Orals Flashcards

Question

59 y/o m LLQ pain, f, diarrhea, happened before and hosp c antibiotics

Answer 1

DDx: diverticulitis Imaging: CT, KUB Labs: CBC, Renal, UA Primary tx for noncomplicated: conservative management (IVF, abx) Tx for complicated c intraabdominal abscess: Percutaneous drain and resect when infxn clears Complications of diverticulitis: Perf, fistulas or obstruction To OR immediately if perf- signs of sepsis/hypotension, obstruction Surgery for perf diverticulitis c significant spillage: Resection and Hartman’s (no anastomosis), or primary anastamosis and divert with a loop (resect bowel, give them loop ileostomy)

Answer 2

Background - Large bowel obstruction classified as mechanical or pseudo-obstruction o Mechanical causes: Colorectal CA most common cause Inflammation Diverticulitis, Crohn’s Adhesions (most common cause for small bowel obstruction, but rarely causes large bowel obstruction) Hernias Volvulus o Pseudo-obstruction Primary–motilitydisorder Secondary–associatedwithneurolepticdrugs,opiates,metabolicillnesses,diabetes, hyperparathyroidism, lupus, scleroderma, Parkinson’s - Clinical presentation: o Abdominal distention, cramping abdominal pain, nausea and vomiting, obstipation b. Large bowel obstruction DDx - abdominal hernia - diverticulitis - colonic polyps - pseudomembranous colitis - toxic megacolon - small bowel obstruction - colon cancer - ileus c. Initial treatment - All patients should be treated with IV fluids, nasogastric suction, continuous observation until diagnosis is established - for pseudo-obstruction: o nasogastric decompression o fluids o correction of electrolyte abnormalities o discontinue all medications that inhibit bowel motility such as opiates d. Diagnosing large bowel obstruction - History and physical examination provide important clues. Abdomen should be palpated for masses, groins inspected for hernias, and a digital rectal exam performed to exclude rectal cancer. o Physical exam usually shows abdominal distention, tympany, high-pitched metallic rushes, and gurgles. Palpation may reveal localized, tender, palpable mass that may indicate a strangulated closed loop or an area of inflamed diverticular disease. - Plain films of abdomen provide considerable information concerning location of obstruction. - Barium enema confirms diagnosis of colonic obstruction and identifies exact location o If plain film shows the obstruction, barium enema is not necessary o Barium should never be given orally in the presence of suspected colonic obstruction because it may accumulate proximal to the obstruction and cause a barium impaction - If pseudo-obstruction is suspected, colonoscopic exam may be used. e. Operation - patients with complete (rather than partial) bowel obstruction should undergo emergent operation - emergency laparotomy is undertaken for acute large bowel obstruction with cecal distention beyond 12cm, severe tenderness, peritonitis, or generalized sepsis

Answer 3

if cause of obstruction is cancer of distal or mid-rectum: o loop colostomy and then neoadjuvant chemoradiation, with plan to resect the primary lesion at a later time - if obstructing cancer is in sigmoid colon, options are: o Hartmann’s operation (sigmoidectomy with descending colostomy and closure of rectal stump) o Sigmoidectomy with primary colorectal anastomosis o Abdominal colectomy with ileorectal anastomosis - for pseudo-obstruction: fiberoptic colonoscopy with decompression and placement of rectal decompression tube - right-sided colonic obstruction, whether caused by cancer or volvulus, is generally treated by resection and primary anastomosis of ileum and transverse colon f. Post-op complications - Wound infection - Small bowel obstruction - Diarrhea - incontinence - post-op ileus (due to leakage from anastomosis) or mechanical obstruction (due to adhesions, internal hernia, or obstructed anastomosis) o This causes failure to propel food and secretions distally, leading to bacterial overgrowth in the stomach and proximal small bowel feculent vomiting - Anastomotic leak o May cause post-op ileus o May also cause wound infection that spontaneously drains to the skin - Obstruction of anastomosis o Causes fistula formation - Abscess g. Dehiscence presentation - In 25% of patients, dehiscence is preceded by a sudden, dramatic drainage of a relatively large volume of clear, salmon-colored fluid - Ripping sensation h. Profuse diarrhea after colectomy - Normally, 1 to 1.5L or fluid enters the colon from the small intestine. It takes time for small intestine to adapt after resecting colon. Adaptation eventually results in decrease in flow from the small intestine. i. Staging of colon CA - Staging of colon CA is based on depth of invasion of the primary lesion, presence of regional lymph nodes, and distant metastasis. The TNM system of staging is as follows: o Stage 0 = Tis, N0, M0 Tumorislimitedtomucosa(insitu) o StageI = T1/T2,N0,M0 Tumor is limited to mucosa and submucosa (T1) OR deeper into, but not beyond, the muscularis propria (T2) Noregionallymphnodeinvolvement Nometastasis >90%5-yearsurvival o StageII= T3/T4,N0,M0 Tumor extends through the full thickness of the bowel wall (T3) OR into adjacent structures (T4) Noregionallymphnodeinvolvement Nometastasis 60-80%5-yearsurvival o StageIII=AnyT,N1/N2/N3,M0 Tumor has metastasized to regional lymph nodes at various levels 20-50%5-yearsurvival o StageIV=AnyT,AnyN,M1 Presenceofliverorotherdistantmetastasis

Answer 4

Hx: Change in bm, hx hysterectomy, bloody stools, last colonoscopy, pain hx, past surgeries DDx: SBO (2/2 adhesions, volvulus, hernias), ileus, cancer, diverticulitis Labs: CBC, renal, CEA, CA19-9, UA, LFTs

Answer 5

Colonoscopy, bx If colon cancer IVF, NGT, plan for OR resection POD #3 develops rush of serous fluid- likely cause and tx: Dehiscence, go back to OR POD #7 spikes f c diarrhea- what tests: CBC, C diff, CT abd (look for abscess) CT shows multiple intraloop abscesses- need to go OR for washout (if only 1 can drain it, if multiple can’t perc drain it)

Answer 6

Clinical presentation of colonic volvulus - Abdominal distention, vomiting, abdominal pain, obstipation, tachypnea - Physical exam shows distention, tympany, high-pitched tinkling sounds and rushes - patients confined to mental institutions or nursing homes have increased risk b. Diagnosing volvulus - abdominal radiographs show a massively dilated cecum or sigmoid without haustra that often assumes a kidney bean appearance - barium enema shows exact site of obstruction, with a characteristic funnel-like narrowing often resembling a bird’s beak c. Initial treatment - hydration is necessary - electrolytes, CBC, abdominal obstructive radiographic series needed to rule out obstruction or other abdominal pathology - In stable patients, it is often possible to “detorse” the sigmoid colon by rigid proctosigmoidoscopy and placement of a rectal tube. o If endoscopic management is unsuccessful, urgent laparatomy is required. Recurrence rate is approximately 30%. d. Definitive treatment - Definitive treatment is either sigmoid colectomy with diverting colostomy OR resection with primary anastomosis – depending on the preoperative condition of the patient - For cecal volvulus: cecopexy (suturing the cecum to the parietal peritoneum) or right hemicolectomy with ileotransverse colostomy

Answer 7

DDx: obstruction, volvulus, colon cancer, diverticulitis, SBO, perf viscus Labs: CBC, comprehensive metabolic panel, CEA, lactic acid (if dead bowel) Imaging: CT, plain film If sigmoid volvulus if can’t do CT- do barium enema If no signs ischemic bowel at presentation before OR- tx: undo sigmoid volvulus by barium enema (not so much for adults as for children), do sigmoidoscopy (colonic decompression c sigmoidscope c rectal tube). Definitive tx for volvulus is sigmoid resection. If presents c intrabdominal abscess at time of operation, the operation you will perform is sigmoidectomy c Hartmann’s pouch. If pt stable and in OR see viable sigmoid after undoing volvulus, do sigmoid resection c primary anastomosis (don’t have to divert bc not perf; trauma literature states that can do primary anatasmosis on colon inj if

Answer 8

Initial treatment for GERD - double dose of PPI o this also serves as a diagnostic tool: more extensive evaluation necessary if symptoms persist after a trial of medical therapy - other medications available include: o antacids, motility agents, H2 blockers, b. Refractory GERD workup - pH monitoring (24-hour pH test) – gold standard for diagnosing and quantifying acid reflux - endoscopy - manometry – rules out primary motility disorders such as achalasia - esophagography c. Standard operation - Total fundoplication (360-degree wrap) o gastric fundus is wrapped around the lower end of the esophagus and then sutured to reinforce the function of the lower esophageal sphincter o whenever stomach contracts, it also closes off the esophagus instead of squeezing gastric acids into it. d. GERD complications - Barrett’s esophagus (esophageal mucosa changes from squamous epithelium to columnar) - Shortened esophagus as a result of repeated injury - Extraesophageal symptoms: hoarseness, laryngitis, cough, wheezing, aspiration e. Alternative operation if there is esophageal motility disorder - partial fundoplication

Answer 9

Initial treatment for lower GI bleed - Resuscitation first (e.g. transfusion) - Endoscopic control (e.g. endoscopic clip placement, cautery) - Angiographic control (e.g. intra-arterial injection with vasoconstrictors) b. DDx - hemorrhoids - colonic polyps colon cancer - rectal cancer - bowel obstruction - inflammatory bowel disease (Crohn’s, Ulcerative colitis) - diverticulitis - AV malformation (angiodysplasia) - Mesenteric ischemia - Meckel’s diverticulum - trauma c. Localizing bleed - Colonoscopy is mainstay - Adjuncts to colonoscopy: o tagged RBC scan – most sensitive but least accurate o angiography o push enteroscopy d. Diagnosis - rule out upper GI bleed by NGT aspirate or EGD - colonoscopy for minor bleeding - for major bleeding: o if stable: tagged RBC scan o if unstable: e. Indications for surgery - hymodynamic instability despite vigorous resuscitation (>6 units transfusion) - failure of endoscopic techniques to arrest hemorrhage - recent hemorrhage after initial stabilization (with up to 2 attempts at obtaining endoscopic hemostasis) - shock associated with recurrent hemorrhage - continued slow bleeding with a transfusion requirement >3U/day f. Extent of standard colon resections o for cancer: need histologically cancer-free margin at the distal extent of the resection. Minimum of 10cm of grossly normal bowel on both sides of the tumor is required to keep the risk o for inflammatory bowel disease: need to evaluate the extent of pericolic inflammation first

Answer 10

Hypertrophic Pyloric Stenosis - Common between ages 2 and 8 weeks - Boys affected 4x as often than girls, 1st born male highest risk - Hypertrophy of the circular muscle of the pylorus results in constriction and obstruction of the gastric outlet, leading to nonbilious, projectile emesis, loss of hydrochloric acid with the onset of hypokalemic hypochloremic metabolic alkalosis, and dehydration. - Clinical Presentation: progressively worsening nonbilious emesis and with time, emesis becomes more frequent, forceful, and projectile in nature. - Diagnosis: Palpation of the pyloric tumor (olive-shaped) in the epigastrium or right upper quadrant is pathognomonic o A plain abdominal radiograph shows an upper abdominal gas bubble in the stomach o When the olive is nonpalpable, the diagnosis of HPS can be made by ultrasound. A persistent pyloric muscle thickness more than 3 to 4 mm or a pyloric length more than 15 to 18 mm in the presence of functional gastric outlet obstruction is generally considered diagnostic o With equivocal clinical history, an upper GI contrast study is useful to evaluate for other causes of vomiting. - Renal compensatory mechanism: o Vomiting/loss of gastric acid hypochloremia impairs kidneys’ ability to excrete bicarbonate. o Hypovolemia hyperaldosteronism retention of Na and excretion of increased amounts of K hypochloremic, hypokalemic metabolic alkalosis. o Body compensates to metabolic alkalosis by hypoventilation resulting in elevated PaCO2 - Tx: Pyloromyotomy

Answer 11

Bilious Vomiting in a Newborn DDx: - Duodenal Atresia o Associated with Down Syndrome o Presents a few hours after birth o Findings: Abdominal film, “double bubble” sign - Malrotation with V olvulus o Incomplete bowel rotation during 7th -12th weeks of gestation o Presents at 3-7 days, rapid deterioration with volvulus o Findings: UGI spiral sign on ultrasound; abnormal location of superior mesenteric vessels - Jejunoileal Atresia o Mesenteric vascular accident during fetal life o Presents within 24 hours of birth o Findings: Air fluid levels on abdominal film - Meconium Ileus o Genetic, 15% of newborns with cystic fibrosis o Presents immediately after birth o Findings: abdominal film; distension, air-fluid levels, sweat test, “ground glass” sign - Necrotizing Ileus o Presents 10-12 days after birth o Findings: Abdominal film; distension, pneumatosis, air in the aortal vein

Answer 12

Differential Dx of Acute Epigastric Pain - Cardiac: MI, pericarditis, myocarditis - Gastric: esophagitis, GERD, gastritis, peptic ulcer - Biliary: cholecystitis, cholelithiasis, cholangitis - Pancreatic: mass, pancreatitis - V ascular: aortic dissection, mesenteric ischemia Perforated Duodenal Ulcer - Sudden onset, frequently severe epigastric pain; localized peritoneal signs - Free air in CXR - Usually in 1st portion of duodenum - Tx: Emergent surgical intervention o If smaller than 1cm: close primarily and buttressed with well-vascularized omentum o Larger perf: Graham patch repair with a tongue of healthy omentum o Very large perf greater than 3 cm: close with application of healthy tissue like omentum or jejunal serosa, with placement of a duodenostomy tube and wide drainage Or antrectomy and Bilroth II reconstruction - Stable patient with chronic DU indications for ulcer surgery: o Elective operative intervention has become rare as medical therapy has become more effective. o Indications for ulcer surgery: Intolerant of medications or do not comply with medication regime High risk of complications (ex: transplant recipients, pt dependent on steroids or NSAIDs) H.pyloricannotbeeradicated Pt with large ulcers that fail to heal with adequate treatment o Options: Truncal V agotomy TruncalVagotomyandAntrectomywithgastroduodenostomy(BilrothI)orgastrojejunostomy (Bilroth II) SelectiveVagotomy:preservingthehepaticandceliacbranchesofthevagus Highly selective vagotomy: division of only the gastric branches of the vagus, preserving Latarjet’s nerve to the pylorus Partialgastrectomy

Answer 13

Ulcerative Colitis - Initial Treatments: o Aminosalicylates Most common therapy for mild to moderate UC Sulfasalazine,5-ASA,Mesalamine o Corticosteroids ForactiveUC o Immunomodulatory medication ForlongtermmanagementofUC 6-Mercaptopurine,Azathioprine,Cyclosporine,Infliximab See UC Vs Crohn's comparison chart UC Long term complications: o Fulminant colitis and toxic megacolon o Massive bleeding o Dysplasia or Carcinoma - UC Recommendation o Prophylactic colectomy Total proctocolectomy with ileostomy; Segmental colectomy has been shown to be inadequate for controlling disease, Recommended in: Inflammatory Bowel Disease Polyposis syndromes Lynch syndrome High risk for development of CRC

Answer 14

Common presentations of Inguinal Hernia - Aching in groin, may radiate to area of hernia - Pain in medial thigh (femoral hernia) - If strangulated/ incarcerated: o Increased pain o Increased size o No reduction in size with recumbency o Fever o N/V o Severe constipation - Palpable and/or visible lump in groin - Lump decreases in size with recumbency, increases in size with standing and with increased intra-abdominal pressure (ex: Valsalva) - If strangulated/ incarcerated: o Irreducible o Tenderness o Abd distention o Tympany o Hyperperistalsis early but with advancing peritonitis BS may be absent o Erythema of skin overlying it Inguinal Canal - Oblique space, 4 cm in length - Lies above medial half of the inguinal ligament - Beneath EO aponeurosis, between: o External/ Superficial Inguinal Ring MedialopeninginEOapnoneurosis Liesaboveandlateraltothepubiccrest o Internal/ Deep Inguinal Ring Lateralend Opening within the transversalis fascia lateral to inferior epigastrics - Males: o spermatic cord o Cremasteric muscle fibers o Testicular artery and veins o Genital branch of genitofemoral nerve o Vas deferens o Cremasteric vessels o Lymphatics o Processus vaginalis - Females: o round ligament of the uterus - Boundaries o Anterior/superficial: EO fascia with contribution of IO fascia in lateral 1/3 o Posterior: fusion of the transversalis fascia and transversus abdominis fascia o Inferior/ floor: inguinalligament o Superior/ roof: arch formed by IO and transversus abdominis (Conjoint Tendon) o Think of it as a cylinder! - Hesselback’s Triangle – margins of the floor of the IC Superolateral: inferior epigastrics o Medial: rectus sheath o Inferior: Inguinal ligament Complications of Hernia Repair - Infection - Recurrence 1.7-10% o Tension free repairs have a lower rate of recurrence than tissure repairs o 50% of recurrences are found within 3 years after primary repair

Answer 15

Bleeding Disorders and ITP Approach to patient with bleeding diathesis- History- bleeding disorders- menorrhagia, epistaxis, bleeding after dental procedures, family history of abnormal bleeding, medication use. Physical- pallor and additional signs of anemia, petechiae, ecchymosis Laboratory Evaluation- platelet count (quantitative not qualitative), bleeding time (measures platelet function), coagulation studies- PT (extrinsic pathway), PTT (intrinsic pathway), INR, factor deficiency tests (vwd, hemophilia), fibrinolysis tests, fibrinogen levels, ristocetin aggregation studies (causes vwf to bind to gp1b- fixed with addition of vwf with VWD, not with Bernard Soulier) Common Bleeding Disorders- refer to page 387 of FA2012 21 ITP Coagulation disorders (macrohemorrhages, hemarthrosis, easy bruising, elecated PTT, PT)- Hemophilia A, B (Christmas Disease), Vitamin K Deficiency Platelet Disorders (microhemorrhage- mucous membrane bleedin, epistaxis, petechiae, purpura, increased bleeding time and decreased platelet count)- Bernard-Soulier (GP1b defect- defect in platelet to collagen adhesion), Glanzmann’s thrombasthenia (GP2b3a defect- defect in platelet to platelet aggregation- low clumping on blood smear), ITP (discussed below), TTP (deficiency of ADAMTS13- a vwf metalloproteinase causing a decreased degradation of VWF multimers- get increased platelet aggregation and thrombosis- see schistocytes (MAHA) and increased LDH- pentad of symptoms- neurological deficits fever, hemolytic anemia, thrombocytopenia, renal symtpoms) Decreased platelet survival due to premature destruction by antibodies (often against GPIIB/IIIa). Labs show increased megakaryocytes. Initial treatment with glucocorticoids – dexamethasone, methylprednisone Treatment with IV immunoglobulin (IVIG) which blocks macrophage Fc receptors Second line- Splenectomy if medical management fails (unresponsive to steroids or requiring chronic treatment- over 1 year). Complications include: overwhelming sepsis from encapsulated bacterial infection (must be immunized for S. pneumo, H. influenza, and N. meningitides), arterial and venous thrombosis, increased risk of cardiac events, increased risk of pulmonary hypertension Rituximab (anti-CD20) is another second line therapy

Answer 16

Etiology A spectrum of infections diseases result in necrosis of skin and soft tissue. These NI include clostridial infections, which are rare, or necrotizing soft tissue infections of various types, which are more common. The broad categories within the latter group include necrotizing fasciitis, bacterial synergistic gangrene, and streptococcal gangrene. The bacteriology of the various disease processes included in the infectious gangrenes is complex. The majority of NIs resulting in necrotizing fasciitis consist of a mixture of β-hemolytic streptococci (90%), anaerobic Gram-positive cocci, aerobic Gram-negative bacilli, and Bacteroides species. A single organism, with the unusual exception of Group A β- hemolytic streptococci (GAS), rarely causes an infection resulting in necrotizing fasciitis. Bacterial synergistic gangrene is primarily a subcutaneous gangrenous infection caused by the same organisms as those that cause necrotizing fasciitis, but there is no involvement of any fascial tissue. Classically, cultures yield the combination of a microaerophilic nonhemolytic streptococcus in the spreading periphery of the lesion and Staphylococcus aureus found in the zone of gangrene. Streptococci can be accompanied by a variety of other organisms, such as Proteus, Enterobacter, Pseudomonas, and Clostridium species. Streptolysin S-producing strain of Group G hemolytic streptococci recently was reported to produce NI. Clostridial and mycotic infections must be considered in any initial evaluation of skin and soft tissue NIs, despite their relatively rare occurrence. Clostridial infections should be suspected when necrotic muscle is found during debridement of an infectious gangrene with severe systemic toxicity associated with clinical central nervous system manifestations. Patients with malignancies are particularly prone to NIs caused by Clostridium septicum Predisposing events include: mild trauma, insect bites, drug reactions, illicit drug injections, perirectal abscesses, major traumas, and surgical procedures. Some may occur without an inciting event or portal of entry. The frequent association of soft tissue NIs with underlying chronic diseases such as diabetes mellitus, hypertension, congestive heart failure, obesity, renal insufficiency, cancer, malnutrition, arteriosclerosis, alcoholism, autoimmune disease, acquired immunodeficiency syndrome, and immunosuppression, as well as with patients older than 60 years of age, is diagnostically helpful. Signs: elevated WBC, hypoNa, inc BUN, hypoCa,prot, alb elevated glucose Diagnosis Often presents as mild cellulitis or ulcer. Spontaneous gangrenous infection often on perineum but most often occurs on the extremities. Neither clostridial nor nonclostridial infections initially demonstrate prominent external evidence of skin death. Severe pain and systemic symptoms that occur out of proportion to the local infection characterize clostridial infections. As the clostridial infection progresses, the skin may develop a bronze color, followed by hemorrhagic bullae, then dermal gangrene, and finally crepitus. Clostridial exotoxins produce extensive tissue necrosis, with minimal hyperemia, fibrin formation, or neutrophil infiltration seen within the affected tissue. Nonclostridial infections are most likely to be associated with erythema, pain, and swelling but frequently are initially identical to simple cellulitis. Failure to respond to antibiotics, rapid progression, or evolving systemic signs of infection are significant clues that NI may be present. The patient generally appears ill and has a rapid pulse and significant temperature elevation. An occasional unique finding of necrotizing fasciitis is numbness of the involved area. Skin anesthesia probably is due to infarction of the cutaneous nerves located in necrotic subcutaneous fascia and soft tissue. Some patients with necrotizing fasciitis may present with localized pain of the involved site, and the overlying skin is erythematous, hot, and edematous. TMT: H&P, WBC Ca lytes, XR consult with ID and surg Gram's stain central line and foley fluids, cardio, preop check IV Abx, tetanus Surgical debridement --> amputation post op nutrition and physical therapy

Answer 17

Penicillin or ampicillin for clostridia, streptococci, and Peptostreptococcus. Clindamycin or metronidazolefor anaerobes, Bacteroides fragilis, Fusobacterium, and Peptostreptococcus. Clindamycin may be useful for treating GAS in patients with the toxic streptococcus syndrome because it inhibits toxin production. Gentamicinor another aminoglycoside for Enterobacteriaceae (ie, Gram-negative organisms). Gentamicin has a synergistic effect with penicillin against streptococci. Imipenem and meropenem by virtue of their high β-lactamase resistance, wide-spectrum efficacy, and inhibition of endotoxin release from aerobic (ie, Gram-negative) bacilli, may be the initial agents of choice for treatment of the frequent polymicrobial infections that result in necrosis or skin and soft tissue. Postoperative antibiotic coverage is adjusted on the basis of microbiologic testing results from cultures of tissue and blood

Answer 18

Hx: OLD CARTS for pain, trauma, exposure/break in skin, drug use, DM, HIV status DDx: Infxn- cellulitis, necrotizing fasciitis, compartment syndrome PE: VS (can be septic shock bc of infxn- need to know if hypotensive or tachycardic). If soft tissue infxn look for erythema, induration, fluctuance, edema. ROM. Sensation. Neurovascular. Dx tests: Blood cx, CBC, renal panel, CT or plain film (look for air) Tx: For necrotizing skin infxn- IVF, resus, abx, foley. Likely microbes for necrotizing soft tissue infxn: polymicrobial (GPC, GNB, anaerobes- staph, strep, Clostridium, Pasturella, Sporothrix) Discuss role of hyperbaric oxygen in recovery after debridement Wounds that fail to heal are usually hypoxic. Wound healing process affected by O2 concentration/gradients. Angiogenesis occurs in response to high O2. Fibroblast proliferation and collagen synthesis are O2 dependent (collagen is the foundational matrix for angiogenesis). HBOT also likely stimulates growth factors in angiogenesis. HBOT also shown to have antimicrobial activity (increases intracellular leukocyte killing). Options to close wounds after recovery Primary intention Clean and clean-contaminated All layers closed Secondary intention Infected wounds Deep layers closed, subcutaneous and skin left open Wound care consists multiple dressing changes per day c wound irrigation, packing and sterile dressings Open portion granulates and re-epithelializes Delayed primary Contaminated Deep layers closed while subcutaneous and skin open and packed Skin graft Block coverage

Answer 19

Presentation History- family history of skin cancer, personal history, sun exposure, irregular moles Whole body physical, exam nevi for ABCDEs. Asymmetry, irregular Borders, Color change (to dark black or blue), Diameter greater than 6mm, Evolution. Also do a lymph node examination DDX- BCC, SCC, dysplastic nevus, pigmented actinic keratosis, metastatic tumors to the skin, histiocytoid hemangioma, spindle and epithelioid nevus, etc Workup for malignant melanoma CMP- AST, ALT (liver mets), ALP (bone or liver mets), creatinine (baseline before chemo which is often nephrotoxic), total protein and albumin (measure of overall health and nutrition) LDH (measure of distant metastases, part of staging, poor prognosis) CXR/CT of lungs for metastasis MRI of brain in patients with evidence of distant metastases (esp if on IL-2 therapy) PET Scans (not indicated for stages I and II)- good for patients with known nodal involvement or satellite migration Biopsy of suggested lesion- excisional, with 1-2cm margins. Surgical excision or re-excision after biopsy- (if not done, associated with a 40% chance of local recurrence)- based on thickness. Less than 1mm, 1cm margins, 1-4mm, 2cm margins, greater than 4mm- greater than 2cm (usually 3cm). Elective lymph node dissection (ELND)- found only to be useful in patients with thickness 1.2-2mm Sentinel lymph node dissection- currently recommended for those patients with intermediate Breslow thickness (1- 4mm). Complete lymph node dissection (CLND) is recommended for all patients with positive SLND Histologic findings of melanoma: cellular atypia, pleomorphic nuclei, enlarged nucleoli, pagetoid upward growth of melanocytes no longer confined to the basal layer, positive stains for S-100 (highly sensitive, not specific) and HMB45 (higher specificity). Classification Superficial spreading (most common type, prolonged radial growth phase) Nodular sclerosis (second mot common, aggressive vertical growth phase, poorer prognosis) Lentigo maligna- long radial growth phase and good prognosis Acral lentigious melanoma (common in African Americans, Asians, and Hispanics) and appears primarily on palms and soles. Aggressive vertical growth phase, poor prognosis. Treatment Surgical excision and lymph node dissection as discussed above Pharmacologic treatment includes interferon 2a for stage III disease and IL-2 for metastatic melanoma (stage IV) CTLA4 blocker Iplimumab for stage IV

Answer 20

1A: ≤0.1 mm no ulceration, no node, no mets 1B: ≤0.1 mm w/ ulceration, 1-2 mm no ulceration, no node no mets 2A: 1-2 mm with ulceration, 2-4 mm w/o ulceration, no mets, no node 2B: 2-4 mm w/ ulceration, >4mm w/o ulceration, no node, no mets 2C: >4 mm w/ ulceration, no node, no mets 3A: any thickness, 1-3 + nodes, micromets 3B: any thickness 1-3 +nodes, macromets, 3C: any thickness 1-3 + nodes + ulceration, macromets 4: distant mets

Answer 21

HPI: How long, changing (size, color, shape), sun exposure, presence other nevi, FHx Detailed description of lesion: ABCDE, look at LNs and other part of body Do not observe this lesion- excisional unless huge then do incisional bx Know Clark and Breslow Clark Based on level of invasion of dermal layers Breslow Based on depth of invasion, which is vertical height of melanoma from granular layer to area of deepest penetration Histological types matter- explain Superficial spreading Most common Long radial growth phase, delayed vertical growth phase Favorable prognosis Nodular sclerosis Second most common No radial, aggressive vertical, spreads quickly Poorer prognosis Lentigo maligna Long radial Good prognosis Acral lentiginous Palms and soles hands and feet, nail beds Very aggressive vertical and poor prognosis Mets w/u for melanoma: PET scan Role sentinel LN dissection (bx?) in melanoma (for certain ones only- thin, intermediate questionable, deep don’t do it- do PET and if + do complete LN dissection): staging Investigative tx for met dz: IFN and surg resection

Answer 22

Workup History- duration, associated symptoms (especially constitutional), recent illnesses, infection, local trauma, bites, exposure to drugs or antibiotics, travel, vaccination status, social (including sexual contact) Physical exam- characteristics of the lymph node (soft/indurated, compressible/not, mobile/fixed, tender/nontender), accompanying cellulitis or inflammation Acutely infected nodes tend to be large, warm, tender with surrounding erythema and edema. Causative organisms usually S. aureus or group B strep Chronically infected nodes tend to have discrete margins, few signs of inflammation, and be adherent to underlying tissues Nodes associated with malignancy- firm, rubbery, discrete, fixed, tend to be larger than 2cm Lab studies- CBC, LDH (rapid turnover for lymphoma and leukemia), tuberculin skin tests, titers for EBV, CMV, catscratch disease, toxoplasmosis (in general indices of inflammation such as ESR and CRP are non-specific and noncontributory to making the diagnosis) CXR (for hilar adenopathy and to r/o tuberculosis, pneumonia, etc) U/S can help distinguish a node that is difficult to palpate and can distinguish the mass from other anatomic abnormalities (thyroglossal duct cyst, branchial cleft cyst, dermoid cysts). Can also describe as solid, liquid gas, heterogenous, homogenous CT scanning can help assess deep lymph nodes in abdominal and thoracic cavity- can look for other causes of malignancy such as Burkitt’s, neuroblastoma, rhabdosarcoma, 18FDG-PET scanning for Hodgkins and NHL FNA for biopsy, or core needle with CT or U/S guidance Etiologies Immune response to infective agents (bacterial- including mycobacteria, viral, fungal) Inflammatory cells in infections involving the lymph node Collections of neoplastic cells carried to node by lymphatics or blood vessels (distant metastasis) Neoplastic proliferation of lymphocytes or macrophages (leukemia or lymphoma-HL, NHL, Burkitts) Collections of macrophages filled with metabolite deposits (storage diseases, granulomas) Kawasaki disease, Langerhans cells histiocytosis, SLE Treatment of lymphoma HL- MOPP (mechlorethamine (nitrogen mustard), vincristine (oncovarin), procarbazine, and prednisolone) or ABVD (Adriamycin, bleomycin, vinblastine, dacarbazine). ABVD causes less infertility than MOPP, but bleomycin can cause fatal pulmonary toxicity. For advanced stages use chemotherapy in conjunction with radiation NHL- CHOP- (cyclophosphamide, hydroxydaunorubicin, vincristine, and prednisolone. May use radioimmunotherapy using anti-CD20. Aggressive B cell lymphomas (DLBCL, burkitts, mantle cell lymphoma, lymphoblastic lymphoma/ALL)- systemic chemotherapy followed by radiotherapy. Rituximab may be added for NHL (anti-CD20) Surgery is very rarely indicated for the treatment of lymphoma due to its systemic nature.

Answer 23

Hx: OLD CARTS, recent illness (f/c), thyroid (radiation exposure, prior cancer, sweats, malaise, weight loss, FHx), trauma PE Know size, location, characteristic of mass Examine thyroid, examine oral and nasal areas Endoscopy- laryngoscopy and exam oro- naso- pharynx Know LN anatomy of neck- all the diff levels Know DDx of both benign and neoplastic Benign: thyroglossal duct cyst, brachial cleft cyst, thyroid nodule, abscess Neoplastic: thyroid cancer, lymphoma, lipoma Workup and staging for lymphoma PE: Most are firm and rubbery, non-hodgkin’s in upper cervical nodes, hodgkin’s in nodes throughout chain Studies Most common sites extranodal involvement in Non-Hodgkin’s in head and neck (Waldeyer’s tonsillar ring, nasal cavity, paranasal sinuses, orbit and salivary glands) Endoscopy to r/o primary epithelial tumor Biopsy of lymph nodes (tissue dx via bx- FN, core, open excisional) and CT Once dx, chest radiograph, CT abd, bone marrow bx Staging I: Single LN region or single extralymphatic site II: 2+ LN regions same side diaphragm or local involvement extranodal site and 1+ LN regions same side diaphragm III: LN regions or extranodal sites both sides diaphragm IV: Diffuse or disseminated involvement of 1+ distant extranodal organs Indications for splenectomy in lymphoma: Symptomatic splenomegaly Pain from recurrent splenic infarctions Hematologic depression from hypersplenism

Answer 24

Malignancy / DCIS Fibroadenoma Fibrocystic change Cyst Cystic vs. solid? Cyst: cyst, fibrocystic change Solid: fibroadenoma, malignancy / DCIS What imaging modalities? Ultrasound- ddx solid vs cystic mass Mammogram- Used for screening or evaluation of palpable mass. Detects 85% of breast cancers. CT- Used for guiding biopsy. MRI- Detects cancers that mammography misses. How do you make a diagnosis? Core biopsy – for readily palpable masses Excisional biopsy – for masses likely to be cancer Stereotactic biopsy – for non-palpable masses or suspicious microcalcifications What are the surgical options for breast cancer? Lumpectomy with sentinel node biopsy- Contraindicated in multi-centric disease. Radical mastectomy Modified radical mastectomy What is the significance of receptor status? Effects treatment options. Only hormone receptor positive cancers are eligible for treatment with hormonal agents. What are the adjuvant therapies? Hormonal o Tamoxifen – benefit restricted to ER or PR positive tumors o Aromatase inhibitors – used in metastatic hormone receptor positive disease or in combination with tamoxifen for early disease. Radiation o Indicated post lumpectomy o Indicated in patients with 4 or more positive lymph nodes Chemotherapy o Trastuzumab for the treatment of ERBB2 positive breast cancer as part of a regimen with dozorubicin, cyclophosphamide, and paclitaxel

Answer 25

How long been there, growing/changing, asymmetry, painful, nipple discharge, skin changes/rashes Breast hx: Age of menarche, age of first child, age of menopause, birth control, estrogen, FHx, Fibrocystic changes, fibroadenoma (Phalloydes tumor similar), DCIS, cyst (tender, well-circumscribed), breast cancer Dx of cyst via u/s, tx by aspiration PE findings that suggest breast cancer: non-mobile, hard, unilateral, skin changes, nipple discharge, adenopathy Diagnostic tests for suspected breast cancer- mammography, u/s, bx If breast cancer confirmed, surg tx- lumpectomy, sentinel LN bx, radiation, chemotherapy If considering hormonal tx, what are the considerations- est or prog +, pre- or post- menopausal Pre- or post- menopausal imp bc Tamoxifen can be used in both groups and aromatase inhibitors can only be used in post. Both take away estrogen but aromatase inhibitors don’t work in pre. Chemo for breast cancer pts, what are your considerations? Chemo given when + LNs, mets, if ER PR – (chemo only option), menopausal status, size of tumor

Answer 26

LUQ or epigastric pain that may radiate to back. May improve by leaning forward. n/v low grade fever tachypnea Abdomen is tender with guarding but no rebound. Retroperitoneal fluid Cullen (periumbical ecchymosis) and Grey-Turner (flank ecchymosis) signs are indicative of sever hemorrhagic pancreatitis. Elevated amylase – not seen in chronic pancreatitis Elevated lipase AXR – sentinel loop sign ( distention and/or air fluid levels near a site of abdominal distention. In pancreatitis it is secondary to pancreatitis associated ileus) What prognostic criteria are helpful? Ranson’s Criteria – predicts risk of mortality o On admission Age>55 Bloodsugar>200 WBC >16,000 Serum glutamic oxaloacetic transaminase (SGOT) > 250 LDH>700 o After 48 hours DropinHct>10% IncreaseinBUN>5 Ca4 Fluiddeficit>6 o # of risk factors above predict mortality 6 risk factors 70-100% What is the initial therapy? Hydration Electrolyte monitoring NG Tube for severe disease with vomiting NPO Abx if infection is identified What are the indications for surgery? Secondary infected necrosis Correction of associated biliary tract disease Progressive deterioration despite medical care

Answer 27

DDx: acute pancreatitis, pancreatic cancer, cholangitis Etiology for acute pancreatitis “ I GET SMASHED” Idiopathic, gallstones, ethanol, trauma, steroids, mumps, autoimmune, scorpion, hypertriglyceridemia, ERCP, drugs Know Ranson’s criteria At dx Age > 55 WBC > 16000 Glucose > 200 AST > 250 LDH > 350 At 48 hours Calcium 10% Hypoxemia with PO2 5 mg/dl Base deficit > 4 Sequestration of fluids > 6L Tx for pancreatitis: conservative management (NPO/bowel rest/IVF, NGT, foley) Indications for surgery for pancreatitis: necrosis, infxn, hemorrhagic, biliary pancreatitis (so can take gallstones out that are causing the problems)`

Answer 28

How do you work up painless jaundice or bilary obstruction? 1. HPI: Weight loss, diarrhea, recent onset of diabetes may indicate cancer. History of hemolytic anemia or blood transfusion may cause non-obstructive painless jaundice. 2. PE:. Courviosier’s sign in chronic progressive biliary obstruction rather than acute choledocolithiasis. 3. LFT: Alk phos elevation indicates biliary tract inflammation. Elevated direct bilirubin in obstructive jaundice. Elevated indirect bilirubin in non-obstructive jaundice. 4. US and CT 5. ERCP: If tumor is visualized, it can be biopsied. Can also perform a sphincterotomy to relieve obstruction at the ampulla of vater. How do you diagnose and treat a pancreatic mass? Dx o ERCP can diagnose peri-ampullary lesions and treat biliary obstruction. o CT can localize lesion for biopsy. Tx o Resectable tumors: Whipple with adjuvant chemoradiation o Unresectable (180` abutment of SMA, abutment of celiac axis, occlusion of portal vein or SMV): Palliative treatment of biliary obstruction, duodenal obstruction or chemical splanchiectomy. How do you do a Whipple resection? Remove gallbladder, CBD, antrum of stomach, duodenum, proximal jejunum and hed of pancreas. See Mingle for technical details. What makes a periampullary cancer unresectable? 180` abutment of SMA, abutment of celiac axis, occlusion of portal vein or SMV What palliative procedures can you perform? Treatment of biliary obstruction, duodenal obstruction or chemical splanchiectomy for pain control. How do you treat gallbladder cancer? Tumor confined to gallbladder mucosa: Cholecystectomy Tumor involving muscularis or serosa: radical cholecystectomy, wedge resection of overlying liver, and lymph node dissection Tumor involving liver: palliative measures such as decompression of proximal biliary tree or a bypass procedure of the obstructed duodenum

Answer 29

DDx: pancreatic cancer, hepatocellular carcinoma, cholangiocarcinoma, hepatitis, choledocolithiasis (benign ones down on list) W/u: CT, ERCP, u/s Tx pancreatic cancer: Whipple, if unresectable palliation, bypass, ERCP c stent Tx GB cancer: cholecystectomy (if just mucosa), cholecystectomy c wedge resection of liver, too (if invades submucosa, too)

Answer 30

What is the differential diagnosis of an anterior neck mass? Thyroglossal duct cyst, thyroid carcinoma, thyroid nodule, thyroiditis, goiter, laryngeal carcinoma, lymphoma, infection of the anterior neck space. If this is a thyroid mass, how do you work it up? US: cystic vs solid FNA: differentiate between cancer and benign nodule What are the different types of thyroid cancer? Papillary Follicular Medullary anaplastic What treatment do you recommend for papillary cancer? Total thyroidectomy – most patients Lobectomy with isthmusectomy – only for low risk patients with tumor

Answer 31

DDx: LN, thyroid, congenital cysts, soft tissue masses Upon PE: 3 cm firm nodule appears to involve L lobe thyroid Know risks for malignancy: cold nodule, radiation hx, family hx (MENs syndromes, LAD, fixation of mass, hoarseness) Know at least 2 studies useful for isolated thyroid nodules and know value of abnormal Know serum thyroid levels, u/s (looks for isolated vs multiple, looks for LNs, too), radioactive scans (hot vs cold), CT scan, FNA Know 3 most common types of thyroid cancer and typical pathways of spread: Papillary, follicular, medullary Papillary – associated w/prior exposure to ionizing radiation, well behaved tumors that spread to cervical lymph nodes but have a good prognosis; appear as cold masses on scintiscans and demonstrate Orphan Annie cells on FNA Follicular – associated w/dietary iodine deficiencies, likes to metastasize hematogenously and prognosis is dependent on extent of invasion; appears as cold mass on scintiscan and demonstrates follicular cells on FNA Medullary – associated w/MEN 2A or 2B syndrome, comes from parafollicular C-cells and secretes calcitonin; those associated w/congenital syndromes metastasize wider and earlier; appears as a cold mass on scintiscan and amyloid is present on FNA What are the important adjacent structures to avoid in thyroidectomy: recurrent laryngeal, superior laryngeal, parathyroids, trachea When do you do a complete thyroidectomy for pt c unilateral cancer? No clean margins, MEN syndrome, multifocal, large tumor Benefit of complete thyroidectomy: recurrence lower, can also tx c radioactive iodine Drawbacks of complete thyroidectomy: life time hormonal replacement, life time trach (injury to both laryngeal nerves)

Answer 32

In a cirrhotic patient with a liver mass, what are you most concerned about? Hepatocellular carcinoma How do you make the diagnosis? Symptoms: o RUQ pain o Weight loss o May be associated with malaise, anorexia, abdominal pain Signs: o Hepatomegaly o Ascites, o Periumbilical ecchymosis (Cullen’s sign) o Flank ecchymosis (Turner’s sign) Labs: o Alpha fetoprotein o LFTs o Alpha-1 antitrypsin Imaging: o Ultrasound o MRI o CT Biopsy o Fine needle aspiration How do you assess his perioperative risk? Standard for assessing perioperative morbidity and mortality in patients with cirrhosis has been the Child-Turcotte- Pugh (CTP) scoring system, which is based on the patient's serum bilirubin and albumin levels, prothrombin time, and severity of encephalopathy and ascites Child Class A: 5 to 6 points o Life expectancy: 15 to 20 years o Abdominal surgery peri-operative mortality: 10% Child Class B: 7 to 9 points o Indicated for liver transplantation evaluation o Abdominal surgery peri-operative mortality: 30% Child Class C: 10 to 15 points o Life expectancy: 1 to 3 years o Abdominal surgery peri-operative mortality: 82% When do you recommend resection vs. transplantation? Hepatic resection beneficial with small solitary lesion with good liver function Liver transplantation if advanced liver dysfunction, solitary tumor

Answer 33

Encephalopathy, ascites, bili (2-3), albumin (3.5-2.8), PT (4-6)

Answer 34

HPI DDx: hepatocellular carcinoma, hepatitis, worsening of cirrhosis Also hepatic adenoma Mets W/u: CBC, renal panel, LFTs, lipase, amylase, UA, AFP (Alpha-fetoprotein dx for hepatocellular carcinoma, will be off charts- 20,000-25,000), CEA, CA19-9, u/s, abd + pelv CT, If mass on u/s or CT, bx Pts c cirrhosis- for surg risk know Child classification (need to know nutritional assessment to calc score) According to NMS, Child’s classification determines operative risk of a shunting procedure in pt c portal HTN. Categories include bili, albumin, ascites, encephalopathy, nutrition Operative mortality rate A (5-6): 2% B (7-9): 10% C (10-15): 50% Pt receives points depending on values of 5 categories- albumin, bilirubin, PT, ascites, encephalopathy Depending on score, pt placed in class A-C, which predicts prognosis of pt Tx hepatocellular CA: resection, transplantation (for bridging to get them to transplant for liver failure- tx c chemo- intraarterial embolization- cryoablation, radio frequency ablation of alcohol injection) Hepatocellular CA Most common primary malignant liver tumor. Solitary or multiple, local invasion (diaphragm) as well as distant mets (lung) Incidence: M:F 2:1, 50 y/o Associations: HBC, HCV, cirrhosis, hemochromatosis, parasites, carcinogens Clinical presentation: HPI: Small- asymp, larger- RUQ pain, jaundice, malaise, f PE: hepatomegaly, weight loss, cirrhosis findings, hemorrhage, paraneoplastic (Cushing’s) Dx: LFTs, AFP, CT and MRI c IV contrast, u/s > 2cm Tx: Surgery- resect, transplantation Chemo- administration of drugs into hepatic artery Combination therapy- chemoembolization (embolizing arterial supply tumor c chemotherapeutic agents mixed c thrombus), local ablation (instillation absolute ethanol into lesion or insertion of probe and delivery of radio frequency energy into lesion) may be palliative for unresectable lesions. Both cause local necrosis of tumor and combo may improve survival.

Answer 35

Biliary colic Cholecystitis Choledocholithiasis Cholangitis Gastritis Peptic ulcer Hepatitis Pancreatitis Pyelonephritis Pancreatic CA/hepatic CA/gastric CA/cholangio CA Gastroenteritis MI Pneumonia (right lower lobe) How do you diagnose biliary colic? Symptoms: o Severe right upper quadrant or epigastric pain that can radiate to the back, right scapula or shoulder o Pain waxes and wanes in intensity o May be associated with fever, nausea, vomiting, fatty meals Labs: o CBC, LFTs, amylase and lipase Imaging: o Ultrasound o HIDA o ERCP o CT What is biliary dyskinesia? Biliary dyskinesia is a motility disorder that affects the gallbladder and sphincter of Oddi. Patients with this condition present with biliary-type pain, and investigations show no evidence of gallstones.

Answer 36

HPI PE (remember vitals) DDx: Biliary colic (gallstones) bc lab nl, symptomatic cholelithiasis, cholangiocarcinoma, biliary dyskinesia W/u: CBC, renal panel, LFTs, amylase, lipase, UA, pregnancy, u/s (r/o cholecystitis), CT abd, HIDA scan (to see that GB functioning properly) Know anatomy of GB- arterial supply off aorta c variations. Extrahepatic biliary tree Ducts of Luschka R and L hepatic ducts common hepatic duct Cystic duct Variations consists of abnormal connections c common hepatic duct and accessory hepatic ducts CBD CBD and pancreatic duct enter duodenum/ampulla of Vater in 3 configurations GB: Fundus (ant), body (storage), infundibulum (post), neck Arterial supply Cystic artery 95% time branch of R hepatic artery that passes behind cystic duct Can arise from R hepatic artery outside Calot’s triangle Can arise from L hepatic artery Can arise from proper hepatic artery Can arise from gastroduodenal artery Can arise from celiac trunk Can arise from abnormal R hepatic (from SMA) Can have double (both from R hepatic, one from R hepatic other from gastroduodenal, both from abnormal R hepatic from SMA) Triangle of Calot: cystic duct, common hepatic duct and inferior border of liver c cystic artery within the triangle Biliary dyskinesia: Abnl contraction of GB. Dx via HIDA EF

Answer 37

``` Symptoms: o RUQ or epigastric pain lasting more than 6 hours o Fever and chills o Nausea and vomiting o Jaundice Signs: o Murphy Sign Labs: o CBC, LFTs, amylase and lipase, CRP Imaging: o Ultrasound o CT o HIDA o ERCP o MRI ```

Answer 38

Leukocytosis present in more than 70% of patients CRP frequently elevated Liver function tests (serum bilirubin, serum alkaline phosphatase, ALT, AST) may be mildly elevated Ultrasound o Thickened gallbladder o Enlarged gallbladder o Pericholecystic fluid collection o Incarcerated gallstone HIDA o Nonvisualized gallbladder with normal uptake and excretion of radioactivity o Rim sign (augmentation of radioactivity around gallbladder fossa) MRI o Pericholecystic high signal o Enlarged gallbladder o Thickened gallbladder wall CT o thickened gallbladder wall o pericholecystic fluid collection o enlarged gallbladder o linear high-density areas in pericholecystic fat tissue

Answer 39

for mild cholecystitis, recommended antimicrobials include o oral fluoroquinolones such as levofloxacin or ciprofloxacin o oral cephalosporins such as cefotiam or cefcapene o first-generation cephalosporin such cefazolin o broad-spectrum penicillin/beta-lactamase inhibitor such as ampicillin-sulbactam for moderate cholecystitis, first-line antimicrobials o broad-spectrum penicillin/beta-lactamase inhibitor such as piperacillin-tazobactam or ampicillin-sulbactam o second-generation cephalosporin such as cefmetazole, cefotiam, oxacephem, flomoxef for severe cholecystitis, initial antibiotic options: third/fourth-generation cephalosporins such as cefoperazone/sulbactam, ceftriaxone, ceftazidime, cefepime, cefozopran OR aztreonam + metronidazole when anaerobic bacteria are detected or expected to coexist secondary options: fluoroquinolones such as ciprofloxacin, levofloxacin, pazufloxacin, and metronidazole (when anaerobic bacteria are detected or expected to coexist) OR carbapenems such as meropenem, imipenem-cilastatin, panipenem/betamipron

Answer 40

Chronic cholecystitis Cholelithiasis (biliary colic) HPI: Risks- fat, female, forty, fertile Usually asymp. If symp- RUQ pain worse after eating (especially fatty food). Studies U/s (acoustic shadow- headlight, gravity-dependent movement gallstones), plain film Tx Asymp: surgery usually not indication (exceptions) Symp: lap chole, medical Acute calculous cholecystitis Inflammation GB usually 2/2 obstruction cystic duct by gallstones HPI: Pain > 3 hrs, f, n/v, anorexia PE: Murphy’s, sonographic Murphy’s Dx: Labs: CBC, LFTs, amylase, lipase, UA Imaging: U/s (inflammation wall > 4mm, pericholecystic fluid, stones in GB, dilation CBD if stone passed), HIDA (radionucleotide scan c Technetium-99m labeled iminodiacetic acid injected IV into hepatocytes. Nl GB visualized w/in hour) Tx: NPO, IVF, IV abx, IV analgesia, chole w/in 24-48 hrs (lap or open) Acalculous cholecystitis Biliary stasis. No stones. 10% cases of acute cholecystitis ICU pts, TPN Choledocolithiasis Studies: ERCP, endoscopic u/s, transabdominal u/s Tx: ERCP or CBD open surgically Ascending cholangitis HPI: f/c, n/v, jaundice, altered mental status, septic shock Dx CBC, LFTs U/s (dilation CBD and intrahepatic bile ducts) Tx If stable- conservative (NPO, IVF, abx) c definitive tx later If in shock- ERCP/percutaneous transhepatic cholangiography (PTC). If unsuccessful, intraop decompression c T-tube placement Sclerosing cholangitis Gallstone pancreatitis Hepatitis HPI: Illicit drug use, sexual practices, blood, travel Studies: LFTs, serology HCC Acute pancreatitis HPI: EtOH, gallstones, pain radiating to back Studies: Lipase, amylase Gastroenteritis HPI: Diet, anorexia Appendix Studies: CBC, CT Pyelonephritis HPI: Kidney stones, kidney surgery, catherization, DM, pregnancy. F/c, flank pain, CVA tenderness, hematuria Studies: UA Leukocyte esterase, WBC casts, nitrite UTI Nephrolithiasis Lower lobe pneumonia HPI: cough, sputum, fever, SOB, hx of pulm conditions, smoking PE: Breath sounds Studies: CBC, CXR Angina HPI: Cardiac hx, chest pain, SOB upon exertion PE: Heart sounds Studies: Cardiac enzymes, EKG and CXR Ulcers HPI: Pre- vs post- prandial pain and relief EUrease breath test, serology, endoscopy c bx

Answer 41

Pertinent hx to narrow DDx Association c food Worse or better, f/c, bm, recurrent, etc. Physical findings Murphy’s: Stop of insp upon palp RUQ Jaundice Rebound, guarding Breath sounds for pneumonia Kidney symptoms, appendicitis Labs and dx studies and why Lipase (pancreatitis) CBC (infxn) LFTs CXR UA U/s Sources of alk phos and how to determine source if elevated Bone, bilary GGT Fractionation Upon heating, isozymes diff levels of activity Pathophysiology of gallstone formation Supersaturation of bile c cholesterol or bilirubin salts predisposes stone formation, which can be made of cholesterol monohydrate stone (crystallizes when bile supersaturated) or bilirubin calcium salt Cholesterol Supersaturation, nucleation, stasis and mucus trapping Types of gallstones and risk factors each type Cholesterol Risks: Native American, industrialized societies, age, fat, fertile, forty, female, estrogens, pregnancy, rapid weight loss, hyperlipidemia syndromes Pigmented Risks: Asians, chronic hemolytic syndromes, biliary tract infections (bacterial microbial beta-glucuronidases that hydrolyze bilirubin glucuronides), ileal dz, CF c panc insufficiency Significance of inc bili and/or dilation intra- and extra- hepatic bile ducts and how to approach DDx: choledocolithiasis, cancer or stricture (from pancreatitis) ERCP see stone or strictures (can remove stone)

Answer 42

In a non-cirrhotic woman with a liver mass, what is differential diagnosis? Liver hemangioma Focal nodular hyperplasia Hepatic adenoma How do you work it up? History Physical Labs Imaging Biopsy Liver hemangioma o Most are asymptomatic, may present with pain o Usually a normal physical exam and found on imaging only o Usually appears as a solitary lesion o Ultrasound: usually shows well-defined, homogenous, hyperechoic lesions o CT: usually shows well-defined, homogenous hypodense lesions o Biopsy: histology characterized by vascular blood-filled spaces line by endothelium and separated by fibrous septa Focal nodular hyperplasia o Usually asymptomatic, rarely abdominal pain o Rarely palpable abdominal mass, non-tender o LFTs are usually normal o CT shows well-circumscribed mass of low density o Arteriogram shows hypervascular mass o Normal uptake on liver nuclear scan o Biopsy: single or multiple lesions with nodular appearance, central scar with radiating septa on cut section, hyperplastic hepatocytes with inflammatory cells, bile duct epithelium prominent Hepatic adenoma o Usually asymptomatic, RUQ fullness, 25% palpable mass or abdominal pain o Abdominal tenderness if there is hemorrhaging o Associated with oral contraceptives and anabolic steroids o Normal AFP o Normal LFT o CT hepatic mass, liver scan cold spot, ultrasound, angiography o Biopsy with fine needle aspiration o Soft, sharply circumcised edges, no true capsule What are the different histologic findings between adenoma and FNH? Hepatic adenoma o Sheets of normal to slightly atypical hepatocytes which are frequently vacuolated. Only an occasional fibrous septum traverses lesion. No bile ducts or Kupffer cells. FNH o Single or multiple lesions with nodular appearance, central scar with radiating septa on cut section, hyperplastic hepatocytes with inflammatory cells, bile duct epithelium prominent What is the treatment for adenoma? Stop oral contraceptives and anabolic steroids Surgical removal to prevent rupture o if large and superficial or pregnancy anticipated If spontaneous rupture with hemorrhage o surgery when stable o hepatic artery ligation - if liver not cirrhotic o hepatic resection - high mortality when acute, elective resection later o if very unstable - open packing or angiographic embolization of hepatic artery may control hemorrhage

Answer 43

The liver is divided into three functional lobes: the right lobe, the left lobe, and the caudate lobe. The right and left lobes are further divided into 2 segments each: The anterior and posterior segments of the right lobe. The medial and lateral segments of the left lobe. Look at photo.

Answer 44

Work-up: CBC, Complete Metabolic Panel, Lactate Dehydrogenase, ultrasound Lab and imaging findings: leukocytosis, increased bilirubin, AST, ALT, Alk Phos, BUN, Creatinine, Glucose, LDH Options to relieve: if stable make NPO, IVF and antibiotics with definitive treatment later. If in shock: ERCP or percutaneous transhepatic cholangiography. If unsuccessful, intraoperative decompression with T-tube placement

Answer 45

If the patient will be NPO for more than 7 days. Patients with severe illness who will be unable to eat for approximately more than 7 days should receive nutritional support earlier because it takes several days for nutritional support to take effect, it is more effective to begin such support if there is any question of nutritional deficit rather than to wait until there is a severe deficit to correct. If there are increased risk of complications of the planned surgery, if intervention will help (i.e. 7-10 days of nutritional support may decrease post-op complications and infections). Also, patients with enterocutaneous fistulas, short bowel syndrome or prolonged ileus Nutritional requirement calculations: Total Energy Requirement is the BEE x Activity Factor x Stress Factor where BEE can be calculated using the Harris-Benedict Equation or the estimated BEE shown below. -Harris-Benedict Equation: IDEAL body weight is in kg, height in cm, age -Male: 66 + (13.7 x W) + (5 x H) – (6.8 x A) - Female: 655 + (9.6 x W) + (1.8 x H) – (4.7 x A) PLUS: 0.8 to 1 gram protein/kg/day -Estimated BEE: 30 cal/kg/day in adults PLUS 0.8 to 1 gram protein/kg/day

Answer 46

Enteral: less defined, more difficult to maintain, less expensive, less infection and complication Parenteral: well-defined, easy to initiate, assured delivery, costly, unused gut SEs

Answer 47

In starvation the secretion of insulin is decreased in response to a reduced intake of carbohydrates. Instead fat and protein stores are catabolised to produce energy. This results in an intracellular loss of electrolytes, in particular phosphate. Malnourished patients' intracellular phosphate stores can be depleted despite normal serum phosphate concentrations. When they start to feed a sudden shift from fat to carbohydrate metabolism occurs and secretion of insulin increases. This stimulates cellularuptake of phosphate, which can lead to profound hypophosphataemia.This phenomenon usually occurs within four days of starting to feed again. Serum phosphate concentrations of less than 0.50 mmol/l (normal range 0.85-1.40 mmol/l) can produce the clinical features of refeeding syndrome, which include rhabdomyolysis, leucocyte dysfunction, respiratory failure, cardiac failure, hypotension, arrhythmias, seizures, coma, and sudden death

Answer 48

Nl: 20-25 kcal/kg/day non-protein calories (protein cals 1 g/kg/day) Trauma pts: 20-40% Postop feeding options for this pts: J tube c tube feeds, TPN Complications of TPN (sepsis, acalculous cholecystitis, fatty liver) Pt c pancreatic leak, what are your options: Conservative manangement (NPO, TPN), somatostatin Define refeeding syndrome and how to prevent it Starvation leads to decreased insulin secretion as body utilizes fats and protein instead of carbs, resulting in intracellular loss of electrolytes, particularly phosphate. When nutrition resumed, there’s a sudden shift to carb metabolism and a rush of insulin stimulates cellular uptake of phosphate, leading to symptoms of hypophosphatemia (rhabdo, leukocyte dysfunction, resp failure, cardiac failure, hypotension, arrhythmias, seizures, coma and sudden death). Prevent this by using a low caloric diet initially and correcting electrolyte imbalances slowly How do you determine nutritional optimization Albumin Pre-albumin Nitrogen balance What if pt on vent- metabolic cart

Answer 49

Nl albumin > 4 and prealbumin > 16 How to optimize status preop? Inc protein (protein shakes), vitamins, supplements, nutritional consults, calorie count Complication if fail to optimize them? Poor wound healing, dehiscence, break down of anastomosis

Answer 50

Assessment: albumin levels (which helps you evaluate nutrition in the past few months), prealbumin (helps evaluate nutrition in the past 1-2 weeks) and C-reactive protein (helpful to assess inflammatory state) Also look at history and PE findings: >15% weight loss, anorexia, organ failure, cancer, HIV, sepsis. Temporal wasting, tricep skin fold, enlarged liver, ascites, ileostomy, prior bowel resection. Routes of supplementation for cachectic patients: enteral or parenteral TPN: Na (40-50 mEq/L), K (40 mEq/L), Cl (50 mEq/L), Mg (4-6 mEq/L), Ca (2.5-5.0 mEq/L), HPO (20-25 mmol/L), and acetate (40 to 60 mEq/L), and other additives including P, Folic Acid, Vitamin B, C, D, K, micronutrients, amino acids, lipids. Contents important for wound healing: vitamin C, micronutrients (zinc, copper, chromium, selenium, manganese), amino acids.

Answer 51

Do an initial assessment for trauma: Mechanism of injury- C-spine, and then ABCDE A: airway: make sure patent B: breathing: B/L breath sounds C: circulation: pulses If patient doesn’t respond to initial resuscitation (i.e. 2 L crystalloids) start blood Places of hemorrhage: chest, abdomen, pelvis, thigh and external. Use vitals, FAST, CXR, labs and CT to determine whether bleeding is occurring and where. Common sourves of intraabodominal bleeding are the spleen and liver.

Answer 52

Possible injuries - Traumatic brain injury, diffuse axonal injury o Brain MRI (CT less sensitive) o Tx – controlling ICP - Vascular injury o Kidney/spleen/small & large intestines – sheering of points of attachment to the retroperitneum and of pedicle vasculature. o Thoracic aorta injury – from compression onto bony structures and torsion; usually fatal o Superior mesenteric artery – intestinal loops that stretch may tear the mesenteric attachments injuring the SMA Diagnoses and Treatment - Diagnoses – history, clinically, FAST, DPL, exploratory lapraotomy - Treatment – resuscitation followed by lapraotomy and repair of damage vessel Signs of vascular injury - Pain - Paralysis - Pallor - Paresthesia - Poikilothermia – cold - Pulselessness Diagnoses - Clinically – the 6P’s although pain and paresthesia are the two most reliable indicators. Pulselessness is rarely present. Paresthesia and paralysis are late symptoms. May have tense/swollen shiny skin with bruising. - Direct compartment pressure measurement – transducer with catheter introduced into the compartment to be measured. Most accurate method of measuring compartment pressure and diagnosising compartment syndrome.

Answer 53

Start blood.

Answer 54

Management of thoraco-abdominal penetrating injuries. 1) ABCs o Airway 100%oxygenbag+mask IntubationGCS Breathing circulation: Hemodynamics Pulses,capillaryrefills,coldextremities Fluid resuscitation with LR or crystalloids infused through two large bore IVs Foley for measuring UOP . Cricothyroidotomy if intubation not feasible because of C-spine injury or laryngeal obstruction. 2) CXR – signs of pneumothorax/effusion; widening mediastinum 3) FAST – pericardial/intraperitoneal bleeding 4) Exploratory lapraotomy/thoracotomy – hemodynamically unstable despite resuscitation, signs of peritonitis, tamponade, hemothorax Life threatening injuries and treatments - Pneumothorax/Tension pneumothorax o Needle thoracostomy o Tube thoracostomy - Hemothorax o Tube thoracostomy - Cardiac tomaponade o Pericardiocentesis or pericardial window to drain and assess for presence of blood o Median sternotomy to treat cardiac injury - Splenic injury o Stable patient – nonoperative managmenet o Unstable patient – splenectomy or splenorrhapy - Large vessel injury o Emergent thoracotomy with cross clamping of vessels (e.g cross clamp descending aorta in patients with intra-abdominal bleeds and cannot maintain BP; cross clamping aorta in patient with subclavian arterial injury). o Internal cardiac massage in absence of pulse or cardiac activity. - Small/Large bowel/mesentary o Laparotomy Indications for ED thoracotomy - Penetrating traumatic cardiac arrest o Persistent BP

Answer 55

Management - Airway o Inhalation injury – requires intubation (can cause laryngeal edema); look for signs of inhalation injury (red oropharynx, facial/upper torso burns) o CO poisoning – assess COhgb (>30% may indicate significant CNS dysfunction, >60% may cause coma/death). o Smoke inhalation – can cause chemical injury to alveolar basement, pulmonary edema; can also lead to secondary infection (bronchopneumonia) - Resuscitation o Patients with 80% TBSA, or pediatric burns usually require larger fluid requirements than calculated o Urinary output Assessadequacyoffluidresuscitation UOPshouldnotbeinexcessunlesstotreatmyoglobinuria - Calculate burn area o Rule of nines Adults–9%head,18%frontoftorso,18%backoftorso,9%eacharm,9%eachleg. Keep in mind, only applies to 2nd, 3rd, and 4th degree burns. 1st degree burns are not counted. So if patient has 10% first degree burns, 15% second, 15% third, the TBSA is only 30%. - Wound coverings o Antimicrobial topical Silver sulfadizine – does not penetrate eschar so not helpful in already infected burn; more preventative; side effect is leukopenia Sulfamylon – penetrates eschar and useful for full-=thickenes infected burns - side effect is carbonic anhydrase inhibitor causing metabolic acidosis, painful application Acticoat–broadspectrumanti-microbialdressing Pigskin–coverflatcleanwounds o Grafts – autograft, allograft, exnograft, artificial, cultured. - Skin debridement o Allows for quicker healing o Decreases infection Treating circumferential burns - Escharotomy to prevent compartment syndrome Complications of burn wounds - Renal failure for hypovolemia - Gi bleed for curlings ulcer - Burn wound sepsis (give a tetanus shot) - Progressive pulmonary insufficiency - Burn scar o Avoid exposure to sunlight o Contractures/hypertrophic scar formation o Marjolin’s ulcer (ulcerating squamous cell carcinoma) o Destruction of skin appendages requires creams/lotions to prevent drying/racking.

Answer 56

singed hair, carbonaceous sputum, altered mental status, ABG c carboxyhemoglobin

Answer 57

Management – mostly same as in question 36 except with some special types of injury. Usually mandates more fluid resuscitation than calculated. - Types of injuries o Current injury Due to heat generated as it flows through tissues Moresevereintissuewithhighresistance(bone>fat>tendon>skin>muscle>vessel>nerves). o Vascular injury - thrombosis o Cardiac injury Atrial/ventricular arrhythmias ImmediatelygetanEKG o Renal injury Due to hemoglobin/myoglobin deposits in renal tubules. Alkalinze urine to keep hemoglobin and myoglobin in more soluble state. o Fractures Tetanic muscle contraction cause bone fractures especially in spine o Neuro/Spinal cord injury Demyelination Cancauseseizures Canbesecondaryfromfracture - Factors to consider o Type of circuit o V oltage of circuit o Resistance offered by body o Amperage of current flowing through tissue o Pathway of current through body o Duration of contact. Significant muscular injury - Excessive myoglobinuria can lead to renal failure. Treat with HCO3 to alkalinze urine and solubilize myoglobin.

Answer 58

Myoglobinuria

Answer 59

Ulcer prophylaxis, DVT prophylaxis, fluid, | tetanus (burns and trauma)

Answer 60

Alkalinize urine, fluid resus, mannitol (to push kidney).

Answer 61

Pain, impaired ambulation, tiredness, cramping, most commonly in the calves which occurs after physical exertion of the affected muscles over an extended period of time. Pain is relieved by resting the effected muscles. Can also get hair loss, exertion dependant rubor, loss of sensation, shiny skin if it is chronic. Ankle brachial index first, Doppler. Normal abi is more than 1.0. Mild claudication 0.6-0.8. Initial treatment for mild claudication is exercise, which develops collateral circulation. Smoking cessation and statins helpful. If worsens revascularization via av graft or amputation may be necessary depending on the degree of ischemia. If there is absence of a femoral pulse, aortoiliac disease. This is typically more progressive, and will require balloon dilation, stent placement, av graft. If pt. returns after initial workup with ulceration, must determine if there is sufficient flow to heal ulcer. In diabetics, get toe bp. Repeat abi. Arteriogram to assess location and formulate revascularization plan. If ulcer is unable to be reperfused, amputation likely necessary. Tx for specific levels of occlusion- superficial femoral artery: saphenous vein graft, iliac artery: balloon dilation/stent placement, superficial femoral and/or popliteal: femoropopliteal bypass.

Answer 62

Embolus (usually concurrent with pvd), compartment syndrome,

Answer 63

Severe ischemia is almost always an embolic event. Time is critical. Revascularization after more than 6 hrs can result in permanent impairment. Initiate heparin therapy immediately, and proceed with urgent operative therapy. Thrombolysis, preoperative angiogram will delay the tx without modifying its need, and should not be performed in most cases. Thrombolysis with tpa or ultrasound are other options that can be considered in certain cases where the ischemia is not severe enough to threaten function. Compartment syndrome will have sensory and motor deficits, and present with an inciting event such as trauma or ischemic injury. Tx is fasciotomy. 6 ps of arterial occlusion: pain, pulselessness, paralysis, pallor, paresthesia, poikilothermia.

Answer 64

Scenarios: Ulcer in critical care setting w/coag blood in ng-initiate ppis and/or h2 blockade, scope not necessary. Bright red blood in ng tube- resuscitation w/ 2l ns, cross and match. Scope is necessary here. Duodenal Ulcer c fresh clot: all ulcers maintain ph above 5. Endoscopic hemostasis. Ulcer c white base: no recent bleed, observe for changes. Duodenal ulcer c visible artery at base: or for operative therapy. Ulcer c acute renal failure: platelet dyfn or uremia. Dialysis c mentioned therapies. Gastric varices: cyanoacrylate glue, tips, splenectomy if there is splenic vein thrombosis. Less amenable to tx than esophageal varices.Esophageal varices c cirrhosis: vit k and ffp. Vasopressin or octreatide to lower portal pressure. Endoscopic sclerotherapy. Acute bleeding of varices: 1. Band the bleeding vessels 2. Correct coagulopathy ffp and platelets. 3. Iv octreotide or vasopressin. 4. Repeat endoscopy. 5. Tips if amenable. High morbidity. Can proceed with balloon tamponade alternatively. In all cases- give beta block.

Answer 65

TIA, amaurosis fugax: ophthalmic artery first branch of internal carotid, aphasia, stroke, bruit -procede with carotid Doppler. 70 percent or more stenosis with sx should have endarterectomy. Cardiac evaluation should be performed as well. Risk of perioperative stroke 1-3 percent.

Answer 66

``` Small cell lung cancer: o Central location o Sensitive to chemotherapy o Surgery is not indicated. o Poor prognosis (2 to 4 months from diagnosis to death) Non–small cell lung cancer: o Includes squamous, large cell, and adenocarcinoma o Poor response to chemotherapy o Treated with surgery (debulking) o Prognosis varies with stage ```

Answer 67

ANESTHESIA: The primary functions of the respiratory system are: 1. Ventilation; the movement of air into and out of the lungs. 2. Gas exchange; the transfer of oxygen into the blood and the removal of carbon dioxide. General anesthesia has a number of effects on both of these key functions. The passage of gas into the lungs may be impaired by obstruction of the airway; the drive to ventilation may be reduced or cease altogether; the distribution of gas within the lungs may change and the transfer of oxygen (and anesthetic gases) into the blood may be impaired. Most of these adverse effects can be seen during anesthesia and in many patients these extend into the post-operative period. SEPSIS (ARDS): Acute lung injury caused by inflammatory process in both lungs causing increased permeability of the capillaries and severe V/Q mismatch. These patients are tachypneic and hypoxic and have bilateral crackles on lung exam. The diagnostic criteria are: 1. Bilateral, fluffy infiltrates on chest x-ray; 2. Refractory hypoxemia; 3. No evidence of heart failure (PCWP ≤ 18 mm Hg). The diagnosis requires all three criteria. CAUSES There is a wide variety of causes of ARDS. The most common are: Sepsis (most common), Infectious pneumonia, Blood products, Aspiration, Severe trauma, burns MANAGEMENT It is often necessary to intubate because of hypoxemia. Treat underlying cause. PEEP is often used

Answer 68

DEFINITION: Autosomal dominant inherited hypermetabolic syndrome occurring after exposure to an anesthetic agent (very rare, but life threatening). ETIOLOGY: Impaired reuptake of calcium by sarcoplasmic reticulum in muscles. SIGNS AND SYMPTOMS: Tachycardia, Hyperthermia, Hypercarbia, Hypoxemia, Acidosis, Muscle rigidity, Ventricular dysrhythmias TREATMENT: Discontinue anesthetics, Benzodiazepines (work fastest to control hypermetabolic state). Dantrolene (considered more definitive treatment, but onset of action takes about 30 minutes).

Answer 69

DEFINITIONS -Dysphagia: Difficulty swallowing, occurs when there is obstruction to the passage of food from the mouth to the stomach. Odynophagia: Pain on swallowing. May or may not accompany dysphagia. TYPES -Mechanical: Patient typically reports difficulty swallowing solids more than liquids. -Neuromuscular: Patient typically reports difficulty swallowing both solids and liquids. CAUSES Mechanical -Foreign body -Inflammation (infectious esophagitis, caustic exposure) -Strictures (inflammatory, post-irradiation) -Neoplasms -Extrinsic compression (aortic aneurysm, retropharyngeal abscess, thyromegaly, etc.) Neuromuscular -Tongue paralysis -Lesions of cranial nerves IX and/or X -Disorders of the neuromuscular junction (NMJ) (e.g., myasthenia gravis) -Primary disorders of muscle (e.g., polymyositis, dermatomyositis) -Disorder of esophageal smooth muscle (scleroderma, achalasia, diffuse esohageal spasm)

Answer 70

The source of RBCs in the urine can be anywhere from the kidney glomerulus to the urethral meatus. Causes of hematuria may be generally grouped into the site of origin: glomerular and non-glomerular. Non-glomerular can be subdivided by whether the process is located in the upper urinary tract (kidney and ureter) or the lower urinary tract (bladder and urethra). Glomerular: IgA nephropathy (Berger’s), glomerulonephritis (ie: poststreptococcal, diffuse proliferative, hereditary), RPGN, Alport syndrome Non-glomerular: Upper tract: Urolithiasis, pyelonephritis, renal cell cancer, transitional cell carcinoma, urinary obstruction, benign hematuria Lower tract: Bacterial cystitis, BPH, strenuous exercise, transitional cell carcinoma, spurious hematuria (ie: menses), instrumentation, benign hematuria.

Answer 71

Neurogenic shock refers to diminished tissue perfusion as a result of loss of vasomotor tone to peripheral arterial beds. Loss of vasoconstrictor impulses results in increased vascular capacitance, decreased venous return, and decreased cardiac output. Neurogenic shock is usually due to injuries to the spinal cord from fractures of the cervical or high thoracic vertebrae that disrupt sympathetic regulation of peripheral vascular tone. Occasionally, an injury such as an epidural hematoma impinging on the spinal cord can produce neurogenic shock without an associated vertebral fracture. Penetrating wounds to the spinal cord can produce neurogenic shock as well. The classic findings of neurogenic shock consist of decreased blood pressure associated with bradycardia (absence of reflexive tachycardia due to disrupted sympathetic discharge), warm extremities (loss of peripheral vasoconstriction), motor and sensory deficits indicative of an injury to the spinal cord, and radiographic evidence of a fracture in the vertebral column

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