexate (MTX), taxanes, vinblastin

Contributing factors:
-ral infection (HSV, candida)
mainly in immunosuppressed patients
-local trauma

115
Q

Oral mucositis secondary to cancer therapy Management (prevention/treatment)?

A
  1. Hold ice cube in mouth while radiated or chemo
    (influencing on heat-activated ion-channels and receptors TOO)
  2. palifermin- Keratinocyte Growth Factor
  3. low level laser
  4. analgesia by morphine
  5. Benzydamine 0.15% mouth wash (NSAID)
116
Q

Immune Derangement and Associated Pathogens?

A

Granulocytopenia
Gram + bacteria
Gram – bacteria
Fungi

Impaired cellular immunity
Herpes viruses (HSV, VZV…)
Mycobacteria (TB)
Fungi

Impaired humoral immunity
S. pneumoniae

Asplenia
S. pneumoniae
N. meningitidis

117
Q

Febrile Neutropenia Predominant pathogen?

A

P. aeruginosa, E.coli

118
Q

Typhlitis?

A

(necrotizing colitis): ulcerations 🡪 opportunistic bacterial invasion 🡪 local proliferation and tissue destruction by exotoxins + mononuclear inflammatory cells

119
Q

Empiric Therapy of neutropenic patient?

A

anti-pseudomonas
ß-lactam +/- aminoglycoside 🡪 Dramatic reduction in mortality 🡪 broad spectrum antibiotic therapy

Emergence of fungi with prolongation of neutropenia 🡪 add antifungal antibiotic.

30-days mortality
gram-negative 10%
gram-positive 6%

120
Q

hematologic malignancy pathogens?

A

Aspergillus species ~60%:
Fluconazole, Caspo/Anidulafungin, Amphotericin B

Candida species ~30%: Amphotericin B , Voriconazole

Zygomycoses or Fusarium: Posa/Isavuconazol e, Amphotericin B

121
Q

MM diagnostic criteria?

A

plasma cells >10%
+
one of CRAB:

Hemoglobin <10 g/dL or >2 g/dL below normal

Serum calcium >11 mg/dL (>2.75 mmol/liter)

Estimated or measured creatinine clearance <40 mL/min or serum creatinine >2 mg/dL (177 micromol/liter)

One or more osteolytic lesions ≥5 mm in size on skeletal radiography,CT, or PET-CT

or one of SLIM

122
Q

PE or DVT treatment?

A

anticoagulation:
LMWH (calexan)
coumadin (require calexan first)
Noacs

thrombolysis:
PE- systemic if big enough
iliofemoral DVT or PE if hemodynamically unstable - locally, catheter directed

thrombectomy- only hemodynamically unstable PE after thrombolysis failure

IVC filter-
if recurrent or resistive to treatment
contra indication for anticoagulation

123
Q

emicizumab

A

hemophilia treatment

connects factor 9 and 8 to create Xase

מבואות (8 decks)

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