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Heme Flashcards

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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
Seven causes of increased platelet destruction
``` Immunologic: ITP HIT infection Leukaemia, lymphoma Mechanical: TTP HUS DIC HELLP ```
26
Four causes of decreased platelet production
Marrow infiltration Drugs Toxins Infections
27
Treatment of ITP
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
28
9 causes of DIC
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
29
Laboratory findings in DIC
Coagulation product consumption: prolonged PT and PTT, low platelet, low fibrinogen, increased thrombin time Active clot formation: elevated dimer Microangiopathic hemolytic anemia:
30
Treatment of DIC
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)
31
Function of vWF and treatment of Von willebrand disease
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
What should you consider in someone with bleeding disorder but normal platelet, PT, PTT?
Von willebrand disease
33
Which factors are deficient in hemophilia a and b
``` A= VIII B= IX ```
34
Clinical symptoms hemophilia
Easy bruising, hemarthrosis, hematuria, muscle hematoma | excessive bleeding after procedures, severe/delayed bleeding with minor trauma
35
Management of bleeding or trauma in hemophilia A
Factor VIII replacement by site (weight based and dependent on intrinsic factor activity) DDAVP in mild to moderate bleeding in hemophilia a
36
Treatment of hemophilia B
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
9 massive transfusion complications
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
How much does one unit of platelets elevate platelet level by
30
39
Three situations where you want to avoid platelet transfusion
ITP, TTP, HIT
40
What is in fibrinogen, how is it administered
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
What is in Cryo and when is it indicated
VIII, XIII, vWF, fibrinogen Indicated in low fibrinogen state plus hemorrhage Consider in hemophilia and vW
42
What is in PCC
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
Diagnostic findings in hereditary spherocytosis | Treatment
Hemolytic anemia (extravascular) Negative Coombs Positive osmotic fragility test Spherocytes on smear Folic acid supplementation, some need splenectomy
44
Precipitants of G6PD Lab findings Treatment
Infection, fava beans, drugs (eg post malarial treatment) Hemolytic anemia, hemoglobinuria, hyperbilirubinemia, Heinz bodies on smear and bite cells Supportive treatment
45
Difference between warm and Cold autoimmune hemolytic anemia
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
Two examples of alloimmune hemolytic anemia
Transfusion reaction | Hemolytic disease of the newborn
47
6 causes of microangiopathic hemolytic anemia
``` DIC TTP HUS pregnancy (HELLP) Malignant hypertension Malignancies ```
48
Hallmarks of TTP-HUS spectrum
Microangiopathic hemolytic anemia Thrombocytopenia Plus minus renal and neuro involvement
49
Clinical picture HUS
Children, bloody diarrhea Renal dysfunction, anemia, thrombocytopenia, microangiopathic anemic Can see jaundice, fever, purpura
50
Pathophysiology of renal failure and neuro involvement in HUS-TTP
Fibrin deposition and platelet aggregation lead to intravascular hemolysis, microthrombi in renal and CNS vasculature
51
Work up of TTP HUS
``` 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
Classic cause of TTP
Congenital or acquired deficiency in ADAMTS13 protein activity
53
Management HUS
Supportive care Plasma exchange in severe No antibiotics
54
Management of TTP
Plasma exchange
55
Four types of thalassemia
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
Pathophysiology of sickle cell
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
3 most common precipitants sickle cell
Hypoxia Dehydration Infection
58
Possible indications of exchange transfusion in sickle cell disease
Acute CNS event Acute chest syndrome Cardiopulmonary collapse Priapism
59
Work up of possible sickle cell pain crisis
CBC, retics (hemolysis or aplastic crisis), smear, urine, chest X-ray, culture
60
Bugs implicated in acute chest syndrome in sickle cell
Staph strep chlamydia and mycoplasma | RSV
61
Treatment acute chest syndrome
``` Oxygen Iv hydration Antibiotics Analgesia Exchange transfusion if multiple lobe involvement, severe hypoxia, refractory to antibiotics ```
62
Age of splenic sequestration crisis in sickle cell
6 mo to 6 years
63
9 possible presentations and complications of sickle cell disease
``` Stroke Acute chest syndrome Acute pain crisis Osteomyelitis (staph aureus, salmonella) Osteonecrosis Cholelithiasis Priapism Ulceration Aplastic anemia ```
64
Definition of polycythemia
165 women, 185 men
65
Causes polycythemia | Treatment
Primary (myeloproliferative) Secondary (increased epo eg lung disease, high altitude, expo secreting tumor) Phlebotomy is treatment
66
Complications polycythemia
Both thrombosis from hyperviscosity and bleeding from platelet dysfunction Hypervolemia syndrome
67
Pathophysiology of methemoglobinemia
Oxidizing agents cause ferrous iron to change to ferric iron which can't bind O2
68
5 causes of methemoglobinemia
``` Nitrates Lidocaine Benzocaine Sulfa Dapsone Pyridium ```
69
Clinical presentation methemoglobinemia
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
Causes of neutrophilia
``` Infection or inflammation (esp w left shift or increase in immature neutrophils) Stress reaction (exercise, seizures, trauma, ketosis) ```
71
What is a leukemoid reaction
Nonleukemic leukocytosis> 50 | See in sepsis, tb, Hodgkins, metastatic non hem cancers
72
Four types of leukaemia
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
Pathophysiology of multiple myeloma
Single plasma cell clone and immunoglobin proliferation
74
Complications of multiple myeloma
Hypercalcemia, pathological fracture, hyperviscosity syndrome, spinal cord compression syndrome
75
What type of malignancy has the Reed-Sternberg cell or owl eye cells
Hodgkin lymphoma
76
Which type of non Hodgkin lymphoma tends to be curable
Aggressive (eg diffuse large B cell, anaplastic large cell, brukittm peripheral T cell, lymphoblastic)

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