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Hb Structures Flashcards

1
Q

Slight pallor and tachycardia Hb level?

A

9-11

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2
Q

More pronounced pallor, plus dyspnea on exertion Hb level?

A

7-8

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3
Q

Pallor, tachycardia, dyspnea, plus many complain of weakness Hb level?

A

6

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4
Q

Pallor, tachycardia, weakness, plus people complain of dyspnea at rest Hb level?

A

3

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5
Q

Pallor, tachycardia, dyspnea, weakness plus many complain of CHF Hb level?

A

2-2.5

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6
Q

Normal RBCs lifespan

A

120 days

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7
Q

Acute anemia (2)

A

Blood loss and hemolysis

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8
Q

4 chronic anemia situations

A
  1. Hemolytic (G6PDH-deficiency, immune mediated, drug induced)
  2. Hemoglobinopathies (sickle cell, thalassemia)
  3. Nutritional/consumptive
  4. Folate deficiency
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9
Q

Shortening of RBC survival to less than 100 days due to an increased rate of destruction of RBCs

A

Hemolytic anemia

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10
Q

2 mechanism for hemolytic anemia?

A
  1. Abnormalities within RBC &/or it’s membrane

2. Abnormalities in environment (extrinsic due to immune mechanisms due to warm and cold agglutinin)

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11
Q

4 hemolytic anemia’s

A
  1. Disorder of RBC structure
  2. Disorder of RBC metabolism
  3. Immune hemolytic anemia
  4. Non immune hemolytic anemia
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12
Q

Most common enzyme defect?

A

G6PDH

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13
Q

Treatment for G6PDH deficiency (3)

A
  1. Remove trigger or stop drug
  2. O2 and fluids
  3. Transfusion
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14
Q

Main G6PDH deficiency anesthesia consideration?

A

Some pts cannot reduce methemoglobin

  • lidocaine and nitroprusside are contraindicated
  • methylene blued can be life threatening
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15
Q

Detected at birth but some present during times of great physiological stress such as pregnancy, or acute illness

A

Pyruvate kinase deficiency

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16
Q

Destruction of RBCs by autoantibodies may occur suddenly, or it may develop gradually.

A

Immune hemolytic anemia

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17
Q

What is more common immune hemolytic anemia: cold antibody or warm antibody?

A

Warm antibody

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18
Q

Cold antibody hemolytic anemia temp:

A

28-31

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19
Q

Warm antibody hemolytic anemia temp:

A

37

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20
Q

Severity of anemia is determined by what?

A

Length of time that RBCs survive and by rate at which bone marrow continue to create new RBC production

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21
Q

CAHA is associated with? (2)

A
  1. Idiopathic cold hemagglutinin syndrome

2. Infectious mononucleosis and mycoplasma pneumonia

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22
Q

WAHA is associate with? (3)

A
  1. Systemic lupus erythematosus (SLE)
  2. Lymphoma
  3. Chronic lymphocytic leukemia
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23
Q

Occurs if body makes antibodies against RBCs that you get from an incompatible blood transfusion; occurs during pregnancy if woman has Rh- and baby is Rh+; drug induced (chemo, acetaminophen, quinine, PCN,)

A

Alloimmune hemolysis

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24
Q

Non immune hemolytic anemia direct Coombs test result?

A

Negative

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25
Q

Common causes of non immune hemolytic anemia (7)

A
  1. Drugs (ribavirin)
  2. toxins (snake venom, plant poisons)
  3. trauma
  4. mechanical
  5. Microangiopathic hemolytic anemia (TTP, HUS, DIC, HELLP)
  6. Infection malaria (babesiosis, sepsis)
  7. Membrane disorders (liver disease, paroxysmal nocturnal hemoglobinuria)
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26
Q

Minimize disruption of O2 delivery to tissues by avoiding what? (6)

A

Oxyhemoglobin dissociation curve to the L

  1. Alkalosis
  2. Hypocarbia
  3. Decreased temp
  4. Carbon monoxide
  5. Methemoglobin
  6. Hypophosphatemia
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27
Q

Consider blood transfusion when Hb is what for:

  • acute blood loss from healthy person <60
  • healthy person with asymptomatic chronic anemia
A

<6.4g/100ml

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28
Q

Consider blood transfusion when Hb is what for:

  • acute blood loss from healthy >60 yrs
  • acute blood loss from multi trauma pt
  • preop in pt with periop blood loss >500ml
  • fever
  • postop after uncomplicated cardiac surgery
  • uncomplicated operation in pt with ASA 2and3
A

<8g/100ml

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29
Q

Consider blood transfusion when Hb is what for:

  • ASA 4 pts
  • HF or valvular disease unable to raise CO
  • severe lung disease (COPD)
  • septic and toxic
  • symptomatic cerebrovascular disease
A

<10g/100ml

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30
Q

Underlying genetic defect of sickle cell disease

A

1 amino acid exchanged in beta-chain of hemoglobin

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31
Q

Suckling and subsequent hemolysis starts at what and becomes pronounced at what?

A

PaO2 50 and 20

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32
Q

Sickle cell disease occurs when (3)

A
  1. High altitude
  2. Severe dehydration
  3. Very high intensity physics activity
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33
Q

Complications with sickle cell disease (3)

A
  1. Muscle breakdown (rhabdomyolysis)
  2. Reduced blood supply to spleen
  3. Increased pressure in eye (glaucoma)
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34
Q

How to prevent sickling? (6)

A
  1. Avoid excessive premed with vent depression
  2. Adequate hydration
  3. Maintain normothermia
  4. Tourniquet
  5. Transfuse to reduce fraction of HbS
  6. Volatile anesthetics prompt sickling
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35
Q

Abnormal formation of hemoglobin with tendency for hemolysis; defect in either alpha or beta globin chain

A

Alpha and beta thalassemia

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36
Q

What is the main consideration for thalassemia and anesthetic considerations?

A

Maintenance of sufficient O2 carrying capacity, often require frequent blood transfusions (every few weeks)

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37
Q

Polycythemia causes: an increase in HCT from reduction in plasma volume with no increase in red cell mass

A

Relative

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38
Q

Polycythemia causes: increased number of RBCs

A

Absolute

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39
Q

Polycythemia causes: over transfusion

A

Latrogenic

40
Q

Polycythemia causes: blood cancers known as “myeloproliferative neoplasms”

A

Polycythemia Vera

41
Q

DNA of developing stem cell in bone marrow is damaged, “acquired mutation”

A

Polycythemia Vera

42
Q

Can minimize need for allogenic blood products; removed blood is replaced with IV fluids to maintain euvolemia

A

Preop phlebotomy

43
Q

Iron in heme group is what for methemoglobinemia pts?

A

Fe3+ NOT Fe2+

44
Q

What can cause methemoglobinemia (2)

A

Sodium nitroprusside and benzocaine

45
Q

3 benzocaine toxicity treatment

A
  1. Supplemental O2
  2. 1% methylene blue IV administration
  3. Ascorbic acid (give slower than methylene blue)
46
Q

4 methemoglobinemia treatment:

A
  1. 100% O2
  2. 1% methylene blue (1-2mg/kg over 5min and repeat after 1hr)
  3. ABGs
  4. A-line placement
47
Q

CF 1:

A

Fibrinogen

48
Q

CF 2:

A

Prothrombin

49
Q

CF 3:

A

Thromboplastin (tissue factor)

50
Q

CF 4:

51
Q

CF 8:

A

Von willebrand factor

52
Q

Normal blood clotting factor level:

53
Q

Mild hemophilia blood clotting factor level:

54
Q

Moderate hemophilia blood clotting factor level:

55
Q

Severe hemophilia blood clotting factor level:

56
Q

Bleeding occurs only after injury, trauma, or surgery (25% of population)

A

Mild hemophilia

57
Q

Bleeding tends to occur after minor injuries, spontaneous bleeding episodes may occur (15% of population)

A

Moderate hemophilia

58
Q

Bleeding after injury, trauma, or surgery, spontaneous bleeding into joints and muscles, average 2-5 spontaneous bleeding episodes each month (60%)

A

Severe hemophilia

59
Q

Factor 8 is what hemophilia?

60
Q

Factor 9 is what hemophilia?

61
Q

Factor 8 and 9 PT, PTT, BT?

A

PT: normal
PTT: prolonged
BT: normal

62
Q

Hemophilia A affects what gender mostly?

63
Q

Treatment of hemophilia A (4)

A
  1. Factor 8
  2. Cryoprecipitate
  3. FFP
  4. Desmopressin (DDAVP)
64
Q

FVIII content in cryoprecipitate per bag?

A

60-100 in 30-40ml

65
Q

1ml of FFP contains how much CF 8?

66
Q

Synthetic vasopressin analogue; increase CF8 and VWF

A

Desmopressin DDAVP

67
Q

DDAVP pretesting?

A

Infusion: slowly over 15-30 min

Post infusion: 30-60min

68
Q

Desired factor level change with DDAVP?

A

2-3 fold increase

69
Q

Hemophilia B is also called what?

A

Christmas’ Disease

70
Q

Hereditary pattern with hemophilia B?

A

X-linked recessive

71
Q

Hemophilia B treatment? (2)

A
  1. Pure coagulation F9 products

2. FFP; only in life threatening emergency and F9 isn’t available (15-20ml/kg)

72
Q

Hemophilia A and B goal for surgical prophylaxis?

A

Level 80-100% for 72hrs

73
Q

Works fine, not enough; have reduced level of vWD

A

Type 1 vWD

74
Q

What is vWD gender affect?

A

Autosomal (F and M)

75
Q

Enough, factor doesn’t work properly

A

Type 2 vWD

76
Q

Platelets don’t bind

77
Q

Platelets bind in blood stream

78
Q

Most severe and rarest; very low levels

A

Type 3 vWD

79
Q

Treatment for vWD for type 1and2, type 2and3, and both

A

Type 1and 2: DDAVP
Type 2 and 3: factor 8
Cryoprecipitate, FFP
Antifibrinolytic drugs

80
Q

Elective procedure levels of hemophiliac should be at what?

A

Stabilized to 40% of normal

81
Q

What to avoid in hemophiliac pts? (2)

A
  1. IM injections, spinal, epidural

2. NSAIDs

82
Q

Most common cause of AKI in children; occur when small blood vessels in kidneys become damaged and inflamed

A

Hemolytic uremic syndrome

83
Q

Low plt count leading to bruising

A

Thrombotic thrombocytopenic purpura (TTP)

84
Q

Excessive shear or turbulence in the circulation causes trauma to RBCs

A

Microangiopathic hemolytic anemia

85
Q

Mild DIC (3)

A
  1. Prolonged PT, PTT, TT
  2. Decreased PLTs
  3. Increase fibrin degradation products
86
Q

Severe DIC (2)

A
  1. Reduced fibrinogen

2. Fragmented RBCs

87
Q

Main clinical feature for DIC?

A

Bleeding at sites of vein puncture/IV catheters

88
Q

Blood transfusion is recommended for what DIC situations? (2)

A
  1. Bleeding type

2. Massive bleeding type

89
Q

Heparin is recommended for what DIC situation?

A

Non-symptomatic type

90
Q

Treat thrombocytopenia

91
Q

Treat elevated PT and PTT

92
Q

Treat low fibrinogen level

A

Cryoprecipitate or fibrinogen

93
Q

Heparin induced thombocytopenia (HIT) treatment (3)

A
  1. PLTs
  2. Corticosteroids
  3. Direct thrombin inhibitor
94
Q

Managing anticoagulation therapy: warfarin

A

Stop 5 days before

95
Q

Managing anticoagulation therapy: heparin

A

Started 36 later

96
Q

Managing anticoagulation therapy: bridging choice

A

Unfractionated LMWH

97
Q

Managing anticoagulation therapy: last dose heparin stopped; infusion and bolus

A

Infusion: 6 hrs
Bolus: BID 18hrs, OD 30hrs

Co-Exisiting Disease 2 (11 decks)

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