Exam II: Hematological System and Diseases Flashcards
Anemia Definition: Deficiency of ____
RBCs
Anemia H&H: ___/___ for women; ___/___ for men
11.5/36
12.5/40
Anemia Primary adverse effect: Decreased ____ ____ content
arterial oxygen
Anemia ___ ____ of OxyHgb Dissociation Curve (_____ affinity - increased O2 to tissues)
R shift
decreased
Anemia Increased _____ d/t decreased viscosity
CO
Anemia - Decreased tissue O2 causes _____ (___) stimulation which increases ____ production
erythropoietin (EPO)
RBC
Anemia: Many causes. Most common: ___ deficiency, ____ disease, acute ____ loss
iron
chronic
blood
Anemia decreases CaO2 leads to R shift
(decreases Hgb’s affinity for O2 which increases tissue O2)
AIs: What is minimal acceptable pre-op Hgb???
Hgb of 10g/dL commonly used but age, chronic disease and anticipated surgical blood loss must be considered.
AIs: No studies point to ____ ____ to prevent MIs, ischemia, infection or improve outcomes.
recommended Hgb
AIs: In vitro: Peak O2 carrying occurs with Hct of ____%.
30%
(<30 causes decreased carrying capacity, >30 causes increased viscosity)
AIs: Chronic anemia increases ___-___ and ___ shift
2,3-DPG and R shift
AIs: ____ increase Hgb 2 x more than whole blood
PRBCs
AIs: Decrease temp causes ___ ____ of OxyHgb D curve
left shift
AIs: Consider ____ _____ or cell saver.
normovolemic hemodilution
AIs: IN THE PRESENSE OF _______, transfuse when symptomatic.
NORMOVOLEMIA
AIs: As a general rule: Transfuse with acute blood loss when Hgb drops to ___g/dL, especially with ______.
7
comorbidities
RBC structure: Bi-concave disc with no _____, no _____, 33% ______
nucleus
mitochondria
hemoglobin
RBC structure: ____ and ____ provide intracellular energy.
2,3-DPG
ATP
RBC: life span ___-___ ___
100-120 days
RBC: _____ ____ _____ regulate erythropoietin (EPO).
renal O2 sensors
RBC: EPO stimulates RBC production in ____ ____.
bone marrow
Hereditary Spherocytosis: Abnormal ____ ____, most common inherited hemolytic anemia, 1/3 very mild, 5% can have life-threatening hemolytic crises usually d/t ____ ____. Prone to ______.
membrane protein
infectious illness
cholithiasis
Hereditary Spherocytosis AIs: Episodic anemia with _____ and ______
infection
cholelithiasis
Hereditary Elliptocytosis: Abnormal membrane protein, prevalent in areas with ____, heterozygous is ____, homozygous can be ____.
AIs: Like _____
malaria
mild
severe
anemia
Paroxysmal Nocturnal Hemoglobinuria: Abnormal membrane protein, increased risk of ____ ____, chronic hemolytic anemia, life expectancy __-__ yrs after diagnosis.
AIs: Anemia, h______
venous thrombosis
8-10
hypercoagulability
Glucose-6-Phosphate Dehydrogenase (G6PD) ______.
_____ affected, mostly in Asia and the Mediterranean areas.
deficiency
MANY
Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency
Can cause acute, chronic or very mild ______ disease.
Precipitated by:
hemolytic
drugs (forane, sevo, diazepam, lidocaine, prilocaine), infections, fava beans.
Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency
Therapeutic _____ _____ (for ______ or vasoplegic syndrome) can be life threatening.*
methylene blue
methemoglobinemia
Pyruvate Kinase Deficiency
Can cause life-threatening congenital hemolytic anemia requiring ____ ____.
exchange transfusion
Pyruvate Kinase Deficiency
Usually ____ with varying severity.
______ may prevent hemolysis.
chronic
splenectomy
AIs for Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency and Pyruvate Kinase Deficiency - Dependent on degree of ______. Caution with pre-op infection and drugs known to ______.
hemolysis
precipitate
Hgb molecule made up of __ ____, __ ____ and ____ _____.
α chains
β chains
heme groups
Each heme group binds an ___ ____.
O2 molecule
Most disorders related to ____ ____ substitution on α or β chains.
amino acid
Sickle S Hgb (Hgb SS) Disease: disorder of the ___ ____
β chain
Sickle S Hgb (Hgb SS) Disease: Membrane distortion leads to _____ (_____)
clumping (sickling)
Sickle S Hgb (Hgb SS) Disease: Homozygous (SS anemia) leads to severe hemolytic anemia, ___-____ crises, ____ and ____ infarcts.
vaso-occlusive
splenic
renal
Sickle S Hgb (Hgb SS) Disease: Leading M&M d/t _____ and _____ complications.
pulm and neuro
Sickle S Hgb (Hgb SS) Disease:
Acute Chest Syndrome __-__ days post-op
Lobular _____-like illness with severe chest pain, fever, tachypnea, cough
Tx: T_____, ___, a_____, inhaled Nitric Oxide (?)
2-3 days
pneumonia
transfuse, O2, analgesia,
Sickle S Hgb (Hgb SS) Disease: SS children & adolescents have _____ CVAs; adults have _____ CVAs.
infarct
hemorrhagic
Anesthesia Implications for Hgb SS
Trait (Ss) carries ___ ____ risk.
no increased
Anesthesia Implications for Hgb SS
Old tx: Aggressive _____ transfusion
intraoperative
Anesthesia Implications for Hgb SS
Current tx: Pre-op transfusion to Hct at (or near) ___%
30%
Anesthesia Implications for Hgb SS
Anesthetic technique ___ ___ ____ to matter.
does not appear
Anesthesia Implications for Hgb SS
“____, wet, ____”
“Warm, wet, green”
Anesthesia Implications for Hgb SS
Good ___ management to decrease sickling/crisis trigger
pain
Anesthesia Implications for Hgb SS
May be tolerant to ___ meds.
pain
Sickle C Hgb (Hb C): ¼ the prevalence of Hgb SS.
Hgb C leads to ____ _____ and _____ anemia
AIs: Treat like anemia.
cellular dehydration
hemolytic
Sickle β-Thalassemia (β-thal): 1/10 the prevalence of Hgb SS
Severity depends on Hgb __ levels (decreased Hgb __ leads to Hgb ___ symptoms).
A
A
SS
Hemoglobinopathies: >____ identified, most without implications
100
Hgb chain fragments and heme form ____ bodies which destabilize ____ membrane.
Heinz
RBC
Level of Heinz body formation dictates degree of ____.
hemolysis
Can have _____ and/or renal impairment.
hemoglobinuria
______ reduces or eliminates symptoms.
Splenectomy
Macrocytic Anemias: Folate and B12 Deficiency
Folic acid & B12 essential for ___ synthesis so high turnover tissue (marrow) quickly affected.
DNA
Macrocytic Anemias: Folate and B12 Deficiency
Marrow precursors appear ___ and cannot ____ (macrocytic).
large
divide
Macrocytic Anemias: Folate and B12 Deficiency
***Prolonged N2O exposure causes ____ ____inhibition which leads to impaired ____ activity. (Major culprit: poor scavenging)
methionine synthetase
B12
Macrocytic Anemias: Folate and B12 Deficiency
Alcoholism and malabsorption leads to f____ deficiency
folate
Macrocytic Anemias: Folate and B12 Deficiency
Severe macrocytic anemia causes impaired m____, p_____ n_____ (regional techniques?)
memory
peripheral neuropathies
Macrocytic Anemias: Folate and B12 Deficiency
Tx: _____ therapy (oral or parenteral) and/or ____s
vitamine
PRBCs
Lisa’s main reasons for avoiding N2O:
Expansion of air-filled spaces (cuffed ETTs, lap cases, VAE risk), inhibited meth synth (chronic exposure), bone marrow depression (heme-onc pts), OR contamination (pregnant staff).
Microcytic Anemias:
Iron Deficiency – _____ in children; chronic ___ ____ in adults. Treat with iron, EPO or transfusion.
nutritional
blood loss
Microcytic Anemias:
Thalassemias – Defective _____ chains
globin
Thalassemias – Defective globin chains
Minor: Usually clinically _____
insignificant
Thalassemias – Defective globin chains
Intermediate: More severe. Can have h_____, c_____, s_____ changes.
hepatosplenomegaly, cardiomegaly, skeletal
Thalassemias – Defective globin chains
Major: Severe, life-threatening childhood anemia
Long-term transfusion therapy causing ____ overload and _____, R heart failure and requires _____ (pheresis?)
_____ helpful but increases risk of sepsis, especially in children <5 years.
____ ____ transplants
iron
cirrhosis
chelation
splenectomy
bone marrow
Thalassemias – Defective globin chains
AIs dependent on severity of anemia. Similar to ___ ____.
Hgb SS
Hgb with INCREASED O2 Affinity
Chesapeake, J-Capetown, Kemsey, Creteil
Normal ___, mild ____ ____, increased EPO leading to polycythemia/increased _____/hyper_____
Hct
tissue hypoxia
viscosity
hypercoagulability
Hgb with INCREASED O2 Affinity
AIs: Hct >___% may require pre-op exchange transfusion.
Hemo_____ (NPO?) must be avoided.
Hemo_____ and blood loss can cause even less O2 to tissues.
> 55%
hemoconcentration
hemodilution
“does this cause a L or R shift of the OHD curve?”
Methemoglobinemia causes: _____ mutation, inefficient or overwhelmed _____, ______
globin
sysem
toxins
Methemoglobinemia: Ferrous iron (Fe2+) oxidized to Ferric (Fe3+) state leads to ___ shift of OxyHgb D curve causing ____ tissue hypoxia.
L
severe
MetHgb - Normally controlled by RBC ____ ____ system
reductase enzyme
MetHgb: < 30% has ____ compromise
little
MetHgb: 30-50% you see _____ _____
symptomatic hypoxia
MetHgb: > 50% can cause ____ or ____
coma or death
MetHgb: Cyanotic appearance with _____ PaO2
adequate
MetHgb: ER treatment: IV ____ ____ (only effective with normal G6PD function)
methylene blue
Aplastic (Fanconi) Anemia:
Severe ______ presents in children & young adults which leads to _____ and other malignancies later in life
pancytopenia
leukemia
Aplastic (Fanconi) Anemia:
Can be c______ (autosomal recessive), d______ drug/radiation induced, v____, c_____ induced. Usually reversible if drug/radiation/viral induced.
chromosomal
dose-dependent
viral
cancer
Aplastic (Fanconi) Anemia:
C______ and v_____ hepatitis can cause irreversible anemia.
choramphenicol and viral
Aplastic (Fanconi) Anemia:
Only cure for irreversible: ___ ____ transplant
bone marrow
Aplastic (Fanconi) Anemia AIs:
Transfuse for significant anemia, t_______
A_____ coverage d/t immunocompromise
thrombocytopenia
Antibiotic
Polycythemia: Increased RBC ___ and ___
mass and Hct
Polycythemia
Tissue oxygenation best at Hct __-__% or Hgb __-___ g/dL
33-36%
11-12 g/dL
Polycythemia
Hct >50% leads to increased _____, decreased ____ (especially cerebral)
viscosity
flow
Polycythemia
Hct 55-60% causes h_____, f_____. Seen with chronic lung dz.
headaches, fatigues
Polycythemia
>60% leads to life threatening loss of ____ ____ and ______.
organ perfusion
thrombosis
Polycythemia AIs:
Pre-op _____ if severe
May be hypercoagulable with paradoxical ____-like bleeding.
Good ____ management. Caution with ____ time (dehydration).
phlebotomy
DIC
fluid
NPO
Polycythemia vera (PV)
“Primary” and chromosomal. Causes increased ___s, ____s & _____s. Usually appears >50 yrs old.
RBCs, WBCs, and platelets
Polycythemia vera (PV)
Thrombosis (usually cerebral) often ____ event.
1st
Polycythemia vera (PV)
Tx with p_____ and/or h_____.
phlebotomy
hydroxyurea
Polycythemia vera (PV)
PV leads to acquired von Willebrand’s leading to consumptive c______ and abnormal clotting, increased b_____.
coagulopathy
bleeding
Polycythemia vera (PV)
High M&M d/t t____, c____, m_____, l_____.
thrombi, cancer, myelofibrosis, leukemia
_____ (___) is approved by the Food and Drug Administration to treat people with polycythemia vera who don’t respond to or can’t take hydroxyurea. It helps your immune system destroy cancer cells, and can improve some polycythemia vera symptoms.
Ruxolitinib (Jakafi)
Hypoxia Induced
Living at >_____ ft. Usually clinically insignificant high Hct. Acute or chronic “____ _____” with headaches, N/V, cerebral edema.
7,000 ft
“mountain sickness”
Hypoxia Induced
Cardiac dz – especially congenital __ to __ ____ with associated cyanosis. Low cardiac output states cause ____ stimulation.
R ro L shunts
EPO
Hypoxia Induced
Pulmonary dz. Ex: ____ _____ (morbid obesity with hypoventilation)
Pickwickian syndrome
Hypoxia Induced
________globinemia
Methemoglobinemia
EPO Induced
____ dz and ____ secreting tumors
Athletic “_____”
renal
EPO
doping
“Old School”: Coagulation cascade with _____ and _____ pathways. In vitro model.
Developed approx. 50 years ago to guide anticoagulant therapy.
NOT an accurate representation of in vivo clotting
intrinsic and extrinsic
New Coagulation Model:
Initiation Phase: Vessel damage causes ___ ____ (___) release which binds with VIIa causing conversion of X to ___ which leads to small amounts of ____
tissue factor (TF)
Xa
thrombin
New Coagulation Model:
Amplification Phase: ___ ____ & ____ activated by thrombin
Plts, V & XI
New Coagulation Model:
Propagation Phase: VIII, IX and calcium on plts leads to activation of X while thrombin activates plts, V, VIII and then get a ___-___ ____.
VIIIa-IXa complex
New Coagulation Model:
The VIIIa-IXa complex switches reaction to intrinsic tenase (Xase) pathway which is ___x more efficient at ___ generation.
50x
Xa
New Coagulation Model:
So increased Xa leads to large amount of t____
thrombin
Thrombin converts _____ to fibrin
fibrinogen
fVII: Rare, variable severity, most ______
Unique lab: Prolonged ___, normal ____
Tx: FFP, fIX complex, recombinant fVII (Novo7®)
asymptomatic
PT
PTT
Congenital fX, fV and fII (prothrombin): Autosomal recessive, severe deficiencies rare.
Lab: Prolonged PT & PTT
Tx: ____, _____
FFP, concentrates
Disadvantage of FFP: ___ ___ needed to significantly increase factor levels. (Caution with CV pts/overload.)
large volume
Disadvantage of concentrates: Increased risk of ____ and ____. Varying levels of _____ factors with different commercially prepared concentrates exist.
thrombus and DIC
Hemophilia A (fVIII)
__ linked, several mutations, most severe have fVIII activity <__% of normal.
X
1
Hemophilia A (fVIII)
Usually diagnosed in childhood d/t spontaneous _____.
hemorrhage
Hemophilia A (fVIII)
Require frequent ____ transfusion.
fVIII
Hemophilia A (fVIII)
Levels of __-__% mildly affected but at risk for major bleeding with surgery. (May be undiagnosed until that time.)
6-30%
Hemophilia A (fVIII)
10% of female carriers have fVIII activity <___%.
< 30%
Hemophilia A (fVIII)
Prolonged ___, normal ___.
PTT
PT
Hemophilia A (fVIII) AIs: Bring fVIII activity up to ___% pre-op.
100%
Hemophilia A (fVIII)
Half-life: ___ hrs in adults, 6 hrs in children. Confirm with ___. Therapy to keep 50% activity or better must continue up to __ _____ post-op depending on procedure.
12
labs
6 weeks
Hemophilia A (fVIII)
30% develop inhibiting _____. Recombinants do NOT reduce _____ formation.
antibodies
antibody
Hemophilia B (fIX)
Clinically similar to Hem A. Activity <1% leads to significant _____.
bleeding
Hemophilia B (fIX)
5-40% activity is very ____ dz. May also go _____ until surgery.
mild
undetected
Hemophilia B (fIX)
Prolonged ____, normal ___.
PTT
PT
Hemophilia B (fIX)
Caution with recombinant combos (PCCs – prothrombin complex concentrates). To get significant fIX, large amount needed for thrombus (especially in ortho). So – use only ___ ___ for Hem B.
pure fIX
Hemophilia B (fIX)
____ absorption of fIX requires ____ the higher dose, but half-life much longer.
collagen
doubling
Up to 40% of severe Hem As develop circulating inhibitors to ____. Much lower incidence in Hem __/fIX.
fVIII
B
Novo7® is current tx of choice for _____ inhibitors d/t DIC-like response to PCCs.
ACQUIRED
May require Novo7® infusion. (VERY _____!!!)
expensive
THROMBOCYTOPENIA
Categorized as disorder of p____, d____ or d_____
production, distribution or destruction
THROMBOCYTOPENIA
Minimal pre-op platelet count: Minor procedures: ___ – ___,
Major: >50K, Neuro: >____
Spontaneous _____ occurs at <15K.
Bad sign: _____ rash
20-30k
100k
bleeding
petechial
THROMBOCYTOPENIA
1 U apheresis plts or 4-8 U donor plts causes plt ct ____ by ____
increase by 50k
THROMBOCYTOPENIA
I_____, CMV-, Rh-, HLA matching, etc. may be required.
New paradigm in platelet transfusion therapy?
Irradiated
Platelet Production Disorders (congenital)
Hypoplastic ______ with ____ ____ (TAR syndrome): Severe (<30K) but slowly improves. Often have bilateral radial deformities.
Thrombocytopenia with absent radius
Platelet Production Disorders (congenital)
Fanconi’s Anemia: Usually diagnosed after ___ yrs old. ____ ____ transplant is only cure.
7
bone marrow
Platelet Production Disorders (congenital)
Wiskott-Aldrich: E____, i______. Small, dysfunctional plts.
Eczema, immunodeficient
Platelet Production Disorders (acquired)
Due to ___ ____ damage from radiation, chemo, toxins, ETOH, hepatitis, Vit B12 or folate deficiency, malignancies (multiple myeloma, leukemia, lymphoma).
bone marrow
Platelet Production Disorders (acquired)
AIs: Plt transfusion, treat cause of t______.
thrombocytopenia
Marked ___disruption –> a consumptive coagulopathy with microvascular ___ –bleeding
[Platelet Destruction Disorders (nonimmune)]
endothelial, clotting (thrombi)
Can have ___ ___ with heavy bleeding, prolonged ___times or low grade with less bleeding.
[Platelet Destruction Disorders (nonimmune)]
severe thrombocytopenia, coag
Etiology can be ___, ___, d/t malignancy, chemo, vasculitis, ___.
[Platelet Destruction Disorders (nonimmune)]
viral, bacteremic, AIDS
Most significant platelet destruction from thrombotic thrombocytopenic purpura, (TTP), ___ HELLP syndrome (___ ___ ___ ___ ___).
[Platelet Destruction Disorders (nonimmune)]
hemolytic uremic syndrome (HUS), hemolysis, elevated liver enzymes, low plt coun
Disseminated Intravascular Coagulation (DIC):
Marked endothelial disruption causes a ____ _____ with microvascular clotting (thrombi) which leads to _____
consumptive coagulopathy
bleeding
Disseminated Intravascular Coagulation (DIC):
Can have severe thrombocytopenia with heavy bleeding, prolonged ____ times or ____ grade with ____ bleeding.
coag
low
less
Disseminated Intravascular Coagulation (DIC):
Etiology can be v___, b_____, d/t malignancy, chemo, vasculitis, AIDS.
viral, bacteremic
Disseminated Intravascular Coagulation (DIC):
Most significant platelet destruction from thrombotic thrombocytopenic purpura, (TTP), hemolytic uremic syndrome (HUS), HELLP syndrome (h_____, e_____ l____ enzymes, l___ p____ count).
(hemolysis, elevated liver enzymes, low plt count).
Disseminated Intravascular Coagulation (DIC):
All can lead to widespread thrombus with ____ ____ damage.
end organ
Nonimmune platelet destruction-Thrombotic Thrombocytopenic Purpura (TTP)-
Platelet thrombi in microvasculature leads to decreased _____ and _____ ______
platelets and hemolytic anemia
Nonimmune platelet destruction-Thrombotic Thrombocytopenic Purpura (TTP)-
Frequent 5 symptoms:
Fever, renal insufficiency, low platelets, anemia, neuro symptoms
Nonimmune platelet destruction-Thrombotic Thrombocytopenic Purpura (TTP)-
Can be familial, idiopathic (ITP), chronic/relapsing, complication of ___ ____ _____ or ____.
bone marrow transplant or drugs
Nonimmune platelet destruction-Thrombotic Thrombocytopenic Purpura (TTP)-
Preeclampsia/HELLP can lead to ____ ____
postpartum TTP
All can lead to widespread ___ with ___ damage.
[Platelet Destruction Disorders (nonimmune)]
thrombus, end organ
Platelet thrombi in microvasculature –> decreased ___ and ___
Frequent 5 symptoms: Fever, renal insufficiency, low platelets, anemia, neuro symptoms
Can be familial, idiopathic (ITP), chronic/relapsing, complication of bone marrow transplant or drugs.
Preeclampsia/HELLP postpartum TTP
[Nonimmune platelet destruction -Thrombotic Thrombocytopenic Purpura (TTP)]
platelets and hemolytic anemia
Frequent 5 symptoms:
[Nonimmune platelet destruction -Thrombotic Thrombocytopenic Purpura (TTP)]
Fever, renal insufficiency, low platelets, anemia, neuro symptoms
Preeclampsia/HELLP –> postpartum ____
[Nonimmune platelet destruction -Thrombotic Thrombocytopenic Purpura (TTP)]
TTP
Non-immune platelet destruction- Hemolytic Uremic Syndrome - (HUS):
Similar to TTP but usually in children and secondary to ___ ____infection.
E. coli
Non-immune platelet destruction- Hemolytic Uremic Syndrome - (HUS):
HUS causes ___ ____ ____ (temporary or permanent). May require short or long-term hemodialysis
acute renal failure
Non-immune platelet destruction- Hemolytic Uremic Syndrome - (HUS):
Most recover spontaneously with <__% mortality.
< 5%
Non-immune platelet destruction- Hemolytic Uremic Syndrome - (HUS):
Adults and older children have higher mortality. Often require ___ ____ and/or _____.
plasma exchange
hemodialysis
Mild thrombocytopenia (__-__K) often seen in pregnancy d/t ___ anemia.
[Nonimmune platelet destruction -HELLP Syndrome-]
70 – 150, dilutional
___% of pre-eclamptics –> DIC-like thrombocytopenia (___-___K) (H=___, EL=___, LP =___)
[Nonimmune platelet destruction -HELLP Syndrome-]
50, 20-40
hemolysis, elevated liver enzymes, low platelets
BP control and delivery –> ___ of ___
[Non-immune platelet destruction-Hemolytic Uremic Syndrome - (HUS)]
regression of symptoms
Some progress to postpartum ___ and/or ___which is life-threatening with poor prognosis.
[Non-immune platelet destruction-Hemolytic Uremic Syndrome - (HUS)]
TTP, HUS
Plasma ___ and/or ___ not very effective.
[Nonimmune platelet destruction -HELLP Syndrome-]
exchange, immunoglobulins
Delay surgery if possible until coags normalized/___
[AIs for TTP, HUS and HELLP]
underlying disorder controlled.
If part of DIC: ___, ___ supportive therapy, treat underlying cause.
[AIs for TTP, HUS and HELLP]
Platelets, FFP
TTP or HUS: Platelets for ___ only (platelet transfusion can –> thrombosis with ___damage).
[AIs for TTP, HUS and HELLP]
severe bleeding, organ
HUS: ___ and/or ___for unresolving renal failure.
[AIs for TTP, HUS and HELLP]
Dialysis, pheresis
HELLP:___ if unresolved after delivery.
[AIs for TTP, HUS and HELLP]
Plasma exchange
Thrombocytopenic Purpura
___, ___, drug-induced
[Platelet Destruction (autoimmune)]
Toxins, post-transfusion
Heparin-induced thrombocytopenia (HIT) usually d/t ___ ___but can also be d/t ___ ___
Type 1 (___-___)
Type 2 (___ ___)
More common with ___ v ___. More common in ortho.
[Platelet Destruction (autoimmune)]
unfractionated heparin, LMW heparin (Lovenox®).
non-immune
immune mediated
bovine v. porcine
Increases risk of ___, ___, ___ in coronary bypass pts and unstable angina.
[Platelet Destruction (autoimmune)]
CVA, MI, death
Symptoms of acute HIT: ___, ___ hypertension, tachycardia. At risk for ___ embolus.
[Platelet Destruction (autoimmune)]
Dyspnea, diaphoresis, fatal
D/C heparin (including ___) immediately.
[Anesthetic Implications for HIT]
LMW
Thrombotic events with HIT must be treated with ___ (Hirudin, Bivalirudin, Desirudin, Lepirudin, Argatroban, Dabigatran, Efegatran, Inogatran, Melagatran, Ximelagatran)
[Anesthetic Implications for HIT]
direct thrombin inhibitor
Direct thrombin inhibitory: (10)
[Anesthetic Implications for HIT]
Hirudin, Bivalirudin, Desirudin, Lepirudin, Argatroban, Dabigatran, Efegatran, Inogatran, Melagatran, Ximelagatran
Oral anticoagulant (warfarin) without direct thrombin inhibitor can –>___ thrombosis –> ___ –>___.
Reverse warfarin with ___.
[Anesthetic Implications for HIT]
increased, necrosis, gangrene
Vit K
Platelets for life-threatening ___ or ___ into closed space.
[Anesthetic Implications for HIT]
hemorrhage or bleeding
Steroid therapy for ___clinical picture.
[Anesthetic Implications for HIT]
ITP-type
Special considerations for HIV/AIDS pts (___ therapy, ___).
[Anesthetic Implications for HIT]
zidovudine [AZT], splenectomy
HIT pts for non-elective CP bypass: Anticoagulate with ___ ___ __ (If elective, delay until HIT resolved.)
[Anesthetic Implications for HIT]
direct thrombin inhibitor.
___ (unrelated to drugs, infection or autoimmune disease)
[Idiopathic Thrombocytopenic Purpura -ITP-]
Autoimmune
Diagnosis of ___
[Idiopathic Thrombocytopenic Purpura -ITP-]
exclusion
Most proceed to chronic thrombocytopenic state (___-___K).
____ may be helpful.
[Idiopathic Thrombocytopenic Purpura -ITP-]
20K – 100K
Splenectomy
Severe, acute episodes with bleeding treated with ____ ____
[Idiopathic Thrombocytopenic Purpura -ITP-]
high-dose steroids.
For ER surgery or IVH: ___, ___
[Idiopathic Thrombocytopenic Purpura -ITP-]
platelets, immunoglobulins
Pregnancy: Treat significant thrombocytopenia during last ___ ____.
Neonatal platelet count usually ___but may be ___.
[Idiopathic Thrombocytopenic Purpura -ITP-]
few weeks
normal, low
Congenital disorder affecting ___function.
[Von Willebrand’s Disease (vWD)]
platelet
Severe vWD with life-threatening bleeding is ___.
[Von Willebrand’s Disease (vWD)]
rare
Basic screening: ___, ___ bleeding time, ___
[Von Willebrand’s Disease (vWD)]
PT, PTT, plt count
Full vWD screen: ___ activity and___ antigen activity to determine which type
[Von Willebrand’s Disease (vWD)]
fVIII, vWF
3 types
Type 1: ___%of total vWD. Low vWF levels (___) with varied degrees of severity
[Von Willebrand’s Disease (vWD)]
80%, quantitative
Types 2 & 3: Mix of ___ and ___, varied degrees of severity
[Von Willebrand’s Disease (vWD)]
quantitative and qualitative
Dependent on ___ and ___ of procedure
[AIs for vWD:]
type and acuity
IV or nasal desmopressin (DDAVP), ___, ___complex.
[AIs for vWD:]
cryoprecipitate, vWF-fVIII
Commercial ____complex preferred over ____ to decrease risk of infection.
[AIs for vWD:]
vWF-fVIII, cryoprecipitate
Myeloproliferative disease, ___, ___, drugs.
[Acquired Platelet Dysfunction]
dysproteinemia, liver diseas
Aspirin –> irreversible cyclooxygenase inhibition –> ____.
[Acquired Platelet Dysfunction]
platelet Thomboxane A2 inhibition
Other NSAIDs also inhibit ____ but only until drug is ____(reversible).
[Acquired Platelet Dysfunction]
cyclooxygenase, metabolized
Specific foods, vitamins and herbals affect ____ like NSAIDs.
[Acquired Platelet Dysfunction]
cyclooxygenase
Certain antibiotics, especially ____, interfere with ___ activation and ____.
[Acquired Platelet Dysfunction]
penicillins, platelet adhesion, aggregation
Dextran interferes with ____(disadvantage with trauma) but can be an advantage to prevent ____.
[Acquired Platelet Dysfunction]
aggregation, thrombosis
Hetastarch (Hespan®) more safe than ____
[Acquired Platelet Dysfunction]
dextran
Absolute platelet number ___ ___ predict risk.
[AIs with Platelet Disorders]
DOES NOT
DDAVP works well for mild bleeding, ____ transfusion required for ___ ___.
[AIs with Platelet Disorders]
platelet, heavy bleeding
Normal bleeding time and ___ may not predict surgical risk.
[AIs with Platelet Disorders]
TEG
Hypothermia (<____ C) and acidosis (pH ___) –>platelet dysfunction (including ____platelets).
[AIs with Platelet Disorders]
35°, <7.3, transfused
ASA given >___ hrs pre-op will not affect ____ platelets.
[AIs with Platelet Disorders]
2, transfused
______ ____: Most important defense to clot formation in healthy vessels.
Antithrombin III
Hereditary Antithrombin III Deficiency leads to undesired ___ ____ in ____ vessels.
AIs: Anticoagulate, maintain antithrombin III level >80% for ___ ___ post-op with antithrombin III concentrates.
clot formation
healthy
5 days
Hereditary Protein C and S Deficiency
Thrombin_____ causes risk of thrombus similar to antithrombin III deficiency.
Pro C & Pro S synthesis is ___ ___dependent, so warfarin therapy can actually____ coagulability.
May need FFP or prothrombin concentrates.
restricted
Vit K
increase
Factor V Leiden
Resistant to inactivation, fV circulates longer and there is ____ thrombin.
Mild to moderate _____ risk of thrombus.
increased
increased
Prothrombin Gene Mutation
Similar risk to ____ ____ ____.
Factor V Leiden
Hereditary Protein C and S Deficiency
Thrombin restricted –> risk of thrombus similar to ___ ___ ___.
antithrombin III deficiency
Pro C & Pro S synthesis is___ ___ dependent, so warfarin therapy can actually ____coagulability.
Vit K, increase
May need ____ or ___ concentrates.
FFP or prothrombin
Factor V Leiden
Resistant to inactivation –> ___ circulates longer –> ____thrombin.
Mild to moderate ____ risk of thrombus.
fV, increased, increased
Prothrombin Gene Mutation
Similar risk to ___ ___ ___.
Factor V Leiden
Factor V Leiden and ____ ____ ___ much higher in European descent, rare in African and Asian descent.
Prothrombin Gene Mutation
Myeloproliferative disorders such as ____ ___
[Hypercoagulation (acquired)]
polycythemia vera
Malignancies, especially ___, ____, ___, ___
[Hypercoagulation (acquired)]
pancreas, colon, stomach, ovaries
Pregnancy, especially with ____, ___, ___, bed rest
[Hypercoagulation (acquired)]
hx of thrombi, PE, obesity
Pts taking oral contraceptives (especially with smoking), migraines and inherited hypercoagulability have___x higher risk of DVT, PE, ____ thrombi.
[Hypercoagulation (acquired)]
30, cerebral
Nephrotic Syndrome, especially ___vein
[Hypercoagulation (acquired)]
renal
Antiphospholipid Antibodies (such as with lupus) can progress to catastrophic ____ ___with widespread thrombosis, ARDS, DIC, multi-organ failure, death.
[Hypercoagulation (acquired)]
antiphospholipid syndrome
Early ambulation, ____, sub-cu heparin, ____warfarin.
[AIs for Hypercoagulation]
elastic stockings, outpatient
Must balance bleeding risk with problematic ___ risk.
Risk stratification system to guide ____ with ____ risk. (As high as ____% - Stoelting, p. 505)
[AIs for Hypercoagulation]
clotting, prophylaxis, VTE, 80
ASA is poor ____.
Pneumatic compression hose almost as good as heparin.
Regional? Increased regional did not significantly lower risk.
Current standard: Post-op heparin or warfarin for high risk pts.
FDA Advisory:
Avoid SABs and epidural anesthesia on pts receiving heparin d/t increased risk of epidural bleeding.
Do not withhold post-op anticoagulants to allow for epidural anesthesia.
Vena Caval filters.
[AIs for Hypercoagulation]
prophylaxis
Pneumatic compression hose almost as good as ____.
[AIs for Hypercoagulation]
heparin
Regional? Increased regional did not significantly ___risk.
[AIs for Hypercoagulation]
lower
Current standard: ___ or ____ for high risk pts.
FDA Advisory:
Avoid ___ and ___ anesthesia on pts receiving heparin d/t increased risk of ____ bleeding.
[AIs for Hypercoagulation]
Post-op heparin or warfarin
SABs and epidural
epidural
Do not withhold ____ ___ to allow for epidural anesthesia.
___ ___ filters.
post-op anticoagulants
Vena Caval
Minor procedures require ____ therapy.
[AIs for Long-term Anticoagulation]
no interrupted
Bleeding risk must be balanced with ___ ___.
[AIs for Long-term Anticoagulation]
post-op clotting risk
For moderate and high risk pts, “bridge” with ___ or ___.
[AIs for Long-term Anticoagulation]
unfractionated or LMW heparin
D/C warfarin___ days pre-op, start heparin___hours after warfarin D/C’d.
[AIs for Long-term Anticoagulation]
5, 36
Stop heparin infusion ____ ___ pre-op.
[AIs for Long-term Anticoagulation]
6 hours
Stop LMW heparin ____ hours pre-op depending on ____.
[AIs for Long-term Anticoagulation]
18 -30, dose
ASA recommendation for regional anesthesia: D/C LMW heparin ____-___ hours pre-op depending on dose.
[AIs for Long-term Anticoagulation]
12-24
Post-op: Warfarin effects ___ ___ hours so resume immediately post-op unless high risk of ____. Consider “___”.
delayed 24, bleeding
bridging
Post-MI wall motion dysfunction –> risk of____.
Usually treated with ____ for several months post-MI.
[AIs of Arterial Hypercoagulation]
thrombi
warfarin
A-fib needs long-term ____ therapy.
[AIs of Arterial Hypercoagulation]
warfarin
____scoring system for estimating A-fib stroke risk.
[AIs of Arterial Hypercoagulation]
CHADS2
Pts with ____ ____ ___ at high risk of arterial AND venous thrombi.
[AIs of Arterial Hypercoagulation]
lupus antiphospholipid antibodies
Some procedures –>___% increased risk of thrombi.
[AIs of Arterial Hypercoagulation]
100%
Venous thrombi: 2 million/year, ____die from PE.
[AIs of Arterial Hypercoagulation]
150,000
C___
H___
A___
D___
S____
CHF 1
HTN 1
Age >/= 75. 1
DM 1
S Prior stroke of TIA. 2
