Download Surgery Study Guide

Surgery Study Guide
Abdominal Hernia
 Hernia – abnormal protrusion of abdominal contents through a defect in the abdominal wall; definitive tx
of hernia is early operative repair
 Anatomy
o Internal (deep) inguinal ring (lateral) – opening in the transversalis fascia halfway between the
ASIS and pubic tubercle
o Inguinal ligament – between pubic tubercle and anterior iliac spine formed by external oblique
aponeurosis
o Lacunar ligament – deep and parallel to inguinal ligament inserts into pubic ramus and
responsible for strangling femoral hernia
o Hesselbach’s triangle – inguinal ligament (inf), epigastric vessels (lateral), and lateral border of
rectus abdominus (medially)
o Nerves of inguinal region
 Iliohypogastric, Ilioinguinal – T12, L1
 IH – suprapubic skin, II – lateral scrotum, medial thigh
o Ilioinguinal – most injured anterior open inguinal repair
 Genitofemoral, lateral femoral cutaneous
 Scrotum, anteromedial and lateral thigh
 May be injured during laparoscopic repair
 Femoral
 Types
o Incarcerated – an “irreducible” hernia whose contents cannot be returned to the abdomen
o Strangulated – compromise to the blood supply of the contents of the sac
o Reducible – contents can be returned to abdomen
o Complete – hernia passes fully into scrotum
o Processus vaginalis – peritoneal extension of accompanying the testis in its descent into the
scrotum
o Inguinal hernia
 Direct – formed by defect in the floor of Hesselbach’s triangle
 Indirect – abdominal contents through inguinal ring through patent processus vaginalis;
internal inguinal ring, superior to inguinal ligament
o Richter hernia – part of bowel wall through defect in anterior abdominal wall
o Obturator hernia – through the obturator canal alongside the obturator vessels; “HowshipRomberg” sign (pain mid-anterior thigh w/ abduction and internal rotation of knee)
o Femoral hernia – highest risk of incarceration and strangulation; inferior to inguinal ligament and
medial to femoral vessels
o Umbilical hernia – improper healing of umbilical scar; simple transverse repair of fascial defect;
females 10x
o Spigelian hernia – lateral to rectus sheath at semilunar line at lower limit of sheath; along
semilunar line (lateral edge rectus @ arcuate line)
o Sliding hernia – one wall of hernia is made up of an intra-adbominal organ, usually sigmoid
o Pantaloon hernia – combination of direct and indirect hernias
o Epigastic hernia – defect in linea alba above umbilicus
o Incisional – most common ventral hernia
o Perineal hernia – pelvic floor
o Peristomal – adjacent to ostomy
 Causes
o Indirect inguinal – congenital internal inguinal ring, goes into scrotum, firm on palpation
o Direct – acquired as result of developing weakness in transversalis fascia in Hesselbach’s triangle,
symmetric, circular at ring while erect, palpation – posterior wall, soft
o Femoral – acquired protrusion of peritoneal sac through femoral ring
 Clinical findings – mostly no symptoms, usually notice a lump, dragging sensation, pain in scrotum,
aching;


o Direct herniae produce fewer symptoms and less likely to incarcerate or strangulate
Treatment
o Operative
 Indirect
 Direct – reinforce floor
 Femoral – pectineal (Cooper’s) ligament repair
 Bilateral repairs can be done w/ low risk of recurrence
 Recurrent hernia – early  inadequate repair; years later  weakening of fascia; repeat
recurrence  collagen disorder
 Marcy repair – simple high ligation of the sac w/ tightening of the internal ring. Useful
in infants and children
 Types
 Bassini – conjoined tendon approximated to Poupart’s ligament. Spermatic cord
remains in normal position under external oblique aponeurosis
 Halsted – external oblique placed beneath cord
 Lotheisson-McVay – femoral hernia repair; Cooper’s ligament sutured to
transversus abdominis aponeurosis/conjoint tendon
 Shouldice – transversalis fascia divided. Imbricated to Poupart’s ligament. Not
widely used
 Laparoscopic repair – higher complications and recurrence rate but pt will
return to work sooner; indicated for bilateral hernias, recurring hernias, and need
to resume full activity as soon as possible
o Pre-operative
 Treat prostatic hyperplasia first since urinary retention and UTI are common after repair
o Incarcerated – attempt reduction, operation, use tension-free reapproximation
o Inguinal – transversus abdominus sutured to Cooper’s ligament or inguinal ligament
Prognosis
o Adults – indirect hernia repair recur in 5-10%; direct 1-18%; use of mesh decreases recurrence by
50-75%
Gallbladder Disease
 Anatomy
o Triangle of Calot – common hepatic duct, cystic duct, and cystic artery (or liver)
o Extrahepatic biliary tree
 Structure
 L and R hepatic ducts  common hepatic duct
 Common hepatic duct + cystic duct  common bile duct
 Common bile duct joins pancreatic duct and enters ampulla of Vater
 Sphincter of Oddi controls bile flow
o Gallbladder – fundus, body, infundibulum, neck
 Cystic artery from right hepatic 75% of time
 Cystic vein  portal veins
 Lymphatic – both to the liver and hilar nodes
 Gallbladder innervation
 Motor – vagal postganglionic celiac ganglia
 Sensory – sympathetic fibers from celiac plexus
 Valves of Heister – mucosal folds in cystic duct
 Functions – store bile, concentration (absorbs water and secretes mucus), and releases
bile (GB contracts, Sphinter of Oddi relaxes)
 Gallstones
o Cholesterol – 75% of gallstones in western countries; 75% of American Indian women over 40 y/o
o Pigment – chronic hemolysis
o 30% of patients w/ cholelithiasis end up with surgery
o Prophylactic surgery if large stone >2cm or calcified gallbladder (increased incidence of cancer)
 Radiologic diagnosis
o Plain abdominal films demonstrates 15% of stones that are opaque and may show porcelain
gallbladder
o Ultrasound – best for evaluating gallstones in GB and intrahepatic ductal dilatation
o HIDA or DISIDA – Cholescintigraphy; best for evaluating cholecystitis, also used for common
bile duct obstruction or leak
o Chalangiagraphy – best for intra- or extrahepatic ductal obstruction; can be done fluroscopically
by ERCP or by MRCP
o CT/MRI – best for hepatic parenchyma
 History and Physical
o Most pts w/ cholelithiasis are asymptomatic
o Biliary colic – pain RUQ radiating to scapula, postprandial, associated w/ nausea or vomiting
o Cholecystitis – implies infection, usually w/ stones, constant pain, fever, and chills
o Choledocholithiasis – stones in CBD, RUQ pain, fever, chills, dark urine, light stools
o Murphy’s sign – arrest of inspiration on deep RUQ palpation as pressure from the examiner’s
hand contacts inflamed gallbladder
o Charcot triad – fever, RUQ pain, jaundice
o Reynold’s pentad – fever, RUQ pain, jaundice, hypotension, mental status change
o Courvoisier’s law – a nontender, palpable gallbladder in a jaundiced patient indicates malignant
common duct obstruction
 Cholecystitis – majority of cases result from calculi, bile stasis, and bacteria
o Chronic – RUQ pain which may radiate to back/scapula, N&V; dx w/ ultrasound; tx surgically w/
elective lap cholecystectomy or medically w/ bile salt therapy (15% of patients are candidates,
takes 2 years, and 50% of stones recur)
o Acute – most causes due to stone in neck or cystic duct; women 30-80 y/o, dx w/ US, CBC,
amylase, liver profile, ECG, CXR, HIDA/DISIDA; tx – immediate surgery w/in 72 hours or IV’s
and antibiotics then sx after 6 weeks
o TX
 Open – right subcostal incision, GB dissected off liver starting at top, cystic duct and
artery divided









Laparoscopic – place 10-mm and 5-mm ports, fill abdominal cavity w/ CO2; GB
dissected form the bottom after cystic duct and artery are divided; conversion rates = 10%
in good hands
 CBD Cholangiogram – suspect CBD stones, biliary tract anatomy unclear
Lap cholecystectomy
o Advantages – cosmetic, short hospital stay, rapid return to activity
o Contraindications – cirrhosis, portal hypertension, pregnancy, generalized peritonitis, prior
surgery, severe cardiopulmonary disease, hypotension esp. d/t hypovolemia
Acalculous cholecystitis – acute or chronic cholecystitis w/o stones; develops as complications of burns,
sepsis, trauma, collagen vascular disease; chronic form is referred to as biliary dyskinesia; causes –
kinking of GB, thrombosis of cystic artery, sphincter spasm, prolonged fasting, dehydration, generalized
sepsis; tx: lap cholecystectomy
Gallstone Ileus – mechanical intestinal obstruction cause by gallstone lodged in lumen; signs- small bowel
obstruction signs, distended abdomen, dx: plain films may help if examiner is aware, pneumobilia is
helpful sign; tx emergency laporotomy and removal of the obstructing stone through a small enterotomy,
examine proximal intestine for second stone, leave GB alone, usually fistulae close spontaneously, elective
cholecystecomy
Bacterial cholangitis – flow is disturbed by partial to complete obstruction which sets up bacterial
infection of the biliary ducts; caused by choledocholitihiasis, biliary stricture, neoplasm; symptoms –
Charcot’s triad; labs: leukocytosis, elevated serum bilirubin and alkaline phosphatase, E. coli most
common; US is helpful and cholangiography is dangerous in this setting; most cases controlled w/
antibiotics, endoscopic sphincerterotomy may be needed
Choledocholithiasis – calculi within the bile ducts; 50% of pts are asymptomatic; CBD may dilate to 2-3
cm proximal to the lesion; fluctuating jaundice; tx w/ lap choly w/ laparoscopic operative cholangiogram
Carcinoma of the gallbladder – most common malignancy of biliary tract, 3x more common in females;
risk factors: gallstones, porcelain gallbladder, adenoma; adenocarcima most common; pts present late w/
weight loss, anorexia; RUQ mass may be felt w/ ascites in advanced cases; tx cholecystecomy w/ hepatic
resection; 5 year survival is 4%
o Staging
 I – mucosa/submucosa
 II – muscle layer of GB
 III – + lymph node or liver extension (<2 cm)
 IV – liver extension (>2cm)
Carcinoma of bile duct – rare; risk factors ulcerative colitis, sclerosing cholangitis, and infection w/
Clonorchis sinensis; RUQ pain, juanice, and pruritis; Couvosier’s sign
Remember
o Cholelithiasis – asymptomatic gallstones w/in the GB
o Biliary colic – symptomatic gallstones causing transient RUQ pain w/o inflammation or infection
o Cholecystitis – inflammation, often infection of the GB
o Choledocholithiasis – stones in common bile duct
o Cholangiitis – infection in the bile ducts extending to the liver
o Courvoisier’s sign – jaundiced patient w/ a palpable nontender GB indicates distal common bile
duct obstruction (Courvoisier’s law)
GI Hemorrhage
 Anatomy
o Portions of stomach
 Cardia – most proximal, gastroesophageal junction
 Fundus – most superior extension, Angle of His
 Body – largest portion, incisura angularis marks beginning of antrum
 Antrum – distal 25%
o Sphincter of the stomach
 Lower esophageal sphincter – physiologic sphincter, high pressure zone of muscular
activity in distal esophagus
 Pylorus – controls flow of food into duodenum
o Blood supply of stomach – complex
o Nervous innervation
 Vagus (parasympathetic)
 Branches (LARP) – left/anterior and right/posterior
o Right first branch – criminal nerve of Grassi which causes recurrent
ulcers when left undivided
 Sympathetic via greater sphlancnic (T5-T10)
o Lympatics – superior/pancreaticolienal/suprapyloric/subpyloric
 Types of GI bleeding
o Hematemesis – vomiting of bright red or “coffee-ground” blood; source is proximal to the
ligament of Treitz
o Hematochezia – passage of bright red blood by rectum, not specific to level
o Melena – passage of black, tarry stools, does not guarantee it is from upper GI
 Identifying source of bleeding
o Fiberoptic endoscopy – only safe w/ stable vital signs
o Upper GI series
o Passage of nasogastric tube
o Angiography and radionuclide scanning
 Pathogenesis of Upper GI – acid-peptic erosion into the submucosal or extraluminal vessels
o Posterior duodenal ulcers dangerous d/t proximity to gastroduodenal and superior
pancreaticoduodenal
o H. pylori – causative agent of duodenal, gastric ulcers and gastritis in 80% of pts not taking
NSAIDs
 Types of Gastric ulcers
o Type 1 – most common, located w/in 2cm of the boundary between parietal cells gastric mucosa,
95% are on the lesser curvature; H. pylori
o Type 2 – duodenal ulcers
o Type 3 – w/in 3cm of pyloris
o Type 4 – adjacent to esophagus
o Type 5 – anywhere due to NSAIDs
 Upper GI – treatment
o Endoscopic therapy
 Bipolar and heater probe therapy – decrease rebleeding rates by 50%
 Lasers generally not used
 Majority of rebleeding occurs within 2-3 days
o Indications for surgery
 Exsanguinating hemorrhage
 Profuse bleeding
 Continued hemorrhage – mortality increases
 Recurrent bleeding
 Pathologic features of bleeding site, e.g. posterior duodenal ulcer, giant gastric ulcer
o Gastric ulcer
 Type 1 – hemigastrectomy, excision of distal 50% of the stomach w/ excision, Billroth I
(stomach  duodenum) or II (stomach  jejunum)

 Type 2 and 3 – vagotomy w/ antrectomy and extension to include excision of ulcer
 Type 4 – antrectomy w/ extension of resection to include ulcer
 Type 5 – stop NSAIDs, primary closure, omental patch, or wedge resection
o Duodenal ulcer – most d/t acid hypersecretion; goal of surgery is to reduce acid via vagotomy w/
antrectomy
Lower GI Bleeding
o Anorectal disease – anal fissure
o Diverticular disease
o Angiodysplasia of colon
o Polyps
o Colon carcinoma
o Inflammatory bowel disease
o Ischemic colitis
o Mechel’s diverticulum
Lung Nodules
 Benign lung disease
o Pulmonary tuberculosis
 Mycobacterium tuberculosis
 Most common path organism seen in lungs
 Spread by aerosolization
 Present w/ necrotizing pneumonia which may go to hilar nodes  caseating
granulomas
 Tx: isoniazid, rifampin, ethmabutol, pyrazinamide
 Indications for surgery include: + sputum and cavitary lesion after > 5 months of
tx, severe hemoptysis, bronchopleural fistula, empyema, lung mass w/ TB,
disease from drug-resistant strain
o Bronchiectasis
 Abnormal dilatation of bronchi from chronic smoldering infection; usually in more distal
bronchial tree
 Presents w/ persistent productive cough, hemoptysis, recurrent pulmonary infections
o Lung abscess
 Etiologies – aspiration, infection distal to occluded bronchi, septic emboli
 Typically resolve w/ medical therapy
 Sx: cavity >2 cm lasting >8 weeks, persistent bacteremia or hemoptysis, or malignancy
suspected
o Massive hemotysis
 >500cc/24hrs
 Mortality >10% resulting from asphyxia rather than exsanguination
 Diagnose and treated w/ bronchoscope
 Balloon catheter or angiographic embolization may be required
 Angio embolization may cause quadriplegia (posterior branch of posterior intercostal
arteries divides into spinal and muscular branches)
o Benign lung tumors
 Hamartoma – most common, usually found incidentally on chest x-ray
 Other – hemangiopericytoma, sclerosing hemangioma, granular cell tumor, fibroma,
lipoma
 Lung Cancer – most common cause of cancer-related deaths in both sexes; etiology: tobacco, hereditary,
environmental (asbestos, radon chromium), genetic (K-ras –NSCLC)
o NSCLC – 80%, most common type is adenocarcinoma; TNM staging
o SCLC – 20%, 2/3 pts present initially w/ disseminated and thus inoperable disease; most common
presentation is pt w/ asymptomatic pulmonary nodule noted incidentally on chest x-ray – assumed
malignant
o Staging (both listed are surgical candidates)
 T1 - <3cm; T1a – no nodes involved
 T2a - <3cm w/ nodes involved
o Mid tracheal lymph nodes important for resection considerations
o Treatment – complex and depends on physical condition of pt, tumor size, lymph node status,
metastases; surgical resection – stage I and II NSCLC’s
o Medical and surgical contraindications to pulmonary resection
 Absolute: MI w/in 3 months, SVC syndrome d/t mets, bilateral endobronchial tumor,
contralateral lymph node metastases, malignant pleural effusion, scalene node mets,
FEV1 <0.8 L,
 Relative – MI w/in 6 months, Horner’s syndrome, small cell histology, main pulmonary
artery involvement, pericardial involvement, recurrent laryngeal nerve paralysis d/t
primary tumor in aorticopulmonary window, FEV1 <50% <0.8L, issuffienct pulmonary
reserve
 Chemotherapy and radiation therapy – not indicated for stage IA dz, all other stages
should be referred to oncologist



The pathological stage of a patient’s tumor is the best predictor of survival with lymph
node status have the greatest effect on long-term survival
o Small cell lung cancers (SCLC)
 Present on imaging as bulky mediastinal lymphadenopathy and are assumed metastatic
 Tx w/ chemo; 80% recurrence
o Carcinoid tumor
 Presents w/ hemoptysis, dyspnea, or recurrent pulmonary infections
 Tx resection
o Others: bronchial adenomas, adenoid cystic carcinomas, mucoepidermoid carcinomas
o If preop FEV1 > 50% of predicted, pt can tolerate pulmonary resection w/ little risk of postop
pulmonary complication
Pulmonary nodule
o Review prior films if available
o CT scan w/ contrast helps determine location of mass
o PET differentiates between benign and malignant masses
o Common sites for mets – brain, adrenals, bone
Solitary pulmonary nodule
o Definition: round lesion <3 cm in diameter surrounded by lung parenchyma
o Size is important predictor of the likelihood of malignancy. Nodule <4cm have an extremely
small risk of cancer
o In some cases benign lesion can be diagnosed by CT b/c of distinct pattern of calcification (e.g.
hamartoma or granuloma)
o 1st step – establish if nodule is new or not and whether it is stable or increasing. CT should be done
if there are no previous images
o 2nd step
 Nodules with low to intermediate risk for cancer
 <4 mm; >1%
 4-8 mm; 6%
 >8 mm; 50%
 Nodules suspicious for malignancy
 >8mm in pt w/ hx of cancer or in a case in which a nodule is increasing in size,
has speculated margins or mixed solid/ground glass attenuation
 Pts w/ hx of cancer should have close follow up intervals
o Diagnostic intervention can include: percutaneous needle aspiration biopsy, FDG-PET scans,
VATS
 PNAB – provide definitive diagnosis w accuracy of about 90% for malignant
lesion and 60-80% for specific benign lesions
 If not possible to perform PNAB, the choices are to surgically remove the
nodule using video assisted thoracoscopic surgery (CATS), or perform followup CT scan
 FDG-PET scans (fluorodeoxyglucose-positron emission tomography) –
identifies metabolically active nodules
 Follow up is not necessary once a nodule has been demonstrated to be stable for 24
months, with the exception of nodules that have ground glass features on CT
 Longer follow up is warranted b/c these features can be indicative of indolent cancers that
can be stable or very slowly growing over several years
o Guidelines
 Solitary pulmonary nodule found on X-ray
 Compare w/ old study
o If growth, consider diagnostic intervention
o If solid or no growth after >2 years, no action
 If no previous studies, do CT
o If calcification or fat, no action
o Nodule of any size needs to be investigated
 If CT shows nodule of any size



With no hx of malignancy or =/- smoking
o <4 mm
 Age >35 follow up CT as 12 and 24 mos
 Age 18-35 follow up CT after 12 mos
 All ages use longer follow up for ground glass nodules
 If growth occurs, consider PNAB or VATS
o >4-8 mm
 Age >35 follow up CT after 3, 9, and 24 mos
 Age 18-35 follow up CT after 6-12 and 24 mos
 All ages use longer follow up for ground glass nodules
 If growth occurs, consider PNAB or VATS
o >8 mm
 Consider PNAB, VATS, FDG-PET. Attention to part
solid/ground glass nodule
 If co-morbitiies and PET neg, then consider follow
up CT after 3, 9, and 24 mos
 If not growth, no action
With Hx of malignancy – follow up CT after 3, 6, 12 mos w/ nodule of any
size
o If growth occurs, consider PNAB, VATS
o If no growth, no action
In immunocompromised pt or pt w/ fever
o Follow up in <4-6 weeks and then to resolution OR
o Consider PNAB, bronchoscopy, or VATS
Neck Masses
 Cervical regions
o Anterior cervical region (anterior triangle)
o Lateral cervical (posterior triangle) – sternocleidomastoid, trapezius,
 Great auricular nerve near external jugular vein
 Spinal accessory nerve – damaged w/ thyroid surgery
 Lateral spinalclavicular nerve
o Carotid triangle
o Occipital triangle
 Thyroid anatomy
o Innervation of the thyroid gland
 Derived from superior, middle, and inferior cervical ganglia
 They reach the gland through plexuses that accompany the thyroid arteries
o Innervation of larynx
 Extrinsic – inferior laryngeal nerve off of the recurrent laryngeal nerve from CN X
 Intrinsic – external laryngeal nerve off of the superior laryngeal nerve from CN X
 Muscles of the larynx
o Cricothyroid – external laryngeal nerve (only this muscle), stretches and tenses vocal ligament;
damage causes bowing of larynx
o Thyroartenoid – relaxes vocal ligament, inferior laryngeal nerve (from recurrent laryngeal nerve)
o Posterior cricoarytenoid – abducts vocal folds
o Lateral cricoarytenoid – adducts vocal folds
o Transverse and oblique arytenoids
 Examination
o Ascultation
 Bruit over both subclavian and common carotid  aortic stenosis
 Bruit over single artery  localized stenosis
o Enlarged nodes
 Enlarged LN or normal structure – greater cornua of hyoid moves w/ swallowing (most
lymph nodes do not move)
 Physical characteristics
 Metastatic – discrete, nontender, unilateral, firm/hard
 Hodgkin’s – discrete, nontender, large, firm/rubbery
 Tuberculosis – conglomeration, fluctuation, nontender
 Acute pyogenic – enlarged, tender, discrete
 Primary lesion
 Posterior triangle – scalp
 Thyroid mets – either to superficial or deep cervical nodes
 Mirror exam of nasopharynx and tonsils may be helpful
 Lesions in children
o Cervical lymphadenopathy
 Don’t worry if it’s small, mobile, rubbery, in anterior cervical triangle
 Worry if its >2cm, nontender, fixed supraclavicular region, hard; hx of weight loss, night
sweats
 If need for Bx is questionable – do CXR and/or CT first to R/O airway obstruction during
induction
o Branchiogenic anomalies
 Mature structures of head and neck are derived from six pairs of branchial arches, their
intervening clefts externally, and pouches internally. The lesions are a result of failure of
these structures to regress
 Second brachial cyst remnants – most common, anterior border of SCM, step-ladder
incision needed to completely excise
o Thyroglossal duct cysts
 One of the most common midline masses most commonly presenting in pre-school age
children



o
o
o
o
o
o
Thyroglossal remnants are involved with the embryogenesis of the thyroid gland
Most cysts are found at or below the hyoid bone
Sistrunk procedure: excise cyst and tract, excise central portion of hyoid bone
extending to base of tongue
Torticollis
 “Twisted neck”; tilted towards, rotated away; mass can be palpated, birth trauma +/-, tx
conservatively
Cystic hygroma
 Mal-developed lymphatic network which fails to connect or drain into venous system.
Complete surgical excision is treatment of choice
Lymphoma – most common malignant neck mass in children
Malignancies
 FNA biopsy for definitive diagnosis
 CT of head and neck – choice for advanced squamous carcinoma
 Modified radical neck dissection-preserves spinal accessory nerve, SCM, and internal
jugular vein
 Post op radiation if:
 More than two nodes contain mets
 Cervical nodes at more than two levels contain mets
 Extracapsular spread of cervical node mets
 Prophylactic radiation of all cancers is not recommended
Thyroid nodules
 Thyroid moves cephalad w/ deglutition, nodes do not
 Isthmus of thyroid is caudad to cricoid cartilage
 Acute thyroiditis (low TSH and low radioactive Iodine uptake)
 Hyperthyroidism (Grave’s disease)
 Nervousness, sweating, infertility
 Goiter, tachycardia, warm most skin, gynecomastia, exopthalmus
 Tx propylthiouracil (PTU)
 Pts over 40, poor surgical risks, or recurrent hyperthyroidism tx w/ Radioiodine
– 100% of young pts will become hypothyroid
 Surgery indications – very large goiter, malignant tissue, opthalmopathy,
pregnancy/children, pt taking Amiodarone, psychologically impaired
o Remove all but 5 gms sparing parathyroid and recurrent laryngeal nv
Thyroid malignancies
 Types of thyroid cancer
 Papillary adenocarcinoma – 75% 10 year survival
o Appears early in adult life as a solitary nodule
o May metastasize to lungs or bones
o Rate of growth may be stimulate by TSH
 Follicular adenocarcinoma – 65%
o Greater tendency to metastasize to lungs, bone, and liver
 Medullary carcinoma – 35%
o Screen all pts w/ medullary carcinoma for a RET point mutation on
chromosome 10
 Undifferentiated (anaplastic) carcinoma – 5%
o Cervical lymphadenopathy and pulmonary metastases
 Wide range of growth and malignant behavior
 Anaplastic – local recurrence or pulmonary mets in 6 mos
 Papillary – slow growth, long life
 Surgery – preserve SCM, spinal accessory nerve, and sensory nerve
 Medullary – high incidence of nodal involvement; post-surgery if calcitonin or CEA are
elevated then order US or MRI of neck and MRI mediatstinum
 All pts w/ thyroid cancer should be maintained on suppressive doses of thyroid hormone
 For follow up, it is helpful to measure serum thyroglobulin
Perianal Problems
 Anatomy
o Anal borders
 Posterior – coccyx
 Bilaterally – ischiorectal fossa
 Anterior – perineal body and vagina in women; urethra in men
o External anal sphincter
o Levator ani muscles
o Anal valves, anal (Morgagnian) columns, longitudinal muscle, internal pudental artery
o Venous drainage for rectal – common iliacs, superior rectal veins 
o Vessels and nerves superior to the pectinate line are visceral; those inferior to the pectinate line are
parietal or somatic. This orientation reflects the embryological development of the anorectum
 Above pectinate line: arteries from inferior mesenteric artery; veins to portal venous
system
 Below pectinate line: arteries from internal iliac artery; vein to caval venous system
 H&P
o Anorectal exam – left lateral decubitus; inspection, palpation, anoscopy, proctosigmoidoscopy
 Pelvic floor disorders
o Incontinence
 Causes
 Obstetric trauma – 3rd degree perineal tears, multiple deliveries, infection of
episiotomy repairs
 Neurogenic cause – pudendal nerve injury d/t delivery or straining at stool
 Iatrogenic – division of external sphincter in fistula surgery
 Other – DM, MS, scleroderma, dermatomyositis, sever diarrhea, fecal impaction
w/ over flow phenomenon, radiation proctitis
 Physical signs of incontinence – patulous anus, loss corrugation anal verge, flattening and
maceration perineal floor, decreased sphincter tone, diminished voluntary squeeze
pressures, and loss of anal sensation
 Work up – anorectal manometry, transrectal US (evaluates internal and external sphincter
abnormalities), pudendal nerve latency studies
 Treatment – biofeedback (1st line tx), anal encircling procedures
o Obstructed defecation
 Anal stenosis
 Causes – circumferential hemorrhoidectomy, trauma, radiation
 Tx – repeated dilatation
 Nonrelaxation of the puborectalis
 Functional disorder
 Symptoms – need for digital maneuver to eliminated stool, pelvic pain,
incomplete emptying, severe straining during evacuation
 Diagnosis – inability to expel 60 cc balloon
 Tx - biofeedback
 Internal intusseseption (internal prolapse of the rectum)
 Cause – solitary rectal ulcer
 Tx – increase dietary fiber, stool softeners, glycerin suppositories
 Indications for surgery – debilitating symptoms, impending anal incontinence,
chronic bleeding
 Low anterior resection of sigmoid and proximal rectum w/ anorectal
anastomosis and rectal fixation
o Rectal prolapse – protrusion of the full thickness of rectum through the anus
 Epidemiology & etiology
 Long-term internal intussusception, women in mental institutions, elderly
women, hx hysterectomy
 Symptoms – mucosa-lined bowel protruding through anus, bleeding, anal pain, mucous
discharge, anal incontinence of varying degrees

o
o
o
Tx surgically
 Pts in fair health w/ good continence – low anterior resection w/ rectopexy or fix
rectum to sacrum w/ synthetic sling (Ripman’s procedure)
 Pts in poor health (perineal proctectomy w/ low colorectal or coloanal
anastomosis of anal encircling procedure
 Pts w/ total incontinence – anterior resection of rectum and colostomy (low
Hartman’s procedure)
Hemorrhoids
 Internal – located above dentate line, rectal mucosa; symptoms – bleeding, mucous
discharge, prolapse, pruritus, anal pain should not be attributed to thrombosed internal
hemorrhoids
 Classification
o 1st degree – bleed
o 2nd – bleed and prolapse
o 3rd – manual reduction
o 4th – non-reducible
 External – below anal verge, covered w/ squamous epithelium
 Diagnose w/ anoscope
 Treatment depends on symptoms
 Thrombosed external – most resolve w/in 2 weeks
 1st degree – medical therapy
 2nd and 3rd – internal – rubber band ligation
 3rd and 4th – surgical excision
 No more than two should be excised-anal stenosis
Anal fissure
 Linear ulcer of the lower half of the anal canal usually locate in the posterior commissure
in the midline
 Best seen by inspecting the anal verge w/ gentle separation of the gluteal cleft
 Associated findings include sentinel pile or tag externally and an enlarged anal papilla
internally
 Involves squamous epithelium thus condition is painful
 Diagnosis is made by history – pain/bleeding w/ defecation, digital exam may be too
painful, delay 4-6 weeks until pain managed medically then scope
 Uncertain etiology – may be due to large hard stools, diet, previous anal sx, childbirth,
laxative abuse, etc
 Tx – warm sitz baths w/ bran or bulking agents, add nitroglycerin and diltiazime
(reversible chemical sphincterotomy) for chronic cases, surgery
 Reversible chemical sphincterotomy – botox transiently caused striated muscle
denervation leading to muscle paralysis and relaxation
Anorectal suppuration – abscess/fistula
 Involves anal glands
 Spreads in intersphincteric plane
 Infection may extend upwards, downwards, horizontally, or circumferentially (horseshoe
abscess)
 An anal fistula may result from the spread of an anal infection and cryptitis. One end of
this abnormal canal opens into the anal canal, and the other end opens into an abscess in
the ischioanal fossa or into the perianal skin
 Pain constant but no associated w/ defecation
 Fever and leukocytosis may be present
 Tx – drain when diagnosed
 Goodsall’s rule – external openings posterior to a transverse line that bisects the anus will
connect to the posterior midline crypt; external openings anterior to this line will
communicate to an anterior crypt by a short direct route
 Exception – anterior, >3cm from anal margin
o
o
Pilonidal disease – hair from the skin of the postsacral superior gluteal cleft that drills below the
skin level causing foreign body reaction and localized inflammation
 Tx w/ drainage, extract hair
Tumors of the anal area
 Squamous cell carcinoma – large, central ulceration w/ rolled edges, <4cm – wide local
excision
 Basal cell carcinoma – tx w/ wide excision
 Bowen’s disease – indolent in situ squamous cell carcinoma w/ anal verge, appearance
usually plaque-like, presents w/ burning and pruritus, tx w/ wide local excision
 Paget’s disease – shallow intraepithelial tumor presenting as a plaque
 Condyloma acuminata – HPV, most common perianal sexually transmitted disease, tx
fulguration w/ electrcautery and direct excision may be required
The Acute Abdomen
 History and physical
o Pain is the most common presenting symptom
o Visceral pain – abdominal viscera innervated by autonomic nerve fibers C and respond mainly to
the sensations of distention and muscular contraction – not to cutting, tearing, or local irritation;
most often felt in midline, slow in onset, dull, poorly localized, and protracted
o Sensory levels (structures – nervous system pathway; sensory level
 Liver, spleen, central diaphragm – phrenic; C3-5
 Peripheral diaphragm, stomach, pancreas, GB, small bowel – celiac plexus, greater
splanchnic, T6-9
 Appendix, colon, pelvic viscera – mesenteric plexus, lesser splanchnic, T10-11
 Sigmoid, rectum, kidney, ureters, testes – lowest splanchnic, T11-L1
 Bladder, rectosigmoid – hypogastric, S2-4
o Parietal pain – afferent C and A delta fibers elicited by direct irritation; pain is localized b/c
somatic afferent fibers directed to only one side of nervous system, cutaneous distribution
corresponds to T6-L2, conveniently describe –RUQ, LLQ, epigastric, ect.
o Referred pain – pain perceived distant from its source and results from convergence of nerve
fibers at the spinal cord
 Subdiaphragm – goes to shoulder C4 phrenic
 Biliary – often perceived in R scapula; can mimic anginal pain
 Retrocecal appendicitis – posterolateral right flank
o Location of pain – spreading or shifting pain (parallels the course of the underlying condition),
location serves as “rough guide” only, “typical” descriptions of pain in only 2/3rd of causes
o Character of pain – steadying pain (most common), biliary pain, colicky pain
 Colic – pain free intervals that reflect intermittent smooth muscle contraction
 Sharp, constant worsened by movement (peritonitis)
 Tearing pain (dissecting aneurysm)
 Dull pain (appendicitis, diverticulitis, pyelonephritis)
o Other symptoms – vomiting (1st then pain), constipation/obstipation, diarrhea
o Physical exam
 Palpation – guarding – place both hands on abdomen and gently depressing fingers have
patient inhale deeply and gently
 Rectus rigidity – peritoneal inflammation
 Ipsilateral rigidity – renal colic
 Carnett’s test – raise head, muscles tense (relief of pain indicates
intraperatoneal)
 Punch tenderness – costal area, costovertebral
 Murphy’s sign – palpate right subcostal, have patient breath deeply and inspiration will
be stopped abruptly, indicates gallbladder disease
 Iliopsoas sign – pain w/ passive hip extension or active hip flexion against resistance;
indicates psoas abscess, Crohn’s disease
 Obturator sign – internal and external rotation of flexed thigh may exert pressure on
entrapped small bowel – obturator hernia
 Costovertebral angle tenderness may indicate pylonephritis
 Investigative studies – lab
o 2/3 of diagnoses of acute abdomen are made w/ history and physical
o Immediate – CBC, BUN, Creat, ABG, UA w/ micro, check stool for blood, chest/abdominal X-ray
o Same day – clotting, amylase, liver fx, stool culture, ultrasound/CT proctosigmoid, upper
endoscopy, paracentesis, culdocentesis
o Next day – specific tests, ERCP, colonoscopy, Lap
o X-ray – plain films are indicated w/ appreciable tenderness/distention, abnormal BS, hx of
abdominal surgery, decreased sensorium, and/or
 Chest x-ray is essential in all acute abdomen cases
 Look for gas patterns, outline of solid organs, outline of fat lines, radiopaque objects; free
gas under diaphragm 80% of time is perforated ulcer
Angiography or MRA – ischemia/hemorrhage
GI contrast – if no clinical evidence of bowel perforation, BE large bowel obstruction; only if no
likelihood of large bowel obstruction
o US – 80 % sensitive in appendicitis, pregnancy
o CT scans – for pts w/o clear indications for laparoscopy
o Proctosigmoidoscopy – large bowel obstruction, bloody stools, rectal bleed
o Colonoscopy – lower GI bleed
o Gastroduodenoscopy and ERCP – gastritis or PUD
Laparoscopy – therapeutic and diagnostic; esp useful for young women, elderly, and critically ill
Differential diagnosis
o Young children – mesenteric adenitis
o Young woman – tubo-ovarian disease
o Elderly – malignancy
Appendicitis – most common cause of cause of ileus or intestinal obstruction; 50% children have facial
flush; nonspecific abdominal pain in 1/3 of all cases; most common cause of acute abdomen in children
Indications for surgery
o Involuntary guarding or rigidity, severe localized tenderness, tense distention, abd/rectal mass w/
high fever/hypotension
o Radiologic findings – pneumoperitoneum, bowel distention, extravsation of contrast, space
occupying lesion w/ fever
o Endoscopic findings – perforated or uncontrollably bleeding lesion
o Paracentesis – blood, pus, urine, etc
Preoperative management – give analgesics, meds for cardiac, corticosterioids, diabetes, antibiotics; place
NG tube, urinary catheter, informed consent
o
o





Fluid, Electrolyte, and Acid-Base Disorders
 Total body water = 60% body weight
o Compartments
 Intercellular – 66%
 Extracellular – 33%
 Interstitial – 66% ECF
 Intravascular – 33% ECF
o Body fluid distribution by weight
 T – total body weight = 60%
 I – intracellular = 40%
 E – extracellular = 20%
o Blood volume: 7% of body weight; ex: 70kg x 0.07 = 5 L blood
o Electrolyte composition
 Intracellular – K+
 Extracellular – Na+
o Maintenance
 Sodium – 1-2 mEq/kg = 70-140 mEq/day
 Potassium – 0.5-1 mEq/kg = 35-70 mEq/day
o Fluid requirements for 24 hours – 100/50/20
 100 mL/kg for first 10 kg
 50 mL/kg for second 10 kg
 20 mL/kg for ever kg over 20
o Hourly rate – 4/2/1
o Maintenance rates – change w/ fever, environmental temperature, respiratory rate, urine output,
age (elderly don’t produce as much urine), total parenteral nutrition – rarely need fluids
o Water
 Hypovolemia
 Acute – tachycardia, hypotension, concentrated urine
 Gradual – skin, thirst, mental status change
 Treatment
o Replace acute losses acutely
o Replace chronic losses half 1st 8 hrs, remainder in next 24-48 hrs
 Hypervolemia
 Acute – tachycardia, tachypnea, sacral edema, JVD
 Chronic – peripheral edema, pulmonary edema
 Treatment
o Mild – Na restriction
o If hyponatremia – water restriction also necessary
o If severe – diuretics
o Sodium – close relationship to volume status
 Hyponatremia <130 mEq/L
 Hyperosmolar – dilutional hyponatremia fro hyperglycemia, mannitol infusion
or other osmotically active particles
 Normo-osmolar – pseudohypotnatremia
o Hyperglycemia, hyperlipidemia, hyperproteinemia interferes with lab
measurement of Na
 Hypo-osmolar – true hyponatremia
o Hypovolemic – total body sodium is usually ow
o Hypervolemic – TBS usually high; cardiac output low, hypoalbumenia
o Euvolemic – syndrome of inappropriate antidiuretic hormone
(hyponatremia, concentrated urine, elevated urine Na, normal or mild
elevated ECF volume)
 Symptoms
o Acute – cerebral edema, seizures, coma
o Chronic – <110 mEq/L well tolerated, irritability

o
Diagnosis
o Hypo-osmolar, hypovolemia – urine osmolality low, urine Na low
o Hypo-osmolar, hypervolemic – similar
o Hypo-osmolar euvolemic – urine osmolality high; urine Na high
o Lab error is #1 cause of misdiagnosis
 Treatment
o Hyperosmolar – correct hyperglycemia or other osmotic particles
o Normo-osmolar – no tx needed
o Hypo-osmolar
 Hypovolemic – isotonic fluid infusion, consider sodium
replacement if severe
 Hypervolemic – tx underlying cause first, then salt and free
water restriction are appropriate
 Euvolemic – restrict water is SIADH and don’t give Na since
can paradoxically ower sodium as kidney extrete sodium and
conserves water
 Hypernatremia >150 mEq/L
 Types
o Hypovolemia: represents a volume deficit
o Hypervolemia: rare but cause by iatrogenic infusion of too much
sodium
 Symptoms
o Tachycardia, hypotension, dry mucous membranes, lethargy,
confusion, and coma as water shifts form intracellular compartment in
CNS
 Diagnosis
o High serum sodium w/ obvious fluid losses d/t:
 Extrarenal: fever, mechanical ventilation, diarrhea, etc.
 Renal – osmotic diuresis from hyperglycemia, mannitol; high
output dilution from acute tubular necrosis
 Treatment
o Hypovolemic
 Replace volume with D5W, ¼ NS, or ½ NS slowly over days
 Lower Na about 12 mEq/L per day
 Seizures will develop if sodium is lowered too fast
o Hypervolemic
 First decrease sodium being administered
 Diuretics can be used
Potassium
 Hypokalemia <3.5 mEq/L
 Symptoms
o Ileus, weakness, cardiac dysrhythmias
o ECG – flattening or inversion T-waves, depressed ST segments, U
waves, prolonged QT interval, ventricular tachycardia
 Treatment
o Renal – diuretics
o Extrarenal – diarrhea, burns
o Intracellular – insulin, alkalotic state
o Medical – hyperaldosteronism, Cushing syndrome
o 10 mEq/hr of K should raise serum K by 0.1 nEq/L
 Hyperkalemia > 6mEq/L
 Symptoms – cardiac manifestations, peaked T waves, decreased DTR,
weakness, respiratory failure, paralysis
 Etiology
o Renal failure

o

o Extracellular shift – Rhadbdomyolysis
o Medical disease – Addison’s
Treatment
o Stabilize cardiac membrane and lower serum K
 1 gram calcium gluconate IV
 Glucose/insulin to shift K intracellularly
 Bicarbonate will also shift K
o To lower K permanently – ion-exchange resin, lasix, dialysis
Chloride
 Hypochloremia < 90 mEq/L
 Symptoms – associated with dehydration or low K, vomiting
 Etiology – HCL lost from stomach d/t vomiting  metabolic alkalosis
 Treatment – replace chloride and K with IV’s
 Hyperchloremia >100 mEq/L
 Cause – too much in IV fluids
 Tx – decrease amount of CL in fluids
o Calcium
 Hypocalcemia < 8mg/dL
 Symptoms neuromuscular irritability, PVC’s
o Trousseau’s sign – carpal spasm after occlusion of blood in FA
o Chvostek’s sign – facial muscle spasm with tapping facial nerve
 Etiology – removal parathyroid gland
 Treat the cause – asymptomatic – po Ca
o Usually oral Ca will suffice
 Hypercalcemia >10.5 mg/dL
 Symptoms – fatigue, confusion, NV, diarrhea, dehydration, anorexia
 Tx the cause – primary hyperparathyroidism
o Cancer
o Thiazides
 Treatment
o Severe – isotonic resuscitation leading to diuresis and excretion of Ca
o If unsuccessful add Lasix
Acid-Base disturbances (pH = 7.35-7.45)
o Regulatory system
 CO2 – increased CO2  decreased pH
 Strong Ions – Na, Cl, K, etc
 Pure salt solution, ion concentration is equal, pH neutral
 Plasma has more cations than anions
 To maintain neutrality, H2O dissociates, H+ excreted, HCO3 increases and pH
7.4 instead of 7.0
 Weak acids – act as buffers, proteins and phosphates
o Acidosis – occurs when PCO2 increases, HCO3 decreases, concentration of strong ions increase,
concentration weak acids increase
 Respiratory acidosis
 Most common cause is decreased alveolar ventilation
 Tx – increase alveolar ventilation
 Metabolic acidosis
 Loss of bicarbonates – diarrhea, ileus, fistula
 Increase in acids – lactic acidosis, ketoacidosis, renal failure
 Tx – correct underlying metabolic problem
o Alkalosis
 Metabolic alkalosis
 Most common cause is loss of gastric contents



Tx – stop Cl loss and replace with isotonic saline and potassium
supplementation
Respiratory alkalosis
 Most common cause is increased alveolar ventilation
Acid-base using blood gas
o <7.35 acidosis
 HCO3
 Low – metabolic acidosis
 High – mixed
 CO2
 High – respiratory acidosis
 Low – mixed
o >7.45 alkalosis
 HCO3
 High – metabolic acidosis
 Low – mixed
 CO2
 Low – respiratory alkalosis
 High – mixed
o pH normal – mixed or compensated
Misc
Shock
 SIRS criteria (Systemic Inflammatory Response Syndrome) – two or more of the following:
o Body temperature <36 C or >38 C
o Tachycardia
o Tachypnea
o White blood cell count <4,000, >12,000, or >10% immature neutrophils
 Sepsis – same criteria as for SIRS but w/ a clearly established focus of infection
 Severe sepsis – sepsis associated w/ organ dysfunction and hypoperfusion
o Systolic blood pressure <90 mm Hg
o >40 mm Hg fall from normal systolic blood pressure
o Lacticacidemia
o Oliguria
o Acute mental status changes
 Septic shock – patients w/ severe sepsis who:
o Are not responsive to IV fluids for resuscitation
o Require inotropic or vasopressor agents to maintain systolic blood pressure
Wound healing
 Phases (think: in every fresh cut)
1. Hemostasis
2. Inflammation – vasoconstriction followed by vasodilation, capillary permeability
3. Epithelialization – epithelial coverage of wound
 Sutured wound epitheliaizes in 24-48 hours (then dressing can be removed and pt can
shower)
 Marjolin’s ulcer (aka burn scar carcinoma) – malignant ulcer
4. Fibroplasia – fibroblast and accumulation of collagen, elastin, and reticulin
5. Contraction – myofibroblasts contract wound
6. Scarring
7. Remodeling
 Wound closure
1. Primary intention – suture wound closed immediately
2. Secondary intention – wound is left open and heals over time without sutures; it heals by
granulation, contraction, and epithelialization over weeks (leaves a huge scar)
 Used for dirty wounds to prevent abscess from forming
3. Delayed primary closure – suture wound close 3 to 5 days after incision
Postoperative complications
 Fever (wind, water, wound, wonder drug, walking)
o Atelectasis – first 24 to 48 hours
o UTI – Anytime after POD #3
o Wound infection – usually after POD #5 (but it can be anytime!)
o DVT/PE/thrombophlebitis – POD #7 to #10
o Drug fever – anytime
Anesthesia
 Malignant hyperthermia
o Inherited predisposition to an anesthetic reaction causing uncoupling of the excitation-contraction
system in skeletal muscle; hypermetabolism is fatal if untreated
o Causative agents – general anesthesia, succinylcholine
o Signs/symptoms – increased body temperature, hypoxia, acidosis, tachycardia, increase pCO2
o Tx – IV dantrolene
Trauma/burns
 Glasgow coma scale
o Eyes (4 eyes)
1. Does not open eyes
2. Opens eyes to painful stimulus
3. Opens to voice command
4. Opens spontaneously
o Motor response (6-cylinder motor)
1. No movement
2. Decerebrate posture
3. Decorticate posture
4. Withdraws from pain
5. Localizes painful stimulus
6. Obeys commands
o Verbal response (Jackson 5)
1. No sounds
2. Incomprehensible sounds
3. Inappropriate words
4. Confused
5. Appropriate and oriented
Breast
 Anatomy
o Borders




o

Superior – axillary vein
Posterior – long thoracic nerve
Lateral – latissimus dorsi muscle
Medial – lateral to, deep to, or medial to pectoral minor muscle, depending on level of
nodes taken
Nerves
 Long thoracic – innervates serratus anterior; “winged scapula”
 Thoracodorsal – innervates latissimus dorsi
 Medial pectoral – innervates pectoralis minor and major
 Lateral pectoral – innervates the pectoralis major
 Intercostobrachial nerve – cutaneous nerve that transverses the axilla
o Lymphatic drainage
 Lateral – axillary lymph nodes
 Medial – parasternal nodes that run w/ internal mammary artery
Breast cancer
o History risk factors (NAACP)
 Nulliparity
 Age at menarche (<13 years)
 Age at menopause (>55 years)
 Cancer of the breast (in self or family)
 Pregnancy w/ first child (>30 years)
o Types
 Infiltrating ductal carcinoma (most common)
 Medullary carcinoma
 Infiltrating lobular carcinoma
 Tubular carcioma
 Mucinous carcinoma (colloid)
 Inflammatory breast cancer – associated w/ Peau d’orange
 Ductal carcinoma in situ – cancer cells in the duct w/o invasion; microcalcifications on
mammography
 Lobular carcinoma in situ
 Intraductal papilloma – bloody discharge in a young woman

o
Fibroadenoma – most common breast tumor in pts <30 years; well-circumscribed;
surgical resection for large or growing lesions
 Paget’s disease of breast – scaling rash/dermatitis of the nipple caused by invasion of
skin by cells from a ductal carcinoma
 Cystosarcoma phyllodes – typically benign, mesenchymal tumor arising from breast
lobular tissue; mobile, smooth breast mass on mammogram/ultrasound
Detection
 Self-exam – monthly
 Ages 20-40 years: breast exam every 2-3 years by a physician
 >40 years: annual breast exam by a physician
 Mammogram
 Baseline mammogram between 35-40 years
 Mammogram every year or every other year for ages 40-50
 Mammogram yearly after age 50
Staging





Stage I – tumor <2 cm w/ no nodes
Stage IIA – tumor <2 cm w/ mobile axillary nodes OR 2-5 cm w/ no nodes
Stage IIB – tumor 2-5 cm w/ mobile axillary nodes OR tumor >5 cm w/ no nodes
Stage IIIA – Tumor >5 cm w/ mobile axillary nodes OR any size tumor w/ fixed axillary
nodes, no metastases
 Stage IIIB – Peau d’orange, chest wall invasion/fixation, inflammatory cancer, breast
skin ulceration, breast skin satellite metastases, or any tumor and + ipsilateral internal
mammary lymph nodes
 Stage IIIC – any size tumor, no distant mets; positive: supraclavicular, infraclavicular, or
internal mammary lymph nodes
 Stage IV – distant metastases
o Treatment
 Stage I and II – lumpectomy and radiation
 Stage III A/B – modified radical mastectomy
Benign breast disease
o Fibrocystic disease – green, straw-colored, or brown nipple discharge
o Fat necrosis – breast mass following trauma
o Mondor’s disease
o Prolactinoma
Gastric cancer
 Risk factors
o Diet – smoked meats, high nitrates, low fruits and vegetables
o Environment – pernicious anemia, H. pylori
 Blummer’s shelf – sold peritoneal deposit anterior to the rectum, forming a “shelf”, palpated on rectal
examination
 Virchow’s node – metastatic gastric cancer to the nodes in the left supraclavicular fossa
Crohn’s disease/Ulcerative Colitis
 Crohn’s – abdominal pain, diarrhea, fever, weight loss, anal disease
o Mouth to anus
o Skip lesions, cobblestoning
o Transmural bowel wall involvement
o Anal involvement is common (fistulae, abscesses, fissures, ulcers)
 Ulcerative colitis – bloody diarrhea (hallmark), fever, weight loss
o Colon only; lead-pipe appearance on barium enema
o Begins with rectum involvement and moves proximally

o Mucosa/submucosa bowel wall envolvement
o Anal involvement rare; 100% rectal involvement
o Crypt abscesses and psuedopolyps
o Complications include cancer, toxic megacolon, perforation
Extraintestinal manifestations in both
o Aphthous elcers
o Pyoderma gangrenosum
o Iritis
o Erythema nodosum
o Sclerosing cholangitis
o Arthritis, Ankylosing spondylitis
o Clubbing of fingers
o Kidney (amyloid deposits, nephritic syndrome)
Diverticular disease
 Diverticulosis – false diverticula consisting of only mucosa and submucosa that herniated through the
bowel musculature; caused by weakness in the bowel wall where nutrient blood vessels enter
o Most commonly involves the sigmoid colon
o Risks – low-fiber diets, chronic constipation, family hx
o Symptoms – bleeding, diverticulitis, asymptomatic
 Diverticulitis – infection or perforation of a diverticulum
o Pathophysiology – obstruction of diverticulum by a fecalith leading to inflammation and
microperforation
o Signs/symptoms – LLQ pain, change in bowel habits, increased WBC
o Colovesical is most common fistula type
o Best test – CT
o Indications for elective resection – two episodes of diverticulitis; should be considered after the
first episode in a young, diabetic, or immunosuppressed patient
o Elective surgery for recurrent bouts – one-stage operation: resection of involved segment and
primary anastomosis (with preoperative bowel prep)
o Hartmann’s procedure: resection of involved segment with an end colostomy and stapled rectal
stump (will need subsequent reanastomosis of colon usually after 2-3 postoperative months)
Colon cancer
 Colonic and rectal polyps
o Anatomical classification
 Sessile (flat)
 Pedunculated (on a stalk)
o Classification
 Inflammatory (pseudopolyp) – as in Crohn’s disease or UC
 Hamartomatous – normal tissue in abnormal configuration
 Hyperplastic – benign, normal cells, no malignant potential
 Neoplastic
 Tubular adenomas – 5% cancerous
 Tubulovillous adenoma – 20%
 Villous adenoma – 40%
 Colorectal carcinoma – adenocarcinoma of the colon or rectum
o ACS recommendations – starting at age 50, at least one of the following test regimens is
recommended:
 Colonoscopy – q 10 years
 Double contrast barium enema – q 5 years
 Flex sigmoidoscopy – q 5 years
 CT colonography – q 5 years
o
o
ACS recommendations if there is a hx of colorectal cancer in 1st degree relative less than 60 years
old
 Colonoscopy at age 40, or 10 years before the age of diagnosis of the youngest firstdegree relative, and every 5 years thereafter
Staging
 Stage I – invades submucosa or muscularis propria (T1-2 N0 M0)
 Stage II – invades through muscularis propria or surrounding structures but with negative
nodes (T3-4 N0 M0)
 Stage III – positive nodes, no distant metastasis (any T, N1-3, MO)
 Stage IV – positive distant metastasis (any T, any N, M1)
Pancreas
 Ranson’s criteria – score of 3 or more is indicative of severe pancreatitis
o At presentation
 Age >55
 WBC >16,000
 Glucose >200
 AST >250
 LDH >350
o With first 48 hours
 Base deficit >4
 BUN increase >5 mg/dL
 Fluid sequestration >6 L
 Serum Ca++ <8
 Hct decrease >10%
 PO2 (ABG) <60 mm Hg
o Predictor of mortality
 1-2: 2%
 3-4: 15%
 5-6: 40%
 7-8: 100%
OTHER TOPICS:
Splenic trauma
Acute thromboembolic
Venous insufficiency
Metastatic liver disease
Cirrhosis
Thyroid
Abdomen
Hernias
Acute Abdomen
Acute gastrointestinal hemorrhage
Peptic Ulcer Disease
Anal conditions
Biliary system
Preoperative care
Large bowel obstruction
Benign gastric lesions – bezoars, volvulus