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Prodigy > Week 1 > Flashcards

Week 1 Flashcards

1
Q

When/why does anaphylaxis occur?

A

pt previously exposed to antigen, develops antibodies to it, and reacts to it on subsequent exposure

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2
Q

What are 2 of the major immune cells and the Ig_ released in anaphylaxis?

A

mast cells, basophils, IgE

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3
Q

How is cell mediated immunity different from anaphylaxis?

A

antigen is presented to T lymphocyte by infected/antigen presenting cells

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4
Q

Initial reaction to anaphylaxis occurs w/in how many min of exposure?

A

5-10

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5
Q

What is responsible for the urticaria, pruritus, and vascular collapse?

A

histamine

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6
Q

Why do anaphylactic pts have hypotension?

A

increased capillary permeability so up to 50% of the intravascular vol can go in to extracell space

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7
Q

histamine also causes?

A

increased HR and myocardial contractility, laryngeal edema, bronchospasm, and hypoxemia

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8
Q

3 other conditions anaphylaxis resembles?

A

MI, PE, acute aspiration

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9
Q

First line tx of anaphylaxis?

A

several L crystalloid and epi in doses from 10-100 mcg IV

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10
Q

How does epi help in anaphylaxis?

A

increases cAMP which restores normal cap permeability

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11
Q

Can antihistamines reverse the negative inotropic sx by leukotrienes? What do they help w?

A

no; help w pruritus and bronchospasm

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12
Q

What is a good class of drugs to give for bronchospasm?

A

beta agonists

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13
Q

What class of drugs is useful for inhibiting the release of leukotriene-mediated arachidonic acid and may be especially helpful in allergic reaction caused by activation of the complement system

A

corticosteroids

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14
Q

What cells make IgE antibodies?

A

b cells

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15
Q

60% of intraop drug rx are d/t what class of drugs? 15% are d/t? 5-10%?

A

muscle relaxants; latex; antibiotics

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16
Q

Opioids are responsible for what % of drug reactions?

A
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17
Q

How do anaphylactoid reactions differ from anaphylactic?

A

anaphylactoid does not release IgE antibodies, but they’re instead mediated by mast cell and basophils

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18
Q

Angioedema usually involves what 3 areas?

A

GI tract, face, extremities

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19
Q

What is the principal indications for antacids prior to surgery?

A

neutralize gastric acid that is present in the stomach.

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20
Q

How effective are antacids at raising the gastric pH?

A

antacid dose administered 15-30 minutes prior to induction is 100% effective at raising the pH of gastric fluid above 2.5

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21
Q

What are preferred methods for raising the gastric pH?

A

Nonparticulate antacids such as sodium citrate are preferred over particulate antacids such as Maalox or Mylanta because the particles can cause pulmonary injury if aspirated. Given a few hours preoperatively, famotidine increases gastric pH and reduces gastric volume. Sodium citrate (15-30ml) increases gastric pH to >2.5. This dose should be administered within 1 hour prior to surgery.

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22
Q

How does the administration of antacids affect drug absorption?

A

Antacids can slow the absorption of PO digoxin, cimetidine, and ranitidine, but speed the absorption of phenobarbital

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23
Q

How do antacids affect gastric emptying time?

A

slow gastric emptying and increase gastric volume

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24
Q

The administration of antacids obviously increases the gastric fluid volume. Is this a concern with regard to increased risk of aspiration?

A

risk of aspiration depends upon both the pH of the fluid in the stomach as well as the volume. The fact that antacids increase the volume of fluid in the stomach, however, does not warrant witholding antacids. It has been shown that the mortality rate of aspiration is increased when small volumes (0.3 mL/kg) of acidic fluid is aspirated compared to larger volumes of buffered solution

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25
Q

Is the administration of an antacid useful in an emergency setting?

A

Yes. In fact, because it has an almost immediate and short-lived peak effect (15-20 minutes), it is more useful as an adjunct to emergency procedures rather than outpatient procedures where the time between administration of the antacid and induction of anesthesia may be prolonged

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26
Q

What is the pediatric dose of sodium citrate?

A

0.4 mL/kg of 0.3 M sodium citrate

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27
Q

What is the adult dose of sodium citrate?

A

30 mL

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28
Q

What are two examples of nonparticulate antacids?

A

Sodium citrate (Bicitra) and two Alka-Seltzer Gold tablets (which contains both sodium citrate and potassium citrate) dissolved in 30 mL of water are both options for nonparticulate antacids

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29
Q

Angioedema characterized by swelling of what?

A

submucosal, subcutaneous

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30
Q

How are the 2 types of angioedema diff?

A

one is d/t release of bradykinin (no sx of allergic reaction) and the other is d/t release of mast cells (sx of allergic reaction)

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31
Q

The most prevalent hereditary form of angioedema is the result of?

A

dysfunction or an autosomal dominant deficiency of C1 esterase inhibitor

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32
Q

C1 esterase inhibitor controls?

A

contact activation, complement, and fibrinolytic pathways

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33
Q

Why is the absence of C1 esterase inhibitor bad?

A

vasoactive mediators such as bradykinin are released that produce edema and increased vascular permeability

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34
Q

Patients who are deficient in C1 esterase inhibitor have recurrent episodes of ?

A

facial and/or laryngeal edema lasting 24-72 hours

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35
Q

Triggers of facial/laryngeal edema?

A

trauma, infection, menses, stress, or estrogen-containing oral contraceptives

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36
Q

Laryngeal attacks can be triggered by?

A

dental surgery

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37
Q

Who can an acquire a C1 esterase inhibitor deficiency? Why?

A

Patients with lymphoproliferative disorders; they have C1 ihibitor antibodies

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38
Q

Why can ACEI cause angioedema?

A

increased availability of bradykinin brought about by the ACE inhibitor-mediated blockade of bradykinin catabolism

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39
Q

Prophylactic therapy (both long-term and preoperatively) for patients with angioedema? Why these drugs?

A

androgens such as stanozolol and danazol; these drugs increase hepatic synthesis of C1 esterase inhibitor

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40
Q

Why have antifibrinolytic drugs been used in the tx of angioedema?

A

they exert their action by inhibiting the activation of plasmin

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41
Q

How do you treat an acute episode of angioedema?

A

25 units/kg of C1 inhibitor concentrate or 2-4 units of FFP in order to replace the deficient enzyme

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42
Q

Prophylactic treatment for patients with recurrent angioedema is necessary before any treatment requiring?

A

intubation or a stimulating procedure like dental surgery

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43
Q

What types of patients typically have AICDs placed?

A

otherwise healthy young patients with supraventricular dysrhythmias such as Wolff-Parkinson-White syndrome to elderly patients with significant coronary artery disease or congestive heart failure who have survived a previous life-threatening arrhythmia such as ventricular tachycardia or ventricular fibrillation

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44
Q

What type of anesthesia is typically utilized for the implantation of an AICD?

A

sedation in EP lab

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45
Q

How long will the battery of an AICD last?

A

designed to deliver 120 shocks and typically lasts 3-6 years

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46
Q

How long after sensing ventricular tachycardia or ventricular fibrillation will an AICD discharge an electric shock?

A

usually discharges about 10-15 seconds after detecting VT or VF. Most of the time, delay is attributed to the charging of the capacitor

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47
Q

Can a healthcare provider be shocked by a patient’s AICD?

A

If in physical contact with a patient who has an AICD that is discharging, a healthcare provider can receive a mild shock that is not capable of causing fibrillation in the caregiver

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48
Q

Is the presence of an AICD of special concern in patients undergoing extracorporeal shock wave lithotripsy (ESWL)?

A

Pacemakers and AICDs are no longer considered contraindications to ESWL. AICD and lithotripter manufacturing companies generally state that AICDs are a contraindication to lithotripsy, but patients with AICDs have been shown to complete the procedure successfully. Older abdominally-implanted AICDs present a greater hazard than transvenous pacemakers. The AICD should be shut off prior to treatment and then reactivated immediately after the procedure.

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49
Q

Can monopolary electrocautery be used in a patient with an AICD?

A

Although bipolar cautery is preferred, monopolar cautery may be used in patients with an AICD as long as it is set at the lowest possible energy setting, used in short bursts, the cautery tip is kept at least six inches away from the AICD, the grounding pad is placed so that the energy flow does not pass through the AICD, and a defibrillator is available for immediate use

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50
Q

To what family of viruses does HIV belong?

A

retrovirus

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51
Q

What type of lymphocyte is destroyed by the AIDS virus?

A

T-helper lymphocytes (also called CD4 T cells)

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52
Q

Where are T-helper lymphocytes predominantly located?

A

98% in lymph nodes

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53
Q

What are the odds of seroconversion from an HIV contaminated needlestick?

A

0.4%

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54
Q

What is the most common opportunistic pathogen associated with AIDS?

A

Pneumocystis jiroveci (formerly Pneumocystis carinii)

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55
Q

What are the potential respiratory complications from pneumocystis carinii pneumonia?

A

Breathlessness, night sweats, bacterial lung abscesses, tuberculosis, fungal infections, pneumothorax, pulmonary Kaposi’s sarcoma, and respiratory failure. Pulmonary adenopathy can be so severe that it results in tracheobronchial and pulmonary vessel compression. Kaposi’s sarcoma within the lungs can result in massive hemoptysis. HIV can also lead to an emphysematous destruction of the alveolar tissue

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56
Q

Pneumocystic carinii pneumonia usually doesn’t develop until the CD4 T cell count reaches what level?

A

200 cells/mL

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57
Q

How does the chest xray of a patient with pneumocystis carinii pneumonia appear?

A

often appears normal. A ‘ground-glass’ appearance may be apparent on xray, but often requires high-resolution CT to identify. Pneumothoraces may sometime be present

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58
Q

A patient with AIDS has a positive acid-fast bacillus test. What does this signify?

A

TB

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59
Q

With relation to HIV, what does the acronym HAART stand for?

A

Highly active antiretroviral therapy, which represents the current drug regimen used to prevent the advancement of HIV infection into AIDS.

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60
Q

What are the potential cardiac complications of AIDS?

A

echocardiogram will be abnormal in about 50% of AIDS patients. Approximately 25% will exhibit pericardial effusions. Infections from opportunistic organisms such as cryptococcus, coxsackie B virus, cytomegalovirus, toxoplasmosis, and aspergillus can cause myocarditis with ventricular dilation

61
Q

An HIV-positive patient takes a non-nucleoside reverse transcriptase inhibitor. How might this affect your anesthetic management plan?

A

NNRTIs can prolong the half-life and effects of drugs such as diazepam, midazolam, fentanyl, and meperidine

62
Q

What are the five major classes of antiretroviral drugs used in the treatment of HIV?

A

Nucleoside analogue reverse transcriptase inhibitors, non-nucleoside reverse transcriptase inhibitors, protease inhibitors, entry inhibitors, and integrase inhibitors

63
Q

What is zidovudine and what is its principal side effect?

A

nucleoside analogue reverse transcriptase inhibitor used in the treatment of HIV. Its principal side effect is bone marrow suppression

64
Q

An anesthetist suffers a needle-stick that was contaminated with blood from an HIV-positive patient. According to current recommendations, how soon should a postexposure prophylaxis medication regimen be started?

A

within 1-2 hours if possible

65
Q

What is Alpha-1 antitrypsin deficiency?

A

rare, homozygous syndrome in which a defective form of alpha-1 antitrypsin is produced

66
Q

What does alpha 1 antitrypsin do?

A

protects the elastic tissue of the lungs from neutrophil elastase

67
Q

What organs do alpha 1 antitrypsin effect?

A

defective form of alpha-1 antitrypsin accumulates in the liver, resulting in cirrhosis and the lack of the normal form in the lungs results in pulmonary diseases such as asthma and emphysema

68
Q

How can you measure the alveolar to arterial oxygen gradient in the OR?

A

subtract the arterial oxygen (PaO2) from the ideal alveolar oxygen (PA02)

69
Q

The normal A-a gradient in non-smokers is?

A
70
Q

The normal A-a gradient increases how much per decade of life?

A

1 mm Hg

71
Q

A useful estimate of the normal A-a gradient is?

A

age/4 + 4

72
Q

The ideal PAO2 is what would exist if there were?

A

no VQ mismatches and normal lungs

73
Q

At room air, the normal PAO2 is about?

A

100-105 mm Hg

74
Q

What is the equation to calculate PAO2?

A

PIO2- (PACO2/R)

75
Q

How do you arrive at PACO2, PIO2, & R?

A

PIO2 is the 3rd potential equation, PACO2 is estimated as the PaCO2, and R is the resp exchange ratio or ratio of VCO2/VO2

76
Q

Why is the respiratory exchange ratio or VCO2/VO2 usually less than 1?

A

you inhale more molecules of O2 than you exhale of CO2

77
Q

What is the normal value of respiratory exchange ratio or VCO2/VO2?

A

0.8

78
Q

Why is R also a measure of metabolism?

A

it expresses the difference in oxygen inspired and carbon dioxide exhaled

79
Q

The use of fat as the primary source of fuel can produce an R closer to?

A

0.7

80
Q

The use of carbohydrates as fuel (such as occurs during intense exercise) can produce an R around?

A

greater than 1

81
Q

If you are not supplied with a value for R, then use the value of?

A

0.8

82
Q

Normal atmospheric pressure at sea level?

A

760 mm Hg

83
Q

If you are at sea level, the partial pressure of oxygen in the alveoli if you’re breathing 21% O2 is?

A

150 mm Hg

84
Q

What is the equation for PIO2?

A

FiO2 x (atmospheric pressure in mm Hg (760) - water vapor pressure in mm Hg (47))

85
Q

We breathe in a combination of (3)?

A

water, nitrogen, and oxygen

86
Q

What is the partial pressure of water in the alveolar air when it is in gas form and when the air is completely saturated?

A

47 mm Hg

87
Q

What is the pathologic process that results in the neuronal degradation associated with Alzheimer’s disease?

A

Deposition of amyloid beta peptides produces neuritic plaques and neurofibrillatory tangles that result in disruption of neurotransmitter function and the death of neurons

88
Q

What is the incidence of Alzhemier’s and what population does it affect the most?

A

most common form of neurodegenerative disease and is responsible for 40-80% of all cases of dementia. It affects approximately 20% of of patients over 80 years of age

89
Q

What test is diagnostic of Alzheimer’s disease?

A

Although computed tomography may demonstrate ventricular dilation and cortical atrophy and positive emission tomography may exhibit areas of decreased cerebral blood flow, only postmortem examination of the brain tissue is definitively diagnostic of Alzheimer’s

90
Q

What is the standard medical treatment for patients with Alzheimer’s disease?

A

Cholinesterase inhibitors such as rivastigmine, donepazil, and galantamine

91
Q

What are the side effects of the most common drugs used to treat Alzheimer’s?

A

Acetylcholinesterase inhibitors are the most common treatment and may result in nausea, vomiting, bradycardia, syncope, and fatigue

92
Q

How is the function of choline acetyltransferase affected in patients with Alzheimer’s disease?

A

significant decrease in the activity of choline acetyltransferase

93
Q

What are the anesthetic management implications for the patient with Alzheimer’s disease?

A

Preoperative sedation is usually avoided because it may aggravate dementia and precipitate postoperative confusion

94
Q

How would you expect a patient with Alzheimer’s to respond to succinylcholine?

A

Patients taking acetylcholinesterase inhibitors may have a prolonged duration of action with succinylcholine

95
Q

How would you expect a patient with Alzheimer’s disease to respond to muscle relaxants?

A

resistance to nondepolarizing muscle relaxants due to the use of acetylcholinesterase inhibiting drugs as part of their medical management. They will also exhibit a longer duration of action with succinylcholine

96
Q

If you need to administer an anticholinergic to a patient with Alzheimer’s disease, which one is preferred and why?

A

Glycopyrrolate is preferred because it doesn’t cross the blood-brain barrier. Atropine and scopolamine may result in increased confusion

97
Q

Enzymes called what break down ACh in brain?

A

cholinesterase

98
Q

People w alzheimers have low levels of what in their brain?

A

ACh

99
Q

What do cholinesterase inhibitors do?

A

stop or inhibit enzymes from breaking down the drug

100
Q

What does choline acetyltransferase do?

A

it is responsible for the synthesis of ACh

101
Q

In reference to ABGs what does the P stand for?

A

partial pressure of that gas in relation to other gasses

102
Q

What is a better indicator of how well you are breathing: O2 or CO2?

A

CO2

103
Q

CO2 is converted to what in your blood stream?

A

carbonic acid

104
Q

How do ACEI work?

A

prevent conversion of angiotensin I to II

105
Q

What is ATII and how does it work?

A

powerful vasoconstrictor that works by increasing aldosterone levels and stimulating SNS

106
Q

If ATII levels are low what happens to Na/H2O retention?

A

less Na/H2O retention

107
Q

What do ACEI do for bradykinin?

A

prevent degredation of bradykinin, an endogenous vasodilator

108
Q

2 most common side effects of ACEI?

A

allergic rhinitis and cough (d/t increased bradykinin)

109
Q

2 less common but more serious side effects of ACEI?

A

angioedema and decreased GFR

110
Q

What K abnormality may occur w ACEI and why? This K abnormality is most common in pts w what?

A

hyperkalemia bc it reduces aldosterone levels; CHF and renal insufficiency

111
Q

What is the long acting form of vasopressin?

A

terlipressin

112
Q

ACEI should be held how many hours before surgery?

A

12-24

113
Q

What is the duration of lisinopril?

A

18-30 hours

114
Q

What is the shortest duration ACEI?

A

captopril

115
Q

How does acetaminophen differ from salicylates?

A

Acetaminophen does not cause gastric irritation, affect platelet aggregation, or have anti-inflammatory properties. It also does not affect the levels of uric acid

116
Q

What are the two primary indications for the use of acetaminophen?

A

Analgesia and antipyrexia

117
Q

What is the adult oral dose of acetaminophen in the treatment of fever and acute pain?

A

325-650 mg every 4-6 hours

118
Q

What is the half-life of acetaminophen?

A

2-3 hours

119
Q

What is the lethal dose of acetaminophen?

A

15 g or greater

120
Q

List symptoms associated with larger doses of acetaminophen

A

Dizziness, disorientation, and excitement

121
Q

What are some early symptoms associated with acetaminophen-induced liver damage?

A

Abdominal pain, diarrhea, nausea, and vomiting

122
Q

What drug is administered in the treatment of acetaminophen toxicity?

A

Acetylcysteine. It is most effective if administered within the first 8 hours of overdose

123
Q

What is the definition of metabolic acidosis?

A

presence of a metabolic acid, which lowers the pH to less than 7.35

124
Q

What is the definition of respiratory acidosis?

A

occurs when alveolar ventilation decreases enough that the PaCO2 rises, leading to a pH less than 7.35

125
Q

What are the major cardiac effects of acidosis and at what pH does this occur?

A

Acidosis decreases myocardial contractility. The effects are usually not clinically evident until the pH is less than 7.2 when the ability of the heart to respond to catecholamines is decreased. It is more evident, however, in patients with impaired left ventricular function, those on beta-blockers, or patients under general anesthesia

126
Q

What is the most likely cause of respiratory depression in the perioperative period?

A

Drug-induced depression of ventilation due to opioids or general anesthetics

127
Q

A patient is suffering from an exacerbation of chronic ventilatory failure and exhibits severe acidosis. You are about to intubate the patient and place him on the ventilator. Should the acidosis be corrected urgently or slowly? Why?

A

Chronic respiratory acidosis should not be corrected too rapidly because the lungs are able to eliminate CO2 much more quickly than the kidneys can eliminate bicarbonate. If the CO2 is eliminated too quickly, the patient will suffer from a metabolic alkalosis that can lead to neuromuscular irritability and CNS excitation that can lead to seizures.

128
Q

What are the primary causes of respiratory acidosis?

A

two categories: those due to alveolar hypoventilation and those due to increased CO2 production. Factors that impair CO2 elimination such as pulmonary diseases, neuromuscular disorders, chest wall abnormalities, and obtundation can potentially result in alveolar hypoventilation. Factors such as intense shivering, malignant hyperthermia, prolonged seizure activity, thyroid storm, and extensive burns result in an increase in CO2 production.

129
Q

What is the formula for anion gap?

A

[Na+] - ([Cl-] + [HCO3-])

130
Q

What is normal anion gap level?

A

7-12 mEq/L

131
Q

What are the two major classifications of metabolic acidosis?

A

normal anion gap acidosis and high anion gap acidosis

132
Q

What are the characteristics of normal anion gap acidosis?

A

Normal anion gap acidosis is due to an increase in chloride concentration. This usually occurs in instances where bicarbonate is lost, so the kidneys retain chloride ions to maintain electrical neutrality

133
Q

What are the most common causes of a normal anion gap acidosis?

A

Conditions that result in an increased production of nonvolatile acids such as renal failure, ketoacidosis, nonketotic hyperosmolar coma, and rhabdomyolysis or the ingestion of toxins such as salicylates, methanol, paraldehyde, and ethylene glycol can result in an acidosis with an increased anion gap. Acidosis with a normal anion gap can be produced by increased gastrointestinal losses of HCO3- from diarrhea, fistulas, or ingestion of CaCl2 or MgCl2. Other factors that can produce a normal anion gap acidosis include hypoaldosteronism, renal tubular acidosis, carbonic anhydrase inhibitors or the administration of large volumes of bicarbonate-free intravenous fluids.

134
Q

How does acidosis affect the oxyhemoglobin dissociation curve?

A

shifts to the right in acidosis to allow for a greater unloading of oxygen from the hemoglobin in the tissue bed. Other factors that shift the oxyhemoglobin dissociation curve to the right include: increased 2,3 DPG, fever, elevated CO2, and low carbon monoxide levels.

135
Q

What is another name for normal anion gap acidosis?

A

Hyperchloremic metabolic acidosis

136
Q

How does high anion gap acidosis occur?

A

A high anion gap acidosis occurs when a fixed acid is introduced into the extracellular space. As the acid dissociates, the hydrogen ion bonds with bicarbonate to form carbonic acid. It is the drop in bicarbonate that produces the anion gap.

137
Q

What systemic abnormalities may occur with acidosis?

A

Severe acidosis is associated with decreased cardiac contractility, decreased responsiveness to catecholamines, sensitization to re-entrant tachydysrhythmias, lowered threshold for ventricular fibrillation, hyperkalemia, hyperventilation, insulin resistance, and inhibition of anaerobic glycolysis

138
Q

What are the symptoms of Addison’s disease?

A

Weakness, anorexia, nausea, vomiting, hyperpigmentation, chronic hypotension, hypovolemia, hyponatremia, and hyperkalemia

139
Q

What are the two types of adrenal insufficiency?

A

primary and secondary. In primary adrenal insufficiency the adrenal glands cannot produce enough hormones. Secondary adrenal insufficiency is due to suppression or disease of the hypothalamic/pituitary axis. Addison’s disease is the idiopathic autoimmune destruction of the adrenal gland and is a form of primary adrenal insufficiency.

140
Q

How do the effects of primary adrenal insufficiency differ from secondary insufficiency?

A

Primary adrenal insufficiency results in the inadequate release of glucocorticoid, mineralocorticoid, and androgen hormones. Secondary adrenal insufficiency results in the inadequate release of glucocorticoid only.

141
Q

What is the most potent mineralocorticoid produced by the adrenal gland?

A

aldosterone

142
Q

Which is the most potent endogenous glucocorticoid and produced by the adrenal cortex?

A

cortisol

143
Q

What are the most common causes of secondary adrenal insufficiency?

A

Iatrogenic causes are the most common and include administration of synthetic glucocorticoids and pituitary surgery or irradiation

144
Q

What patients are at risk for adrenal insufficiency?

A

Any patient on chronic exogenous steroid therapy is at risk for adrenal insufficiency during periods of stress such as surgery.

145
Q

What plasma cortisol level is diagnostic of adrenal insufficiency?

A

less than 20 mcg/dL indicate adrenal insufficiency

146
Q

How does general anesthesia affect activation of the HPA axis? How does regional anesthesia affect it?

A

both postpone the increase in plasma cortisol secretion until the postoperative period.

147
Q

What are the surgical factors that influence the activation of the hypothalamic-pituitary-adrenal axis? How does surgery affect it?

A

magnitude and duration of surgery determine the degree to which the HPA axis is stimulated. Increases in adrenocorticotropic hormone begin immediately after incision, remain elevated during surgery, and peak at the time neuromuscular blockade is reversed. Major surgery can elevate plasma cortisol secretion from a normal of about 20 mg/day to 75 to 150 mg/day.

148
Q

How long after abrupt withdrawal of steroids would symptoms begin to appear in a patient on a long-term exogenous steroid regimen?

A

24-36 hours

149
Q

How long after discontinuation of long-term steroid use will it take for adrenal function to return to normal?

A

6-12 mos

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