McNeil's notes - stats/epi, coagulation cascade, trauma, cancer (gen, uro only), ICU, fluids, anesthesia, Neurology, SCI/nerve injuries Flashcards

Question

When using median as a measure of central tendency, when is it best? a. slightly skewed b. normal distribution

Answer 1

Answer: Normal distribution The median is primarily used for skewed distributions, which it summarizes differently than the arithmetic mean. Consider the multiset { 1, 2, 2, 2, 3, 9 }. The median is 2 in this case, as is the mode, and it might be seen as a better indication of central tendency than the arithmetic mean of 3.166. - for a normal distribution, mean = median = mode.

Answer 2

Answer: Positively skewed This is a positively skewed curve, because the mean is greater than the mode. In probability theory and statistics, skewness is a measure of the asymmetry of the probability distribution of a real-valued random variable. The skewness value can be positive or negative, or even undefined. Qualitatively, a negative skew indicates that the tail on the left side of the probability density function is longer than the right side and the bulk of the values (possibly including the median) lie to the right of the mean. A positive skew indicates that the tail on the right side is longer than the left side and the bulk of the values lie to the left of the mean. Negative skew: The left tail is longer; the mass of the distribution is concentrated on the right of the figure. The mean is smaller than the median. Positive skew: The right tail is longer; the mass of the distribution is concentrated on the left of the figure. The mean is larger than the median.

Answer 3

Answer: Analysis of variance Analysis of variance compares mean values from three or more groups simultaneously. Chi-square test tests difference between proportions or tests for association between categories. Used when variable is categorical.

Answer 4

Answer: 1:20 (ie 5%)

Answer 5

e) Recurrence of breast malignancy, when patient has entered a clinical trial of adjuvant therapy They consent to this

Answer 6

- Med student observer

Answer 7

- The secretaries he employees in his office

Answer 8

- disclosure is in keeping with principles of automony?

Answer 9

Answer: responsibility for content of the publication

Answer 10

Disregard Mom, take kid to OR, give blood as needed to save her. Kid is too young/does not have the capacity to reject treatment/be Jehovah? No time to call CAS - deal with it later. Rule: Must contact CAS but if threat is imminent, then transfuse right away

Answer 11

- give the patient a forum to ask about operative findings and their interest in knowing all details

Answer 12

- Explain to the family your obligation to your patient and tell the patient

Answer 13

Answer: Tell the police Duty to Warn (look it up) If there is a threat, then you should tell police, person in question, or holding person against will

Answer 14

Answer: See the patient and ask a doctor who was not involved in his treatment before to look after him

Answer 15

Answer: Arbitration Arbitration – legal technique for the resolution of disputes outside of courts, wherein the parties to a dispute refer it to one or more persons, by whose decision they agree to be bound Negotiation – a process of resolving disputes and conflicts via talks and discussions without using force Rationalism – any view appealing to reason as a source of knowledge or justification Autonomy – capacity of a rational indivdual to make a informed, uncoerced decision

Answer 16

Answer: Tell the chief.

Answer 17

A? The legal standard of risk disclosure expected of a physician hinges on the interpretation of the entity called "material risk." Any impairment of the physician related to drug usage, disease, or alcohol which compounds the risk of a procedure is very likely to be considered material by a patient. This paper argues that physician inexperience is a factor that a reasonable patient would attach significance to and that it should therefore be viewed as a "material risk" requiring disclosure.

Answer 18

c) Give your patients advantages d) Treat patients on first-come first-serve basis (also a silly thing since a prescription refill should not be seen before a trauma)

Answer 19

d) Inform the police (this is legally what you should be doing) Duty to warn

Answer 20

c) Tell patient about intra-op complication, possible sequelae, and what to look for (i.e., symptoms of CSF leak)

Answer 21

5) Physician provides good care Negligence = Not doing the standard of care, which is what another reasonable physician would have done in the same situation. NB: cannot be blamed unless this would have affected the patient → poor outcome (doesn’t count if it doesn’t influence management).

Answer 22

Answer given: Liable for negligence One could argue hemodialysis is not a heroic measure.

Answer 23

Answer: Not take anything

Answer 24

Answer: draw blood for you and give result only if court order The confidentiality of patient information is prescribed in law. For example, physicians in Ontario are prohibited from providing information to third parties regarding a patient's condition or any professional service performed for a patient without the consent of the patient or his or her authorized agent unless such disclosure is required by law.[2] A breach of confidentiality that is not required by law may prompt disciplinary action by the College of Physicians and Surgeons of Ontario. Similar provisions concerning confidentiality exist in other provinces. Moreover, a breach of confidentiality may result in a civil suit. CMAJ ethics online http://collection.nlc-bnc.ca/100/201/300/cdn_medical_association/cmaj/vol-156/issue-4/0521.htm

Answer 25

d (consent)

Answer 26

e. special and unique risks The law presumes that an adult is mentally competent to make medical decisions and that the competent adult is entitled to sufficient information to make an informed decision concerning the physician's proposed course of examination and treatment.[74] Under the doctrine of informed consent, physicians have the duty to disclose the following information to patients[74-76]: 1. The patient's condition and/or diagnosis 2. The nature and purpose of the proposed treatment, including the likelihood of success in the physician's practice 3. Reasonable alternative measures related to the diagnosis and treatment, including the probable outcome of those alternatives 4. The particular known inherent risks that are material to make an informed decision about whether to accept or reject the proposed treatment, including the consequences of refusing that treatment - Marx: Rosen's Emergency Medicine, 7th ed.

Answer 27

Answer: Has to be written (implied consent ex: lifting up your sleeve for someone to give you a vaccine)

Answer 28

b) the patient’s common-law partner order of SDM when patient is not capable (ex: under GA?)

Answer 29

For consent to be valid, it must be informed. The patient must be provided all relevant information. To be valid, it must also be voluntary, that is, as free from coercion as possible while recognizing that in extremis the patient's condition itself may be inherently coercive. The surgeon's ethical objective is to judiciously provide the patient sufficient information with which to decide what course to follow. This entails selectively presenting all information pertinent to the patient's condition regarding benefits, risks, and alternatives while avoiding overwhelming the patient with extraneous data. To walk the line between what is pertinent and what is extraneous requires prudent judgment. - Townsend: Sabiston Textbook of Surgery, 18th ed.

Answer 30

Answer given: Ask a next of kin or a patient advocate to assess the risks and benefits

Answer 31

Answer: Support with crystalloid but don’t give blood

Answer 32

Answer: explain to the patient what has happened

Answer 33

Answer: stage migration (???) Bias is a systematic error in making inference (assumptions). Any bias would invalidate results, therefore a), b) and d) are not correct answers. Stage migration describes change in the distribution of stage in a particular cancer population induced by either a change in the staging system itself or else a change in technology which allows more sensitive detection of tumor spread and therefore more sensitivity in detecting spread of disease (e.g., the use of MRI scan). Stage migration can lead to curious statistical phenomena. - http://en.wikipedia.org/wiki/Cancer_staging

Answer 34

Answer: CHF Based on goldman classification CHF has the highest score

Answer 35

``` Answer: intraoperative hypotension or class II angina ?? ```

Answer 36

Answer: Spontaneous abortion [...] Nevertheless, as late as 1997 a meta-analysis of over 19 studies completed between 1984 and 1992 reported an RR of abortion in females exposed to anesthetic gases to be 1.48 (CI 95%) 1.4-1.58. [...] This preliminary report showed the incidence of infertility, spontaneous abortion and children with congenital abnormalities in female anesthesiologists to be the same as that in other physicians […] No definitive evidence has shown that trace concentrations of anesthetics in the ambient air of the operating room present a health hazard. - Miller: Miller's Anesthesia, 7th ed.101 – Environmental Safety Including Chemical Dependency There used to be “strong” evidence but now mostly debunked.

Answer 37

Answer: ASA III I. A normal healthy patient. II. A patient with mild systemic disease. III. A patient with severe systemic disease. IV. A patient with severe systemic disease that is a constant threat to life. V. A moribund patient who is not expected to survive without the operation. VI. A declared brain-dead patient whose organs are being removed for donor purposes.

Answer 38

CABG 3 years ago

Answer 39

Presence of heart failure

Answer 40

3) Angina functional class II Perioperative MI probably is the leading cause of death in elderly after noncardiac surgery; - presence of CAD increases the incidence of peri-op MI from 0.1 to 0.7-1.1%; >40 with or without CAD: infarction rate is 1.8%; previous MI, reinfarction rate is 5-8%; MI within 3 months: reinfarction rate is 27%; 3-6 months: 11%; >6months: 5%; - patients with EF 35%); thus, CHF is a higher risk. a. mi within the previous 6 months - 10 points b. angina functional class II - not on the cardiac risk index (class III and IV are) c. s3 gallop (CHF) - see above d. aortic stenosis - 20 points for critical aortic stenosis e. age > 70 years- 5 points

Answer 41

Answer: High postoperative complication

Answer 42

c. Reschedule surgery and arrange a pre-operative anesthesia consult A patient with a new LBBB could have had an infarct. Considering this is elective surgery, the best course of action is to delay the operation and has the patient assessed by anesthesia. Unlike RBBB, which is occasionally seen without evident cardiac disease, LBBB is usually a sign of organic heart disease. LBBB may develop in patients with long-standing hypertensive heart disease, a valvular lesion (e.g., calcification of the mitral annulus, aortic stenosis, or aortic regurgitation), or different types of cardiomyopathy (see Chapter 11 ). It is also seen in patients with coronary artery disease and often correlates with impaired left ventricular function. Most patients with LBBB have underlying left ventricular hypertrophy (see Chapter 6 ). Rarely, otherwise normal individuals have an LBBB pattern without evidence of organic heart disease by examination, echocardiogram, or even invasive studies. Important clinical consideration: LBBB may be the first clue to four previously undiagnosed but clinically important abnormalities. These are advanced coronary artery disease, valvular heart disease, hypertensive heart disease, and cardiomyopathy. - Goldberger: Clinical Electrocardiography: A Simplified Approach, 7th ed.

Answer 43

The liver is the major site of synthesis of all the coagulation factors except factor VIII - Townsend: Sabiston Textbook of Surgery, 18th ed.

Answer 44

10 (actually Xa and Va)

Answer 45

Answer: give replacement factor before the surgery and for 10 days following In elective surgery, levels of the deficient coagulation factor should be assayed 48 hours before surgery and the level restored to 40% of normal before surgery. Because the half-life is 6 to 10 hours for factor VIII (8h for factor 8) and 8 to 16 hours for factor IX, approximately 1.5 U/hr/kg of factor VIII or 1.5 U/2 hr/kg of factor IX should be given. Additional administration of factors VIII and IX should be guided by the activity of the clotting factors for about 6 to 10 days postoperatively. - Miller: Miller's Anesthesia, 7th ed.

Answer 46

D. nothing. unlikely spontaneous bleed if >5-10% Hemophilia A is inherited as a sex-linked recessive deficiency of factor VIII, with fewer cases secondary to spontaneous mutation. The incidence of this abnormality is about 1 in 10,000 births. Clinical findings range from bleeding into joints and muscles, epistaxis, hematuria, and bleeding after minor trauma to prolonged postoperative bleeding, retroperitoneal bleeding, and intramural bowel hemorrhage. Laboratory screening tests usually reveal a prolongation of aPTT, with other tests being normal. The minimum level of factor VIII required for hemostasis is 30%, and spontaneous bleeding is uncommon with factor VIII levels greater than 5% to 10% of normal. Levels less than 2% constitute severe, 2% to 5% moderate, and greater than 5% mild deficiency. Severe deficiency with levels less than 1% are at risk for spontaneous bleeding episodes. Although the half-life of factor VIII is 2.9 days in normal subjects, the half-life of factor VIII concentrates is only 9 to 18 hours. Levels between 80% to 100% of normal should be attained for surgical bleeding or life-threatening hemorrhage. Acquired deficiency has been reported to occur with the development of antibodies to factor VIII after therapy. - Greenfield CD, ch 4

Answer 47

In elective surgery, levels of the deficient coagulation factor should be assayed 48 hours before surgery and the level restored to 40% of normal before surgery. Additional administration of factors VIII and IX should be guided by the activity of the clotting factors for about 6 to 10 days postoperatively - Miller: Miller's Anesthesia, 7th ed. To achieve hemostasis for major surgical procedures, an initial level of 60 to 100 percent is achieved. This level is followed by a prophylactic level of 30 to 50 percent until the wound is healed, typically 10 to 14 days. After some orthopedic procedures, factor level may need to be maintained for a longer period of time.

Answer 48

(depends on the site of operation/risk of bleeding): a. 10% b. 20% c. 40% = elective surgery d. 60% = major surgery and high risk of bleeding To achieve hemostasis for major surgical procedures, an initial level of 60 to 100 percent is achieved. This level is followed by a prophylactic level of 30 to 50 percent until the wound is healed, typically 10 to 14 days. After some orthopedic procedures, factor level may need to be maintained for a longer period of time.

Answer 49

Answers: | 1) Medication induced (most likely heparin for inpatients)

Answer 50

b. deficiency of factor VIII a. deficiency of factor VII (INR) b. deficiency of factor VIII (yes, intrinsic pathway) c. dysfibrogenemia (both) d. X inhibitor (both)

Answer 51

Undiagnosed bleeding dyscriasis. a. Platelet dysfunction. (depends, may be both) b. Drug induced coagulation defect. (depends on factors inovolved) c. Undiagnosed bleeding dyscriasis. d. Cirrhosis. (Both)

Answer 52

4) lack of factor XIII When aPTT is performed in conjunction with PT (INR), a further clarification of coagulation defects is possible. For example, a normal INR with an abnormal aPTT means that the defect lies within the first stage of the (intrinsic) clotting cascade (factors VIII, IX, X, XI, and/or XII). The pattern of a normal aPTT with an abnormal INR suggests a possible factor VII deficiency (extrinsic). If both INR and aPTT are prolonged, a deficiency of factor I, II, V, or X is suggested (common pathway). Used together, APTT and INR will detect approximately 95% of coagulation defects.

Answer 53

Answer: a. VW vWF has 2 functions 1) platelet aggregation (bleeding time) 2) carrier for factor 8 (intrinsic pathway – PTT) - aPTT prolonged in (Factor 12, 8, 9, 11 – deficiencies), Lupus Anticoagulant, 1. Activated partial thromboplastin time (aPTT): Measures intrinsic system; requires factors V, VIII, IX, X, XI, XII, fibrinogen, and prothrombin. May be prolonged in heparin administration, in hemophilia, in von Willebrand disease (vWD), in DIC, and in the presence of circulating inhibitors (e.g., lupus anticoagulants or other antiphospholipid antibodies). 2. Prothrombin time (PT): Measures extrinsic pathway; requires factors V, VII, X, fibrinogen, and prothrombin. May be prolonged in warfarin administration, in deficiencies of vitamin K–associated factors, in malabsorption, in liver disease, in DIC, and in the presence of circulating inhibitors. 3. Bleeding time (BT): Evaluates clot formation, including platelet number and function, and von Willebrand factor (vWF). Performed at patient's bedside. Always assess the platelet number and history of ingestion of platelet inhibitors, such as nonsteroidal anti-inflammatory drugs, before a BT test. The Platelet Function Analyzer-100 (PFA-100) system is another in vitro method for measuring platelet and vWF function. - Johns Hopkins: The Harriet Lane Handbook, 18th ed.

Answer 54

Answer: Acidosis and hypothermia The wording of this question is a bit misleading. The acidosis and hypothermia are usually associated with transfusion, not the shock itself.

Answer 55

Easy way to remember: factor 8 = 8 hours. vWF stabilizes factor VIII, which has a half-life of about 2.4 hours when free and 12 hours when bound to vWF in the circulation. - Kumar: Robbins and Cotran Pathologic Basis of Disease, Professional Edition , 8th ed. In its circulating form, factor VIII is inactive or minimally active as a cofactor in blood coagulation. It circulates in the blood at very low concentration (100 ng/mL) bound to vWF. Its plasma half-life is approximately 8 to 12 hours. - Hoffman: Hematology: Basic Principles and Practice, 5th ed. Because the half-life is 6 to 10 hours for factor VIII …. - Miller: Miller's Anesthesia, 7th ed.

Answer 56

Answers given: 1) VII INR : 1972 : X, IX, VII, II (rules out B and D in 1st stem) Hemophilia B is Factor IX deficiency : elevated PTT (rules out C) Also, VIII, IX, and XI are in intrinsic (PTT) pathway, while VII is extrinsic pathway (INR) Profiles of Hemostasis Screening Tests in Patients with Bleeding Disorders

Answer 57

b. Factor VII Extrinsic pathway - The ONLY Factor Deficiency that DOES NOT prolong aPTT = 7 Disorders of the Extrinsic Pathway of Coagulation A prolonged prothrombin time and a normal aPTT suggest an isolated deficiency of factor VII, which is rare and may be the result of an inherited or an acquired abnormality. Less commonly, inhibitors to factor VII have been reported. Additionally, certain cases of DIC or dysfibrinogenemia may present with isolated prolonged PT values. Because factor VII is essential only in the tissue factor-activated extrinsic pathway of coagulation, the coagulation time and the Stypven time are normal in patients with this disorder. - Lee: Wintrobe's Clinical Hematology, 10th ed., Copyright © 1999 Lippincott Williams ; Wilkins

Answer 58

Factor XI deficiency a) Factor II deficiency (affects both - common pathway) b) Factor V deficiency (affects both - common pathway) c) Factor VII deficiency (only INR - extrinsic pathway) d) Factor X deficiency (affects both - common pathway) e) Factor XI deficiency (intrinsic pathway only)

Answer 59

1) Increase functional protein S protein C + S are "anticoagulants" Protein C and S deficiencies lead to a hypercoagulable state

Answer 60

2) Low protein C protein C + S are "anticoagulants" Protein C and S deficiencies lead to a hypercoagulable state

Answer 61

B+F: Increased factor VII, decrease in protein S a. Increased antithrombin III (bleeding) b. Decreased Protein S (clot) c. Increase protein S (bleeding) d. Factor II deficiency (bleeding) e. Platelet dysfunction (bleeding) f. Increased factor VII (clot) The mechanism by which oral contraceptives are prothrombotic is complex and uncertain. Prothrombotic effects include modest increases in the levels of procoagulant factors (factor VII, factor VIII, factor X, prothrombin, fibrinogen) and decreases in the levels of anticoagulant proteins (antithrombin III, protein S). The development of acquired APC resistance has been demonstrated, by means of a thrombin generation assay, in women taking oral contraceptives. Although the molecular basis for this phenomenon is unknown, it provides a plausible explanation for the greatly increased thrombotic risk among oral contraceptive users who are carriers of the factor V Leiden mutation.[4] - Hoffman: Hematology: Basic Principles and Practice, 5th ed. Oral contraceptives cause alterations of the vessel wall with intimal hyperplasia. They also increase blood viscosity. There are decreased levels of protein S, antithrombin activity, and plasminogen activator content in women taking oral contraceptives. There also may be an increase in the levels of fibrinogen, factor VII, and factor X. - Bradley: Neurology in Clinical Practice, 5th ed. The estrogen component of combination OCs increases hepatic production of serum clotting factors, particularly factors I (fibrinogen), VII, and X - Noble: Textbook of Primary Care Medicine, 3rd ed., Mosby, Inc. p.332

Answer 62

Not sure.. Factor VII has the shortest half-life of all the factors carboxylated by vitamin K; therefore, when deficient, it is the PT that rises first, since the activated Factor VII is the first to "disappear." In later stages of deficiency, the other factors (which have longer half lives) are able to "catch up," and the PTT becomes elevated as well. old answer: This isn't mentioned in common texts. The following might suggest factor II is most sensitive marker .... When there is mild vitamin K deficiency, the PT is normal, but there are elevated levels of the undercarboxylated forms of the proteins that are normally carboxylated in the presence of vitamin K. These undercarboxylated proteins are called proteins induced by vitamin K absence (PIVKA). Measurement of undercarboxylated factor II (PIVKA-II) can be used to detect mild vitamin K deficiency - Kliegman: Nelson Textbook of Pediatrics, 18th ed.

Answer 63

Answer: Conversion of plasminogen to plasmin (well, almost) Plasminogen activators convert plasminogen to plasmin. Plasmin then degrades fibrin into soluble fibrin degradation products. - Hoffman: Hematology: Basic Principles and Practice, 5th ed.

Answer 64

Answer: A and D. I think A makes most sense based on below explanation and the fact that A and B are contradictory (so one must be the right one) Laboratory abnormalities in DIC are variable and related to the many diseases associated with this condition. Common abnormalities include an abnormal PT and aPTT with depressed fibrinogen levels and abnormal platelet counts. Levels of fibrin degradation products and d-dimer are elevated. The peripheral smear reveals fragmented RBCs, but this finding is not specific. Because of the continued activation of coagulation, thrombin/antithrombin complexes will be formed. Levels of thrombin/antithrombin and AT-III are depressed. Fragments of coagulation factor degradation are elevated, including F1.2 and FpA. Because of activation of the fibrinolytic system, plasminogen and α2-antiplasmin inhibitor levels are decreased. - Townsend: Sabiston Textbook of Surgery, 18th ed. Another feature of disseminated intravascular coagulation, hypofibrinogenemia, is unlikely to contribute to a defect in platelet aggregation, except in extreme cases, as fibrinogen concentration in plasma exceeds by at least 10-fold the quantity needed to saturate fibrinogen receptors on platelets. - Hoffman: Hematology: Basic Principles and Practice, 5th ed. Hmmm … based on the stem both A and D are possible.

Answer 65

Answer: decreased fibrinolysis by inhibiting plasminogen activators (similar to tranexamic acid) Amicar is an antifibrinolytic that inhibits plasminogen to plasmin conversion thereby inhibiting fibrinolysis by plasmin An antifibrinolytic for treatment of excessive bleeding from fibrinolysis. Competitively inhibits activation of plasminogen to plasmin, also, a lesser antiplasmin effect

Answer 66

Logical answer: inhibiting factors would prevent further thrombosis without lysing current clots. fibrin causes clots. therefore plasminogen/plasmin is the answer (Urokinase and Streptokinase increase Plasminogen → Plasmin formation) ⇒ Increase Plasmin activity ⇒ Increase Fibrinolysis

Answer 67

Answers: - a. Prothrombin (factor II) The uptake of the vitamin is intimately linked to the liver, as biliary salts are required for intestinal absorption.[10] Vitamin K deficiency can therefore be caused by anything that impairs the metabolism of bile acids. This includes intra- or extrahepatic cholestasis, biliary system fistulae or obstruction, primary biliary cirrhosis, or treatment with bile acid binders (i.e., cholestyramine). Vitamin K serves as a coenzyme in the post-translational carboxylation of factors II, VII, IX, and X.[18] This modification creates sites on these proteins for calcium ion coordination and thereby renders them functional

Answer 68

b. Decreased absorbtion of Vit K The uptake of the vitamin is intimately linked to the liver, as biliary salts are required for intestinal absorption.[10] Vitamin K deficiency can therefore be caused by anything that impairs the metabolism of bile acids. This includes intra- or extrahepatic cholestasis, biliary system fistulae or obstruction, primary biliary cirrhosis, or treatment with bile acid binders (i.e., cholestyramine). Vitamin K serves as a coenzyme in the post-translational carboxylation of factors II, VII, IX, and X.[18] This modification creates sites on these proteins for calcium ion coordination and thereby renders them functional

Answer 69

Answer: b. VII (extrinsic pathway, trauma) Activator of extrinsic Pathway: -Tissue factor comes into contact with factor 7 Activator of Intrinsic Pathway: -Factor 12 binding to negatively charged surfaces (ex proteins) Tissue kallikrein can also form bradykinin. Plasma kallikrein and bradykinin are activated during the acute and chronic phases of several experimental rat models of small intestinal ulceration and granulomatous enterocolitis, with a pathogenic role indicated by suppression of inflammation by a specific kallikrein inhibitor. [243] [244] Of considerable interest, genetic susceptibility to intestinal and systemic inflammation in inbred rat strains correlated with activation of the contact system[245] and is mediated by a single nucleotide polymorphism in kininogen that encodes a defect in glycosylation that accelerates cleavage by kininogen. - Feldman: Sleisenger amp; Fordtran's Gastrointestinal and Liver Disease, 8th ed. Inflammation and blood clotting are often intertwined, with each promoting the other.[74] The clotting system is divided into two pathways that converge, culminating in the activation of thrombin and the formation of fibrin ( Fig. 2-15 ) ( Chapter 4). The intrinsic clotting pathway is a series of plasma proteins that can be activated by Hageman factor (factor XII), a protein synthesized by the liver that circulates in an inactive form. ***Factor XII is activated upon contact with negatively charged surfaces, for instance when vascular permeability increases and plasma proteins leak into the extravascular space and come into contact with collagen, or when it comes into contact with basement membranes exposed as a result of endothelial damage. Factor XII then undergoes a conformational change (becoming factor XIIa), exposing an active serine center that can subsequently cleave protein substrates and activate a variety of mediator systems (see later). Inflammation increases the production of several coagulation factors, makes the endothelial surface pro-thrombogenic, and inhibits anticoagulation mechanisms, thus promoting clotting. - Kumar: Robbins and Cotran Pathologic Basis of Disease, Professional Edition , 8th ed.

Answer 70

Answer: c. Factor VIII vWF is actually more common > VIII > IX > XI a. Factor V deficiency (1 in million) b. Factor VII (1/500 000) c. Factor VIII (1/5000, X linked) d. Factor IX (1/30 000) vWF deficiency 1/100 (asymptomatic) - 1/10000 (symptomatic)

Answer 71

Answer: b) heparin In addition to the administration of warfarin, there are other causes of prothrombin time prolongation. These include (show table 1): - Vitamin K deficiency due, for example, to poor nutrition, or prolonged use of broad spectrum antibiotics. - Severe liver disease, which decreases the synthesis of both vitamin K-dependent and -independent clotting factors. - Deficiency or inhibition of factors VII, X, II (prothrombin), V, or fibrinogen - The infrequent antiphospholipid antibodies (lupus anticoagulant phenomenon) with antiprothrombin activity. In such patients, the acquired prothrombin deficiency may be severe enough to cause clinical bleeding. ( - While treatment with heparin does not normally prolong the PT (due to the addition of heparin-neutralizing materials to the PT reagent), the PT may be transiently elevated after heparin bolus administration. Increase INR (Extrinsic pathway) - Warfarin, Vitamin K deficiency - Factors 10, 9, 7, 2 Deficient (7 MOST IMPORTANT) - Liver Disease, DIC

Answer 72

a. Glutamine The pattern of changes in amino acid concentration in muscle during catabolism shows an increase in branched-chain amino acids, aromatic amino acids, and methionine, and a decrease in glutamine and basic amino acids (lysine and arginine). A uniform reduction of approximately 50% of free muscular glutamine associated with negative N balance seems to be one of the most typical features of the response to trauma and infection Glutamine is the most abundant amino acid in the human body, comprising nearly two thirds of the free intracellular amino acid pool. Of this, 75% is found within the skeletal muscles. During stress states such as sepsis, or in tumor-bearing hosts, peripheral glutamine stores are rapidly depleted, and the amino acid is preferentially shunted as a fuel source toward the visceral organs and tumors, respectively. (Schwartz)

Answer 73

Answer: fluid resuscitation until u/o > 0.5 cc/kg/hr Rhabdomyolysis is the breakdown of muscle fibers with leakage of potentially toxic cellular contents into the systemic circulation. The final common pathway of rhabdomyolysis may be a disturbance in myocyte calcium homeostasis.[ Vigorous hydration with isotonic crystalloid is the cornerstone of therapy for rhabdomyolysis. Administer isotonic crystalloid 500 mL/h and titrate to maintain a urine output of 200-300 mL/h Urinary alkalinization is recommended for patients with rhabdomyolysis and CK levels in excess of 6000 IU/L. Alkalinization should be considered earlier in patients with acidemia, dehydration, or underlying renal disease. A suggested regimen is 0.5 isotonic sodium chloride solution with one ampule of sodium bicarbonate administered at 100 mL/h and titrated to a urine pH higher than 7. After establishing an adequate intravascular volume, mannitol may be administered to enhance renal perfusion. Loop diuretics may be used to enhance urinary output in oliguric patients, despite adequate intravascular volume. - http://emedicine.medscape.com/article/827738-treatment Clinical sequelae of rhabdomyolysis include the following: • Hypovolemia (sequestration of plasma water within injured myocytes) • Hyperkalemia (release of cellular potassium into the systemic circulation) • Metabolic acidosis (release of cellular phosphate and sulfate) • Acute renal failure (nephrotoxic effects of liberated myocyte components) • Disseminated intravascular coagulation (DIC) • Hypocalemia (from phospate binding to calcium)

Answer 74

Answer: delay to OR Synonyms: "high-pressure injection injury," "grease gun injury," "paint gun injury," "pressure gun injury," and "high-pressure injection." Worsens with: • Greater time from injury to decompression/debridement o>10 hours – very high rate of amputation • Chemical/toxic nature of injectant o Amputation rate 60-80% paint/solvents; 7000 -100% rate of amputation • Velocity of injectant • Secondary infection oMay develop oleogranulomas (grease and oil based compounds) – drain through skin (fistulas/sinus) • Portals of entry o more distal worse o digits: into tendon sheath poor o palm: better because not governed by fascial planes • MUST warn patients even if digit survives – will be left with painful, stiff, atrophic digit. Prepare for poor outcome and possible later ankylosis/amputation

Answer 75

Answer: Perform a mechanical debridement

Answer 76

Answer: Thigh compartment syndrome a. Open femur fracture – embolis and infection b. B/L femur fracture – embolis c. Traumatic arm amputation – bleed out d. Thigh compartment syndrome

Answer 77

Answer: Trauma ``` #1 Unintentional Injury Age 1-4 11.1/100000, 5-14 6.8/100000 (of this MVA>drowning (1-4) and firearms (5-14)) #2 Congential Malformations 3.6/100,000(1-4) amp; Malignant Neoplams 2.4/100,000(5-14) (source National Center for Health Statistics 2001) ```

Answer 78

Answer: Intubate and ventilate

Answer 79

a. Post tib. Nerve injury b. Vascular injury - fix the vascular injury c. Segmental bone loss - bone graft d. Contamination - debride Posterior tibial nerve doesn't exist. I think they mean tibial nerve. If you don't have tibial nerve you can't feel the sole of your foot, and it's a contraindication to salvage "two absolute contraindications for lower limb salvage: anatomical complete disruption of the posterior tibial nerve in adults and crush injuries with warm ischemia time of more than 6 hours" - again, posterior tibial nerve isn't technically correct but it's cited in this article http://www.hindawi.com/journals/tswj/2014/640430/

Answer 80

c) Patient temp 34 degrees (a core body temp less than 32 during laporotomy is considered universally fatal) There is convincing evidence from multiple clinical series that a damage control strategy can be lifesaving in patients with severe injury. With such a strategy the surgeon limits interventions during the first operation to those that stop the bleeding and enable the patient to be resuscitated from hemorrhagic shock. In damage control, the surgeon selects a point in the first operation when the basic life-threatening problems have been managed and then decides to stop operating and return the patient to the ICU for resuscitation and correction of body temperature, acidemia, and coagulation disorders. - Townsend: Sabiston Textbook of Surgery, 18th ed. Indications for damage control surgery Thoracic trauma • Penetrating injury and SBP 5 (indication of anerobic metabolism and possible loss of blood)

Answer 81

c. After the primary survey. Based on ATLS, the phases of emergency department care are divided into the primary survey with interventions, initial diagnostics and imaging, the secondary survey, and disposition. - Marx: Rosen's Emergency Medicine, 7th ed. Radiographs of the chest, pelvis, C-spine, and FAST are adjuncts to the primary survey. Imaging is considered helpful but should be used judiciously and should not interrupt or delay the resuscitation process. When appropriate, radiography may be postponed until the secondary survey. - Kool, Blickman. Advanced Trauma Life Support®. ABCDE from a radiological point of view. Emerg Radiol. 2007 July; 14(3): 135–141. ``` Order from ATLS : Primary survery Resuscitation Adjuncts to primary surgery and resuscitation Consider need for patient transfer Secondary survery Continued post-resuscitation monitoring and re-evaluation Definitive care ```

Answer 82

Answer: deltoid Anterior Shoulder Dislocations A careful assessment of the neurovascular status of the affected extremity is essential. Injury to the axillary artery is rare, usually occurring in the elderly,[13] and can be quickly assessed by palpation of the radial pulse or the presence of an expanding hematoma. It is important to assess the status of the axillary nerve, because this is the most common nerve lesion resulting from anterior dislocations.[14] The sensory component of the axillary nerve is assessed by testing for sensation over the lateral aspect of the upper arm ( Fig. 49–5 ). The motor component of the axillary nerve would be tested by assessing the strength of the deltoid muscle, a difficult undertaking in the patient with a dislocated shoulder. - Roberts: Clinical Procedures in Emergency Medicine, 5th ed.

Answer 83

Answer dilantin.

Answer 84

ATLS book 15% of patients with severe brain injury will have seizure Severe definted as GCS 3-8 Approximately 5-10% of individuals with traumatic brain injury (TBI) experience new- onset seizures. The risk of seizure increases with increasing injury severity, depressed skull fracture, intracranial hematoma, and penetrating trauma. The risk is greatest in the first two years after injury and gradually declines thereafter. All types of seizures may occur as a result of trauma, but the most frequent are focal or partial complex seizures. Generalized complex seizures (what are commonly called "grand mal' seizures) occur in approximately 33% of cases. Immediate onset seizures, those that occur immediately or in the first few hours after a brain injury, do not suggest a chronic seizure disorder. Early onset seizures and those which develop within the first 7-8 days after trauma require prophylaxis for up to one year. Spontaneous resolution of seizure activity has been noted in this group. The highest risk group for persisting seizures are those individuals who experience seizure 7-8 days or longer following injury. Current recommendations for seizure prophylaxis suggest that patients who have not suffered a seizure within the first 7-8 days following a closed head injury, probably do not require prophylaxis ``` Posttraumatic seizures (PTS) frequently occur after moderate or severe TBI. Seizures are usually general or partial, and absence seizures are uncommon. Seizures are classified according to the time elapsed after the initial injury: Immediate seizures occur in the first 24 hours. Early seizures occur in the first 2-7 days, and late seizures occur after 7 days. The incidence of late PTS is in the range of 5-18.9%. Risk factors include chronic alcoholism, older age at the time of injury, and a history of seizure disorder. Approximately one half to two thirds of patients with these risk factors develop late PTS within the first year after injury.16 If a patient with TBI has 1 PTS, his or her likelihood of having another is approximately 50%. - http://emedicine.medscape.com/article/326643-overview ```

Answer 85

Answer: 20 degrees extension Examination of a child with a suspected spinal injury is carried out with the patient supine, in a neutral position, after the head and neck have been stabilized. In small children, it is appropriate to place a pad beneath the trunk to avoid hyperflexion of the neck because of the disproportion in head size. - Green amp; Swiontkowski: Skeletal Trauma in Children, 4th ed.

Answer 86

B. Lasix, 40mg IV and G. Dexamethasone Glucocorticoids — Glucocorticoids were associated with a worse outcome in a large randomized clinical trial (CRASH) of their use in moderate to severe head injury. They should not be used in this setting. Other agents — Furosemide, 0.5 to 1.0 mg/kg intravenously, may be given with mannitol to potentiate its effect. However, this effect can also exacerbate dehydration and hypokalemia (this patient is hypotensive) Management of Elevated Intracranial Pressure - Prevention of venous engorgement - CO2 control (mild hyperventilation) NORMOCAPNEA and NORMOXIA - Sedation and pain control - Cerebrospinal fluid drainage - Mannitol - Lasix - Hypertonic saline - Decompressive craniectomy - Pentobarbital coma - used as last-ditch effort Bope: Conn's Current Therapy 2010, 1st ed ICP is normally 0–10 mm Hg; at 20–25 mm Hg, the upper limit of normal, treatment to reduce ICP is needed. Propofol decreases intracranial pressure (ICP) in patients with either normal or increased ICP.

Answer 87

Propofol does not increase ICP and can be run as an infusion. Sedation — Keeping patients appropriately sedated can decrease ICP by reducing metabolic demand, ventilator asynchrony, venous congestion, and the sympathetic responses of hypertension and tachycardia [72]. Establishing a secure airway and close attention to blood pressure allow the clinician to identify and treat apnea and hypotension quickly. Propofol has been utilized to good effect in this setting, as it is easily titrated and has a short half-life, thus permitting frequent neurologic reassessment.

Answer 88

Answer: Brown-Sequard - the flexed view is usually most helpful in detecting ligamentous injury that is not apparent on the neutral view - typically, this view is ordered at 7 to 10 days post injury when C-spine is less tender Contraindications : - known cervical spine fracture or dislocation - Brown sequard, central cord - not with anterior cord syndrome In alert patients with normal plain radiographs but persistent symptoms, flexion-extension views, especially of the cervical spine, can be obtained to look for ligamentous instability. - Townsend: Sabiston Textbook of Surgery, 18th ed. Central cord syndrome is a contraindication to flex-ex. Flex-ext stress views should obtained for only those who are alert, cooperative, and neurologically intact and patients who can describe pain or early onset of any subjective neurologic symptoms Brown-sequard: hemisection of cord. Asymmetric paresis and jt position/vibration loss (ipsilateral) with contralateral pain and temperature loss. Ant. Cord syndrome: disproportionately greater motor impairment in upper compared to lower extremities, bladder dysfunction, and variable degree of sensory loss below the level of injury. Typically after hyperextension injury. Flex-Ext views indicated

Answer 89

Answer: perfusion In addition, polytrauma patients can present with hypotension caused by ongoing hemorrhage, resulting in a critically low perfusion to a potentially swollen, injured spinal cord. As with brain injury, prolonged hypoperfusion and hypoxia may be harbingers of poor outcome. - Bradley: Neurology in Clinical Practice, 5th ed.

Answer 90

Answer: unrecognized intra-abdominal injury SIADH would make you hypertensive

Answer 91

Not sure what the answers are... probably A for the second question PROGNOSIS — Outcome from severe head injury is dependent on a range of factors including baseline patient characteristics, severity of TBI, and the occurrence of medical complications and secondary brain insults. Specific negative outcome predictors that have been identified from these factors include : ●GCS at presentation (especially the GCS motor score) ●Presence and severity of CT abnormalities (subarachnoid hemorrhage, cisternal effacement, midline shift) ●Pupillary function ●Age ●Associated injuries and complications ●Hypotension ●Hypoxemia ●Pyrexia ●Elevated ICP ●Reduced CPP ●Bleeding diathesis (low platelet count, abnormal coagulation parameters)

Answer 92

Hypotension is always hemhorrage until proven otherwise ?

Answer 93

CN 1 Posttraumatic single nerve palsy was observed in 38 patients (77.6%), and multiple nerve injuries were observed in 11 (22.4%). Cranial nerves were affected in 62 cases. The most affected CN was the olfactory nerve (CN I), followed by the facial nerve (CN VII) and the oculomotor nerves (CNs III, IV, and VI). Other cranial nerve injuries — The risk of injury to other cranial nerves increases with the severity of brain injury, but these can also occur in mild TBI with an incidence of 0.3 percent according to one case series [143]. The distribution is similar to that for moderate or severe head injuries: ●Anosmia and hyposmia, which are often reported by the patient as impaired taste as well as smell, occur following injury to olfactory filaments as they enter the brain through the cribiform plate. While recovery occurs in about one-third of patients, loss of smell is likely permanent if present one year after the injury [144]. (See "Anatomy and etiology of taste and smell disorders".) ●Diplopia may result from injury to cranial nerves III, IV, and VI. In the setting of mild TBI, injury to cranial nerve IV is most common, followed by VI. Cranial nerve III is less commonly affected by mild TBI. (See "Overview of diplopia".) ●Facial pain and occipital neuralgia may occur in association with mild TBI. The former usually occurs in the setting of blunt force injury to the trigeminal nerve in the face, while occipital nerve injury may be indirect from a contiguous musculoskeletal injury in the neck. (See "Overview of craniofacial pain".)

Answer 94

d. 9 E1V3M5 = 9 his eyes are closed (do not open to command) = 1, he is mumbling incoherently = 3, and he localizes to pain = 5 Defintion of incoherent: without logical or meaningful connection; disjointed; rambling

Answer 95

Answer: Basal skull fracture Raccoon eyes, battle's sign

Answer 96

e- Observe and consult if drainage continues Realistically should get neurosurg assessment, but the key to answering this question is to know that 1. usually the CSF leaks stop on their own (so don't need urgent OR), and 2. you don't need to give prophylactic antibiotics. See below for more details. Basal skull fractures involve the floor of the skull. Bruising may occur about the eye (raccoon sign) or behind the ear (Battle's sign), suggesting a fracture involving either the anterior or middle fossa, respectively. Isolated cranial nerve deficits can be seen in association with this fracture type because the nerves' exit foramina lie at the skull base. The facial nerve is frequently affected, with injury due to laceration or swelling. Most facial nerve deficits resolve spontaneously, so no specific therapy is warranted. On the other hand, complete transections of the facial nerve are usually explored, although the timing of exploration remains a matter of debate. Any associated CSF rhinorrhea or otorrhea should be treated expectantly. Traumatic CSF leaks typically stop within the first 7 to 10 days. If a leak persists, lumbar CSF drainage can be implemented to seal the leak by lowering CSF volume and ICP. If drainage therapy fails, surgical exploration is indicated and accomplished by oversewing the defect with an intradural fascial patch graft. Fewer than 5 percent of patients require surgical repair. Prophylactic antibiotics are not used routinely because recent prospective studies have failed to demonstrate any benefit from their use. - Schwartz Uptodate Basilar fractures — Intracranial hemorrhage caused by a basilar skull fracture frequently represents a surgical emergency and requires immediate neurosurgical consultation. All patients with basilar skull fractures require admission for observation, regardless of the need for surgical intervention. Basilar skull fractures can produce a dural tear, which can cause a cerebral spinal fluid (CSF) leak. Clinically, this is suggested by the presence of clear or blood-tinged rhinorrhea or otorrhea in a head-injured patient. If the fluid is blood tinged, the "halo" sign (also called the "ring" or "target" sign) may be useful to determine the presence of CSF. To perform the test, a drop of the fluid is placed on a tissue or filter paper. A rapidly expanding ring of clear fluid around red blood defines a positive test. Of note, the halo test does NOT differentiate among CSF, saline, saliva, and other clear fluids and has not been formally studied in a clinical setting. (See "Facial trauma in adults", section on 'Examination of specific body parts'.) The majority of CSF leaks resolve spontaneously within one week of injury and without CNS complications. The risk of meningitis has been estimated at 3 percent in the first week. Retrospective observational studies suggest that the administration of prophylactic antibiotics during the first week of a CSF leak is unnecessary [46-49]. The incidence of bacterial meningitis rises substantially if the leak persists past seven days and we suggest that prophylactic antibiotics be given in such cases [46]. Antibiotic selection is identical to that for penetrating head trauma. (See 'Penetrating injuries' below.) Cranial nerve palsies are a delayed complication of basilar skull fractures. They generally present two to three days following injury and are due to nerve compression or contusion [50,51]. These palsies may respond to treatment with glucocorticoids, although no large clinical trials have been performed to support this approach. Common treatment regimens are similar to those used for nontraumatic palsies (eg, Bell's palsy). We suggest starting such treatment in consultation with otolaryngology or neurosurgery. (See "Bell's palsy: Pathogenesis, clinical features, and diagnosis in adults".) Facial nerve palsies that appear acutely in association with basilar skull fractures are due to nerve transections. These injuries do NOT respond to glucocorticoid therapy and carry a poor prognosis for recovery of nerve function [45].

Answer 97

Answer: CT Head because he is >65 years old Canadian CT Head Rule CT Head Rule is only required for patients with minor head injuries with any one of the following: ``` High risk (for neurological intervention) ● GCS score 30 min ● Dangerous mechanism (pedestrian struck by motor vehicle, occupant ejected from motor vehicle, fall from height >3 feet or five stairs) ``` Minor head injury is defined as witnessed loss of consciousness, definite amnesia, or witnessed disorientation in a patients with a GCS score of 13–15.

Answer 98

? I think further details on stem would help. Unsure if this is a syncope question or CT head rule question For the second, CT is likely the answer. Hard to argue EKG vs. stress EKG so likely those two are not the answer. MRI is almost always contraindicated if you have a pacemaker

Answer 99

Answer: Linear fracture is critical if occurred over a vessel The great majority of linear skull fractures have minimal or no clinical significance. However, fractures that cross the middle meningeal groove in the temporal bone or major venous dural sinuses may disturb these vascular structures causing significant extraaxial bleeding (ie, bleeding beneath the skull but outside the brain parenchyma). Separation (ie, diastasis) of skull sutures can occur following trauma and most often involves the coronal or lambdoid sutures. Uptodate Linear skull fracture — A linear skull fracture is a single fracture that most often extends through the entire thickness of the calvarium. They occur most often in the temporoparietal, frontal, and occipital regions.

Answer 100

Answer: Decrease cerebral oxygenation by the effect of other injuries

Answer 101

Answer: hyponatremia SIADH is the most common abnormality after CHI, thus hyponatremia is correct. SIADH causes a dilutional hyponatremia secondary to inappropriate renal water conservation. Relatively less common post-TBI endocrinopathies include anterior hypopituitarism (AH), DI, cerebral salt wasting (CSW), and primary adrenal insufficiency (PAI)

Answer 102

Answer: Transtentorial herniation An evaluation of the patient’s pupil size and responsiveness must be done early in the initial assessment of the head-injured patient. A large fixed pupil suggests herniation syndrome; it is usually on the side of the expanding lesion. Traumatic mydriasis, resulting from direct injury to the eye and periorbital structures, may confuse the assessment of the pupillary responsiveness. The most common clinically significant traumatic herniation syndrome is uncal herniation, a form of transtentorial herniation. Uncal herniation is often associated with traumatic extraaxial hematomas in the lateral middle fossa or the temporal lobe. The classic signs and symptoms are caused by compression of the ipsilateral uncus of the temporal lobe on the U-shaped edge of the tentorium cerebelli as the brain is forced through the tentorial hiatus. As compression of the uncus begins, the third cranial nerve is compressed; anisocoria, ptosis, impaired extraocular movements, and a sluggish pupillary light reflex develop on the side ipsilateral to the expanding mass lesion. This phase may last for minutes to hours, depending on how rapidly the expanding lesion is changing. As the herniation progresses, compression of the ipsilateral oculomotor nerve eventually causes ipsilateral pupillary dilation and nonreactivity. Initially in the uncal herniation process, the motor examination can be normal, but contralateral Babinski’s responses develop early. Contralateral hemiparesis develops as the ipsilateral peduncle is compressed against the tentorium. With continued progression of the herniation, bilateral decerebrate posturing eventually occurs; decorticate posturing is not always seen with the uncal herniation syndrome. In up to 25% of patients the contralateral cerebral peduncle is forced against the opposite edge of the tentorial hiatus. Hemiparesis is then detected ipsilateral to the dilated pupil and the mass lesion. This is termed Kernohan’s notch syndrome and causes false-localizing motor findings. - Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 5th Edition, pg 290

Answer 103

The prevention of deep venous thrombosis (DVT) is a difficult management issue in TBI. Patients with TBI are at increased risk of DVT which can be reduced by the use of mechanical thromboprophylaxis using intermittent pneumatic compression stockings [50,51]. While DVT risk can be further reduced with antithrombotic therapy, this has to be weighed against the potential risk of hemorrhage expansion, which is greatest in the first 24 to 48 hours [52-54]. The use and timing of antithrombotic agents in patients with TBI must therefore be individualized according to the degree of intracranial bleeding and the perceived risk of DVT. Observational studies suggest that antithrombotic therapy may not be associated with the increased risk of intracranial hemorrhage expansion previously thought to occur in this setting, even when administered early on [55,56]. But based on newest evidence, it appears that enoxaparin may be used in these patients without increased risk of bleeding.

Answer 104

Cavernous sinus thrombosis usually presents with visual symptoms as CN 3,4,6 and sensory 5 pass through there. Superior sagiall sinus thrombosis can get focal findings with weird hemorrhades in weird places, typically involving the abduces nerve (it is the longest nerve) Meningitis , cerebral edema and saggitial sinus thrombosis are less likely to be focal seizures in nature This patient has a bilateral loss of sense of smell – olfactory nerve is CN I and the receptors are located in the roof and walls of the nasal cavity. CN I and II are derived from the forebrain - also, the fever and leukocytosis are more suggestive of infection, therefore making a) the more likely answer

Answer 105

Answer: Zone I is clavicle to cricoid Zone I, the base of the neck, is demarcated by the thoracic inlet inferiorly and the cricoid cartilage superiorly. Structures at greatest risk in this zone are the great vessels (subclavian vessels, brachiocephalic veins, common carotid arteries, aortic arch, and jugular veins, trachea, esophagus, lung apices, cervical spine, spinal cord, and cervical nerve roots. Signs of a significant injury in the zone I region may be hidden from inspection of the chest or the mediastinum Zone II encompasses the midportion of the neck and the region from the cricoid cartilage to the angle of the mandible. Important structures in this region include the carotid and vertebral arteries, jugular veins, pharynx, larynx, trachea, esophagus, and cervical spine and spinal cord. Zone II injuries are likely to be the most apparent on inspection and tend not to be occult. Additionally, most carotid artery injuries are associated with zone II injuries. Zone III characterizes the superior aspect of the neck and is bounded by the angle of the mandible and the base of the skull. Diverse structures, such as the salivary and parotid glands, esophagus, trachea, vertebral bodies, carotid arteries, jugular veins, and major nerves (including cranial nerves IX-XII), traverse this zone. Injuries in zone III can prove difficult to access surgically.

Answer 106

Answer: 1) Likely question/answer is q) for asymptomatic patients, which would you explore a) zone II 2) posterior (given) When would you explore the neck? - Any Region with SHOCK or STROKE ⇒ Surgery - Region 2 with SYMPTOMS ⇒ Surgery * * All others cases ⇒ Angiography, CXR, +/- Esophagus Scope, +/- Tracheal Scope Asymptomatic patients with penetrating injuries to the base of the neck (zone 1) require four-vessel arch angiography either to exclude major arterial injury or to plan the operative approach if an injury is present. The same applies to penetrating injuries above the angle of the mandible (zone 3), where both exploration and distal control are technically difficult; therefore, an endovascular solution, if feasible, may be the safest option. Patients with asymptomatic midcervical injuries (zone 2) may undergo either neck exploration (a straightforward procedure associated with very low morbidity) or a combination of four-vessel angiography, esophagoscopy, and barium swallow to rule out significant arterial and esophageal injury. Both pathways are acceptable alternatives, and thus choice between operative exploration and a sequence of diagnostic procedures reflects individual preferences or institutional policies. - Townsend: Sabiston Textbook of Surgery, 18th ed. Zone I Injuries - At risk: great vessels; esophagus; trachea - Symptomatic: angio, then explore - Asymptomatic: needs angio, laryngoscopy and esophagoscopy - Mandatory esophageal evaluation is also recommended because a missed esophageal injury in Zone I may be clinically silent until mediastinitis and sepsis develop - Contrast esophagram may also be useful (sensitivity and specificity as high as 90% to 100%) - Flexible or rigid esophagoscopy has high specificity and sensitivity - CT can show path of projectile Zone II Injuries - At risk: everything - Symptomatic: explore - Asymptomatic: either - Directed evaluation with serial exam - Mandatory neck exploration Zone III Injuries - At risk: great vessels and cranial nerves at skull base - Symptomatic: angio, then explore and/or interventional radiology - Asymptomatic: angio +/- exploration - Bailey: Head and Neck Surgery – Otolaryngology

Answer 107

Answer: Delayed repair of facial fractures

Answer 108

Answer: Lefort I Seminar Plastic Surgery 1. Le Fort I (Gueurin fracture or Horizontal fracture) - Fracture line passes through - Base of pyriform aperture (above roots of maxillary teeth) - Base of maxillary sinus and nasal septum - Pyramidal process of palatine bone ; pterygoid plates - Separates maxillary alveolus from superior midfacial skeleton - 30% of maxillary fractures 2. Le Fort II (Pyramidal fracture) - Fracture line passes through - Across nasal bones, nasofrontal suture and septum - Into medial wall of orbit (lacrimal bone) - Diagonally downward and outward through maxilla (involves inferior orbital rim and orbital floor) - Through pterygoid plates - Central pyramidally shaped nasomaxillary segment separated from the zygomatic and upper, lateral midfacial skeleton - Bony fragment contains - Lacrimal crests → possible lacrimal duct injury - Bulk of maxilla (displaces backward and up) → anterior open bite - Pyriform margin (incorporates nasal skeleton including: nasal bones, bony septum, perpendicular plate of ethmoid, lower half of vomer and infra-orbital foramen) → transient or permanent infra-orbital nerve injury - Alveolus - Palate - Above or below medial canthal ligament (attached to frontal process of maxilla); low and high varieties - Telecanthus may result if disrupted - 42% of maxillary fractures 3. Le Fort III (Craniofacial dysjunction or transverse fracture) - Cranial base completely separated from the mid-facial skeleton (free floating maxilla) - Fracture line passes through - Nasofrontal (NF) suture - Across orbital floor to ZF suture - Zygomatic arch and pterygoid plates - Usually will develop anterior open bite (as per II) - Anesthesia of maxillary teeth will usually resolve - 28% of maxillary fractures 4. Le Fort IV - Not described by Le Fort - Fractures consisting of frontal bone, sinus, superior orbital rims and anterior cranial base

Answer 109

Answer: depends on neurological status - awake = repair - coma = close monitoring If awake should repair or ligate. Ligate if uncontrolled hemorrage or no antegrade flow. Penetrating carotid artery injuries, regardless of the patient's neurologic status, usually require repair, except in comatose patients. Inaccessible carotid artery injuries near the base of the skull can be treated by interventional radiologists with a stent if the anatomy of the injury is favorable. Otherwise the artery will need to be thrombosed or ligated. If ligation is necessary, the patient should be given anticoagulation therapy with heparin followed by warfarin sodium (Coumadin) for 3 months. This treatment may prevent a stroke by inhibiting the generation of thrombi from the surface of the clot at the circle of Willis while the endothelium heals. Without anticoagulation therapy the risk of stroke with ligation has been approximately 20 to 30 percent, and most strokes occur a few days after ligation. - PRINCIPLES OF SURGERY, SEVENTH EDITION

Answer 110

Answer: Tension pneumothorax

Answer 111

Answer: clinically Tension pneumothorax is a clinical diagnosis and treatment should not be delayed by radiologic confirmation ``` Tension pneumothorax is characterized by: o chest pain o respiratory distress o tachycardia o hypotension o tracheal deviation o unilateral absence of breath sounds o neck vein distention o cyanosis (late) Reference: ATLS manual ```

Answer 112

Answer: Pulmonary contusion

Answer 113

Answer: Thoracotomy and pericardial window. Fluid that is not clotting suggest pericardial fluid. Treatment of traumatic pericardial temponade is immediate drainage. emedicine Pericardial window involves the excision of a portion of the pericardium, which allows the effusion to drain continuously into the peritoneum or chest.[2] The fluid can be drained in any of 3 ways: via a small subxiphoid incision, thoracoscopically,[6] or via a thoracotomy indications for a pericardial window: -Symptomatic pericardial effusions -Asymptomatic pericardial effusions that warrant a pericardial window for diagnosis -Hemodynamically stable patients with an undiagnosed pericardial effusion (a thoracoscopic approach is ideal) -Coexisting pericardial, pleural, or pulmonary pathology that requires diagnosis or therapy (a thoracoscopic approach is ideal) -Known benign effusions that reaccumulate after aspiration -Drainage of a purulent pericardial effusion -Early fungal or tuberculous pericarditis in which resection of the pericardium is required to prevent future pericardial constriction etc

Answer 114

Answer: Obtain an aortogram Aortic dissection 2016: CT-angiogram is more practical

Answer 115

Answers: - Needle decompression in 2ed I.C.S - Intubation ABCDE Emergent needle decompression for tension pneumothorax is carried out on the affected side by placing an 18-gauge needle or angiocatheter into the hemithorax at the midclavicular line in the second anterior intercostal space. This emergency maneuver relieves the tension created within the thorax. It does not treat the pneumothorax; subsequent chest tube insertion is required. [no mention of intubation] - Townsend: Sabiston Textbook of Surgery, 18th ed. When the diagnosis of tension pneumothorax is suspected clinically, the pressure should be relieved immediately with needle thoracostomy, which is performed by inserting a large-bore (14-gauge or larger) catheter, at least 5 cm in length, through the second or third interspace anteriorly or the fourth or fifth interspace laterally on the involved side. This method can be easily performed in the field or ED, allowing vital signs to improve during transport or preparation for a tube thoracostomy. [no mention of intubation] - Marx: Rosen's Emergency Medicine, 7th ed.

Answer 116

c? a) subq emphysema (most common physican finding; high sensitive) b) mediastinal emphysema c) massive air leak and failed re-exapansion lung after chest tube (highly suggestive of tracheobronchial injury; high specificity) Diagnosis is difficult and often delayed [86]. Intrathoracic injury can be subtle and indolent, presenting with retained secretions, recurrent pneumothoraces, and obstruction. The sine qua non ("[a condition] without which it could not be", or "but for..." or "without which [there is] nothing".) of intrathoracic tracheobronchial injury is a significant air leak and pneumothorax or pneumomediastinum that reaccumulates despite tube thoracostomy. A cervical injury may present without a significant air leak, if the tear or rupture is contained by the adventitia. Signs of cervical tracheal injury include dyspnea, hoarseness, and subcutaneous emphysema.

Answer 117

Answer: Tube thorocotomy and laparotomy Airway, breathing and then circulation. With decreased breath sounds, this is a clinical diagnosis of a pneumothorax, although its only tension if he is hypotensive or hypoxic. Therefore he needs a chest tube(tube thoracostomy) and since he has a tender abdomen, he likely has a perforated bowel which necessitates a laparotomy.

Answer 118

Answers: - pleural effusion (?) Patients with diaphragmatic injury due to blunt trauma usually have associated injuried that demand first attention and prevent detailed initial evaluation. The first chest X-ray after rupture of either hemidiaphragm may show nothing more than a blurring of the diaphragm with or without evidence of a small hemothorax. - Schwartz Rupture of the diaphragm may occur after blunt trauma. The diaphragm most frequently is ruptured on the left side, perhaps because the liver may dissipate some of the force of an abdominal blow, lessening the likelihood of rupture of the right hemidiaphragm. The most common appearance is loops of bowel protruding into the lower chest cavity without the normal dome-shaped structure of the hemidiaphragm ( Fig. 3–91 ). - Mettler: Essentials of Radiology, 2nd ed.

Answer 119

Answer: Amylase more than 20 IU/dl Positive DPL criteria (8): 1. > 10 mL of gross blood aspirated 2. Bloody lavage effluent 3. RBC count > 100 000/ml (> 5000/mL in penetrating trauma to the low chest) 4. WBC count > 500/ml 5. Amylase > 175 IU/dl 6. Bile 7. Bacteria 8. Food

Answer 120

EXPLORE: penetrating trauma, zone 1, or rapidly expanding/rupture/pulsatile? DO NOT EXPLORE: blunt zone 2 and 3 The location of a retroperitoneal hematoma and mechanism of injury guide the decision to explore the hematoma. The retroperitoneum is divided into three anatomic zones: the midline retroperitoneum (Zone 1), the perinephric space (Zone 2) , and the pelvic retroperitoneum (Zone 3) . Any hematoma in zone 1 mandates exploration for both penetrating and blunt injury because of the high likelihood and unforgiving nature of major vascular injury in this area. A hematoma in zone 2 is the result of injury to the renal vessels or parenchyma and mandates exploration for penetrating trauma to assess the damage and repair the injuries. A pelvic retroperitoneal hematoma (zone 3) secondary to penetrating trauma mandates exploration because of the likelihood of iliac vessel injury. However, zone 3 hematomas resulting from blunt trauma are usually associated with pelvic fractures and are not explored because the effective management of this type of bleeding is based not on operative control (which rarely proves effective) but on external fixation or angiographic embolization of the bleeding vessels. The only exception is a rapidly expanding hematoma in which the surgeon suspects a major iliac vascular injury that requires operative repair. - Townsend: Sabiston Textbook of Surgery, 18th ed. After blunt trauma, selected retroperitoneal hematomas in the lateral perirenal and pelvic areas do not require operation and should not be opened if discovered at operation. Midline, lateral paraduodenal, lateral pericolonic not associated with pelvic, and portal hematomas are opened after proximal vascular control has been obtained, if appropriate. Retrohepatic hematomas without obvious active hemorrhage are not opened. After penetrating trauma, most retroperitoneal hematomas are still opened. Exceptions include isolated lateral perirenal hematomas that have been carefully staged by CT and some lateral pericolonic hematomas. As with blunt trauma, retrohepatic hematomas without obvious active hemorrhage are not opened. - Feliciano. Management of traumatic retroperitoneal hematoma. Ann Surg. 1990 February; 211(2): 109–123

Answer 121

Answer: laparotomy Given the kinetics of bullet wounds, this pt probably has a bullet that has entered him through the buttock and traversed through to the retroperitoneal and abdominal organs. The bullet also forms a cavitation, injuring tissues not in the actual path of the bullet. Exit wounds are usually larger than entrance wounds. This pt has probably sustained an intrabdominal injury in addition to possible msk injury. The basic principles of patient care for abdominal gunshot wounds is: A,B,Cs NG tube Foley Chest and abdominal X-rays if pt stable Antibiotics and Tetanus Surgery Advanced Surgical Recall, blackbourne et al P329-334 Uptodate: Clinical indications for laporotomy -Unexplained signs of blood loss or hypotension in a patient who cannot be stabilized and in whom intraabdominal injury is strongly suspected -Clear and persistent signs of peritoneal irritation -Radiologic evidence of pneumoperitoneum consistent with a viscus rupture -Evidence of a diaphragmatic rupture -Persistent, significant GI bleeding seen in nasogastric drainage or vomitus

Answer 122

(there are multiple references for both liver and spleen but the consensus was spleen) Injuries to the spleen are the most common injuries in pediatric abdominal trauma. The liver is the second most commonly injured solid organ in the pediatric patient with abdominal trauma. However, it is the most common cause of lethal hemorrhage, with a mortality of 10 to 20% in severe liver injury. - Marx: Rosen's Emergency Medicine, 7th ed. The liver and spleen seem to be the most frequently injured organs, although reports vary. Small and large intestines are the next most injured organs, respectively. Recent studies show an increased number of hepatic injuries, perhaps reflecting increased use of CT scanning and concomitant identification of more injuries. - http://emedicine.medscape.com/article/821995-overview

Answer 123

Answer: D is true. C may be true, but is based on expert opinion. Answer key says C An important technical aspect to keep in mind is that in major perinephric hematomas, proximal control of the renal pedicle before opening Gerota's fascia is advisable. Renal contusions encompass the vast majority of minor renal trauma and can almost invariably be treated nonoperatively. It is our opinion that all perinephric hematomas caused by penetrating mechanisms that have not previously been evaluated by IVP should be explored. If preoperative IVP shows renal pedicle injury, extensive parenchymal laceration, or urinary extravasation, surgical exploration remains the best option. - Townsend: Sabiston Textbook of Surgery, 18th ed. D is true. C may be true, but is based on expert opinion. Answer key says C

Answer 124

Answer: Observation Renal contusions encompass the vast majority of minor renal trauma and can almost invariably be treated nonoperatively. - Townsend: Sabiston Textbook of Surgery, 18th ed.

Answer 125

Answers given: - Reassure - IVP (disagree) If patient was hemodynamically unstable and microscopic hematuria, then requires CT scan with and without control, including delayed phases. All blunt trauma patients with gross hematuria and those patients with microscopic hematuria and shock (systolic blood pressure

Answer 126

Answer: observe (Disagree. Likely get an ultrasound at least.) Need to get a Doppler us first Most testicular injuries are manage conservatively Hematocele is due to either testicular contusion or rupture. If rupture is present, then surgery is indicated to drain and repair. Early exploration and repair of testis injury is associated with increased testis salvage, reduced convalescence and disability, faster return to normal activities, and preservation of fertility and hormonal function ( Kukadia et al, 1996 ). Minor scrotal injuries without testis damage can be managed with ice, elevation, analgesics, and irrigation and closure in some circumstances. Significant intratesticular hematomas should be explored and drained even in the absence of testis rupture to prevent progressive pressure necrosis and atrophy, delayed exploration (40%), and orchiectomy (15%) ( Cass and Luxenberg, 1988 ). Significant hematoceles should also be explored, regardless of imaging studies, since up to 80% are due to testis rupture. - Wein: Campbell-Walsh Urology, 9th ed.

Answer 127

Answer: Retrograde urethrogram Blood at meatus = buzz word for retrograde urethrogram, don't put in a foley yet In the clinically stable patient, triphasic abdominal and pelvic CT (precontrast study, followed by a study immediately after injection of contrast agent, and then a 15- to 20-minute delayed study) is the most sensitive method for diagnosis and classification of genitourinary trauma” - Cambell’s Urolog In trauma patients with clinical evidence of urethral injury (scrotal hematoma, blood at the meatus, high-riding prostate), do not pass foley catheter since may increase damage If urethral injury is suspected, before any attempts to insert a foley, do a retrograde urethrogram as the study of choice to investigate A scout film is obtained with the patient at 25-30 degrees in oblique position. Then insert 14 or 16 Fr foley a few cm into urethra. Inflate balloon with 1-2ml and inject contrast through catheter and take X-ray. If no extravasation, deflate balloon, advance and place in bladder. A cystogram is then done to evaluate the bladder - Schwartz

Answer 128

Answer: fractured kidney I don't even think this is an accepted terminology. The American Association for the Surgery of Trauma (AAST) classifies renal injuries into five grades (Figs. 1 and 2): • Grade 1: Nonexpanding subcapsular hematoma/contusion with absence of parenchymal injury • Grade 2: Less than 1cm laceration into the renal cortex, not extending into the collecting system, with a nonexpanding hematoma confined to the perirenal fascia • Grade 3: Greater than 1cm laceration, extending through the renal cortex and medulla but not the collecting system • Grade 4: Laceration extending to the collecting system with urinary extravasation or a segmental vascular injury with contained hematoma; renal artery thrombosis • Grade 5: Shattered kidney or renal pedicle avulsion Follow-up imaging is indicated for patients with grade 4 or 5 injuries with urinary extravasation to assess for worsening urinoma or hematoma that might require further intervention. - Bope: Conn's Current Therapy 2010, 1st ed. In intraperitoneal bladder injuries, open surgical repair of the laceration is the recommended treatment modality. This allows the surgeon to reduce any herniating omentum or small bowel from the confines of the bladder and allows careful intravesical inspection of the bladder neck at the time of surgical exploration. - Wein: Campbell-Walsh Urology, 9th ed. Intraperitoneal bladder rupture accounts for 25% of all bladder injuries. The postulated mechanism of intraperitoneal bladder injury is thought to be rapid rise of intra-abdominal pressure during a blunt trauma.[6] In contrast to extraperitoneal bladder injuries, intraperitoneal bladder rupture requires operative repair with two-layer closure of the bladder injury and placement of a perivesical drain. - Townsend: Sabiston Textbook of Surgery, 18th ed.

Answer 129

Probably obsolete question given that no one does IVP's anymore Answers provided: (???) - focal or global filling defect - leakage into retroperitoneum 80% of bladder rupture is extraperitoneal - secondary to bone puncture from pelvic fracture - contrast most commonly extravasates into the retropubic space of Retzius - usually managed conservatively with foley catheter decompression unless laparotomy required for other reasons, then can fix primarily 20% of bladder rupture is intraperitoneal -secondary to blunt trauma to distended bladder with rupture at the dome -contrast extravasates into the paracolic gutters and outlines loops of bowel BUT, apparently the kidney is the most commonly injured structure in the urinary tract (see above question) in traumatic injury ALSO, hydronephrosis takes time to occur (days to week) and less than 1% of people have a single kidney, therefore these answers are less likely correct - Fundamentals of Diagnostic Radiology, 2nd Edition. Brant Blunt renal injuries are divided into minor and major injuries. Minor injuries make up approximately 85% of cases. Renal contusions encompass the vast majority of minor renal trauma and can almost invariably be treated nonoperatively. Major renal trauma includes deep cortical medullary lacerations with extravasation, large perinephric hematomas, and vascular injuries of the renal pedicle. Injury to the ureter is uncommon and occurs mostly after penetrating trauma. - Townsend: Sabiston Textbook of Surgery, 16th ed., Copyright © 2001

Answer 130

a. nonop The American Association for the Surgery of Trauma (AAST) classifies renal injuries into five grades (Figs. 1 and 2): - Grade 1: Nonexpanding subcapsular hematoma/contusion with absence of parenchymal injury - Grade 2: Less than 1cm laceration into the renal cortex, not extending into the collecting system, with a nonexpanding hematoma confined to the perirenal fascia - Grade 3: Greater than 1cm laceration, extending through the renal cortex and medulla but not the collecting system - Grade 4: Laceration extending to the collecting system with urinary extravasation or a segmental vascular injury with contained hematoma; renal artery thrombosis - Grade 5: Shattered kidney or renal pedicle avulsion Routine early follow-up imaging for grades 1 to 3 blunt renal injury is unnecessary. Grade 4 renovascular injuries can be followed up clinically. Follow-up imaging is indicated for patients with grade 4 or 5 injuries with urinary extravasation to assess for worsening urinoma or hematoma that might require further intervention. - Bope: Conn's Current Therapy 2010, 1st ed.

Answer 131

Answer: loss of both alleles The proto-oncogene can become an oncogene by a relatively small modification of its original function. There are three basic activation types: 1) A mutation within a proto-oncogene can cause a change in the protein structure, causing - an increase in protein (enzyme) activity - a loss of regulation 2) An increase in protein concentration, caused by - an increase of protein expression (through misregulation) - an increase of protein (mRNA) stability, prolonging its existence and thus its activity in the cell - a gene duplication (one type of chromosome abnormality), resulting in an increased amount of protein in the cell 3) A chromosomal translocation (another type of chromosome abnormality), causing -an increased gene expression in the wrong cell type or at wrong times the expression of a constitutively active hybrid protein

Answer 132

Oncogenes encode proteins that control cell proliferation, apoptosis, or both. The products of oncogenes can be classified into six broad groups: transcription factors, chromatin remodelers, growth factors, growth factor receptors, signal transducers, and apoptosis regulators

Answer 133

Answer: imbalance between cell growth and cell death [M]alignant transformation is the process by which a clonal population of cells acquires alterations that confer a growth advantage over normal cells. - Townsend: Sabiston Textbook of Surgery, 18th ed.

Answer 134

Answer: Genetic mutation of clonal cells leads to cancer formation [M]alignant transformation is the process by which a clonal population of cells acquires alterations that confer a growth advantage over normal cells. - Townsend: Sabiston Textbook of Surgery, 18th ed.

Answer 135

Answer: Cellular response (T-cells) decreases tumour growth The immune system is mediated by helper T lymphocytes (CD4); cytotoxic T lymphocytes (CD8), which directly lyse neoplastic cells, and natural killer (NK) cells and macrophages, which destroy tumor cells through secretion of cytokines such as interleukin-2 (IL2) and interferon-γ (IFN-γ). - Walsh: Palliative Medicine , 1st ed. T cells or T lymphocytes belong to a group of white blood cells known as lymphocytes, and play a central role in cell-mediated immunity. - http://en.wikipedia.org/wiki/T_cell

Answer 136

Answer: CMV (controversial) - found others say that Hep C is the correct answer HBV infection is also a risk factor for hepatocellular carcinoma. Hepatocellular carcinoma may ensue in 1% to 4% of chronic active hepatitis C patients per year. - Townsend: Sabiston Textbook of Surgery, 18th ed. However, found source that Hep C predisposes to cirrhosis which can lead to HCC but it is the cirrhosis, not the Hep C that is correlated. Although human cytomegalovirus (HCMV) is generally not regarded to be an oncogenic virus, HCMV infection has been implicated in malignant diseases from different cancer entities. Detection of viral DNA, mRNA, and/or antigens in tumor tissues as well as seroepidemiologic evidence suggested a role of HCMV infection in the etiology of several human malignancies. Transforming infections: This group includes several viruses that have been implicated in the causation of human cancer: EBV, HPV, HBV, and HTLV-1 - Kumar: Robbins and Cotran Pathologic Basis of Disease, Professional Edition , 8th ed.

Answer 137

??E helps select treatment but even within same TNM group? TNM on initial presentation

Answer 138

``` Top 3 as per CDC.gov - Rate per 100000 Prostate cancer (105.3) - adenocarcinoma makes 90% of it Lung cancer (71.6) Colorectal cancer (44.8) ``` Men Incident: Prostate, lung, colorectal Mortality: lung, colorectal, prostate

Answer 139

- most common (by mortality) - women o lung cancer (26%) o breast cancer (15%) o colorectal cancer (9%) Women Incident: breast, lung, colorectal Mortality: lung, breast, colorectal

Answer 140

Answer: Primary tumor not controlled

Answer 141

Tumor growth follows a gompertzian exponential model ( Fig. 217-5 ). There is exponential growth in vitro and in vivo; it is fast in the beginning, and becomes slower as the tumor attains a larger size, tending to form a plateau that never completely arrives and that is fully achieved only in normal tissues. - Walsh: Palliative Medicine , 1st ed.

Answer 142

Answer: SCC Can get SCC after chronic wound/chronic draining sinus/ostemoyelitis sinus Squamous cell carcinoma may arise in the chronically infected granulation tissue that is adjacent to a chronically infected bone. This rare complication can occur in areas of burn scars, chronic pressure ulcers, and ostomies, as well as at sites of chronic draining osteomyelitis. The patient usually has had stable chronic osteomyelitis for an average of approximately 20 years, although the latent period can be as little as 18 months. The tumor can be difficult to distinguish visually from the granulation tissue. The focus of carcinoma appears to be an exuberance of proliferative, lobulated, and friable "granulation tissue." A recent and progressive worsening of the soft-tissue defect in an otherwise stable case of chronic osteomyelitis is a clue that carcinoma has developed. Liberal sampling of the wound can easily be done in a clinic setting with a disposable skin punch biopsy trephine that dermatologists use for skin biopsies. Histologic examination of the biopsy specimens enables the pathologist to distinguish readily between squamous cell carcinoma and chronic granulation. Marjolin’s ulcer: aggressive ulcerating squamous cell carcinoma presenting in area of previously traumatised , chronically inflammed, or scarred skin. Commmonly present in the context of chronic wounds including burn injuries, venous ulcers, ulcers from osteomyelitis and post-radiotherapy scars

Answer 143

Answer: Calcitonin- medullary carcinoma (???) Poor specificity of PSA screening, a great number of men who do not have prostate cancer will be subjected to biopsies, thus causing morbidity and increasing the cost of health care without any benefit. In fact, nearly 75% of men with a PSA between 4 and 10 ng/mL do not have prostate cancer. Measurement of the free β-subunit is useful for the detection of recurrence or metastasis for choriocarcinoma when the intact hCG may remain normal. Analysis of serum hCG subunits is especially useful for managing patients with germ cell tumors ( von Eyben, 2003 ). However, elevated hCG can be found in trophoblastic tumors, choriocarcinoma, and testicular tumors. More than 60% of patients with nonseminomatous germ cell tumors and 10–30% with seminomas have elevated free β-hCG. - McPherson ; Pincus: Henry's Clinical Diagnosis and Management by Laboratory Methods, 21st ed. CA119-9 not sensitive or specific calcitonin is sufficiently elevated to be diagnostic of the presence of the tumor. In the early stages of the disease, however, the basal concentrations of calcitonin cannot be readily distinguished from normal. In these circumstances, provocative testing of calcitonin secretion can reveal the presence of the abnormal C-cells.

Answer 144

Answer: Detecting a cancer early when it is more amenable to successful therapy Primary prevention avoids the development of a disease. Most population-based health promotion activities are primary preventive measures. Secondary prevention activities are aimed at early disease detection, thereby increasing opportunities for interventions to prevent progression of the disease and emergence of symptoms. (ex: screening) Tertiary prevention reduces the negative impact of an already established disease by restoring function and reducing disease-related complications.

Answer 145

b. Early cancer detection and treatment.

Answer 146

``` Incidence of Skeletal Metastases from Autopsy Studies Incidence (%) Primary Tumor No. of Studies Median Breast 5 73 Prostate 6 68 Thyroid 4 42 Kidney 3 35 Bronchus 4 36 Esophagus 3 6 Gastrointestinal tract 4 5 Rectum 3 11 ``` ``` Bitches Like Penis that Kill Breast Lung Prostate Throid Kidney ```

Answer 147

Metastatic destruction of bone reduces its load-bearing capabilities, resulting initially in trabecular disruption and microfractures and, subsequently, in total loss of bony integrity. Rib fractures and vertebral collapse are the most common occurrences, resulting in loss of height, kyphoscoliosis, and a degree of restrictive lung disease. - Abeloff: Abeloff's Clinical Oncology, 4th ed.

Answer 148

C or D? 1 organ 30% 2 organ 50-60% (40-45%) 3 organ 80-90% (55-60%) 4 organ 100% (75-85%) Other studies show diversity of results with rates varying from 14% to 40% with 1 system failure; 20% to 76% with 2 system failures; 30% to 90% with 3 system failures; the majority of studies showed mortality of 100% for 4 or more system failures.

Answer 149

1 organ 30% 2 organ 50-60% (40-45%) 3 organ 80-90% (55-60%) 4 organ 100% (75-85%) Other studies show diversity of results with rates varying from 14% to 40% with 1 system failure; 20% to 76% with 2 system failures; 30% to 90% with 3 system failures; the majority of studies showed mortality of 100% for 4 or more system failures.

Answer 150

Answer: neurogenic shock Traditionally bradycardia with hypotension but are not always bradycardic. For this exam probably brady = neurogenic, tachy = something else Complete injury to the cervical or upper thoracic spinal cord may result in sympathetic denervation manifested as loss of vasomotor tone in the periphery. Neurogenic shock should be considered in any trauma patient who is hypotensive but not actively bleeding. - Goldman: Cecil Medicine, 23rd ed.

Answer 151

Answer: Unrecognized intraabdominal injury Traumatic Spinal Cord Injury Other immediate concerns are bleeding and circulation. Hypotension may be due to either neurogenic shock or hypovolemia. For neurogenic shock, vasopressive pharmacologic agents such as phenylephrine (beginning as a continuous intravenous infusion at 100 μg/min with titration to clinical effect) may be needed. If tachycardia is present, hypovolemia is more likely, so fluid resuscitation would be more appropriate. If the lesion is at T3 or above, sympathetic tone to the heart is compromised. In this setting, hypotension is accompanied by bradycardia, thus producing the neurogenic shock triad of bradycardia, hypotension, and peripheral vasodilation. - Goldman: Cecil Medicine, 23rd ed.

Answer 152

Obsolete question since the criteria changed in 2016 and I doubt they updated the information. BP not in this definition Criteria for SIRS were established in 1992 as part of the American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference.[2] The conference concluded that the manifestations of SIRS include, but are not limited to: - Body temperature less than 36°C or greater than 38°C - Heart rate greater than 90 beats per minute - Tachypnea (high respiratory rate), with greater than 20 breaths per minute; or, an arterial partial pressure of carbon dioxide less than 4.3 kPa (32 mmHg) - White blood cell count less than 4000 cells/mm³ (4 x 109 cells/L) or greater than 12,000 cells/mm³ (12 x 109 cells/L); or the presence of greater than 10% immature neutrophils (band forms)

Answer 153

Answer: CVP 18 CI (N=2.4-4.0) PCWP (N=6-12) SVR (N = 900–1200 dyn·s/cm5 [90–120 MPa·s/m3]) CVP (N=8-12) high CVP means volume overloaded a. Cardiac Index 3.5 – can be high in early sepsis b. CVP 18 - volume depleted and usually reduced venous return c. SVR 300 – true d. Hypotension –true

Answer 154

Answer: CVP 18 CI (N=2.4-4.0) PCWP (N=6-12) SVR (N = 900–1200 dyn·s/cm5 [90–120 MPa·s/m3]) CVP (N=8-12) high CVP means volume overloaded a. Cardiac Index 3.5 – can be high in early sepsis b. CVP 18 - volume depleted and usually reduced venous return c. SVR 300 – true d. Hypotension –true

Answer 155

Answer: 15, 1.5, 35 increased, decreased, decreased Cardiogenic shock is a reduction in the cardiac output, causing elevated central venous pressure and a reflex increased systemic vascular resistance and narrow pulse pressure. - Rakel: Textbook of Family Medicine, 7th ed.

Answer 156

A. increased cardiac index a. Increased cardiac index. (can be increased in early sepsis) b. Mostly due to gram positive bacteria. (can be due to gram positive and ned) c. Mortality is 5%. (much higher) d. Increased Arterio-venous O2 difference. (? Mean that SV02 decreases) Findings in sepsis: HR : tachycardic MAP 4 (high) : later can be depressed. heart is compensating Pulmonary artery wedge pressure : decreased SVR : low, distributive shock O2 delivery: decreased (this is another common question) Mixed venous O2 sat

Answer 157

D. CLASSIFICATION OF SHOCK Increased vascular capacitance (venodilation) = Sepsis - Goldman: Cecil Medicine, 23rd ed. Definition of capacitance: The measure of a BLOOD VESSEL's ability to increase the volume of BLOOD it holds without a large increase in BLOOD PRESSURE.

Answer 158

HYPOVOLEMIC/HEMORRHAGIC SHOCK - patient feels cold, postural hypotension and tachycardia, cool, pale, moist skin, low JVP, decreased CVP, increased peripheral vascular resistance (PVR), concentrated urine

Answer 159

SEPTIC SHOCK - clinical features: warm skin (fever), decreased JVP, wide pulse pressure, increased cardiac output (CO),decreased systemic vascular resistance, increased heart rate (HR)

Answer 160

OBSTRUCTIVE - increased JVP, distended neck veins, increased systemic vascular resistance (SVR) - insufficient cardiac output (CO)

Answer 161

CARDIOGENIC | - increased JVP, distended neck veins, increased SVR, decreased CO

Answer 162

ANAPHYLACTIC | - angioedema and hives

Answer 163

C. fluid resusc The first priority in any patient with severe sepsis or septic shock is stabilization of their airway and breathing. Next, perfusion to the peripheral tissues should be restored and antibiotics administered 1: airway + breathing 2: assess perfusion (BP, end-organ function, lactate...) 3: vascular access/fluid resuscitation - This is the answer 3. 5: pressors are second line 4. antibiotics, broad-spectrum uptodate

Answer 164

Answer: Hemorrhage

Answer 165

Answer: Intra-abdominal sepsis From lactate? TPN and Diarrhea cause NAGMA.

Answer 166

A. ETT ABC A lot of questions from POS are like this - airway airway airway

Answer 167

Answer: Hypoglycemia In studies on brain death, the hypothalamic hormones, such as growth hormone–releasing hormone, corticotropin-releasing hormone, thyroxine-releasing hormone, and luteinizing hormone–releasing hormone were found in trace to subnormal levels. When intracranial pressure increases, systemic hypertension occurs as a result of the Cushing phenomenon. This is followed by a sudden decrease in blood pressure because of sudden interruption of vasomotor output from the brainstem and hypothalamus to the spinal cord. After an initial hyperdynamic response consisting of hypertension with or without tachycardia, brain-dead patients brought to the operating room for organ recovery experience hypotension, reduced cardiac output, myocardial dysfunction,[14] and vasodilation (decreased systemic vascular resistance). In addition, diminished oxygenation as a result of neurogenic pulmonary edema and diabetes insipidus secondary to decreased circulating levels of antidiuretic hormone may be observed. The latter also may lead to hypernatremia and hypokalemia. Hyperglycemia, coagulopathy, and hypothermia may be encountered and must be corrected when severe. - Miller: Miller's Anesthesia, 7th ed.

Answer 168

D. Lack of any response to painful stimuli Pain reflex arch (ex: look up Lazarus sign - pretty cool) A. Prerequisites. 1. Clinical or neuroimaging evidence of an acute central nervous system catastrophe that is compatible with the clinical diagnosis of brain death 2. Exclusion of complicating medical conditions that may confound clinical assessment (no severe electrolyte, acid-base, or endocrine disturbance) 3. No drug intoxication or poisoning 4. Core temperature ≥ 32°C (90°F) B. The three cardinal findings in brain death are coma or unresponsiveness, absence of brainstem reflexes, and apnea. 1. Coma or unresponsiveness—no cerebral motor response to pain in all extremities (nail-bed pressure and supraorbital pressure) 2. Absence of brainstem reflexes a. Pupils i. No response to bright light ii. Size: midposition (4 mm) to dilated (9 mm) b. Ocular movement i. No oculocephalic reflex (testing only when no fracture or instability of the cervical spine is apparent) ii. No deviation of eyes to irrigation in each ear with 50 mL of cold water (allow 1 minute after injection and at least 5 minutes between testing on each side) c. Facial sensation and facial motor response i. No corneal reflex to touch with a throat swab ii. No jaw reflex iii. No grimacing to deep pressure on nail bed, supraorbital ridge, or temporomandibular joint d. Pharyngeal and tracheal reflexes i. No response after stimulation of the posterior pharynx with tongue blade ii. No cough response to bronchial suctioning 3. Apnea testing performed as follows: a. Prerequisites i. Core temperature ≥ 36.5°C or 97°F ii. Systolic blood pressure ≥ 90 mm Hg iii. Euvolemia. Option: positive fluid balance in the previous 6 hours iv. Normal Paco2. Option: Paco2≥ 40 mm Hg v. Normal Pao2. Option: preoxygenation to obtain arterial Pao2≥ 200 mm Hg b. Connect a pulse oximeter and disconnect the ventilator. c. Deliver 100% O2, 6 L/min, into the trachea. Option: place a cannula at the level of the carina. d. Look closely for respiratory movements (abdominal or chest excursions that produce adequate tidal volumes). e. Measure arterial Pao2, Pco2, and pH after approximately 8 minutes and reconnect the ventilator. f. If respiratory movements are absent and arterial Pco2 is ≥ 60 mm Hg (option: 20 mm Hg increase in Pco2 over a baseline normal Pco2), the apnea test result is positive (i.e., it supports the diagnosis of brain death). g. If respiratory movements are observed, the apnea test result is negative (i.e., it does not support the clinical diagnosis of brain death), the test should be repeated. h. Connect the ventilator if, during testing, the systolic blood pressure becomes ≤ 90 mm Hg or the pulse oximeter indicates significant oxygen desaturation and cardiac arrhythmias are present; immediately draw an arterial blood sample and analyze arterial blood gas. If Pco2 is ≥ 60 mm Hg or Pco2 increase is ≥ 20 mm Hg over baseline normal Pco2, the apnea test result is positive (it supports the clinical diagnosis of brain death); if Pco2 is

Answer 169

Answer: Give fluid

Answer 170

Previous answer said go back to OR. I disagree. Given the options this person may have cardiogenic shock: Tx of cardiogenic shock = norepinephrine (first line), dopamine (second line). Also, this person sounds like they are not dry based on the fluids received, and they were ok until POD1. So I say D: norepinephrine Complications: From PMHx: heart failure, myocardial ischemia, acute kidney injury, pulmonary insufficiency and pneumonia ``` From surgery (early): lower extremity ischemia, bowel ischemia, pelvic ischemia, renal dysfunction ``` Late complications :incisional hernia, anastomotic aneurysm and graft infection/aortoenteric fistula

Answer 171

Answer: Mixed venous O2 sat. Swan Ganz (pulmonary artery catheter) is on the right side of the heart.. So cannot detect L-sided stuff or peripheral stuff (CI, LA diastolic pressure, SVR) Direct measurements: Right Atrial/Ventricle pressures, Pulmonary artery pressure, PCWP, and mixed venous 02 sat (CvO2) Indirect: CO/C.I. via Fick Principle (CO= V02/CaO2-CvO2) or indicator-dilution technique, PCWP = Left atrial pressure = (assumed) left ventricle end diastolic pressures = LVED volume, Stroke volume

Answer 172

Answer: Reduce mortality No difference in mortality and morbidity, except higher incidence of PE in the PA catheter group. A randomized, controlled trial of the use of pulmonary-artery catheters in high-risk surgical patients. Conclusion: no benefit

Answer 173

Answer: increasing the tidal volume Given that the minute ventilation is constant, we want to increase the % of non-dead-space ventilation per breath. Since the dead-space ventilation is a constant volume, we need to increase the tidal volume to result in increased ventilation. Minute Ventilation = amount of air person inspires or expires in a minute MV = TV X RR MV = volume/breath * breath/min MV = Volume/min

Answer 174

Answer: increase FiO2 to 90% PaO2: hypoxia PCO2: slightly elevated pH: acidotic Needs more oxygen. O2 exchange is not really affected by resp rate so need to increase oxygen supply. (Or increase PEEP but that is not an option) A-a gradient = PAO2 – PaO2 [FiO2(Patm-PH20) – PaCO2/RQ] – PaO2 [.75(760-47) – 38/0.8] – 50 437.25 If A-a gradient > 15 = decreased diffusion capacity, ILD, emphysema Tx = give 100% O2

Answer 175

Answer: At end expiration At the end of expiration, intrathoracic and juxtacardiac pressures approach atmospheric pressure regardless of ventilatory status, and the CVP values will coincide. Proper pressure values can also be determined by visual inspection of the CVP waveform on a calibrated monitor screen or paper recording. This facilitates comparison of CVP values (and other cardiac filling pressures) obtained from the same patient under varying patterns of ventilation, a common situation in anesthesia and critical care. - Miller: Miller's Anesthesia, 7th ed.

Answer 176

Answer: probably pre-op dyspnea at rest Pre-op dyspnea at rest = CHF probably = bad (40 pack-years) • ASA-PS scores higher than 2 • Age >70 years • COPD • Neck, thoracic, upper abdominal, aortic, or neurologic surgery • Anticipated prolonged procedures (>2 hours) • Planned general anesthesia (especially with endotracheal intubation) • Albumin less than 3 g/dL • Exercise capacity of less than two blocks or one flight of stairs • BMI greater than 30 Surprisingly absent predictors in this list are asthma and results from arterial blood gas analysis or PFTs. - Miller: Miller's Anesthesia, 7th ed.

Answer 177

Answers: anything with FEV1 ``` Possible Criteria for Ventilator Weaning TEST CRITERION MECHANICAL FUNCTION Vital capacity (FVC) >10-15 mL/kg FEV1 >10 mL/kg Tidal volume (V T) >5 mL/kg Maximum inspiratory pressure (MIP) 2 times resting V E Respiratory rate (V F) >25/min Respiratory minute volume (V E) 50% predicted ``` GAS EXCHANGE FUNCTION A-a gradient (F IO2 = 1.0) 200 P100 7.30 - Miller: Anesthesia, 5th ed., Copyright © 2000

Answer 178

Answer: decreased central venous pressure The degree of this elevation depends on the compliance of the lungs and intravascular volume and will vary between patients. For this reason, CVP measurements are best made and compared at the same point in the ventilatory cycle⎯usually end-expiration. When positive end-expiratory pressure (PEEP) is applied, the positive pressure is transmitted through to the right atrium, causing a decrease in venous return and a rise in CVP.

Answer 179

Answer: tension pneumothorax Potential risk of PEEP: o pneumothorax can develop at high pressures (>20cm H2O) o tension pneumothorax will subsequently develop as air is forced into the lungs and out the rupture site into the thoracic cavity (one-way leak), thus lung collapse. Results in displacement of mediastinum to opposite side, therefore decreasing venous return causing hypotension Most common cause of tension pneumothorax is mechanical ventilation with PEEP in the patient with visceral pleural injury - Schwartz, ATLS manual

Answer 180

Respiratory Alkalosis - reduced respiratory rate

Answer 181

Answer: Decreased pO2 despite increasing FiO2 Stages of ARDS 1) Injury or Exudative stage (1-7 days) Accumulation of fluid/protein lead to endothelial damage Inflammatory cells in response to the initial injury Proteinaceous fluid flooding in interstitium and alveoli is an early appearance 2) Reparative or Proliferative stage (1-2 weeks) Continued inflammatory response Complete when lung composed of dense, fibrous tissue 3) Fibrotic stage (2-3 weeks) Lung completely remodeled by fibrous tissue Also called chronic or late phase

Answer 182

A Acute respiratory distress syndrome (ARDS), is characterized by hypoxia (despite oxygen therapy), decreased pulmonary compliance, diffuse or patchy infiltrates on chest x-ray, and noncardiac pulmonary edema. ``` ARDS criteria (uptodate 2016): -Resp symptoms started/worsened 5cmH2O: PaO2/FiO2 >200mmHg = mild PaO2/FiO2 100-200mmHg = moderate PaO2/FiO2 ```

Answer 183

Answer: Decrease the tidal volume TV

Answer 184

Answer: Previous answer leaky pulmonary capillaries but uptodate (2016) states ventilation/perfusion mismatch and shunt physiology Consequences — Lung injury has numerous consequences including impairment of gas exchange, decreased lung compliance, and increased pulmonary arterial pressure. ●Impaired gas exchange – Impaired gas exchange in ARDS is primarily due to ventilation-perfusion mismatching: physiologic shunting causes hypoxemia, while increased physiologic dead space impairs carbon dioxide elimination [28,29]. A high minute volume is generally needed to maintain a normal arterial carbon dioxide tension (PaCO2), although hypercapnia is uncommon. (See "Oxygenation and mechanisms of hypoxemia".) ●Decreased lung compliance – Decreased pulmonary compliance is one of the hallmarks of ARDS [30]. It is a consequence of the stiffness of poorly or nonaerated lung, rather than the pressure-volume characteristics of residual functioning lung units [31]. Even small tidal volumes can exceed the lung's inspiratory capacity and cause a dramatic rise in airway pressures [30]. ●Pulmonary hypertension – Pulmonary hypertension (PH) occurs in up to 25 percent of patients with ARDS who undergo mechanical ventilation [32-34]. Causes include hypoxic vasoconstriction, vascular compression by positive airway pressure, parenchymal destruction, airway collapse, hypercarbia, and pulmonary vasoconstrictors [35]. The clinical importance of PH in most patients with ARDS is uncertain. PH severe enough to induce cor pulmonale is rare, but it is associated with an increased risk of death [36,37].

Answer 185

Answer: Positive end expiratory pressure Positive end-expiratory pressure (PEEP) can improve oxygenation by recruiting collapsed alveoli and increasing functional residual capacity. Conventional ventilation generally calls for the minimal PEEP necessary to provide acceptable oxygenation. However, in the setting of ARDS there may be benefit in increasing PEEP to improve oxygenation, as well as protect the lung, by preventing the repetitive recruitment/derecruitment of alveoli and thereby reducing cyclic reopening and stretch during mechanical breaths. - Townsend: Sabiston Textbook of Surgery, 18th ed.

Answer 186

Answer: Increase FRC Patients with ARDS have noncardiogenic pulmonary edema, with a reduced functional residual capacity and a mortality rate of 30 to 60%. - Goldman: Cecil Medicine, 23rd ed.

Answer 187

c. ARDS Hypoxia + low PaO2/FiO2 + bilateral infiltrate + trauma mechanism (?pulm contusion) and massive transfusion (both trauma + massive transfusion can cause ARDS)

Answer 188

Answer: maintenance of cerebral perfusion

Answer 189

Answer: Add oxygen by facemask Once the diagnosis is confirmed, treatment is largely supportive. Satisfactory relief of pain and anxiety is important and cn be accomplished using morphine and sedation. Maintenance of optimal oxygenation is crucial, and effective pulmonary toilet o tclear bronchial secetions is combined with supplemental oxygen to maintain the arterial oxygen saturation at greater than 95%. All patients should be initially treated in an ICU or monitored bed. If evidence of hemodynamic instability or respiratory distress is present, intraarterial catheter monitoring should be utilized. Frequent determinations of fluid status and cardiac output to guide diuretic and vasopressor therapy may require pulmonary artery catheter monitoring. - Schwartz SHOCK trial demonstrated that percutaneous coronary intervention (PCI) or coronary artery bypass are the treatments of choice and that they have been shown to markedly decrease mortality rates at 1 year. PCI should be initiated within *90 minutes* of presentation; however, it remains helpful, as an acute intervention, within 12 hours of presentation. If such a facility is not immediately available, thrombolytics should be considered. However, this treatment is second best. An increased mortality is seen in situations where thrombolytics are used instead of PCI.

Answer 190

B. Electrical cardioversion ATLS - unstable a. fib Test-taking skills: verapamil/amiodarone are both reasonable medications for rapid A.fib, so therefore they are both not the answer to this question

Answer 191

C. Shock (check rhythm then shock, biphasic 200J, monophasic 360J) ATLS

Answer 192

D. zap zap zap ATLS

Answer 193

Previous answer: lidocaine As of 2010, ATLS no longer recommends lidocaine Procainamide if stable is reasonable I would say shock cause she's already intubated - don't need to sedate. Plus electricity is cheap and meds only have ~30% chance to convert and take too long

Answer 194

Answer: dobutamine or dopamine (obsolete - now norepinephrine is the correct answer) Cardiogenic shock management 2016 - uptodate: suggest norepinephrine as first line, dopamine as second line pressors for cardiogenic shock: In patients with cardiogenic shock, norepinephrine is preferred over dopamine as the first-line vasopressor because a subgroup analysis from a randomized trial found that patients with cardiogenic shock who received dopamine had a higher mortality than those who received norepinephrin. In addition, dysrhythmias were more common in the dopamine group.

Answer 195

Answer: increase inotropy Catecholamines are used in cardiac arrest not only in an attempt to achieve better electrical stability (e.g., conversion from fine to coarse VF, or increasing the rate of spontaneous contraction during bradyarrhythmias) but also for their inotropic and peripheral vascular effects. Epinephrine is the first choice among the catecholamines for use in cardiac arrest because it increases myocardial contractility, ele-vates perfusion pressure, may convert electromechanical dissociation to electromechanical coupling, and improves chances for defibrillation. - Libby: Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 8th ed.

Answer 196

Answer: Set up for transcutaneous pacing Bradycardia/Complete heart block

Answer 197

Answer: adenosine Regular narrow complex tachycardia = SVT. In hemodynamic stable patients, the drug of choice is adenosine. 2nd drug of choice is verapamil. If patient is unstable and HR over 150/min : electric cardioversion is the Tx. Adenosine slows conduction through the AV node, interrupts AV-nodal reentry pathways, and can restore normal sinus rhythm in patients with PSVT, including those ass with WPW. - ACLS

Answer 198

B. Insert LMA The goal here is to turn this "can't intubate, can't oxygenate" emergency situation into a "can't intubate, CAN oxygenate" which is less emergent. In any case, you should only try one time to do the LMA before movign on to a cric. Ideally you slam the LMA in while someone else is getting things ready to cricothyroitomize in case you fail. If you get your LMA in - great. If not, cric. Uptodate2016

Answer 199

Answers provided: - oral endotracheal tube - Cricothyrodiotomy In practice you can still intubate these patients... So I vote ETT. Although facial fractures in and of them selves are not an indication for tracheotomy, in cases of severe maxillo-facial trauma, tracheotomy is sometimes used to secure an airway where intubation would be difficult or damaging. - Cummings: Otolaryngology: Head & Neck Surgery, 4th ed. The primary indication for cricothyrotomy is the need for a definitive airway in the victim in whom orotracheal or blind nasotracheal intubation (BNTI) has failed, is contraindicated, or is extremely difficult. Clinical scenarios include the victim with severe facial trauma for whom conventional airway management is extremely complicated or unfeasible, the victim with severe laryngeal edema, or the victim with upper airway foreign-body obstruction that cannot be alleviated by the Heimlich maneuver or direct laryngoscopy. - Auerbach: Wilderness Medicine, 5th ed. Patients with an unstable cervical spine, massive facial injuries, or inability to undergo laryngoscopic intubation benefit from the ease of intubation with the help of the flexible bronchoscope. Bronchoscopic guidance is also valuable in the performance of percutaneous dilational tracheostomy. - Mason: Murray & Nadel's Textbook of Respiratory Medicine, 4th ed

Answer 200

A. ETT Basal skull fracture = DO NOT DO NASOTRACHEAL INTUBATION Wheeless Textbook Facial Fractures and Upper Airway Injuries: -in pts with major frxs of the mandible and maxilla (Lefort III) in whom massive edema has yet to occur, oral intubation is preferred, and if required is usually easily accomplished; - blind nasal intubation following major facial injury is discouraged because of the hazard of potential false passages into nasal sinuses and cranial vault; -injuries of the Larynx may cause rapid respiratory obstruction and require immediate tracheostomy; - in less urgen situation, a history of trauma to the head and neck, stridor, hoarseness, and crepitus in the neck are all suggestive or laryngeal injury;

Answer 201

Answer: Decreased turbulence Gas: Helium 79%: Oxygen 21% used since 1990 to help with upper airway obstruction He: decreased airway resistance therefore decrease mechanical energy to vent

Answer 202

Better answer: ETT was too large Previous Answer: cricoarytenoid dislocation (?? rare) Complications are common during mechanical ventilation. Adverse events that are directly attributable to the ETT include laryngeal injury (eg, laryngeal edema, vocal cord dysfunction), swallowing impairment, tracheal stenosis, tracheoesophageal fistula, cuff leaks, sinusitis, and biofilm formation Risk factors for laryngeal injury that have been described include prolonged intubation (variably defined as ≥36 hours to ≥3 days), traumatic intubation, not using a myorelaxant drug during intubation, a large ETT (>8 mm in men, >7 mm in women), aspiration, and the presence of a nasogastric tube

Answer 203

b? Check for optimal head positioning: neck slightly flexed and head extended on the neck (conditions permitting). May be facilitated by placing a towel under the patient's occiput to raise it 10 cm. Obese patients usually require significantly more occiput elevation. - Roberts: Clinical Procedures in Emergency Medicine, 5th ed.

Answer 204

3. transfer patient to OR for flexible bronchoscopic intubation and possible tracheostomy. Ludwigs angina

Answer 205

c. Fibrin Stimulators of Platelets - ADP = most important - collagen = attracts platelets to the subendothelium - vWF - thrombin Inhibitors - NO - PGI2 (“platelet gathering inhibitor”) - ADPase

Answer 206

Answer: 1-3 days The remaining COX-1 NSAIDs such as naproxyn, ketorolac, diclofenac, piroxicam, ibuprofen, and others also act as prostaglandin synthesis inhibitors. All of them cause reversible competitive platelet inhibition, and platelet function usually returns to normal within 1 to 3 days after stopping the drug

Answer 207

Answer: b. Papaverin ASA inhibits COX decreases Thromboxane A2 which stimulates platelet aggregation Papaverin smooth muscle relaxant. “PVD, CVD” Dipyrimadole (persantine)-impairs platelet function by inhibiting activity of ADP. Used in pulomonary HT. Phenylbutasone-NSAID COX inhibition. dextran 70 may interfere with normal blood clotting, causing a deficiency with crossmatching procedures and possibly a bleeding diathesis

Answer 208

Answer: b. qualitative platelet problem An association between renal failure and bleeding tendency has long been recognized. A qualitative defect in platelet function produced by uremia itself seems to be central. The defect results from accumulation of the compound guanidinosuccinic acid in uremic blood, which inhibits adenosine diphosphate–induced platelet aggregation. - Miller: Miller's Anesthesia, 7th ed.

Answer 209

Answer: C Insensitive to heparin since heparin acts by potentiating antithrombin III The most common thrombotic manifestations in patients with antithrombin deficiency (AT deficiency) include lower extremity VTE, with recurrent VTE being common. Other sites of thrombosis include the inferior vena cava, hepatic and portal veins, and renal, axillary, brachial, mesenteric, pelvic, cerebral, and retinal veins. Arterial thrombosis is strikingly less common. In a patient with a known inherited antithrombin deficiency (AT deficiency), management of the acute thrombotic event depends on the type of antithrombin deficiency, because a variable response to large doses of heparin occurs in some of these patients. When a therapeutic response to intravenous heparin is not achievable, additional support with an antithrombin concentrate may be necessary. Antithrombin concentrates are used to raise the plasma antithrombin level from a reduced value to approximately 120%. - http://emedicine.medscape.com/article/198573-treatment In antithrombin III deficiency, the activity of LMWH is not as reliable as in an otherwise healthy person. Careful monitoring of the anti-Xa activity in the patient should be performed. Consider alternative anticoagulation medications (eg, warfarin) because the effectiveness of LMWH is likely reduced. - http://emedicine.medscape.com/article/954688-treatment

Answer 210

C is true A can also be true I don't know the answer. von Willebrand disease is due to an abnormality, either quantitative or qualitative, of the von Willebrand factor, which is a large multimeric glycoprotein that functions as the carrier protein for factor VIII (FVIII). von Willebrand factor is also required for normal platelet adhesion. As such, von Willebrand factor functions in both primary (involving platelet adhesion) and secondary (involving FVIII) hemostasis. - http://emedicine.medscape.com/article/959825-overview Bernard-Soulier syndrome (BSS) was first described in 1948 as a congenital bleeding disorder characterized by thrombocytopenia and large platelets. - http://emedicine.medscape.com/article/954877-overview Bleeding time is generally very prolonged in patients with uremia, signifying a major defect in platelet function, which improves after dialysis - http://emedicine.medscape.com/article/201722-overview The life span of platelets in circulation is 7 to 10 days. Under normal conditions, the spleen stores about one third of circulating platelets. Circumstances that increase splenic volume, such as hepatic cirrhosis or portal hypertension, cause a reduction in the circulating platelet count by a sequestration within the splenic sinusoids. - Firestein: Kelley's Textbook of Rheumatology, 8th ed.

Answer 211

a. binds to AT3 Like heparin, low-molecular-weight heparin exerts its anticoagulant activity by activating antithrombin Consequently, low-molecular-weight heparin catalyzes factor Xa inhibition by antithrombin more than thrombin inhibition

Answer 212

Answer: Thrombin Like heparin, low-molecular-weight heparin exerts its anticoagulant activity by activating antithrombin. With a mean molecular weight of 5000, which corresponds to approximately 17 saccharide units, at least half of the pentasaccharide-containing chains of low-molecular-weight heparin are too short to bridge thrombin to antithrombin (Fig. 137-4). However, these chains retain the capacity to accelerate factor Xa inhibition by antithrombin because this activity is largely the result of the conformational changes in antithrombin evoked by pentasaccharide binding. Consequently, low-molecular-weight heparin catalyzes factor Xa inhibition by antithrombin more than thrombin inhibition. Depending on their unique molecular weight distributions, low-molecular-weight heparin preparations have anti–factor Xa to anti–factor IIa ratios ranging from 2 : 1 to 4 : 1. - Hoffman: Hematology: Basic Principles and Practice, 5th ed.

Answer 213

There is a decreased incidence of heparin-induced thrombocytopenia and thrombisis associated with LMWH therapy A is partially true. LMWH does bind both but to a lesser extent than heparin does cause the chains are shorter (his arms are too short!!) The binding of LMWH to antithrombin causes less inactivation of coagulation factor IIa (thrombin) when compared with that of unfractionated heparin.[9] This is because inactivation of factor IIa requires the formation of a ternary complex in which heparin binds to both antithrombin and to a binding site on factor IIa (Figure 2).[17] This ternary complex is formed on pentasaccharide containing chains of at least 18 saccharide units. However, unlike UFH, many of the LMWH do not contain sufficient saccharide units to form the ternary complex Low-molecular-weight heparins (LMWHs) derived from UFH have more selective anti-Xa activity than UFH does. LMWH has been associated with less bleeding complications and has become the first-line therapy for prophylaxis and treatment of deep venous thrombosis (DVT) and acute coronary syndromes. LMWH can also cause HIT (

Answer 214

``` Enoxaparin Half-life = 4.5 hours Duration = 12 hours Dalteparin Half-life = 3-5 hours - Medscape ```

Answer 215

Stop the coumadin 5 days prior to surgery and administer LMWH 3 days prior to surgery

Answer 216

7 days pre-op stop coumadin, start on full dose LMWH holding 12 hrs before surgery

Answer 217

Stop warfarin and start heparin infusion 9. 2.5. Bridging Therapy in Patients With Mechanical Valves Who Require Interruption of Warfarin Therapy for Noncardiac Surgery, Invasive Procedures, or Dental Care Class I 1. In patients at low risk of thrombosis, deﬁned as those with a bileaﬂet mechanical AVR with no risk factors,* it is recommended that warfarin be stopped 48 to 72 h before the procedure (so the INR falls to less than 1.5) and restarted within 24 h after the procedure. Heparin is usually unnecessary. (Level of Evidence: B) 2. In patients at high risk of thrombosis, deﬁned as those with any mechanical MV replacement or a mechanical AVR with any risk factor, therapeutic doses of intravenous UFH should be started when the INR falls below 2.0 (typically 48 h before surgery), stopped 4 to 6 h before the procedure, restarted as early after surgery as bleeding stability allows, and continued until the INR is again therapeutic with warfarin therapy. (Level of Evidence: B) - ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guideline

Answer 218

Answer: Decreases thromboxane A2 production Unfractionated heparin effects anticoagulation by enhancing antithrombin activity, increasing factor Xa inhibitor activity, and inhibiting platelet aggregation. - Gabbe: Obstetrics: Normal and Problem Pregnancies, 5th ed.

Answer 219

C. intravascular protein When they say oncotic pressure, this mean colloid-osmotic pressure (which does not include electrolytes!!) By far the most important for osmotic pressure is intravascular Na

Answer 220

A. Intravascular sodium content Osmotic pressure determined by intravascular Na - don't get mixed up with oncotic. Oncotic refers to the colloid-portion of the osmotic pressure, which is less than the osmotic pressure from Na. EXCEPTION: At the level of capillaries, the main pressure is the oncotic pressure because the membrane is readily permeable to ions. Therefore the only except where the osmotic pressure is determined by protein (albumin mostly) is at the level of the capillaries.

Answer 221

In cases of clinical dehydration, children with pyloric stenosis require rehydration with IV fluid therapy before surgery. Administer D5W with 0.45% NaCl IV at 1.5 times the maintenance rate. Severely dehydrated children should receive initial deficit fluid therapy with 0.9% NaCl.When urine output is demonstrated, KCl 10-20 mEq/L can be added to the fluids.

Answer 222

Answer: Low K, Low Cl, metabolic alkalosis Olive = Pyloric stenosis Paradoxically urine is acid because K is so depleted that kidney shifts to H+ excretion. Labs: hypochloremic, hypokalemic metabolic alkalosis. Persistent emesis causes progressive loss of fluids rich in hydrochloric acid, which causes the kidneys to retain H+ ions in favor of potassium. May also have elevated unconjugated bilirubin. Paradoxic acid urea.

Answer 223

Answer: c. 130 2.5 88 28 In gastric losses, loss of Na, Cl, K, but not bicarb

Answer 224

C. Increase intravascular volume - NS will stay extracellular, approx ¾ interstitial and ¼ intravascular. - NS does not go into the ICF - Dextrose is distributed evenly among all compartments - Plasma protein solutions stay intravascular A would be a dextrose B would be a colloid D would be a hypotonic solution?

Answer 225

25% of RL or NS will go intravascular

Answer 226

1200cc/day 4:2:1 4x10, 2x5 = 50cc/h 50cc/h*24h=1200cc

Answer 227

b. 20cc/h Restore cardiovascular stability with a rapid bolus of 20mL/kg over 10 to 30minutes - Bope: Conn's Current Therapy 2010, 1st ed. The child is given a fluid bolus, usually 20 mL/kg of the isotonic fluid, over approximately 20 min. - Kliegman: Nelson Textbook of Pediatrics, 18th ed.

Answer 228

Answer: A. Muscle has more water Old people have less water Seems like babies have the most water content Water is the most abundant component in the body. Total body water (TBW) accounts for approximately 50% of the lean body weight in women and 60% in men. In children, the contribution of the TBW to weight varies with age and constitution: it ranges from 80% or greater in the premature infant, to 70% to 75% in the term infant, to 65% to 70% in toddlers. - Miller: Miller's Anesthesia, 7th ed.

Answer 229

C. Decreased UOP. 25% dehydrate is severe dehydration Clinical Evaluation of Dehydration Mild dehydration (1.5 sec); cool and pale Severe dehydration (>10% in an infant; >6% in an older child or adult): rapid and weak or absent peripheral pulses; decreased blood pressure; no urine output; very sunken eyes and fontanel; no tears; parched mucous membranes; delayed elasticity (poor skin turgor); very delayed capillary refill (>3 sec); cold and mottled; limp, depressed consciousness - Kliegman: Nelson Textbook of Pediatrics, 18th ed.

Answer 230

b. Na 130, K4, CL 109, HCO3 28, Ca 2.7 | Memorize these numbers. Often asked as a "all of these are ringers' numbers except"

Answer 231

B. ECF NS & D5NS > ECF > RL > D5½NS > 2/3 1/3

Answer 232

B. K+Mg Tip: Banana floating in a sea. Or Caleb's "Potassium and magnesium are good for you, so you want them in the cell" ! a. Na + Ca (extracellular cations) b. K + Mg c. PO and protein (intracellular anions) d. Cl and HCO3 (extracellular cations)

Answer 233

60% of body weight is water in male = 42kg of water 2/3 of that is intracellular = 28kg Therefore 14 L of extracellular 1/4 of that is intravascular= 3.5L Tip: remember YOUR plasma volume and then just guess based off that on a whim Total Body Water = 60% of Body Weight (For Male) Total Body Water = 50% of Body Weight (For Female) Extracellular Fluid = Total Body Water / 3 Interstitial Fluid = Total Body Water * 0.25 Plasma = Extracellular Fluid - Interstitial Fluid

Answer 234

D) left lateral decubitus In the later stages of pregnancy, as already described, uterine compression of the vena cava may result in hypotension from diminished venous return, thus the pregnant trauma patient needs to be placed in a left lateral decubitus position - Townsend: Sabiston Textbook of Surgery, 18th ed.

Answer 235

Canadian paper. Advantages over the TT included: increased speed and ease of placement by inexperienced personnel; increased speed ofplacement by anaesthetists; improved haemodynamie stability at induction and during emergence; minimal increase in intraocular pressure following insertion; reduced anaesthetic requirements for airway tolerance; lower frequency of coughing during emergence; improved oxygen saturation during emergence; and lower incidence of sore throat in adults. Advantages over the FM included: easier placement by inexperienced persornel; improved oxygen saturation; less hand fatigue; and improved operating conditions during minor paediatric otological surgery Disadvantages over the TT were lower seal pressures and a higher frequency of gastric insufflation. The only disadvantage compared with the FM was that oesophageal reflux was more likely No difference in the risk of aspiration b/c not enough studies, but with ETT increase complications of voice hoarness, cough, and laryngeal spasms (see article)

Answer 236

Answer: decreases cerebral perfusion pressure Propofol decreases intracranial pressure (ICP) in patients with either normal or increased ICP.[79] The decrease in ICP (30% to 50%) is associated with significant decreases in cerebral perfusion pressure (CPP), however. - Miller: Miller's Anesthesia, 7th ed.

Answer 237

? wrist extension (radial nerve)

Answer 238

Answer: Systemic toxicity happens 30 minutes after removal of tourniquet. Loss of anesthesia after cuff deflation may occur. If the surgeon wants to attain hemostasis and then close the wound, there is only 5 to 10 minutes of post-deflation analgesia, which may be inadequate in some procedures. When the tourniquet is released, a large bolus of anesthetic enters the systemic circulation; the level peaks within 1 minute and falls rapidly thereafter. This brief elevation of the local anesthetic blood level may produce systemic toxic reactions, including convulsions and cardiac irregularities

Answer 239

Morrell • MAC 0.75 • Almost completely replaced by newer agents. • Powerful cardiac depressant (↓ contractility and SV, HR unchanged → overall ↓ CO) •Inhibits baroreceptor-increased HR usually seen with lowered BP. • Sensitizes myocardium to catecholamines. •Associated with fulminant hepatitis. •Suitable for mask induction.

Answer 240

Answer: the presence of parents up until OR time increases separation anxiety it decreases it

Answer 241

Answer: sympathetic block Complications of subarachnoid block include hypotension (sometimes refractory), postdural puncture headache, transient radicular neuropathy, backache, urinary retention, infection, epidural hematoma, and excessive cephalad spread resulting in cardiorespiratory compromise. Frank neurologic injury, although recently described with continuous techniques using small-bore catheters, is rare. Hypotension, occurring as a consequence of sympathectomy, usually responds readily to fluids and small doses of pressors, such as ephedrine. - Townsend: Sabiston Textbook of Surgery, 16th ed., Copyright © 2001 W. B. Saunders Company Pharmacologic sympathectomy with local anesthetics is a very effective way of inducing hypotension. Epidural or spinal anesthesia produces arteriolar and venous dilation and hypotension. These effects are enhanced by a pooling of blood in the venous system that decreases venous return and cardiac output. If the block is extended to the midthoracic region, sympathetic innervation of the heart (T1-T4) is also affected, thereby preventing compensatory tachycardia. [37] The unpredictable degree of hypotension and the necessity for large infusions of fluids are the principal drawbacks of this technique. It was recently demonstrated, however, that if hemodynamic stability is maintained by intravenous infusion of low-dose epinephrine (1-5 mug/min), this technique can be used safely. [25] [35] An epidural anesthetic technique is most commonly used to minimize blood loss during lower abdominal or pelvic surgery. - Miller: Anesthesia, 5th ed., Copyright © 2000 Churchill Livingstone, Inc.

Answer 242

B. autosomal dominant Half of cases are autosomal dominant; others are unknown. Diagnosis rests on acute awareness of the signs and symptoms of this syndrome, of which hyperthermia is a late sign. The increased permeability of skeletal muscle results in increased serum levels of potassium, ionized calcium, CK (although MH-related changes in serum CK do not differ overall from changes in CK observed during surgery[236]), myoglobin, and serum sodium. - Miller: Miller's Anesthesia, 7th ed. Miller describes a variable pattern in C02 rise. Also early vs late hyperthermia … there is no hard and fast rule that says early C02 rise and late hyperthermia. But B is likely the POS answer. Early clinical signs of MH include an increase in end-tidal carbon dioxide (even with increasing minute ventilation), tachycardia, muscle rigidity, tachypnea, and hyperkalemia. Later signs include fever, myoglobinuria, and multiorgan failure.

Answer 243

a. Propofol Triggering Agents * Depolarizing muscle relaxants (eg, succinylcholine) * Volatile general anesthetic agents (eg, ether, cyclopropane, methoxyflurane, halothane, isoflurane, enflurane, sevoflurane, and desflurane) Safe (nontriggering) Agents * All nondepolarizing muscle relaxants (eg, vecuronium, rocuronium, d-tubocurarine, pancuronium, atracurium, cis-atracurium, and mivacurium) * Nitrous oxide * Intravenous anesthetics (eg, ketamine, propofol, etomidate, thiopental, opiates, and benzodiazepines) * All ester and amide local anesthetics - http://cme.medscape.com/viewarticle/491434 Saw in some older literature that local anesthetics were thought to be a cause, but this has been debunked (they do not cause it)

Answer 244

d. diltiazem Acute therapy for MH can be summarized as follows: (1) Discontinue all anesthetic agents and hyperventilate with 100% oxygen. Normal ventilation is that required to remove metabolic carbon dioxide. With increased aerobic metabolism, normal ventilation must increase. However, carbon dioxide production is also increased because of neutralization of fixed acid by bicarbonate; hyperventilation removes this additional CO2. (2) Administer dantrolene (2.5 mg/kg intravenously [IV] to a total dose of 10 mg/kg IV) every 5 to 10 minutes until symptoms subside. (3) Administer bicarbonate (2 to 4 mEq/kg IV) to correct the metabolic acidosis with frequent monitoring of blood gases and pH. (4) Control fever by administering iced fluids, cooling the body surface, cooling body cavities with sterile iced fluids, and if necessary, using a heat exchanger with a pump oxygenator. Cooling should be halted at 38°C to 39°C to prevent inadvertent hypothermia. (5) Monitor urinary output and establish diuresis to protect the kidney from probable myoglobinuria. (6) Further therapy is guided by blood gases, electrolytes, temperature, arrhythmia, muscle tone, and urinary output. Treatment of hyperkalemia with glucose and insulin should be slow. The most effective way to lower serum potassium is reversal of MH by effective doses of dantrolene. (7) Analyze coagulation studies. - Miller: Miller's Anesthesia, 7th ed.

Answer 245

Answer: Succinylcholine

Answer 246

d. preservative free marcaine with epinephrine More likely to be allergic to ester which produced a PABA metabolite (procaine), or preservative (MPB) so give neither of those. This stem is probably incorrect. There can be preservatives in epinephrine. The LEAST allergenic is preservative-free amide (ex: plain lidocaine) Amino ESTERS - cocaine, tetracaine, benzocaine, procaine (1 "i") Amino AMIDES - lidocaine, bupivacaine, prilocaine, mepivicaine (2 "i"s) bupivicane (bupivicaine is also trademarked marcaine, which only has 1 i so you need to know this exception) More info: True allergic reactions are rare, accounting for only 1% to 2% of all adverse reactions, but they are important to recognize because of their serious potential. Ester solutions (procaine, tetracaine), which produce the metabolite para-aminobenzoic acid (PABA), account for the great majority of these reactions. Amide solutions (lidocaine, bupivacaine) are rarely involved, and usually the preservative methylparaben (MPB), which is structurally similar to PABA, is responsible. Generally speaking, the optimal approach to the patient with a presumed anesthetic allergy is to determine the specific anesthetic agent associated with a presumed allergic reaction and then use a preservative-free agent from the other class (see earlier discussion). If the agent is unknown, use an antihistamine or give 0.1 mL of preservative-free lidocaine as a subcutaneous test dose, proceeding with the full dose if no reaction occurs within 30 minutes. Given the studies mentioned earlier, the prudent choices would seem to be diphenhydramine (Benadryl) or benzyl alcohol. Epinephrine (1 : 100,000) can be added to both of these drugs to prolong the duration of action. Ketamine anesthesia is also an alternative. - Roberts: Clinical Procedures in Emergency Medicine, 5th ed. Allergy to lidocaine is very rare. Most patients who claim to be allergic have had a vasovagal response. Bacteriostatic saline is an alternative for patients who are allergic to lidocaine. Commercially available bacteriostatic saline contains benzyl alcohol, which acts as a painless anesthetic. The anesthetic effect dissipates rapidly when injected subcutaneously. The volume of saline required to achieve anesthesia is at least two to three times that required when using 1% lidocaine and is of brief duration. - Habif: Clinical Dermatology, 5th ed. If an allergic reaction cannot be ruled out and the drug previously used is known, use an agent from the other class (whether amide or ester). - Roberts: Clinical Procedures in Emergency Medicine, 5th ed.

Answer 247

a) 10cc 1% xylocaine (lidocaine) lidocaine with epi : 5mg/kg lidocaine without epi: 7mg/kg bupivicaine : 2-3 mg/kg % means % weight so 1% xylocaine is 0.01kg/L = 10g/L =10mg/mL 1 mL = 10 mg

Answer 248

d. hemiparesis * Low levels → depression, lightheadedness, dizziness, circumoral numbness, metallic taste, visual disturbance, tinnitus & slurred speech * High levels → excitation, anxiety, nystagmus, fine tremors: hand and face, seizures * Very high levels →depression, coma, respiratory depression and arrest * Cocaine – euphoria, sense of well being Major Side Effects Side effects are proportional to the plasma concentration of lidocaine. At low concentrations, light-headedness, numb tongue, metallic taste, increased blood pressure, and dizziness can occur. As the plasma concentration increases, visual and auditory disturbances, confusion, muscle twitching, and decreased blood pressure develop. At high plasma concentrations, patients are at risk for arrhythmias, convulsions, coma, and respiratory and cardiovascular system collapse. Hypersensitivity has also been reported. - Walsh: Palliative Medicine , 1st ed.

Answer 249

Answer: Neurological * Initially CNS (excitation followed by depression) then CVS collapse at higher level * Earliest toxic effect circumoral paresthesia, numbness of the tounge/metallic taste, dizziness,hyperacusis and tinnitus

Answer 250

Answer: Decreased with hepatic dysfunction Ninety percent of a dose of lidocaine is metabolized in the liver via N-dealkylation. Urinary excretion is 10%. - McPherson & Pincus: Henry's Clinical Diagnosis and Management by Laboratory Methods, 21st ed. Lidocaine is chiefly metabolized in the liver via de-ethylation. The half-life is prolonged in patients with liver but not renal failure. - Walsh: Palliative Medicine , 1st ed.

Answer 251

Esters - Procaine - Chloroprocaine - Cocaine - Tetracaine Amides (have an “i” early in the name) - Lidocaine - Mepivacaine - Prilocaine - bupivacaine (Marcaine) - etidocaine

Answer 252

E. None of the above. Airway Treatment: • Airway maintenance • Hyperventilation →CO2 reduces seizure threshold • Diazepam or thiopental Na for seizures • Fluid and vasopressors for cardiac depression

Answer 253

b. bupivocaine ``` mepivacaine (120m with epi) bupivocaine (180-240 with epi) lidocaine (120m with epi) procaine (30-45m with epi) - Source: Miller: Miller's Anesthesia, 7th ed. ```

Answer 254

Answer: Ibuprofen (Motrin)

Answer 255

Answer: NSAID’s can help in controling the pain. a. NSAID’s (Yes) b. Meperidine (not recommended) c. Parenteral morphine (oral is preferred) d. Talwin when used inceases the effect of narcotics (not on the WHO ladder)

Answer 256

Answer: Decreased post operative narcotic requirement. Think of pre-op celebrex in our arthroplasty patients

Answer 257

Answer: The dose of acetaminophen would exceed the recommended level

Answer 258

Avoid opioids, and if you need them, hydromorphone is better in elderly (less delirium) ``` A. Rotate to hydromorphone (maybe) B. Rotate to fentanyl as it has less metabolites (no) C. Use haloperidol (no) D. Use a benzodiazepine (no) E. Avoid opioids (probably yes) ```

Answer 259

Answer: active metabolite toxicity Does anyone even use this anymore? keep in mind these questions are old - meds seem to have aged the most so this whole section is probably not super high yield

Answer 260

Answer: epidural A meta-analysis of respiratory complications after various types of surgery has shown that epidural techniques reduce the incidence of respiratory complications.[252] Lumbar epidural analgesia has gradually been replaced by thoracic epidural analgesia for thoracic surgery in the 1990s. - Miller: Miller's Anesthesia, 7th ed. Two very efficacious methods of post-thoracotomy pain treatment have become widely used and are considered by many to be the methods of choice. They are cryoanalgesia and administration of epidural narcotics. In addition, interpleural regional analgesia has recently been introduced as an alternative method for treating pain after thoracotomy. - Miller: Anesthesia, 5th ed., Copyright © 2000

Answer 261

D. Antiemetics to counteract nausea Or laxatives (if it was an answer choice)

Answer 262

Answer: Causes respiratory depression I think depending on the question they may be wanting to see if you know that PCA are less likely to cause respiratory depression because you stop pressing the button when you are comfortable/sleepy (unless someone else is pushing the button for you!) Intravenous PCA is based on the premise that a negative-feedback loop exists; when pain is experienced, analgesic medication is self-administered, and when pain is reduced, there are no further demands. When the negative-feedback loop is violated, excessive sedation or respiratory depression may occur. - Miller: Miller's Anesthesia, 7th ed.

Answer 263

Ketamine has a wide range of effects in humans, including analgesia, anesthesia, hallucinations, elevated blood pressure, and bronchodilation. Ketamine is primarily used for the induction and maintenance of general anesthesia, usually in combination with some sedative drug. Other uses include sedation in intensive care, analgesia (particularly in emergency medicine), and treatment of bronchospasm. - http://en.wikipedia.org/wiki/Ketamine

Answer 264

Answers given: - morphine 1.5 mg IV q3h = Immediate - Codeine 15 mg po q4h prn = Slow release (who uses codeine anymore? doubt this will be in POS post-medieval ages) Both of these drugs could be used as effective pain control in the peds pop. There is no fixed age below which PCA is not offered; however, patients below the age of 7 years generally are poor candidates for PCA. Acetaminophen 160mg po q4h: Insufficient dose – need 240mg - Infants and children

Answer 265

Answer: Increased lacrimation The clinical features of Horner's syndrome can be remembered using the mnemonic, "Horny PAMELa" for Ptosis, Anhydrosis, Miosis, Enophthalmos and Loss of ciliospinal reflex. Ptosis is an abnormally low position (drooping) of the upper eyelid. Anhydrosis means lack of sweating. Miosis is constriction of the pupil of the eye. Enophthalmos (Also Endopthalmos) is recession of the eyeball within the orbit. The ciliospinal reflex (pupillary-skin reflex) consists of dilation of the ipsilateral pupil in response to pain applied to the neck, face, and upper trunk.

Answer 266

Upper arm, lower arm, and hand are involved. Horner syndrome (ptosis, anhydrosis, and miosis) exists if T1 is involved. - Johns Hopkins: The Harriet Lane Handbook, 18th ed.

Answer 267

None of the above Autonomic dysreflexia (AD), also known as autonomic hyperreflexia, is a potentially life threatening condition which can be considered a medical emergency requiring immediate attention. AD occurs most often in spinal cord-injured individuals with spinal lesions above the T6 spinal cord level. Acute AD is a reaction of the autonomic (involuntary) nervous system to overstimulation. It is characterised by severe paroxysmal hypertension (episodic high blood pressure) associated with throbbing headaches, profuse sweating, nasal stuffiness, flushing of the skin above the level of the lesion, bradycardia, apprehension and anxiety, which is sometimes accompanied by cognitive impairment.[1] The sympathetic discharge that occurs is usually in association with spinal cord injury (SCI) or disease (e.g. multiple sclerosis). AD is believed to be triggered by afferent stimuli (nerve signals that send messages back to the spinal cord and brain) which originate below the level of the spinal cord lesion. It is believed that these afferent stimuli trigger and maintain an increase in blood pressure via a sympathetically mediated vasoconstriction in muscle, skin and splanchnic (gut) vascular bed

Answer 268

1st change is decrease in threshold for vibration, thus hypersensitivity to tuning fork. 2 point discrimination is the last sensory modality to go.

Answer 269

e. Uraemia DKA. a. Ketonemia -yes b. High glucose -yes c. Leukocytosis -yes Leukocytosis — The majority of patients with hyperglycemic emergencies present with leukocytosis, which is proportional to the degree of ketonemia [6,61]. Leukocytosis unrelated to infection may occur as a result of hypercortisolemia and increased catecholamine secretion d. Hyperkalemia - ??? e. Uraemia - ???

Answer 270

Answer: c. Intracranial pressure CPP=MAP-ICP Cerebral autoregulation maintains constant blood flow by compensating for changes in CPP, unless -high ICP such that CPP 160 mmHg or

Answer 271

?? Autoregulation of cerebral blood flow (CBF) responds to changes in arterial pressure, arterial Pco2, or Po2, by dynamically altering arteriolar caliber so as to maintain a constantly matched cerebral perfusion sufficient to meet metabolic demands ( Fig. 94-3 ). pH, Paco2, potassium, and adenosine are among many purported metabolic mediators of flow. - Miller: Miller's Anesthesia, 7th ed.

Answer 272

Cubital tunnel syndrome PHYSICAL FINDINGS & CLINICAL PRESENTATION - Paresthesias and numbness along distribution of ulnar nerve (ulnar one and one-half fingers) - Positive Tinel’s sign at elbow - Positive elbow flexion test (flexion of elbow with wrist extended for 30 sec may reproduce symptoms) - May be diminished sensation to tip of small finger - Ulnar nerve may be subluxable with elbow motion or by manipulation - Cubitus valgus may be present if prior bony injury - Interosseous weakness in longstanding cases with atrophy Ferri: Ferri's Clinical Advisor 2010, 1st ed. Carpal Tunnel Syndrome The earliest symptoms are pain and paresthesias, which are characteristically more obvious at night, after prolonged activity, and with positional postural changes at the wrist such as when driving, using a blower hairdryer, or reading a book. The patient may complain of clumsiness and a tendency to drop objects. The paresthesias characteristically follow the distribution of the median nerve, including the thumb and index and middle finger. Physical examination consists of compressing the carpal canal, percussing the median nerve, and hyperflexing the wrist to produce paresthesias (Durkin's sign, Tinel's sign, and Phalen's test, respectively). Pronator Syndrome The symptoms produced are similar to those of carpal tunnel, although nocturnal symptoms are uncommon. The palm may also feel numb because the palmar cutaneous branch is involved, but is specifically spared in carpal tunnel syndrome because that nerve branch passes superficial to the flexor retinaculum and arises proximal to the retinaculum. Cubital Tunnel Syndrome Motor and sensory symptoms develop in the distribution of the ulnar nerve and are worsened by adopting a flexed position at the elbow. Examination reveals a positive Tinel's sign over the tunnel. Paresthesias are described in the distribution of the ulnar nerve to the little and ring fingers and ulnar border of the hand. Thoracic Outlet Syndrome All elements of the brachial plexus, as well as the subclavian artery and vein, pass through this narrow space and can be potentially compressed at this site. - Townsend: Sabiston Textbook of Surgery, 18th ed.

Answer 273

?? Postoperative hypertension in particular has been shown to be associated with increased postoperative stroke and death and with postoperative cardiac complications. - Townsend: Sabiston Textbook of Surgery, 18th ed. Most strokes develop within the first 2 days after surgery, and are up to two times more common in combined cardiac procedures or technically challenging operations. Multivariable analysis has identified 10 variables that were independent predictors of stroke: history of cerebrovascular disease, peripheral vascular disease, diabetes, hypertension, previous cardiac surgery, preoperative infection, urgent operation, CPB time more than 2 hours, need for intraoperative hemofiltration, and high transfusion requirement. Patients with ascending aortic atherosclerosis, older age (70 years), preoperative unstable angina, chronic obstructive pulmonary disease, and carotid artery disease are at risk for late postoperative stroke (new strokes during 5-year follow-up) after CABG. - Libby: Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 8th ed

Answer 274

B. Complete recovery is expected In a Sunderland type 2 injury, the endoneurium, perineurium, and epineurium are still intact, but the axons are physiologically disrupted. Because the endoneurium is intact, the regenerating axons are directed along their original course, and complete functional recovery can be expected. The time for recovery depends on the level of injury, as the axon must regenerate distally to the end-organ. It can usually be measured in months, as opposed to weeks for a Sunderland type 1 injury. Injuries to subsequent connective tissue layers upgrade the Sunderland classification. J Am Acad Orthop Surg 2000;8:243-252 Regeneration is 1mm/day (or 1inch/mo) Recovery is expected in days to weeks for neuropraxia (Sunderland grade I) First-degree injury or Neuropraxia: a localized conduction block is produced that results in at most a segment of demyelination. Since the axons are not injured, regeneration is not required and after remyelination, recovery is complete. Second-degree injury or Axonotmesis: axonal injury occurs and the distal segment undergoes Wallerian degeneration. Proximal nerve fibres will regenerate at a rate of 1mm/day. By definition the connective tissue layers are uninjured. Recovery will be complete unless the distance of the injury from the motor end plate results in such prolonged denervation of the receptor that motor recovery is adversely affected. Third-degree injury: Wallerian degeneration is combined with some fibrosis of the endoneurium. Recovery will be incomplete because scar within the endoneurium may block or cause mismatching of regenerating fibres with the appropriate end organs. Fourth-degree injury: A complete scar block results from injury to the axon, endoneurium and perineurium. Regeneration will not occur unless the block is removed and the nerve is repaired or grafted. Fifth-degree injury or Neurotmesis: the nerve is completely divided at every tissue layer and must be repaired before any regeneration can occur Sixth-degree injury: this represents a combination of any of the previous five levels of injury. Because of the longitudinal nature of crushing injuries, different levels of nerve injury can be seen at various locations along the nerve.

Answer 275

a. Brown-Sequard

Answer 276

b. complete spinal cord injury Return of bulbocavernous reflex = end of spinal shock. Cannot fully diagnose extent of spinal cord injury until spinal shock ends to see what function is left. Complete Spinal Cord Lesion • bilateral loss of motor/sensory and autonomic function at ≥4 segments below lesion/injury, with UMN signs • about 3% of patients with complete injuries will develop some recovery within 24 hours, beyond 24 hours, no distal function will recover Definition: - complete cord injury implies unequivocal absence of motor or sensory function distal to injury in absence of spinal shock; - w/ complete injuries, an improvement of one nerve root level can be expected in 80% of patients, and approximately 20% will recover 2 additional function levels; - there is also evidence that operative decompression can also allow recovery of an additional nerve root level; - incomplete lesion: - present when there is any distal sparing of motor or sensory function along with sparing of perirectal sensation; Anterior Cord Syndrome - syndrome is manifested by complete motor paralysis (corticospinal function) & sensory anesthesia (spinothalamic function); - there is sparing of the dorsal column: - deep pressure and proprioception are only retained sesibility of the trunk and lower extremities; - patient demonstrates greater motor loss in the legs than arms; The bulbocavernosus reflex is a polysynaptic reflex that is useful in testing for spinal shock and gaining information about the state of spinal cord injuries (SCI). The test involves monitoring anal sphincter contraction in response to squeezing the glans penis or tugging on an indwelling Foley catheter.[1] The reflex is spinal mediated and involves S2-S4. The absence of the reflex without sacral spinal cord trauma indicates spinal shock. Typically this is one of the first reflexes to return after spinal shock. Lack of motor and sensory function after the reflex has returned indicates complete SCI. Absence of this reflex in instances where spinal shock is not suspected could indicate a lesion or injury of the conus medullaris or sacral nerve roots. - http://en.wikipedia.org/wiki/Bulbocavernosus_reflex

Answer 277

Answer: Can not determine neurologic prognosis Must wait for the reflex to return for prognosis.

Answer 278

Answer: RCT > Prospective cohort > Case-control Case control is retrospective and suffers from recall bias. Order from least to most bias: Experimental Studies 1. Randomized Controlled Clinical Trial (RCT): Observational Studies 1. Cohort (Incidence, Longitudinal Study) 2. Case-Control Study: 3. Ecologic (Aggregate) Study: 4. Cross-Sectional (Prevalence Study) Study: 5. Case Series: 6. Case Report - http://www.vetmed.wsu.edu/courses-jmgay/GlossClinStudy.htm (great resource)

Answer 279

d) A prospective cohort study Answer: Cohort study (prospective, incidence, longitudinal): follows a group of persons with common characteristics forward over a period of time and determines outcome according to exposure to different factors Provides estimates of incidence, relative risk, attributable risk Cannot by itself, establish causation but can show an association between a factor and an outcome

Answer 280

c. Coin toss everything else could have confounding factors

Answer 281

d. Validity

Answer 282

a. Add more patients need more POWER

Answer 283

d) Class IV The following is a description of the rating scale used to evaluate how strongly supported the evidence supports the use of a PARTICULAR THERAPY. Class I: Prospective, randomized, controlled clinical trial with masked outcome assessment, in a representative population. The following are required: a) primary outcome(s) is/are clearly defined b) exclusion/inclusion criteria are clearly defined c) adequate accounting for drop-outs and cross-overs with numbers sufficiently low to have minimal potential for bias d) relevant baseline characteristics are presented and substantially equivalent among treatment groups or there is appropriate statistical adjustment for differences. Class II: Prospective matched group cohort study in a representative population with masked outcome assessment that meets a-d above OR a RCT in a representative population that lacks one criteria a-d. Class III: All other controlled trials (including well-defined natural history controls or patients serving as own controls) in a representative population, where outcome assessment is independent of patient treatment. Class IV: Evidence from uncontrolled studies, case series, case reports, or expert opinion.

Answer 284

In a single-blinded trial, the participants don't know whether they're receiving a treatment or placebo until the trial is over. In a double-blinded trial, neither the participants nor the researchers know who's receiving treatment or placebo until the trial is over.Both of these designs are meant to eliminate expectations that could bias the trial results. Placebo-controlled, double-blinded trials are the gold standard of clinical trials.

Answer 285

a. smaller difference than expecte So you can get more power/less chance of a type ii error