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Heme > Heme > Flashcards

Heme Flashcards

1
Q

Mechanism of action of unfractionated heparin

A

Antithrombin III inhibits thrombin and factor Xa

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2
Q

5 contraindications to unfractionated heparin

A 
Hypersensitivity
Active GI bleed
ICH
Bacterial endocarditis
HIT
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3
Q

Treatment of major bleeding on heparin

A

Stop heparin

Protamine 1 mg/100 units given over previous 4 hours, administer slowly as risk of anaphylaxis

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4
Q

What is HIT syndrome, diagnosis and treatment

A

Autoimmune response to heparin, presents as >50% reduction platelets or thrombosis. HIT assay confirms
Treat with direct thrombin inhibitor

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5
Q

Mechanism of action of LMWH

A

Inhibits factor Xa

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6
Q

Which patients require monitoring of factor Xa while on LMWH

A

GFR <50 (cleared by kidneys, needs dose adjustment)
Morbid obesity
Pregnancy

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7
Q

Fondaparinux: a) uses b) treatment of major bleeding c) mechanism

A

A) VTE, hip replacement prophylaxis
B) recombinant factor VIIa
C) inhibits factor X

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8
Q

Primary indication for direct thrombin inhibitors (lepirudin, bivalirudin)

A

Patients with HIT

No antidote exists, care is supportive

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9
Q

Which coagulation factors are inhibited by warfarin

A

II, VII, IX, X

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10
Q

90yo on warfarin for mechanical valve, INR is 10 with no active bleeding, how do you reverse

A

Hold warfarin
Vit k 2.5-5 mg po
Recheck INR

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11
Q

Warfarin reversal with any major bleeding

A

Hold warfarin
Vitamin K 10mg iv slow push (risk anaphylaxis)
FFP or PCC or recombinant factor VIIa

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12
Q

4 complications of warfarin

A

Under anticoagulation
Over anticoagulation (bleed)
Paradoxical thrombosis between 2nd and tenth day
Warfarin induced skin thrombosis

Reduce risk of last two by bridging with heparin

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13
Q

Mechanism of action of dabigatran, apixaban and Rivaroxaban

A

Dabi direct thrombin inhibitor

Rivaroxaban and apixaban factor Xa inhibitor

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14
Q

Management of major bleed on DOAC

A

Stop offending drug
Supportive management
PCC, FFP, antifibrinolytics eg tranexamic acid

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15
Q

What is bleeding due to with patients taking aspirin

A

Platelet dysfunction, not thrombocytopenia

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16
Q

Three classes of anti platelets and their mechanism of action

A

Aspirin: cox 1 inhibitor, prevents thromboxane A2 synthesis
Thienopyridines (clopidogrel): irreversibly inhibits platelet aggregation
Glycoprotein IIA/IIIb inhibitors (abciximab): inhibit platelet activation

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17
Q

What additives are in packed RBCs

A

Anticoagulant preservatives; citrate, phosphate, dextrose, adenine

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18
Q

How much volume is in one unit of adult and pediatric pRBCs

A

350 ml in adult

60 ml in peds

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19
Q

What should you do to reduce the risk of febrile nonhemolytic reactions and prevent sensitization in bone marrow eligible patients and reduce risk of CMV and HIV transmission in immunesuppressed

A

Use leukoreduced PRBCs

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20
Q

Indications for transfusion pRBCs

A

End organ damage related to anemia (ie MI, stroke)

Active or recent bleed with Hb level under 70, 80-100 in known cardiac disease

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21
Q

How much does one unit of pRBCs increase hemoglobin

A

10

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22
Q

Mechanism of action of tpa

A

Activates plasminogen to plasmin, breakdown of fibrinogen and cross linked fibrin

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23
Q

Define thrombocytopenia and name four causes

A

Platelets < 100

Decreased production, increased destruction, splenic sequestration

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24
Q

Transfusion threshold for platelets

A

Life threatening hemorrhage and abnormal platelets
Platelets under 10 (except ITP, TTP, HIT, HUS)
Bleeding under 50
Massive transfusion

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25
Q

Seven causes of increased platelet destruction

A 
Immunologic:
ITP
HIT
infection 
Leukaemia, lymphoma
Mechanical:
TTP
HUS
DIC
HELLP
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26
Q

Four causes of decreased platelet production

A

Marrow infiltration
Drugs
Toxins
Infections

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27
Q

Treatment of ITP

A

Treat for severe bleeding under 50, platelet under 10 without bleeding
Steroids, IVIG for unresponsive to steroids, recalcitrant may need splenectomy
Platelet transfusion only for life threatening hemorrhage
Avoid NSAIDS and physical activity for two months

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28
Q

9 causes of DIC

A

Infection (most common): GP and GN sepsis, meningiococcemia, Rocky Mountain spotted fever, typhoid fever
Trauma (burns, crush, head injury)
Shock
Pregnancy complications (abruption, amniotic fluid embolus)
Transfusion and drug reaction
Carcinoma (lymphoma, leukaemia, adenocarcinoma)
Liver disease
ARDS
envenomation
Surgical procedures
Heat stroke

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29
Q

Laboratory findings in DIC

A

Coagulation product consumption: prolonged PT and PTT, low platelet, low fibrinogen, increased thrombin time
Active clot formation: elevated dimer
Microangiopathic hemolytic anemia:

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30
Q

Treatment of DIC

A

Treat underlying cause
Replace consumed coagulation factors: FFP and Cryo
Platelet transfusion under 50 of bleeding, 10 if not
If thrombosis predominated give heparin
Purpura fulminans (protein c deficiency) treat with protein c concentrate (see in severe sepsis, bruising then necrotic centre)

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31
Q

Function of vWF and treatment of Von willebrand disease

A

Facilitates adherence or platelets to injured blood vessels
Stabilized factor VIII in plasma
Treatment:
DDAVP (stimulates release of vWF and factor VIII)
vWF concentrate in all cases serious bleeding
Cryo if no vWF available but carries risk infection

32
Q

What should you consider in someone with bleeding disorder but normal platelet, PT, PTT?

A

Von willebrand disease

33
Q

Which factors are deficient in hemophilia a and b

A 
A= VIII
B= IX
34
Q

Clinical symptoms hemophilia

A

Easy bruising, hemarthrosis, hematuria, muscle hematoma

excessive bleeding after procedures, severe/delayed bleeding with minor trauma

35
Q

Management of bleeding or trauma in hemophilia A

A

Factor VIII replacement by site (weight based and dependent on intrinsic factor activity)
DDAVP in mild to moderate bleeding in hemophilia a

36
Q

Treatment of hemophilia B

A

Factor ix replacement weight based and site based
Use in extreme caution with presence of inhibitors (clotting factor mixing test) as can cause anaphylaxis so use PCC or factor VIIa in these cases

37
Q

9 massive transfusion complications

A

Hypocalcemia
Hypothermia
Acidosis
Hyperkalemia
TACO
TRALI (supportive) – see most commonly w FFP and platelets
Fever transfusion reaction
Acute hemolytic transfusion reaction (ABO incompatibility)
Allergic
Delayed transfusion reaction (extravascular hemolysis from small amounts RBC antibodies)
Graft vs host disease (irradiate platelets in immunecompromised)
Infection

38
Q

How much does one unit of platelets elevate platelet level by

A

30

39
Q

Three situations where you want to avoid platelet transfusion

A

ITP, TTP, HIT

40
Q

What is in fibrinogen, how is it administered

A

All clotting factors, fibrinogen
Given as 4-6 units (250 ml volume each)
Indicated in significant hemorrhage secondary to coagulopathy
Needs to be cross matched

41
Q

What is in Cryo and when is it indicated

A

VIII, XIII, vWF, fibrinogen
Indicated in low fibrinogen state plus hemorrhage
Consider in hemophilia and vW

42
Q

What is in PCC

A

II, VII, IX, X (vit k dependent)
Give in life threatening hemorrhage
Needs to be given with vit k as is transient
Lower volume and faster than FFP

43
Q

Diagnostic findings in hereditary spherocytosis

Treatment

A

Hemolytic anemia (extravascular)
Negative Coombs
Positive osmotic fragility test
Spherocytes on smear

Folic acid supplementation, some need splenectomy

44
Q

Precipitants of G6PD
Lab findings
Treatment

A

Infection, fava beans, drugs (eg post malarial treatment)
Hemolytic anemia, hemoglobinuria, hyperbilirubinemia, Heinz bodies on smear and bite cells
Supportive treatment

45
Q

Difference between warm and Cold autoimmune hemolytic anemia

A

Warm is IgG antibodies against RBCs antigens. Binds at body temp. Associated w lymphoproliferative disorders
Cold is igm antibodies. Binds at cool temp, assoc w EBV, lymphoma, mycoplasma

46
Q

Two examples of alloimmune hemolytic anemia

A

Transfusion reaction

Hemolytic disease of the newborn

47
Q

6 causes of microangiopathic hemolytic anemia

A 
DIC
TTP
HUS
pregnancy (HELLP)
Malignant hypertension
Malignancies
48
Q

Hallmarks of TTP-HUS spectrum

A

Microangiopathic hemolytic anemia
Thrombocytopenia
Plus minus renal and neuro involvement

49
Q

Clinical picture HUS

A

Children, bloody diarrhea
Renal dysfunction, anemia, thrombocytopenia, microangiopathic anemic
Can see jaundice, fever, purpura

50
Q

Pathophysiology of renal failure and neuro involvement in HUS-TTP

A

Fibrin deposition and platelet aggregation lead to intravascular hemolysis, microthrombi in renal and CNS vasculature

51
Q

Work up of TTP HUS

A 
CBC hapto ldh smear
Coombs to rule out autoimmune
D-dimer, fibrinogen for DIC, ptt inr
Stool for shiga toxin producing bacteria (e coli, salmonella, shigella)
Creatinine
Urine r and m
52
Q

Classic cause of TTP

A

Congenital or acquired deficiency in ADAMTS13 protein activity

53
Q

Management HUS

A

Supportive care
Plasma exchange in severe
No antibiotics

54
Q

Management of TTP

A

Plasma exchange

55
Q

Four types of thalassemia

A

Alpha minor: usually mild, asymptomatic
Alpha maj: fetal hydrops and demise
Beta min: asymptonatic, hypochromic, microcytic anemia
Beta maj: severe anemia, splenomegaly, frontal bossing, transfusion dependent (splenectomy can reduce need for this)

56
Q

Pathophysiology of sickle cell

A

Autosomal recessive disease, structure of b globin chain
One chain is carrier, both is disease
Deoxygenated RBCs take on sickle shape, leads to obstruction of RBCs in microcirculatoin and vaso-occlusive ischemic tissue injury

57
Q

3 most common precipitants sickle cell

A

Hypoxia
Dehydration
Infection

58
Q

Possible indications of exchange transfusion in sickle cell disease

A

Acute CNS event
Acute chest syndrome
Cardiopulmonary collapse
Priapism

59
Q

Work up of possible sickle cell pain crisis

A

CBC, retics (hemolysis or aplastic crisis), smear, urine, chest X-ray, culture

60
Q

Bugs implicated in acute chest syndrome in sickle cell

A

Staph strep chlamydia and mycoplasma

RSV

61
Q

Treatment acute chest syndrome

A 
Oxygen
Iv hydration 
Antibiotics
Analgesia
Exchange transfusion if multiple lobe involvement, severe hypoxia, refractory to antibiotics
62
Q

Age of splenic sequestration crisis in sickle cell

A

6 mo to 6 years

63
Q

9 possible presentations and complications of sickle cell disease

A 
Stroke
Acute chest syndrome
Acute pain crisis
Osteomyelitis (staph aureus, salmonella)
Osteonecrosis 
Cholelithiasis
Priapism
Ulceration 
Aplastic anemia
64
Q

Definition of polycythemia

A

165 women, 185 men

65
Q

Causes polycythemia

Treatment

A

Primary (myeloproliferative)
Secondary (increased epo eg lung disease, high altitude, expo secreting tumor)
Phlebotomy is treatment

66
Q

Complications polycythemia

A

Both thrombosis from hyperviscosity and bleeding from platelet dysfunction
Hypervolemia syndrome

67
Q

Pathophysiology of methemoglobinemia

A

Oxidizing agents cause ferrous iron to change to ferric iron which can’t bind O2

68
Q

5 causes of methemoglobinemia

A 
Nitrates
Lidocaine
Benzocaine
Sulfa
Dapsone
Pyridium
69
Q

Clinical presentation methemoglobinemia

A

MI, seizures, coma, death
Cyanosis
Anxiety, headache, tachycardia
Pulse ox 80-85 no response to oxygen with normal PaO2 on abg
Co-oximetry confirms
Mortality with levels over 40%, symptoms over 20%

Treat with methylene blue 1-2 mg /kg contraindicated in G6PD

70
Q

Causes of neutrophilia

A 
Infection or inflammation (esp w left shift or increase in immature neutrophils)
Stress reaction (exercise, seizures, trauma, ketosis)
71
Q

What is a leukemoid reaction

A

Nonleukemic leukocytosis> 50

See in sepsis, tb, Hodgkins, metastatic non hem cancers

72
Q

Four types of leukaemia

A

CML: adult, least common, Philadelphia chromosome, typically asymptomatic. Increased polymorphonuclear neutrophils and myelocytes
Aml: most common adult acute, anemia, thrombocytopenia, variable leukocyte, blasts
CLL: lymphadenopathy, lymphocytosis, neutropenia, anemia, thrombocytopenia
ALL: peds, oancytopenia, blasts.

73
Q

Pathophysiology of multiple myeloma

A

Single plasma cell clone and immunoglobin proliferation

74
Q

Complications of multiple myeloma

A

Hypercalcemia, pathological fracture, hyperviscosity syndrome, spinal cord compression syndrome

75
Q

What type of malignancy has the Reed-Sternberg cell or owl eye cells

A

Hodgkin lymphoma

76
Q

Which type of non Hodgkin lymphoma tends to be curable

A

Aggressive (eg diffuse large B cell, anaplastic large cell, brukittm peripheral T cell, lymphoblastic)

Heme (3 decks)

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