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Surgery > ABSITE > Flashcards

ABSITE Flashcards

1
Q

Define Null Hypothesis

A

No difference exits

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2
Q

Define Type I error

A

Incorrectly rejects null hypothesis - Falsely assumes there was a difference when no difference exists.

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3
Q

Define Type II error

A

Incorrectly accepts the null hypothesis. Treatments are interpreted as equal when a difference exits.

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4
Q

Major cause of Type II error?

A

Small sample size.

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5
Q

Define Type III error

A

Conclusions that are not supported by the data.

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6
Q

Define ‘Mode’

A

The most frequently occurring variable in a data set.

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7
Q

Define ‘Mean’

A

The average

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8
Q

Define ‘Median’

A

The middle value in a set of data when organized in ascending or descending order. (50th percentile).

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9
Q

What is an ANOVA test?

A

A t-test for >2 samples of quantitative data.

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10
Q

What is nominal data?

A

Named categories. For example, color.

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11
Q

What is ordinal data?

A

Scaled data. For example, pain rating on a scale of 1-10.

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12
Q

Define prevalence

A

The number of people in a population who have a disease (or any phenotype)

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13
Q

Define incidence

A

The number of newly defined cases per a given time period.

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14
Q

What information does the sensitivity provide?

A

The ability to detect a disease: i.e number with positive test results who actually have the disease (true positive)

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15
Q

What information does specificity provide?

A

The ability to state no disease is present: i.e., number with negative test results who actually don’t have disease (true negative)

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16
Q

What cells are responsible for fever in atelectasis?

A

Alveolar macrophages.

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17
Q

Where in the cell is the TCA cycle carried out?

A

Inner membrane of the mitochondria.

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18
Q

What does TCA cycle stand for? What are some other names for this process?

A

Tricarboxilic acid cycle. Also known as the citric acid cycle, or the Krebs cycle.

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19
Q

Where are cell surface proteins constructed?

A

The rough endoplastic reticulum (RER)

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20
Q

Where are cytoplasmic proteins constructed?

A

The smooth endoplastic reticulum (SER).

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21
Q

What percentage of the plasma membrane is made of protein?

A

60%

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22
Q

What percentage of the plasma membrane is made of lipids?

A

40%

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23
Q

How does increasing the percent of cholesterol in the plasma membrane affect membrane proteins?

A

Increased cholesterol increases the mobility of proteins in the plasma membrane.

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24
Q

What are the four cardinal signs of Malignant Hyperthermia?

A

Fever, tachycardia, rigidity and acidosis.

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25
Q

What is the first sign of malignant hyperthermia?

A

Increased end tidal CO2.

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26
Q

What is the treatment for malignant hyperthemia?

A

Dantrolene. Stop surgical procedure/anesthesia and provide supportive care.

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27
Q

What is the mechanism of action of dantrolene?

A

Abolishes excitation-contraction coupling in muscle cells; most likely by affecting ryanodine receptors

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28
Q

What is the underlying pathophysiology of malignant hyperthermia?

A

Increased Ca++ release from the sarcoplastic reticulum.

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29
Q

Which muscle is the first to recover from paralytics?

A

Diaphragm

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30
Q

What are the last muscle groups to recover from paralytics?

A

Neck and face

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31
Q

How many ATP are produced by one molecule of glucose after the TCA cycle?

A

38

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32
Q

How many ATP are produced by one molecule of glucose during anarobig glycolysis?

A

2 ATP + 2 Lactate.

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33
Q

What effects do anticonvulsants have on the P450 system?

A

Increases Cyt p 450 activity

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34
Q

What effect does coumadin have on the P450 system?

A

Increases Cyt p 450 activity

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35
Q

What effect does theophylline have on the P450 system?

A

Increases Cyt p 450 activity

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36
Q

What effect does cimetidine have on the P450 system?

A

Decreases Cyt p 450 activity

37
Q

What effect does isoniazide (INH) have on the P450 system?

A

Decreases Cyt p 450 activity

38
Q

What effects do monoamine oxidase inhibitors (MAOIs) have on the P450 system?

A

Decreases Cyt p 450 activity

39
Q

What effect does disulfiram have on the P450 system?

A

Decreases Cyt p 450 activity

40
Q

What is the role of the Macula Densa in the kidney?

A

Secreted by the macula densa of the kidney in response to decrease serum Na/Cl. Renin then converts angiotensinogen to angiotnesin I, which is converted to angiotensin II in the lungs by angiotensin converting enxyme (ACE)

41
Q

What is the role of renin?

A

Senses low Na/Cl. Produces renin, which converts angiotensinogen to angiotnesin I, which is converted to angiotensin II in the lungs by angiotensin converting enxyme (ACE)

42
Q

What is the role of angiotensin II?

A

Acts as a vasoconstrictor and increases aldosterone, which keeps Na+ at the expense of K+/H+ in the urine.

43
Q

What is cimetidine?

A

An antihistamine (H2-receptor antagonist) that inhibits stomach acid production.

44
Q

Major use for theophylline and MOA?

A

Relaxes bronchial smooth muscles. Used in COPD and Asthma.

45
Q

MOA of disulfiram?

A

Inhibits acetylaldehyde dehydrogenase, which prevents the breakdown of alcohol, thus exacerbating the ‘hang-over’ feelings.

46
Q

General MOA for MAOIs>

A

Inhibit the activity of monoamine oxidase, thus preventing the breakdown of monoamine neurotransmitters (seratonin, melatonin, epinephrine, norepinephrine, phenethylamine, trace amines, and dopamine). This increases the levels of these active neurotransmitters in circulation.

47
Q

Major constituents of bile?

A

80% bile salts, 15% lecithin, 5% cholesterol

48
Q

How does the gallbladder concentrated bile?

A

Active re-absorption of NaCl. H2O follows.

49
Q

How much bile is there in the body, how frequently does it circulate? Hoe much is lost daily?

A

5 g of bile makes up the bile pool, which recirculates every 4 hours. 0.5 g (10%) of bile is lost through excrement daily.

50
Q

What are the two primary bile acids?

A

Cholic acid and Chenodeoxycholic acid

51
Q

What are the two secondary types of bile, and where are they formed?

A

Formed by intestinal bacteria. Deoxycholic acid, and Lithocholic acid.

52
Q

What are the four phases of the Migrating Motor Complex (MMC)?

A

Phase I: Quiescence, II: Gallbladder contraction, III; Peristalsis, IV: Subsiding enteric activity.

53
Q

What is the main stimulatory hormone of the migrating motor complex (MMC?

A

Motilin?

54
Q

How does erythromycin simulate enteric motility?

A

Stimulates motilin receptors.

55
Q

Where is most of the Na and water absorbed in the digestive system?

A

Jejunum

56
Q

What is the best single test to evaluate the synthetic function of the liver?

A

PT (INR)

57
Q

Basic pathway of the Intrinsic clotting cascade?

A

Exposed collagen interacts with Factor XII, Activates XI and IX. Activates X, which then activates thrombin to produce fibrin.

58
Q

What is the common factor between the intrinsic and extrinsic coagulation pathways?

A

Factor X

59
Q

Basic pathway of the Extrinsic clotting cascade?

A

Tissue factor (damaged cells) interacts with Factor VII leading to activation of X, which activates thrombin to produce fibrin.

60
Q

What is the role of Factor XIII?

A

Crosslinks fibrin to form a ‘plug’.

61
Q

How do high versus low levels of 2,3-DPG affect hemoglobin oxygen carrying capacity?

A

2,3-DPG lowers hemoglobins affinity for oxygen. Thus, low levels cause increased oxygen-hemoglobin binding (left shit), while high levels decreases oxygen binding to hemoglobin (right shift).

62
Q

How do levels of 2,3-DPG in banked blood affect transfused blood’s oxygen carrying capacity?

A

Banked blood is deficient in 2,3-DPG, thus increasing the affinity of hemoglobin for oxygen and causing left shift.

63
Q

What are the two major components that cryoprecipitate replaces?

A

Fibrinogen , vWF-XIII, and VIII

64
Q

MOA of Protein-C?

A

Degrades active V and VIII

65
Q

MOA of Protein-S

A

Acts as coenzyme for Protein-C, which degrades active Factor V and VIII.

66
Q

What is the only coagulation factor not made in the liver, and where is it produced?

A

Factor VIII is produced by the reticuloendothelial system.

67
Q

What are the Vitamin-K dependent factors?

A

II, VII, IX, X, Protein-C and Protein-S

68
Q

What are three laboratory values affected by Von Willebrand’s Disease, and how?

A

Prolongs PTT, prolongs bleeding time, positive ristocetin test.

69
Q

What are the different types of Von-Willebrand’s disease, and how do they respond differently to DDAVP?

A

Types I and III have low amounts of normal vwf, and both respond well to DDAVP. Type II has qualitatively poor wvf.

70
Q

What is the mode of inheritance of Von-Willebrand’s Disease?

A

Autosomal dominant

71
Q

What is the only inherited bleeding disorder that prolongs bleeding time?

A

Von-Willebrand’s Disease

72
Q

What are three treatments for Von Willebrand’s Disease?

A

Give Factor VIII, vwf, or cryoprecipitate.

73
Q

What is Glanzman’s thrombasthenia?

A

Defect in IIb/IIIa receptor leading to decreased platelet aggregation.

74
Q

What is Bernard Soulier syndrome?

A

A deficiency to Ib receptor. Decreased platelet adherence to exposed collagen.

75
Q

How does Factor VII deficiency effect PT and PTT?

A

Prolongs PT, does not effect PTT.

76
Q

What deficiency is present in Hemophilia A? How is it transmitted? pre-operative treatment?

A

Factor VIII. Sex-linked recessive. Replace 100% pre-operatively.

77
Q

How does Hemophilia A effect PT and PTT?

A

Prolongs PTT. Normal PT.

78
Q

What is the treatment for a hemophiliac joint?

A

Do not aspirate! Treat with ice, range of motion exercises, and replace factor VIII.

79
Q

What deficiency is present in Hemophilia A? How is it transmitted? pre-operative treatment?

A

Factor IX deficiency. Sex-linked recessive. Replace 50% pe-operatively.

80
Q

What laboratory tests demonstrate Lupus Anticoagulant?

A

Long Russel viper venom time, Long PTT that does not correct when normal plasma is added.

81
Q

What is Factor V Leyden?

A

Factor V that is resistant to activated Protein-C -> increases incidence of DVT

82
Q

MOA for heparin

A

Binds ATIII, which inactivates factors IX-XII (intrisinc pathway) leading to an increased PTT.

83
Q

What is the reversal agent for heparin?

A

Protamine

84
Q

What is the treatment for an overdose of thrombolytics?

A

epsilon amino-capoci acid (e-ACA)

85
Q

What five laboratory abnormalities are seen in DIC?

A

Low platelets, prolonged PT, prolonged PTT, low fibrinogen, high fibrin split products (d-dimer)

86
Q

What can be used for anticoagulation in HIT?

A

Dextran

87
Q

What is the effect of endothelial derived prostacyclin?

A

Decreases platelet aggregation, increases vasodilation, leads to bronchial relaxation.

88
Q

What is the role of thromboxane in platelets?

A

Increases platelet aggregation, causes vasoconstriction, increases bronchial constriction

89
Q

What is the best pre-operative test for patients on NSAIDs or ASA?

A

Bleeding time.

Surgery (9 decks)

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