SURGERY EOR-GI 50%, PRE/POST-OP 12%, CARDIO 9%, ENDO 8%, DERM, NEURO, GU 5%, HEME/ONC, PULM, OBGYN 3%

GASTROENTEROLOGY 50%- Perforated Viscus

GI 50%
Hiatal Protrusion of the upper stomach •Type I: sliding hernia (MC) CXR •Type I: same at GERD
Hernia into the chest cavity due to tear •Type II: rolling hernia  fundus protrudes •Type II: surgery

Esophageal Web: thin membrane in mid-upper Dysphagia (especially solid foods) Barium swallow Endoscopic dilation
Webs/Ring esophagus
s Schatzki ring MC in people with sliding hiatal
Schatzki ring: constriction at the hernias
squamocolumnar junction

Esophageal Dilated submucosal veins due to •Acute gastrointestinal hemorrhage Emergent Endoscopy STABILIZE: IV, fluids, blood
Varices portal HTN •Retching, Dyspepsia (+) red wale markings and FFP or plts if INR >2.0 or plt <50,000
•Bright red bleeding in esophagus cherry red spots
Risks: CIRRHOSIS •Hypovolemia w/ postural vitals or shock Pharm:
Vasoconstrict: Ocreotide (Somatostatin)
ABX: IV Rocephin or Fluoroquinolones

Emergent Endoscopy with banding

*Performed with pts stabilized within 2-12
hrs

Prevent Re-bleed: Beta Blockers

Mallory UGI bleeding due to longitudinal
Weiss Tear mucosal laceration at the cardia or
gastroesophageal junction
Due to increase in intragastric
pressure  vomiting after ETOH
•Hematemesis with or without melena Upper endoscopy: Supportive: fluids, transfusions
•H/o retching, vomiting, straining 50% cases Superficial longitudinal
mucosal erosions Severe: epinephrine, sclerosing agent, band
•Upper endoscopy after resuscitation ligation, clipping

GERD Transient relaxation of lower
esophageal sphincter (LES)
*severity not correlated with degree
of tissue damage
•Heartburn (pyrosis) ~30-60min after Upper endoscopy 1st: lifestyle modificiations
meals -elevate head, avoid lying down x3hr, avoid
•Reflux of sour/bitter contents (regurg) Complications: acidic food and alcohol
•Dysphagia (1/3) Esophagitis
•Asthma, cough, laryngitis, CP, altered sleep Stricture Pharm: H2-blockers (Ranitidine), PPI
Adenocarcinoma (Omeprazole),
ALARM: dysphagia, odynophagia, weight Barrett’s Esopagus 
loss, bleeding squamous to columnar

Esophageal Squamous cell: •Solid food dysphagia then fluids Endoscopy with biopsy Curable: surgery and chemo
Cancer -MC type worldwide •Odynophagia
-MC in upper 1/3 esophagus •Tracheo-esophageal fistula  cough, PNA Incurable: chemo, palliative
-risk: smoking, alcohol •Chest or back pain (mediastinal estension)

Adenocarcinoma:
-MC type in US; MC in lower 1/3
 -risk: GERD

GI
Peptic Ulcer Decreased mucosal protective factors and •Epigastric Pain (dyspepsia) worse at night Endoscope: GOLD 1. Triple Therapy x10-14d
Disease increased damaging factors •Dull, aching, “hunger” CAP: Clarithromycin,
•Food relief (duodenum) *returns in 2-4h H. Pylori tests: Amoxicillin, PPI
MCC OF UGI BLEED •endoscopy with biopsy (GOLD)
•Nausea, anorexia •urea breath test; stool 2. Quadruple Therapy
Causes: •GI bleed (melena, coffee ground emesis) •antibodies PPI + Bismuth (pepto) +
H. pylori infection *MC in duodenum *may be asymp until bleed Tetracycline + Flagyl
NSAIDS *MC in stomach Complications:
Zollinger-Ellison syndrome Physical Exam: tenderness over epigastric Bleeding, perforation,
ETOH, smoking, stress, obstruction, malignancy

Gastric Adenocarcinoma MCC worldwide Asymptomatic until advanced Iron deficiency anemia •Surgical resection: gastrectomy
Adeno- Other: lymphoma •Dyspepsia, vague epigastric pain
carcinoma •Anorexia, wt loss, early satiety Diagnostic: EGD & biopsy •Chemotherapy and/or radiation
Risks: H. pylori, high salt or nitrate foods
PE: •Palliative measures
•palpable mass (20%)
•left supraclavicular lymph (virchows)
•umbilical node (sister mary joseph)
•rigid rectal shift (Blumer shelf)

Zollinger- Gastrin-secreting neuroendocrine tumor •Multiple peptic ulcers •Fasting gastrin level HIGH Local: surgical resection
Ellison Associated with MEN1 •Refractory ulcers *best screening test
Syndrome •“Kissing” ulcers (each side of luminal Metastatic: PPIs
MC in duodenum, pancreas, lymph node wall touching each other) • (+) Secretin test: increase
•Abdominal pain, diarrhea gastrin release with secretin seen
in gastrinomas

Pyloric •Projectile vomiting associated with
Stenosis hypertrophy of the pylorus
•Non-bilous vomiting, dehydration,
alkalosis in infants <12 weeks
•MC in males
•Risks: first born, twins, fhx
•mothers who has taken Azithroycin in 3rd
trimester of pregnancy
•Postprandial vomiting
* shoots across the room
•Hungry “hungry vomiter”
Signs:
• “Olive Sign”: palpable oval mass RUQ at
lateral edge of rectus abdominis muscle
•dehydration or emanciation
•CMP: •Pyloromyotoy laparoscopically
-hypochloremic alkalosis
-potassium depletion
-BUN/Cr abnormlaities
-mild hyperbilirubinemia
•CBC: r/o infection
Diagnostic of choice: US
•UGI: long & narrow pyloric
canal "string sign"
•US: muscle ring >4mm x15mm

Small Bowel 24-40% adenocarcinomas in the •Abdominal pain: intermittent & crampy Diagnosis usually delayed  •Surgery
Carcinoma duodenum •N/V, wt loss poor outcomes •Chemo if (+) lymph nodes
•Anemia
Risks: hereditary, CF, Crohns, alcohol, •Jaundice •CT scan
sugar, red meat, salt-cured, smoked foods •Wireless capsule endoscopy
• (+) CEA
GI About/Causes Clinical Presentation Diagnostics Treatment
Paralytic Ileus Loss of peristalsis of the intestine (STOP) •N/V obstipation (severe const.) Plain films *may look nml early •Underlying cause
*more severe that gastroporesis •Abdominal distention with  Distended gas-filled •Complete bowel rest
*no sign of obstruction tympany to percussion loops of bowel  IV fluids/TPN, NG tube
•Diminished/absent BSs *can’t determine between an •Slowly advance diet *gas=good
common causes: surgery (abdominal and ileus and an obstruction on x-ray •Activity
pelvic), peritonitis, medications, severe *mild-moderate diffuse pain •Remove drugs that reduce
medical illness, post-infection •Possible dehydration intestinal motility

Small Bowel Usually tissue within bowel that causes •Moderate-severe localized pain •Leukocytosis on labs •NG tube
Obstruction obstruction; tumor •Mild distention, tenderness •Surgery
•High-pitched BS early •Imaging abnormal

Appendicitis Rectocecal: •dull periumbilical or epigastric •CBC, UA, pregnancy •Consult surgeon
abd and flank pain pain  RLQ •Preoperative preparation
•N/V, anorexia; SX increase over •CT scan: STUDY OF CHOICE IVF, ABX  Zosyn
Pelvic: 24h *don’t need contrast
tender abd and rectal pain
PE: McBurneys point &
Appendicitis signs
Rovsing: RLQ, Psoas: SLR,
Obturator: twist

Volvulus •Torsion bowel  bowel obstruction Infants: bilious vomiting Complications: •Endoscopic decompression
•MC in elderly • intestinal ischemia, gangrene •IV Fluids
•Sigmoid (MC!) 80% Adults: distention, abdominal
pain, N/V Imaging:
Fever, tachycardia •X-ray: SBO, “double bubble”
•GI series & CT: “birds beak”

Acute Mesenteric Decrease of blood supply to bowel •Crampy, abdominal pain DX: CT angiogram •NPO, rest, fluids; SURGERY
Ischemia MCC: emboli, thrombus •Bloody diarrhea •Pain control, anti-emetics
•HALLMARK: pain out of Labs: CBC, lactate
proportion

Ischemia Colitis MCC: hypotension or atherosclerosis •LLQ pain •Colonoscopy •Restore perfusion and observe
•Bloody diarrhea for perforation
Toxic Megacolon Total/segmental non-obstructive colonic •colitis present for at least 1wk XRAY (best!): •Complete bowel rest & NG tube
dilatation (>6cm) + toxicity prior to onset Transverse or R colon is dilated, •DC all antimotility agents
•Severe bloody diarrhea, abd 6-15cm supine (opiates, anticholinergics)
Complication of IBD, radiation, ischemia pain, distention •prophylaxis PPI & DVT
•Malaise •IV steroids & surgical consult
•Flagyl + Amp/Gent or
PE: FAT BAT Ceftriaxone
•Fever, AMS, Toxic
•BP low, abd pain, tachycardia
GI
Acute GI bleed •Ligament of Treitz is
defining location
seperating UGI from LGI
bleed
Medications:
•NSAIDS, anticoags,
antiplatelets,
•Iron (melena)
•Beets (hematochezia)
Social:
•Alcohol  gastris, liver
hx similar sx: 60% UGI
from same lesions
Hematesmesis: bleed proximal to ligament •type and crossmatch Upper GI Bleed
-coffee-ground: mild, frank blood: severe •CBC ALL GET ENDOSCOPY
-normocytic: acute
Hemathochezia: maroon/bright red  LGI -microcytic: chronic Stable: consult GI/surgery
•CMP: high BUN: CR >30-UGI Unstable: IVF, PRBC: FFP (4:1)
Melena: black, tarry stool (altered hgb from •PT/INR: endoscopy can not be
digestive enzymes )  UGI performed until INR <2.5 Lower GI
•consult GI/general surgery
•Pain, dixzzy, syncope, confusion, diaphoresis •EKG & cardiac enzymes •consider endoscopy to r/o UGI
•discuss colonoscopy v angiography
signs of significant bleeding: hypotension, NG Tube (suspected UGI)
tachycardia, low pulse pressure, tachypnea •visual inspection of gastric content Others:
•sign of shock: cool, pale, low cap refill  MOST SENSITIVE PPI: acid suppression
•Pantoprazole 80mg IV bolus
•hyperactive BS: UGI bleed •indicated for bleeding from PUD
•tenderness: inflame/infectious Somatostatin analong
•non-tender: vascular •Ocreotide 50mcg bolus
•ascites/hepatosplenomegaly: liver •use for variceal bleeding
Rectal exam: if LGI suspected  guaiac test

GI
Anal Fissure •Linear tears/ulcerations around anus •Tearing pain with defecation Inspection •Proper toileting, Sitz bath, Fiber
*MC posterior midline •Bleeding
*small amount with bright red Chronic fissures:
•Due to trauma to anal canal during blood (streaking on TP) •Topical NTG, Botulinum injection
defecation  constipation/hard, straining •Surgery- sphincterotomy

Perianal ½ perianal abscesses are caused by fistulas Abscess: swelling, pain Clinical rectal exam •Perianal Abscess: I & D, Antibiotics;
Abscess and MC in posterior rectal wall •worse with sitting, cough, poo sitz baths, high fiber
Fistula Fistula DX: US/CT
Fistula: open tract b/w two epithelium areas Fistula: anal discharge and pain •Fistula treatment: Fistulectomy

Hemorrhoids •Engorged rectal & hemorrhoidal veins
Causes: constipation, low fiber, straining,
pregnancy, obesity
Complications:
•Thrombosed external hemorrhoids *painful
•sitz bath, topical ointments, clot evacuation
Internal (superior vein)
•Bleeding
•Prolapse
•mucoid discharge
External (inferior vein)
•perianal pain and bleeding
PE: inspect, aposcopic evaluation
Staging:
•I: confined in anal canal, no
prolapse
•II: prolapse with straining
•III: require manual reduction
•IV: always out, irreducible
Conservation (stage I and II)
•proper toileting & high fiber diet
Medical (bleed stage I & II; II-IV)
•Preparation H, Anusol, Proctofoam
Surgical (III-IV, recurrent bleed)
•band ligation (MC); sclerotherapy

Diverticulitis Infection/inflammation of diverticuli •Acute LLQ abdominal pain Labs: leukocytosis Diet: Clear liquid initially
•Fever, N/V, Bowel changes *eliminate seed, nuts, popcorn
Diverticuli: outpouching due to herniation of Imaging: CT abdomen/pelvis
the mucosa into the colon wall Physical exam: ***BEST TEST ABX:
*MC in sigmoid colon •LLQ tenderness, Complications: peroration, bleed, •Augmentin 875mg BID x7-10d,
•palpable mass abscess, stricture •Flagyl + Cipro
 •Bactrim

GI About Clinical Presentation Diagnostics Treatment

Fecal Impaction Severe impaction of stool in the
rectal vault may result in
obstruction to further fecal flow
 Partial or complete large
bowel obstruction
Causes: medication, psych,
prolonged bed rest, neurogenic
disorders of colon, spinal cord
disorder
•Decreased appetite •DRE (digital rectal exam) Initial:
•N/V •Firm feces are palpable •Relieve impaction with enemas
•abdominal pain, distention saline, mineral oil, soap suds
•Paradoxical “diarrhea” •digital disruption of fecal material
Long-term: maintain soft stool and
regular bowel movements

GI
Hernia (Inguinal) Indirect (MC!): inguinal ring
•lateral to inferior epigastric
•persistent patent process
vaginalis
Direct: Hesselbachs triangle Incarcerated: •Surgical repair
•medial to inferior epigastric •painful, enlarged and •Strangulated are surgical
•Triangle: “RIP: rectus abdominis, inferior irreducible emergencies
epigastric, pouparts ligament
•Does NOT reach scrotum Strangulated: systemic toxicity

Umbilical Hernia Occurs after closure of the •Increases steadily in size Surgical repair High rate complications:
umbilical ring •Hernia sac may have multiple loculations *surgical repair of the •large size of the hernia
MC in women > men •Umbilical hernias usually contain omentum umbilical defects gives good •old age or debility of pt
•Incarceration and strangulation are common -> results with a low rate of •obesity
emergent repair recurrence •intra-abd disease
Risks: •Umbilical hernias with tight rings are often
•mult pregnancies associated w/ sharp pain on coughing or straining Prognosis: good results with
•ascities •Aching sensation low recurrence
•obesity
•intra-abdominal tumors

Ventral Hernia About 10% of abdominal Risks: •Small incisional hernias *typically, surgeons do not fix this
(Incisional operations result in incisional •Poor surgical technique should be treated early due to rectus abdominus fascia
hernia) hernias •Postop wound infection
•advanced age •Elastic bind if CI to surgery
•general debility
•obesity
•post-op pulmonary comp. that stress the repair
•post-op pulmonary complications that stress the
repair
•placement of drains or stomas through primary
operative fascial defect
•failure to close the fascia of laparoscopic trocar
sites of 10mm+
•defects in collagen
GI
Crohns Transmural inflammation and skip •Crampy RLQ abdominal pain
Disease lesion •Diarrhea (intermittent, non-bloody)
 malabsorptive, steatorrhea
Can occur anywhere in GI •weight loss, fatigue
*MC-ileum and cecum
perianal disease: fistula, abscess
malabsorption: iron and B12 deficiency
extra-intestinal manifestation:
•arthralgia, arthritis, iritis, uveitis
•skin: Pyoderma gangrenosum
erythema nodosum
Labs: (+) ASCA Goal: *NOT curative!
GOLD=Colonoscopy w/ biopsy •Diet
 skip lesions with cobblestone appearance •Stop smoking
•Symptomatic medications
Barium study: “string sign”
 barium flows through narrow 1st line: oral mesalamine
inflammaed/scarred area due to transmural
strictures Maintenance:
5-ASA (Asacol, Pentasa)

Ulcerative Relapsing and remitting episodes of •Crampy lower LLQ abdominal pain Labs: H/H, ESR, albumin, (+) P-ANCA CURATIVE
Colitis inflammation, spreads proximally •BLOODY diarrhea, pus/mucus
*mucosal layer of colon ONLY, •Fecal urgency and tenesmus Imaging: Pharmacology
*can mimic rectum is always involved Gold Standard-COLONOSCOPY 1. Aminosalicyclates
diverticuliti Complications:  uniform inflammation, ulceration, polyps (Sulfasalazine, Mesalamine)
s *smoking decreases risk for UC •Severe bleed -CI IN ACUTE COLITIS 2. Steroids *acute flares only
•fulminant colitis (>10BMs/day) 3. Immunomodulators
•toxic megacolon, perf Barium: “stovepipe sign”  loss of haustra 4. Anti-TNF

IBD Pharmacotherapy Indication MOA Side Effects/Adverse Events/ BBW Notes

Aminosalicylates Induction and maintenance Inhibits prostaglandin •N/V, HA, hypersensitivity *must exert effect directly to
Sulfasalazine** therapy of UC and CD production, producing anti- •CI: sulfa or ASA allergy colon
Mesalamine inflammatory effects
Corticosteroids Most effective to induce *Can use Budesonide (Entrocort)
(Prednisone remission in severe flare for maint. crohns disease for ~3mo
40-60mg daily) *acute flare -> CD and UC
Immunomodulators/ •Steroid dependent CD and UC Leukopenia, thrompoenia, anemia
Immunosuppressants Remission maintenance in mild- Infection, N/V/D
Azathioprine (Imuran) severe disease Malaise, arthralgia
6-Meracaptopurine Adverse: lymphoma, severe
(Pruinethol) (6-MP)
BBW mutagenic potential, rapid growth, CA

Immunomodulators/ Methotrexate: Cyclosporine: Cyclosprine SE: *must put on folic acid if taking
Immunosuppressants •Mild-moderate active C and •Severe UC/CD refractory to •Multiple serious adverse effects to Methotrexate
Methotrexate maintenance *NOT IN CD steroids
Cycosporine
Antitumor Necrosis TREATMENT OF CHOICE for Inhibits TNF (which •Fever, rigors, N/V, myalgia, urticarial,
Factor Antibodies someone with crohns disease promotes inflammation) hypotension
Infliximab (Remicade) and a fistula
Adalimumab (Humira) •Mod-severe active CD and UC BBW severe infection/sepsis, malignancy
Certolizumab (Cimzia) maintenance
Disease About Clinical Manifestation Physical Exam Diagnosis and Treatment
Colon Polyps •Fleshly lesions protruding into •Flat, sessile, predunculated Procedure:
(Adenomatous) intestinal lumen *most benign *flat-more likely •colonoscopy
cancerous •remove and send to pathology
•Growth arises due to DNA changes in •all dysplastic: low or high grade (carcinoma
the lining of the colon •Slow growth in situ)
*cause 95% adenocarcinomas •Typically asymptomatic • “glandular” structure
-Tubular *most common
Risks: Sx with larger polyps *(less likely to be cancerous)
•Genetics •bleeding -Tubulovillous
•age >50 •change in bowel habits -Villous-most likely cancerous
•male •obstruction
•diet (high fat, red meat, low fiber) •abdominal discomfort Treatment:
•obesity Risk factor for high grade dysplasia: •Remove *colonoscopy and polypectomy
*high-grade dysplasia/CA -must remove entire polyp if high grade
•polyps >1cm •colonoscopy screening
•villous histology *all good, repeat 10 years
•number of polyps *high grade-one year
•flat polyps
Prevention: Diet, weight loss

Colon Cancer *3rd most common cancer among men Aymptomatic Screening Staging and Management: TNM system
and women S/S depend on location •FOBT (yearly) CT colonography *tumor, node, metastasis
*2nd leading cause of CA death •flexible sigmoidoscopy
Proximal •colonoscopy (best) Treatment: *good prognosis if caught early
Causes: •Anemia •Surgical resection
•Adenomatous •Weakness, fatigue Procedure: colonoscopy •Chemotherapy/radiation
•Familial adenomatous polyposis •Melena, (+) FOBT *CT/MRI used for staging -stage II-III (node/tissue involvement)
•IBD •Wt loss -stage IV (metastatic ds)
Labs:
Risk factors: Distal colon •H/H
•>50yo •Change in bowel habits •LFTs (elevation-mets to liver)
•family hx •Obstruction •CEA (level suggest prognosis)
•diet (red meat, fat) •Hematochezia *NOT for screening because it can be
•smoking •Urgency/tenesmus (rectal) false (+) w/o other inflammation
•obesity
GI
Cholelithiasis Gallstone form from: Asymptomatic •Ultrasound Symptomatic (Biliary Colic):
•Ratio of cholesterol too high *procedure of choice •Laparoscopic cholecystectomy
•Ratio of bilirubin too high Symptomatic (biliary colic)
•Gallbladder not emptying bile •RUQ pain (hallmark) •CT No surgery:
-follow fatty meals Ursodeoxycholic acid
Types: Cholesterol gallstones (MC!) -may radiate to back and
right shoulder blade! Complications:
Risks: 5 F: fat, female, fertile, fair, forty choledocholithiasis, acute
*don’t typically see N/V, fever, chills cholangitis, acute cholecystitis

Choledocolithiasi Choledocolithiasis: gallstones in Choledocolithiasis Choledocolithiasis •IV fluids, pain control, NPO
s and Cholangitis common bile duct (CBD); symptomatic •Intermittent RUQ pain, N/V Labs: normal •ERCP w/ stone extraction &
-passes are “uncomplicated” •Jaundice sphincterotomy
-typically symptomatic PE: normal Cholangitis
Labs: •ABX with acute cholangitis
Cholangitis: gallstone lodged and Cholangitis •Leukocytosis -mild-moderate: Cipro + Flagyl
obstruction in CBD  infection •Charcot Triad •high alk phos, GGT, bilirubin -severe: IV Zosyn + Flagyl
-Bacterial infection or hepatic injury -RUQ pain, Fever, jaundice
*when become a problem •Reynolds Pentad: Diagnostics: Complications:
-Charcot + low BP + AMS •US/CT (FIRST!) •liver damage
PE: RUQ pain & hepatomegaly •ERCP-diagnostic test of choice •septic shock with cholangitis

Cholecystitis Acute: •RUQ Pain
•MC due to stone lodged in cystic duct -steady, sharp pain, continuous
•Sudden onset, severe -precipitated by meal
•N/V & Fever
Bugs: E. coli, Klebsiella, Enterococci
PE:
(+) Murphy Sign
(+) Boas: referred pain to R shoulder
 irritation of the phrenic nerve
Labs: Leukocytosis Management: NPO, IVF, ABX
•Ceftriaxone +/- Flagyl
Imaging: •IV Morphine or Demerol for pain
•Ultrasound-1st line •Laparoscopic chole in 24-72hr
-thick gallbladder, sludge, stones
Complications:
•HIDA scan: GOLD •Gangrene
(+): no visualization of gallbladder •Chronic Cholecystitis

GI About Clinical Presentation Diagnostics Treatment

Budd-Chiari Hepatic vein obstruction •Insidious onset most common •DOPPLER US •Treat ascites
Syndrome •Tender hepatic enlargement -85% sensitivity
Causes: *clotting •Jaundice -may show prominent caudate lobe •LMWH; Thombrolytic agent
•hypercoagulation •Splenomegaly *require lifelong anticoagulation
•neoplasm •Ascites •MRI with contrast
•protein C or S deficiency -obstructed veins & collateral vessels •Liver transplant considered in pts with
•blunt abd trauma chronic disease: bleeding, hepatic hepatic failure and cirrhosis
•oral contraceptives, prego encephalopathy
•50-90% survival with treatment
GI
Acute Causes: •Epigastric pain that radiates into the back •Serum amylase & lipase Assessment of Severity:
Pancreatiti •gallstone *because retroperitoneal -elevated 3x normal •Ransons Criteria “LAAWG”
s •heavy alcohol -sudden, steady -lipase better for dx 3+ indicates severe course
-worse w/ activity & supine •CBC -age >55
Pathophysiology: -improve w/ leaning forward -leukocytosis -bld random glucose >200
•Edema/obstruction at ampulla of Vater •N/V •CMP -serum LDH >350
•acinar cell injury  premature or over •Weakness, sweating, anxiety -elevated glucose -AST >250
activation of enzymes  self-digestion -electrolyte abnormal b/c N/V -WBC >16,000
PE: *can dehydrate quickly •elevated alk-phos, LFTs
•Epigastric tenderness •High TGs Treatment:
•Distended abdomen •UA: proteinuria, glycosuria **Supportive: IVF, NPO, pain
•Absent BS if with ileus ABX: broad spectrum if severe
•Fever, Tachycardia, hypotension *baseline 3 tests are serum
•Cullens & Grey Turners (side) sign amylase and lipase, CBC, CMP

X-ray: Sentinel loop, colon cut off

CT: diagnostic study of choice

Chronic Chronic inflammation causing •Chronic, steady or intermittent epigastric X-ray: calcifications in pancreas Oral pancreatic enzyme
Pancreatiti parenchymal destruction  loss of pain *often radiates to back replacements
s exocrine function, sometimes endocrine •Anorexia, weight loss CT (best): pancreatic enlargement,
•N/V, constipation pseduocysts, calcifications
Causes:
•Alcoholism –MC! Pancreatic insufficiency Endoscope US: honeycomb
•Recurrent biliary pancreatitis exocrine: malabsorption & steatorrhea
•Severe high TGs endocrine: glucose high or low
•Autoimmune
•Genetic mutations TRIAD: calcifications, steatorrhea,
•Idiopathic diabetes

Pancreatic Cystic collection of tissue, fluid, and •Abdominal pain •Study of choice: CT Scan Persists >4-6 weeks
Pseudocyst necrotic debris surrounding the pancreas •Abdominal mass •Ultrasound -percutaneous drainage
-surgical decompression
Associated with: *NO true epithelial lining in the capsule Complications: (pancreaticogastrostomy)
•acute or chronic pancreatitis •Peritonitis, infection -drain into stomach or bowel
•trauma to chest
 GI Etiology/Pathophysiology
Carcinoma •75% adenocarcinomas
of Pancreas •75% in pancreatic head
*poor prognosis with body and
tail
Risks:
•Advanced age (>45)
•tobacco use
*only consistent exogenous risk
•heavy alcohol use
•obesity
•chronic pancreatitis
•fhx
•new onset DM after 45
Clinical Presentation
•Vague epigastric pain w/ back
radiation
•Weight loss, anorexia, fatigue
•Jaundice, enlarged gallbladder-
palpable?
*due to tumor of pancreatic head
causing obstruction of common bile
duct
-being able to palpate the
gallbladder on exam is BAD
•Malabsorptive diarrhea
Often asymptomatic until metastasis
occurs, especially with body and tail
Labs/Diagnostics Treatment
Labs: Surgical resection if localized disease:
•Amylase nml to high •Whipple Procedure
•Lipase nml to high *radical pancreaticoduodenal resection
•Glycosuria -5year survival rates 25-30%
•Hyperglycemia -surgery carried 4% mortalilty rate
•Elevated LFTs if CBD obstruction -precede by biliary stenting if with
jaundice/CBD blockage
Diagnostics: -often followed with chemotherapy
•1st line-CT w/ FNA biopsy and/or chemoradiation
•Endoscopic U/S *staging laparoscopy performed prior to surgery
•ERCP to determine suitability
*metastasis in nodes-will not do
*open surgical exploration required
for biopsy if unable to get CT Distal Pancreatectomy
guided or ERCP guided bx •Resection of tumor in body and tail
•Peform staging laparoscopy 1st!
Staging: TNM -usually combined with splenectomy
-higher postoperative mortality rates

Nonresectable:
•liver, peritoneum, omentum mets
•encasement of superior
mesenteric
artery/vein
•extension inferior vena cava
Total Pancreatectomy
•Very rare, poor prognosis &survival
Non-resectable:
•liver, peritoneum, omentum mets
•encasement of superior mesenteric
artery/vein
•extension inferior vena cava
Non-resectable Treatment:
•biliary stent if symptoms of obstruction, chemo,
palliative

Endoscopic Retrograde Cholangiopancreatography

 Camera goes into pancreatic duct and can look inside; inject dye and watch it on an xray or just watch visually with a camera
 Requires some sedation

Magnetic Resonance Cholangiopancreatography

 Same thing but with an MRI picture rather than an xray; Less invasive on the patient & easier to be done
 Problem: if there is a stone seen, they will have to undergo ERCP to remove it
GI About/Causes
Alcoholic Liver •Excessive alcohol intake
Disease •Men >2drink/day
•Women >1drink/day
*risk increases if consumed
daily for 10yrs
*risk most in men
Risk of cirrhosis increases if
other associated liver
disease present or obesity
Clinical Presentation
•Fatty liver:
*>5% fatty deposits
-aymptomatic, reversible
-hepatomegaly
•Alcoholic Hepatitis:
-symptomatic, reversible
-fatigue, nausea, anorexia,
recurrent infections
-bouts of jaundice
•Cirrhosis:
-symptomatic, NOT reversible
-end stage liver failure
-ascites, abd pain,
-splenomegaly, fever
Diagnostics
•Fatty liver: *usually incidental
-mild AST/ALT elevations
-anemia
•Alcoholic Hepatitis:
-Greater AST/ALT elevation
-AST not > 300
-AST >ALT is greater 2:1
-ALP elevations
-Elevated total bilirubin
-Leukopenia, thrombocytopenia
Alcoholic Cirrhosis:
-Elevated total bilirubin >10
-Hypoalbuminemia
-Prolonged PT/PTT
-Anemia
-Last disease -> electrolytes,
elevated BUN/CR
Imaging: CT scan
Definitive Dx: liver biopsy
Treatment
Abstinence from Alcohol-most important!
-especially if fatty liver or alcoholic hepatitis
•nutritional support
•folic acid, zinc, thiamine supplementation
Pharmacotherapy:
•Methylprednisolone x1 months
*alcoholic hepatitis
*see improvement in bilirubin in ~7days
•Pentoxifylline 400mg TIX x1 month
*severe alcoholic hepatitis, especially if with
hepatorenal syndrome or hepatic
encephalopathy (elevated ammonia)
Prognosis:
•Fatty liver: good IF stop drinking
•Alcoholic Hepatitis:
-unfavorable if: prolonged PT/PTT
-bilirubin >10, hepatic encephalopathy,
azotemia (renal)
Cirrhosis: poor prognosis

Non-Alcoholic Causes: •Asymptomatic or mild, vague •Mildly elevated AST/ALT •Lifestyle modifications: weight loss, exercise,
Steatohepatitis •Obesity, DM, metabolic, symptoms -AST/ALT ratio <1 dietary fat restriction, glucose control
(NASH) •TGs •RUQ discomfort *differentiate from alcoholic
*benign •Medications •Hepatomegaly steatohepatitis •Hepatic vaccines
~20% progress to •Cushings •Signs of chronic liver disease
cirrhosis •PCOS uncommon •CT scan (do this 1st!) •Medications:
•Genetics •Definitive DX: liver biopsy vitamin E, thiazolidinediones (Actos, Avandia)
and Metformin, Pentoxifylline, wt loss agents

GI About/Causes Clinical Presentation Diagnostics Treatment

Autoimmune Causes: •Insidious onset -> sudden •AST/ ALT >3x normal Prednisone
Hepatitis •autoimmune •Usually follows viral illness •Elevated total bilirubin -improves sx and inflammation
•genetics •Spider Nevi & Hepatomegaly •Positive ANA -Adding Azathioprine lowers steroid dose
•pANCA, anti-SLA (antibodies) ~18-24mo for resolution, flares common
MC in young/ middle age Extrahepatic: arthritis,
women thyroiditis, associated definitive dx: liver biopsy failed therapy -> liver transplant
autoimmune conditions *can progress to cirrhosis

Drug/Toxin Causes: “Herbals” •Elevated ALT >AST •Can progress to liver failure
Induced Hepatitis Acetaminophen *alcohol •Hepatomegaly
Isoniazid *Rifampin •Jaundice •Stop offending agent
ABX-Tetracyclines •Fatigue, N/V •May require transplant if liver failure develops
GI About/Causes Clinical Presentation Diagnostics Treatment
Cirrhosis Causes: S/S: Insidious onset Minimal changes early •No cure w/o liver transplant
“liver failure” •Alcoholic hepatitis •Weakness, fatigue, sleep changes •Treat complications!
•Hepatitis C •N/V, abdominal pain, ascites •AST/ALT & ALP elevated
•NASH •Bilirubin elevated Avoid alcohol
•Drug toxicity •Portal HTN: •Hypoalbuminemia •Strict dietary management: protein, low carb
•Autoimmune hepatitis -esophageal varices, splenomegaly •Anemia and sodium; reduce protein if encephalopathy
•Hemochromatosis •WBC fluctuations •Nutritional supplements
•Genetic, metabolic •Skin: spider angioma, palmar •Thrombocytopenia •Vaccinations: HBV, HAV, flu, pneumococcal
erythema, ecchymosis •Prolonged PT/PTT •Medications not helpful unless viral
*May have normal AST/ALT but •Avoid liver toxic medications
End result of hepatocellular •Menstrual abn, ED, gynecomastia craziness everywhere else
injury Goals:
•Vitamin & nutrient deficiencies: Diagnostics: •Slow progression & prevent further insult
•Fibrosis and nodular regeneration -anemia, glossitis, cheilosis •US: assess size and ascites •Identify medications that require dosage
throughout the liver -> •CT: assess liver nodules adjustments or should be discontinued
replaces functional hepatocytes •Jaundice (late) •Biopsy: definitive DX •Manage symptoms and lab abnormalities
with nonfunctioning fibrotic •Ascites, edema, effusion (late) •EGD: look for varices •Prevent and treat complications
nodules •Recurrent infections *cirrhosis pt -> undergo EGD •Determine appropriateness of liver transplant
•Encephalopathy and ARF (late) *have to be alcohol free for 6 months

Primary Causes: •Insidious onset Early: •Ursodeocyholic acid *only FDA approved tx
Biliary •Autoimmune destruction of •Asymptomatic for years •Elevated ALP & cholesterol -slows progression of disease
Cirrhosis •intrahepatic bile ducts -elevated ALP -reduces toxicity of cholestasis
•Genetics •fatigue, pruritis -> MC early sx Late: Elevated bilirubin -delay or prevent need for liver transplant
•Other autoimmune disorders
Later sx: •Antimicrobial antibodies (95) •Methotrexate
*MC women 40-60yo •hepatomegaly, jaundice, •(+) ANA •Cholestyramine-sx relief of pruritis
steatorrhea, portal HTN, mother •Elevated serum IgM levels
cirrhosis manifestations Definitive treatment: liver transplant
*DX clinically, no imaging

GI About/Causes Clinical Presentation Diagnostics Treatment/Prevention

Hepatocellular Types: Patient that has already had •Alk phos spike (higher then was before) Screening:
Carcinoma •Hepatocellular cirrhosis and now they are •Alpha feroprotein Cirrhosis & chronic HBV/HCV
-parenchymal cells declining patients are screening
•Cholangiocarcinoma Imaging: •Liver US & a-feroprotein q6mo
-ductal cells •Cechexia •CT: 1st line imaging! •US only detects 60%
*wasting of body, weakness •Liver biopsy: CONFIRMS!
Risks: •Severe wt loss, anorexia *can defer if MASS on CT & + alpha fetoprotein Treatment:
•Obesity •Weakness, muscle wasiting •resection if not invading
•male gender •Bloody ascities Staging: TNM •vasculature and preserved liver
•age >55 *necrotic tumor •T0=no tumor function
•DM •Tender hepatomegaly •T1=solitary tumor w/o vascular invasion •liver transplant
•HCV or HBV •T2=solitary tumor with vascular invasions or multiple
•Alcohol tumor <5cm •MELD score 20+ poor prognosis
•fhx •T3=multiple tumor >5cm or tumor involving major
branch of portal or hepatic vein Prognosis:

Cirrhosis Complications
Ascites/Edema
Spontaneous Bacterial Peritonitis
*MCC- E. Coli
Hepatorenal Syndrome
Occurs in 10% of patients with
advanced cirrhosis and ascites
Hepatic Encephalopathy
Anemia and Coagulopathy
Esophageal Varices
50% patients with cirrhosis
•T4=direct invade of adjacent organs (not gallbladder)
•Sodium restriction
•Diuretics (Spironolocatone, Furosemide)
•Paracentesis
-if unresponsive to diuretics, can’t tolerate diuretics, resp sx
-can use with albumin to move fluid
•Ascites with worsening abdominal pain, fever, WBC
•DX: dipstick or culture of fluid
•Azotemia in the absence of intrinsic renal disease
•Two types:
-type I: sudden doubling of Cr >2.5
-type II: slowly progressive
•Stages: mild confusion -> drowsiness, stupor, coma
•Causes: CNS drugs, TIPS
•DX: clinical (elevated ammonia w/ sx), no imaging
•Iron deficiency: ferrous sulfate
•Folate deficiency: folic acid *most common in alcoholics
•DX: EGD *all cirrhosis patients should undergo a EGD
•TX: IV fluids, PRBCs, FFP, Ocretotide, EGD when stable, ABX
•One year ~23%, five year ~5%
•Transjugular Intrahepatic Portosystemic Shunt (TIPS)
-primary indication for variceal bleeding
-shunts blood out of portal system -> reduces portal HTN ->
decreased occurrence of ascites
Problems: bleeding, shunt occlusion, hepatic encephalopathy
•TX: Cefoxaime 2gm IV x5-7d, can follow w/ oral fluoroquinalone
•Prophylaxis: oral fluoroquinalone
Labs: increase BUN/Cr, hyponatremia, oliguria
•TX:
Stop diuretics & Increase blood flow to kidneys
IV albumin, Dialysis; TIPS, Liver transplant
•TX:
reduce protein intake
lactulose (breaks down ammonia)
ABX (Rifaximin, Metronidazole) minimize ammonia producing
bacteria
•Transfusion if due to severe blood loss from bleeding varices
•Vitamin K for severe coagulopathies w/ FFP
•Oral thrombocytopoetin (maybe for thrombocytopenia)
•Procedures: banding, sclerotherapy, balloon tamponade
*balloon tamponade has complications, only do if others don’t work
•Prevention: band ligationg AND BB (Propranolol), TIPS, transplant
GI About/Causes Clinical Presentation Diagnostics Treatment/Prevention
Hepatitis A •Fecal-oral route •Incubation ~30 days •Hep A Antibody (Anti-HAV) Treatment:
•Crowding and poor •Seen in feces 2 wks before onset of sx -IgM peak in first week of sx *active infection •Symptomatic -> rest & fluids
sanitation -IgG rises for months -> years. •Avoid exertion, alcohol, and
•Contaminated food •Malaise, myalgia, N/V, anorexia hepatotoxic drugs
•Aversion to smoking (no craving) •ALT/AST (LT>ST) & bilirubin elevations *recover in ~3months
•RUQ abdominal pain, jaundice
•Mild hepatomegaly, liver tenderness Blood smear: Atypical large lymphocytes Prevention: Hand washing, vaccine

Acute •Double stranded DNA •Incubation 12-14wks (up to 6mo) •HBsAG (surface antigen)-infective state! •Recovery ~3-6 months
Hepatitis B •Insidious onset, variable *first to elevate, first sign
•Inner core protein and •Asymptomatic •Rest, increase fluids, nutrition
outer surface coat •Anti-HBs (surface antibody) •Avoid activity, alcohol, hepatotoxic
•Flu-like: Malaise, myalgia, fatigue *indicates recovery of acute and non-infectivity
Causes: •Low grade fever, anorexia •Hepatitis B Immune Globulin
•Bloodborne •Recurrent infections (URI) •Anti-HBC (antibody to core antigen) (HBIG) *must give within 7d
•Sexual contact •Enlarged lymph -IgM after HBsAG, indicates diagnosis of Hep B -shorten duration & reduce severity
•Mother -> baby •Distaste for smoking -newborns with HBV + mothers
•Mild RUQ pain and hepatomegaly •BEeAG (envelope antigen) *definitely infected
Risk populations: •Jaundice - fter HBsAG, rapid replication & infectivity *HOSPITALIZE FULMINANT
•IV drugs ATTACKS (liver sx)
•inmates •Can become severe fulminant disease •HBV DNA: parallels presence of HBeAG
•healthcare workers Prevent: universal, safe sex, needle
•Acute subsides in ~2-3wks •Elevated ALT/AST (LT > ST), bilirubin & ALP sharing education, vaccination x3
•PT prolongation (fulminant hepatitis)

Chronic 40% develop cirrhosis Periods of remission with acute flares Elevated HBsAG and ALT/AST for >6 months! •Interferon-inhibit viral replication
Hepatitis B Increases CA risk -BBW-infections
Increased risk of hepatocellular Treatment:
carcinoma •Antivirals: Tenofoir, Adefovir, Entecavir •Nucleoside analog (Lamivudine)
-Inhibits reverse transcriptase

Hepatitis C •Bloodborne Incubation period 6 weeks HCV antibodies=INFECTION! Treatment:

•Sex •asymptomatic  Fatigue, myalgia •ALT/AST rise and decline •Direct Acting Antiviral (DAA)
•Jaundice wax and wane •Interferon
Risk populations: •HCV antibodies present (anti-HCV) •Add Ribavirin if no improvement
•IV drugs Complications: *signifies HCV as causes of hepatitis
•inmates •hepatitis C •Non-Hodgkins
•healthcare workers •DM, glomerulonephritis, pulmonary •HCV RNA
fibrosis, thyroiditis -indicates current infection

Hepatitis D Hep B co-infection Increased risk of fulminant hepatitis •serum antibodies •Worse prognosis

Hepatitis E •RNA virus, Waterborne Extrahepatic: “PANT” •IgM anti-HEV in serum •Self-limited *possible cirrhosis
•Pancreatitis, Arthritis, Neuro (Guillan- •Oral Ribavirin x3 months
•Central and SE Asia,
Barre), Thrombrocytopenia •Recombinant vaccines
Middle East, North Africa
Spread: swine, pet, orangs
GI Causes Five Groups Associated Sx Physical Exam/Diagnostics Treatment
Acute *more than 90% diarrhea 1) Travelers diarrhea (Giardia) Fever, abd tender Physical Exam: Diet-BRAT
Diarrhea due to infectious agent •Inflammatory •Note hydration, mental •Hydration (carbs and electrolytes),
2) Consumers of certain foods status abdominal tenderness •bowel rest (no fiber, milk, alc, caff)
Acute Most acquired by: •Chicken-Salmonella, campylobacter, N/V
<4wks Fecal-oral transmission Shigella •S. aureus, B. cerus Diagnostics: self-limited ~5d Rehydration
Ingestion of food/water •Undercooked hamburger-E. coli *begins 1-6h after •Fluids containing glucose, Na, K,
Persistent Disturbances of flora by •Fried rice or reheated-Bacillus cereus •Noro & rotavirus If persists >7 days: Cl, bicarb ~50-200ml/kg/24h
2-4wks antibiotics -> C. diff •Mayo or creams-Staph or Salmonella *begins 24-48h •Stool sample & studies *salt, baking soda, sugar, OJ, water
•Eggs-Salmonella after Orange tube: foodborne ill Other: pedialyte, gatorade
When to admit: •Undercooked food or soft cheese-Listeria Pink and Grey: parasites
Severe dehydration Volume depletion White: C. diff Antidiarrheal agents
organ failure 3) Immunodeficient •Non-inflammatory •Fecal leukocytes *do NOT use in bloody diarrhea,
altered mental status •Vibrio cholera (+)= inflammatory high fever, systemic toxicity
hemolytic-uremic syn. 4) Daycare-shigella, giardia, rotavirus, hep (-)= noninflammatory Loperamide, Pepto-Bismol, Lomotil
(AKI, thrombocytopenia, Immunocomp. •Stool culture (SSYC)
hemolytic anemia) 5) institutionalized •CMV •O/P ABX-Cipro, Levo; Doxy, Bactrim
*MC nosocomial infection •Protozoans •Stool for C. diff *use if high fever, bloody stools,
immunocompromised, dehydration
Diarrhea Causes Evaluation
Chronic •Medications: •Secretory Conditions •Systemic: hyperthyroid disease, Labs: CMC, CMP, TSH, Vit A+D,
Diarrhea Cholinesterase inhibitors, SSRIs, ARBs, Increased intestinal secretion or DM INR, ESR, CRP, B12, folate, iron,
>4 weeks PPIs, NSAIDs, Metformin, Alllopurinol, decreased absorption results in high- •Chronic Infections: celiac disease serologic testing
Orlistat volume water diarrhea with normal Giardia, E. histolytica, Cyclospora,
osmotic gap C. diff, intestinal nematodes Stool studies: O/P, electrolytes,
•Osmotic Diarrheas: * osmotic gap •Motility Disorders: IBS (MC!) staining for fat, occult blood, leuko
Carbohydrate malabsorption (lactose), Causes: endocrine tumors, bile salt •Malabsorptive conditions
laxative abuse, malabsorption syndromes malabsorption •Inflammatory Conditions: Endoscope: exclude IBD or neoplasia
ASK IF GOES AWAY WITH FASTING IBD, UC, crohn disease

GI About Presentation Findings Treatment

Anorexia •Refusal to maintain a minimally normal body LOW BMI (>17.5kg/m2) or body weight <85% ideal Labs: CBC, CMP, UA, 1st line-multimodal
Nervosa weight due to desire for thinness electrolytes, INR, EKG (therapy, SSRI,
•Morbid fear of gaining weight Clinical findings: emancipation (thin), depressed, nutrition)
fatigue, bone pain, amenorrhea, abd pain, constipation, •Leukocytosis & leukopenia
Types: hair loss, brittle nails, Russel Sign (callous on hands), •Anemia Hospital:
Restrictive: reduced calorie intake, dieting, hypothermia, decrease HR and BP, lanugo, petechial, •Hypokalemia •<75% ideal body wt
excessive exercise, diet pills osteoporosis •Hypothyroidism •electrolyte imbalances
•Increased BUN (dehydration) •cardiac abnormalities
Purging: primarily engages in self-induced
vomiting, diuretic, laxative, enema

MC in women and mid-teens

Diarrhea Drugs
Loperamide (Imodium)
Diphenoxylate (Lomotil)
Schedule V; 1st line
Bismuth (Pepto-Bismol,
Maalox, Kaopectate)
Ocreotide (Sandostatin)
Cholestyramine
(Questran)
Antispasmodics
Hyoscyamine (Levisin)
Dicyclomine (Bentyl)
MOA
•Inhibits peristalsis and gut transit
•Opioid receptor agonists (mu receptor
gut)
•Reduces secretions, some antimicrobial
effects
•Inhibits intestinal fluid secretion and
stimulates intestinal absorption
*use-chronic secretory diarrhea
•Binds intestinal bile acids
*use for chronic secretory or
malabsorptive diarrhea
(post small resections,
cholecystectomy)
•Relaxes intestinal smooth muscle,
inhibits spasms and contraction
*diarrhea associated with IBS (Bentyl)
*can use for bladder spasms (Levsin)
Dosing
Imodium OTC 4mg x 1
Lomotil 2.5mg-2 po QID
OTC oral tablet or suspension
50-250mcg SC TID
Powder: 4gm packet
*sprinkle into food QID
*can lower cholesterol too
Bentyl: 20mg tablet QID
Levsin: 0.125mg ODT q4h prn
CI
bloody or C. diff diarrhea; Pts
<2yo
Lomotil:
Acute diarrhea-> toxic megacolon
Caution: DM, thyoid, pancreas,
kidney, liver, arrhythmia
*inhibits hormone production
•Toxic megacolon
•Inflammatory bowel disease
Adverse Effects
•Constipation, abd cramp, dizzy
•Serious: paralytic ileus, toxic
megacolon
•Black stool, black tongue
•Constipation, Tinnitus
•Cholelthiasis/cholecystitis/biliary
tract disease
•Edema, Constipation
•Biliary/intestinal obstruction
•Fecal impaction
•Constipation, abd pain,
flatulence
•Ileus, delirium, nervous,
palpitations, constipation,
xerostomia, mydriasis

Constipation Drugs MOA CI Adverse Effects

Fiber/Bulk Forming Laxatives •Fiber promotes intestinal motility by increasing “bulk” of stool •GI obstruction •GI obstruction
Metamucil Citrucil, •Draws water into stool •Abdominal
FiberCon Benefiber *problem if not drinking water with fiber then can cause constipation cramps/distention
•Flatulence
Stool Softeners/Surfactants •Emollient that covers stool and softens it •Do NOT use for
Ducosate (Colace) •Allows it to pass through colon easier SEVERE
Mineral Oil don’t typically see mineral oil because can interfere with absorption

Osmotic Laxatives •Increases secretion of water into the intestine •Abdominal bloating/cramps
Milk of Magnesia •Softens stool and promotes defecation •Flatulence
Miralax •Usually works within 24h *not immediate relief •Diarrhea
Enulose *use for opioid induced and chronic constipation

Bowel Cleansers •Osmotic laxatice

Polyethylene glycol (GoLYTELY) •More rapid, COMPLETE bowel cleanse
Magensium citrate
Sodium phosphate (Fleets) *used prior to colonoscopy, bowel surgeries

Stimulant Laxatives •Stimulate fluid secretion and colonic contraction -> “irritants” •NOT for long term use •N/V/D, abdominal cramps
Bisacodyl (Ducolax) •Irritate intestinal wall, causing fluid accumulations and increased contractions •Electrolyte abnormalities
Senna (Senekot) of intestines -> increases motility *can become dependent
Cascara
*works within 6-12 hours; can use about 3-4x per week “rescue” agent
Enemas •Commonly used as adjunct to bowel cleanse (osmotic laxative) prior to
Tap water surgical procedures/colonoscopy
Sodium Phosphate (Fleets)
Mineral Oil (ok to use here) *common in hospital setting

N/V Drugs Class Indication Side Effects Safety/Monitoring/CI Dosing/PD

Scopolamine Anticholinergic •Motion sickness *drys everything up Pregnancy Category C Form: patch
(Transderm Scop) •Prevention postop N/V •Xerostomia, dizziness, drowsy, urinary *C=use with caution *can be expensive
retention, mydriasis (pupil dilation)

Ondansetron Serotonin 5-HT3 •Acute N/V •HA •Pregnancy (1st trimester) Form: IM, IV, tab, ODT
(Zofran) receptor agonist •Postoperative N/V •diarrhea/constipation •QT prolongation (sublingual-tongue), liquid
•Chemotrherapy N/V •fatigue, dizziness Dose: 4-8mg
1st line •Hyperemesis •pruritis
gravidarum •liver metabolism
*last resort *pretty well tolerated; NO SEDATION *caution hepatic

Promethazine Dopamine •Acute N/V Common SE: •Pregnancy Category C Forms: IM, IV, oral, tablet,
(Phenergan) Antagonist •Sedation, blurred vision, confusion, *better in 1st trimester rectal suppository
xerostomia, dermatitis, urinary retention,
*1st gen *usually given in the constipation Caution: Dose: 12.5-25mg q4-6h prn
antihistamine hospital for people with •elderly, asthma/COPD,
migraines Serious SE: glaucoma, BPH, cardiac •Liver metabolism
•Respiratory distress, seizure, leukopenia, Ds, hepatic Ds, seizure Ds •CYP450
thrombocytopenia, hallucinations, *caution w/ hepatic
extrapyramidal, bradycardia Labs: obtain CBC

BBW respiratory distress Monitor: ophtho exam with

issue injury/necrosis (with IM injection) prolonged use

Metoclopramide Prokinetic •N/V adjunct Common SE: Pregnancy category B Form: IM, IV, oral tab, liquid
(Reglan) •Gastroparesis (slow •Diarrhea, drowsy, restlessness,
gut) anxiety/depression/insomnia, HA/dizziness, CI: seizure, GI obstruction Dose: 10-20mg BID
increases •GERD hormonal, HTN *causes bigger obstruction
peristalsis by •Liver metabolism
binding to D2 Serious SE: Caution: HTN, Parkinsons, •renal excretion
receptor *usually use in cases •Extrapyramidal, neuroleptic malignant CHF, Depression, DM,
where you want to syn., seizure, depression/suicidal, HTN, Renal impairement
stimulate the bowel leukopenia/agranulocytosis, CHF, arrhythmia
Labs: CrCl baseline
BBW Tardive Dyskinesia (repeat
movements) do not abruptly stop->taper
*usually irreversible; avoid in elderly
GI: BARIATRIC SURGERY

Only proven method to reduce and maintain weight loss

Guidelines:
- BMI >40 or BMI >35 with a medical problem related to morbid obesity
- Failed other non-surgical weight loss programs
- Physiologically stable and can follow post-op instruction
- Obesity not caused by a medical disease (such as endocrine disorders)

Types of Procedures:
- Restrictive: less extensive but less weight loss
o Adjustable Gastric Banding (AGB) *only one for BMI >30
 Proximal gastric puch is created using an inflatable band and an access port
 35-45% EBW lost
 less complications, but frequent follow-ups
o Vertical Banded Gastroplasty (VBG)
o Sleeve Gastrectomy (SG)
 85% stomach removed, leaving pylorus and stomach intact

- Malabsorptive:
o Biliopancreatic Diversion (BPD)
o Biliopancreatic Diversion with/without duodenal switch (BPD/DS)
 Many complications and malnutrition problems
 70-90% EBW lost

- Combo Restrictive & Malabsorptive:

o Roux-en-Y Gastric Bypass (RNYGB)
 MC method for severe obesity
 Proximal gastric pouch created by transecting the stomach & creating gastrojejunostomy
 75-85% excess body weight loss in first 2 years
 nutritional problems less severe
 Complication: dumping syndrome

Early Complications:
- anastomatic leak
- DVT and PE
- Bleeding
- Infection
- Splenic Injury

Late Complications:
- Malnutrition
- Marginal ulcer and anastomotic strictures
- Internal hernia
- Cholelithiasis
 - Band slippage
- Band erosion
- Esophageal dilation

Pre-Op/Post-Op 12% **DVT in cardiology ***Clotting in heme/onc

6 predictors of surgical cardiac complications:
 IHD, CHF, CVD, high-risk operation, pre-treatment with insulin, pre-op creatinine >2.0
 Additional risks: age, smoking, abnormal stress test, long-term BB therapy, COPD

Obtain noninvasive stress test in:

 Anyone with active cardiac conditions
 Patients requiring vascular operations
Coronary revascularization before non-cardiac operations in patients with:
 Significant left main coronary artery stenosis
 Stable angina with three-vessel coronary disease
 Stable angina with two-vessel disease
 Significant proximal left anterior descending coronary artery stenosis with either an ejection fraction <50% or ischemia on noninvasive testing
 High-risk unstable angina or non–ST-segment elevation MI, or acute ST-elevation MI

MC perioperative complications: pulmonary system

- Smokers should ideally stop smoking 8 weeks prior to surgery

Pre/Pos About Wound Cleansing

t
Wound Skin and wound cleansers
•agents: NS, sterile water
•debatable: diluted hydrogen
peroxide, tap water
•avoid: iodine, full hydrogen
peroxide
Mechanical Scrubbing
•sponge/brush works to
dislodge any debris lodges in
wound
•aggressive brush worsens
scarring
•avoid soaking the wound
*increased bacterial
colonization
Debridement:
•selective debdridement safest
-remove wound borders that are
mangled, irregular, nectrotic
Clean and Debride:
•hair can act as a FB & delay healing
•move hair away with sterile liquid,
petroleum-based ointment
NEVER remove eyebrow/eyelash
Lacerations can be closed by:
•sutures
•5-0 or 6-0 for face
•3-0 to 5-0 for scalp, ext., others
•staples: MC on scalp, never on face
•adhesive tape: cant use alone w/ hand
or joints
•tissue adhesives: NO hands or joints
•hair apposition: only on scalp
Primary Closure: immediately after
CI:
•heavy bacterial colonization
•bite wound
•tissue defect or retained FB
•poor perfusion
Secondary Closure: Allowing wound to
heal by secondary intention
Delayed Closure Packing the wound and
performing closure at a later date once
infection ruled out (48-96h)
Procedure:
•after debridement, gently pack wound
with saline moistened fine-mesh gauze
•pt will have to change gauze 1-3x/day
•follow up in 24-48h for wound check
ABX:
•uncomplicated:
Cephalexin, Macrolide of Clinda
•grossly contaminated or retained FB:
Augmentin, Clinda + FQ
•bite wound: Augmentin, Clinda+ FQ
•plantar puncture wound:
Cipro, Cephalexin
•immunocompromised:
Augmentin, Clinda + FQ
•impaired local defense:
Augmentin + Clinda
Wound Cleansing: 8hr later with soap & water
Suture Removal:
•face: 3-5 days
•hands, feet, buttocks, joints: 10-14d
•all other: 7-10d
Tetanus Prophylaxis
Don’t know: IG + toxoid >5-10yr ago: booster
Pre/Post-Op
Wind
MCC fever post-op day 1 is
atelectasis (24-48 hours)
Symptoms:
Fluid overload
Rales
Bronchial breathing
Diagnostics/TX: CXR, BNP,
spirometry, nebulizer
Post-Op Fever
Water
UTI (48-72 hours)
MC nosocomial infection
Cause: catheter, GU instrument
Symptoms:
Dysuria, frequenct, urgency
hematuria
Diagnostics:UA, CBC
Walking Wound
DVT (>72 hours) #1 cause of fever day 3 (>72h)
Superficial or deep MC organism: Staph
*superficial:IV catheter Others: e.coli, enterococcus,
*deep: indwelling central line or DVT clostriudium (bronze-brown)
SX: swollen calf, red, tender DX: WBC, blood cx, CT
DX: Homans, Duplex US Treatment:
change dressing q24 hours
TX: SCDs, Lovenox SQ I&D if abscess + ABX
Wonder Drugs
1 week post-op
Ex: anesthesia, sulfs, ect.
Blood/FFP/plt/RBC/chemo
DX: blood cx x2, check wounds
and central/PICC lines
Treatment:
Prophylaxis tylebol, Benadryl

Substance About Intoxication Withdrawal Treatment

Alcohol Drink: 12oz beer, 8oz malt. 5oz wine
At-Risk Drinking:
-men: 4 drinks/day or 14 drinks/week
-women: 3 drinks/day or 7 drinks/week
Moderate-Severe Drinking:
•Recurrent use of alcohol despite risks
Tolerance: need for increased amounts
of alcohol; diminished effect
Alcohol Intoxication:
•Slurred speech
•incoordination, unsteady gait
•nystagmus
•impairment in memory or attention
Wernickes: confusion, ataxia,
ophthalmalgia
Karsakoff: amnesia, aphasia, apraxia,
agnosia
•uncomplicated (6-24h): increased CNS Withdrawal:
activity (tremors, anxiety, diaphoresis, •Benzos, Clonidine,
palpitations, insomnia) •IV fluids
•Thiamine & Mg & Glucose
•withdrawal seizure (12-24h): tonic-clonic
Chronic use TX:
•alcoholic hallucinosis (48h): hallucinations •Naltrexon
with normal vital signs •Campral
•Thiamine
•delirium tremens (2-5d): delirium, •Antabuse
hallucinations, agitations, abnormal vitals

Substance Intoxication Withdrawal Treatment

Tobacco Withdrawal: (+) effects: decrease anxiety and Surgical Treatment:
•restless, irritable, anxiety appetite, increase mood, alertness, -Buproprion
•sleep abnormalities soling -Nicotine Lozenge *benefits of NRT outweigh the risks
•depression
Surgery Effects: effects wound healing, CV risks
•nicotine craving (-) effects: CA, DM, COPD, asthma,
•weight gain dental, infection Goal:
-stop smoking 8wk prior to surgery
Tolerance due to UP REGULATION -NO nicotine gum around time of surgery

Opioid MOA: mu receptor agonist Withdrawal Intoxiation: Naltrexone (1st line), Methadone, Buprenorphine
heroin, •lacrimation OD: Nalaxone
oxycodone, Intoxication: •HTN, tachycardia Withdrawal: Methadone, Clonidine, Suboxone
morphine, •euphora, sedation & impaired memory •pruritic
meperidine, •slurred speech •piloerections (goose bumps) Surgical Problems:
codeine •pupil constriction •pupil dilation -venous access
•respiratory depression •flu-like symptoms -arterial injury
•bradycardia & hypotension •yawning -DVT
•nausea, vomit, flushing -abscess and gangrene
-tissue compression & injury

Alcohol Chronic Use

Drug MOA Side Effects Dosing CI/DDI
Thiamine •Low BP Acute: 50-100mg IV/po
(B1) •Effect glucose metabolism
Wernicke: 100mg IV
500 BID x2d, qd x5d, then 100mg

Chronic: 50mg po daily

Naltrexone Blocks dopamine release, antagonizes mu BBW: hepatocellular 50mg daily CI: opioid dependency
1st LINE receptor  decreases craving and reward •N/V/D/C, abd pain
•dizzy, HA, anxiety, fatigue Vivitrol: 380mg IM monthly DDI: opioids

Acamprosate Restores glutamate •Diarrhea, nausea, abd pain 66mg TID (333 for renal) CI: renal (Cr <30)
(Campral)  Stops withdrawal S/S •fatigue, HA, amnesia, mood
1st LINE

Disulfiram Inhibits enzyme aldehyde dehydrogenase  •Metallic taste 500mg/d for 1-2wk, 250mg/d CI: heart or CAD, ethanol
(Antabuse) increases acetaldehyde  Fs you up
2nd Line •Effects of drug  sweating, HA, DI: “WAM”
dyspnea, low BP, flushing, palp warfarin, amitriptyline,
metronidazole

Opioid Overdose Treatment

Drug MOA Dose Side Effects
Naloxone Short-acting opioid antagonist Cardiorespiratory: 2mg
ventilations: 0.05mg IV
*titrate up every few minutes until RR
>12/min

Opioid Use Treatment

Drug MOA Dose Side Effects
Naltrexone Blocks dopamine release, antagonizes mu receptor 25-50mg daily BBW: hepatocellular
1st LINE  decreases craving and reward N/V/D/C, abd pain, dizzy, HA, anxiety, fatigue
*opioid antagonist, completely blocks effects Vivitrol (IV): 380mg IM/4wks

Methadone Long-acting opioid agonist 20-30mg po, titrate up (80-120mg) •Constipation, drowsiness, sweating
•peripheral edema, hyperalgesia
•reduced libido, ED
•QT prolongation, OVERDOSE

Buprenorphin Partial agonist *often in combo with Naloxone •HA, nausea, pain
e *take home therapy 4mg B/1mg N daily •insomnia
most stabile on 16-20mg/d B •withdrawal syndrome

Taper by reducing 2mg/1-2wk Rare: liver, necrosis, anaphylaxis

Type I DM no insulin due to destruction of beta-cells (islet 3 Ps: Monitor: •insulin (multiple-dose basal bolus)
cells of the pancreas) *antibodies •polyuria (pee) •check glucose 3x daily -short acting: Humalog, Novalog
•polydipsia (thirst at home, increase fiber in -basal: Glargine, Lantus, Levemir
•Islets of Langerhans infiltrated by lymph •polyphagia (hunger) diet •Pramlitide (Symlin) *adjunct only
islet cell autoantibodies, T-lymph proliferate, •GFR and urine
release of cytokines within infiltrated islets albumin/year Dawn Phenomenon:
•Weight loss (low
•nml glucose until 2-8am
water)
preproinsulin (A, B, and C)  proinsulin (A & Labs: •decreased insulin sensitivity & nightly hormones
B)  insulin (C chain cleaves off) •postural hypotension •treat with bedtime injection of NPH
•weakness, blurred • glucose >200, fast>126
Insulin functions: glucose transport; stops vision, neuropathy, •A1C >6.5%, GGT Somogyi effect:
protein & TG breakdown, and gluconeogenesis fatigue •C-pep/Insulin ratio (low) •night hypoglycemia  rebound hyperglycemia due
to surge of GH
•treat with decreased night NPH dose
Incretin: hormone that stimulates the release of (+)GAD-65 with type IA
insulin and decrease blood glucose
Type II DM Risks: •polyuria, polydipsia •self-check glucose 1- 1st line-Metformin + diet + exercise
•(+) fhx; N. American, AA, Hispanics, Asians •blurred vision 2x/d 2nd line-GLP1 ag., SGLT-2, DPP-4
•overweight (obese), birth wt >9lbs •poor wound heal •weight loss (5-10%) GLP1: “-tide”, DDP4: “-gliptin” SGLT2: “-glifozin”
•hyperglycemia •neuropathy •caloric restriction *insulin 0.1-0.2U if A1C>9 or sig. sx
•dry and itchy skin •eye exam, neuropathy
DM Treatment: •A1C 2x/year
Hypoglycemia: Sulfon, Meglit, Pramlintide, Insulin
Surgery:
Affordable: Metformin, Sulfonylureas -Elevated glucose post-op increases your risk of
Yearly eye exams
Weight Loss: GLP-1 Agonists, SGLT2 inhibitors;
Recheck meds q3mo infection and prolonged stay (>140)
Weight Gain: Sulfonylureas, TZDs, insulin -TX: IV short-acting or sliding scale insulin

Diabetic metabolic acidosis 1+ days of ↑ thirst with •Glucose: 350-900 1-Fluid: 1L/hr 0.9% NS or LR 1-2h
Ketoacidosis polyuria and polydipsia •pH: acidic (6.8-7.3) *if Na rises, change to 0.45%
•Relative/absolute insulin def.
•GI: N/V, fruity breath 2-monitor cap glucose/hr & BMP/4hr for 1st 24hrs
•Excessive counter hormones •Potassium nml or ↑
•↓ Bicarbonate b/c depleted by ketoacids •Cardio: ↓ BP, ↑ HR •Sodium ↓Bicarbonate ↓ 3-IV regular insulin 0.1U/kg/hr
•↓ Insulin, ↑Glucagon *due to volume *change to dextrose when glucose 200mg/dL
-↑ hepatic gluconeogenesis and glycogenolysis depletion •Renal: ↑BUN/Cr, ↓GFR Goal glucose: 150-200mg/dL
-↑ free FA release -> ↑ ketones
•Neuro: •Ketones: acetone, 4-Potassium 10meq if <5.2
*triggered during increased physiologic need
Mild-alert or drowsy acetoacetate, B-hydroxy 5-Bicarb if pH <7.0 (50meq/L/2hrs)
Severe-confusion, coma *serum checks B-hydroxy,
•Respiratory: kussmaul

Hyperglycemi Insulin deficiency and inadequate fluid intake polyuria, polydipsia, •Glucose: 600-1200 1-Fluid management
a weakness, decreased oral Infusion 1-3L/hr 0.9% NS 1-3h
•pH: nml or minimal acid
Hyperosmolar •Triggered by stress: intake, wt loss *if Na rises >150, change to 0.45%
State -infection, infarction, ↓ water •K+ and bicarb nml 2-monitor *same as DKA
•Neuro: altered mental
•Renal: ↑BUN/Cr, ↓GFR 3-IV regular insulin 0.1U/kg/hr *NO if K <3.3
•Cardio: ↓ BP, ↑ HR *change to dextrose when glucose 250mg/dL
•Osmolality: 330-380
Goal glucose: 250-300mg/dL
*often >350
4-Potassium-10meq/hr, ↑ if K+ <3.5

Hypercalcemia Calcium >10.5 “stones, bones, abdominal moans, psychic EKG: shortened QT interval Mild: no treatment
groans”
Causes: •High Ca and PTH Severe/symptomatic:
•hyperparathyroidism •Low Ph •IV saline  Furosemide (Lasix)
•malignancy (low PTH) •NO HCTZ (increases Ca2+)

Hypocalcemia Calcium <8.4 •Chovstek (touching cheek) EKG: prolonged QT internal Mild: oral calcium and vitamin D
(Ergocalciferol, Calcitriol)
Causes: •Trousseu (BP cuff), cramps, spasms, Low Ca and PTH
•hypoparathyroidism (low PTH) tetany  lower action potential threshold High Ph Severe/sympatomatic: Calcium
•Renal disease (high PTH) gluconate IV or calcium carbonate IV
•Hypomagnesemia

Hypermagnesiu Magnesium >2.6 Muscle weknaess EKG: prolonged QT, PR and •IV NS 0.9% (isotonic)
m wide QRS •Loop diuretics

Hypomagensium Magnesium <1.8 Muscle weakness EKG: prolonged QT, •IV magnesium sulfate
Hyperreflexia Torsades, V-tach •Oral magnesium if chronic

Hyperkalemia Potassium >5.5 Muscle fatigue EKG: peaked T waves, •Insulin

prolonged QRS •Sodium bicarbonate and glucose
(drives K+ into the cell)
•Calcium gluconate (antagonize effects
on heart)

Hypokalemia Potassium <3.5 Muscle cramps EKG: Flat/inverted T waves •Potassium repletion
Constipation U waves NO DEXTROSE liquids
Hypernatremia Sodium >145 Poor skin turgor Na >145 •hypotonic fluids
Dry mucous membrances High BUN/Cr -water, 0.45% NS, 5% D5W
Causes: Flat neck veins
•Body loss: diarrhea, sweat, Hypotension
diuretics
•Hyperglycemia CNS dysfunction: confusion, lethargy,
•Burns coma, muscle weakness
•D.I. (low Na in urine, high in
serum)

Hyponatremia Sodium <135 •CNS dysfunction: Na <135 Free water restriction

*cerebral edema IV normal saline 0.9%
 Hypervolemic: CHF, nephrotic, HA, AMS, seizure, decreased DTR Possible loop diuretics
RF, cirrhosis Muscle cramps
N/V, hypervolemic: hypertonic 3% saline
Euvolemic: SIADH, steroids,
hypothyroid
Correct slowely by <10meq/L over 24h
Hypovolemic: sodium loss,
diuretics

Fluid Overload/Depletion: 10-30% patients suffer AKI post-cardiac surgery

Daily fluids: wt (kg) x 30  Fluid over 24 hour period
- Requirement increase for: fever, hyperventilation, increased catabolism IV fluid

MC fluids: 2000 to 2500ml of 5% dextrose in normal saline or LR daily

- Do NOT add potassium in first 24 hour

Don’t need to measure electrolytes post-op unless external losses >1500ml/d

- Replace calcium is thyroidecetomy or parathyroidecetomy

Urinary catheter indications:

- Long procedure
- Urologic or low pelvic surgery
- Need to monitor fluid balance

Causes Labs
Metabolic Anion Gap-MUDPILERS Non-Anion Gap-HARDUPS •Low bicarb
Acidosis •Methanol •Uremia •Hyperalimentation •Acetazolamide •low ph
•DKA •Propylene glycol •Renal tubular acidosis •Diarrhea
•Isoniazid, infection •Lactic acidosis •Ureto-pelvic shunt •Post-hypopcapnis
•Ethylene glycol •Rhabdo.renal failure •Spironolactone
•Salicylates (ASA)

Metabolic CLEVER-PD •Increased

Alkalosis •Contraction •Licorice Bicarb
•Endo (Cushings) •Vomiting (loss of H+ from GI tract) •increased pH
•Excess Alkali •Refeeding Alkalosis
•Post-hypercapnia •Diuretics

Respiratory Hypoventilation-CHAMPP •High CO2

Acidosis •CNS depression) •Hemo/pneumothorax •low ph
•Airway obstruction •Myopathy
•Pneumonia •Pulmonary Edema

Respiratory Hyperventilation-CHAMPS •Low CO2

Alkalosis •CNS disease •Hypoxia •high pH
•Anxiety •Mechanical Ventilators
•Progesterone •Salicylates
Acute “Addisonian Crisis” •Hypovolemic Shock (MC!) •BMP •IVF: normal saline (D5NS if
Adrenal •Sudden worsening of adrenal •Hypotension -hyponatermia hypoglycemia)
Insufficiency insufficiency due to “stressful” event •Hypovolemia -hyperkalemia
•Abdominal pain, N/V -hypoglycemia •IV HIGH dose Hydrocortisone
Triggers: surgery, trauma, volume loss, •Fever
hypothermia, MI, fever, sepsis, •Weakness, lethargy, confusion •Reversal of electrolytes
hypoglycemia, steroid withdrawal •Fludricortisone
CARDIO About Clinical Presentation Diagnostics Treatment
Congestiv •Acute: began last few days to weeks •Chest pain, HTN, Flu-like sx GOAL: confirm sx & Lifestyle modifications:
e Heart •Chronic: sx present for months cause of HF •Wt loss, sodium <2g, fluids <2L
Failure Physical Exam: •Daily weight monitoring
•High: heart can’t meet demands General: tachy, diaphoresis Initial Testing Pharmacotherapy: Loop Diuretics
(supply<demand) •Narrow pulse pressure <25 EKG
-thyrotoxicosis, anemia; decreased CO CXR: kerley B, effusion, Class I:
•Low: insufficiency forward output (low EF) Volume Assessment congestion, cardiomegaly •ACEI (Check BMP for hyperkalemia)
•Rales or dull breath sounds •Entresto (Sabucitril + Valsartan)
•Systolic: reduced EF (HFrEF) •Edema, JVD Initial Labs: •BB (Carvedilol, Metoprolol, Bisprolol)
•Diastolic: preserved EF (HFpEF) •CBC, CMP, coagulation -caution: 1st AVB, asthma, bradycardia
Pulsus Alternans: LV HF studies, glucose, lipids •Aldosterone Antagonists
•Left: DOE, PND, orthopnea, fatigue Precordial: lateral displaced PMI •BNP (>500 very likely) -CI: K+ >5 or GFR <30
•Right *MCC of left sided HF •cardiac enzymes •Hydralazine/Nitrate (if black + ACEI/BB)
-JVD, hepatic congestion, ascities, edema Heart Sounds: S3 & S4
Echo: GOLD Acute: LMNOP: Lasix, Morphine, O2,
Nitrate, position

Aortic Valve General Features Clinical Presentation Diagnostic Studies Management

Aortic Stenosis Congenital v. acquired
-Congenital: bi or quad
-Acquired: *MC in elderly
•rheumatic fever
•degenerative (Ca2+)
-Risks: HTN, HLD, smoke
thickening  narrowing 
LVH  systolic dysfunction
Chronic Causes:
Aortic •Aortic leaflets:
Regurgitation rheumatic fever, congenital
abnormalities, endocarditis
•Aortic root:
dissection or dilation,
Marfan
*LVH due to dilation from
Most asymptomatic for years
Cardinal SX:angina, syncope, CHF
•Murmur:
-Harsh, Mid-systolic at R 2nd ICS
-Crescendo-decrescendo
-worse with leaning forward
-Radiates to CAROTIDS
-Thrill, S4 gallop, displaced PMI
*Asymptomatic for years
•CHF, angina
Murmur:
•Early diastolic, radiate to apex
•Decrescendo, blowing
•High pitch, 2nd and 4th L spaces
•Widened pulse pressure
•S3&S4 gallop
•Austin Flint Murmur maybe
Echo *diagnostic study of choice!
-severe: <1 cm 2 -critical: <0.7 cm 2
•Cardiac Catherization
confirms severe AS and any CAD
EKG: may demonstrate LVH
•Echo*diagnostic of choice
-monitors progression of disease
•1st line-AV Replacement with Sternotomy
-symptomatic patients
•2nd line-Transcutaneous Aortic Valve
Implantation/Replacement (TAVI/R)
*need a good myocardium
-poor candidates for open heart
-multiple comorbidities, high pre-op risk
-higher risk for stroke immediately after
•Balloon Valvuloplast: congenital AS
•Valve Replacement (AVR): those with
symptomatic severe AR or with LV changes
•AR prior to LC dilation greater than 50mm
or reduction in EF to less than 50%
•Vasodilator therapy-unload the ventricle
 Arterodilation
 Reduce afterload -> less pressure to
push back into the ventricle
 accommodating regurg
volume
Acute Aortic Causes:
Regurgitation •infective endocarditis
•trauma rupture of leaflet
EMERGENCY •aortic root dilation
•acute dysfunction of
prosthetic valve
•S/S of cardiogenic shock
•Pale, cool extremities
•Weak, rapid pulse
Murmur:
•low pitch, early diastolic
Echo *diagnostic study of choice
-performed quickly and bedside
*LV in unable to accommodate the
increased diastolic volume -> increased
pressures and pulmonary congestion
SURGICAL EMERGENCY
Vasodilator and diuretic if BP is stable
-Inotropic agents & vasopressors
**Treatment of choice: Urgent AVR

Mitral Valve General Features Clinical Presentation Diagnostic Studies Management

Mitral Stenosis •2/3 are women
•Don’t develop sx until 20-40
years following disease ~30-40yo
Causes:
•Rheumatic fever is MCC!
•congenital abnormalities,
connective tissue disorders, left
atrial tumors, aggressive surgical
repair of MR
•Dyspnea, orthopnea
•Atrial fibrillation *enlarged atria
•Hemoptysis (rupture of dialted bronchi)
•Blood tinged sputum *pulmonary edema
Additional findings:
•PE, edema, Ortner Syndrome (L recurrent
laryngeal nerve compression)
Murmur:
•Diastolic, Low-pitch, rumbling
•Heard at apex in LLD position w/ bel
•Opening snap following S2
EKG: LAE, RVH, A-fib
Echo: *diagnostic of choice
•Rhematic deformitity-doming
(hockey stick)
•Large LA compared to LV
-normal MV area: 4-6cm 2
-critical: <1cm 2
•smoke in left atrium
Cardiac cath: measure CO
Mild to moderate: CONTROL HR
Moderate to Severe (NYHA III-IV):
•Percutaneous balloon valvuloplasty
*not common or definitive treatment
Surgery is definitive treatment with
bioprosthetic or valve replacement

Mitral Valve •1-3% population; MC in women Nonspecific sx (MVP syndrome): DX: Echo •NO TREATMENT if mild prolapse
Prolapse •superior displacement in systole •chest pain, palpitations, dizzy, anxiety *diagnostic study of choice and asymptomatic

Causes: Murmur: *treat when regurgitation occurs!

-connective tissue disorder •Mid-systolic click, usually followed by
-Marfans or SLE late-systolic murmur
-Autosomal dominant •Heard at the apex
•Squatting: delays click
•Standing: earlier click
*gallops won’t change with position!

Chronic Abnormalities of mitral leaflets, •fatigue EKG: Reduce Afterload: *less regurg
Mitral annulus, chordae, papillary •dyspnea on exertion •LA enlargement, LVH, A-fib •vasoduilators (ACEI, hydralazine)
Regurgitation muscles •peripheral edema •diuretics
-MVP, LV dilation, posterior MI Echo: *Diagnostic of choice
-rheumatic fever Murmur: Surgery: annuloplasty
-endocarditis •blowing holosytolic murmur Cardiac Cath: *DEFINITIVE
•heard at apex & radiates to axilla/back •Assess function & filling pressures •should be performed before
•Regurgitating blood flow from •mid-systolic click irreversible myocyte damage and left
LV to LA in systole centricular remodeling occur

Monitoring: annual echo

Acute Mitral •Life threatening
Regurgitation •LA does not dilate to
accommodate regurg volume -
increase in LA and pulmonary
EMERGENCY venous pressure  congestion
Causes:
•acute MI, trauma, endocarditis
•tachyarrhythmia w/ chronic MR
•MVP
Tricuspid Valve Causes/
Tricuspid *MC in women •Uncommon
Stenosis •Usually associated with AS or MS
Causes
•rheumatic heart disease MCC!
•carcinoid, congenital valve
abnormalities, tumors
•Reduced RA emptying 
Increased venous congestion and
reduced RV CO  fluid overload
Tricuspid •Regurgitating blood flow from RV
Regurgitation to RA
•Secondary to dilation of the RV
and tricuspid annulus due to RV
failure (pulm HTN or L failure)
•Increased RA pressure -> increased
venous congestion & reduced RV
output -> volume overload
Pulmonic Valve Causes
Pulmonic CONGENITAL (peds pt)
Stenosis •Rheumatic disease is RARE
•Noonan, Trisomy 13
•Isolated congenital lesion
fusion of pulmonary leaflets ->
pressure overload -> RVH
Pulmonic •Result of dilation of the PV annulus
Regurgitation secondary to pulm HTN
Signs of cardiogenic shock SURGICAL EMERGENCY
Murmur: Urgent valve replacement
•Soft, low-pitched sound in early systole
*have high index of suspicion
S&S/Physical Exam/Murmur Diagnostics Treatment/Management
•Liver congestion •Echo-significant: <1cm 2 Diuretics
•Varices, Ascites, JVD, LE edema •Loop diuretics are best
•Palpable presystolic pulsation with •EKG: RA enlargement •ascites  ADD aldosterone
atrial contraction over liver antagonists (Spironolactone)
*always palpate liver with ascites •CXR: cardiomegaly from
enlarged R atrium Surgery:
Murmur: •TV replacement if symptomatic
•soft, high-pitch, mid-diastolic, L 4th ICS
•Accentuated with inspiration
•Opening snap at left sternal border
•Well tolerated without pulmonary HTN CXR: •Treatment of underlying cause
•As it progresses, may have RV failure:
-fatigue, abd bloat & peripheral edema •Repair TV with annuloplasty
*persistent symptoms
Physical Exam:
•JVD, hepatic congestion and palpable •TV replacement
systolic pulsation *pts with underlying primary leaflet
pathologic condition
Murmur:
•High pitch, pansystolic, tricuspid post
•accentuated with inspiration or leg raise
S/S Murmur Management/Treatment
Critical at birth: Murmur:
•Central cyanosis at birth •systolic at pulmonic post Mild: (pressure <30mmHg)
•otherwise asymptomatic until •increases with inspiration •asymptomatic and no intervention
adolescence or young adulthood •RV lift on palpation of
precordium Moderate-Severe: (>50mmHg)
Moderate-Severe: •S1 followed by opening click •Balloon valvuloplasty or surgical
•fatigue, dyspnea that’s louder with expiration valve replacement
•-> RV dysfunction -> RV failure
•Sx due to primary disease and secondary Murmur: TREAT PULMONARY HTN!
to RV failure •High pitched, blowing
•Heard at 2nd L ICS •PV replacement is rare because its
 being cause by pulmonary HTN, so it
will come back if that is still present

Sinus Dysrhythmias About Symptoms Management

Sinus Arrhythmia •Cyclic increase in normal heart rate with reflex changes in vagal influence on the normal No treatment required
inspiration and decrease with expiration pacemaker and disappears with breath holding or *not pathologic
increase in heart rate

Sinus Bradycardia Heart rate <60bpm
Rate increases with exercise, atropine
Causes:
•Increased ICP: hemorrhage
•Anterior MI: Inf. wall MI -> RCA supply SA
•OSA: decreased Hr <30bpm in apnea
•Other: hypothermia, hypothyroidism
•Increased vagal influence on the normal pacemaker •1st line-permanent pacemaker
or organic disease of sinus node
- Fear, bearing down, SSS Acute setting: transcutaneous pacing, temporary
transvenous pacing, Atropine (ACLS protocol)
•Severe <45bpm-sinus node pathology
SX:
•weakness, dizziness, confusion, syncope

Sick Sinus Syndrome •Commonly have recurrent supraventricular “When they go into AFIB its really fast then when Symptomatic  Pacemaker (PPM)
arrhythmias and bradycardia “tachy-brady” they go out of afib they go into a really slow sinus
brady”
•MC in elderly
•Cause: medications

Sinus Tachycardia •HR >100bpm Symptoms: palpitations, lightheadedness Physiologic: none needed, try massage
•Onset & termination usually GRADUAL *usually related to the cause *usually a compensatory mechanism

Causes: •2 types: inappropriate, POTS Symptomatic pts w/ or w/o correctable:

•MC-exercise, anger/stress *inappropriate sinus tach, POTS
- Beta-blockers (Metoprolol) or CCB

Dysrhythmia About Causes Signs and Symptoms Diagnose/Management

Premature ectopic focus in the atria that fires *frequently occurs in nml hearts Palpitations •Not required most of the time
Atrial before the next sinus node impulse •increased frequency with age
Contractions *diff P wave morphology •structural changes •Beta Blockers if significant symptoms
•precuroseor to afib, aflutter •Class IC antiarrhythmis is second-line

Premature Premature depolarization originates *frequently in normal heart •Many are completely asymptomatic •Symptomatic: BB (Metoprolol)
Ventricular from the ventricles •caffeine, stress, alcohol •Palpitations MC complaint •2nd line: Class Ic or III AAD
Contractions - wide QRS complex w/ pause •electrolyte abnormalities
•thyroid •Significant burden: cath ablation
Atrial About
Atrial Results from an ectopic atrial focus firing at a rate
Tachycardia faster than the sinus rate -> becomes pacemaker
•Onset and termination occur abruptly
•Atrial rate about 100-160bpm
•Unifocal or multifocal
Dysrhythmia About
AV Block •First degree: PR >0.21 with all atrial
impulses conducted
•2nd-degree: intermittent blocked beats
Mobitz type I (Wenckebach) AV block:
AV conduction time (PR) progressively
lengthens with the RR interval
shortening before the blocked beat
*abnormal conduction AV node
Mobitx type II AV block: there are
intermittently non-conducted atrial beats
*block in HIS bundle
•Third degree: complete heart block, in
which no supraventricular impulses are
conducted to the ventricles
Dysrhythmia About
Paroxysmal •Common cause of paroxysmal
Ventricular tachycardia
Tachycardia
Two common types of reentry:
•AVNRT (AV node reentrant tachy)
*within the node
*Most Common
•AVRT (AV reciprocating tachy)
 WPW: accessory path
*accessory path outside AV node
Causes Symptoms
•severe COPD -palpitations
•structural heart disease -heart racing sensation
•may occur in normal hearts -SOB
*not commonly -dizziness
•digoxin toxicity -near syncope
Causes Signs and Symptoms
First Degree and Mobitz Type I: First Degree Block:
•may occur in normal individuals -diagnosed by EKG alone
with heightened vagal tone
•drug effect Mobitz type I:
•electrolyte abnormalities -most commonly asymptomatic
•organic disease: ischemia, infarction, -may note palpitations, DOE,
inflammatory, fibrosis, calcification, dizziness
infiltration
Mobitz type II:
Mabotiz type II and 3rd degree: irregular rhythm
•ORGANIC DISEASE involving the -may be asympatomatic
infranodal conduction system -palpitations, DOW, weakness, dizzy
•transient or permanent
Third-Degree block:
-sx vary; worse w/ exertion
-palpitations, DOE, weakness, near
syncope, syncope, and/or HF
Causes Signs & Symptoms//Diagnosis
•MC mechanism for •Awareness of rapid heart beat
paroxysmal supraventricular •Chest pain, SOB
tachycardia is reentry •Dizziness, syncope
- typically initiated by •Abrupt onset and termination, last
a PAC or PVC seconds to several hours or longer
EKG:
•Tachycardia (140-240)
•regular rhythm
•QRS most commonly narrow
•P wave is often buried in QRS
Management
•treat underlying conditions
•CCB 1st line option
*especially if have COPD
•refractory: class IC or III
Diagnose/Management
Diagnostic Studies:
•Review medications & HX
*REVIEW FIRST!
•12 lead EKG
•telemetry monitoring (inpt)
•echo to r/o structural disease
•S/S ischemia -> cath
Labs: CBC, CMP, TSH
Management:
•First Degree:
-avoid medications that may prolong PR
interval and slow AV conduction
•Mobitz type I:
-avoid meds that slow AV conduction
•Mobitz type II/Third-Degree:
-unstable, usually require pacemaker
Management
Acute Management: STABLE PT
1. Mechanical measures *done by pt
•valsalva*
•stretching the arms and body, lowering the head
between knees*
•coughing, breath holding*
•cold water
•carotid sinus massage-> PROVIDER
2. Drug Therapy (IV therapy): “ABCD”
•Adenossine, CCB, BB (Esmolol, Metoprolol)
3. Cardioversion (shock) *sedate if awake
•FIRST LINE if hemodynamically unstable
•synchronized electrical cardioversion at 100J

Arrhythmias Phases Risks/Causes/Complications
Atrial Paroxysmal: in and out on own Risks:
Fibrillation •CHF* & HTN*
Persistent: >7 days •Old age, CAD, valvular disease
Long Standing Persistent: 1 year Causes:
-alcohol
Permanent (Chronic): staying in -thyroid disease, lung, heart
-fhx
-pericarditis
Complications: HF, thromboemboli
Rhythm Control Anticoagulation
Hemodynamically unstable: CHA2DS2SASc Score
Cardioversion *calculate on EVERY Afib pt
•Score 0: no therapy
*any unstable patient in a fast heart •Score 1: consider oral anticoag or
rate needs to be carvioverted antiplat (ASA 81)
•Score 2: oral anticoagulant
•Valvular (mitral stenosis or
regurg) heart disease: Coumadin
Atrial Causes/Risks/Presentation Treatment
Atrial Flutter Presentation, risk factors, causes are Higher rate of cure with catheter-
the same as afib based radiofrequency ablatation
- FIRST LINE
Prevention:
•Catheter Ablation: recurrent, sympt. PSVT
•Medication Therapy: BB & CCB are 1st LINE
** pts w/ AVRT (WPW) are prone to afib and
aflutter -> class IC or III or ablation
Symptoms Management
Symptoms: Three-Fold:
-may be asymptomatic 1. Rate control
-palpitations, heart racing 2. Rhythm control
-chest pain, SOB, fatigue, CHF 3. Thromboembolic event prevention (ALL)
Physical Exam: Rate Control:
-irregularly irregular rhythm •CCB (Verapamil, Diltiazem) *NOT in HF!
-signs of CHF •Beta Blockers (Metoprolol)
-distal pulses may be difficult •Digoxin
Rhythm Control: dependent on comorbidities
Maintenance/Education
Long-Term: “P-SEX” Maintenance:
*bridge with LMWH or Heparin •CBC and BMP q6months
•Warfarin (INR goal 2-3) •outpatient ambulatory monitoring
*if on Amiodarone, then make sure they are
•Pradaxa (reduce if CrCl 15-30) getting routine imaging and labs
•Xarelto (reduce if CrCl 15-50) Patient Education:
•avoid alcohol ANYTIME
•Eliquis (reduce if 2+: 80+, wt •control underlying risk factors
</=60kg, Cr 1.5+) •monitor for signs of bleeding if
anticoagulated
•Savaysa (reduce if CrCl 15-50)
-antiarrhythmics, cardioversion, -anticoag same as AF
rate control same as AF (4 weeks post ablation then no more)
Arrhythmias Definition/ Causes Symptoms Management
Ventricular •Three or more consecutive ventricular Patient may be asympatomatic, Acute sustained VT Long-Term therapy
Tachycardia premature beats especially with nonsustained •if hemodynamically unstable: immediate (prevention/recurrence):
-nonsustained: less than 30 seconds, synchronized direct current cardioversion •ICD
-sustained: greater than 30 seconds Majority have symptoms: •BB
•usual rate is 160-240bpm -palpitations, heart racing If stable and tolerating: •Amiodarone, Sotalol (class III)
-near syncope, syncope •IV Amiodarone likely will convert to sinus •catheter ablation
-confusion, fatigue •IV Lidocaine *MI or still in VT with Amio
-chest pain, SOB •Add IV Magnesium *everyone Non-sustained VT: Beta Blockers

Arrhythmias Definition
Ventricular •Not a sustainable rhythm IMMEDIATE UNSYNCHORNIZED
Fibrillation •Leading cause of sudden death DEFIBRILLATION

Arrhythmia About Mechanisms Causes/Management

Accelerated Regular wide complex rhythm with a rate Two possible mechanisms: 2. escape rhythm due to suppression of No treatment unless UNSTABLE
Idioventricular of 60-120bpm 1. Slow ventricular tachycardia higher pacemakers resulting from sinoatrial
Rhythm due to increased automaticity and AV block or depressed sinus node

IVC Delays About Causes Evaluation Management

Left Bundle •MC in pts with underlying heart
Branch Block disease; Can also be seen in
(LBBB) structurally normal heart
*Left anterior descending artery
provides the primary blood
Causes: Evaluation: Asymptomatic and isolated LBBB:
-structural heart disease •chest pain/ACS sx -no specific therapy
-functional LBBB (rate-related) -treat underlying cause (treat like MI)
Diagnostics:
•echo symptomatic pts with LBBB and low EF:
•stress test or LHC CRT

Right Bundle Receives blood supply from septal Conduction can be compromised by: Generally asymptomatic Do not require further dx or tx
Branch Block branches of the left anterior •Structural heart disease
(RBBB) descending •Functional factors
Bifasicular
Block
CARDIO About
HTN Causes:
1. Sympathetic NS & RAAS
2. Pressure/natriuretic
3. Renal/cardio development
4. Increase in Na & Ca levels
HTN Hypertensive Urgency
Urgency v. *>220/125 WITHOUT end-
Emergenc organ damage
y failure  brain, kidney, heart
Hypertensive Emergency
*>220/125 WITH end-organ
damage
Angina Substernal chest pain usually
Pectoris brought on my exertion
•Class I: strenuous activity
•Class II: more prolonged
rigorous activity
•Class III: daily activity
•Class IV: at rest
Clinical Presentation
Risks:
OSA, smoking, alcohol, obesity,
metabolic syndrome, NSAIDs,
high sodium in diet (low K+)
•Urgency: poorly controlled
•Emergency: identify organ
History:
•Chest pain: poorly localized,
substernal
•Radiation: arm, teeth, jaw
•Duration: Short (<30 minutes)
•Alleviating: rest, NTG
•Aggravating: exertion
Other SX: diaphoresis, dyspnea,
fatigue, numbness, nausea
Exam: usually normal
•Asymptomatic (BENIGN) Asymptomatic:
- no further dx tests •Screen carefully for symptoms and signs
suggesting occult cardiac disease
•Presyncope or syncope
- ECG monitor 24-48h Symptomatic:
- Echocardiography •Pacemaker if CHB is identified
Diagnostics Management
•UA, BMP, EKG, lipids •healthy >60yo-150/90;
•<60yo, CKD, DM-140/90
Evaluation goals: assess target-organ
damage, other risks, secondary causes; •1st line-ACE/ARB
•AA 1st line-CCB/thiazide, HF/MI-BB
**control STAGE II PRIOR TO SURGERY
**take anti-HTN DAY OF surgery
•CBC, CMP, UA; EKG, CXR Hypertensive Urgency: adjust medications
•CT if neuro sx in emergency -hospital: Clonidine, Captopril, Nifedipine
-oral: labetolol, captopril, NTG, clonidine
Complications:
•Renal-nephrosclerosis Hypertensive Emergency: 1st line: BB, CCB
•Eye-retinopathy, cotton wool -ischemic CVA: keep BP 180-200
•Vascular-atherosclerosis, aneurysm -hemorrhagic CVA: <130
•CVA (SPB); S4, heave -dissection: 100-110
ALL: EKG and CXR Lifestyle modifications
NSTEMI: high troponin, ST depressed
Unstable: normal troponin, ST depressed Pharmacotherapy: M.O.N.A. (162-325mg)
*goal is to increase supply and decrease
Exercise Stress Test: demand on the heart
• (+) if ST-depressions, hypotension/HTN, •NTG
arrhythmias, symptomatic •Beta-Blockers
•CCB (Diltiazem, Verapamil)
Imaging Stress Test: •Aspirin: does not work with supply/demand,
•thallium-201 or technetium-99 but prevents progression of stable angina to
•patient with baseline EKG abnormalities acute coronary syndrome
•Adenosine or Dipyridamole
•CI: asthmatics Classic TX: ASA, BB, NTG, statin
 Coronary Angiography (GOLD) “Cath”

History of MI prior to surgery:

- Pre-op EKG if >40yo
- Cardiac clearance

PULM 15%
COPD Irreversible airflow obstruction •cough, dyspnea with exertion Screening: annual screen with Cat A (GOLD 1-2):
- Loss of elastic recoil of alveoli •excess sputum production CT in adults 55-80yo with 30yr •SABA, possible LABA
- Increased airway resistance pack history and currently smoke
or smoked within past 15 years Cat B (GOLD 1-2):
Risks •LABA or LAMA
•SMOKING (>15 pack years) CXR: hyperinflation
•secondhand smoke CT: better for emphysema Cat C (GOLD 3-4):
•alpha-1-antitrypsin deficiency •LAMA, + LABA, LABA +
Spirometry: inhaled steroids + SABA
FEV1/FVC <70%, FEV1 <80%
COPD •Productive cough x3mo for 2 consecutive years •Productive cough Cat D (GOLD 3-4):
(Chronic •cyanotic, edema, RHF A: mMRC 0-1, CAT <10, 0-1 •LABA/LAMA, triple
Bronchitis) •Chronic airway inflammation  hypersecretion of •rales and rhonchi exacerbation
mucus, airway narrowing, increased airway B: mMRC 2+, CAT 10+, 0-1 SABA: Albuterol
resistance  obstruction •respiratory acidosis exacerbation LABA/ICS: “SAD”
•V/Q mismatch (normal in C: mMR 0-1, CAT <10, 2+ LABA: Salmeterol,
emphysema) exacerbation, 1+ hospital
D: mMRC 2+, CAT 10+, 2+ Combo LABA/LAMA: Bevespi
exacerbation, 1+ hospital Triple (D): Trelegy

COPD •Irreversible enlargement of air spaces distal to •dyspnea with exertion GOLD 1: mild-FEV1 80%+
(Emphysema terminal bronchioles  destruction of air spaces; •pink complexion GOLD 2: moderate-FEV1 50- Surgery:
) loss of elastic recoil in acinus  air trapping •thin, barrel chest, no edema 70% -one week of therapy
•respiratory alkalosis GOLD 3: severe-FEV1 30-49% -smoking cessation
“lean forward w/ pursed lips” GOLD 4: very severe-FEV1 -ABX for purulent sputum
>30% -bronchodilators

Asthma Reversible; airway inflammation & •Dyspnea Pulmonary Function Test 1. SABA (all)
bronchoconstriction in response to trigger •Wheezing  Spirometry *GOLD 2. +ICS
•Cough (worse at night) low FEV1/FVC and FEV1 3. +ICS/LABA or med ICS
Pathophys: •Chest tightness
 1. airway hyperactivity (IgE  T-cell) •Fatigue Bronchoprovocation: Admit if:
2. bronchoconstriction: airway narrowing due to Bronchodilator  FEV1 •PEFR <50%
smooth muscle contraction, edema, mucus, Physical Exam: increases by 12% and 200ml •ER within past 3 days
hypertrophy  air trapping •Prolonged expiration •status asthmaticus
3. inflammation •Hyperresonance to percussion Peak Expiratory Flow (PEFR)
•Decreased breath sounds *assesses asthma exacerbation
Uncontrolled prior to Surgery:
Mild Intermittent: •Tachycardia, tachypnea severity and response
•Accessory muscles •Normal is 400-600 -step up in therapy; steroids
•SX ≤2d/wk, night awake ≤2x/mo, FEV1 >80%
Mild Persistent: Samter’s Triad: asthma, nasal Culture: curschmann’s spirals, Surgery goal: NO wheezing,
•SX >2d/wk, night 3-4x/mo, FEV1 >80% polyps, ASA or NSAID allergy Charcot-Leyden crystals peak expiratory flow >80%
Moderate Persistent:
•SX daily, night awake >1x/wk, FEV1 60-80% Intubation for surgery:
Severe Persistent: -rapid acting beta-agonist or
•SX throughout day, awake nightly, FEV1 <60% nebulizer tx within 30 min

Cardiovascular 9% ***CP/Angina in Pre-Post Op, Claudication in Heme/Onc

Dyspnea on Exertion: PE, MI, Angina, HF, cardiomyopathies, valvular
Syncope: Aortic stenosis, subclavian steal syndrome, HF, valvular problems, vasovagal, arrhythmia, orthostatic hypotension, pericarditis

Cardio About Clinical Presentation Diagnostics Treatment

Deep Vein Virchows Triad: Unilateral swelling of LE (>3cm), tender Venous duplex US: 1st line LMWH or heparin IV AND oral
Thrombosis 1. Venous stasis -noncompressible echogenicity *rec. for med/high risk surgical patients
(DVT) 2. Endothelial damage Exam: *A-fib, CVA, TIA, HTN, DM, HF,
3. Hypercoaguability (factor V •WARM skin & Dusky cyanosis Venography: GOLD mechanical mitral valve, age >75yo
leiden, cancer, OCP + smoke, •Palpable cord, normal pulses
pregnancy) •Homans sign: calf pain with Heparin (antithrombin III): PTT
dorsiflexion (unreliable) -Risks: HIT, bleeding, hematoma
Warfarin(Vit K ant): extrinisic, PT/INR

Varicose Veins •Varicose veins develop in LE
Dilated, tortuous superficial veins
Increased intraluminal pressure 
reverse venous flow
Hallmark: venous reflux & HTN
•Dull, aching heaviness or feeling of
fatigue in legs brought on by periods of
standing, relieved with elevation
•Itching , palpable
•No diagnostic evaluation
•Imaging needed for surgical
intervention-duplex US
•Nonsurgical: Elastic compression
stocking (20-30mmHg), leg elevation
•Surgical:
-sclerotherapy: inject sclerosing agent
-laser therapy: wavelength
-endovenous ablation
-vein stripping (last resport)

Cardio About Clinical Presentation Diagnostics Treatment

Chronic Venous •Severe manifestation of venous
Insufficiency hypertension
•Valve leaflets that do not coapt
because thickened and scarred or
in a dilated vein so impaired
function
Burning, aching, heavy leg pain Compression stockings, leg elevation
-worse with standing/sitting Regular exercise
-better with walking & elevation lipodermato
Ulcer: UNNA boot, wet to dry dressings
Edema, hyperpigmentation,
•Venous ulcers: medial malleolus atrophic blanche
  legs develop venous
HTN and high
hydrostatic force
MCC-prior deep venous
thrombophlebitis
•Lipodermatosclerosis
-pigmented, swelling, red, “bowling pin”
•Atrophie Blanche
-star shaped ivory-white depressed
atrophic plaque; red dots within scar
•Corona Phlebectatica
-dilated veins around the ankle
corona
Trendelenburg test: elevate one
leg at 90 degrees, occlude great
saphenous vein, have patient
stand for 20 sec  slow ankle
fillings suggests competency

Cardio About Clinical Presentation Diagnostics Treatment

PAD Stenosis or occlusion in artery due
to atherosclerosis
•Coronary artery: angina
•Carotid artery: stroke, TIA
•Renovascular: HTN, renal
•PAD: claudication, limb
ischemia
•Distal aorta & proximal iliac:
smokers
•Femoral & popliteal: 60+,
minorities
•Tibial artery: Diabetics
Atypical leg pain (MC)
•Intermittent Claudication
-aching, pain, tightness
-brought on by EXERCISE
-relieved with rest within 10 minutes
•Functional Impairement
-do not have claudication but have rest
pain or ulceration
•Limb ischemia: ulcer, gangrene
•Skin: COLD
Leg Lift Test: 60 degrees x1min
(+) if feet turn white when you
lower down
Dependent Rubor: seated to
supine, assess blood flow;
longer red is more severe
ABI: BEST TOOL
Abnormal is 0.90 or less
*TBI if non-compressible >1.40
GOLD: ANGIOGRAPHY
•Lifestyle: smoking cessation
•Exercise therapy
Pharm: Aspirin or Plavix
•Cilostazol (Pletal)
-supress cAMP degredation
-reversibly inhibits platelete
aggregation
-SE: edema, GI, HA, bleed
-CI: HF
Others: ACEI, statin, glycemic control
BETA BLOCKERS CI

Acute Arterial Causes: 5 Ps: •MEDICAL EMERGENCY! Acute Arterial Occlusion of a Limb
Occlusion of a •thrombus: stable atheroma with -pallor
Limb fibrous cap  plaque rupture  -pain/ paresthesias (numbness/tingling) •Doppler: little to now flow
acute occlusion -pulseless •EKG: determine if Afib
-paralysis (muscles w/ no perfusion) •Labs: CBC, PT/INR, PTT
•embolus  AFIB MC cause -polar (cold) •Echo: done LATER if embolic
source is suspected (TEE w/
MEDICAL EMERGENCY! bubble)

Thrombo-angiitis NOT ATHEROSCLEROSIS •Starts at toes/feet  hand/fingers Thrombo-angiitis Obliterans

Obliterans •Segmental, inflammatory, -severe ischemia  tissue loss (Buerger Disease)
(Buerger Disease) thrombotic processes that occur in
small distal arteries •Presents with distal ischemic rest pain
or ischemic ulceration on the toes, feet,
 •Closely linked to tobacco use or fingers
•Males <40, smokers

Cardio About/Risks Clinical Presentation Diagnostics/Screening Management

Abdomina •Dilation of the infrarenal aorta
l Aortic is a normal part of aging ~2cm
Aneurysm -AAA when >3cm
(AAA)
Risks:
Male, smoking, fhx, old age
Two major groups:
Fusiform: circumferential
Saccular: outpouching of a
*NOT around entire aorta
*higher risk of rupture
Symptomatic: *more concerning
•PAIN
-Mild to severe mid-abdominal discomfort
often radiating to lower back
-Constant or intermittent
-Exacerbated by gentle pressure
-Distal embolization is rare
•RUPTURE *lethal
-Sudden blood into retroperitoneal space
-Severe pain, palpable mass, hypotension
-Free rupture into peritoneal cavity is
LETHAL *bruising on the back
DX: Repair for:
CBC, BMP, PT/INR, PTT -aortic aneurysm larger than 5.5cm
Abdominal US- study of choice -rapid expansion (>0.5cm in 6mo)
-symptomatic pain & tenderness
•CT scan provide a more reliable
assessment of diameter
-perform when >5cm & surgery
Screening:
•One-time screening for:
-men 65-75 and have smoked 100
cigarettes in a lifetime

Thoracic Risks: •Most asymptomatic •CXR: widened mediastinum •Repair when 6cm or larger
Aortic •Most due to atherosclerosis *easiest initial tool, do 1st Treatment: endovascular grafting
Aneurysm •Symptoms depend on size and position
•CT disorders: Ehlers-Danlos, -Substernal back or neck pain •CT scan: modality of choice Involvement of proximal aortic arch:
Marfan Syndrome -Hoarseness due to L recurrent laryngeal -open surgery *substantial risk
-aortic regurg due to dilation -may need replacement/repair of AV
•Bicuspid aortic valve -performed by CT surgeon

Aortic •MC in men over 50 S/S: EKG: LVH BP Control:

Dissection
Risks:
•aging, atherosclerosis, HTN
•blunt trauma to chest wall,
aortic valve defect, aortic
coarctation, preexisting, prego
•CP radiating to back or neck
•hypertensive
•syncope, hemiplegia, paralysis of LE
•ischemia (MI)
•diminished peripheral pulses distally,
diastolic murmur
CXR: widened mediastinum
*initial screening
Multiplanar CT of chest/ abdomen:
immediate diagnostic study
•lower SBP 100-120 &pulse pressure
•BB first line! (Lebetolol, Esmolol)
-can add CCB or Nitroprusside
Pain: Morphine (pain & vasodilation)
Cardio 20% About Clinical Presentation Diagnostics Treatment
Myocarditis Inflammation of heart muscle due to 1. Viral prodrome: fever, myalgia, •CXR: cardiomegaly •supportive symptomatic therapy
myocellular damage malaise, HF symptoms •beta blockers
•EKG: dysrhythmias •IVIG
MCC: Viral infection 2. Heart Failure: dyspnea, exercise
intolerance, syncope, tachypnea, •Labs: cardia enzymes, ESR
Etiologies: tachycardia, impaired systolic
•Infectious: Enterovirus (MC), function, megacolon •TTE Echo: ventricular dysfunction
adenovirus, parovirus, HHV-6, EBV,
HIV, VZV 3. Pericarditis: fever, CP, friction •Endomyocardial biopsy-GOLD
•Toxic: diphtheria, scorpion rub, effusion STANDARD!
•Autoimmune: SLE, rheumatic fever,
RA, Kawasaki, UC
•Systemic: Uremia
•Medications: Clozapine
Dilated MC CARDIOMYOPATHY Heart Failure symptoms •CXR: cardiomegaly •Treat underlying source
Cardio- -left ventricular dilation •EKG: arrhythmias, tachycardia •CHF management
myopathy Systolic dysfunction, LVEF <40% -decreased ejection fraction •Prevention of sudden cardiac arrest
 ventricular dilation  dilated -arrhythmias

Causes: Exam: S3 gallop

Idiopathic (MC)
Viral: Enterovirus, PB19, Chagas
Toxic: Alcohol, cocaine,
Doxorubicin
Other: pregnancy

Hypertrophic Inherited genetic disorder (autosomal •Dyspnea (MC complaint) Murmur: •Avoid volume depletion
Cardio- dominant) •Angina, Syncope, Arrythmias Harsh, mid-systolic crescendo-
myopathy  mutation of sarcomeres •Sudden cardiac death decrescendo murmur, at 3rd/4th ICS •Beta-blockers or Verapamil (CCB)
louder with valsalva, quiet w/ squat *1st line!
 •MC effects interventricular septum
 LVH  diastolic dysfunction
•Impaired ventricular relaxation/filling
Restrictive •Ventricle is STIFF and has impaired
Cardio- filling  diastolic dysfunction
myopathy
Cause: Amyloidosis (MCC),
sarcoidosis, hemochromatosis,
scleroderma, fibrosis, cancer
Stress- •Can cause an ACS or STEMI
Induced *MC in postmenopausal women
(Takotsubo)
Cardio 20% About
Pericarditis Inflammation in pericardial sac
Causes:
•Idiopathic *MC
•Viral (enterovirus) (MC!)
•Systemic: thyroid, lupus, RA
•Neoplasms: lung & breast CA
•Drug Toxicity
•Myocardial Injury
•Pericardial Injury
Pericardial •Fluid in pericardial space
Effusion
•MCC: pericarditis
•Others: infection, radiation, cancer
Cardiac Effusion causing significant pressure
Tamponade on the heart  restricted filling 
decreased CO
Constrictive Thick, fibrotic and calcified heart
Pericarditis  diastolic dysfunction
MCC=TB *underdeveloped
MC is radiation, surgery, and viral
pericarditis *developed
•Right sided HF sx
•Pulmonary HTN
•Normal ejection fraction
Exam: Kussmaul sign
• psycho or physiological stress
 Systolic dysfunction of apex
and/or mid segments
Clinical Presentation
•PLEURITIC CHEST PAIN
-worse with inspiration
-worse when supine
-relieved with sitting up and leaning
forward
•Fever
Auscultation: pericardial friction
rub *washing machine sound
Distant (muffled) heart sounds
BECKS TRIAD:
•JVD
•Muffled heart sounds
•hypotension
Exam: Pulses paradoxus
•Dyspnea (MC sx)
•RHF: JVD, edema, N/V
Murmur: pericardial knock
-high pitched 3rd heart sound due to
sudden cessation of ventricular filling
from thickened pericardium
•EKG: LVH (V5, V6, aVL) •Septal myetomy/alcohol septal
•Echo: DIAGNOSTIC-assymetrical ablation *inject alcohol-kill off part
wall thickeness
•Echo: non-dilated ventricles with •Treat underlying cause if known
normal wall thickness  dilation of
both atria
Echo/LV angiography: •Recover in a few weeks
•LV apical ballooning •Beta Blockers for one year
Diagnostics Treatment
•Viral titers •FIRST LINE-NSAIDS
•Cardiac enzymes -Ibuprofen 600-800mg TID or
•Echo Indomethacin TID for 1-2 weeks
*likely normal unless significant -ASA post MI
effusion present
•CBC, BMP, ESR/CRP 2nd line: Colchicine
-use for recurrence
EKG: diffuse ST segment elevation
-smiley face &diffuse
CXR: cardiomegaly Small/no tamponade: observe
EKG: low QRS voltage
Echo: increased pericardial fluid
Echo: effusion + diastolic collapse of Pericardiocentesis
cardiac chambers
EKG: electric alternans
Echo: thickening of pericardium, Diuretics for sx improvement
CXR: pericardial calcificiation Definitive: pericardiectomy
-if unresponsive to diuretics
Cardiac CT/MRI: thickening
Cardiac Cath: *CONFIRMATORY
Endocrinology 8% **Tremors in Neuro
Fatigue: Addisons, Hypothyroidism, DM, Pituitary Insufficiency, Hypercalcemia, Chronic Renal Failure, Hepatic Failure (GI)
- Labs: CBC, SER, CMP, TSH, T3/T4, HIV, Pregnancy test
Palpitations: Hyperthyroidism, Pheo
Tremors: Rest (Parkinsons, Wilsons, Essential), Postural & Action (Physiologic, essential, writing tremor, Parksinsons, Charcot-Marie, Cerebellar Tremor) *NEURO

Adrenal Gland: Cortex = GFR-ACE outer  inner: Glomerulosa (Aldosterone-Na+), Fasciculata (Cortisol), Reticularis (Estrogen/Androgens)

Disease Epidemiology Presentation/Labs & Testing Work-Up Treatment/Management

Pheo- Average age=40yo “the great masquerader” Plasma Free Metanephrines Management:
chromocytoma *most sensitive test •resection of tumor
Rule of 10s: Triad: episodic palpitations, HA, diaphoresis •sit 15min before, if elevated repeat after •refer to surgeon (BP labile!)
•10% bilateral •Anxiety, pallor, syncope, tachycardia supine for 30min •post-surgery assess ACTH level
•10% extra-adrenal •Paroxysms <1hr •elevated -> assess urine
•10% malignant •emotions/physical stressors, change in position, •interf factors-stress, apnea, drugs Awaiting Surgery:
urination, various medications •Maintain VP < 160/90
Urine Fractionated Metanephrine and •Alpha-Adrenergic Blockers
Hypertension (episodic or sustained) Creatinine Cardura, Minipress, Hytrin
*triad + HTN is HIGHLY suggestive •24hr, overnight, or shorter Diet-high salt and water intake
• (+) if >2.2mcg/mg of creatinine •3 days after alpha adrenergic

Imaging: Complications
•CT/MRI with contrast C/A/P •hypertensive crisis, cardiac
*MRI preferred in child/pregnant arrhythmias
•PET-rule out malignancy •stroke, MI
Adrenal Nonfunctional: Nonfunctional:  Detailed HP  Surgery referral
Adenoma Benign, does NOT  Asymptomatic
secrete steroids Functional:  Labs based upon suspected
*related to cellular involvement adrenal zone affected
Functional:  Glomerulosa-hyperaldosteronism
•Benign >1cm  Fasiculata-cushings
•Secrete steroids ind.  Reticularis-hyperandrogenism
ACTH/ RAAS  Medulla-pheochromocytoma

Adrenal Functional-MC Functional*: •Hormonal evaluation  Staging (TNM)

Carcinoma Nonfunctional •virilization, cushinoid, hyperaldosteronism  Refer to Surgeon
•gynecomastia in males •Fine Needle Aspiration
2 peaks: •precocious sexual development in females *only to r/o metastasis in patient with
•birth-10 years* known malignancy
*functional Nonfunctional: *must r/o Pheochromocytoma
•30-40yo •fever, wt loss, abdominal s/s, back pain
*non-functional •PE: palpable, firm, adherent mass of abd *not recommended to differentiate
adenoma and carcinoma

ENDO
Hyper- Causes: HIGH BMR
thyroidism •Graves Disease (MC) •Heat intolerance
•Toxic multinodular goiter •Weight loss, hyperglycemia
•TSH secreting pituitary adenoma •Diarrhea
•Excess intake •Warm, moist skin & hair
•Iatrogenic thyrotoxicosis •Hyperactive: anxiety, tremor, nervous,
fatigue, weakness
•Tachycardia, high output HF
•Scanty period
Graves Eyes: lid lag with downward
gaze, “staring” appearance
Graves dermopathy (pretibial
myxedema): red, rough plaques
Thyroid labs:
•Primary: ↓TSH, ↑ FT4
Hypercalcemia, ↑ alk phos, Anemia
Decreased granulocytes
•Graves-(+) TSI,(+) anti-TPO, anti-Tg
increased RAI and vascularity
•Thyroiditis: ↑ ESR
Treatment: PTU
Thyroid Storm:
•marked delirium, tachy, V/D,
dehydration, high fever
•Thiourea Methimazole or PTU
•Iodinated contrast
•Beta Blocker
•Hydrocortisone
Thyroid Storm Definitive tx:
radioactive iodine surgery

Thyroid •Potentially fatal complication of HYPERMETABOLIC •Insulin resistance 1. Propranolol

Storm untreated thyrotoxicosis •N/V/D •Increased free T3 & T4 2. PTU
•Tremors, psychosis (AMS) •Decreased TSH 3. Iodine
Triggers: surgery, trauma, infection, •Lid lag 4. Glucocorticoids
illness, pregnancy •High fever
•Palpitations, tachycardia Definitive: radioactive iodine
•Liver failure surgery

Hypo- Causes: LOW BMR •serum TSH +/- FT: ↑ TSH, ↓ FT4 Treatment: Levothyroxine
thyroidism •Iodine deficiency (MC worldwide) •Cold intolerance
•Hashimotos thyroiditis (autoimmune) •Weight gain, hypoglycemia Hashimoto: Myxedema Crisis-
 •Potpartum thyroiditis
•Pituitary hypothyroidism
•Hypothalamic hypothyroidism
Primary: failure of thyroid T3, T4
Secondary: failure of pituitary TSH
Tertiary: Failure of hypothalamus TRH
•Constipation
•Dry, thick skin; brittle nails
•Loss of outer 1/3 eyebrows
•Hypoactivity: fatigue, sluggish,
memory loss, depression
•Bradycardia, decreased CO
•Menorrhagia
• (+) (anti-TPO) *MC and (=) anti-Tg
Imaging:*not indicated in simple cases
•thyroid US
•CT MRI views gland
*triggered by infection, illness,
cold, drugs
•Treament Myxedema:
IV levothyroxine (LT4)
•Supportive Myxedema: blankets,
intubation, tx underlying

ENDO
Hyper- Primary: increased PTH (MC) •Signs of hypercalcemia •Increased PTH and Ca2+, vit D Primary:
parathyroidism •parathyroid adenoma •Decreased DTR •Low phosphate •Parathyroidectomy

Secondary: 24 urine calcium: HIGH Secondary:

•hypocalcemia or vitamin D deficiency •Vitamin D, calcium supplementation
•CKD

Disease Signs/Symptoms Labs Imaging Results Management

Thyroid Small, solitary nodules
Nodules and •Asymptomatic
Goiters •Accidently found on exam
Large, multinodular goiters
•Swelling, hoarseness, dysphagia
*compression on venous return
Abnormal thyroid function
*hypo or hyper
Order TSH Multinodular Goiter •Follow-up with regular palpation
•Multiple hyperechoic discrete and •US every 6mo
Thyroid US nodules
*size, characteristic •Enlargement of isthmus and •LT4 suppression for nodule >2cm
•cystic lesions benign thyroid lobes and normal or high TSH
•concerning-irregular margins, solid *reduces emergence of new nodules
•lesions, heterogenous texture, >1cm Thyroid nodule
•Single nodule •Ethanol Injection
RAI Uptake •color flow Doppler *shrink benign nodules
*evaluate hyperfunctioning tissue
•hypofunction=cold, high cancer risk Solitary Thyroid nodule Toxic Multinodular Goiter:
•hyperfunction=hot, low cancer risk •Discrete hypoechoic nodule •Methimazole +/- BB
•Surgery
CT Scan Multinodular Goiter
*differentiate large nodules or MNG, •CT scan Cancer, Hyperfunctioning, Toxic
degree of mediastinum involvement, •SVC compression MNG
tracheal compression •Tracheal deviation •Surgery

FNA Biopsy Toxic adenoma, Tosic MNG, Graves

•Evaluate thyroid nodules for malignancy •RAI therapy
*solitary hypechoic nodule *shrinks nodules by ~60%
*MNG-biopsy 4 largest >1cm
•Solitary nodules-biopsy if suspicious
appearance, >2cm
Thyroid papillary thyroid carcinoma *MC
Cancer •single thyroid nodule
•least aggressive, slow, confined
for
Follicular Thyroid Carcinoma
•metastasize, ↑ iodine uptake
Medullary Thyroid Carcinoma
•Secrete calcitonin, prostaglandins,
5HT, ACTH, CRH, other chemicals
•Local mets, NO good iodine uptake
Anaplastic Thyroid Carcinoma
•Most aggressive, worst survival
•Rapidly enlarging mass in MNG
•Does not have good iodine uptake
*local resection and radiation
Dermatology 5% *zinc deficiency, pagets, fat emboli
Infectious About
Trichomonal •unicellular flagellate
Vaginitis protozoan
•MC non-viral STD in US
•perinatal complications,
increased HIV transmission
Bacterial •overgrowth of abnormal
Vaginosis bacterial flora
-often polymicobial
-Gardnerella vaginilis
-not an STI
Candidal •75% of women will
Vulvovaginitis experience at some point
(MC-Candida albicans)
•often associated with DM,
HIV, obese, pregnancy, ABX,
steroids, OCPs, chronic
debilitation
•Palpable, firm, nontender nodule/mass
Symptoms:
•Asymptomatic
•Metastasis ~3% cases
*MC sites-lymph, lungs, bone
•Anaplastic-s/s of metastasis
•Medullary-flushing, diarrhea
*rare Cushing-like syndrome
Presentation
•profuse extremely frothy, greenish,
at times foul-smelling vaginal
discharge
•erythema, petechial
-strawberry cervix
•milky, homogenous, malodorous
•noticeable after unprotected sex
•”fishy” smell, enhanced w/ KOH
•lack vaginal mucosal inflammation
on exam
•increased risk of preterm delivery
•intense vulvar pruritus
•thick, white cottage cheese
discharge
•minimal odor
•vulvar erythema, edema
•burning sensation after peeing
Serum Tg
•↑-metastatic papillary and
follicular
Serum Calcitonin
•↑-medullary thyroid carcinoma
Serum CEA
•↑-medullary thyroid carcinoma
Thyroid US *size, location of mass
RAI Scan *use after thyroidectomy
•reveal metastatic tissue
High uptake: follicular
CT or MRI: Distant metastases
Malignant:
COLD & LOW UPTAKE
Diagnostic
•pH: elevated 5-5.5
•saline prep: actively motile trichomonads
•immunochormatographic: 10min
•nucleic acid: 45 minutes
•pap smears, culture
•pH: elevated 5.5-7
•saline prep: “Clue Cells”
•KOH: (+) “whiff test” with fishy odor
•Vaginal pH: elevated 4-5
•saline prep: 1 drop discharge & NS
-branching filaments, pseudohyphae
•KOH: 1 drop 10% KOH
-dissolves epithelial cells & debris
and facilitates visual of fungal
Surgery-First Line
>1cm cancer: total
<1cm cancer: lobectomy
<4cm inderterminate: lobectomy
>4cm indeterminate: total
RAI therapy
CI-prego, nursing
*low iodine diet for 2wkbefore
Chemo: aggressive CA
Treatment
•Metronidazole or Tinidazole x1dose
-or Metronidazole 500mg BID x7d
Resistant: Tinidazole 500mg TID x 7d
•treat partner & screen for other STIs
•Metronidazole (Flagyl) x7d
•Clindamycin (Cleocin) x3-7d
•Tinidazoel (Tindamax) x3-7d
Prevention:
•avoid factors altering flora
•probiotics
•acidifying douches (not general)
Pharm: Fluconazole once
•topical or oral antifungals
•boric acid or gentian violet
Complicated:
•4+ episodes/yr, severe symptoms, non-
albicans, uncontrolled DM, HIV, steroid,
pregnancy
-topical x7-14d, fluconazole x2 dose

Gonorrheal •MC infects glands of cervix,
urethra, vulva, perineum, anus
Chlamydial
Non-infectious •topical: sanitary & hygiene
supplies, spermicidices,
•allergen: latex, cream
•atrophy: postmenopausal
•sex, hygiene, stress, sweat
About
Thermal •MCC: scalding, direct
Burn thermal and flame burns
•descriptions based on
% of body surface area
-rule of 9s
-lund and broder
-palmar method
Depth
•old: 1st, 2nd, 3rd, 4th degree
•new systemic: superficial
partial thickness, deep partial
thickness, full thickness
Labs
•lab evaluation: assess
complications of burn injury
•ABG, CBC, CK, CMP
•80-85% of women asymptomatic
•copious mucopurulent discharge
possible
•often asymptomatic
•may see mucopurulent cervicitis,
dysuria, and/or postcoital bleed
•can progress to PID or
lymphogranuloma venereum
Varying degrees of pruritus, irritation,
burning, erythema, vaginal discharge
Rules
•Rule of 9s: easy, 2nd and 3rd degree
•Palmar: palm equates to 1%
•1st degree (sunburn): erythema, skin
blanches with pressure
•2nd degree (partial): red and blistered
•3rd degree (full): tough, lethargy, non-
tender
•4th degree: bone and muscle
Complications
•inhalation injury, carbon monoxide,
bacterial super infection, sepsis, multiorgan
failure
•Culture: GOLD STANDARD
•nuclei probe or culture of discharge
-gram (-) diplococci
•culture, immunoassay, nucleic acid
•can be found on pap smear
Treatment
Identify and removal offending agent
Atrophy: lubricant/moisturizer, HRT
-warm sitz baths, topical steroid
Management
Management:
•supplemental O2 & intubation if
needed
-complication of airway edema or
inhalation injury
•Monitor VS
-pulse ox may be falsely high by CO
-BP monitoring: utilize a radial or
femoral arterial cath if unable to
utilize extremity cuff
•assess & treat trauma, inhalation, CO
•IV opiates for pain control (opiotes)
•urinary cath: measure I&Os (US at 0.5-
1ml/kg/h)
Minor Burns
•clean with mild soap and water
•large bullae (>2cm) or over mobile
-culture to confirm dx, boric acid
•single IM dose of Ceftriaxone 250mg
•usually receive TX for chlaymdia
-Azithromcyin 1g orally or Dozy
•Azithromcyin 1g po once
•Doxycyline 100mg po DIB x 7 days
•treat partner
CAM
Intravaginal
•white vinegar, herbal combination
•povidone iodine, tea tree oil
•probiotic supplements
IV Fluids:
•IV lactated ringer via 2 bore needle in
unburned area
•Parkland formula to determine fluid
Adults >15% total body surface area
LR 4ml x wt (kg) x % BSA burned
over initial 24 hours
-half over first 8 hours
-other hal over subsequent 16h
Children: >10% total body area
LR 3ml x wt(kg) x % BSA burned over
initial 24h plus maintenance
-half over first 8h
-other hald over subsequent 16h
Moderate and Severe
•cover with dry sterile sheet
•admit
-moderate (hospital), severe (burn)
 •UA, carboxyhemoglobin joints  drain and debride, 1% silver

About Types Management

Chemical •results from exposure to strong
Burn acids/alkalis
•historical information needed
-type and concentration
-duration of exposure
-extent of prenetration
Acid Burns: •remove clothing (prevent self exposure) •contact poision control
•results in a coagulation necrosis
leading to eschar formation •copious irrifation with tap water •after approparite decontamination
•partial thickness with erythema and -IVF, pain control
erosion •cover elemental metals (Na, lithium, CA, -assess for systemic toxicity
Mg) with mineral oil -hypotension, acidosis, shock
Alkali: -water will cause exothermic reaction -TD updates
•results in liquefaction necrosis resulting worsening burn
in deeper damage •consult surgeon/burn center to
•full-thickness, appears pale, feel leathery detmine need for excision
and slippery

Urticaria •Pruritic, raised, well-circumscribed areas of
erythema and edema
Pathogenesis
•mast cells and basophils release vasoactive
substances (histamine, leukotriene C4,
prostaglandins) resulting in extravasation of
fluid into the dermis
•Type I IgE: foods, meds, insects, latex,
contact allergen
•Complement: infectious, serum
sickness, transfusion
•Physical: pressure urticarial, cold
urticarial, cholinergic urticarial
•Autoimmune: SLE, RA, thyroid
•Acute: <6 weeks (infection, allergy)
•Chronic: recurrent and >6 weeks
(physical, autoimmune)
Clinical Findings
•raised, erythematous-pink-skin
color wheals with central pallor
•shape and size change rapidly
•resolves within 24 hours
•+/- dermatographism
•H&P should focus on underlying
cause
Lab/Diagnostics
•acute: clinical dx
•chronic: look for other cause
Management: Acute Urticaria
•ED evaluation, can be life-threat
-angioedema/anaphylactic shock
•Triple Regimen
-H1 + H2 + steroid
Management: Chronic Urticaria
•antihistamines (Allegra, Claritin)
•refer to dermatology

About, Pathophys, Risks
Pressure •Breakdown of the skin and
Injury underlying tissue resulting from
unrelieved soft tissue pressure
between bony prominence and
external surface
Pathophys:
•non-reliving pressure shearing
forces results in diminished blood
Location & Scale Diagnostics and Scaling Management
Location: Signs: Management:
•sacrum/hip (70%) •deviated tissue (Eschar/slough) at •reduce/eliminate underlying risk factors if
base increases risk of infection possible
Pressure injuries place pts with •purpulent exudate and surround •optimize nutrition
same risk factors at 4.5 times erythema indicated infection •redistribute pressure every 2hr
greater risk of death •foul odor  anaerobic infection -elevate head 30 degrees
•clean skin with mild cleansing agents and
Pressure Ulcer Scale for Healing: Labs: keep skin dry
•size in cm -ESR, WBC (elevated with OM and
 supply leading to cell death
Etiology/Risks:
-impaired mobility (MC)
-contractures/spasticity
-imapired sensation
-aging skin
-incontinence/fistula (skin
maceration)
•exudate amount
•tissue type (sloughing, eschar)
•score (0-17) will decrease with
healing
bacteremia)
-wound cultures
-bacterial cx: punch bx 
culture for aerobic/anaerobic
-viral cx: r/o chronic HSV ulcer
Local wound care
•Stage I: cover with film
•Stage II: trnasparant or hydrocolloid
dressing *CI in active infection
•Stage III/IV: debridement
Course and Prognosis:
•Stage I & II in 1-2 wks, III & IV 6-12wk
•MC complication: infection

Stage I and II Stage III Stage IV Unstageable

Stage I •full thickness skin loss •full thickness skin/tissue loss Unstageable
•intact skin •exposed SC tissue/adipose •exposed fascia, muscle, tendon, •full thickness skin and tissue loss obscured
•non-blanchable hyperemia ligament, cartilage, and/or bone by slough or eschar
Granulation: scar tissue •eschar tissue •removal of obscuring tissue will reveal
Stage I Eschar: dry, dark scab of skin stage III or IV
Stage II: Slough: moist, thick, stringy, •do not remove a stable eschar
•intact blister or loss of epidermis Epibole: rolled wound edge
with exposed dermis Suspected deep tissue
•SC not visible •intact skin
•wound viable, pink/red, moist •deep red, maroon, purple discolor
Stage II •no granulation or eschar tissue •blood filled blister, unable to visualize

About Clinical Presentation Diagnostic Treatment

SCC •Malignancy of cutaneous
epithelial cells on sun-exposed
area
MC Areas & people:
•face and dorsal hands
•Light skin individuals
•MC skin cancer in AA
•AK may be a precursor
•Greater risk of mets on the lip
and oral mucosa
Risks:
-chronic sun exposure
-fair skin and blue eyes
-fhx skin cancer
-increased age
-scarring processes
-ionizing radiation
-immunosuppression
-HPV
-tattoos, piercing, burn
Differentiated: Squamous in situ (SCCIS):
•Hard, firm papule, plaque, nodule with a •confined to epidermis
thick adherent keratotic scale •bowen disease and erythroplasia or
•+/- erosion, ulcerated, umbilicated Queyrat (on male genitalia)
•Erythematous, yellow, skin colored •more frequent and more aggressive in
•Lesions in sun exposed areas immunosuppressed individuals
 head, neck, dorsal hands, legs (women) •prevalent in organ transplant
•LAN with mets recipients and HIV/AIDS
Undifferentiated: *large, irregular border Tumor Subtypes:
•soft, fleshy, erosive papule/nodule •bowen diseae (SCCIS)
•papillomatous, cauliflower-like •acantholytic, adenoid, psuedoglandular
•bleeds easy •well v poorly differentiated
•found on less sun exposed areas (genitalia,
trunk, LE, face) Best Tests: BIOPSY!!!
•regional LAN •most effective: history and PE
•pleomorphic and hyperchromatic SCC
Diagnostic Pearls: with variable nuclear size
•skin often displays other evidence of sun •loss of full-thickness epidermal
exposure (solar elastosis, AK, solar letingines) maturation
•burn scars, chronic ulcers, inflammation, •overlying parakeratotis
chronic lymphedema, venous stasis, irradiation •keratinocute motses
•Can occur in scars and non-exposed areas in •dykeratosis
darker skin phototypes •squamous pearls
•occasional features
Treatment:
•excision w/ margins (3-5mm) & Mohs
*TREATMENT OF CHOICE
-6mm margin in high risk
Non-surgical Candidates
Superficial: electrodessication, curettage
(x3) with margins of 3-4mm, radiation
Others: Imuquimob, 5-FU, photodynamic
therapy, electrochemotherapy, Intralesional
interferon-alpha
-CAN NOT USE PICATO
Education:
watch lesions (open sore, pink/red, irritate,
shiny papulae/nodule, scar-like), SPF 30+,
protective clothes
 •presence of an adjacent solar/AK

CA Pharm MOA Dosing SE/CI/Caution Education

5-FU •Blocks DNA synthesis: apoptosis and selective •BID to affected region x2-4wk •localized skin reaction Education: success is
cell death -Alt: daily for face & anterior scalp only burn, itch, erythema, parallel to compliance
•D/C once erythema, erosion, crusting, and necrosis erosion, crusting, ulceration
have occurred •F/U in 2 weeks

Imiquimob •Stimulates local cytokine induction •5% (starting dose), 3.75%, 2.5% •Localized skin reaction use if insurance doesn’t
•Used for non-hypertrophic AK on face or •Lower doses if unable to tolerate SE cover 5-FU
scalp; Not used in SCC •Apply to area nightly, wash off 8hr; 2x/wk x16wk

Ingenol •Plant derivative •0.015% gel: face/scalp once daily x3days •Localized skin irritation; AK ONLY
Mebutate 1. disrupt cell membrane & DNAcell necrosis •0.05% gel: trunk/extremities, apply nightly x2d erosions
(Picato) 2. Neutrophil-mediated cytotoxicity that
eliminates remaining tumor cells •Caution: risk of SCC?

Diclofenac •COX-2 inhibitor (inhibits prostaglandin) •3% Gel-Apply to treatment area BID x60-90d •Localized skin reaction

About Clinical Presentation

Basal Cell •MC type of skin cancer
Carcinoma •neoplasm of basal keratinocytes
(BCC) •Largely a non-mets form of
cancer, although lesions become
locally destructive w/o treatment
Nodular Sclerosing Pigmented
•translucent “pearly” papule/nodule •plaque, scar like lesion •firm papule/nodule +/- umbilications
•well defined borders (rolled-edge) •pink/white in color •smooth pearly surface
•smooth, firm surface with •telangiectasia •generally pigmented or stippled globules
telangiectasias •ill-defined borders
•+/- erosions, sporadic pigmentation

MC locations:
•head and neck
•upper chest and back
•upper extremities

4 types:
-nodular (MC overall)
-infiltrattive Ulcerating
-pigmented (MC in AA, Hispanic, Superficial Multicentric
•translucent-pearly, smooth, firm,
Asians) *can rub alcohol pad over it
telangiectasia with a central ulcer Diagnostic Pearls
-superficial •thin plaque/patch
•+/- elevated border (rodent ulcer) • >1 BCC before 30yo suggests nevoid basal
-sclerosing/morpheaform •pink/red
•+/- scaling cell
-metaplastic/basosquamous *usually larger then clinically appear

Risks:
•light skin phototype
•sun exposure
•radiation
•advanced age
 •immunosuppression
•personal hx

Hereditary conditions associated:
•albinism
•xeroderma pigmentosum
•nevoid basal cell carcinoma
•rasmussen syndrome
•rombo syndrome
•bazex-dupre-christol syndrome
•darier disease
Diagnostics Treatment
•skin biopsy (shave or punch) •Good prognosis w/ tx •mohs (MAIN TX)
•likely recurrence in 5 years •Imiquimob
Histology: •Photodymaic Therapy
•nests and cords of basaloid Education:
keratinocytes with peripheral palisading •Avoid sun exposure
and a central arrangement •Followed by dermatology
•watch for suspicious lesion
•SPF30+
•protective clothing

About Clinical Presentation Diagnostic Treatment

Common •benign overgrowth of skin cells •asymptomatic without •clinical diagnosis with •none if diagnosis is confirmed
Melanocytic change dermatoscopy
Nevi Types: •symmetric -will not appreciate Indications for excision:
•congenital (CMN): develop defect in melanoblasts •sharp borders neoplastic changes •locations: scalp, anogenital, mucosa
 increased risk of melanoma development if large •uniform color •rapid change
•irregular borders
•Acquired (MN): develops early in childhood •erosions
 often regresses by age 6 •persistent itching, pain, bleeding

Dysplastic •pigmented lesion from proliferation of atypical •asympatomatic •clinical diagnosis & •observe with dermoscopy +/- digital
Melanocytic melanocytes •irregular shape confirmed w/ histopathology dermoscopy
Nevi (DN) •MC onset in late childhood-early adulthood •sharp and ill-defined
•precursor to superficial spreading melanoma (SSM) bordered Education: •surgical excision w/ biopsy-r/o melanoma
-one lesions increase risk by 2x •varigated color •monthly self-exams -indications: changing, cant observe
-10+ lesions increase risk by 12x •maculopapular •sun protection
•family member skin checks •routine exams q3-12mo

About Risk Factors & Sites Clinical Presentation Types and Presentation
Melanoma •malignancy of melanocytes Risk Factors: Classifications: Superficial spreading melanoma (MC)
•increasing age •de novo melanoma (70%) •asymmetric macule with variegated pigmentation &
 •MC cancer in young women •photo-skin type I-II
between 25-29yo • > 25 nevi
•atypical nevi
Sites: •immunosuppression
•skin, mucous membranes, •personal or fhx of
nail apparatus, eye melanoma
•UV exposure (blistering
4 Types: sunburn before puberty,
•superficial spreading tanning beds)
melanoma (MC!)
•nodular melanoma MC Sites of Mets
•lentigo maligna melanoma •skin/subcutaneous
•acral lentiginous melanoma •lymph
•lungs
Associations: •liver
•genetics •brain
•exposure to UVA/
-new pigmented papule, plaque or nodule notched/ragged borders
•precursor melanoma (30%) •May occasionally be somewhat elevated
-develop from precursor (DN or CMN) •MC on trunk in men and LE in women
2 phases of growth: Nodular melanoma (2nd MC) RAPID GROWTH
•radial (thin): remains in epidermis •dark brown to bluish-black nodule
 good prognosis if treated early •ulcerate or bleed
•vertical: extends to dermis/vessels  mets •MC on trunk, head, and neck
Clinical Presentation: Lentigo maligna melanoma SLOW GROWTH
ABCDS: •asymmetric brown/black macule or patch with color
•asymmetric variegation & irregular borders
•irregular borders •dermal induration or nodularity
•change in color
•large diameter (>6mm) Acral lentiginous melanoma SLOW GROWTH
•evolution •Asymmetric brown/black macule
•MC on palms, soles, or nail apparatus
Late signs: ulceration and bleeding

Diagnostics Staging Treatment Education

Best test: 3 ways: Surgical excision Exams: age 18+ should have yearly skin exams
•excisional biopsy •Clark •In situ: margins at least 0.5cm
•TNM (tumor, node mets) •tumor <1mm: margins of 1cm •BCC and SCC: skin exam every 6 months
•Breslow (>0.76mm) •tumor 1-2mm: margins 1-2cm •melanoma: skin exam every 3 months
•tumor 2+: margins 2cm

Infection About Clinical Presentation Risks/Diagnostics Diagnostics/Management

Necrotizing •Rapid progression, extensive
Fasciitis necrosis of soft tissues & skin
•Bacteria release enzymes that
degrade fascia  proliferation,
thrombosis, ischemia, necrosis
Causes: GABHS, Pseudomonas,
Clostridium
•MC in middle age
Erysipelas •Acute superficial infection
(dermis and dermal lymphatic
vessels)
•MCC: GABHS
•MC in young children & adults
Cellulitis •Acute infection of the dermis
•Begins at site of non-penetrating Risks: Surgical Debridement
trauma  bruise, muscle, or strain •DM; malnutrition
-minor trauma, laceration •ETOH abuse & liver disease Broad Spectrum ABX:
-needle puncture -surgical incision •CKD •Carbepenem
•malnutrition •Ampicillin/Sulbactam
S/S: severe pain, indurated swelling, •Clindamycin
bullae, cyanosis, skin pallor, skin
hypesthesia, crepitation, muscle MRSA: Vancomycin
weakness, foul smelling
•Pain, redness, warmth, edema
Prodrome: fever, chills, anorexia, malaise DX: CBC, CMP, ESR, blood cx, US or MRI
General: +/- sepsis Complications:
•abscess formation
Lesion: painful, tender, hot •bacteremia, endocarditis
-bright red, raised, swollen, indurated •osteomyelitis
plaque with SHARP borders •metastatic infection
•sepsis, toxic shock syndrome
•Prodrome: fever, chills, anorexia, Risks:
 and subcutanoues tissue
•MC in middle age adults
Causes:
•S. aureus (MC), GABHS
•Cat/dog: Pasturella multocida
•Freshwater: Aeromonas
•Salt water: V. vulnificus
Lymphangitis •Acute inflammatory process
involving subcutaneous
lymphatic channel
•Acute Causes:
-GAS, S. aureus, HSV
•Chronic cause: Mycobacterium
Infection About
Abscess •Acute or chronic localized
inflammation  collection of
pus in tissue  inflammation
•Bugs: MSSA or MRSA
Furuncle •Infected nodule evolving from
folliculitis
Carbuncle •Deeper infection composed of
interconnecting
abscess/furuncles usually arising
in several contiguous hair
follicles
malaise
•General: +/- sepsis
•Lesion: painful, tender, hot
-bright red, raised, swollen, indurated
plaque with INDISTINCT borders
•Portals: break in the sin, wound,
paronychia (breaks around cuticles),
primary herpes simplex
•Symptoms: pain +/- erythema proximal
break in the skin, red linear streaks and
palpable lymphatic cord
Clinical Presentation
Any organ or tissue
-tender, red, hot, indurated nodule, +/- fever
-constiutional symptoms
•days  weeks=pus formation
DX: Gram stain & culture
 usually MSSA or MRSA
•Acute, deep seated, red, hot, tender nodule
or abscess (boil)
•1-2cm & fluctuant
•Nodule with cavitation after drainage
•Ill appearing, fever & constitutional symptoms
•Painful, tender
MC locations: nape of neck, back, thighs
*usually occur in folds or at base of fold
•minor skin trauma Management:
•body piercing •MRSA: IV Vancomycin, Daptomycin
•IVDU -Oral: Clindamycin, Amoxi + Bactrim, Doxy
•tinea pedis infection •MSSA: IV Cefazolin, Clindamycin, Nafcillin
•animal bites -Oral: cephalexin, Nafcillin, Clindamycin
•peripheral vascular disease
•immunosuppressed •Dog/cat: Augmentin
-•lymphatic damage •Human bite: Augmentin
•Fresh water: Ciprofloxacin
•Salt water: Doxycycline
•DX: cx if open & weeping •Oral ABX:
•Labs: CBC, CMP, blood cx -Dicloxacillin or 1st generation cephalosporin
•MRSA: Clindamycin or Bactrim
•Follow up in 24-48 hours
Diagnostics/Management Management
•Incision and drainage IV ABX if:
•toxic: fever, low BP, tachycardia-
ABX Therapy (Doxycyline): •rapid progression after 48h of PO
-single 2cm+ •inability to tolerate orals
-multiple lesions •close to indwelling device
-extensive cellulitis
-immunoscuppression Large Lesions: *surgery
-toxicity (fever >100.5, hypotension, •palms, soles, nasolabial, genitalia
sustained tachycardia) •avoid squeezing; ABX soap, BPO
Location: •Warm compress x10min/d
•hair bearing regions: beard, •PO ABX if red, hot and tender:
posterior neck, occipital scalp, axillae, -Bactrim (1st line), Clinda,
buttocks Doxycycline x7 days
Admit if: Uncomplicated:
•toxic appearing •Bactrim (1st line), Clindamycin,
•rapid growth Doxycycline x7 days
•no improvement w/ 24-48h of po
ABX Complicated: ADMIT IV Vanc
Folliculitis •Infection of the hair follicle
Causes:
•bacteria, fungi, mites, virus
Predisposing factors:
•shaving hairy areas
•occlusion of hair bearing
•hot tub
•topical CS, systemic ABX
•diabetes, immunocompromised
•Non-tender or slightly tender DX: clinical Mild (few):
•Pruritic •warm compress
•Can progress to abscess or furuncle formation •gram stain, C/S •BPO wash or antibact soap-dial
•KOH if fungal •ABX if spontaneous resolution
•Hot tub: Pseudomas (trunk) *KOH dissolves the skin so you see does not occur in 2-3weeks
•Viral: herpetic and molluscum the actual fungus
•Fundal: candida, malassezia Moderate (multiple): TOPICAL
•Other: syphilis •Clindamycin or Bactroban x10d
*GRAM NEGATIVE MSSA: ORAL Cephalexin
MRSA: Doxycycline, Bactrim
Prevention: BPO body wash

Herpes •dermatomal infection
Zoster reactivation of VZV
•Passes via sensory fibers
centripetally to sensory ganglia
 lifelong latent
•Triggers: immunosuppression,
trauma, tumor, irradiation
•prodrome pain, tenderness, flu-like •New lesions appear for up to 1wk
•active: papules  vesicles  pustule Other involvement:
•mucous, lymph, sensory
•opthalmic zoster
•postherpatic neuraligia
 (+) hutchinsons (CN V-V1)
•New lesions appear for up to 1wk
Diagnosis:Clinical, Tzanck test
Treatment
•Acyclovir 1000mg TID x7d
•Valcyclovir 500mg q8h x7d
PHN: NSAIDS (1st line),
gabapentin, pregablin, TCAs, nerve
block (severe)

Herpes HSV-1: oral HSV-2: genital Prodrome: pain, burning, tingling, paresthesias PCR (most sensitive) •Acyclovir 1000mg TID x7d
Simplex •Valcyclovir 500mg q8h x7d
*Bells Palsy with HSV-1 Active: painful, grouped vesicles on an Tzanck smear: multinucleated giant
*HSV MCC of encephalitis erythematous base cells and intranuclear inclusion bodies
Rashes About Phases Presentation Diagnosis and Treatment
Systemic Juvenile •Autoimmune mono or •Daily arthritis, diurnal high fever •Clinical Diagnosis •NSAIDS
Idiopathic Arthritis polyarthritis in children <16yo •Salmon-colored/pink migratory rash •Steroids
(Stills Disease) •Large and small joints •HSM, LAN, hepatitis •HIGH ESR and CRP •Methotrexate

About Clinical Presentation Minor V Major Diagnostics & Treatment

SJS and •Cytotoxic event caused by an •Fever, chills, malaise, HA, sore throat, N/V/D, skin tender Emergency SX: •D/C offending agent
TEN immune response  destruction of •Macule  papulae  central vesicle/bullae  erosions •fever •IV fluids
keratinocytes •Target lesions-2 zones of color •Rapid confluence •(+) Nikolsy •HR >120bpm •Parenteral nutrition
•sloughing of epidermis •IV pain meds
Causes: •Distribution: face and extremities  generalized •IV steroids/IVIG early
•drugs-MC •Mucosal (lips, buccal, eye, genitalia, anal): PAIN,red Diagnostics:
•chemicals •Eyes: conjunctivitis, keratitis, synechia •SJS: <10% surface Wound care: wet dressing
•mycoplasms, viral, vaccine •Hair and nail (TEN ONLY): lose lashes & nails •SJS/TEN: 10-30% Eye: saline and erythromycin
•TEN: >30% surface

Risks Immediate v Delayed Exanthematous Reaction

Adverse HISTORY IS IMPORTANT Immediate: <1hr of last dose •MC of all drug reactions Reaction Possibility
Drug •urticaria, angioedema, anaphylaxis •EBV and CMV with PCN •High risk: PCN, carbamazepine,
Reactions Risks: allopurinol, gold salts
 •females
•hx drug reaction
•recurrent drug exposure
•EBV/CMV infection w/ PCN
•HIV with sulfonamides
Delayed: occurring after 1 hour,
usually before 6 hours, occasionally
weeks-months after use
•exanthematous eruptions v. fixed
drug eruptions v. systemic reactions
•Bright red, maculopapular rash
•Symmetric: trunk  extremities
•Scaling/desquamation w/ healing
Immediate: 2-3 days *previously sensitized
Delayed: 7-10 days  3 weeks
*due to sensitization requirement
•Medium: sulfonamides, NSAIDS,
isoniazid, chloramphenicol,
erythromycin, streptomycin
•Low: barbituates, BZDs,
phenothiazines, tetracyclines

Fixed Drug Eruption Pustular Drug Eruptions Drug-Induced Hypersensitivity

•Solitary erythematous •An acute febrile eruption •Skin eruptions with systemic symptoms and Diagnostics:
patch/plaque that will recur at internal organ involvement •leukocytosis, eosinophilia
same site if re-exposure Clinical Findings:
•sterile pustules on an erythematous Causes: Diagnostic Criteria: NEED 3
Lesion: base, often start in the intertriginous •antiepileptic drugs: phenytoin, •cutaneous drug eruption
•sharply marginated macule fold and/or face carbamazepine, phenobarbital •hematologic abnormalities
•erythema; dusky-red color •fever •sulfonamides: antimicrobials agents, •systemic involvement
•edematous & bullous  erode dapsone, sulfasalazine -LAN >2cm
Labs: leukocytosis -elevated LFT (hepatitis)
Management *remove agent Clinical Findings: -elevated BUN/Cr (nephritis)
•non-eroded: steroid ointment Course/Prognosis: •fever, malaise, facial edema, LAN,
•eroded: topical ABX (Bactroban •pustules resolve over 2 weeks then hepatosplenomegaly Treatment:
or Mupiciron) desquamation for 2 weeks •maculopapular eruption: starts on face, •stop/substitute all suspected meds
•SX: antihistamines for pruritis upper trunk and UE •consult dermatology
liquid compound for oral lesions •mild-moderate rxn: topical steroid
•moderate-severe/organ failure: oral
steroid with long gradual taper
•symptomatic: oral antihistamines
Neurology 5% Change in speech: migraine, recurrent laryngeal injury, apraxia of speech, Tumor
Perioperative vision loss is very rare, occurring at a frequency of 0.002% after non-ocular surgeries and 0.2% after cardiac and spine surgeries
 Increased prevalence after cardiac, spine, head and neck, and some orthopedic procedures.
 The most common cause of postoperative ocular injury is corneal abrasion, which may or may not be associated with visual loss.
 The most common causes of permanent POVL are central retinal artery occlusion, ischemic optic neuropathy, and cerebral vision loss
 Ischemic optic neuropathy (ION) is the most frequent clinical presentation of perioperative vision loss
Perioperative visual changes range in severity from a transient blurring of vision to irreversible blindness
 Transient blurring of vision often is associated with the intraoperative use of ocular ointments, excessive drying of the cornea, or corneal trauma
 Complete or partial visual loss after neurovascular, cardiopulmonary bypass and ocular procedures is well recognized as a potential complication that is likely related to
direct surgical trauma, embolic events, acute anemia, hypotension, or other undefined etiologies

Glycine-induced visual loss — Transient perioperative visual loss can occur after absorption of glycine solution used as a non-electrolyte bladder irrigant during transurethral
resection of the prostate (TURP) or as a uterine irrigant during hysteroscopy
Acute Vision Loss About Diagnostics Treatment/Management
Acute Angle •Obstruction of aqueous humor History: dark room (movie), reading, dilating, anticholinergics, coke •Immediate consultation & supine position
Closure outflow due to the lens or peripheral •Timolol  wait one minute 
Glaucoma iris blocking the trabecular network •Sudden onset of eye pain & HA Acetazolamide IV if >50mmHG, severe
•Blurred vision colored halos around light loss, or unable to tolerate po therapy  if
•N/V elevated-IV Mannitol
 •Fixed mid-position pupil, hazy cornea, conjunctival injection •Pilocarpine once below 40mmHg
•Increased IOP 60-80 (normal 10-20): tonometry; firm to palpation

Optic Neuritis Inflammation along optic nerve •PAINLESS vision loss Fundoscopic exam: swollen & edematous
•reduction in color vision, complete loss of light disk (anterior) or normal appearing disk
•red desaturation test: look at dark red object with unaffected eye, (retroulbar)
then look with affected eye (affected eye sees a lighter red or pink)
• (+) afferent pupillary defect •Consult

Anterior Ischemic •Most frequent clinical presentation •PAINLESS, abrupt vision loss; optic disc pallor & swelling
Optic Neuropathy of perioperative vision loss •Small cup-to-disc ratio
•Due to hypoperfusion •Systemic low BP, Anemia, Atherosclerosis

Central Retinal •History of amaurosis fugax •PAINLESS monocular vision loss Fundoscope: pale & infarct retina, red
Artery Occlusion  intermittent quick episodes of • (+) afferent pupillary defect “cherry” macula
vision loss
•Urgent consult; Permanent vision loss in 4hr

Central Retinal •PAINLESS monocular visions loss Fundoscope: edema optic disc, diffuse
Vein Occlusion -ranges from vague blurring to rapid loss retinal hemorrhages “blood and thunder”
• (+) afferent pupillary defect
•Urgent consult

Retinal •PAINLESS monocular “floaters”, “flashes”, dark veil curtain •Bedside US

Detachment •Normal exam except decreased VA and confrontation •Urgent consult for dilated exam

NEURO
CVA A sudden onset of neurologic deficit
resulting from a loss of blood flow
to a part of the brain
*cell death and irreparable damage
to brain tissue w/n 5min
Types:
Ischemia: thrombotic, emboli
*MCC is atrial fibrillation
Hemorrhagic: intracerebral (HTN),
subarachnoid (aneurysm, AV
malformation)
•hemi/mono/quadriparesis
•hemisensory deficit
•visual loss; one or both eyes, diplopia
•dysarthria, facial droop, ataxia, vertigo
•aphasia (Brocas or Wernickes)
•decrease in LOC
Exam:
ABCs and vitals
Skin: petechial, janeway, osler, livedo
reticularis, purpura
HEENT: trauma, funcoscope, mouth
Cardio: rhythm, M/R/G, bruit
Respiratory: breath sounds
Neuro: CNs, NIHSS sale
•Oxygen Saturation
•Finger stick blood glucose
•CT brain w/o contrast
-GOAL: w/n 25min of arrival
Other Immediate Studies:
•CBC, BMP, PT/PTT, troponin
•EKG/cardiac monitoring
•Keep NPO  IVF
•Hypoglycemia: dextrose
•Blood pressure: Labetolol,
Nicardipine, Clevedipine
•Cerebral edema: Mannitol
•Seizure: Lorazepam
Ischemic Stroke
•goal of SBP < 185 + DBP < 110
•TPA (Altepase): maintain BP
<180/105 for 24 hours after
Intracerebral Hemorrhage
-lower BP within one hour to 140

Transient •transient episode of neurologic Assessing severity of symptoms ABCD2 scoring: 1. Order US of carotids (CAD)
Ischemic dysfunction caused by cerebral 3+ should be admitted 2. EKG, Echo (emboli)
Attack (TIA) acute infarction 3. MRA/CTA (vessel disease)
-most resolve within 1-2 hours
 Pharm: Plavix, Control BP, Statin

NEURO 8% About Cardiac/Other Neuro Diagnostics and Treatment

Syncope Cardiac: carotid sinus,
aortic stenosis, HOCM
Neurologic: basilary artery,
subclavian steal syndrome
Other: orthostatic,
vasovagal
Carotid sinus: slow SA and AV node due
to pressure on carotids (turtleneck)
Aortic Stenosis: low CO due to stenosis
HOCM: murmur increases with valsalva
Vasovagal: decrease in arterial pressure
and HR mediated by parsympathetic tone
Basilary Artery: vertigo, visual
dysfunction, perioral numbness, ataxia
Subclavian Steal: Stenosis of subclavian
artery proximal to the vertebral artery 
sx with left arm exertion  angina, finger
ulceration
Orthostatic: rapid change from lying to
sitting or sitting to standing
Diagnostics:
•Head CT: focal neuro, hx SAH
•Position of patient at time of syncope
-lying: seizure, cardiac arrhythmias
-standing: orthostatic, vasovagal
Orthostatic vital signs: SBP drop >20
or SBP <90 or pulse increase >30bpm
Treatment: varies on cause

Epidural •middle meningeal artery •LOC, HA, N/V, focal sx, CN III palsy •CT of brain: convex (lens) bleed •high ICP: Mannitol
Hematoma •MCC: temporal FX •LUCID INTERVAL  coma -does NOT cross suture lines

Subdural •cortical bridging veins •varies, may have focal neuro sx •CT of brain: concave (cresecent) •evacuate with massive 5mm+ midline
Hematoma •MC in elderly -DOES cross suture lines shift
•MCC: blunt trauma

Subarachnoi •berry arterial aneurysm •”thunderclap” sudden HA •CT of brain •supportive tx: bed rest, stool soft
d •MCC: rupture, AVM •meningeal symptoms, no focal neuro •LP: CT (-)  xanthrochromia, high CSF •lower BP: Nicardipine, Nimodipine,
Hemorrhage Labetalol

NEURO
Guillain- •Acute inflammatory •Onset 1-4wks after respiratory of GI illness Labs: CMP, CK, ESR, thyroid, stool IMMUNOTHERAPY WITHIN
Barre polyradiculoneuropathy with culture for C. jejuni, rheumatologic, 4WK OF ONSET
resultant weakness with possible Symptoms: vit B12, folic acid, A1C,
paralysis and diminished •dyesthesias (finger/toes and move proximal) electrophoresis, metal •Plasmapheresis
reflexes •proximal muscle weakness of LE ascending -removes autoantibodies, immune
symmetrically Electrodiagnostic (EMG/NCS) complexes, cytotoxic constituents
•Age: bimodal •diminished or loss of DTRs early on •confirms polyneuropathy
(15-35yo, 50-75yo) •pain-throbbing, aching •IVIG: donated plasma
*shoulder, back, buttocks, thighs Lumbar Puncture -requires less time, once daily
Variants: •progression of weakness over hrs -> days •reveals albuminocytologic
•acute inflammatory -CN involvement dissociation  high protein, normal •Pain: NSAIDS, Gabapentin
demyelinating polyneuropathy -respiratory: dyspnea, SOB, diminished WBC
(AIDP)=MC •ANS dysfunction (dysautonomia) •Motor Dysfunction: PT, OT
-tachycardia(MC), bradycardia, arrhythmias MRI with Gadolinium
•other neurological findings •spine: thick intrathecal spinal nerve •DVT Prophylaxis: LMWH
-neuro: unsteady to complete gait loss roots and cauda equine
-sensory: impaired proprioception •brain: enhanced CN III, VI, VII

Myasthenia •Autoimmune disorder with •Fluctuating skeletal muscle weakness and fatigue Ice Pack Test x 2 minutes 4 treatment option available:
Gravis progressively reduced muscle •worse later in the day/evening or after exercise •(+) if improvement 1. symptomatic therapy
 strength with repeated use
•Females 20-30; Males 50-70
eye/face -> neck -> UE
-> hands -> LE
•Antibodies are produced (by
thymus) against the ACH
nicotinic postsynaptic receptors
(AChR) at the neuromuscular
junction
 AChR destruction and a
loss of postsynaptic
folds
 Over release of Ach
Etiology:
•Idiopathic derangement of
immune system regulation
-anti-AChR antibody (MC!)
-anti-MuSK antibodies
•Thymic disease found in 75%
•Various drugs
•Ocular (CN II, IV, VI): EOM weak  diplopi
-diplopia disappears when close one eye Serology:
-unilateral or bilateral ptosis •AChR antibodies (85%)
•MuSK Antibodies (if AChR (-))
•Bulbar muscle weakness (CN IX-XII) -not likely to have thymic
-weakness with prolonged chewing •Seronegative MG (both (-))
-dysphagia, dysarthria(speech), dysphonia(voice) -purely ocular disease
•Anti-striated Muscle(anti-SM)
•Facial Muscles (CN VII) -(+) in about 80% w/ thymoma
-flat affect, cant smile or close eye
Imaging: CT chest  thymoma
•Neck Muscle Weakness *anterior mediastinal mass
-“dropped syndrome” later in day  weak
extensor muscles Electrodiagnostic Studies
•Repetitive Nerve Stimulation
•Limb: proximal muscle weakness, UE>LE (RNS) *MC study for MG
-repetitively stimulated the NMJ of a
•Myasthenia Crisis (resp. muscles) specific muscle
-diaphragm and IC muscle weakness (+) test: smaller EPSPs due to
repetitive stimulation
•Single-Fiber Electromyopgraphy
*Most sensitive test for MG
-2 muscle fibers w/ same axon
-(+) if increased time frame between
1st and 2nd AP
 anticholinesterase
(Pyridostigmine)
2. Chronic immunomodulating
therapy  glucocorticoids
3. immediate immunomodulating
therapy Prednisone
-Other immunomodulators:
Azathioprine, Mycophenolate
mofetil, Cyclosporine
4. Surgery (thymectomy)
Rapid Immunomodulating
Therapy
Indications: myasthenic crisis,
pre-op, bridging meds, maintain
remission
•Plasmapheresis
•IVIG

NEURO
Essential MC adult onset movement disorder •Rapid action/kinetic tremor of arms Clinical Diagnosis •1st line-Propranolol (off label)
Tremor -trouble writing, eating, fine motor skills •Primidone + Propranolol if no response
Defined by: •Head and arm tremor MC *speech *refer if 1st line options don’t work
-enhanced by emotional stress changes
-decreased with ETOH •NO tremor at rest •2nd-Alprazolam, Topiramate, Gabapentin
-fhx common (dominant)
-no other abnormal findings •3rd line-Deep brain stimulation, botox

Parkinson’s •Uncommon under age 40, increase after •resting tremor, rigidity, bradykinesia Clinical features from hx •Aim: blocking the effect of Ach or
Disease age 60 & PE administration of Levodopa
Tremor
•MC in men •resting tremor of distal muscles; “pill Must have bradykinesia •1st line: Levodopa & Carbidopa
roll” with either rigidity
•Reduced Risk: caffeine, coffee, ibuprofen, •less with voluntary movement and/or tremor •Dopamine Agonist: <65 and mild sx
statins, cigarette smoking, moderate alcohol •spreads unilaterally up the body -Bromocriptine (Cycloset)
-Pramipexole (Mirapex)
•Increased Risk: age, fhx, Rigidity -Ropinirole (Requip)
herbicide/pesticide exposure •unilat  spread up then contralateral -Amantadine
• “cogwheel” rigiditiy & lead pipe
Pathophysiology: •Anticholinergic-Benztropine
 Degeneration of the dopamine-producing
neurons in the pars compacta of the
substantia nigra and locus coeruleus in
brainstem Dopamine/Ach imbalance
•Lewy bodies within neurons
Bradykinesia 80% of patients -young patient w/ tremor as primary sx
•generalized slow movement
•starts distally: fingers  loss of arm •COMT Inhibitors
swing  feet and legs (shuffling) -Talcapine, Entacapone
-extend life of Levodopa; adjunct tx

Huntingtons •Incurable, inherited, autosomal •Characterized by motor, cognitive, and •History and PE *Symptomatic; No cure
dominant neurodegenerative disorder psychiatric deficits with cell loss in
neurons of basal ganglia and cortex •CT/MRI: cerebral & •Tetrabenazine for dyskinesia
•Chromosome 4 caudate nucleus atrophy -MOA: blocks Dopamine release
•Expanded & unstable CAG trinucleotide •Chorea, Dystonia -SE: extrapyramidal
repeat in HTT gene at 4P16 •Eye movement abnormalities •PET scan: reduced •Reserpine for chorea
•Wt loss and cachexia striatal metabolic rate •Haloperidol for behavior & chorea
•Psych: irritable, moody, antisocial •Amantadine for chorea
•Cognitive: judgement, memory •Genetic Testing •Supportive care
•Behavior changes: dementia *gradual

•Initial: abnormal movements or

intellectual changes

•Early: abnormal behavior & restless

•Later: dementia & choreiform, dystonia

NEURO
Multiple •MC autoimmune inflammatory
Sclerosis demyelinating disease of CNS
•Cause: autoimmune
•Women > Men
Pathophysiology:
•lesions effect white matter in the optic
nerve, brainstem, basal ganglia and
spinal cord
-demyelinating lesions (plaques)
-myelin loss, destruction of
oligodendrocytes, reactive
astrogliosis (increase in astrocytes)
•lesions affecting signal in grey matter
Risks: far from equator, viral
infections, HLA on chromosome 6
Spinal cord
•sensory loss, weakness, numbness,
sphincter (urgency, hesitancy, sexual)
brainstem: optic neuritis, diplopia,
lateral gaze, dysphagia
psychological: cognitive disability,
depression, euphoria
motor: unsteady, spastic, cramp, gait
transient features
•lhermitte sign: electric shock like
sensation that runs down back or
limbs upon neck flexion (looking
down)
•uhthoff phenomenon: worsening sx
when overheated
CLINICAL
•2+ attacks followed by objective
evidence on exam & 2 lesions
McDonald Criteria
•clinical findings + MRI
•2+ regions of central white matter
(space)
•different times (time)
Imaging:
T1/T2 MRI of brain/cervical cord
-T1: hypointense “black holes”
showing axonal damage
-T2: high signal intesntity lesions
associated with total # of lesions,
highlight active inflammation
LP: oligoclonal IgG
Acute Attacks
•Methylprednisolone
•Plasma exchange if steroids CI
Symptomatic
•fatigue: Amantadine, Methypheidate
•Depression: SSRI
•Spasticity: Baclofen, Diazepam
•Pain: TCAs
•Optic Neuritis: Methylprednisolone
Disease-Modifying
RRMS, SPMS with exacerbations
relapse prevention 1st line
•IFN B-1a (Avonex, Rebif)
•IFN B1b (Betaseron or •Extavia)
•Glatiramer acetate (Copaxone)
•Fingolimod (Gilenya)
•progressive MS
 -SPMS: high dose IFN-B
-PPMS: Ocrelizumab (Ocrevus)

•Aggressive MS: Cyclophosphamide

Amyotrophi •MC degenerative disease of the •Limb onset (75-80%) USUALLY CLINICAL Riluzole (Rilutek)
c Lateral motor neuron system *initial complaint (bottom up) -antiglutamatergic, reduces damage to
Sclerosis -tripping, stumbling, awkward run •Labs: blood, urine, CSF the motor neurons by decreasing the
(ALS) •Muscle weakness & atrophy -foot drop & wrist drop •Imaging: MRI release of glutamate -> reduces
(Lou throughout the body due to -reduced finger dexterity, stiff, •Genetic testing stimulation and regulates intracellular
Gehrigs) degeneration of the UMN and LMN cramp, weak •Muscle biopsy calcium
•Neuromuscular US: detect
•Loses ability to initiate & control all •Bulbar onset (20-25%) fasiculations Supportive:
voluntary movements: eyes, bladder, (brain down) •therapy: PT/OT, braces
bowel (spared until final stages) -slurred speech, hoarse, decreased •EMG & NCS -nutrition: percutaneous endoscopic
volume of speech/nasal standard in evaluation of motor gastrotomy (PEG)
•Cognitive function spared -aspiration or choking neuron disease •breathing support
•palliative
•Sporadic (MC!) or familial with •Emotional:
autosomal dominant -involuntary laughing, crying, Prognosis:
•fatal
•Increases with decade after age 40 PE/Diagnosis: •respiratory failure #1 cause of death
-MC whites and males •UMN and LMN dysfunction in one in ALS
•2x greater in smokers of the four categories: •rate measured by ALS
-cranial/bulbar, cervical, thoracic,
•Risks: age and family history lumbosacral Progression Rate:
SX are PROGRESSIVE, not •Functional Rating Scale:
remitting -0(severe)-48 (normal)

Anterior Cord Syndrome: Loss of pain and temperature below the level with preserved joint position/vibration sense

Central Cord Syndrome: Loss of pain and temperature sensation at level of the lesion where spinothalamic fibers cross the cord

Complete Cord Transection: Rostral zone of spares sensory, no sensation in levels below injury, urinary retention and bladder distention

Brown-Sequard Syndrome: Loss of joint position sense and ibration sense on the same side as lesion and pain ant temp on the opposite side a few levels below

NEURO
Lyme Disease Deer tick  Ixodes tick early localized: erythema migrans •ELISA test  if (+) then Doxycycline; Amoxi (<8, prego)
(Spirochete) summer & spring confirm with Western Blot
early disseminated: arthritis, CN VII palsy, cardio Prophylaxis: <72hr of rick
 Borrelia burgdorferi late: neurologic worsening, synovitis, arthritis removal if the tick present >36h

HIV (Viral) Retrovirus: changes RNA into
DNA via reverse transcriptase
Transmission: sex, IVDU,
mother, blood contact
Acute seroconversion: flu-like illness •ELISA  western blot 2 NRTIs: nucleotide reverse
transcriptase inhibitor
AIDS: CD4 <200, diarrhea, wt loss, dementia •HIV RNA viral load -Zidovudine (Retrovir)
-Tenofivir
Prophylaxis
<200: Bactrim
<150: Itraconazole
<100: Fluconazole
<50: Azithromycin;
Valgangcilovir

Syphillis Trepenoma pallidum Primary painless chancre on genital, painless lymph •RPR/VDRL Pen G Benzathine
(Spirochete) •dark field microscopy
Secondary: mucous patch, condyloma, scaly papule

Latent: first year=contagious, > one year=not contagious

Tertiary: anytime after untreated secondary  gummas

Neurosyphillis: asymptomatic invasion  meningeal 

tabes dorsalis (wide gait)  paresthesia (cerebral cortex)

Urology/Renal 5%
Edema:
- Lymphedema: surgical removal of lymph nodes for CA treatment (MC breast) can cause swelling of a limb or limbs with thickening of the skin
- Angioedema: reactions to some medications (ACE, ARB) can cause fluid to leak out of blood vessels into surrounding tissues
- Drugs: oral DM meds, BP meds, Ibuprofen, Estrogen
- Infection: peritonitis

Urinary retention: common complication of spinal and epidural anesthesia

- Obstructive: urethral stricture, bladder calculi or neoplasm, FB
- Neurogenic: MS, Parkinsons, CVA, post-op retention
- Traumatic: urethral, bladder, or spinal cord injury
- Extraurinary: fecal impaction, AAA, rectal or retroperitoneal mass
- Infectious: local bascess, cystitis, genital herpes, herpes zoster

Acute Urinary retention: inability to void with a full bladder

- Risks: male, enlarged prostate, anesthesia, antihistamine and narcotis use, pelvic and perineal procedures
- SX: painful, vomiting, palpable bladder, LOW BP & HR

Chronic Urinary retention:

- SX: painless, develops gradually , suprapubic dullness, rounded midline mass
Orthostatic Hypotension: drop >20 systolic or 10 diastolic, 15bpm increase in pulse 2-5 min after supine to stand

GU About/ Causes Signs/ Symptoms Diagnosis Treatment

Testicular Tumor •MCC solid testicular tumor in •Painless enlargement of testis Labs: •Inguinal exploration with vascular
men 18-40 -testicular or scrotal heaviness •Alpha-fetoprotein (AFP) control of spermatic cord
-painless nodule on testicle •Hcg (not good for a male!) •Radical inguinal orchiectomy
•MC cancer in males 20-35 •LDH •Radiation/chemo depends on subtype
•90-95% are germ tumors •acute testicular pain -10% •Advanced: anemia, LFTs, renal
•metastatic symptoms-10% Follow-Up:
Risks:
Imaging/diagnosis: •Monthly for 1st 2 years, bimonthly 3rd yr
•Cryptorchidism
MC site of metastasis- •Scrotal US-initial evaluation •Tumor markers at each visit
•Exogenous estrogen in prego
retroperitoneal abd lymph nodes •Definitive dx-radical inguinal •CXR and CT every 3 months
•Infertility
*Back pain, cough, SOB, anorexia, orchiectomy •80% relapse in 1st 2 years after tx
•Fhx HIV, ethnicity
N/V, bone pain, LE swelling
*transscrotal biopsy Prognosis:
contraindicated •90% + 5 years survival rates
•>10cm retroperitoneal disease 55-80%

Wilms Tumor •Mainly in PEDIATRIC patients Often a single unilateral lesion, but Imaging: •Surgical resection followed by chemo +/-
(Nephroblastoma •95% renal carcinoma in children may be multifocal or bilateral •Abdominal US=initial study radiation
) <15yo •CT or MRI to further investigate
*primary •Abdominal mass (MC!) •CXR or CT for lung mets Prognosis:
Abnormal renal development  •Abdominal pain •more anaplastic and metastasis are worse
*MC renal cancer loss of tumor suppressor and •HTN Labs: rates
in kids <15yo transcription gene functions •Hematuria •CBC, CMP •recurrent disease is possible
•UA *MC in anaplastic tumors (bad)
•Coagulation studies

GU
Renal *MC in males *stone size does NOT Labs: •Pain control-NSAIDS, opioids
Calculi •Calcium oxalate- MC! correlate with severity •hematuria (micro or gross) •Hydration-NO FORCED IV because may worsen pain
(Nephro- •<5.5: uric acid or cysteine
lithiasis) Risks: S/S: • 5.5-6.8: calcium oxalate •Alpha-1 blocker-Tamsulosin
•high protein and salt •Acute, severe pain (flank) • >7.2: calcium phosphate/struvite
•inadequate hydration •radiate to abdomen or groin •Steroids-Prednisone 10mg daily for 3-5d
•humidity & elevated temp. •Urgency and frequency Frequent or + family history:
•sedentary lifestyle •Nausea/Vomiting •Low Na & protein, high fluid Prevention:
•GI malabsorption syndromes •Increase fluids-best thing to do! 1.5-2L of urine/d
•HTN, obesity, gout <5mm pass spontaneously Diagnostics: •Diet (Eat bran to decrease calciuria)
10mm+ do NOT pass •KUB abdominal xray (cheapest) *do not need to decrease calcium!
•Renal US (good if noradiation)
•Spiral CT-most accurate
Acute E. coli •Irritative voiding (dysuria) Labs: Short term antimicrobial Therapy
Cystitis Proteus •Frequency urgency •Pyuria •Nitrofurantoin (Macrobid) 100mg po BID x5-7d
“Bladder Klebsiella •Suprapubic pain •Hematuria •Bactrim 800/160mg po BID x3d
Infection” Pseudomonas •+/- gross hematuria •Bacteriuria •Fosfomycin (Monurol) 3g po x1
“UTI” Staph •Leukocyte esterase •Fluoroquinalones, Augmentin, Cephalosporins
Exam: •Urinary nitrate
MC route: •Suprapubic tenderness •Urine culture + bacteria Urinary Analgesics: Phenazopyridine (Azo)
ascent up urethra •NO CVA!
•NO TOXICITY! COLONY COUNT >100,000 Non-Pharm: *in addition to antibiotics
*MC in women •Sitz baths, fluids +/- crandberry juice, probiotics

Acute G-bacteria MC •Irritative void (dysuria) Labs: Outpatient:

Pyelo- E. coli •Suprapubic pain •Pyuria, hematuria, bacteriuria •1st line: FQ (Cipro or Levo); Bactrim, Augmentin
nephritis Proteus •+/- gross hematuria •+/- WBC Casts
“kidney Klebsiella •Fever, chills, N/V/D •Leukocyte esterase & Urinary nitrate •Adjunct Tx: if high risk for fluoroquinalone resistance
infection” Pseudomonas •Flank pain •CX: + heavy growth of bacteria or if using 2nd line tx  1g Ceftriaxone (Rocephin)
•CBC: leukocytes w/ left shift
MC route: Exam: Inpatient:
ascent up urethra •Fever Imaging: •IV ampicillin/gentamicin, FQ, fluoroquinalone
hematologic route •Tachycardia •CT (preferred): renal arcino, abscess •IV carbapenem (Imipenem)
•CVA tenderness •US: hydronephrosis, abscess •IV extended-spectrum cephalosporin (Cefepime)

GU
Chronic Epidemiology: Early: asymptomatic •↓ RBC, H/H SLOW PROGRESSION
Kidney •70%+ cases due to DM or Late CKD: waste build-up, uremia •↓ Ca, Na+, pH (acidosis)
Disease HTN/vascular •↓ GFR •HTN & proteinuria: ACE/ARB
(CKD) •Independent risk of cardio disease Stage I-II: no sx from low GFR •↓ vitamin D •Reduce further kidney damage
•possible edema, HTN •↓ HDL *obstruction, nephrotoxins, flare of
↑↓ Risk Factors: underlying disease
Patient demographics: old, AA Stage III and IV: all organs affected •↑ K+, Phosphate •Control bld glucose AIC <7%
•Anemia, fatigue, anorexia •↑ uric acid
Historical Factors: •Abnormal Ca, Ph, vit D, PTH •↑ BUN/Cr Dialysis Indications:
•previous AKI •Abnormal Na, K, water, acid/base •↑ PTH •GFR 10 or less
•fhx renal disease •↑ triglycerides •Uremic symptoms
•smoking Stage V/ESRD: uremia syndrome •metabolic disturbances
•lead exposure •Marked disturbance in ADL, well-being, Urinalysis: •Fluid overload unresponsive to
nutrition, water, electrolytes •broad, waxy cast (dilated nephron) diuretics
Comorbid Conditions: •proteinuria
 •GU-structural, proteinuria, sediment Physical Exam:
•Metabolic-DM, HDL, obese, •MC=hypertension!
•Other-HTN, autoimmune •Uremic frost

Bladder 2nd most common urologic cancer
Cancer MC in men and older patients (~73yo)
MC-epithelial cell malignancy
(urothlial cell carcinoma)
Hematuria, painless
Weight loss
+/- irritative voiding
Large: possible abdominal mass
Labs: Hematuria +/- pyuria, anemia
Cytology: epithleial cells
Imaging: CT, MRI, or US
Superficial (Ta and T1):
•transurethral resection of tumor
Invasive (T2+): radical cystectomy
•+/- chemotherapy, radiation

Risks:Smoker; Industrial solvents Metastatic: Hepatomegaly, LAN Cytoscopy with biopsy-GOLD!

 Local anesthesia, local resection

Renal Cell •Peak incidences in 60s
Carcinoma •2x more common in males
*primary •MC cause=sporadic tumors
*most •most are clear cell carcinoma
common  arise from proximal tubules
renal
cancer Risks: obesity, HTN, chronic
analgesics, environmental toxin
exposure, chronic HCV,
nephrolithiasis, smoking
•Gross or microscopic hematuria Labs: •Surgical excision
•Flank pain •Hematuria -standard: radical nephrectomy
•Abdominal mass •Anemia (MC!) or erythrocytosis - kidney & adrenal, lymph nodes
•Hypercalcemia
Classic triad: •Stauffer syndrome: hepatic •very limited effective chemotherapy
•flank pain dysfunction with elevated LFTs for RCC
•hematuria
•abdominal mass Imaging: Prognosis: 5 years survival rates
•Solid renal mass •renal capsule only 90-100%
Metastatic: cough, bone pain •Standard-CT abd/pelvis •beyond renal capsule 50-60%
•MRI-evaluates spread into IVC •lymph node involvement 0-15%

Renal Atherosclerotic occlusive disease
Artery 5% of pts with HTN have RAS
Stenosis
*MC >45yo w/ atherosclerotic disease
*suspect if unexplained HTN in
woman <45 year old
•HTN (refractory new onset)
•Pulmonary edema with poor HTN
PE:
•HTN
•audible abdominal bruit
Elevated BUN/Cr if ischemia
Imaging:
•US: asymmetric kidney (unilat) or
small hyperchoic kidney (bilat)
•Doppler US *BEST
•Renal angiography *GOLD
don’t use ACE if BILATERAL
•Medical management
•Angioplasty +/- stent
•Surgical bypass
*more risks, no greater efficacy

GU 8% Causes Labs Treatment

Metabolic Anion Gap-MUDPILERS Non-Anion Gap-HARDUPS •Low bicarb Correct underlying
Acidosis •Methanol •Hyperalimentation •low ph
•Uremia •Acetazolamide
•DKA •Renal tubular acidosis
•Propylene glycol •Diarrhea
•Isoniazid, infection •Ureto-pelvic shunt
•Lactic acidosis •Post-hypopcapnis
•Ethylene glycol •Spironolactone
•Rhabdo.renal failure
•Salicylates (ASA)

Metabolic CLEVER-PD •Increased Bicarb

Alkalosis •Contraction •increased pH
•Licorice
 •Endo (Cushings)
•Vomiting (loss of H+ from GI tract)
•Excess Alkali
•Refeeding Alkalosis
•Post-hypercapnia
•Diuretics

Respiratory Hypoventilation-CHAMPP •High CO2

Acidosis •CNS depression (acute/chronic resp failure) •low ph
•Hemo/pneumothorax
•Airway obstruction
•Myopathy
•Pneumonia
•Pulmonary Edema

Respiratory Hyperventilation-CHAMPS •Low CO2

Alkalosis •CNS disease •high pH
•Hypoxia
•Anxiety
•Mechanical Ventilators
•Progesterone
•Salicylates

GU 8% About Clinical Presentation Diagnostics Treatment

Hydronephrosis Water inside kidney  distention/dilation of •May be palpable abdominal or •Increased BUN/Cr •Remove obstruction/drain urine
pelvis and calyces by obstruction of free flow of flank mass •Electrolyte imbalance
urine from kidney •IV urogram, US, CT, MRI •Nephrostomy tube: upper tract
•Catheter: lower tract

Hematology 3%

HEME/ONC
Iron •MCC blood loss •Fatigue, hair thinning •High TIBC, RDW Ferrous Sulfate
Deficiency •pallor, pica, cheilitis •Low iron, ferritin, transferrin *take with Vitamin C
Microcytic •koilycia, plummer vinson syndrome •Low MCV, low MCH, nml MCHC

Alpha •Decreased alpha-globin •¼-silent •Smear: target cells •Moderate: folate, avoid oxidative
Thalassemia •MC in Asians •2/4- minor (trait) stress, avoid iron supplementation
•¾- HbH •Electrophoresis:
Microcytic •4/4- hydrops fetalis all equal b/c all contain A •Severe: transfusions, splenectomy
iron chelation (IV Deferoxamine),
Beta •Decreased beta-globin •½: Minor (trait)-asymptomatic electrophoresis: Major: blood transfusions
Thalassemia •MC in Mediterranean •2/2: major (cooleys) •increased HbA2 and HbF,
-symptomatic around 6 months definitive=bone marrow transplant
Microcytic HbF=2a2y -Frontal bossing & maxillary smear: target cells, nucleated cells
HbA=2a2b, HbA2=2a2d growth X-ray: crew-cut skull appearance

Folate •MCC=diet  leafy greens •Glossitis, cheilosis •high MCV and homocysteine Folate supplement
Deficiency •NO NEUROPATHY •normal MMA
Macrocytic
Smear: hypersegmented
neutrophils, macro-ovalocytes

B12 •MCC=pernicious anemia  damaged glossitis, NEUROPATHY high MCV, homocysteine & B12 Injections
Deficiency parietal cells  lack of intrinsic factor *B12 needed to convert MMA to ScoA MMA
Macrocytic
Smear: hypersegmented, macro-
ovalocytes, basophilic stippling

Anemia of increased hepcidin and decreased EPO Increased ferritin EPO

Chronic  not able to produce heme Rest of labs are low
Disease
Normocytic •MCC: Chronic Kidney Disease (CKD)

Sick Cell •Autosomal resessive Jaundice, HSM, cardiomegaly •Electrophresis: HbS •PCN at 2 months, folic acid at 1 yr
Anemia •Abnormal substitution of B chain Ill appearing, poor healing, •Smear: Howell-Jolly •Hydroxyurea
Normocytic retinopathy •Labs: increased reticulocytes
•Unstable HbS  abnormal shape  vaso- Acute: HOP: hydration, oxygen, pain
occlusive episodes  destroyed by spleen Triggers: SHITAE Definitive: stem cell

G6PD •X-linked recessive; MC in AA males •Jaundice, dark urine Smear: Prevent: avoid oxidative drugs,
Normocytic •Malaise, weakness, pain •Bite & Blister cells; Heinz Bodies triggers
•Deficit in G6PD enzyme
Labs: •Folic acid supplementation
•RBC is vulnerable to oxidative state  Triggers: •Low hgb & hct
hgb denatures  forms Heinz bodies  infection, food (fava beans), ABX •High reticulocytes & High MCH
damages membrane  destroyed by spleen •G6PD assay

HEME/ONC
Aplastic Failure of hematopoietic bone marrow
Anemia due to suppression or injury of stem cells
MC: idiopathic autoimmune
Hypoplasia of hematopoietic bone
marrow  decrease in hematopoietic cell
lines (WBC, RBC, platelets)
Exam: pallor, purpura, petechial
*no hepatomegaly, splenomegaly,
bone tenderness, lymphadenopathy
Low WBC, RBC, Plt
Low reticulocyte count
Normal MCV
Bone marrow biopsy: hypocellular
aspirate, limited/no hematopeitic
precurosors
Meds: EPO, Darbepoetin
Supportive: transfusions, ABX
Mild: growth factors
Severe:
neutrophil count <500, plat <20000,
reticulocyte <1, bone marrow <20
-bone marrow transplant pt <40

Spherocytosis inherited genetic defect  abnormal *jaundice, enlarged spleen Smear: Spherocytosis All: folic acid (1mg daily)
 formation of proteins in RBC skeleton *+/- gallstones (50%) Definitive: splenectomy
*most autosomal dominant LOW: hgb, hct, *delay until 5+yo or puberty
HIGH: reticulocytes, MCHC
*trapped in small red pulp fenestrations Normal MCV -pneumococcal vaccine
which leads to phagocytic destruction -transfusions of EPO if severe

Autoimmune Antibody forms against RBC antigen (IgG) Abrupt, rapid, life-threatening Smear: Prednisone 1-2mg/kg/day orally
Hemolytic Marked microspherocytosis
Anemia Diseases-lupus, leukemia, lymphoma Fatigue, jaundice, splenomegaly Polychromataphils/reticulocytes Severe: splenectomy

RBC tagged  macrophages remove Low: hgb, hct Comorbitities: treat underlying
membrane  spleen destroys High: reticulocytes Transfusion: required
*give without type/cross matching
Complement can tag Kupffer cells in liver Diagnostic: Coombs testing

HEME
ITP • antibodies against platelets •Bleeding, petechiae, bruising ISOLATED •Steroids
•MC after URTI thrombocytopenia •IVIG, splenectomy

TTP •deficiency in ADAMTS13 • “FATRN”  fever/FFP, anemia, •increased vWF, low FFP
“Adults, fever, neuro, vWF” thrombocytopenia, renal(hematuria), ADAMTS13
neurp •smear: shistocytes

DIC Pathologic activation of coagulation system  •Widespread hemorrhage & •Increased PTT/PT/INR •Treat underlying cause
widespread microthrombi  consumes clotting thrombosis •Decreased fibrinogen •FFP if severe bleeding
factors  thrombocytopenia and diffuse bleeding •MC at venipuncture sites •Increased D-dimer

vWF Disease •Autosomal Dominant •recurrent nose bleeds, heavy •Decreased vWF, DDAVP
periods decreased VIII
•family history •prolonged PTT and
bleeding time

Hemophilia X-linked recessive •hemarthrosis (joints, MC ankle) •prolong PTT & bleeding •Hemophilia A: Factor VIII or DDAVP
MC in children •hemorrhage due to trauma time •Hemophilia B: Factor IX
A: factor VII B: Factor IX C: factor XI •possible purpura/petechiae •normal platelets •Hemophilia C: Factor XI

HEME
Disseminated *lots of clotting with bleeding (using Uncontrolled local or systemic Bleeding Prolonged PTT and PT
Intravascular up all clotting factors) activation of coagulation (multiple sites) Low fibrinogen
Coagulopathy -> bleed from ALL orifices ->depletes coagulation factors Elevated D-dimer
(DIC) Pupura *activating coagulation and cross-
Petechiae linking fibrin

Smear: shistocytes (10-20%)

*shearing through microvasculature

Heparin Induced Acquired Onset 5-7d post therapy Prior heparin use or use in those *resolves around detecting heparin-
Thrombocytopeni Heparin +PF4 forms a neoantigen on who started past 5-10d or those dependent antibody
a (HIT) the platelet -> immune antibody
response -> platelet clearance->
HITT=HIT and thrombocytopenia (85-90%)
thrombosis
*can be hypercoaguable (50%) too
because destroyed platelets release
granules/activate
Early exposure can occur within
24hrs if been exposed and have
circulating antibodies
*Venous thrombosis:
Legs, cardiac, skin
-> necrosis, gangrene
receiving LMWH:
-new thrombocytopenia
-platelet drop of > 50% of prior
value
-venous or arterial thrombosis
-necrotic skin at injection site
-acute systemic reactions
*Begin anticoagulation with non-
heparin: Argatroban
*Can be Warfarin once the pt is stable
and plt >150,000
Duration:
No thrombosis: 2-3 months
Thrombosis: 3-6 months

Disease Cause Labs Presentation Treatment

Thrombotic Thrombocytopenia due to incorporation of vWF LOTS! Acute/subacute onset of Plasma exchange with FFP
Thrombocytopeni platelets into thrombi in vessel -> shearing of plasma protease (ADAMTS13) low neurologic symptoms, *reinstitute with relapse
c Purpura (TTP) erythrocytes in microcirculation anemia, or thrombocytopenia
Hgb: decreased if FFP not available perform
Adults Fibrinogen: high Fever 50% pts a simple plasma infusion
Brain *ultimate cause unknown LDH: 1000
Fever could have antibodies against ADAMTS13 Bilirubin: high Hemoglobinuria mortality rate >95% without
vWF plasma exchange
Direct Coombs: (-)
Smear: moderate-to-severe
schistocytosis

Hemolytic-Uremic Progressive renal failure with microangiopathic BMP: elevated BUN/CR Prodromal gastritis Typical:
Syndrome (HUS) hemolytic anemia and thrombocytopenia CBC: severe anemia, varying (Fever, blood diarrhea for 2-7d Supportive care
-> damages endothelial cells thrombocytopenia before onset of renal failure) *plasma exchange NOT
Kids beneficial
Kidney Typical: Stx*, secondary to E. coli O157:H7 Smear: schistocytes Irritability, lethargy
NO fever  diarrhea in 2-3yo Seizure Atypical:
Diarrhea  acute renal failure *obtain stool sample for E. coli and Acute renal failure Plasma exchange ASAP
Atypical: non-STx, sporadic or familial Shigella Anura
(complement abnormalities) HTN
 may not have gastric Edema
 poor outcome Pallor (due to anemia)

HEME
Factor V Leiden Factor V: activated by thrombin and helps •DVT Activated protein C Anticoagulant
convert prothrombin to thrombin •PE resistance assay
•Clotting  confirm with DNA test
MCC inherited thrombophilia

Mutation of Factor V  does not respond to

protein C  does not turn off and keeps clotting
 Protein C/S Autosomal dominant •DVT Heparin  oral
Deficiency Vitamin K dependent •PE anticoagulation

Protein C: risk warfarin induced necrosis

Anti-thrombin Autosomal dominant •Venous thrombosis, DVT, PE Asymptomatic: anticoag

III deficiency •MC in deep veins and mesenteric veins before surgery
Normal: inactivated thrombin, IX-XII
Thrombosis: high-dose IV
heparin  oral
Antiphospholipi •Acquired hypercoaguable condition •Thrombotic events Antibodies
d Syndrome •Cardiac: Libman-Sacks, endocarditis
•Autoantibody antiphospholipid antibody (aPL) •pulmonary HTN
in plasms •necrosis of hip
•Livdeo reticularis
HX: pregnancy complications •adrenal insufficiency

Pulmonology 3% *SOB: rib fracture

Obstructive: *FVC and TLC: normal, FV1 & FEV1/FVC ratio (normal >80%): decreased (because FEV1 decrease, FVC normal)

Disease About Pathophysiology History/Symptoms

Tuberculosi (Mycobacterium tuberculosis) cough >3 weeks DX: “RIPE  Rifampin (orange fluids  “ripe
s fever •sputum cultures & acid-fast stain orange”), Isoniazid (hep, neuropathy),
Transmission: person to person by night sweats •Mantoux TB skin test Pyrazinamide (hep), Ethambutol (eye)
airborne droplets weight loss • (+) 5mm+ 
hemoptysis HIV/immunosuppressed, (+) CXR, latent=Isosinizid x9mo *not contagious in
close contact latent period
 • (+) 10mm+  high risk: IVDU,
homeless, <5yo, immigrant, travel
• (+) 15mm+  no risk factors
CXR: apical cavities of upper lobes
(+) PPD & (-) CXR: Isosinizid + Rifampin
Smartypance: Enterecept can activate dormant
TB  test for TB first before prescribing

Acute MC in the winter, self-limited ~5 days- •non-productive cough CLINICAL *Reassurance and education
Bronchitis 3 weeks •Wheezing •rest and hydration, NSAIDs
MCC: Adenovirus; Others: S. pneumo, •Rhonchi (clear with cough) CXR: usually normal
M. cat, H. flu •Pharyngitis AVOID ABX unless indicated!
•Fatigue/Malaise •Procalcitonin *bacterial •Atypicals: Macrolide, FQs
Pathophys: infection  inflamed  •Fever (low-grade) >0.25 (non-ICU)
exudate  spasm - >0.5mcg (ICU)

Two phases:
1. direct inoculation of tracheobronchial
epithelium
2. Hypersensitivity of airway receptors
(persistent sx 1-3wks)  increased
sputum

Epiglottitis Inflammation of the epiglottis
•Bugs: H, influenza B (HIB)
•MC in children 3 months-6 years
•classic “tripod” position
•drooling & dysphagia
•fever
•stridor, toxic
Lateral cervical x-ray: secure airway with larygoscopy &
“thumbprint sign” intubation
DEFINITIVE: laryngoscope ABX: Rocephin, Unasyn (Vanc, Clinda if
PCN allergy), racemic EPI, steroids

FB choke, cough, insp. stridor CXR: endoscope (flexible, rigid-child)

Aspiration nml inspiratory
expiratory-hyperinflation

Rheumatoid •Chronic inflammatory disease with
Arthritis persistent symmetric polyarthritis  T-
cell mediated
•Formation of pannus  erodes
cartilage, bone, ligaments, tendons
•MC in PIP of fingers and
MCP of wrists, knees, ankles
Worse in the morning,
improves with movement
Complications: ulnar
deviation, swan neck
boutonniere deformity
•High ESR and CRP
• (+) RF *best initial test
• (+) anti-CCP *most specific
X-ray: joint space narrowing
Joint fluid: inflammatory
1. NSAIDs *symptom control
2. DMARDs (Methotrexate)
3. TNF-inhibitors
*give NSAIDs with DMARDS; NSAIDS don’t
prevent disease course

PULM
Idiopathic *MC interstitial lung disease Clinical Findings: PFT: restrictive (low TLC, RV) Early referral for lung
Pulmonary •gradual dyspnea with nonproductive cough DLco: reduced transplant
Fibrosis Pathophysiology:
diffuse epithelial cell activation and PE: HRCT: ground glass opacities,
abnormal repair  fibrosis •fine inspiratory crackles/rale traction bronchiectasis,
•maybe digital clubbing honeycomb
Black Lung Pathophysiology:
*coal workers alveolar macrophages ingest coal 
pneumoconiosis form coal macules (2-5mm) that
deposit in the lungs (MC upper)
Silicosis •Rock or coal mining, stone cutting,
*pneumoconiosi tunneling, sandblasting, pottery
s •dust containing crystalline silica
Pathophysiology:
alveolar macrophages ingest particles
 inflammation  fibrosis
Asbestosis workers exposed to asbestos fibers
pneumoconiosis over many years (old homes, ships)
Pathophys:
macrophages ingest  inflammation
 fibroblasts  fibrosis
Sarcoidosis •Inflammatory Disease, immune
•Noncaseating (non-necrotizing),
granulomas involving 2+ organs
•Organs: lungs (MC!); skin, eye
Granuloma:
mass of immune •MC in black, N. European, females
cells made by
macrophages, Pathophysiology:
epithelioid, giant T-cell response to variety of antigens
cells  immune activation and immune
depression  granuloma formation
 disrupt normal structure
PULM
Cor Pulmonale Risks: pulm disease  COPD, ILD, pulm HTN
Pulmonary Increased pulmonary vascular resistance  RHF
HTN
WHO Group1: pulmonary arterial hypertension
•muscle hypertrophy & endothelial dysfunction
WHO Group 2: *lungs  L heart disease
CXR: small upper lobe nodules Supportive
and hyperinflation
•Asymptomatic CXR Supportive
•Dyspnea on exertion •diffuse multiple small (<10mm) -bronchodilators
•Non-productive cough nodular opacities in upper lobes -oxygen
•”egg shell” calcifications of -vaccinations (flu, PNA)
PE: crackles on exam hilar and mediastinal nodes -pulmonary rehab
CT: masses of small nodules Increased risk of TB
Symptoms: CXR/HRCT: LOWER LOBES Supportive
•after a latent period of 20 years + DOE -linear (reticular) opacities
-pleural plaques INCREASED RISK OF
PE: -honeycomb bronchogenic carcinoma &
•bibasilar, fine end-inspiratory crackles malignant mesothelioma
•clubbing Lavage: asbestos bodies
Pulmonary: (MC) Labs: High Ca2+, ESR, ACE 1st line: watch and wait
•dyspnea & dry, non-productive cough x2-4wks *granulomas produce Vit D
•Fatigue, fever, night sweat, wt loss Standard: steroids
Pulmonary Function Tests: *reduce granulomas
Skin: (2nd MC organ) •DLco: <80% (most sensitive)
•erythema nodosum: bilat tender red nodules •restrictive disease (all low Second Line:
on anterior legs except ratio is normal or high) Immmunomodulators if no
•lupus pernio (pathognomonic): violaceous, improvement in 6 months
raised discoloration of nose, ear, cheek, chin CXR:
•maculopapular rash (MC chronic) •Stage I: bilat hilar adenopathy Advanced: Lung transplant
•Stage II: combo
Ocular: Anterior uveitis  blurred vision, •Stage III: infiltrates *upper Follow-Up:
discomfort, photophobia, floaters •Stage IV: fibrosis -min yearly exam
-yearly PFTs, labs, CXR, EKG
Biopsy: noncaseating granuloma
HRCT: hilar adenopathy,
nodules, ground glass, infiltrates
Lavage: high CD4/CD8
JVD, ascites, edema DX: echo, R cath •diuretics & oxygen, anticoag
Symptoms: •Echo: *begin with echo Who Group 1:
•dyspnea, chest pain •EKG: RHF, RVH, RAD 1st line  CCB: Verapamil
•cough
•fatigue, lightheadedm syncope •CXR: increased pulm arteries Other options:
•hemoptysis •PDE-5 (Sildenafil),
•R Heart Cath (Swan-Ganz) •Prostacyclins (Epoprostenol),
 -pulmonary venous hypertension (heart) Classification: NYHA 1-4
1-no limitation
WHO Group 3: secondary to lung disease 2-mild sx with normal activities
3-marked limitation
WHO Group 4: pulm HTN secondary to 4-severe sx with rest
thromboembolism  occludes pulm arteries
Signs/Physical Exam:
WHO Group 5: heme, systemic & metabolic -JVD, LE edema  RHF
(sickle cell, sarcoidosis) - S2 & P2; tricuspid regurg
*GOLD STANDARD
-MAP >25, Wedge <15
•Vasoreactivity Testing
-vasodilator and measure
hemodynamic response
-Epoprostenol, Adenosine, NO
(+) if pressure decreases <10 and
to a value <40
•Endothelin antagonists
(Bosentan)
Who Group 2: tx underlying
Who Group 3: Oxygen
Who Group 4: anticoagulant

Hypoventilation Risks: obesity, structural, fhx, alc, hypothyroid •snoring, interrupted sleep •Polysomnography (sleep study) weight loss, exercise, nonsupine,
Syndrome •daytime sleepiness, fatigue, avoid alcohol and sedatives
(sleep apnea) 1. pharyngeal wall collapse repetitively •wake up with breath holding, •Alternative: home sleep apnea
2. failure of upper airway dilator muscle gasping, choking testing (HSAT) Mild/moderate: CPAP
3. sleep-related obstruction and breath cessation •HTN, CAD, DM, mood Severe: CPAP, surgery

PULM
Solitary Nodule: <3cm; Mass: >3cm Benign: SLOW GROWTH Malignant: RAPID GROWTH Low (<5%): watch
Pulmonary -round, smooth -irregular, speculated “<50yo and no smoking”
Nodule Risks: Thymomas (MC) -calcifications “popcorn” -cavitation with thick walls Intermediate (5-60%): biopsy
-cavitation High (>60%): resect

Carcinoid Neuroendocrine tumor •Asymptomatic (25-40%) •Secrete serotonin, ACTH, ADH, Definitive: surgical excision
Tumor •Wheezing, cough, recurrent PNA, hemoptysis melanocyte stimulating hormone
MC sites: GI tract, lungs •Ocreotide may reduce SX
Carcinoid syndrome: diarrhea due to serotonin Bronchoscope: pink-purple tumor
•Increased bradykinin and histamine  flushing, *well vascularized MC complication: bleeding
tachycardia, bronchoconstriction, acidosis
Bronchogenic MCC cancer deaths SCLC: fast growing, starts in bronchi (central) CXR & CT Scan NSCLC:
Carcinoma •SVC syndrome, SIADH/hyponatremia, cushing •Surgical resection treatment of
Risks: cigarettes, asbestosis •lambert-eaton (weakness improves WITH use) Central lesions: sputum, bronchoscope choice
*squamous cell, SCLC
Adenocarcinoma (MC!!): slow, periphery SCLC:
Peripheral lesions: FNA biopsy •Chemo treatment of choice
Squamous: central (bronchial) *large NSCLC, adenocarcinoma
•CCCP: central, cavitation, hypercalcemia,
Pancoast (shoulder pain, horners, hand atrophy)

Large: rapid, periphery, AGGRESSIVE

Disease About Pathophysiology History/Symptoms Physical Exam

Pleural •Fluid in the pleural space from a
Effusion disruption in the normal pleural
homeostasis
Pleural Fluid Homeostasis achieved by:
•constant movement of fluid from
capillaries of parietal & visceral into the
Two types:
•Transudates
-fluid passes through a membrane (capillary
wall) which filters the cells and protein
yielding a watery solution
-filtrate of blood caused by imbalance in
hydrostatic & colloid osmotic pressure
CC: “I can’t breath” •diminished or absent breath sounds
•dullness to percussion
Detailed History •decreased tactile fremitus
•recent illness •diminished or delayed chest
•chronic medical conditions expansion on side of effusion
•trauma •displacement of trachea away from
•recent travel (risk for PE) effusion
 pleural space
•absorption of pleural fluidthrough parietal
pleural lymphatics
•leaves 5-15ml of fluid in normal pleura
5 pathophysiologic processes:
1. increased fluid production due to
increased hydrostatic or decreased oncotic
capillary pressures (transudates)
2. increased fluid due to abnormal
capillary permeability (exudates)
3. decreased lymphatic clearance of fluid
from pleural space (exudates)
4. infection in pleural space (empyema)
5. bleeding in pleural space (hemothorax)
•Exudates
-fluid rich in protein & cellular elements
oozes out of blood vessels due to inflame
-impermeability of vessel permits the
passage of large molecules and solid matter
•occupational history
•medication history
•TB exposure (homeless shelter,
migrant farm camp, prison or jail,
nursing home)
Symptoms:
•MC presenting symptoms
(dyspnea, cough, pleuritic CP)
•other symptoms related to
underlying cause
-large effusions due to
increased intrapleural pressure
PE findings of uderlying etiology:
•CHF: edema, neck veins, S3
•Nephortic/Pericardial: edema
•Liver: jaundice, ascites
•Maliganncy: lymphadenopathy,
palpable mass
Smaller effusions:
•less sx with normal PE
Large effusion:
•more sx with abnormal PE

Diagnostics Thoracocentesis Lights Criteria and Management

CXR
•PA
-blunting of the costophrenic angle if
>175ml of fluid
-loculation
-tracheal deviation with large effusions
•Lateral Decubitus
-better for smaller effusions
•Lateral View: fluid appears opaque
•Supine: generalized hazing of lung field
CT of Chest: *more sensitive
-helpful in determining underlying cause
Thoracocentesis
•procedure where a needle is inserted into
the pleural space between the lungs and the
chest wall to remove fluid
 ultrasound guidance
Diagnostic Indications:
•new onset effusion without a clinically
apparent cause
•atypical presentation in HF:
-unequal bilat effusions, pleurisy, fever,
•concern for CA/infection, echo
inconsistent with HR, lack of improvement
after acute tx of HF
Therapeutic Indications
•symptomatic relief
•evidence of loculation on imaging
•risk of pleural thickening/restrictive
•functional impairment
Absolute CI: uncooperative pt
Relative CI:
•small volume of fluid (<1cm
thickness of a lateral decubitus)
•bleeding diasthesis or systemic
anticoagulation
•mechanical ventilation
•cutaneous disease over proposed
puncture site
Complications:
•pain at puncture site
•cutaneous or internal bleeding
•pneumothorax (guage <20)
•empyema
•reexpansion pulm edema
•malignant seeding of tract
•adverse reactions to anesthetics
Light Criteria:
•pleural fluid to serum protein >0.5
•pleural fluid to serum LDH >0.6
•pleural fluid LDH >2/3 ULN serum
Management:
•treat underlying condition
•thoracocentesis
•tube thoracostomy: empyema,
complicated effusion, hemothorax
•repeat CXR when drainage decreased
<100ml/day
•Pleurodesis
-indication: recurrent effusions
(malignancy)
-instillation of sclerosing agent to
cause inflammatory changes
-due to limited life expectancy, the
goal of therapy is to palliate sx

PULM
Pneumonia rust: S. pneumo (MC)  RLL •productive cough CXR (PA and Lateral)  GOLD CAP Out: No comorbid/ABX:
(Bacterial) green: H, flu, pseudomonas •fever CT if unclear Azithro, Clarithro, Doxycycline;
red currant jelly: Klebsiella  upper lung •dyspnea Comborbid/ABX: Levofloxacin,
Foul smell/bad taste: anaerobic •pleuritic CP Azithro+Rocephin
•chills Labs: hospital: cx, NP, CBC, CMP;
•tachypnea HAP: new infiltrate CAP Inpatient:
Ventilator: Pseudomonas, Acinetobacter •accessory muscles Non-ICU: Levo; Moxifloxacin;
PSI: >90=hospital Rocephin+Azithro
 CAP: within 48 hours of hospital or outpatient Dullness to percussion CURB-65 (2+=hospital): ICU: Rocephin + Azithro or Levo
-S. pneumo, Mycoplasma pneumo Increased TF confusion, urea >19 (>7mmol), RR
(+) egophony 30+, BP <90/60, age >65 HAP (low risk drug-resistant):
HAP/VAP/HCAP: develops 48hours AFTER Levofloxacin, Zosyn, Cefepime
-Pseudomonas, Klebsillea, S. aureus
HAP (high): Vanc +
1. Cefepime or Ceftazadime
2. Imipenem or Carbapenem
3. Zosyn+Cipro
4. Gent or Amikacin

Pneumonia •Influenza •Fever, chills •NP swab O2, rest, fluids, antipyretics,
(Viral) •adenovirus, parainfluenza, RSV, HMNV •nonproductive cough •CXR analgesics, IVF
•rhinorrhea, myalgia
•HA, sore throat

Pneumonia •Unicellular, Fungal pneumonia •Fever Labs: Elevated LDH & B-D-glucan •ART initiated if not already
(HIV/Fungal) •Associate with immunocompromised, esp HIV •dry cough, dyspnea
P. jivoreci •Person-person through airborne spread •respiratory failure CXR: diffuse, bilateral infiltrates •BACTRIM
CT scan: ground glass opacities •Prophlylaxis: CD4 <200

Pulm
Pneumo- spontaneous:
thorax •primary: no lung disease
-rupture of subpleural apical bleb
-tall, thin males 10-40yo
•secondary: underlying lung dx
traumatic: penetrating or blunt,
iatrogranic ((+) pressure)
Sudden chest pain-pleuritic,
unilateral, non-exertional
Dyspnea
Physical Exam:
•diminished breath sounds & TF
•increased resonance to percussion
•mild tachypnea
CLINICALLY
•PA CXR with expiratory view:
diagnostic *stable pt
•Chest CT, bedside US *large
Tension Pneumothorax:
Needle decompression
•large-bore needle (14-16 guage) at 2nd ICS at
midclavicular line-leave in until thoracostomy
tube places
•Oxygen 2-4L nasal cannula
Small Primary (<15-20%): observe x6hr

tension (EMERGENT)
-air entering pleural sac
-MCC: cardiopulm, (+) pressure
Pulmonary Thrombus of the pulmonary artery
Embolism or its branches
Types: thrombus MC!
Risks (Virchows Triad):
•venous stasis
•injury (to vessel wall)
•hypercoagulability: medications
Acute MC form non-cardiogenic
Respirator pulmonary edema
y Distress
•acute hypoxemic respiratory
failure following systemic or pulm
insult WITHOUT evidence of HF
•inflammatory alveolar damage 
increased permeability of
alveolar-capillary barrier 
pulmonary edema  low O2
Causes: MCC-sepsis
-critically ill, trauma, aspiration
OBGYN 3%
Adenopathy: enlargement of lymph nodes due to gynecologic infection, malignancy or inflammation *MC is axillary
About
Abnormal Fluid expressed from ducts in:
Nipple •40% premenopausal
Discharge •55% parous women
•75% of women who have
lactated within 2 years
•pneumothorax under tension
-resp. compromise & CV collapse
-tracheal deviation, displaced PMI
Symptoms:
•Dyspnea (sudden onset)
•Pleuritic chest pain
•Hemoptysis (pulm infarction)
•Cough, wheeze
•DVT symptoms (Homans sign)
-dorsiflexion causing pain
PE:
-tachypnea, tachycardia
-hypoxemia; rales
-hypotension and syncope
-JVD & S3 and S4 sounds
(+) homans: calf pain w/ dorsiflex
•rapid onset of profound DYSPNEA
within 12-48h after event
•SOB, tachypnea, intercostal
retractions, crackles
•hypoxemia (no response to O2)
•multiple organ failure: kidney,
liver, CV, CNS
HALLMARK: diffuse alveolar
damage
•Multiduct discharge elicited ONLY
following manual pressure and NO
blood
-likely physiologic and no
further evaluation needed
EKG: sinus tachycardia, S1Q3T3
CXR: Hamptoms Hump or westmark
VQ Scan: poor perfusion, good vent
Spiral CT: BEST
Pulmonary angiography: GOLD
Wells Score >6: high, 2-6: mod
+3: DVT, alt dx not likely
+1.5: HR >100, VTE hx,
immobilization for 4 weeks
+1: malignancy, hemoptysis
•CXR: bilateral pulmonary infiltrates
-AIR BRONCHOGRAMS
-spares costophrenic angles
•ABG: PaO2/FIO2 <200 and is NOT
responsive to 100% O2 (refractory
hypoxemia)
•Swanz-Ganz cath: pressure <18
*differentiates from pulm edema
Causes
•normal lactation
•galactorrhea
•benign physiologic nipple discharge
(manual pressure, multi)
•pathologic nipple discharge
Large: chest tube (thoacostomy) & admit
1. Oxygen, IV Fluids if needed
2. Anticoagulation
•Anti-thrombin III: Heparin (renal), LMWH
•Factor Xa inhibitor: Xarelto, Eliquis
*good for outpatient, no heparin
•Direct thrombin inhibitor: Pradaxa
*requires Heparin for 5-10d
•Vitamin K inhibitor: Warfarin
TPA: *hemodynamic compromise
•begin UFH or LMWH after infusion
Thromboembolectomy:
•pts with life-threatening PE and CI to TPA
Non-invasive or mechanical ventilation
PEEP ((+) end-expiratory pressure)
-prevents alveolar collapse
-give at lowest effective levels
-does not improve mortality
-risks: barotrauma, pneumothorax, auto-peep
Treat underlying disease
Questions to Ask
Location: unilat/bilat, single or mult. ducts
Qualities
•spontaneous or manual; constant?
•pressure at single site or general pressure

•Usually multi-duct
•milky white, dark green, brown
-green: cholesterol diepoxides
*not totally infection or CA
Spontaneous or single duct
discharge  needs evaluation
MCC bloody: intraductal papilloma
-MCC: intraductal papilloma
-other: carcinoma, fibrocystic changes Menses/Hormonal
-usually unilateral and single duct •menstrual cycle, menopausal status,
hormones

Breast CA About Presentation Diagnostics Treatment

Pagets •Eczematoid eruption and •pain, itching, burning •Full-thickness biopsy of lesion •Mastectomy is traditional
Disease ulceration •erosion, ulceration •Insitu: no lymph biopsy therapy
•Arises from NIPPLE can •may see bloody nipple discharge •Invasive: biopsy lymph
spread to areola •retracted nipple •May try excision of nipple,
•1% of breast CA areola, local mass
•often mistake for dermatitis or •palpable mass: 50% (9% invasive cancer)
infection •no palpable mass: noninvasive cancer or
ductal carcinoma in situ in 7% causes

Inflamamtory •Aggressive but rare •Diffuse, brawny edema of skin with •Suspected mastitis does not rapidly •Multiple round of chemo,
Carcinoma erysipeloid border response (1-2wk to ABX  biopsy followed by surgery and
•blocked dermal lymphatics by tumor emboli radiation
• “Peau d orange” (orange peel) skin
•usually NO palpable mass

Infections About Presentation Causes Breast Abscess

Mastitis •Typically seen with lactation
and nursing
•typically primiparous (first
pregnancy) nusing patients
•rare prior to 5th day
postpartum
•MCC: S. aureus
•RARE if patient is not nursing
and no other obvious cause
(radiation)
•prompt w/u to exclude
inflammatory breast CA
Classic:
•painful erythematous lobule in
outer quadrant of breast noted
during 2nd or 3rd week of
puerperium
•Systemic signs: fever, malaise,
myalgia, leukocytosis
•Abscess: edema and fluctuation
•Antibody-coated bacteria in milk supports
diagnosis *look under microscopy
Treatment
•avoid milk stasis  continue breastfeeding or
use breast pump *wont hurt baby to feed
•local heat warm compresses
•well-fitted bra
•instruct on proper breastfeeding techniques
ABX x10-14d
-Dicloxacillin or Augment
-Cephalexin, Clinda, Erytho, Bactrim
-Severe: inpatient IV with Vanc or Clinda
•May arise from pre-existing mastitis
-redness, tender, induration
-palpable mass or fluctuance
-I&D with ABX
Non-puerperal: peripheral or subareolar;
peripheral: skin infection
 TX with I/D and ABX
Subareola: keratin-plugged milk ducts
-fistulas between multiple abscesses
-simple I & D (40% recurrence)
-requires subareolar duct excision and
complete removal of sinus tracts
-biopsy wal ot rule out breast CA

Benign Mass About Causes Questions to Ask

Fibrocystic •MCC cyclic breast pain or •Common affect >50% of •Pain or tenderness DX:
breast mastaglgia in reproductive age women of reproductive age associated with a mass •US or mammogram (not indicated <30)
Chnges women -does not necessarily present •pain 2nd degree proliferation •aspiration and/or US may be useful in determining
disease of normal glandular tissue cystic v solid mass
•MC age 30-50 years; rare after •estrogen stimulates ducts, •if dominant mass: biopsy
menopause unless pts is on HRT •Thought to be due to progesterone stimulates
 -E/P makes it develop then
undergoes apoptosis
*once cyclic change stops then you
wont see this anymore
-benign change sin breast
epithelium
hormonal imbalance that may
produce asymptomatic breast
lumps on palpation
•estrogen considered a
causative factor
•May be increased risk in
women who drink alcohol
(especially ages 18-22)
stroma
•change in pain/tenderness
over the course of menstrual
cycle
-usually present or worse
during premenstrual phase
•fluctuations in size
multiplicity of lesions
•+/- nonbloody green or
brown nipple discharge
•caffeine may worsen sx
Treatment
•reassurance of benign findings
•avoidance of trauma
•well-fitting, supportive bra
•abstaining from caffeine, coffe, chocolate
•low-fat diets may help
•CAM: evening primrose oil, vit E 400U
•OTC analgesics: Tyneol, Ibuprofen
•severe pain: Danazol, Tamoxifen
•Refractory: surgery
Prognosis: exacerbation may occur until menopause,
*SX usually resolve following menopause

Fibro- •Common, benign neoplasms
adenoma •focal abnormality of breast lobule
•Usually in young women (within
20 yrs of puberty)
•more frequent and earlier age of
onset in black women
•etiology unknown: suspected
possible hormonal link
•increased in size during pregnany
and with estrogen therapy
•decrease in size after menopause
•Round, firm, discrete,
relatively, mobile, non-tender
mass
•1-5cm in diameter
•usually discovered by accident
•often can make clinical
diagnosis
•definitive diagnosis: core
biopsy
•US: well-defined solid mass
with benign features
•Simple fibroadenoma are benign
•Do no increase risk of breast CA
•May be consumed with Phyllodes tumor: a
fibroepithelial tumor that clinically resemble
fibroadenomas and has a small chacce of becoming
malignant
Unclear diagnosis or rapid growth: surgery
•excision with margin of normal tissue
•phyllodes tumors: also treatment with excision with
wide local margins
Asymptomatic: monitor, core needle biopsy to confirm
OR repeat US and exam in 3-6 months

Skin Changes:
- Melasma (mask of pregnancy): hyperpigmentation of the face in pregnant women, can occur in non-pregnat women on OCPs
- Vascular: spiger angiomas, varicosities
- Striae Gravidarum: connective tissue stretch marks
- Pruritis: TX with Chlorpheniramine
- Hirsutism: hair growth
- Nails: nails grow faster
- Vaginal *blue due to increased blood flow
o Chadwick Sign: bluish/purplish coloration of vagina
o Goodell Sign: discoloration of cervix

Breast CA Causes Breast Abscess

•MCC of cancer in women
other than non-melanoma skin
cancers
•MCC cancer (after skin CA)
in all ethnic groups
•Chances of developing increases with age
-average age: 60-61
-main cause of death in women 40-59
-1/8 in a lifetime risk
•Over 50% of women who develop breast
CA do not have significant identificable risks
(+) fhx
-1st degree relative: 2x risk
-2nd degree relative: 3x risk
Genes: BRCA1 and BRCA 2 *dominant
-BRCA 1: higher breast and ovarian
-BRCA 2: lower breast and ovarian
•Most are diagnosed after
abnormal mammogram, instead of
discovery of a breast mass
>90% dx by mammogram
Initial evaluation:
•CBE and assessment of lesion
 •2nd MCC cancer death in •Nulliparity •bilateral mammogram (if not already
women (after lung CA) •First full-term pregnancy after age 30 done) & breast US if indicated
•Early menarche (befre age 12)
•Incidence and mortality slowly •Late natural menopause (After 50) Initial labs:
decreasing due to improved •Postmenopasual combination HRT •CBC, LFT, alkaline phosphatase
screening and treatment •Hx uterine CA
•Greatest risk factors: personal hx

History Symptoms
•Age at menarche Usual presentation: •Inspect breasts in multiple positions Usual finding on exam:
•Prengancy history and parity •painless breast mass •nontender, firm or hard lump with
•Menopause •hard, fixed, irregular margins, nonmibile •Concerning: change in breast poorly delineated margins generally
•LKMP •upper outer quadrant size/contour, nipple or skin retraction, cause by local infiltration
•Previous breast lesiosns or edema or erythema •watery, serous bloody discharge p
biopsies Less frequent:
•History of hormonal •breast pain •axillary nodes >85% of lymph drainage Suggestive of advanced cancer:
medication use •nipple discharge, erosion, retraction, •edema, redness, nodularity
•Radiation exposure enlargement, itching -firm or >5mm: highly suspicious •ulceration of skin
•Fhx breast CA •redness, generalized hardness, breast -matted or fixed axillary: locally •fixation to chest wall
enlargement/shrinking advanced disease •enlargement or shrinkage of breast
•retraction of breast
Metastatic symptoms •lymphadenopathy
•axillary mass or swelling of arm •edema of ipsilateral arm
•bone pain or back pain •large primary tumor (>5cm)
•weight loss

Diagnostics Screening SubTypes

Breast CA Mammography 1st line
•breast imaging modality of choice
•may detect CA as early as 2 years
before CA is palpable
•false +/- possible but usually right 90%
of cases
•general sensitivity 70-90% specificity
Cytology
•helpful on rare occasional for
cyst fluid or nipple discharge
Biopsy: definitive diagnosis
•FNA: simple, cant distinguish
invasive or noninsace
mammograms: one every 1-2 years
for women 50-69
•ACS: CBE q3yrs 20-39, mammo +
CBE age 40
•ACOG: CBE + mammo q1-2yr 40-
•ductal: large or intermediate sized ducts
•lobular: epithelium of terminal ducts
•most arise from intermediate ducts and are
invasive
•noninvasive cancers though to lack ability
to spread

US and MRI not recommended for
general population
*may consider adding on for patients at
very high risk
Surgery
Treatment Radical mastectomy:
•removal of breast, pectoral muscles,
axillary lymph nodes
•rarely indicated or performed currently
Modified radial mastectomy:
•removal of breast and underlying
pectoralis major fascia with eval of
selected axillary lymph nodes
•better cosmetic and functional result
•no difference in survival
Breast Conservation: excise tumor with
negative margins, axillary evaluation,
postop irradiation
•stage I & II and some III
Medication and Usage
SERM •Tamoxifen (Nolvadex)
•Raloxifene (Evista)
•Toremifene (Fareston)
•Used for treatment of breast CA and
chemoprevention of breast CA in
some high-risk women
•core needle biopsy: determine
invasive from noninvasive
•open surgical biopsies: if core
needle cannot be done
Labs: CBC, LFT, b-Hcg, ALP
or combo CT and PET
If positive for ER/PR -
•hormonal therapy indicated
•Regardless of age, menopausal
status, lymph node involvement
or tumor size
Systemic chemotherapy: reduce
occult metastases
Polychemotherapy for 3-6 months
or 4-6 cycles
MOA
•binds to estrogen receptors and
blockes estrogen activity
•Tamoxifen & Toremifene -
blocks in breasts; mimics in
uterus, bone
50, annually 50+
•USPSTF: mammo +/I CBE q1-2
yrs, age 50-69
CBE+mammo annually age 40-50
Follow-Up
Follow-Up:
•Close follow-up needed due to high
risk of recurrences
•Exam: Q 4 mo x 2 yrs, then Q 6
mo x 3 yrs, then yearly
-Mammogram 6 months after
radiation, then yearly
-Routine laboratory tests
-Median time to recurrence: 4yrs
-Varies with stage of cancer
Side Effects
•Common
hot flashes, nausea, muscle aches and
cramps, hair thinning, headache,
paresthesias
•Increased risk of thrombosis, fatty
liver, endometrial cancer
Hormone Receptor Sites
•presence of absence of E/P sites is
critically important for management
•ER (+) tumor: slightly lower liklihood of
early recurrence
•ER (+): bone, soft tissue, genital organs
•Er (-): mets to liver, lung, brain
Prognosis
Prognosis:
•Largely dependent on stage
•ER/PR negative cancers: higher chance
of recurrence
•If cancer is localized to breast with no
regional spread: cure rate is 75-80%
•If axillary lymphadenopathy present:
-Survival rate drops to 50-60% at 5 year
-Survival rate is < 25% at 10 years
DDI
•Not for use with other hormone-
modulating anti-CA therapy
•SSRIs, cimetidine can reduce efficacy
•Avoid with QT-prolonging agents

•May be used off-label to treat other
estrogen-sensitive neoplasms
Aromatase •anastrazole (Arimidex)
Inhibitors •exemestane (Aromasin)
•letrozole (Femara)
Fulvestrant •used for metastatic breast cancer
(Faslodex) •attaches to and causes destruction of
estrogen receptors
•does not mimic effects of estrogen
•raloxifene - blocks in breasts,
uterus; mimics in bone
•inhibit aromatase (enzyme that
produces estrogen)
•GnRH agonists/antagonists
•Impaired cognition
•False thyroid function studies
•Common: •Caution when using with, or do not use
hot flashes, GI upset, muscle with, other hormone-modulating anti-CA
weakness, joint pain, headache, therapy
worsened ischemic heart disease
•May increase serum concentration of
•Hypercholesterolemia methadone or L-methadone
•Insomnia, impaired cognition,
fatigue, mood changes •Do not use with estrogen or
•Thinning hair immunomodulating drugs
•CI: pregnancy
•Used to reduce release of GnRH and
FSH/LH