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Heme/Onc Flashcards

1
Q

Platelet transfusion target if no bleeding

A

Transfuse if less than 10

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2
Q

One diagnosis you need to rule out in iron deficiency?

A

G.I. bleed

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3
Q

What’s the MCV in anaemia of chronic disease?

A

Normocytic or microcytic

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4
Q

Typical transfusion threshold for RBC’s and one time you would use a different one?

A

Transfuse below 70 consider using 80 CAD

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5
Q

Signs and symptoms of hemolysis

A

Generally, those associated with anemia: shortness of breath, fatigue, pallor.
Can’t have dark urine from haemoglobinuria or pale skin from unconjugated hyperbilirubinaemia

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6
Q

Lab abnormalities as part of haemolysis work up?

A

LDH is increased, haptoglobin decreased. Can see sphereocytes or schistocytes on peripheral smear.
Unconjugated hyperbili
DAT can be abnormal if d/t membrane antibodies

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7
Q

2 hereditary causes of hemolysis

A

G6PD deficiency
Hereditary spherocytosis

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8
Q

Warm vs cold antibody immune mediated anemia?

A
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9
Q

What is a MAHA?

A

Mechanical destruction of RBC in circulation, caused by damage from fibrin containing vessels

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10
Q

Causes of MAHA?

A
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11
Q

What is TTP-HUS

A

Spectrum of illness with MAHA and thrombocytopenia with varying degrees of renal failure and neurological symptoms

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12
Q

What is classic HUS

A

Occurs in children, MAHA with thrombocytopenia and renal dysfunction following diarrheal illness

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13
Q

Pathophysiology of TTP-HUS?

A

Phibro deposition and platelet aggregation in capillaries/arterials leads to MAHA and thrombocytopenia. Micro thrombi lead to renal failure and CNS symptoms.

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14
Q

What should raise clinical suspicion for TTP – HUS?

A

Anaemia with findings of hemolysis, jaundice, and thrombocytopenia

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15
Q

Management for TTP?

A

Plasma exchange therapy (PLEX)

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16
Q

Management for HUS

A

Usually supportive care is enough in typical HUS, PLEX for severe case cases

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17
Q

What is the cause of TTP?

A

Congenital or acquired deficiency in ADAMTS-13

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18
Q

Why consider reticulocyte count in sickle cell dz if hgb lower than baseline?

A

Low retics would be concerning for aplastic crisis

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19
Q

What do reticulocytes do in hemolysis versus aplastic anemia?

A

Will be elevated in haemolysis and not in aplastic anemia

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20
Q

how is thalassemia inherited?

A

autosomal recessive

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21
Q

4 types of thalassemia and a 1 liner on them:

A

alpha minor: usually asymptomatic
alpha major: fetal death
beta minor: microcytic anemia, usually asymptomatic
beta major: severe anemia

minor vs major comes from the amount of mutated genes they have

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22
Q

sickle cell dz vs sickle trait

A

dz: both chains affected –> sickling of deoxygenated blood

trait: one chain affected –> sickling only occurs under conditions of severe hypoxia, but in general is less severe condition

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23
Q

3 common triggers for sickling?

A

hypoxia, infection, dehydration

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24
Q

what is vaso-occlusive crisis in SCD
mgmt of same

A

-most common SCD manifestation
-caused by sickled RBCs blocking microvasculature
-presents as pain (commonly ribs, back, limbs)
-diagnosis is one EXCLUSION and is clinical
-mgmt analgesia and PO/IV hydration
-consider sepsis/infection in anyone with a fever.

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25
what is acute chest syndrome? how is it dx'd? what is mgmt?
- combo of pulmonary infarct/infection - cxr shows multiple pulmonary infiltrates - mgmt is supportive with O2, ABX consider PLEX for severe cases
26
signs/symptoms of splenic sequestration crisis in sickle cell?
severe anemia, splenomegaly, supportive care, transfuse prn most common age 6 months to 6 years.
27
possible presentations of sickle cells disease
vaso-occlusive acute chest syndrome splenic sequestration aplastic crisis
28
WTF is methemoglobinemia? what can trigger it
in the presence of oxidizing agents, ferrous iron change to ferric (dont really need to know that), and ferric doesn't bind O2 triggers: nitrates of any kind, lidocaine, benzocaine, dapsone
29
methemoglobinemia dx and tx
co-oximetry (>20% is symptomatic, >40% high mortality) ; methylene blue is tx
30
methemoglobinemia presentation
spo2 in 80s, not responding to supp o2. tachycardia, tachypnea, seizure, coma, MI
31
difference between methemoglobinemia and sulfhemoglobinemia?
they have similar pathophys, sulf causes rightward shift of o2 dissociation curve whereas methemoglobinemia causes leftward shift); therefore sulf is usually less severe also methylene blue doesn't help in sulf
32
Causes of thrombocytopenia
33
Briefly what is the path of physiology of DIC and what is the most common presentation?
Widespread activation of coagulation and fibrinolytic cascade. Bleeding is the most common manifestation whereas Thrombosis is very uncommon.
34
Lab abnormalities in DIC
Low fibrinogen, prolonged INR and PTT, elevated D dimer
35
Treatment for DIC
Treat underlying cause, otherwise treatment is basically supportive. Consider platelet transfusion for any platelets less than 50, can use FFP to replace consumed coagulation factors.
36
Common causes of DIC
37
what is a neutrophil count with left shift
predominance of immature neutrophils indicating infection or inflammation opposed to demargination as seen with corticosteroids
38
what happens in primary hemostasis
primary plug via VWF and platelets
39
what is role of fibrinogen?
it is the precursor to fibrin. "fibrin clot" is the final common pathway of intrinsic and extrinsic paths of secondary hemostasis
40
when to suspect issues with primary vs secondary hemostasis
primary: mucocutaneous bleeding secondary: intraarticular
41
platelet levels associated with risk of: -increased bleeding -risk of life threatening bleed -significant risk of life threatening bleed
less than: 50 20 10
42
platelet transfusion targets
< 50 if significant bleeding < 10 regardless of bleeding
43
What do labs show in ITP?
isolated thrombocytopenia
44
mgmt of ITP 2 meds to consider in ITP?
IVIG, steroids, sometimes nothing, but transfuse for severe bleeding under 50 and any values under 10
45
MHP transfusion ratio
Unsure: 2:1:1 or 1:1:1 or prbc, plts and FFP
46
Bleeding disorder with normal platelets, INR and PTT?
Won willebrand disease (4 types)
47
Which factors can you consider replacing in hemophilia?
Factor eight in type, a and factor nine in type B
48
List some prbc transfusion reactions
49
Most common transfusion reaction
Febrile transfusion reaction
50
Dose of prbc in kids
15 mL/kg
51
How much will one unit of prbcs raise hgb?
10
52
How much will one unit (dose) of platelets raise plt count
30 pts?
53
Dose of PCC (aka prothrombin complex concentrate or octaplex)
2000 units for adults
54
Symptoms of hypercalcaemia
Stones, bones, abdominal groans, and psychiatric overtones
55
Emergency department management of hypercalcemia? One additional test to order?
Aggressive, fluid hydration, its fascinates, and consider calcitonin until bisphosphonates reached their therapeutic effect, (about 48 hours) Test to order is PTH, also probably should just look at ionized calcium
56
Classic presentation of hyperviscosity syndrome?
Blurred vision, mucosal, bleeding, neurologic symptoms [headache, dizziness, altered mental status, dyspnea.)
57
Pathophysiology of hyperviscosity syndrome
Microvascular sludging related to increased quantity of cells or para proteins (i.e. in hematologic, malignancies or multiple myeloma)
58
Management of hyperviscosity syndrome
Emergent haematology or medical oncology consult
59
Definition of febrile neutropenia
Sustained temperature over 38 or single temperature over 38.3 in the presence of neutropenia (absolute neutrophil count less than 500 cells per microliter (or 0.5 depending on units)
60
Antibiotic choice in febrile neutropenia
Pip taz Or clavulin if oral
61
Common malignant etiologies of spinal cord compression
Multiple myeloma, lymphoma and metastatic cancer (lung, breast, prostate)
62
What is SVC syndrome?
Compression or invasion of superior vena cava by tumour
63
SVC syndrome, presentation and diagnosis?
Generally diagnosed with CTA of the chest. Presents with dyspnea, oedema of the face trunk, and upper extremities. If presenting with neurologic symptoms, like headache, altered mental status can represent cerebral edema, which is a true emergency
64
what is tumor lysis syndrome (TLS)?
rapid destruction of large number of neoplastic cells from chemo or rapidly growing malignancy leading to release of intracellular contents
65
lab abnormalities seen in tumor lysis syndrome (TLS)?
hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia
66
initial mgmt of tumor lysis syndrome (TLS)?
hydration to protect kidneys from uric acid, manage hyperK in usual fashion, can give allopurinol to reduce uric acid production, refractory cases may need dialysis

CCFP EM (23 decks)

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