Exam II: Hematological System and Diseases Flashcards by Linsley Lloyd

Anemia Definition: Deficiency of ____

RBCs

How well did you know this?

Not at all

Perfectly

Anemia H&H: ___/___ for women; ___/___ for men

11.5/36
12.5/40

How well did you know this?

Not at all

Perfectly

Anemia Primary adverse effect: Decreased ____ ____ content

arterial oxygen

How well did you know this?

Not at all

Perfectly

Anemia ___ ____ of OxyHgb Dissociation Curve (_____ affinity - increased O2 to tissues)

R shift
decreased

How well did you know this?

Not at all

Perfectly

Anemia Increased _____ d/t decreased viscosity

How well did you know this?

Not at all

Perfectly

Anemia - Decreased tissue O2 causes _____ (___) stimulation which increases ____ production

erythropoietin (EPO)
RBC

How well did you know this?

Not at all

Perfectly

Anemia: Many causes. Most common: ___ deficiency, ____ disease, acute ____ loss

iron
chronic
blood

How well did you know this?

Not at all

Perfectly

Anemia decreases CaO2 leads to R shift
(decreases Hgb’s affinity for O2 which increases tissue O2)

How well did you know this?

Not at all

Perfectly

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.

How well did you know this?

Not at all

Perfectly

AIs: No studies point to ____ ____ to prevent MIs, ischemia, infection or improve outcomes.

recommended Hgb

How well did you know this?

Not at all

Perfectly

AIs: In vitro: Peak O2 carrying occurs with Hct of ____%.

30%

(<30 causes decreased carrying capacity, >30 causes increased viscosity)

How well did you know this?

Not at all

Perfectly

AIs: Chronic anemia increases ___-___ and ___ shift

2,3-DPG and R shift

How well did you know this?

Not at all

Perfectly

AIs: ____ increase Hgb 2 x more than whole blood

PRBCs

How well did you know this?

Not at all

Perfectly

AIs: Decrease temp causes ___ ____ of OxyHgb D curve

left shift

How well did you know this?

Not at all

Perfectly

AIs: Consider ____ _____ or cell saver.

normovolemic hemodilution

How well did you know this?

Not at all

Perfectly

AIs: IN THE PRESENSE OF _______, transfuse when symptomatic.

NORMOVOLEMIA

How well did you know this?

Not at all

Perfectly

AIs: As a general rule: Transfuse with acute blood loss when Hgb drops to ___g/dL, especially with ______.

7
comorbidities

How well did you know this?

Not at all

Perfectly

RBC structure: Bi-concave disc with no _____, no _____, 33% ______

nucleus
mitochondria
hemoglobin

How well did you know this?

Not at all

Perfectly

RBC structure: ____ and ____ provide intracellular energy.

2,3-DPG
ATP

How well did you know this?

Not at all

Perfectly

RBC: life span ___-___ ___

100-120 days

How well did you know this?

Not at all

Perfectly

RBC: _____ ____ _____ regulate erythropoietin (EPO).

renal O2 sensors

How well did you know this?

Not at all

Perfectly

RBC: EPO stimulates RBC production in ____ ____.

bone marrow

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

Hereditary Spherocytosis AIs: Episodic anemia with _____ and ______

infection
cholelithiasis

How well did you know this?

Not at all

Perfectly

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

Exam II: Hematological System and Diseases Flashcards

(246 cards)