המטולוגיה Flashcards
(123 cards)
1
Q
Pseodo pelger form in blood smear?
A
גרנולוציטיים דיספלסטיים בצורת משקפיים
מאפיין MDS
2
Q
macrocytic anemia DD?
A
חסר B12 חסר חומצה פולית
MDS
אנמיה אפלסטית
אנמיה המוליטית
תרופות
היפותירואידיזם
אלכוהול
3
Q
Polychromasia
A
reticulocytosis
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)
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
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
7
Q
microcytic anemia DD (tails)?
A
חסר ברזל מתקדם מחלה דלקתית תלסמיה עופרת אנמיה סידרובלאסטית
8
Q
normocytic anemia DD?
A
חסר ברזל כרוני
טלסמיה מינור
אנמיה סידרובלסטית (דפקט בסינטזת heme)
אנמיה כרונית/ דלקתית
9
Q
low MCV and low reticulocytes anemia DD?
A
חסר ברזל בינוני או בתחילתו
אנמיה כרונית/ דלקתית
כימו
כשל כלייתי
10
Q
high MCV and low reticulocytes anemia DD?
A
אנמיה מגלובלסטית
MDS
אנמיה אפלסטית
תרופות
היפוטיירודיזם
אלכוהוליזם
11
Q
DD אנמיה עם רטיקולוציטים גבוהים?
A
MCV נורמאלי/נמוך:
תלסמיה מג’ור
ספרוציטוזיס
MCV גבוה:
אנמיה חרמשית
G6PD
IHA
מלריה
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
13
Q
מה נבדוק אם רואים סכיסטוציטים (שברי תאים) במשטח עם חשד לאנמיה המוליטית?
A
פרוטזה- לא?
נבדוק תפקודי קרישה לDIC- לא?
TTP/HUS
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
15
Q
באיזו אנמיה נראה-
רמות EPO גבוהות
הפטוספלנומגליה, הרחבת מח עצם, המטופואיזה חוץ- מדולרית, כולליטיאזיס
A
תלסמיה מייג’ור
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
17
Q
סיבוכים של עירויים
A
עודפי ברזל
התפתחות נוגדנים
זיהומים- HCV
18
Q
איברי מטרה לעודפי ברזל
A
עור
לב- אי ספיקה, הפרעות קצב (שקיעה במערכת ההולכה)
כבד- carcinoma
מערכת אנדוקריני
19
Q
Deferoxamime (Desferal)
A
תרופה לפינוי ברזל- עושה כלציה בזרם הדם. מתן בזריקה ופינוי ברזל בשתן.
ת”ל- הפרעות ראייה ושמיעה.
20
Q
Deferasirox (Exjade)
A
תרופה לסילוק ברזל דרך המעי.
POx1xD
ת”ל: GIT, kidney, liver
21
Q
(Deferiprone (L1, ferriprox)
A
תרופה לסילוק ברזל דרך המעי.
POx3xD
ת”ל: arthralgia, agranulocytosis, GIT
22
Q
Luspatercept
A
תרופות המשפרות הבשלת התאים האדומים במח העצם
23
Q
מהי ההמלצה לגבי שילוב תרופות פומיות וזריקות לסילוק ברזל?
A
שילוב של זריקות ומתן פומי
24
Q
לאילו מחלות ניתן תרופות שעושות אינדוקצייה של המוגלובין F?
A
תלסמיה- בעיקר אינטרמדיה ואנמיה חרמשית
25
RBC - Storage Limitations
PH (down)
plasma K (up)
plasma LDH (up)
plasma HB (up)
(down) 2,3-BPG
ATP (down)
26
PLT collection characteristics
seperation from blood:
unit volume: 50 ml
dose for transfusion: 4-6 units
apheresis:
unit volume: 200 ml
dose for transfusion: 1 unit
27
Indications for Granulocytes Transfusion
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
28
Indications for FFP transfusion
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
29
Cryoprecipitate Characteristics
von Willebrand factor
factor VIII
factor XIII
fibrinogen
fibronectin
30
blood typing unexpected results
1. Direct typing: no antigens present (O)
reverse typing: only anti-B present (A)
The reason: weak A
2. 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
3. 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.
31
how to Type and Match bloods?
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)
3. If auto-antibody is suspected - direct anti
globulin (Coombs) test
32
how does Antibody Screening performed?
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
33
Antibody Screening pan agglutination reasons?
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)
34
Transfusion Reactions
immunological:
hemolytic (rbc)
Febrile non-hemolytic reactions (wbc, plt)
Allergic reactions (plasma proteins)- most common
GVHD
TRALI
non- immunological
35
Transfusion hemolytic Reactions mechanism
immidiate: ABO, IgM
renal failure, bronchospasm, anaphylaxis and DIC
delayed: Rh (D, C, c, E, e), Kell, Kidd, S/s
fever, rash, jaundice
36
Transfusion immediate hemolytic Reactions treatment
stop the transfusion;
fluids, oxygen, anti-histamines, vasopressors;
DIC- give FFP;
ventilatory support
send the unit back to the blood bank for repeated testing
37
Transfusion delayed hemolytic Reactions treatment
fluids, steroids
anti-histamines and anti-pyretics;
send a new sample of recipient's serum to the blood bank
38
Transfusion Febrile Non-Hemolytic Reaction mechanism
immediate/delayed
Antibodies to granulocytes in recipient's plasma
Cytokine accumulation by WBCs in stored blood components
fever, usually with chills
'impending doom'
39
Transfusion Febrile Non-Hemolytic Reaction treatment
stop the transfusion;
supportive: steroids, anti-histamines, Morphine
40
Transfusion Febrile Non-Hemolytic Reaction prevention
Leukoreduction
FNHTR <5x10^8
CMV <5x10^7
alloimmunization to HLA <5x10^6
41
transfusion allergic reaction mechanism
most frequent (1%)
Antibodies to transfused plasma proteins
more common in IgA deficient patients
pruritus, urticaria, Anaphylaxis
42
transfusion allergic reaction prevention
wash cellular blood products
43
TRALI (transfusion related acute lung injury)
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
44
TRALI (transfusion related acute lung injury) treatment
treat with o2 or ventilation (self limited)
45
TRALI (transfusion related acute lung injury) prevention
wash cellular blood products
Disqualification of multiparous female donors
46
transfusion GVHD mechanism
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)
47
transfusion GVHD prevention
irradiation of blood products
48
transfusion Non-Immunological Reactions
Volume overload
Metabolic (hypothermia, hypocalcemia, hyperkalemia)
Infections:
- Bacterial (PLT transfusion)
Gram negative < Gram positive
- Viral
49
Weibel-Palade bodies
sub endothelial vesicles of vWF multimers
stress brings a release to blood
50
Von Willebrand Disease
chromosome 12
Type 1 VWD - Partial deficiency of VWF
Type 2 VWD - Qualitative defects of VWF
Type 3 [AR] - Complete deficiency of VWF
51
Type 2 VWD sub classes
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
in which VWD types is there a reduction in F8 lvls?
2N thus soft tissue and joint bleadings
3 bleed all around
53
WVD treatment?
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
Acquired VWD etiology?
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
Aggregometry test conduction
1. Ristocetin (antibiotic) induced activation of platelets in FFP through vWF.
2. aggregation and plug sinking.
3. measuring transmittance of light beam percentage.
56
Aggregometry in VWD?
2a- no rising in transmittance due initial lack of large multimers
2b- too early rising in transmittance due increased affinity to platelets GPIb
57
Western Blotting in VWD?
1- semi reduction in all proteins
2a+b- no large multimers (heavier- first lines)
3- complete disappearance of all VW proteins
58
Glanzmann's thrombasthenia
chromosome 17 [AR]
Type 1 : GPIIb-IIIa receptor is not expressed
Type 2 : Non functional GPIIb-IIIa
59
most common Bleeding symptoms in GT?
Menorrhagia 98%
Easy bruising 86%
60
laboratory finding of GT?
Platelet count - normal
PT, PTT, fibrinogen - normal
FACS- GPIIb-IIIa expression (CD41, CD61) - reduced /absent
61
aggregometry in glazmann's?
no response to ADP, EPI and Collagen
| normal response to Ristocetin
opposite to VWD and Bernard-soulier
62
Treatment of GT
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
Hemophilia A and B inheritance
X linked (more men)
30% sporadic
A- F8 gene inversion (intron 22)
64
Hemophilia A and B Bleeding symptoms
hemarthrosis- originates from the synovial vessels
internal organs
3-5% develop significant subgaleal or ICH in the perinatal period
65
Hemophilia A and B Classification
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
Moderate aplastic anemia CRITERIA?
Bone marrow cellularity <30 percent
Absence of severe pancytopenia
Depression of at least 2 OF 3 blood elements below normal
67
Severe aplastic anemia (SAA) criteria?
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
Very severe aplastic anemia criteria?
Severe aplastic anemia (SAA) criteria met
+
ANC is <200/microL
69
Moderate AA treatment?
close follow up
| rarely blood products
70
SAA and VSAA treatment?
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
MPN associated thrombosis?
unprovoked VTE? 🡪check for MPN (JAK2-V617F) mute
72
NOAC antidotes?
idarucizuman- dabigatran
| Andexanet alfa- Xabans
73
ITP (immune thrombocytopenia)- Treatment?
“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
Wiskott-Aldrich syndrome triad?
thrombocytopenia
immune def.
eczemaD
75
Tumor Lysis Syndrome treatment?
Hydration 3000ml/24h
Allopurinol 300mg/day- prevent uric acid formation
Phosphate binders if needed
Rasburicase in severe cases- degrades uric acid in blood
76
Neutropenic Fever treatment?
Broad Spectrum AB
77
High suspicion for Leukostasis treatment?
Leukophersis
Hydroxyurea
Hydration
78
AML induction therapy?
7 days of continuous Cytarabine
3 days of Daunorubicin
D14 Assessment
Repeat BM on D28
79
AML consolidation therapy?
```
Allogeneic BMT (graft vs leukemia risks)
NOT AUTOLLOUGUS!
```
chemotherapy-based consolidation:
High dose Ara-c and BM check alternation
80
non-chemo based AML therapy (elders?)?
Induction:
| Combination of Vidaza- Venetoclax
81
ALL: HIGH RISK PATIENTS- MRD BASED?
ההנחה: תאי הדגימה ממח העצם מייצגים את מספר התאים הממאירים במחלה, אי לכך כמותם מהווה עדות או פרוגנוזה או תגובה טיפולית
pcr identification
82
ALL therapy agents?
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
leukocytosis inducing drugs?
BM immobilization and production?
ATRA
G-CSF
84
most common cause of leukocytosis in adults?
smoking:
WBC up by 25%
ANC doubled after 2 years
85
LEUKEMOID REACTION etiology?
CDT
TB
Pertussis
Visceral lava migrans
תרופות
Asplenia
ממאירות לא המטלוגית
86
LEUKOSTASIS?
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
LEUKOSTASIS treatment?
לויקופרזיס
88
PV criteria?
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
most common cause of thrombocytosis?
Iron deficiency anemia
in hospitalized: infection!
90
reactive thrombocytosis pathogenesis?
IL-6 stimulates TPO and CRP production in the liver
91
ET criteria?
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
anti emetic drugs?
5-HTR antagonist
glucocorticoids
aprepitant
olanzapine (anti psychotics with anti emetic effects)
93
MCV in children between 2-10 years?
lower limit 70fl + age (years)
| upper limit 84fl + age x 0.6
94
decreased red cell production etiology?
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
most common Acute blood loss etiology in children?
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
Clinical diagnosis of Fanconi anemia?
Phenotypic features:
digital and facial dysmorphism
short stature
Progressive thrombocytopenia
Progressive macrocytic anemia
Progressive neutropenia
Increased chromosomal fragility
97
Diamond Blackfan Syndrome (pure red cell aplasia)?
```
[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
MM prognosis criteria?
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
MM treatment (multiple myeloma)?
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
ROULEAUX FORMATION?
characteristic of MM
| protein in blood elevated thus masking RBS negative charge, allowing them to rouleaux
101
pre-engraftment (phase 1) bacterial complications?
```
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
Acute Graft Versus Host Disease?
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
Acute Graft Versus Host Disease risk factors?
```
HLA disparity
age
female to male tranplantation
strong pre-engraftment treatment (eradication)
peripheral blood graft
```
104
clinical manifistation of acute GVHD?
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
acute GVHD treatment?
steroids
| immunosuppressants
106
post-engraftment (phase 2) bacterial complications?
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
CMV In BM transplant treatment?
do PCR every weak to detect CMV at beginning
if serum positive than :
ganciclovir
108
Chronic Graft Versus Host Disease?
main cause of death after 100d post transplant
109
Chronic Graft Versus Host Disease risk factors?
```
age
aGVHD
HLA disparity
female to male transplantation
peripheral blood graft
```
110
Chronic Graft Versus Host Disease clinical features?
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
latephase graft complications?
CMV, VZV
Encapsulated bacteria
aspergillus
pneumocystis
112
Bisphosphonates kinds?
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
Medication-related osteonecrosis of the jaws cretiria?
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
Oral mucositis secondary to cancer therapy Causing agents?
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
Oral mucositis secondary to cancer therapy Management (prevention/treatment)?
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
Immune Derangement and Associated Pathogens?
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
Febrile Neutropenia Predominant pathogen?
P. aeruginosa, E.coli
118
Typhlitis?
(necrotizing colitis): ulcerations 🡪 opportunistic bacterial invasion 🡪 local proliferation and tissue destruction by exotoxins + mononuclear inflammatory cells
119
Empiric Therapy of neutropenic patient?
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
hematologic malignancy pathogens?
Aspergillus species ~60%:
Fluconazole, Caspo/Anidulafungin, Amphotericin B
Candida species ~30%: Amphotericin B , Voriconazole
Zygomycoses or Fusarium: Posa/Isavuconazol e, Amphotericin B
121
MM diagnostic criteria?
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
PE or DVT treatment?
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
emicizumab
hemophilia treatment
| connects factor 9 and 8 to create Xase
