Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Anesthesia MM/TL > Heme > Flashcards

Heme Flashcards

1
Q

What are the effects of sodium bicarbonate ?

A
  1. Increased preload
  2. Decreased left ventricular contractility
  3. Increased hemoglobin affinity for oxygen
  4. Intracranial hemorrhage with rapid administration
  5. Increased lactate production
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How does sodium bicarbonate increase preload?

A

It is very hypertonic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does it cause intracranial hemorrhage?

A

Through rapid administration due to volume expansion

Increased PaCO2 and subsequent cerebral vasodilation due to conversion of bicarbonate to PaCO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How does bicarbonate cause decreased left ventricular contractility?

A

Decrease in serum ionized calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the Bohr effect?

A

Increased H or CO2 concentration reduces the oxygen affinity of hemoglobin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is R time?

A

The time to the start of clot formation from initiation of the test
Normal = 1-3 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What does R time reflect?

A

Heparinization

Factor deficiencies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the alpha angle or K time?

A

The time from clot initiation to clot thickness of at least 20 mm
RELIES ON FIBRINOGEN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is MA?

A

Maximal clot thickness/strength as measured by platelet number and function
MEASURE OF PLATELET FUNCTION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What does the alpha angle, k time, and MA indicate?

A

Fibrin polymerization

Platelet function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is LY30?

A

The ratio of clot thickness at 30 minutes post MA relative to MA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What does LY30 tell you?

A

The degree of fibrinolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What happens in altitude sickness?

A

The increase in minute ventilation causes a respiratory alkalosis from decreased PaCO2 and increased CSF bicarbonate. Over the next 48-96 hours the CSF normalizes it’s oh by decreasing bicarbonate production allowing the chemoreceptors to be more sensitive to high PaCO2.

The kidneys increase bicarbonate excretion over the week to restore normal blood ph

There is also an increase in 2,3DPG in response to respiratory alkalosis and thus a shift of the oxygen dissociation curve to the right.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Why and when do you start making more hemoglobin for oxygen transport at higher altitudes?

A

After a while the decrease in PaCO2 and PaO2 cause a left shift in the oxygen dissociation curve. Renal hypoxia triggers erythropoeitin secretion. This happens over 1-3 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How can you diagnose CO poisoning?

A

Blood sample (stable levels for several days after exposure)
Co-oximetry
Exhaled CO
Carboxyhemoglobin levels over 5% in no smoker
Over 10-15% in smoker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the treatment of choice for methemoglobinemia in a patient with G6PD deficiency?

A

Vit C because it functions as an electron acceptor and aids in reduction of Fe 3+ to Fe 2+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What does methylene blue do in G6PD patient?

A

It causes hemolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Why does the pulse ox read 85% in methemoglobinemia?

A

Because methemoglobin has an absorbance of 630 nm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is used to treat cyanide toxicity?

A

Amyl nitrite

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How does indigo carmine affect pulse oximetry?

A

Causes a decrease in the oximetry due to absorption at 600 mm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What medications does methylene blue interact with?

A

MAOi because it is a potent MAOi. Careful for serotonin syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What electrolyte abnormality occurs in hyperventilation?

A

Hypocalcemia because hydrogen unbinds albumin and calcium then can bind albumin

Hypokalemia due to hydrogen being pumped out of cell and K pumped in

Hypophosphatemia due to increased glycolysis with increased Ph

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Which coagulation factors does PT measure?

A

Factors I, II, V, VII, IX, X

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Where is factor 13 made and what does it do?

A

Stabilizes fibrin

Made by megakaryocytes, macrophages, platelets and liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is factor I?

A

Fibrinogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what is factor II?

A

Prothrombin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the 4Ts?

A

Thrombin, Timing of platelet decrease (5-11 days after heparin), oTher things have been ruled out, TCP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is involved in a type and cross?

A

Mixing patient red cells with antibodies A, B, AB to determine ABO status, mix patient red cell with anti-D to determine RH status, mix patient serum with donor red cells, mix patient serum with red cells with known antigens on the surface.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What does Factor V do?

A

Increases thrombin levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What does factor II do?

A

Converts fibrinogen to fibrin to strengthen a clot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is Factor V Leiden deficiency?

A

A mutation in the factor V gene that makes it resistant to inactivation by protein C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

When should a patient with Factor V leiden deficiency have lifetime anticoagulation?

A
  1. 2 or more spontaneous thromboses
  2. Life-threatening thromboses
  3. Has another prothrombotic disorder
  4. Gets clot in an unexpected place (cerebral, mesenteric)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the initial treatment for a first time clot with a normal patient?

A

3-6 months anticoagulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is leukoreduction?

A

The process of depleting donor blood products of leukocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the advantages of leukoreduction?

A

Reduced CMV transmission
Reduced febrile reactions
Reduced alloimmunization
Reduced proinflammatory mediators in the storage
Reduced LOS, mortality, transfusion-related tumor occurrences

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are the risk factors of heparin resistance?

A

Platelet count > 300K
Previous use of heparin or LMWH
Antithrombin III levels < 60%
Age over 65

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is heparin resistance?

A

ACT <480 after giving 500 U/kg of heparin

ACT < 400 s with heparin anytime during CPB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

How much citrate is in 1 unit of blood?

A

3 g

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Where is citrate metabolized?

A

The liver converts it to bicarbonate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

When does hypocalcemia begin to happen?

A

When infusion of blood exceeds 1 unit per 10 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What does a decrease in MA mean?

A

Platelet dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is a normal MA?

A

50-60 mm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

How does a TEG work?

A

A sample of citrated blood is injected into a sample cup with a stationary pin attached to a torsion wire.
The cup oscillates at a set rate
When fibrin and platelets form, they cause connection of the inner wall of the cup to the pin, causing the pin to oscillate within the phase of the clot. The pin is attache d to a transducer to an electrical signal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are the effects of garlic?

A

Potentiates the action of warfarin
Inhibits platelet aggregation

Used in HTN and HLD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are the effects of St. John’s Wort?

A

Antibacterial
Antioxidant
Potent inhibitor of CYP3A4 - may potentiates NMB because blocks this metabolism
*does not effect bleeding

46
Q

What are the effects of ginkgo?

A

Potent antagonist of platelet activating factor

47
Q

What is ginkgo used for?

A

Dementia
PVD
CAD
Reynaud’s

48
Q

What are the effects of ginger?

A

Inhibition of platelet function in high doses
Antispasmodic
Antinausea

49
Q

What are the effects of vitamin E?

A

Inhibits platelet aggregation
Enhances wound healing
Decreases thromboembolic events, synergistic with warfarin because blocks epoxide reductase at high levels
Antioxidant

50
Q

Why might patients with cystic fibrosis have prolonged prothrombin time?

A

Due to inability to absorb fat soluble vitamins (K, E)

51
Q

How does warfarin work?

A

It inhibits gamma-glutamyl carboxylase which is the enzyme that allows the carboxylation of vitamin K dependent clotting factors and protein C and S

52
Q

What is type I vWD?

A

Quantitative defect: decreased vWF production, shortened VIII half life

53
Q

what is the treatment for type I vWD?

A

1st line: Desmopressin

2nd line: Factor VIII-vWF

54
Q

What is vWF 2A?

A

Qualitative defect: decreased ability of vWF to bind to platelet glycoprotein-1
Unable to bind and form multimers

55
Q

What is vWF 2B?

A

Enhanced bind of vWF to platelets and formation of multimers –> rapid clearance, potential for TCP

56
Q

What is the treatment for vWD 2A/B?

A

Factor VIII-vWF concentrate

57
Q

What is vWF 2M?

A

Decreased ability for vWF to bind to platelet glycoprotein1

58
Q

What is the treatment for vWF 2M/2N?

A

1st line: Factor VIII-vWF concentrate

2nd: Desmopressin

59
Q

What is vWF 2N?

A

Decreased ability to bind factor VIII, may be mistaken for hemophilia A

60
Q

What is vWF 3?

A

Complete absence of vWF with resultant severe factor VIII deficiency

61
Q

What is the treatment for vWF 3?

A

Factor VIII-vWF concentrate

Recombinant factor VIII

62
Q

What is platelet-type vWF?

A

Platelet defect where glycoprotein 1b has higher affinity for binding vWF –> rapid clearance of multimers, TCP common

63
Q

Why are morbidly obese patients at risk for DVT?

A

They have increased levels of fibrinogen, factor VII, and factor VIII, plasminogen activating factor

64
Q

What is the test with the high specificity for HIT?

A

Serotonin assay

65
Q

What is the test with the highest sensitivity?

A

detection of anti platelet factor 4 antibodies

66
Q

What are the CV effects of acute normovolemic anemia?

A

Increased CO from increased SV due reduced blood viscosity and venoconstriction

67
Q

What are the effects of chronic anemia?

A

Increased CO: Increased SV due to reduced blood viscosity and venoconstriction, increased HR and contractility due to increased catecholamines
Increased oxygen offload to tissues (right shift)
Decreased after load due to decreased blood viscosity

68
Q

What are the most unstable factors in FFP?

A

Factor VIII and factor V

69
Q

What is TRALI?

A

Noncardiogenic pulmonary edema occurring within 6 hours of transfusion due to donor leukocytes attacking recipient leukocytes in the pulmonary microcirculation

70
Q

What is the most common source for TRALI?

A

FFP from multiparous women (alloimmunization)

71
Q

What are the clinical features of TRALI?

A

Pa/Fi ratio between 200-300 mm Hg
Sudden hypoxia
Bilateral infiltrates on CXR
No other source for pulmonary edema (normal cardiac filling pressures)

72
Q

What are the contraindications to acute normovolemic hemodilution?

A

Pre-op anemia, cardiac disease, recent MI, recent CVA, renal or liver disease, active infection

73
Q

What is the mechanism of action of a febrile transfusion reaction?

A

Donor leukocytes are attacking recipient leukocytes, the binding of these antibodies cause hemolysis and cytokine release (IL1 and TNF alpha) which increase the temperature set point in the hypothalamus to cause shivering and fever

74
Q

What is the test for diagnosing hemolytic reactions?

A

Direct Coombs:

75
Q

What is TRIM?

A

Transfusion related Immune modulation that occurs because of leukocyte mediators in product (more common in older product).
Increases cancer occurrence and recurrence

76
Q

How much fibrinogen is in 1 unit of cryo?

A

200 mg

So there is 2 grams in the 10 unit pack

77
Q

How is cryo precipitate made?

A

Thawed FFP - high in factor VIII, factor XIII, vWF

78
Q

What is an acute hemolytic reaction due to?

A

IgM antibody mediated complement activation from ABO incompatibility leading to massive hemolysis –> release of bradykinin and histamine –> flushing, bronchospasm, renal failure, DIC, death

79
Q

How long can blood be stored at room temperature in the OR?

A

Up to 6 hours

80
Q

What does metformin do?

A

Inhibits pyruvate dehydrogenase and other reducing factors forcing anaerobic metabolism and lactic acidosis.

81
Q

How is metformin metabolized?

A

it is excreted unchanged in the urine 90%

82
Q

What is the recommended dose of FFP for reversal of warfarin?

A

10-15 ml/kg for INR goal of 1.4-1.7

83
Q

What are the contraindications to using FFP?

A
  1. Sole use for plasma volume expander
  2. To correct INR that can be corrected by vit K
  3. To correct a factor deficiency when recombinant is available
84
Q

What are the indications of FFP?

A
  1. To correct INR > 1.8 in a massive bleeding situation
  2. To correct dilution coagulopathy
  3. Heparin resistance
  4. TTP
  5. HUS
85
Q

What drug should be used in patients undergoing cardiac surgery who have a history of HIT?

A

Bivalirudin (direct thrombin inhibitor)

86
Q

What is Type I HIT?

A

Platelet glycoprotein 1B release ADP causing platelet aggregation –> mild TCP, no thrombosis
Occurs within 2-5 days of heparin administration

87
Q

What is type II HIT?

A

IgA, IgM, IgG mediated against heparin-antiplatelet 4 complexes causing platelet activation and clot formation.
TCP < 100K
5-9 days after heparin administration

88
Q

What blood product is most likely to cause sepsis?

A

Platelets because stored at room temperature

89
Q

What happens to a patient with IgA deficiency given a blood transfusion?

A

Anaphylaxis from making anti-IgA antibodies from a previous transfusion

90
Q

Which vWD should you not give desmopressin to and why?

A

Type 2B because it may cause severe TCP

91
Q

What is CPDA-1?

A

Citrate - binds calcium so it cannot be used in clot formation
P - phosphate for ATP and cellular function
D - energy for glycolysis
A- adenosine for ATP production

92
Q

Why is FFP a treatment for TTP?

A

It replaces the missing enzyme ADAMST13, which normally degrades vWF multimers.

93
Q

What is a direct Coomb’s test?

A

anti-Ig antibody is added to the patient’s serum. If + : will see agglutination of RBCs

94
Q

What does factor V do?

A

Acts with calcium and factor X to convert prothrombin (factor II) to thrombin

95
Q

What does factor V do?

A

Binds factor X to activate factor II (prothrombin to thrombin)

96
Q

What does factor VIII do?

A

Bind factor IX to activate factor X

97
Q

What is the intrinsic pathway?

A

Tissue factor secreted by endothelium binds with VII to form VIIa which activates factor X

98
Q

What is the contact activation pathway?

A

Starts due to factor 12–> 11 –> 9 a–> 9+8 –> 10!

99
Q

What happens in fibrinolysis?

A

Plasminogen is converted to plasminogen via tissue plasminogen activator

Plasminogen binds fibrin causing degradation

100
Q

What amino acid blocks fibrinolysis?

A

Lysine by binding to site on plasminogen

101
Q

What are the two main things seen in acute hemolytic reactions?

A

Renal failure and DIC

102
Q

How does an acute hemolytic reaction cause renal failure?

A

The hemoglobin accumulated in the distal tubules causing blockage and failure

103
Q

What is the treatment for acute hemolytic renal failure?

A

IV fluids and diuretics

104
Q

What happens to ABGs when they are corrected to a colder temperature?

A

The PaO2 and PaCO2 decreases and the ph increases

PaO2: 5 mmHg per degree Celsius
PaCO2: 2 mmHg per degree Celsius
pH: 0.17 per degree Celsius decreases

105
Q

What happens to the solubility of a gas in colder temperatures?

A

It increases

106
Q

What happens when LMWH is used?

A

There is an increased antiXa-IIa ratio due to thrombin binding

107
Q

Why does LMWH have a longer half life than heparin?

A

It has smaller segments that are not as bound by macrophage so it is cleared Renally

108
Q

Which ADP receptor inhibitor has the longest half life?

A

Ticlodipine

109
Q

How far out should you stop Ticlodipine before surgery?

A

10-14 days

110
Q

What is the duration of action of argagroban?

A

2-4 hours

Stop 4-6 hours before surgery

111
Q

At what level of SNP do you see cyanide toxicity?

A

Greater than 100 mg/dl (1 mg/kg in less than 2 hours)

Anesthesia MM/TL (36 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions