Surgery EOR

GI/Nutritional 50%
Abdominal RUQ LUQ Epigastric Lower Abdominal Pain
Pain Biliary Colic Splenomegaly Acute Myocardial Infarction Appendicitis
•intense, dull discomfort located in the RUQ or •pain or discomfort in LUQ, left shoulder pain, &/or •may be associated w/ SOB & exertional sxs •periumbilical pain initially that radiates to the
epigastrium early satiety RLQ
•associated w/ N/V, & diaphoresis Acute Pancreatitis •associated w/ anorexia, N/V
•generally lasts at least 30min, plateauing within 1hr Splenic Infarct •acute onset, persistent upper abdominal pain Diverticulitis
Acute Cholecystitis •severe LUQ pain radiating to the back •generally LLQ pain, usually constant & present
•prolonged (>4-6hrs) RUQ or epigastric pain, fever for several days prior to presentation
•pts will have abdominal guarding & Murphy’s sign Splenic Abscess Chronic Pancreatitis •may have associated N/V
Acute Cholangitis •associated w/ fever & LUQ tenderness •epigastric pain radiating to the back Nephrolithiasis
•fever, jaundice, RUQ pain •pain MC symptom varies from mild to severe
Sphincter of Oddi Dysfunction Splenic Rupture Peptic Ulcer Disease •generally, flank pain, but may have abdominal
•RUQ pain is similar to other biliary pain •may complain of LUQ, left chest wall, or left •epigastric pain or discomfort is the most prominent or back pain
Acute Hepatitis shoulder pain that is worse w/ inspiration symptom Pyelonephritis
•RUQ pain w/ fatigue, malaise, N/V, anorexia •associated w/ dysuria, frequency, urgency,
•pts may also have jaundice, dark urine, & light- GERD hematuria, fever, chills, flank pain, & CVA
colored stools •associated w/ heartburn, regurgitation, & dysphagia tenderness
Perihepatitis (Fitz-Hugh-Curtis Syndrome) Acute Urinary Retention
•RUQ pain w/ a pleuritis component, pain is Gastritis/Gastropathy •present w/ lower abdominal pain & discomfort;
sometimes referred to the right shoulder •abdominal discomfort/pain, heartburn, N/V, inability to urinate
Liver Abscess hematemesis Cystitis
•fever & abdominal pain are MC sxs •associated w/ dysuria, frequency, urgency, &
Budd-Chiari Syndrome Functional Dyspepsia hematuria
•sxs include fever, abdominal pain, abdominal •the presence of one or more of the following: Infectious Colitis
distention (from ascites), lower extremity edema, postprandial fullness, early satiety, epigastric pain, or •diarrhea is the predominant symptom, may
jaundice, GI bleeding, &/or hepatic encephalopathy burning also have associated abdominal pain, which may
Portal Vein Thrombosis be severe
•sxs include abdominal pain, dyspepsia, or GI Gastroparesis
bleeding •N/V, abdominal pain, early satiety postprandial
fullness, & bloating

GI About Diagnostics Management

Anorexia Appendicitis Lower GI Bleed Appendicitis: spiral CT, U/S (may see a large, noncompressible appendix or Depends on the cause
•periumbilical pain (intermittent & crampy) •hematochezia (bright red blood per rectum), w/ fecalith), abdominal x-ray
•N/V or w/o abdominal pain, melena, anorexia, fatigue,
•anorexia syncope, SOB, shock Gastric Ulcer: HX/PE, EGD w/ multiple bx (looking for gastric cancer)
•pain migrates to RLQ (constant & intense
pain), usually in 24hrs Carcinoma of the Gallbladder Duodenal Ulcer: HX/PE, EGD, UGI series (if the pt is not actively bleeding)
•biliary colic, weight loss, anorexia
Gastric Ulcers •many pts are symptomatic until late; may present Gastric Cancer: EGD w/ bx, endoscopic U/S to evaluate the level of invasion, CT of
•epigastric pain & vomiting, anorexia, & nausea as acute cholecystitis abdomen/pelvis for metastasis, CXR, labs

Duodenal Ulcers
•epigastric pain – burning or aching, usually
several hours after a meal (food, milk, or
antacids initially relieve pain)
•bleeding, back pain N/V, anorexia, ↓ appetite
Gastric Cancer
•weight loss, emesis, anorexia, pain/epigastric
discomfort, obstruction, nausea
Pancreatic Carcinoma Lower GI Bleed: HX/PE, NGT aspiration (to r/o UGI bleeding; bile or blood must be
•painless jaundice from obstruction of the seen; otherwise, performed EGD), anoscopy/proctoscopic exam
common biliary duct
•weight loss, abdominal pain, back pain, weakness Carcinoma of the Gallbladder: U/S, abdominal CT, ERCP
•pruritis from bile salts in the skin; anorexia
•Courvoisier’s sign Pancreatic Cancer: abdominal CT, U/S, cholangiography (ERCP to r/o
•acholic stools choledocholithiasis & cell brushings), endoscopic U/S w/ bx
•dark urine, diabetes
 Gallbladder About
Cholelithiasis Gallstones in the biliary tract (usually in the
gallbladder) w/o inflammation
Types of Gallstones:
•cholesterol (MC)
•black stones: hemolysis or ETOH-related cirrhosis
•brown stones: ↑ in Asian population, parasitic,
bacterial infections
Risk Factors: 5Fs (fat, fair, female, forty, fertile)
•OCPs (increased estrogen), Native Americans, bile
stasis, chronic hemolysis, cirrhosis, infection, rapid
weight loss, IBD, TPN, fibrates, increased triglycerides
Acute Cholecystitis Inflammation & infection of the gallbladder due to
obstruction of the cystic duct by gallstones
Etiologies: E. coli MC, klebsiella, other gram-neg
enteric organisms
Chronic Cholecystitis:
•fibrosis & thickening of the gallbladder due to
chronic inflammatory cell infiltration of the
gallbladder evident on histopathology – almost
always associated w/ gallstones
Choledocholithiasis Gallstones in the common bile duct (can lead to
cholestasis due to blockage)
Acute Ascending •biliary tract infection secondary to obstruction of
Cholangitis the common bile duct – e.g., gallstones, malignancy
Etiologies: E. coli MC
Primary Sclerosing Autoimmune, progressive cholestasis leading to
Cholangitis diffuse fibrosis of intra/extrahepatic biliary ducts
Risk Factors:
•MC associated w/ IBD – UC (90%)
•men 20-40yrs
Complications: cirrhosis, liver failure,
cholangiocarcinoma
Clinical Manifestations
Most are asymptomatic – may be an incidental
finding
Biliary colic: episodic, abrupt RUQ or epigastric
pain, resolves slowly, lasting 30min-hrs; may be
associated w/ nausea & precipitated by fatty
foods or large meals
Continuous RUQ or epigastric pain – may be
precipitated by fatty foods or large meals
•may be associated w/ nausea, guarding, anorexia
PE:
•fever (often low-grade); enlarged, palpable
gallbladder
•MURPHY’S SIGN: RUQ pain or inspiratory arrest
w/ palpation of the gallbladder
•Boas sign: referred pain to the right shoulder or
subscapular area (phrenic nerve irritation)
Prolonged biliary colic: RUQ or epigastric pain,
N/V – pain usually more prolonged due to the
presence of the stone blocking the bile duct
PE: RUQ or epigastric tenderness, jaundice
Charcot’s Triad: fever + RUQ pain + jaundice
Reynold’s Pentad: + shock or AMS
Jaundice, pruritis, fatigue, RUQ pain,
hepatomegaly, splenomegaly
Diagnostics
U/S – initial TOC: stone in GB or cystic duct
U/S – initial TOC: thickened or distended gallbladder,
pericholecystic fluid, sonographic Murphy’s sign
CT scan: alternative to U/S; can detect complications
Labs: ↑ WBCs (leukocytosis w/ left shift), ↑
bilirubin, alk phos, & LFTs
HIDA scan: most accurate test – cholecystitis present
if there is no visualization of the gallbladder
Labs: ↑ AST/ALT, alk phos, & GGT (cholestasis)
U/S – initial
ERCP: dx TOC – diagnostic + therapeutic
Labs:
•leukocytosis
•cholestasis: ↑ alk phos & GGT
•↑ bilirubin > increased ALT/AST
U/S – initial
MRCP
Cholangiography via ERCP: gold standard
Cholestatic pattern: ↑ alk phos & GGT, ↑ AST/ALT,
bilirubin, IgM
+ P-ANCA hallmark
MRCP, ERCP – most accurate test: beaded
appearance of biliary ducts (narrowing, strictures)
Liver bx – rarely used
Management
Observation if asymptomatic
Symptomatic: ursodeoxycholic acid may be
used to dissolve the gallstones (takes 6-
9mo); elective cholecystectomy
Complications: choledocholithiasis, acute
cholangitis, acute cholecystitis
NPO, IV fluids, abx (ceftriaxone +
metronidazole) followed by
cholecystectomy (usually within 72hrs;
laparoscopic preferred)
Cholecystostomy (percutaneous drainage)
if nonoperative
Cholesterolosis: fat deposits on GB à
“strawberry GB”; tx is cholecystectomy
ERCP stone extraction preferred over
laparoscopic choledocholithotomy
•IV abx
•piperacillin/tazobactam
•metronidazole + cephalosporin
•metronidazole + cipro/levofloxacin
•CBD decompression & stone extraction
(ERCP)
Eventually à elective cholecystectomy
Stricture dilation for symptomatic relief
Cholestyramine for pruritis
Liver transplant definitive
GI About Clinical Manifestations Diagnostics Management
Acute Pancreatitis •acinar cell injury à intracellular activation Epigastric pain Criteria: 2/3 “rest the pancreas”
of pancreatic enzymes à autodigestion of •radiates to back (1) acute onset epigastric pain radiating to back
pancreas •exacerbated if supine, relieved leaning forward (2) ↑ lipase/amylase ≥3xULN Supportive:
(3) CT, MRI, or U/S findings of acute pancreatitis •NPO
Etiologies: •N/V, fever *no imaging required if pt meets first 2 criteria •high-volume IVF (LR preferred)
•gallstones (MC), ETOH abuse (2nd MC) •analgesia (Meperidine)
•meds: thiazides, protease inhibitors, PE: Labs:
exenatide, valproic acid •epigastric tenderness •↑ lipase/amylase (lipase more specific) Antibiotics:
•others: iatrogenic (ERCP), malignancy, •tachycardia •ALT 3-fold ↑ à gallstone pancreatitis •indicated only if >30% necrosis seen
scorpion sting, trauma, CF, •adynamic ileus à decreased bowel sounds •hypocalcemia: necrotic fat binds calcium
hypertriglyceridemia, hypercalcemia, •severe à dehydration, shock •leukocytosis Ranson’s Criteria:
infection, mumps (children) •↑ glucose, bilirubin, triglycerides Admission:
Necrotizing, hemorrhagic: (1) glucose >200mg/dL
•Cullen’s sign (periumbilical) Abdominal CT: dx imaging of choice (2) age >55yrs
•Grey Turner sign (flank) •also perform in pts who fail to improve/worsen (3) LDH >350IU/L
after 48hrs (4) AST >250IU/dL
(5) WBC >16,000/µL
Transabdominal U/S: Within 48hrs:
•assess for gallstones & bile duct dilation (6) calcium <8mg/dL
(7) hematocrit fall >10%
Abdominal x-ray: (8) PO2 <60mmHg
•“sentinel loop” = localized ileus of small bowel (9) BUN >5mg/dL
segment in LUQ (10) base deficit >4mEq/L
•colon cutoff sign: abrupt collapse of colon near (11) sequestration of fluid >6L
pancreas Interpretation:
•calcification à chronic pancreatitis ≥3 à severe pancreatitis likely
<3 à severe pancreatitis unlikely
MRCP: stones, stricture, tumor
0-2: 2% mortality
CXR: 3-4: 15% mortality
•mod-severe à L-sided, exudative pleural effusion 5-6: 40% mortality
7-8: 100% mortality
Chronic Progressive inflammatory changes to the Triad: calcification + steatorrhea + DM (seen only Amylase & lipase usually normal ETOH abstinence, pain control, low fat diet, vitamin
Pancreatitis pancreas that lead to loss of pancreatic in 1/3 of pts) supplementation
endocrine & exocrine function •weight loss; epigastric &/or back pain may be CT scan: calcification of the pancreas – often done
atypical or completely absent in pts w/ acute pain to r/o other causes of Oral pancreatic enzyme replacement
Etiologies: ETOH abuse MC, idiopathic abdominal pain
•hypocalcemia, hyperlipidemia, islet cell Pancreatectomy only if retractable pain despite
tumors, familial, trauma, iatrogenic; Abdominal x-ray: calcified pancreas medical therapy
gallstones not significant as in acute
Pancreatic function testing: fecal elastase most
sensitive & specific; pancreatic stimulation w/
secretin & CCK (not usually done)

GI About Clinical Manifestations Disagnostics Management

Achalasia Loss of peristalsis & failure of relaxation of the LES •dysphagia to both solids & liquids at the same time Barium esophagram: Decreased LES pressure:
•regurgitation of undigested food •”bird’s beak” appearance of the LES •botulinum toxin injection (requires re-
PATHO: idiopathic proximal degeneration of Auerbach’s •chest pain, cough treatment in 6-12mo)
plexus leads to increased LES pressure & impaired LES Manometry: increased LES pressure, lack of •nitrates
relaxation May develop à malnutrition, weight loss, peristalsis
dehydration Pneumatic dilation of LES
MC presents <50yrs of age Endoscopy: usually performed prior to tx to
r/o esophageal SCC Esophagomyomectomy (definitive)
GI About Clinical Manifestations Diagnostics Management
Anal Fissure Painful linear tear/crack in the distal anal canal Severe painful rectal pain & bowel movements causing the pt to Clinical >80% resolve spontaneously
refrain from defecating, bright red blood per rectum Supportive measures: first line
Etiologies: low fiber diets, passage of large, hard management – warm sitz baths, analgesics,
stools, constipation, or other anal trauma PE: high fiber diet, increased water intake,
•longitudinal tear in the anoderm that usually extends no more stool softeners, laxatives, mineral oil
proximally than the dentate line – MC at the posterior midline Second line tx: topical vasodilators: NTG
(99% M, 90% W) (ADRs: HA, dizziness) nifedipine ointment
•skin tags seen in chronic
Botox injections: to reduce spasm of the
internal sphincter (may be more effective
that topical dilators)

Surgery: lateral internal sphincterotomy

Perianal Abscess ½ perianal abscesses are caused by fistulas
and Fistula MC in posterior rectal wall
Abscess: infection MC from an obstructed anal crypt
gland, w/ resultant pus collecting in the
subcutaneous tissue, intersphincteric plane, or
beyond
Fistula: epithelialized tract that connects an abscess
w/ skin or adjacent organs
reserved for refractory cases
Complications: fecal incontinence
Abscess: severe pain in anal or rectal area Clinical rectal exam, DRE Perianal Abscess: I&D, Antibiotics; sitz
•fever, malaise baths, high fiber
Fistula DX: MRI & endosonography •Augmentin, cipro + metronidazole
Fistula:
•“non-healing” anorectal abscess Fistula: surgical
•chronic purulent drainage
•pain w/ defecation, sitting, & activity
•malodorous perianal drainage & pruritis

GI About Clinical Manifestations Diagnostics Management

Hemorrhoids Internal Hemorrhoids: Internal Hemorrhoids: Visual inspection, DRE, fecal Conservative tx: high fiber diet, increased
•originate from superior hemorrhoid vein; above dentate line •intermittent rectal bleeding MC – painless occult blood testing fluids; warm sitz baths; topical rectal
•tend to bleed, usually painless bright red blood (hematochezia) – seen on corticosteroids (analgesics like lidocaine) may
I Does not prolapse (confined to anal canal); may bleed w/ toilet paper, coating the stool, or dispersed in Anoscopy for internal allows for be used for pruritis & discomfort or thrombosis
defecation toilet water direct visualization & diagnosis
II Prolapses w/ defecation or straining but spontaneously reduce •may have rectal itching & fullness or mucus Procedures: if failed conservative, debilitating
III Prolapses w/ defecation or straining, requires manual reduction discharge Proctosigmoidoscopy or pain, strangulation
IV Irreducible & may strangulate •uncomplicated internal are usually not tender colonoscopy may be indicated in •rubber band ligation (MC), sclerotherapy,
External Hemorrhoids: & not palpable (unless they are thrombosed) – pts w/ hematochezia to r/o infrared coagulation; excision of thrombosed
•originate from inferior hemorrhoid vein; below dentate line rectal pain w/ internal suggests a complication proximal sigmoid disease external hemorrhoids may be performed
•do not tend to bleed, usually painful
External Hemorrhoids: Hemorrhoidectomy: for stage IV or those not
Risk Factors: increased venous pressure: straining during defecation •perianal pain aggravated w/ defecation responsive to other therapies; surgical
(constipation), pregnancy, obesity, prolonged sitting, cirrhosis w/ portal HTN •may have tender palpable mass; +/- skin tags management used for external hemorrhoids

GI About Clinical Manifestations Diagnostics Management

Zollinger-Ellison •gastric-secreting neuroendocrine tumor leading to •severe, recurrent, multiple, or refractory ulcers + •endoscopy – confirm presence of ulcer Local: tumor resection
Syndrome severe PUD & diarrhea diarrhea •elevated basal or stimulated gastrin levels
(Gastrinoma) Metastatic, unresectable:
MC seen in duodenal wall, pancreas, lymph nodes, Severe PUD: Screening: elevated fasting gastrin levels •lifelong high dose PPIs
other sites •multiple peptic ulcers •>1000pg/mL + gastric pH <2
•refractory ulcers *liver & abdominal LN MC sites for METS
•abdominal pain Confirmatory: secretin test
•persistent gastrin elevations
Diarrhea
•increased acidity inactivated the pancreatic
enzymes, leading to malabsorption
 GI About
Appendicitis •obstruction of the lumen of the appendix, resulting in
inflammation & bacterial overgrowth
•MC 10-30yrs
•MC cause of acute abdomen in children 12-18yrs
Etiologies: fecalith & lymphoid hyperplasia MC,
inflammation, malignancy or foreign body, lymphoid
hyperplasia due to infection MC cause in children
Clinical Manifestations Diagnostics Management
Classic presentation: anorexia & periumbilical or epigastric pain Adults – CT scan preferred Refer to GI surgery STAT
followed by RLQ pain (12-18hrs), N/V (vomiting usually occurs
after the pain) U/S, MRI – reserved for radiosensitive Nonsurgical: may be treated w/ abx but
populations (pregnant, children) high likelihood of recurrence
Retrocecal appendix à atypical pattern (diarrhea), + rectal or
gynecologic examination; appendix may also be pelvic In children à surgical consult often Surgical: appendectomy (laparoscopic
obtained prior to imaging to preferred)
Appendiceal inflammation stimulates nerve fibers around T8- determine if imaging is needed, •board spectrum abx prior to surgery w/
T10, causing vague periumbilical pain – once the peritoneum depending on the risk gram neg & anerobic coverage
becomes irritated, it radiates to the RLQ -cephalosporins + metronidazole
-piperacillin-tazobactam
PE: rebound tenderness, rigidity, guarding; retrocecal appendix
may have atypical findings
•Rovsing: RLQ pain w/ LLQ palpation
•Obturator: RLQ pain w/ internal & external hip rotation w/
flexed knee
•Psoas: RLQ pain w/ right hip flexion/extension (raise leg against
resistance)
•McBurney’s point tenderness: point 1/3 the distance from the
ASIS & navel

GI About Clinical Manifestations/Diagnostics Management

Bowel Mechanical: ⊕physical barrier preventing passage ⇢ Simple or Complicated: •N/V, colicky abdominal pain, obstipation SMALL BOWEL:
Obstruction •extrinsic (adhesion, hernia, cancer, abscess) •Simple: ⊘evidence of complications •peristalsis (bowel sounds) ⇡⇡ in early phases of mechanical obstruction •NPO, IV fluids, foley to monitor urine output
•intraluminal (gallstone ileus, FB, intussusception) ▪i.e., bowel ischemia, perforation, red flags d/t intense intestinal muscular contraction (“peristaltic rush”) •NGT for gastric decompression (⇣ N/V,
SBO •intramural (Crohn’s, lymphoma, radiation enteritis) •Complicated: strangulation, ischemic ▪progressively ⇣ & eventually disappears in late obstruction distention)
necrosis, or perforation •strangulation: fever, crampy abdominal pain ⇢ peritonitis •monitor electrolytes for hypokalemia,
LBO •vitals: initially normal ⇢ tachycardia & hypotension d/t dehydration metabolic acidosis (signs of ischemia)
•pts w/ suspected strangulation need fluid
Volvulus Proximal SBO: profuse emesis containing undigested food, upper resuscitation prior to surgery
abdominal discomfort, epigastric distention
Paralytic Ileus: temporary functional impairment of peristalsis, ⊘physical barrier Distal SBO: diffuse, poorly localized crampy abdominal pain 24h w/o improvement, deterioration:
•postoperative, peritonitis, meds (e.g., opioids, anticholinergics) •laparotomy, procedure depends on cause
•electrolyte abnormalities (e.g., hypokalemia) LBO: ▪adhesions: lysis of adhesions (LOA)
•hemoperitoneum/retroperitoneal hematoma •emesis is late finding, may be absent if ileocecal valve prevents reflux ▪hernias: reduced/repaired
•deep, visceral, cramping pain from colonic obstruction usually referred ▪Crohn’s: resection or stricturoplasty
Partial: only part of lumen is occluded, allowing some passage of intraluminal contents to hypogastrium •entire small bowel should be examined
Complete: no passage of intraluminal content distal to obstruction •cancer ⇢ gradually progressive pain/symptoms, volvulus ⇢ acute •resect nonviable intestine
•primary anastomosis of resected segments
Closed Loop Obstruction: both proximal & distal ends of obstructed loop closed (e.g., volvulus, LABS: ⇡ Hct (hemoconcentration), leukocytosis (d/t dehydration/acute
obstructed inguinal hernia); can rapidly lead to ischemia & perforation ⇢ surgery necessary stress response), ⇡ SCr indicative of hypovolemia w/ prerenal failure LARGE BOWEL:
•surgery almost always required
SBO MCC: adhesions from prior abdominal surgery (75%) > hernia > neoplasms DX: plain abdominal x-rays (supine/standing), CT w/w/o contrast •goals ⇢ resection of necrotic bowel &
LBO MCC: adenocarcinoma > scarring secondary to diverticulitis > volvulus •dilated bowel loops w/ air-fluid levels in ladder-like appearance decompression of obstructed segment
•major factor in clinical course of LBO is competence of ileocecal valve ▪3-6-9 rule: small bowel >3cm, large bowel >6cm, cecum >9cm Options:
▪30% ⇢ incompetent ileocecal valve: allows decompression of large bowel into ileum ▪SBO dilated loops ⇢ central, LBO dilated loops ⇢ peripheral •resection + primary anastomosis
▪MC ⇢ ileocecal valve does NOT allow reflux to occur: closed loop obstruction w/ rapidly ⇡ •little/no air distal to obstruction •resection + diversion, diversion alone
intraluminal pressure ⇢ impaired capillary circulation, mucosal ischemia, bacterial translocation •pneumoperitoneum ⇢ perforation •endoscopic stent placement
w/ systemic toxicity ⇢ gangrene, perforation SIGMOID Volvulus: coffee bean sign (bent inner tube, kidney bean)
•dilated loop w/ absent haustrae, arises in LLQ & extends ⇢ RUQ Cecal: ileocecal resection or R colectomy w/
VOLVULUS: torsion of bowel on its axis ⇢ closed loop obstruction; sigmoid MC (75%), cecal (25%) •proximal colonic/small bowel dilation w/ air-fluid levels, ⊘distally ileocolic anastomosis
•torsion of mesenteric vascular pedicle ⇢ occlusion/thrombosis of mesenteric vessels ⇢ bowel CECAL Volvulus: Sigmoid:
strangulation, ischemia, & gangrene •dilated loop w/ maintained haustrae, arises in RLQ & extends ⇢ LUQ ⊘signs of peritonitis:
•upward displacement of appendix, ⊘colonic dilation distally •sigmoidoscopy w/ rectal tube insertion for
•dilated small bowel loops w/ multiple air-fluid levels decompression, detorsion, & reduction
CT (volvulus): whirl sign pathognomonic •surgery if fails
⊕signs of peritonitis/ischemia:
•sigmoid colectomy & primary anastomosis
GI
Bariatric Indications: Prerequisite: participation in supervised Common Postoperative Concern ⇢ nutrient deficiencies ▪micronutrient supplementation recommended for all patients
Surgery •BMI >35 + comorbidity (e.g., HTN, diabetes) dietary program without success ▪postop screening: q3-6mo x1y, then annually following bariatric surgery
•BMI ≥40 +/- comorbidity
Fat-Soluble Vitamins: Absorption: Highest Risk: S/SXS of Deficiency:
Restrictive: limit caloric intake by ⇣ stomach’s reservoir capacity A, D, E, K ▪jejunum & ileum ▪BPD-DS > RYGB A ⇢ night blindness, xerophthalmia, keratomalacia,
Sleeve Gastrectomy (SG): resection of greater curvature Bitot spot, follicular hyperkeratosis
•restrictive + hormonal changes •60% weight loss @2y D ⇢ Rickets, osteomalacia, craniotabes, rachitic rosary
▪less hunger, improved insulin resistance & glycemic control E ⇢ sensory/motor neuropathy, ataxia, retinal
Laparoscopic Adjustable Gastric Banding (LABG): *RARELY PERFORMED degeneration, hemolytic anemia
•tight, adjustable prosthetic band around stomach entrance ⇢ purely restrictive K ⇢ hemorrhagic disease
•replaced by other procedures that offer better results for weight loss/comorbidity resolution
Water-Soluble Vitamins: Absorption: Highest Risk: S/SXS of Deficiency:
Malabsorptive: bypass duodenum & small intestine to limit nutrient absorption Vitamin B1 (thiamine) ▪duodenum & ▪RYGB & BPD-DS ▪Beriberi – CHF (wet beriberi), aphonia, peripheral
Restrictive + Malabsorptive: combination of both mechanisms proximal jejunum neuropathy, confusion, coma
Biliopancreatic Diversion w/ Duodenal Switch (BPD-DS): ▪Wernicke encephalopathy (nystagmus, ataxia,
•use limited by high rates of malnutrition, anemia, diarrhea, & stomal ulceration ophthalmoplegia)

Single-Anastomosis Duodenoileal Bypass w/ Sleeve Gastrectomy (SADI-S): Vitamin B12 ▪gastric acid cleaves ▪RYGB ▪megaloblastic anemia (pernicious anemia)
▪restrictive + malabsorptive + hormonal mechanisms ▪85% weight loss @2y B12 into its free form for absorption ▪peripheral neuropathy w/ impaired proprioception
▪primary bariatric procedure; also used as conversional procedure for inadequate weight loss ▪may include axonal or optic neuropathy & slowed
after RYGB or SG mentation

Roux-en-Y Gastric Bypass (RYGB): Folate ▪small intestine ▪BPD ▪megaloblastic anemia, may include sensory
▪small stomach pouch created & connected directly to small intestine ▪70% weight loss @2y *less common w/ RYGB/SG predominant neuropathy
▪restrictive + malabsorptive + hormonal mechanisms
▪Dumping Syndrome: nausea, weakness, sweating, faintness, & possibly diarrhea soon after Vitamin C (ascorbic acid) ▪scurvy ⇢ fatigue, petechiae, ecchymosis, bleeding
eating within first few years after surgery ⇢ symptoms intensify w/ high-sugar foods *uncommon as long as patient consumes fruits & vegetables gums, depression, dry skin, impaired wound healing

One-Anastomosis Gastric Bypass (OAGB): “mini-gastric bypass” Trace Minerals: Absorption: Highest Risk: S/SXS of Deficiency:
▪narrow stomach pouch made from lesser curvature & connected to small intestine Iron *one of the ▪duodenum & ▪RYGB, BPD-DS, SG* ▪anemia, pica, impaired learning
▪weight loss outcomes comparable to RYGB MC deficiencies proximal jejunum *requires cleavage by gastric acid in stomach, SG ⇣ stomach size
•restrictive + malabsorptive, probably hormonal after bariatric surgery

Zinc ▪duodenum & ▪BPD-DS > RYGB > LAGB ▪growth retardation, delayed sexual maturity, impaired
proximal jejunum immune function, impotence

Other:
Calcium ▪duodenum & ▪BPD-DS, RYGB, SG ▪metabolic bone disease, 2° hyperparathyroidism
proximal jejunum *best absorbed in acidic environment
Constipation About Management
Etiologies: Fiber, laxatives
•disordered movement of stool through colon/anus/rectum (usually proximal GI tract intact)
•slow colonic transport: idiopathic, motor disorders (CRC, DM, hypothyroid), adverse effects of drugs (verapamil, opioids); outlet delay: Hirschsprung’s disease

Gastroparesis: condition that affects the stomach muscles & prevents proper stomach emptying
•MCC: diabetes; others: anorexia, bulimia, scleroderma, Ehlers-Danlos, adnominal surgery
•S/SX: nausea, full feeling after little food is eaten; palpitations, heartburn, bloating, decreased appetite, GERD
•DX: KUB, manometry, gastric emptying scan
•TX: low fiber & low residue diets, restrict fat intake, smaller meals spaced 2-3hrs apart; metoclopramide

Ileus: ileus that persists >3d following surgery is termed postoperative adynamic ileus or paralytic ileus
•PATHO: hypomobility of the GI tract in the absence of mechanical bowel obstruction
•S/SX: absent bowel sounds
•DX: CT scan w/ gastrografin – must exclude mechanical obstruction
•TX: spontaneously resolves after 2-3d; D/C opiates

PHARM About
Fiber MOA: retains water & improves GI transit
Bulk Forming Laxatives MOA: absorbs water & increases fecal mass; increases the frequency & softens the consistency of stool w/ minimal effects
Psyllium Methylcellulose •dietary fiber + bulk forming laxatives most physiologic & effective approach
Polycarbophil Wheat dextran ADRs: flatulence, bloating
Osmotic Laxatives Sorbitol MOA: causes water retention in stool (osmotic effect pulls water into gut)
Polyethylene glycol (PEG) Lactulose ADRs: flatulence, bloating
Saline Laxatives: milk of magnesia, mag citrate •saline laxatives à hypomagnesemia (esp. w/ chronic renal disease)
Stimulant Laxatives MOA: increases acetylcholine-regulated GI motility (peristalsis) & alters electrolyte transport in the mucosa
Bisacodyl Senna ADRs: diarrhea, abdominal pain

GI About Clinical Manifestations Diagnostics Management

Colorectal Most arise from adenomatous polyps Iron deficiency anemia (fatigue, weakness), Colonoscopy w/ bx: diagnostic TOC Localized: surgical resection (radical vs.
Cancer (CRC) MC cause of large bowel obstruction in adults rectal bleeding, abdominal pain, change in endoscopic) + post-op chemo to destroy
bowel habits Barium enema: apple core lesion residual cells & micrometastases
Risk Factors:
•age >50yrs (peak 65yrs), AA, family hx of CRC Advanced disease: ascites, abdominal masses, Labs: iron deficiency anemia, (CRC is MC cause of occult Metastatic: palliative chemo
•IBD: UC > Crohn hepatomegaly GI bleeding in adults)
•diet (low fiber, high in red or processed meat, animal fat) Chemotherapy:
•obesity, smoking, ETOH Right-Sided (Proximal): chronic occult Tumor markers: CEA is MC monitored •FOLFOX
bleeding (iron deficiency anemia, + guaiac), -folinic acid (leucovorin calcium)
Protective Factors: physical activity, regular use of ASA, NSAIDs diarrhea Screening: any of the 3 approaches -fluorouracil
•fecal occult blood test annually starting at 50yrs -oxaliplatin
Genetics: Left-Sided (Distal): bowel obstruction; •colonoscopy q10yrs for ages 50-75 •FOLFIRI
Familial Adenomatous Polyposis: genetic mutation of APC present later & cause changes in stool •flexible sigmoidoscopy q5yrs + fecal occult blood testing -folinic acid (leucovorin calcium)
gene; adenomas begin in childhood – almost all will develop diameter – may develop Streptococcus bovis q3yrs -fluorouracil
colon cancer by age 45yrs; prophylactic colectomy best for endocarditis -irinotecan
survival Lynch Syndrome: colonoscopy q1-2yrs beginning at 20- •VGEF inhibitor: bevacizumab
↓ risk: 25yrs
Turcot Syndrome: FAP-like syndrome + CNS tumors •pedunculated
(medulloblastoma, glial tumors) •tubular FAP: flexible sigmoidoscopy annually beginning 10-12yrs
•<1cm
Lynch Syndrome (Hereditary Nonpolyposis CRC): autosomal Colonoscopy Screening:
dominant; d/t loss of function in DNA mismatch repair genes ↑ risk: •no risk: q10yrs
(MLH1, MSH2/6, PMS3); 40% risk of colon cancer – mean age •sessile •low risk: q5-10yrs
late 40s •villous 1-2 polyps, <1cm, tubular, low grade
•type I: esp. seen on right side •>1cm •high risk: q1-3yrs
•type II: ↑ risk of extra-colonic cancers (esp. endometrial) ≥3 polyps, ≥1cm, sessile/villous, high grade
•mega risk: q2-6mo
Puetz-Jegher’s Syndrome: autosomal dominant; associated w/ ≥10 polyps
hamartomatous polyps, mucocutaneous hyperpigmentation
(lips, oral mucosa, hands) – risk of breast/pancreatic cancer
Gastroenteritis About
Infection of the VIRUSES (75-90%):
GI tract 1) Rotavirus – children <5y, peaks in cooler months
associated w/
vomiting &
diarrhea 2) Norovirus – outbreaks in care centers, cruise ships
*MCC of foodborne disease outbreaks
>3 episodes of
loose/watery 3) Sapovirus, Adenovirus, Astrovirus – primarily <4yo
stools per day
BACTERIAL (10-20%):
1) Campylobacter jejuni – poultry, unpasteurized milk,
untreated water, new pets, dairy farms
2) C. diff – spectrum: mild diarrhea –
pseudomembranous colitis – toxic megacolon
3) E. coli, Shiga-toxin-producing (STEC) – beef, greens,
unpasteurized milk, petting zoos, person-person
3) E. coli, Enterotoxigenic – “Traveler’s diarrhea”
(resource-limited settings)
4) Nontyphoid Salmonella – poultry/beef, dairy,
contaminated water, reptiles/amphibians, MC <4yo
4) Salmonella typhi – humans are only hosts;
resource-limited settings
5) Shigella – infection requires low inoculum; childcare
outbreaks
7) Vibrio cholerae – shellfish; “rice water diarrhea”
8) Yersinia enterocolitica – SWINE; pork, milk, well
water, chitterlings, tofu; uncommon in US
PARASITES (up to 5%):
1) Giardia lamblia – daycare, camping trips,
contaminated water; “backpacker’s diarrhea”
2) Entamoeba histolytica – resource-limited
Clinical Manifestations
S/SXS: generally begins w/ vomiting followed by
watery diarrhea; high fevers in 1/3 of cases
S/SXS: sudden onset vomiting, watery diarrhea,
abdominal pain, fever
S/SXS: milder than rota/nora; watery diarrhea
(vomiting/fever less common)
S/SXS: bloody diarrhea w/ severe abdominal
pain, fever, occasional bacteremia
•Immune-Mediated Manifestations: Guillain-
Barre, Miller-Fisher, reactive arthritis
S/SXS: fever, crampy abdominal pain, foul-
smelling, watery stools
•Pseudo Colitis: diarrhea w/ blood/mucus,
abdominal pain, fever, systemic toxicity
S/SXS: hemorrhagic colitis w/ bloody diarrhea
appearing 3-4d after sxs onset; *may cause HUS
S/SXS: watery diarrhea, abdominal cramping
S/SXS: diarrhea, abdominal cramps, fever
•Complications – bacteremia, osteomyelitis,
brain abscess, meningitis
S/SXS: initially – fever, malaise, myalgias,
abdominal pain, constipation or bloody diarrhea;
then – HSM & rose spots by wk2
•Associated w/ bacteremia & meningitis
S/SXS: varies; watery stools w/o other sxs –
bloody stools + high fever, abdominal pain,
tenesmus
•S. dysenteriae – HUS; seizures, reactive arthritis
S/SXS: painless, watery diarrhea w/ significant
electrolyte imbalances
S/SXS: fever, abdominal pain, bloody diarrhea in
young children
•Pseudo-Appendicitis: mesenteric lymphadenitis
w/ fever, abdominal pain/tenderness,
leukocytosis – older children
S/SXS: acute – watery diarrhea, foul-smell,
flatulence, anorexia; can à FTT
S/SXS: intestinal amebiasis MC – gradual onset
bloody diarrhea, lower abd. pain, tenesmus, wt
loss; complications: toxic megacolon, fulm. colitis
Diagnostics
DX: antigen detection via EIA, PCR
DX: PCR; stool antigen tests have lower s/s
DX: sapovirus/astrovirus: PCR; adenovirus: EIA
DX: culture using selective media (preferred), EIA,
PCR
DX: two-step: enzyme immunoassay for glutamine
dehydrogenase w/ confirmatory toxin testing by
NAAT or toxin immunoassay
•CBC: leukocytosis; anemia possible if bloody
DX: culture on sorbitol containing selective media,
EIA for Shiga toxin – monitor: CBC/BUN/Cr for HUS
DX: clinic; PCR; *culture cannot distinguish from
normal flora
DX: stool culture
DX: blood culture, bile culture, bone marrow
aspirate *stool cultures often negative
DX: stool culture
DX: stool culture (must request selective media)
DX: stool culture (must request selective media)
DX: stool EIA or DFA
DX: stool O&P, serologic testing
Management
TX: supportive; prevention – rotavirus vaccine
TX: supportive
TX: supportive
TX: usually supportive; azithromycin x3d or
erythromycin x5d can shorten duration when
given early in illness
TX: metronidazole 30mg/kg/d divided 4x daily
x10d; vancomycin 40mg/kg/d divided 4x daily
x10d if severe; *fidaxomicin for continuous
relapse
TX: supportive; abx not recommended d/t HUS
risk
TX: azithromycin or cipro x3d may ↓ duration
TX: initial dose of ceftriaxone followed by PO
(azithromycin or amoxicillin or Bactrim)
• only in pts @ high risk of invasive disease –
<3mo, chronic GI dz, HIV/immunocompromised
TX: empiric – ceftriaxone or azithromycin; then
definitive therapy based on cultures x7-14d
•steroids may be beneficial in children w/ enteric
fever (delirium, coma, shock)
TX: azithromycin, ceftriaxone, or FQ
TX: single dose doxy or azithromycin;
erythromycin, cipro, or tetracycline x3d
TX: parenteral 3rd gen ceph, Bactrim,
aminoglycosides, FQs, tetracycline, doxy,
chloramphenicol – only for neonates/IC
TX: tinidazole x1, metronidazole x5-10d,
nitazoxanide x3d
TX: metronidazole or tinidazole then iodoquinol
or paromomycin
PHARM About ADRs/Contraindications
ANTI-DIARRHEALS
Bismuth Subsalicylate MOA: antimicrobial properties; salicylate: anti-secretory & anti-inflammatory properties •dark colored stools, darkening of tongue
Pepto-Bismol Indications: safe in pts w/ dysentery = significant fever, blood diarrhea Contraindications: children w/ viral illness (↑ risk of Reye syndrome)
Kaopectate
Diphenoxylate MOA: binds to gut wall opioid receptors, inhibiting peristalsis •CNS (central opiate effects), anticholinergic, N/V, abd. pain, constipation
Loperamide MOA: binds gut wall opioid receptors, inhibiting peristalsis; ↑ anal sphincter tone •avoid in pts w/ acute dysentery or colitis
Indications: noninvasive diarrhea
Anticholinergics MOA: anticholinergic; inhibits Ach-related GI motility, relaxes GI muscle (antispasmodic), ↓
Phenobarbital, Hyoscyamine, Atropine, Scopolamine gastric secretions
ANTIEMETICS
Ondansetron, Granisetron, Dolasetron MOA: blocks serotonin receptors •neuro: HA, fatigue, sedation •GI: bloating, diarrhea,
•cardiac: QT prolongation, arrhythmias constipation
Dopamine Blockers MOA: blocks CNS dopamine receptors; mild antihistaminic/antimuscarinic •QT prolongation, anticholinergic, drowsiness, hypotension, hyperprolactinemia
Prochlorperazine •EPS: rigidity, bradykinesia, tremor, akathisia
Promethazine Dystonic Reactions (Dyskinesia): tx – IV diphenhydramine
Metoclopramide Parkinsonism: rigidity, tremor

About Clinical Manifestations Diagnostics Management

Diverticulosis Diverticula: outpouchings due to herniation of the
mucosa into the wall of the colon along natural
openings at the vasa recta of the colon
L colon MC in incidence, R colon MC for bleeding
Asymptomatic – incidental finding Colonoscopy Bleeding usually stops spontaneously
Lower GI bleeding: diverticulosis MCC of acute High fiber diet, Bran, psyllium
lower GI bleed
•painless hematochezia

Risk Factors: low fiber diet, constipation, obesity

Diverticulitis Microscopic perforation of a diverticulum leads to •LLQ pain, LLQ tenderness CT scan Uncomplicated:
inflammation & focal necrosis •low grade fever •metronidazole + (ciprofloxacin or levofloxacin)
Labs: x7-10d
Complicated: bowel perforation, abscess, fistula, +/- N/V/D/C, flatulence, bloating, changes in •leukocytosis •clear liquid diet
bowel obstruction bowel habits
ADMIT: complicated, high-risk Surgery: refractory to medical therapy, frequent
Sigmoid colon MC area; onset usually >40yrs PE: +/- tender mass d/t inflammation or abscess recurrences, perforation, strictures

About Clinical Manifestations Diagnostics Management

Esophageal Adenocarcinoma •progressive dysphagia – solid food dysphagia Upper endoscopy w/ bx •esophageal resection combined w/ chemo
Neoplasms •MC in the US progressing to include fluids •radiation, chemo (5-FU)
•MC in distal esophagus, esophagogastric junction •odynophagia •palliative stenting (advanced)
•Risks: Barret’s esophagus (complication of GERD), •weight loss
smoking, high BMI Barrett’s: endoscopic eval q3-5yrs

Squamous Cell
•MC worldwide – increased incidence in AA
•MC in mid to upper third of the esophagus
•Risks: smoking, alcohol
Esophageal Esophageal Web: noncircumferential thin membrane in Dysphagia (esp. to solids) Barium esophagram (swallow) Symptomatic: dilation
Strictures the mid-upper esophagus
Plummer-Vinson Syndrome:
Shatzki Ring: circumferential diaphragm of tissue that •dysphagia + webs + iron deficiency anemia
protrudes into the esophageal lumen •may be associated w/ atrophic glossitis
•MC at the lower esophagus (at the squamocolumnar •increased risk for esophageal SCC
junction)
•Risks: hiatal hernia
GI About Clinical Manifestations Diagnostics Management
Gastric Types: •weight loss & persistent abdominal pain MC Upper endoscopy w/ bx Early local disease: endoscopic resection
Carcinoma •adenocarcinoma MC (90%) •early satiety
•lymphoma, carcinoid tumors, stromal, sarcomas Endoscopic U/S – eval level of invasion •gastrectomy, chemo, radiation
PE: Abdominal/pelvic CT (METS)
Risk Factors: •supraclavicular lymph nodes (Virchow’s node) CXR *poor prognosis – usually presents late in the
•H. pylori biggest risk factor •umbilical LN (Sister Mary Joseph’s node) disease
•preserved foods (salted, cured, smoked, pickled, •left axillary LN (Irish sign) Labs: microcytic/hypochromic anemia
nitrites, nitrates) •palpable nodule on rectal exam (Blumer’s shelf) + guaiac

GI About Diagnostics Management

Dyspepsia •acute, chronic, or recurrent pain/discomfort centered in the upper abdomen (epigastric) HX: clarify chronicity, location, & quality of epigastric UPPER ENDOSCOPY:
•may be associated w/ heartburn, nausea, postprandial fullness, or vomiting pain & its relationship to meals •mainly indicated to look for upper gastric or
•family hx of UGI cancer esophageal malignancy in ALL patients >60yo
Heartburn: retrosternal burning – should be distinguished from dyspepsia •recent employment changes, marital discord, physical w/ new-onset dyspepsia (if ⇡ malignancy risk)
•when heartburn is predominant complaint ⇢ gastroesophageal reflux nearly always present & sexual abuse, anxiety, depression, fear of serious •guidelines recommended against routine
disease endoscopy for pts <60yo (risk of cancer <1%)
FOOD/DRUG INTOLERANCE: acute, self-limited FUNCTIONAL DYSPEPSIA: ⊘organic etiology found +/- postprandial fullness, heartburn, N/V unless alarm features
•overeating, eating too quickly, eating high-fat foods by endoscopy/other testing •may also be warranted if symptoms fail to
•eating during stressful situations, alcohol/coffee •MCC of chronic dyspepsia, often difficult to treat Functional Dyspepsia ⇢ younger patients respond to initial empiric tx or when there is
•MEDS: ASA, NSAIDs, metronidazole, macrolides, •PATHO: ⇡ visceral afferent sensitivity, delayed •report variety of abdominal & non-GI complaints frequent symptom relapse after empiric tx DC
metformin, GLP-1 antagonists, ACEI/ARBS, SSRIs, gastric emptying or impaired accommodation to •show signs of anxiety/depression
SNRIs, Parkinson RX (DA agonists, MAO-B), steroids, food/psychosocial stressors •use/used psychotropic medications TX:
estrogens, iron, opioids, digoxin ⊕H. pylori: bismuth quadruple therapy x14d
H. PYLORI INFECTION: chronic gastric infection w/ *symptom profile alone does NOT differentiate •PPI + Bismuth subsalicylate 262mg +
LUMINAL GI TRACT DYSFUNCTION: H. pylori important cause of PUD but may cause between functional dyspepsia & organic disorders tetracycline + metronidazole
•PUD present in 5-15% of patients w/ dyspepsia dyspepsia in a subset of patients in absence of PUD •PCPs misdiagnose nearly half of pts w/ PUD/GERD •alternative ⇢ rifabutin-based triple therapy
•GERD present in up to 20%, even w/o significant HB ▪omeprazole + rifabutin + amoxicillin
•gastric/esophageal cancer <1%, rare if <60yo PANCREATIC DISEASE: pancreatic carcinoma & chronic ALARM: weight ⇣, persistent vomiting, constant or *standard triple therapy w/ clarithromycin
•gastroparesis (diabetics) pancreatitis may cause chronic epigastric pain, but usually severe pain, progressive dysphagia, hematemesis, no longer recommended
•parasitic infections (Giardia, Strongyloids, Anisakis) more severe, radiates to back, & associated w/ anorexia, melena, family hx of UGI cancer, abdominal mass
rapid weight ⇣, steatorrhea, or jaundice ⇢ endoscopy or abdominal CT indicated ⊖endoscopy, <60yo w/o response to PPI:
BILIARY TRACT DISEASE: ⇢ presumed to have functional dyspepsia
•abrupt onset epigastric/RUQ pain d/t cholelithiasis OTHER: diabetes, thyroid disease, CKD, myocardial <60yo, uncomplicated dyspepsia, gastric cancer rare: •reassurance, lifestyle/dietary changes
or choledocholithiasis ischemia, intra-abdominal malignancy, gastric volvulus or •H. pylori testing: urea breath test, fecal antigen test •herbal therapies: peppermint, caraway
paraoesophageal hernia, chronic gastric or intestinal ▪⊖ + not taking NSAIDs ⇢ PUD virtually excluded •low-dose TCAs (desipramine or nortriptyline)
ischemia, pregnancy >60yo: CBC, electrolytes, liver enzymes, calcium, TFTs
GI About Clinical Manifestations Workup Management
Upper GI Ligament of Treitz: separates UGIB from LGIB Hematemesis – vomiting blood, “coffee-ground” PMH – previous episodes of bleeding, Hemodynamically unstable:
Bleeding •bleeding proximal à hematemesis, melena •bloody: suggests moderate-severe bleeding comorbid conditions •IV access
•bleeding distal à hematochezia •coffee ground: suggests more limited bleeding •fluids
Medication hx •transfusion
Etiologies: Melena – black, tarry stools •aspirin/NSAIDs predispose to PUD
•PUD *hematochezia usually indicates LGIB but can occur in massive UGIB •anticoagulants/antiplatelets ↑ bleed risk Once underlying cause is identified, treat the
•esophagitis •SSRIs/CCBs/aldosterone antagonists have underlying cause
•portal HTN Symptom assessment: been associated w/ GI bleeding •endoscopic thermal probe
•Mallory-Weiss tear •PUD – upper abdominal pain •endoscopic clips
•angiodysplasia •esophageal ulcer – odynophagia, reflux, dysphagia Labs: CBC, CMP, electrolytes, lipids, liver •endoscopic injection
•mallory-weiss tear – emesis, retching, or cough prior to bleeding enzymes, albumin, creatinine, BUN, •angiographic embolization
•variceal hemorrhage or portal HTN gastropathy – jaundice, thyroid, coagulation studies •endoscopic intravariceal cyanoacrylate injection
abdominal distention (ascites) •monitor Hgb every 2-8hrs •band ligation
•malignancy – early satiety, dysphagia, weight loss, cachexia •typically have ↑ BUN-to-creatinine ratio
- >30:1 suggest UGIB PPI (esomeprazole, pantoprazole)
PE to assess hemodynamic stability:
•mild-mod hypovolemia (<15% volume loss): tachycardia UPPER ENDOSCOPY (within 24hrs) Octreotide for esophageal varices or cirrhosis
•≥15% volume loss: orthostatic hypotension
•≥40% volume loss: supine hypotension

*any sxs of acute abdomen, must r/o perforation prior to endoscopy

Lower GI Ligament of Treitz: separates UGIB from LGIB Hematochezia – maroon/bright red blood, blood clots Labs: CBC, CMP, electrolytes, lipids, liver Hemodynamically unstable:
Bleeding •bleeding proximal à hematemesis, melena •L colon origin: bright red enzymes, albumin, creatinine, BUN, •IV access
•bleeding distal à hematochezia •R colon origin: dark/maroon colored thyroid, coagulation studies •fluids
•typically have normal BUN-to-creatinine •transfusion
Etiologies: Symptom assessment: ratio
•diverticulosis •hemorrhoids: painless bleeding w/ wiping - <20:1 Once underlying cause is identified, treat the
•angiodysplasia •anal fissures: severe rectal pain w/ defecation +/- upper endoscopy to r/o UGIB underlying cause
•colitis (infectious, ischemic, IBD) •proctitis: rectal bleeding & abdominal pain •endoscopic thermal probe
•colon cancer •polyps: painless rectal bleeding, no red flag signs COLONOSCOPY, CT angiography, •endoscopic clips
•hemorrhoids •colorectal cancer: painless rectal bleeding & a change in bowel radionucleotide scanning •endoscopic injection
•anal fissures habits in a pt 50-80yrs •angiographic embolization
•polyps, proctitis •endoscopic intravariceal cyanoacrylate injection
•rectal ulcers PE to assess hemodynamic stability: •band ligation
•mild-mod hypovolemia (<15% volume loss): tachycardia
•≥15% volume loss: orthostatic hypotension
•≥40% volume loss: supine hypotension

GI About Clinical Manifestations Diagnostics Management

Carcinoid •rare, well-differentiated neuroendocrine tumor that
Tumors arise from enterochromaffin cells
•55% occur in the GI tract, 30% in the lungs
•carcinoid tumors are thought to arise from
transformation of enterochromaffin-like cells (ECL
cells, which are responsible for histamine secretion)
due to chronic stimulation by gastrin; autoimmune
atrophic gastritis is associated w/ hypergastinermia
Many are asymptomatic (incidental finding on endoscopy) •24hr urinary 5-hydroxyindoleacetic acid/5-HIAA excretion Surgical resection
-the end product of serotonin metabolism
Carcinoid syndrome: periodic episodes of •contrast-enhanced, triple-phase CT scans of
•diarrhea (serotonin release) abdomen/pelvis
•flushing
•tachycardia
•bronchoconstriction (histamine release)
•hemodynamic instability (e.g., hypotension)
Hernias About Clinical Manifestations Management
Inguinal Hernias Indirect: (MC!!) Direct: Asymptomatic: swelling or fullness at the hernia Surgical repair
•bowel protrusion @ •MEDIAL to the inferior epigastric site; enlarges w/ increased intraabdominal
internal inguinal ring artery pressure &/or standing; may develop scrotal Strangulated: surgical emergency!
•LATERAL to inferior •Hesselbach’s triangle: “RIP” rectus swelling
epigastric artery abdominis, inferior epigastric, poupart’s Incarcerated: painful, enlargement of an
(inguinal) ligament irreducible hernia
•MC found on the right side Strangulated: painful d/t impaired blood flow,
ischemia, & necrosis, overlying skin changes
Femoral Hernias Protrusion of the contents of the abdominal cavity through the Often become incarcerated or strangulated
femoral canal (below the inguinal ligament) because femoral ring is smaller in women

MC seen in women
Umbilical Hernias Hernia through the umbilical fibromuscular ring Observation: usually resolves by
Congenital (failure of umbilical ring closure) 2yrs of age
- usually due to loosening of the tissue around in the ring in adults
Surgical repair
Incisional Herniation through weakness in the abdominal wall Mostly occur w/ vertical incisions & in obese pts
(Ventral) Hernias
Obturator Hernias Rare hernia through the pelvic floor in which abdominal/pelvic MC in women (esp. multiparous) or women w/
contents protrude through the obturator foramen significant weight loss

Howship-Romberg sign: inner thigh pain w/

internal rotation of the hip

GI About Clinical Manifestations Management

Hiatal Hernia Herniation of structures from the abdominal cavity through the esophageal hiatus of Usually an asymptomatic incidental finding Sliding: management of GERD
the diaphragm •may develop intermittent epigastric or substernal pain, •PPIs + weight loss
postprandial fullness, retching, or nausea, chest pain,
Type I: Sliding (95%) dysphagia Paraoesophageal: surgical repair for complications
•GE junction “slides” into the mediastinum (increases reflux) •volvulus, obstruction, strangulation, bleeding, perforation
DX: barium upper GI series, upper endoscopy
Type II: Paraoesophageal (“rolling hernia”)
•fundus of stomach protrudes through diaphragm
w/ the GE junction remaining its anatomic location

Inflammatory Bowel Disease (IBD)

RF: MC in Ashkenazi Jews, onset MC 15-35y, genetics (10-30% have 1st degree relative affected), smoking (↑ incidence of CD, may be protective in UC), western style diet, infections, medications (NSAIDs, OCPs, HRT)
Extra-Intestinal Manifestations: see w/ both UC & CD
• Rheumatologic: MSK pain, arthritis, ankylosing spondylitis, osteoporosis
• Dermatologic: erythema nodosum, pyoderma gangrenosum
• Ocular: conjunctivitis, anterior uveitis/iritis (ocular pain, HA, blurred vision), episcleritis (mild ocular burning)
• Hepatobiliary: fatty liver, primary sclerosing cholangitis
• Hematologic: B12/iron deficiency (esp. w/ CD), ↑ r/o thromboembolism
Workup: CBC, ESR/CRP, albumin, electrolytes, AST/ALT, creatinine, urea nitrogen, fecal calprotectin, stool microscopy, stool cultures, testing for C. diff

ULCERATIVE COLITIS (UC): chronic, recurrent disease involving only the colon characterized by diffuse CROHN’S DISEASE (CD): transmural process involving any segment of GI tract, resulting in mucosal
mucosal inflammation that results in friability, erosions, & ulcers w/ bleeding; mucosa + submucosa inflammation/ulceration, stricturing, fistula development, & abscess formation
Bimodal: 15-25, 55-65, slightly more common in males RF: cigarette smoking strongly correlated, slightly more common in females
*MC in nonsmokers & previous smokers RF for aggressive disease course: young age at onset, early need for steroids, deep ulcerations, perianal
disease, fistulizing or stricturing disease, or upper GI involvement, ⇣ albumin, ⇡ CRP,
*RECTUM ALWAYS INVOLVED ⇡ fecal calprotectin
Complications: *MC in terminal ileus
•Primary Sclerosing Cholangitis Complications:
•Colon Cancer •Perianal disease: fistulas, strictures, abscesses, granulomas
•Toxic Megacolon •Malabsorption: iron/B12 deficiency
IBD Clinical Manifestations Diagnostics Management
Ulcerative Montreal Classification of Extent of UC: Sigmoidoscopy: mucosa – edema, friability, mucopus, Mild/Moderate UC:
Colitis (UC) ▪E1: ulcerative proctitis ⇢ limited to the rectum erosions; UNIFORM inflammation Induction TX: ▪proctitis/proctosigmoiditis: topical (rectal) mesalamine
▪E2: left-sided UC ⇢ limited to colon distal to splenic fixture ▪left-sided/extensive: PO 5-ASA + rectal mesalamine
▪E3: extensive UC ⇢ extends proximal to splenic fixture ▪topical/PO steroids if no improvement after 2-4wks
Maintenance TX:
Hallmark: bloody diarrhea** ▪continue w/ same agent that induced remission except for steroids
S/SXS: fecal urgency, abdominal pain & cramps, tenesmus
Moderate/Severe UC:
*NO COLONOSCOPY W/ FULMINANT DZ (r/o perforation) Induction TX: ▪anti-TNF +/- immunomodulator
▪anti-integrin (Vedolizumab)
Abdominal radiograph, CT: pts w/ severe colitis to look for ▪anti-interleukin 12/23 (Ustekinumab)
significant colonic dilation ▪steroids for symptom control short-term
Barium studies: “stovepipe sign,” loss of haustral markings Maintenance TX:
*little use, can precipitate toxic megacolon in pts w/ severe ▪continue w/ same agent that induced remission except for steroids
disease

Labs: Hct, albumin (⇣), ESR/CRP, fecal calprotectin

*POSITIVE P-ANCA

Crohn Cardinal SXS: Initial DX: compatible clinical picture + supporting Induction TX (acute flares): agents w/ rapid onset ⇢ steroids, biologics
Disease ▪abdominal pain (crampy), RLQ pain if limited to terminal ileum (MC location) endoscopic, pathologic, & radiographic findings Maintenance TX: biologics & immunomodulators
(CD) ▪diarrhea (+/- bleeding)
▪systemic symptoms ⇢ fatigue, weight loss (d/t ⇣ intake, malabsorption) Colonoscopy: aphthoid, linear, or stellate ulcers; strictures; Mild/Low-Risk CD:
segmental involvement w/ areas of normal-appearing Induction TX: ▪limited to ileum/R colon: Entocort (controlled ileal
Transmural Inflammation mucosa adjacent to inflamed mucosa (“skip lesions”); release Budesonide) x4-8wks
•associated w/ sinus tracts that may lead to fistulas & phlegmon formation cobblestone appearance ▪colonic: PO Prednisone, Sulfasalazine alternative
▪fistulas: enterovesical (bladder), enterocutaneous, enterovaginal BX: granulomas (seen in <25%) Maintenance TX:
▪phlegmon: walled-off inflammatory mass w/o bacterial infection ▪remission via steroid ⇢ taper then DC, f/u ileocolonoscopy in 6-12mo
▪abscess: acute ⇢ localized peritonitis + fever, abdominal pain, tenderness CT/MR enterography: for suspected small bowel ▪remission via Sulfasalazine ⇢ continue for long-term maintenance
▪perianal disease: perianal fistula, perianal abscess involvement
Malabsorption: small bowel CD ⇢ bile salt malabsorption •ulcerations, strictures, fistulas Moderate-Severe/High-Risk CD:
▪watery diarrhea, steatorrhea •bowel wall thickening & vascularity, mucosal Induction TX: ▪Combination: TNF-inhibitor + immunomodulator
enhancement, fat stranding •TNF-inhibitor: Infliximab or Adalimumab preferred
Crohn Disease Activity Index (CDAI): liquid stools/d, abdominal pain, general Barium studies: “string sign,” barium flow through •Immunomodulator: Azathioprine, 6-MP, or MTX
condition, extraintestinal features or complications, use of antidiarrheals, narrowed inflamed/scarred area d/t transmural strictures *combination therapy first line for fistulizing disease
presence of abdominal mass, hematocrit, & body weight *only performed when CT/MR enterography unavailable ▪Steroids used for more immediate symptom relief
▪CDAI <150 = clinical remission ▪CDAI 220-450 = moderate-severe CD •use x8wks then taper
▪CDAI 150-220 = mild CD ▪CDAI >450 = severe-fulminant CD Labs: inflammatory markers – albumin, CRP, fecal Maintenance TX:
calprotectin; CBC (anemia), C. diff testing ▪continue anti-TNF & immunomodulator, taper steroid if used
Disease Characterization: •⇣ albumin
Mild/Low-Risk: no/mild symptoms, normal/minimally ⇡ CRP/fecal •⇡ ESR/CRP during active inflammation
calprotectin, diagnosis at >30yo, limited distribution of bowel inflammation, •⇡ fecal calprotectin correlates w/ active inflammation
no/superficial ulceration on colonoscopy, ⊘perianal disease, ⊘penetrating or *POSITIVE ASCA
stricturing disease Moderate-Severe: CRP >5mg/dL, anemia, ⇣ albumin, fecal
Moderate-Severe/High-Risk: diagnosis at <30yo, current/past tobacco use, ⇡ calprotectin >150-200mcg/g
CRP/fecal calprotectin, deep ulcers on colonoscopy, perianal disease, extra-
intestinal manifestations, intestinal fistula
Maintenance Therapy About ADRs
5-Aminosalicyclic Acid Formulations: sulfasalazine (PO), balsalazide (PO), mesalamine (PO, topical) PO mesalamine ADRs: N/D, rash, pancreatitis, AIN
(5-ASA) •PO: mesalamine (Asacol, Apriso, Lialda, Pentasa); sulfasalazine (Azulfidine); balsalazide (Colazal, Giazo) PO sulfasalazine/balsalazide ADRs: *always admin w/ folate
•Topical: mesalamine suppositories (Canasa, 1000mg); mesalamine enema (Rowasa, 4g/60mL) •nausea, oligospermia, leukopenia, agranulocytosis
MOA: anti-inflammatory; sulfasalazine & balsalazide – 5-ASA linked by azo bond to prevent small intestine absorption, released in colon •impaired folate metabolism, HSN (rash, fever, hemolytic
Indications: during active inflammation + remission maintenance anemia, pneumonitis)
Corticosteroids Formulations: methylprednisolone (IV, 40-60mg/d; PO), prednisone (PO), budesonide (PO; foam, 2mg), hydrocortisone (suppositories, 25 & PO prednisone, methylprednisolone:
Methylprednisolone 30mg; foam, 10%, 80mg; enema, 100mg) •short term: mood changes, insomnia, dyspepsia, weight
Prednisone Indications: short-term tx of mod-severe disease while other agents take effect *calcium + vitamin D supplementation w/ long-term use gain, edema, ↑ BG, acne, moon facies
Budesonide •PO budesonide: Entocort targets terminal ileum & proximal colon, Uceris releases budesonide throughout colon •long term: osteoporosis, osteonecrosis of femoral head,
Hydrocortisone *less suppression of HPA axis + fewer ADRs myopathy, cataracts, susceptibility to infections
Immunomodulators About ADRs
Thiopurines MOA: azathioprine converted in vivo to mercaptopurine, mercaptopurine active metabolite is 6-thioguanine (6-TG) •allergic reactions (fever, rash, arthralgias), nonallergic
Mercaptopurine (6-MP) Indications: mainly used in combo w/ anti-TNF agents in pts w/ mod-severe disease to reduce antibody formation against the biologic agents reactions (N/V, pancreatitis, hepatotoxicity, bone marrow
Azathioprine (AZA) & to increase the likelihood of clinical remission through increased anti-TNF drug levels & possible synergistic effects suppression, infections)
Prior to initiation: obtain TPMT functional activity to assess for mutations, HOLD tx in pts w/ absent TPMT •2.5-fold ↑ r/o Non-Hodgkin lymphoma, ↑ r/o HPV-related
Monitoring: CBC q1wk x4wks, then q2wks x4wks, then q1-3mo for duration of therapy; LFTs periodically cervical cx & non-melanoma skin cx, EBV in younger pts
*if WBC <4000/mcL or platelet <100,000/mcL, DC medication x1wk, then reduce dose by 25-50mg
Methotrexate (MTX) MOA: low dose (12.5mg q1wk) has anti-inflammatory properties, including inhibition of TNF expression in monocytes & macrophages •N/V, stomatitis, infections, bone marrow suppression,
Indications: used in combo w/ anti-TNF agents to prevent immunogenicity hepatic fibrosis, life-threatening pneumonitis, TERATOGENIC
*folate supplementation Monitoring: CBC + LFTs q3mo
Tofacitinib MOA: JAK 1/3 inhibitor, which is involved through the JAK-STAT pathway in modulation of multiple interleukins ↑ r/o Herpes Zoster infection: pts w/o hx of varicella
Indications: SECOND-LINE therapy for the tx of mod-severe ULCERATIVE COLITIS (not CD) that has not responded to anti-TNF therapy vaccination should undergo testing for antibodies & receive
vaccination (Shingrix) if antibody negative prior to initiation
BLACK BOX WARNING: ↑ risk of blood clots/deaths in rheumatoid arthritis patients ↑ LDL/HDL: seen within 4-8wks, monitor lipid panel within
first 8wks & LFTs/CBC q3mo
Ozanimod MOA: PO agent that binds to lymphocyte sphingosine 1-phosphate receptors (1 & 5), thereby blocking their ability to leave lymph nodes Serious, but rare: HTN, bradyarrhythmia, ↑ AST/ALT,
Indications: tx of mod-severe ULCERATIVE COLITIS (not CD), leads to ~45% ↓ of peripheral lymphocytes that may last up to 2wks after DC macular edema; herpes simplex reactivation or herpes zoster
Monitoring: LFTs/CBC 3-6mo after initiation; severe
Prior to initiation, pts w/o hx of varicella vaccination should be tested for antibodies & given Shingrix if negative lymphopenia <200x109 should prompt dose ↓ or DC
Biologic Therapies About ADRs
Anti-TNF agents Formulations: infliximab (IV), adalimumab & golimumab (SQ), certolizumab (SQ) Infliximab: reactions are uncommon, usually mild/mod
Infliximab •Infliximab: 5mg/kg @0, 2, 6wks for acute induction à infusions q8wks for maintenance •nausea, HA, dizziness, urticaria, diaphoresis, mild
Adalimumab •Adalimumab: 160mg @0wk, 80mg @2wks for acute induction à 40mg SQ Q2wks for maintenance cardiopulmonary sxs (chest tightness, dyspnea, palpitations)
Golimumab •Golimumab: 200mg @0wk, 100mg @2wks for acute induction à 100mg SQ q4wks for maintenance *tx w/ slower infusion rate, Tylenol, Benadryl
MOA: bind/neutralize TNF (proinflammatory cytokine) on macrophages/activated T lymphocytes, preventing TNF stimulation of effector cells •severe (<1%): hypotension, SOB, rigors, chest pain; require
Indications: used in BOTH mod-severe UC & CD in combo w/ a thiopurine for induction & maintenance of remission O2, Benadryl, hydrocortisone, epinephrine
*Warning: may worsen HF in pts w/ cardiac disease General ADRs for anti-TNF agents:
Monitoring: LFTs routinely, dermatologic exams q1y (↑ r/o skin cx), drug trough levels, anti-drug antibodies •serious (2-5%): sepsis, pneumonia, abscess, cellulitis
↑ r/o opportunistic infections: TB, candidiasis, histoplasmosis, coccidioidomycosis, listeriosis *PPD/CXR for TB prior to use •r/o non-Hodgkin lymphoma (↑ risk if combo w/ thiopurine)
↑ r/o reactivation of HBV, herpes simplex, VZV, EBV •rare: optic neuritis, MS
Anti-Integrins MOA: decrease trafficking of circulating leukocytes through the vasculature, reducing chronic inflammation •infusion reactions uncommon, NO ↑ r/o serious infections
Vedolizumab Indications: mod. active UC or CD who have an inadequate response to or intolerance of steroids, immunomodulators, or anti-TNF agents or malignancy
•induction – 300mg IV @0, 2, 6wks à maintenance – 300mg IV q4-8wks (based on response/trough) Monitoring: therapeutic drug levels
Anti-IL-12/23 Antibody MOA: binds to p40 subunit of IL-12/IL-23, interfering w/ their receptor binding on T/NK/antigen presenting cells •NO ↑ r/o serious infections or malignancy, other serious
Ustekinumab Indications: mod-severe CD & UC; induction w/ single IV dose (5-7mg/kg) à maintenance w/ 90mg SQ q8wks (monitor drug levels) events rare

GI About Clinical Manifestations Diagnostics Management

Meckel’s (Ileal) •persistent portion of embryonic vitelline duct (yolk sac, Usually asymptomatic – often an incidental Meckel scan: loos for ectopic gastric Surgical excision if symptomatic
Diverticulum omphalomesenteric duct) in the small intestine finding during abdominal surgery for other tissue
•MC congenital anomaly of the GI tract causes
•Rule of 2s: 2% of population, 2 feet from ileocecal valve, 2% Mesenteric arteriography or abdominal
symptomatic, 2 inches in length, 2 types of ectopic tissue (gastric •painless rectal bleeding or ulceration exploration
MC or pancreatic), 2yrs MC age, 2x MC in males •if pain à periumbilical

PATHO: ectopic gastric or pancreatic tissue may secrete digestive *may cause intussusception, volvulus, or
hormones, leading to bleeding obstruction; may cause diverticulitis in adults
 GI
Jaundice Yellowing of the skin, nail beds, & sclera by
bilirubin deposition as a consequence of
hyperbilirubinemia
FIRST SIGN à scleral icterus
Serum bilirubin >2.5mg/dL – not a disease but a
sign of disease
Occurs w/ increased bilirubin overproductions
(hemolysis)/ineffective erythropoiesis, decreased
hepatic bilirubin uptake, impaired conjugation,
biliary tract obstruction, viral hepatitis, physiologic
jaundice of newborn, Gilbert syndrome, Dubin-
Johnson syndrome
Causes:
Extravascular hemolysis/ineffective erythropoiesis
•increases the level of UCB which overwhelms the
liver’s ability to conjugate UCB
•dark urine & increased risk for pigmented bilirubin
gallstones results
Physiologic jaundice of the newborn
•newborn has transient low UGT which increases
UCB
•it can present w/ kernicterus leading to neuro
deficits & death
•tx w/ phototherapy
GI About
Hepatocellular •5th MC malignancy worldwide, M > F
Carcinoma •MC primary liver malignancy in adults, peak 70-75yo
(HCC)
Etiology: cirrhosis MCC (80%)
•chronic HBV, HCV •alcoholic liver disease
•nonalcoholic steatohepatitis •hemochromatosis
•Wilson disease •alpha-1 antitrypsin def.
•aflatoxin (Aspergillus flavus) •autoimmune hepatitis
Gilbert Syndrome Initial lab tests:
•mildly low UGT activity which increases UCB •serum total & unconjugated bilirubin
•jaundice occurs during stress like a severe infection; otherwise, •alk phos
pts are asymptomatic •AST/ALT
•PT/INR
Crigler-Najjar Syndrome •albumin
•the absence of UGT which increases UCB causing kernicterus Interpretation:
which is usually fatal Normal alk phos & aminotransferases
•jaundice likely not due to hepatic injury or biliary tract disease
Dubin-Johnson Syndrome
•deficiency of bilirubin canaliculi transport protein which Predominant alk phos elevation
increases CB •suggests biliary obstruction or intrahepatic cholestasis
•the liver is pitch-dark
•Rotor syndrome – liver is not dark Predominant aminotransferase elevation
•suggests jaundice is caused by intrinsic hepatocellular disease
Biliary tract obstruction (obstructive jaundice)
•associated w/ gallstones, pancreatic carcinoma, liver fluke, & Elevated INR
cholangiocarcinoma •an elevated INR that corrects w/ vitamin K admin suggests impaired intestinal absorption of
•this also increases the CB, & alkaline phosphatase & decrease fat-soluble vitamins & is compatible w/ obstructive jaundice
urine urobilinogen
•dark urine, pale stool, pruritis due to increased bile acids, Unconjugated hyperbilirubinemia
steatorrhea •typically involves evaluation for hemolytic anemia, drugs that impair hepatic uptake of
bilirubin, & Gilbert syndrome
Viral hepatitis
•disrupts both hepatocytes & small bile ductules which increase Conjugated hyperbilirubinemia
both the CB & UCB •evaluation will be based on whether the abnormalities are likely due to biliary obstruction,
•dark urine due to elevated urine bilirubin intrahepatic cholestasis, hepatocellular injury, or an inherited condition
Clinical Manifestations Diagnostics Management
•usually asymptomatic early on LABS: ⇡ alk phos, ⇡ AST/ALT, ⇡ GGT, ⇡ α-fetoprotein (AFP) Early stage: surgical resection
▪sxs from underlying cirrhosis/hepatitis *AFP ≥20ng/mL w/ liver lesions of any size ⇢ CT/MRI
Intermediate: locoregional therapy
Advanced disease: CT w/ contrast: 1+ lesions w/ irregular borders •transarterial chemoembolization (TACE)
▪weight loss, anorexia •arterial phase hyperenhancement •transarterial radioembolization (TARE)
▪hepatomegaly & RUQ tenderness •nonperipheral washout: hypointense compared to
▪jaundice, ascites surrounding in portal venous or delayed phase Advanced: systemic chemotherapy
•enhancing capsule •atezolizumab/bevacizumab
Liver biopsy ⇢ definitive
•liver transplant
Screening Indications: Modality: U/S
•cirrhosis from any cause
•chronic HBV + either ⇢ active infection, family hx of HCC
Findings: Interval:
▪no lesion ▪repeat in 6mo
▪lesion <10mm ▪repeat in 3-6mo
▪lesion ≥10mm ▪further imaging (CT)
HEPATITIS Transmission Acute/Chronic Incubation Period Clinical Manifestations Serology/Diagnostics Management
HAV Fecal-oral ACUTE 15-45d (4wks) Prodromal sxs: Acute: IgM anti-HAV No treatment needed (self-limiting)
•anorexia, N/V Past exposure: IgG HAV Ab
•fatigue, malaise, arthralgias, myalgias Post-Exposure Prophylaxis:
•HA, photophobia LFTs: ↑ AST/ALT & bilirubin •healthy, age 1-40: HAV vaccine preferred over
•pharyngitis, cough, coryza immunoglobulin (within 2wks of exposure)
•immunocomp, chronic liver disease: HAV vaccine +
1-2wks later à jaundice, +/- RUQ pain HAV immunoglobulin (within 2wks)
HBV Sex & blood BOTH 30-180d (8-12wks) HBsAg (surface antigen): (+) in acute & chronic Supportive – majority will not become chronic
Dark urine, clay-colored stools – may Anti-HBs (surface antibody): (+) if recovered/immunized
appear 1-5d before onset of jaundice Anti-HBc (core antibody): Chronic Mgmt:
•acute: IgM •antiviral therapy may be indicated if persistent,
•chronic/recovered: IgG severe sxs, marked jaundice, (bilirubin >10),
HbeAg (envelope antigen): replicative (chronic) inflammation on liver bx, ↑ ALT or (+) HB envelope
Anti-Hbe (envelope antibody): non-replicative (chronic) antigen present
•entecavir, tenofovir
LFTs: ↑ bilirubin •tx can be stopped after confirmation pt has cleared
•acute: AST/ALT in the thousands HBsAg
•chronic: AST/ALT in the hundreds
Vaccine: derived from yeast, CI if allergic to baker’s
HBV DNA: best way to assess viral replications activity yeast
•infant: given @ birth, 1-2mo, 6-18mo
Liver bx •adult: 3 doses @ 0, 1, 6mo
HCV Blood (IVDU MC) BOTH 15-160d (7wks) Screening test: HCV antibodies 12wks PO therapy:
•ledipasvir-sofosbuvir
Confirmatory: HCV RNA •elbasvir-grazoprevir
•ombitasvir-paritaprevir-ritonavir + dasabuvir
HCV RNA (+): acute or chronic •simeprevir + sofosbuvir
Anti-HCV (+): chronic •daclatasvir + sofosbuvir
Response determined by PCR-RNA viral load @ 12 &
24wks after therapy

*some tx may activate HBV, so perform HBV testing

before initiating therapy
HDV Blood BOTH 30-180d (8-12wks) Screening: total anti-HDV – confirmed by No FDA approved management
immunochemical staining of liver bx for HDAg or RT; PCR
assays for HDV RNA in serum (HBV serologies also Interferon alpha has been used in management of
performed) chronic HDV

Liver transplant definitive

Prevention: hepatitis B vaccine

HEV Fecal-oral ACUTE 14-60d (5-6wks) LFTs: ↑ AST/ALT, bilirubin No treatment needed (self-limited) – not associated
w/ a chronic state
3rd WORLD, IgM anti-HEV: (+) = infected
PREGNANT Highest mortality due to fulminant hepatitis during
pregnancy

About Clinical Manifestations Diagnostics Management

Alcoholic Progressive inflammatory liver injury due to Mild forms may be asymptomatic AST:ALT >2, ↑ bilirubin & GGT, ↑ INR AVOID alcohol, nutritional support,
Hepatitis long-term heavy alcohol use hydration
Anorexia, N/V, malaise, fever, jaundice, RUQ pain, hepatomegaly, CBC: leukocytosis
Can progress to cirrhosis or hepatic failure if ascites Severe: glucocorticoids
alcohol use continues Liver bx – steatosis, neutrophil or lymphocyte
infiltration, Mallory-Denk bodies, cholestasis
Nonalcoholic Inflammation & fibrosis of the liver Mostly asymptomatic U/S, CT, MRI Weight loss, statins, vitamin E
Steatohepatitis Mild abnormalities in LFTs
(NASH) Etiologies: obesity, hyperlipidemia, Fatigue, malaise, vague RUQ discomfort, hepatomegaly
glucocorticoids, DM Liver bx
GI
Cirrhosis •result of chronic hepatic injury w/ inflammation that leads to hepatic fibrosis & regenerative nodules, HCC PRECURSOR**
•prevalence rate 0.27%, ♂ > ♀ (2:1)
MCC ⇢ ▪chronic viral hepatitis (HBV, HCV**) Others ⇢ ▪meds (e.g., MTX, APAP, ISN)
▪alcohol-associated liver disease
▪hemochromatosis
▪nonalcoholic fatty liver disease (NAFLD)
Clinical Manifestations:
▪muscle cramps (can be severe), easy bruising, LE edema
▪fever, diarrhea, pruritis, muscle wasting
▪⇣ MAP (contributes to hepatorenal syndrome)
▪hepatosplenomegaly, ascites
▪caput medusae ⇢ dilated abdominal veins
▪palmar erythema, clubbing (MC in 1° biliary cirrhosis)
Wilson Disease *ATP7B gene mutation
▪copper accumulation results from impaired excretion
▪S/SXS: Parkinsonism, mood disturbances, cirrhosis
▪Kayser-Fleisher rings (corneal copper accumulation)
COMPLICATIONS:
Hepatic Encephalopathy ⇢ ammonia accumulation in brain
▪cognitive deficits + impaired neuromuscular function
▪asterixis: flapping tremor
About Diagnostics Management
LABS: ▪alcohol abstinence most important
▪hepatic studies: Modest ⇡ AST & alk phos ▪treatment of underlying conditions
▪autoimmune hepatitis ⇡ bilirubin, ⇣ albumin, ⇡ GGT
▪primary biliary cirrhosis ▪Wilson disease ▪avoid hepatotoxic drugs: NSAIDs, opiates,
▪primary sclerosing cholangitis ▪right-sided HF ▪coagulation studies ⇡ PT, ⇡ INR BDZs (HE)
▪α1-antitrypsin deficiency ▪veno-occlusive disease
i.e., Budd-Chiari ▪CBC: thrombocytopenia (MC), anemia, leukopenia ▪vaccinations: PPSV23, HAV/HBV, influenza
▪hyponatremia (common in cirrhosis + ascites) ▪adequate nutritional intake
▪anovulation (♀): amenorrhea, menstrual irregularities
▪hypogonadism (♂): gynecomastia, ⇣ libido, testicular atrophy IMAGING: Definitive ⇢ liver transplant
▪Skin: jaundice, dark urine, spider angiomata (telangiectasia) ▪U/S: surface nodularity, ⇡ echogenicity, small liver ▪indications: index complication (e.g.,
⇡⇡ bilirubin: jaundice usually not detectable until >2-3mg/dL ▪Caudate/left lobes: hypertrophy ascites, HE, variceal hemorrhage) &/or
▪Fetor hepaticus (sweet, pungent smelling breath): dimethyl ▪Right lobe: atrophy MELD score ≥15
sulfide accumulation, suggests severe portal-systemic shunting
▪Dupuytren’s contractures (i.e., thickening/shortening of palmar LIVER BX ⇢ confirmatory Hemochromatosis: phlebotomy,
fascia causes flexion deformities of fingers) Deferoxamine (iron-chelation)
Hemochromatosis:
Hemochromatosis (bronze diabetes) *HFE gene defect ▪transferrin sat ≥45%, ⇡ ferritin >200-300ng/mL Wilson: Penicillamine, avoid seafood &
▪excess iron deposition as a result of ⇡ iron absorption ▪BX: ⇡ hemosiderin other high-copper foods
▪S/SXS: diabetes + dark (bronze) skin + cirrhosis
Wilson: ⇣ ceruloplasmin, ⇡ urinary copper excretion
▪slit lamp (Kayser-Fleischer rings)
▪BX: ⇡ copper content
Hepatic Encephalopathy:
▪lactulose + rifaximin, liver transplant

Portal Vein Thrombosis (PVT) ⇢ thrombus in the portal vein PVT: anticoagulation (enoxaparin)
▪contributes to development of portal HTN

Cirrhosis Complications of Portal HTN

Esophageal varices ⇢ UGIB Ascites ⇢ accumulation of fluid within the peritoneal cavity TX: therapeutic paracentesis
S/SXS: hematemesis &/or melena S/SXS: abdominal distention/pain, early satiety ▪salt restriction ≤2g/d, +/- fluid restriction
DX: EGD – prediction of variceal hemorrhage: location, size, appearance, clinical features, variceal pressure DX: paracentesis ▪diuretics (spironolactone, furosemide)
▪⊕red signs associated w/ ⇡ bleeding risk
Spontaneous bacterial peritonitis (SBP) ⇢ infection of ascitic TX: IV cefotaxime 2g q8h x5d, IV albumin,
TX: bleeding prophylaxis ⇢ beta blockers (e.g., propranolol or nadolol), endoscopic variceal band ligation fluid w/o an intraabdominal secondary source repeat paracentesis 48h later
TX: variceal hemorrhage ⇢ PRBCs to maintain Hgb ≥7g/dL, octreotide (preferred) or vasopressin ▪common pathogens: E. coli, strep, Klebsiella
▪ABX prophylaxis: IV ceftriaxone x7d S/SXS: fever, abdominal pain/tenderness, AMS
▪endoscopic variceal band ligation** (1st line), sclerotherapy, balloon tamponade, TIPS (alternatives) DX: paracentesis ⇢ PMN (neutrophil) count ≥250 cells/mm3
Hepatorenal syndrome ⇢ development of renal failure in a patient who has advanced liver disease d/t Portopulmonary HTN ⇢ pulmonary HTN + portal HTN Cirrhotic cardiomyopathy ⇢ normal CO &
cirrhosis, severe alcoholic liver disease, acute liver failure, etc. S/SXS: fatigue, dyspnea, peripheral edema, CP, syncope contractility at rest & a dysfunctional or
blunted response to stress
DX: ⇡ creatinine, normal urine sediment, no/minimal proteinuria (<500mg/d), urine Na <10mEq/L DX: initial ⇢ TTE, confirmatory ⇢ right heart catheterization
TX: improve hepatic function, liver transplant TX: liver transplant definitive
Hepatic hydrothorax ⇢ pleural effusion in a patient w/ cirrhosis & no evidence of underlying cardiopulmonary Hepatopulmonary syndrome ⇢ triad of abnormal arterial oxygenation + intrapulmonary vascular dilatations
disease resulting from movement of ascitic fluid into the pleural space through defects in the diaphragm (IPVDs) + liver disease
▪most commonly right-sided S/SXS: dyspnea, platypnea (⇡ dyspnea when upright vs supine), orthodeoxia (⇣ arterial O2 saturation when
S/SXS: dyspnea, nonproductive cough, pleuritic CP going from supine to upright), SpO2 <96%

DX: thoracentesis ⇢ transudative DX: ABG (⇡ A-a gradient ≥15mmHg), TTE (⊕IPVDs)
TX: diuretics, sodium restriction, therapeutic thoracentesis, TIPS, NO CHEST TUBE* TX: medical therapies not effective, liver transplant*
GI About Clinical Manifestations Diagnostics Management
Primary Biliary Idiopathic, autoimmune d/o of Most are asymptomatic – incidental finding of high alk Cholestatic pattern: ↑ alk phos & GGT Ursodeoxycholic acid first line
Cirrhosis/Cholangitis intrahepatic small bile ducts that leads to phos
(PBC) decreased bile salt excretion, cirrhosis, Antimitochondrial antibody hallmark; Cholestyramine & UV light for pruritis
and ESLD Fatigue (usually first symptom), pruritis, RUQ hypercholesterolemia
discomfort Liver transplant definitive
MC in middle-aged women (30-60) U/S – often initial dx test
PE: hepatomegaly, jaundice, xanthelasma, osteoporosis
•signs of cirrhosis may occur late in the disease Liver bx – definitive

GI About Risk Factors Management

Nausea/Vomiting Postoperative N/V (PONV) – complication affecting 30% of children •female gender 0 – 10% risk Preoperative fasting – fasting guidelines often restrict the intake of
& adults after anesthesia •nonsmoker 1 – 20% risk any oral fluid for 2-6hrs preoperatively
•vomiting or retching can result in wound dehiscence, esophageal •hx of motion sickness or previous PONV 2 – 40% risk •it has been demonstrated that clear oral fluids right up until
rupture, aspiration, dehydration, increased intracranial pressure, •expected administration or postoperative opioids 3 – 60% risk transfer to theatre could significantly reduce the incidence of PONV
& pneumothorax 4 – 80% risk w/o an increased risk in the adverse outcomes for which such
conservative guidance exists
Emetogenic drugs commonly used in anesthetic procedures:
•nitrous oxide Antiemetics
•opioids •scopolamine patch
•physostigmine •dexamethasone
•ondansetron
Type of surgery – studies of the effect of the type of surgery on the
incidence of PONV have reported conflicting results Rescue antiemetics – if N/V occur in the post-anesthetic care unit
•the best evidence suggests that cholecystectomy, gynecologic, & (PACU), we administer an antiemetic from a different class of drug
laparoscopic procedures are associated w/ modestly increased risk from those used for prophylaxis
of PONV compared w/ other general surgical procedure •prochlorperazine
•droperidol
The intravenous anesthetic propofol is current the least
emetogenic general anesthetic – these medications are thought to
trigger the CTZ

GI About Clinical Manifestations Diagnostics Management

Pancreatic Cancer 70% found in the head of the pancreas, 20% body, 10%
tail
Types: adenocarcinoma (ductal) MC (90%), islet cell (5-
10%)
•ampullary & duodenal carcinomas; cystadenoma &
cystocarcinoma
Risk Factors: smoking (>20%), >55yrs, chronic
pancreatitis, DM, males, obesity, AA
•usually presents late in the disease course – METS often
present (regional lymph nodes & liver)
•painless jaundice classic (common bile duct
obstruction); weight loss
•abdominal pain radiating to the back; may be
relieved w/ sitting up & leaning forward; tumors
in body or tail produce sxs later than in the head
so usually more advanced at diagnosis – new
onset DM, depression
•pruritis (due to increased bile salts in the skin),
anorexia, acholic stools, dark urine (due to
common bile duct obstruction)
PE:
•trousseau’s malignancy sign = migratory phlebitis
associated w/ malignancy; nonspecific
•Courvoisier’s sign: palpable, nontender,
distended gallbladder due to common bile duct
obstruction (esp. if head of pancreas is involved)
CT scan: initial test of choice
(-) à endoscopic U/S w/ bx
(+) à simultaneous surgical removal/bx
Tumor markers: CA 19-9 (often used to
monitor after treatment), CEA
Surgical: Whipple procedure
(pancreaticoduodenectomy) if confined to the
head or duodenal area; tail (distal resection);
post-op chemo (5-FU, gemcitabine) or
radiotherapy
Advanced or inoperative: ERCP w/ stent
placement palliative for intractable itching
Prognosis: only 20% resectable at time of dx;
overall 5yr survival rate is 5-15%

GI About Clinical Manifestations Diagnostics Management

Pancreatic Cystic collection of tissue, fluid, and necrotic debris •Abdominal pain •Study of choice: CT Scan Persists >4-6 weeks
Pseudocyst surrounding the pancreas •Abdominal mass •Ultrasound -percutaneous drainage
-surgical decompression
Associated with: *NO true epithelial lining in the capsule FNA (pancreaticogastrostomy)
•acute or chronic pancreatitis •elevated amylase -drain into stomach or bowel
•trauma to chest •low CEA
•low fluid viscosity Complications:
•Peritonitis, infection
GI About Clinical Manifestations Diagnostics Management
Peptic Ulcer Duodenal Ulcers: 4x more common, usually Dyspepsia (burning, gnawing, epigastric pain) hallmark; N/V Upper endoscopy w/ bx – all GU need H. pylori positive:
Disease benign repeat endoscopy to document healing •bismuth quadruple therapy: bismuth
(PUD) Gastric Ulcers: 4% associated w/ gastric DU: dyspepsia classically relieved w/ food subsalicylate + tetracycline + metronidazole +
adenocarcinoma GU: sxs worsened w/ food H. pylori testing: PPI x14d
•endoscopy w/ bx – gold standard
PATHO: imbalance between •urea breath test (H. pylori converts H. pylori negative:
•↑ aggressive factors in DU (hydrochloric acid, labeled urea à labeled CO2; breathing •PPI; H2 blocker, misoprostol, antacids, etc.
H. pylori) out labeled urea = +)
•↓ protective mechanisms w/ GU (mucus,
bicarb, PGs)

Etiologies:
•H. pylori MC cause of gastritis
•NSAIDs/ASA – 2nd MC cause (GU – PG Bleeding ulcer: hematemesis, melena, hematochezia – PUD is MC cause
inhibition) of upper GI bleed
•Zollinger-Ellison Syndrome: gastrin-producing
tumor (1%) Perforated ulcer: sudden onset of severe abdominal pain (may radiate to
•ETOH, smoking, stress (burns, trauma, shoulder); peritonitis (rebound tenderness, guarding, rigidity)
surgery, severe medical illness); males, elderly,
steroids, gastric cancer

PHARM Drugs About

PPIs “azoles” Omeprazole Rabeprazole MOA: block H/K ATPase (proton pump) of parietal cell, reducing acid secretion ADRs: diarrhea, HA, hypomagnesemia, B12 deficiency, hypocalcemia
Lansoprazole Esomeprazole •associated w/ faster sxs relief & healing •Omeprazole: associated w/ C. diff infections & hip fractures
Pantoprazole Dexlansoprazole •taken 30min before meals in AM
Indications: most effective drug to treat PUD; gastritis, ZES DI: omeprazole causes P450 inhibition à increases levels of theophylline, warfarin,
•90% healing of duodenal ulcers after 4wks & gastric ulcers after 6wks phenytoin
H2 Blockers Cimetidine Famotidine MOA: histamine 2 receptor blocker (indirectly inhibits proton pump) reducing ADRs: B12 deficiency, ↑ LFTs
“tidines” Ranitidine Nizatidine acid/pepsin secretion •Famotidine, Nizatidine: blood dyscrasias; Famotidine can prolong QT
•90% healing of duodenal ulcers after 6wks & gastric ulcers after 8wks -CNS: confusion, dizziness, HA
•Cimetidine
-P450 inhibition à increases levels of theophylline, warfarin, phenytoin
-CNS: confusion, HA; gynecomastia, impotence
-caution if renal/hepatic dysfunction
Misoprostol MOA: PG E1 analog that increases bicarbonate & mucus secretion, & reduces acid ADRs: diarrhea, abdominal cramping
production
•good for preventing NSAID-induced ulcers but not for healing already existing ulcers CI: premenopausal women – abortifacient & causes cervical ripening
Antacids MOA: neutralize acid, prevents conversion of pepsinogen to pepsin (active form) Nonsystemic:
•Milk of Magnesia (+/- cause diarrhea)
Systemic: calcium carbonate (Tums) •Amphogel (ALOH) (+/- cause constipation, hypophosphatemia)
•ADRs: acid rebound, milk alkali syndrome
Bismuth Pepto-Bismol Kaopecate MOA: antibacterial & cytoprotective that inhibits peptic activity ADRs: darkening of tongue/stool, constipation
Compounds Indications: limited role (used in quadruple therapy in H. pylori management) •salicylate toxicity in OD
•cautious use w/ renal insufficiency
Sucralfate MOA: cytoprotective (forms viscous adhesive ulcer coating that promotes healing, ADRs: metallic taste, constipation, nausea
protects the stomach mucosa)
Indications: MC used as ulcer prophylactic measurement than for tx DI: may reduce bioavailability of H2RAs, PPIs when given simultaneously
GI About Clinical Manifestations Diagnostics Management
Pyloric Hypertrophy & hyperplasia of the pyloric muscles, •nonbilious projectile vomiting Abdominal U/S Initial: rehydration (IV fluids) & potassium
Stenosis causing a functional gastric outlet obstruction •+/- signs of dehydration, weight loss, malnutrition •elongated, thickened pylorus replacement
(preventing gastric emptying into the duodenum)
PE: Upper GI series: Definitive: pyloromyotomy
*MC cause of intestinal obstruction in infancy •palpable pylorus: “olive shaped” nontender, •string sign (thin column of barium through a
mobile hard mass to the right of the epigastrium narrowed pyloric channel), delayed gastric
Risk Factors: emptying
•MC in the first 3-12wks of life •railroad track sign: excess mucosa in the pyloric
•erythromycin use (within the first 2wks of life) lumen resulting in 2 columns of barium
•Caucasians, males 4:1, first-borns
Labs: hypokalemia, hypochloremic metabolic
alkalosis

GI About Clinical Manifestations Diagnostics Management

Small Bowel RARE MC presenting symptom is abdominal pain •CT scan Surgery: wide segmental surgical resection
Carcinoma •delay in diagnosis common •typically intermittent & crampy in nature •wireless capsule endoscopy •adjuvant chemo in pts w/ LN +
•push enteroscopy
Adenocarcinoma MC (25-40%) •N/V •double-balloon endoscopy
•highest in the duodenum •anemia
•GI bleeding Screening for fecal occult blood
Risk Factors: •jaundice
•hereditary cancer syndromes: hereditary •weight loss •CBC, serum electrolytes, LFTs
nonpolyposis colorectal cancer (HNPCC) •obstruction, perforation •tumor marker: CEA
•cystic fibrosis
•Crohn’s disease
•alcohol, refined sugar, red meat, salt-cured &
smoked foods

GI About Clinical Manifestations Diagnostics Management

Toxic Nonobstructive, extreme colon dilation
Megacolon >6cm + signs of systemic toxicity
Etiologies:
•IBD (UC), infectious colitis (C. diff)
•ischemic colitis, volvulus, diverticulitis,
radiation, obstructive CRC
•profound bloody diarrhea Radiologic evidence of colon >6cm: abdominal x-ray Supportive mainstay: bowel rest, bowel
•abdominal pain & distention decompression w/ NG tube, broad spectrum
•N/V, tenesmus 3 or more of the following: abx, fluid & electrolyte replacement
•fever >38C •ceftriaxone + metronidazole
PE: •pulse >120
•lower abdominal tenderness & distention •neutrophilic leukocytosis >10,500/microL Management of underlying cause
•signs of toxicity: AMS, fever, tachycardia, hypotension, •anemia •steroids in ulcerative colitis
dehydration
+/- signs of peritonitis (rigidity, guarding, rebound tenderness) PLUS Surgical: subtotal colectomy w/ end ileostomy

1 of the following:
•hypotension
•dehydration
•electrolyte abnormalities
•AMS
GI About Diagnostics Management
Mesenteric ACUTE (AMI): acute reduction in arterial or venous blood CHRONIC (CMI) ⇢ “Intestinal Angina” •peritoneal signs ⇢ emergent laparotomy AMI – initial Measures:
Ischemia flow to small intestine, may ⇢ bowel ischemia or infarct •atherosclerosis ⇢ ischemia (i.e., hypoperfusion) MCC •IV fluids, NPO, NG decompression
•SMA MC (~90%), SMV LC (<10%), IMA & celiac uncommon •⇣ supply during ⇡ demand (eating) DX: CTA abdomen & pelvis •anticoagulation ⇢ UFH
Etiologies: •2/3 major vessels need to be affected before symptoms •mesenteric stenosis & thromboembolism •empiric broad-spectrum antibiotics
SMA embolism (50%) MCC** •bowel-wall thickening, hypoperfusion •PPI, O2 PRN
•risks ⇢ AFIB, MI, valvular heart disease S/SXS: epigastric/periumbilical postprandial pain, lasts 1-3h •bowel dilation, mesenteric fat stranding
•most acute onset & most severe pain •pain leads to: •pneumatosis intestinalis (gas within walls) Revascularization ⇢ open embolectomy
SMA thrombosis (~25%): ▪limiting food intake ⇢ unintentional weight loss** •thrombosis: mesenteric bypass grafting
•risks ⇢ visceral atherosclerosis, arteritis, aortic aneurysm, ▪sitophobia ⇢ extreme aversion to eating or food
aortic dissection SMA: CMI ⇢ revascularization
Nonocclusive Mesenteric Ischemia (~20%): ▪small intestines •percutaneous mesenteric artery stent
•low flow states (e.g., severe HF, sepsis, hypotension) ▪cecum •angioplasty
Mesenteric Venous Thrombosis LCC (<10%), SMV MC involved ▪ascending colon
▪2/3 transverse colon
S/SXS: pain out of proportion to exam** IMA:
•severe, steady, diffuse abdominal pain +/- N/V/D ▪distal 1/3 transverse colon
•no focal tenderness or distention ▪splenic fixture ▪sigmoid colon
▪descending colon ▪rectum

ISCHEMIC COLITIS: transient colonic ischemia secondary to a nonocclusive reduction in blood flow; MC intestinal ischemia CT abdomen: Ischemic Colitis:
MCC ⇢ nonocclusive (low flow) ischemia (95%) •less common: arterial thromboembolism, venous thrombosis •bowel wall thickening, bowel edema •mild: IV fluids & observation
•IMA distribution MC involved ⇢ LEFT; rectal involvement rare Precipitating Events: hypotension, MI, sepsis, HF, aortic surgery •thumbprint sign: edematous mucosal •moderate: IV antibiotics
•typically involves “watershed” areas w/ limited collateral flow thickening causing indentation in large bowel •severe: exploratory laparotomy w/
▪i.e., splenic fixture & rectosigmoid junction S/SXS: crampy LLQ pain ⇢ rectal bleeding within 24h colonoscopy ⇢ confirms colostomy
•ischemia typically transient, prolonged ⇢ transmural necrosis •abdominal tenderness •clearly defined segmental ischemia in areas of
Risk Factors: age >60, hemodialysis, CVD, diabetes, low albumin low perfusion (e.g., splenic fixture)
•edematous, friable mucosa w/ erosions

GI About Clinical Manifestations Management

Pilonidal Cyst •skin condition caused by local inflammation of superior midline gluteal General features: possible history of trauma or surgery for pilonidal cyst, may be •improved local hygiene, local hair control
(Intergluteal cleft, may progress to local abscess or fistula asymptomatic, simple sinus tract opening in sacrococcygeal region (~5cm from perianal skin)
Pilonidal Disease) •M > F 3:1, peak incidence 15-25y Acute: I&D + local hair removal under
ACUTE (e.g., abscess): anesthesia
•fluctuant, erythematous swelling
Risk Factors: young men w/ excessive body hair, obesity, deep gluteal •painful, tender Chronic/recurrent: surgical resection
cleft, poor anal hygiene/local irritation, sedentary lifestyle, family history •purulent or bloody discharge, fever

Chronic:
•draining sinus w/ pain in sacrococcygeal region/fistula opening
•purulent, mucoid, or bloody discharge

About Clinical Manifestations Diagnostics Management

Boerhaave •full thickness rupture, MC affecting the left •retrosternal chest pain worse w/ deep breathing & Contrast esophagram: leakage Small & stable:
Syndrome posterolateral wall of the lower esophagus swallowing •IV fluids, NPO, broad-spectrum abx, H2
•vomiting, hematemesis Chest CT, CXR receptor blockers
Etiologies: PE: •left-sided hydropneumothorax (MC)
•iatrogenic perforation during endoscopy •crepitus on chest auscultation (subcutaneous •pneumomediastinum Large or severe: surgical repair
(MC) emphysema) •esophageal thickening
•repeated, forceful retching or vomiting •Hamman’s sign: mediastinal “crackling” accompanying
(Bulimia, alcoholism) every heartbeat in the left lateral decubitus position
Mallory-Weiss PATHO: •upper GI bleeding preceded by retching or vomiting Upper endoscopy – superficial longitudinal mucosal Not actively bleeding: supportive
Syndrome •sudden rise in intraabdominal pressure or •hematemesis, melena, syncope erosions •PPIs promotes healing
(Tears) gastric prolapse into the esophagus •may develop abdominal pain, back pain, or
(persistent retching or vomiting after ETOH hydrophobia Severe bleeding:
binge) •thermal coagulation, hemoclips, endoscopic
•may also be associated w/ hiatal hernias band ligation, balloon tamponade
 Preoperative/Postoperative Care 12%
PREOP EVAL PREOP EVAL
Evaluating Approach Low risk surgery, low risk patient: no routine diagnostic testing required
Surgical Indications for Preoperative Testing in Intermediate/High-Risk Surgery
Procedural Hemoglobin *consider in advanced age, liver disease, bleeding disorder
Risk •surgery associated w/ significant blood loss (e.g., major vascular)
•history of anemia or hemoglobinopathy
Platelet count: liver disease, hematologic disorders
BMP:
•older patients, known renal disease, CHF, diabetes, high-risk procedures
Perioperative Mortality by Type of Surgery Mortality •medications that may impair renal function or alter electrolytes (e.g., diuretics, ACEIs, NSAIDs)
HIGHEST >5% •procedures that include exposure to nephrotoxic substances (e.g., iodinated IV contrast)
▪major intraperitoneal, intrathoracic, or vascular surgery Fasting glucose, A1c: known diabetes + no A1c within last 3mo
▪lung/liver transplant, cystectomy LFTs: chronic liver disease, symptoms of liver disease (e.g., jaundice, hepatomegaly)
LOWEST <1% Coagulation studies: AC use, hx suggestive of bleeding d/o, personal/family hx of bleeding d/o
▪superficial, minor ortho, procedures for asymptomatic carotid stenosis UA: urological/gynecological surgery, symptoms of UTI
▪minor gynecological & urological EKG:
Perioperative Mortality by Urgency of Surgery Mortality at 30d •high-risk surgery (e.g., major intrathoracic/vascular), hx of significant arrhythmias
▪EMERGENT: performed ASAP d/t threat to life or limb 3.7% •known ASCVD, BMI >40 + additional risk factors for ASCVD
▪URGENT: performed within 24-48h d/t threat to life or limb 2.3% CXR:
▪Time-Sensitive: performed within 1-6wks to avoid negative outcomes ✗ •thoracic/major upper abdominal surgery + pt >50yo
▪ELECTIVE: performed within 12mo 0.4% •symptomatic cardiopulmonary disease (e.g., COPD, CHF), BMI >40
Cardiac Risk RCRI: predict risk of major adverse cardiac events (MACE) Cardiac Emergent: proceed directly to surgery but identify RFs that affect perioperative management
Assessment •MACE ⇢ MI, cardiac arrest, cardiac death Management All other patients: calculate risk of MACE
Application: screening for all pts undergoing major surgery Approach •RCRI 0-1 (risk <1%) ⇢ proceed to surgery without further testing
•RCRI 2+ (risk ≥1%) ⇢ assess functional capacity (METs)
Functional Capacity in Metabolic Equivalents (METs) ▪Capacity ≥4 METs ⇢ proceed to surgery without further testing
•<4 METs associated w/ ⇡ risk of perioperative complication ▪Capacity <4 METs ⇢ consider stress testing ONLY if result will affect decision for surgery
Activities Associated w/ ≥4 METs:
•climb up a flight of stairs, walk up a hill, walking at ≥4mph •Resting EKG should be obtained in all patients w/ 1+ RCRI prior to major surgery
•heavy housework, yard work •Resting EKG not needed in asymptomatic patients undergoing minor operations
Pulmonary •preoperative evaluation is clinical, PFTs only needed in select cases Pulmonary Main role of PFTs ⇢ identify pulmonary disease in pts w/ unexplained sxs prior to major abdominal
Risk Clinical RFs for Postop Pulmonary Complications: Management or cardiothoracic surgery
Assessment •upper abdominal or cardiothoracic surgery, prolonged anesthesia (>4h), emergency surgery Approach *PFTs often add little information above clinical assessment in pts w/ diagnosed lung disease
•age >60y, COPD, HF, severe systemic disease, tobacco use (>20 pack-years), impaired cognition
•function dependency or prior stroke, preop sepsis, low albumin, OSA Acute RTI: increases risk of perioperative pulmonary/airway complications
•consider delaying surgery to treat infection
ALL patients should be screened for Chronic Pulmonary Disease (asthma, COPD): ⇣ risk by preop optimization of pulmonary function
OSA using validated tool •wheezing ⇢ preop bronchodilator therapy +/- steroids
•e.g., STOP-BANG •COPD ⇢ antibiotics MAY be beneficial in pts w/ increased sputum production or purulence
•OSA associated w/ double risk for
postop pulmonary complications •smoking cessation (only ⇣ risk if initiated 1-2mo before surgery)
Hepatic Risk Chronic Liver Disease ⇢ calculate MELD score or Child-Pugh Class Hepatic
Assessment Management
Approach

Acute Hepatitis: delay surgery until LFTs improve

Chronic Liver Disease:

•MELD <15, Child-Pugh Class A/B: control encephalopathy, coagulopathy, & ascites preoperatively
•MELD >20, Child-Pugh Class C: delay nonurgent surgery until score/class improves
PREOP EVAL PREOP EVAL
Renal Risk •pts w/ CKD are at increased risk of postop AKI Hematologic History unknown/suggestive of bleeding disorder ⇢ PT, aPTT, platelet count
Assessment & •MCC complication for dialysis patients ⇢ hyperkalemia Risk Venous Thromboembolism (VTE):
Management Assessment & •assess all patients for VTE risk factors
Chronic Kidney Disease (CKD) Preop Management: Management Thromboprophylaxis Recommended:
•check preop eGFR ~1mo before surgery, treat associated HTN •pts >40yo or undergoing major general procedures
•dialysis pts should be dialyzed within 24h of surgery to optimize creatinine, electrolytes, & uremic
platelet dysfunction Anemia:
*pts on peritoneal dialysis may temporarily need hemodialysis for intraabdominal procedures •obtain iron studies in anemic pts if planned surgery is associated w/ significant blood loss
•consider delaying elective surgery to correct anemia w/ treatable cause (e.g., iron therapy)
Prevention of Postoperative AKI: AABB recommends preoperative transfusion for:
•optimize kidney perfusion for pts at risk of perioperative hypotension (e.g., IVF, vasopressors) •Hgb <8g/dL
•avoid nephrotoxic agents, adjust doses of renally cleared medications •symptomatic anemia in pts undergoing ortho/cardiac surgery
Endocrine •DKA is an absolute contraindication to surgery Endocrine •hypotension/shock resulting from adrenocortical insufficiency is rare
Risk Preoperative Evaluation: EKG, serum creatinine, A1c if no measurement in last 3mo, blood glucose Risk Steroid Stress Dosing
Assessment & •consider delaying surgery if current A1c >8-9% Assessment & NOT needed:
Management Management •any patient taking any dose of steroid for <3wks
Glycemic Targets: ~110-180mg/dL •patients on morning doses of prednisone <5mg (or equivalent) for any length of time
DIABETES CHRONIC •patients treated w/ prednisone 10mg (or equivalent) every other day
Preoperative Medication Management: STEROID SUGGESTED for:
PO Hypoglycemics: hold morning of surgery THERAPY •any patient taking >20mg/d of prednisone (or equivalent) for >3wks
•SGLT-2 inhibitors: hold 3-4d prior to surgery (long t1/2 & associated ketoacidosis risk) •any patient on steroids w/ clinical Cushing’s syndrome

Insulin:
•Short-acting: hold morning of surgery
•intermediate-acting: give 50% of usual dose morning of surgery
•Long-acting: give 60-80% of usual dose before surgery
•Insulin pump: continue basal infusion at 60-80% of usual rate

Preoperative Preoperative
Medication Medication
Management Management

Other Preoperative Antibiotic Prophylaxis of Surgical Site Infections: Risk Factors:

Preoperative Preparation •determined by type of procedure & patient RFs •advanced age, diabetes, obesity
Assessment •smoking, heavy ETOH consumption
•admit from long-term care facility
•malnutrition, immunocompromised

NPO: DC solids 8h before surgery, liquids 2h before surgery

FLUIDS
Anatomy & Total Body Water (TBW): 50-70% of total body weight, made up of 2 compartments ⇢ ICF & ECF S/SXS of Volume Disturbances: Volume Deficit Volume Excess
Physiology of Intracellular Fluid Volume (ICFV): mostly in skeletal muscle mass, 50% in females, 60% in males Generalized •weight loss •weight gain
Body Fluids Extracellular Fluid Volume (ECFV): made up of plasma & interstitial (extravascular) fluid •⇣ skin turgor •peripheral edema
•Interstitial ECF: anything not inside cells or plasma (i.e., between cells & vasculature)
•Plasma ECF: intravascular volume ⇢ venous circulation contains 70% Cardiac •tachycardia •⇡ cardiac output
•orthostasis/hypotension •⇡ central venous pressure
•collapsed neck veins •distended neck veins
•murmur
Renal •oliguria
•azotemia

GI •ileus •bowel edema

Pulmonary •pulmonary edema

Renal Control Total body sodium content determines ECFV
of Fluids & •total Na content & ECFV LOW: ⇡ kidney reabsorption of Na
Electrolytes •total Na content & ECFV HIGH: ⇡ kidney excretion of Na

FENA: fractional excretion of Na (via urine)

•FENA <1% ⇢ renal reabsorption
•FENA >1% ⇢ renal wasting

•Distal Tubule: reabsorption of Na in exchange for K & H+ secretion

•JG cells release renin ⇢ cleaves angiotensinogen to angiotensin I

•Lungs release ACE ⇢ cleaves angiotensin I to angiotensin II
•Angiotensin II
▪ Stimulates posterior lobe of pituitary to release ADH ⇢ increases H2O reabsorption in collecting duct
▪ Stimulates adrenal cortex to release aldosterone ⇢ stimulates K secretion & Na reabsorption @distal tubule
▪ Leads to ⇡ Na reabsorption, ⇡ vasoconstriction, ⇡ K excretion, & ⇡ H2O retention
Assessing Early Signs of Hypovolemia: tachycardia, decreased pulse pressure, orthostatic BP Input, Output, Weight: daily weight one of the best methods for assessing volume status
Volume •BP not persistently lowered until 20-30% of circulating volume is lost Urine Output (UO) *even without intake, must excrete 800mL/d in urine waste products
Status Hypervolemia HX/PE: •Normal UO: 0.5cc/kg/hr or 1-2L/d (adults), 1cc/kg/hr (kids)
•HX: weight gain, recent MI, SOB, orthopnea •Low UO: hypovolemia, renal failure, low flow states
•PE: JVD, rales, S3, pitting edema, ascites •High UO: hypervolemia, diabetes insipidus, osmotic diuresis, post-obstructive diuresis
Hypovolemia HX/PE: Labs: electrolytes QD for ICU patients
•HX: weight loss, vomiting, diarrhea, burns •Hypovolemia: BUN/Cr >20, FENA <1%
•PE: flat neck veins, poor turgor, dry mucous membranes, cool extremities, slow capillary refill •BUN/Cr <15 ⇢ adequate hydration
Fluid H2O BALANCE: H2O loss ⇢ increased Na/osmolality ⇢ thirst stimulation & ⇡ ADH release
Calculations •minimal obligatory H2O intake/generation: •minimal obligatory H2O output:
▪ ingested water: 500mL ▪ urine, stool: 500mL, 200mL
▪ water in food: 800mL ▪ skin: 500mL
▪ water from oxidation: 300mL ▪ respiratory tract: 400mL
•TOTAL: ~1600mL/d •TOTAL: ~1600mL/d
FLUIDS
IV Fluids
Osmolality: dissolved particles per
unit mass (mOsm/kg)
Osmolarity: solutes concentration
per unit volume (mOsm/L)
PLASMA
Human Plasma
ISOTONIC CRYSTALLOIDS
0.9% NaCl, Normal Saline (NS)
Lactated Ringer’s Solution (LR)
Plasma-Lyte A
HYPOTONIC CRYSTALLOIDS
0.45% NaCl (½NS), Half Normal
Saline
5% Dextrose in Water (D5W)
HYPERTONIC CRYSTALLOIDS
3% NaCl, 5% NaCl
5% Dextrose + 0.45% NaCl (D5½NS)
5% Dextrose + 0.9% NaCl (D5NS)
5% Dextrose + LR (D5LR)
50% Dextrose in Water (D50W)
Crystalloids: aqueous solutions w/ varying concentrations of electrolytes
•Most commonly used fluids in hospital setting, ⇡ intravascular (ECF) volume
Types: isotonic, hypotonic, hypertonic
Colloids: solutions that contain larger molecular weight solutes (e.g., albumin, starch)
•solutes mostly remain confined to intravascular compartment
•NOT routinely used for fluid resuscitation
Natural Colloids: albumin, FFP
Artificial Colloids: gelatins, dextrans, hydroxyethyl starch (HES)
Composition (mEq/L) & Osmolarity (mOsm/L) Tonicity
•Na: 135-145 •Cl: 96-106 Capacity of ECF to create osmotic gradient ⇢ causes H2O to move into or out of ICF
•K: 3.5-5.0 •Ca: 2.2-2.6
•HCO3 (buffer): 22-26 •Mg: 0.8-1.2 •Isotonic (osmolarity ~250-375mOsm/L): •IV solutes = plasma solutes ⇢ increases intravascular volume
•Glucose: 0.07-0.11g/dL •Hypotonic: •IV solutes < plasma solutes ⇢ dilutes intravascular ECF causing H2O ⇢ interstitial/ICF
Osmolarity ⇢ ~290 •Hypertonic: •IV solutes > plasma solutes ⇢ concentrates intravascular ECF causing H2O ⇢ ECF
Composition (mEq/L) & Osmolarity (mOsm/L) Effect on Fluid Compartments Clinical Applications Risks
0.9% NaCl (NS) NO NET H2O SHIFT •fluid resuscitation, maintenance •fluid overload
•Na: 154 •Cl: 154 ⇡ ECFV •mild hyponatremia *caution in HF, edema, renal failure
Osmolarity ⇢ 308 ⊘Δ in ICFV
Lactated Ringer’s (LR) NS: NS:
•Na: 130 •Cl: 109 LR & Plasma-Lyte A ⇢ balanced solutions: •early DKA, shock, blood transfusions •hyperchloremic metabolic acidosis
•K: 4 •Ca: 3 •mild buffer action that counters acidosis •metabolic alkalosis, hypercalcemia, TBI •hypernatremia
•Lactate (buffer): 28 LR: LR:
Osmolarity ⇢ 273 *q1L of blood loss requires 3L of isotonic fluid •hypovolemia due to third spacing •liver failure ⇢ lactate accumulation
Plasma-Lyte A •burns, fistula drainage, trauma •avoid in renal failure ⇢ hyperkalemia
•Na: 140 •Cl: 98 •diarrhea, hemorrhage, pancreatitis •incompatible w/ transfusions
•K: 5 •Mg: 3
•Acetate (buffer): 27 •Gluconate (buffer): 23
Osmolarity ⇢ 294
Composition (mEq/L) & Osmolarity (mOsm/L) Effect on Fluid Compartments Clinical Applications Risks
0.45% NaCl (½NS) Net H2O shift: plasma/interstitial ⇢ ICF •hypovolemic hypernatremia CAUTION ⇢ CEREBRAL EDEMA
•Na: 77 •Cl: 77 ⇡ ECFV, ⇡ ICFV •dialysis, diuretics, DKA •hyponatremia, pulmonary edema
Osmolarity ⇢ 154 •not for rapid rehydration
5% Dextrose ⇢ 5d/dL dextrose = 170cal/L Cell ⇢ SWELLS 0.45%NS (½NS): DKA after NS & before dextrose
Osmolarity ⇢ 252 (iso) ⇢ free water (hypo) D5W: alcohol/starvation ketosis D5W: hyperglycemia, hypokalemia
Composition (mEq/L) & Osmolarity (mOsm/L) Effect on Fluid Compartments Clinical Applications Risks
3% NaCl 5% NaCl Net H2O shift: ICF ⇢ ECF •severe hyponatremia, cerebral edema (⇡ ICP) CAUTION ⇢ CEREBRAL DEMYELINATION
•Na: 513 •Na: 856 ⇡ ECFV, ⇣ ICFV •HF, pulmonary edema, fluid overload
•Cl: 513 •Cl: 856 D5½NS: DKA once BG <250mg/dL
Osmolarity ⇢ 1027 Osmolarity ⇢ 1711 Cell ⇢ SHRINKS *MC postop fluids AVOID ⇢ renal/cardiac disease
5% Dextrose ⇢ 5d/dL dextrose = 170cal/L D5NS: SIADH, Addisonian crisis
Osmolarity ⇢ 406 (hyper) ⇢ ½NS (hypo)
5% Dextrose ⇢ 5d/dL dextrose = 170cal/L D50W: rapid reversal of hypoglycemia D50W: hyperglycemia
D5NS Osmolarity ⇢ 560 (hyper) ⇢ NS (iso) D50W + insulin: adjunctive tx of hyperkalemia •incompatible w/ transfusions
D5LR Osmolarity ⇢ 525 (hyper) ⇢ LR (iso)
50% Dextrose ⇢ 50d/dL dextrose = 1700cal/L
Osmolarity ⇢ 2523 (hyper) ⇢ free water (hypo)
VOLUME D/O About
Volume
Depletion
(Hypovolemia)
*MC fluid d/o
HYPOVOLEMIA:
•secondary to loss of sodium AND water from ECF
•results in compromised tissue perfusion
Etiology:
•GI losses: vomiting, diarrhea, bleeding
•Renal losses: diuretics, hypoaldosteronism, osmotic
diuresis via glucosuria, salt-wasting nephropathies
•Skin losses: sweat, burns
•Third-spacing sequestration: intestinal obstruction,
crush injury, ascites, pancreatitis/peritonitis
Compensatory Mechanisms:
•RAAS activation ⇢ Na & H2O reabsorption
•ADH release ⇢ H2O reabsorption
DEHYDRATION:
•H2O loss from ICF ⇢ ECF hypertonicity (⇡ Na)
•H2O net shift: ICF ⇢ ECF
Etiology: insensible losses, diabetes insipidus
S/SXS: secondary to hypernatremia (e.g., HA,
confusion, dizziness)
Compensatory Mechanisms:
•activation of thirst center ⇢ increased intake
•ADH release ⇢ H2O reabsorption
Volume Isotonic Hypervolemia (salt gain = H2O gain):
Overload •intravascular overload of IV fluids w/ electrolytes
(Hypervolemia) •postop/trauma stress causing ⇣ Na/H2O excretion
•renal insufficiency, cirrhosis, CHF
Hypotonic Hypervolemia (salt gain < H2O gain):
•replacement of GI losses w/ NaCl-poor solutions
•third-spacing, ⇡ ADH w/ surgical stress, SIADH
Hypertonic Hypervolemia (salt gain > H2O gain):
•excessive Na load w/o adequate H2O intake
Clinical Manifestations Diagnostics Management
S/SXS related to VOLUME DEPLETION: LABS: Resuscitation: IV fluid boluses
•lack of energy, easy fatigability, thirst, muscle cramps •low urine volume (oliguria) •20mL/kg IV NS or LR
•postural dizziness, oliguria •BUN/creatinine ratio >20:1
*d/t ⇡ Na reabsorption & resultant ⇣ urea excretion Maintenance:
S/SXS related to FLUID LOSS ETIOLOGY: ▪ ⇡ BUN (ref. 5-20mg/dL) ⇢ prerenal azotemia •calculate maintenance rate
•V/D, polyuria, severe skin burn ▪ creatinine ⇡ only if loss severe enough to ⇣ GFR •D5½NS + 20mEq KCl preferred
•pain caused by underlying third-spacing mechanism •hyponatremia (ref. 135-145mEq/L)
•hyperkalemia (ref. 3.5-5.0mEq/L) Monitor: I&Os, electrolytes, weight
S/SXS related to ELECTROLYTE ABNORMALITIES: •acid-base disturbances *depends on mechanism of loss
•hyponatremia ⇢ N/V, lethargy, confusion, seizures ▪ vomiting, diuretics (H+ loss) ⇢ metabolic alkalosis
•hyperkalemia ⇢ N/V/D, ileus, muscle weakness ▪ diarrhea (HCO3 loss) ⇢ metabolic acidosis
•acidosis ⇢ tachypnea •Hct & albumin *depletion of plasma volume
•alkalosis ⇢ neuromuscular irritability (spasms) ▪ ⇡ Hct (i.e., relative polycythemia)
▪ ⇡ albumin (ref. 3.5-5g/dL)
Physical Exam:
•⇣ interstitial volume ⇢ skin/mucous membrane signs DX: clinical, confirmed by low urine Na concentration
▪ dry skin, ⇣ turgor, tenting, dry mucous membranes •urine Na <20mEq/L
•⇣ plasma (intravascular) volume ⇢ SBP & JVP reductions •FENA <1%
▪ SBPΔ as severity of volume deficit increases •urine osmolality concentration >450mOsm/kg
⤷ ~NML ⇢ orthostasis ⇢ posture-independent low SBP ▪ specific gravity >1.015
▪ ⇣ intensity of Korotkoff sounds & radial pulse •UA normal in hypovolemia since kidney is not diseased
▪ ⇣ JVP ▪ i.e., ⊖protein, ⊖cells/casts
*Hypovolemic Shock ⇢ tachycardia, cold/clammy
extremities, cyanosis, low UO <15mL/h, agitation, confusion
•tachypnea, orthopnea, weight gain DX: mainly clinical •sodium & water restriction
•pulmonary edema, crackles, rales •serum Na (ref. 135-145mEq/L) •loop diuretics
•ascites, pleural effusions •dialysis may be required if severe
•⇡ JVD, peripheral edema, oliguria Supportive labs/imaging:
•CXR, ECHO
Hypertonic ⇢ symptoms of sodium excess •NT-proBNP
•HA, confusion, dizziness, etc.
SODIUM About Diagnostics Management
Hyponatremia Serum Osmolality Type of Hyponatremia: Causes: Normal Serum Sodium: 135-145mEq/L Symptomatic (seizures, confusion):
280-295mOsm/kg •Pseudohyponatremia ▪hyperproteinemia, hyperlipidemia SEVERE HYPONATREMIA: <125mEq/L •emergent tx required regardless of etiology
>295mOsm/kg •Hypertonic Hyponatremia ▪hyperglycemia, mannitol •IV 3% NaCl in 100mL bolus over 10min
<280mOsm/kg •Hypotonic “True “ Hyponatremia •exclude low GFR (<15) & thiazide use ▪can repeat up to 2x if needed
ADH-Dependent *Uosm >100mOsm/kg ADH-Independent *Uosm <100mOsm/kg •exclude hyperglycemia *add 1.6mEq/L to Na for •4-5mEq/L ⇡ of Na usually sufficient to promptly
•Hypovolemic ADH present ADH appropriately absent •psychogenic polydipsia q100mg/dL of glucose above normal reverse neurological symptoms & ⇣ ICP
UNa <10mEq/L ⇢ ▪extrarenal: V/D, sweat/burns, •beer potomania
third-spacing (e.g., pancreatitis) •“tea & toast diet” •urine osmolality (mOsm/kg) Hypovolemic: IV normal saline
UNa >20mEq/L ⇢ ▪renal: thiazides, cerebral salt ≤100 ⇢ ADH-independent Hypervolemic: fluid restriction +/- loop diuretics
wasting, mineralocorticoid ⇣⇣ >100 ⇢ ADH-dependent ⇢ look at urine sodium Euvolemic: fluid restriction
•Hypervolemic •Euvolemic ⇢ UNa >20mEq/L •urine sodium (ref. ~20mEq/L)
UNa <10mEq/L ⇢ ▪heart failure, cirrhosis, ▪severe hypothyroidism ▪adrenal insufficiency <25: extrarenal Warning ⇢ osmotic demyelination syndrome
nephrotic syndrome (rare) ▪CBZ, opioids, SSRIs, MDMA ▪SIADH *dx of exclusion 25-40: give 1L IV NS ⇢ repeat urine Na •result of overly rapid correction of sodium
UNa >20mEq/L ⇢ ▪AKI/CKD (GFR <15) >40: renal ⇢ endo workup (e.g., TSH, cortisol) •correction shouldn’t exceed 8mEq/L within 24h
Acute: <48h ⇢ acute brain swelling, ⇡ ICP Chronic: ≥48h ⇢ brain adapts to hypotonicity ▪⊖further workup⇢ SIADH Risk Factors: Na <120mEq/L, alcoholism, liver
S/SXS: HA, lethargy, N/V, confusion, seizures, •often asymptomatic, may have mild concentration disease, malnutrition, concurrent hypokalemia
brainstem herniation, coma, death or cognitive defects, gait disturbances
Hypernatremia •sodium >145mEq/L **always hyperosmolar •reflects deficit of TBW relative to total body sodium SEVERE HYPERNATREMIA: ≥170mEq/L •requires induction of ⊕water balance
Hypervolemic: Na ⇡, normal or ⇡ TBW Hypovolemic: ⇣⇣ TBW > ⇣ Na DX: often from hx, MCC: water loss w/o replacement •calculate FWD
•Extrarenal ⇢ ⊕polyuria leading to dehydration •Extrarenal ⇢ ⊕oliguria d/t dehydration •If Na >150 in alert patient w/ water access •hypotonic fluids ⇢ D5W most commonly used
▪hypertonic saline, sodium bicarbonate, TPN ▪osmotic diarrhea, vomiting, burns/sweat, third-spacing ⇢ suspect primary hypodipsia
•Renal ⇢ ⊕HTN & hypokalemia, ⊘oliguria •Renal ⇢ ⊕polyuria leading to dehydration If hypovolemic + hypernatremic
▪mineralocorticoid excess (e.g., 1° aldosteronism) ▪loops, osmotic diuresis (e.g., hyperglycemia, uremia) •if etiology unclear ⇢ urine osmolality (mOsm/kg) •FIRST: correct hypovolemia w/ ISOTONIC fluids
Euvolemic: ⇣ TBW, near-nml Na *free water deficit <300: diabetes insipidus ⇢ DDAVP challenge •then correction of sodium w/ hypotonic fluids
•Extrarenal ⇢ ⊕oliguria d/t ⇣ H2O intake Acute: <48h ⇢ neurons shrink from H2O shift into ECF ▪Uosm ⇡ after DDAVP ⇢ central, if not ⇢ nephro
▪unable to access H2O (e.g., dementia) S/SXS (Na >160mEq/L): lethargy, weakness, & irritability 300-600: possible osmotic diuresis: ⊕glucosuria
▪lesions in hypothalamus (i.e., primary hypodipsia) sometimes progressing to ⇢ delirium, seizures, coma >600: extrarenal ⇢ look at urine sodium
•Diabetes Insipidus ⇢ ⊕polyuria, Uosm <300 •urine sodium (mEq/L)
▪Central: ⇣ pituitary release of ADH Chronic: >48h ⇢ Na levels slowly rise, brain adapts <20 ⇢ hypovolemia (e.g., vomiting, diarrhea, etc.)
▪Nephrogenic: renal resistance to ADH •often asymptomatic +/- signs of dehydration >100 ⇢ sodium overload (i.e., iatrogenic)
POTASSIUM About Diagnostics Management
Hypokalemia •serum K <3.5mEq/L, major intracellular cation S/SXS: usually asymptomatic until K <3.0mEq/L •normal K 3.6-5.0mEq/L •PO K replacement for mild/moderate
•magnesium regulates K: low Mg ⇡ renal K excretion •muscle weakness, cramps, ⇣ DTRs •24h-urinary K excretion >30mEq/d ⇢ renal wasting •IV KCl reserved for K <3.0mEq/L
NONRENAL: •constipation, ileus, hyperglycemia, polyuria •spot urine K/UCr ratio >13mEq/g ⇢ renal wasting ▪avoid dextrose fluids ⇢ stimulates insulin
▪insufficient dietary intake (e.g., alcoholics) •cardiac arrhythmias, hypotension, arrest release which shifts K intracellularly
•shift ⇢ ICF: insulin, β-agonists (albuterol), alkalosis •rhabdomyolysis w/ AKI (K <2.5mEq/L) EKGΔ •give Mg w/ potassium replacement
•GI loss (e.g., vomiting & diarrhea) •flat/inverted T waves ⇢ ST depression ⇢ U waves
RENAL WASTING: loop diuretics, RTA, 1° aldosteronism •prolonged QT, PAC/PVCs, bradycardia, VT/VFIB
Hyperkalemia •serum K >5.2mEq/L MEDICATIONS: ACEI/ARBs, NSAIDs, spironolactone, •normal K 3.6-5.0mEq/L Cardiac toxicity, muscle weakness, K >6.5:
EXTRACELLULAR RELEASE: *K shifts from ICF ⇢ ECF trimethoprim, tacrolimus, heparin, cyclosporin •repeat K to exclude pseudohyperkalemia •IV calcium gluconate to stabilize myocardium
•pseudohyperkalemia ⇢ hemolysis MCC
⤷during blood draw d/t fist clenching, tourniquets •tissue injury (e.g., acute tumor lysis, burns, rhabdo) LABS: glucose, electrolytes, CBC, transaminases, ABG Lower extracellular calcium: β-agonists, insulin
•insulin deficiency (hyperglycemia) •metabolic acidosis (intracellular K ⇄ extracellular H+ •chronic ⇡ K ⇢ workup for hypoaldosteronism w/ glucose (NaHCO3 reserved for severe cases)
IMPAIRED RENAL EXCRETION:
•AKI: rapid ⇣ in kidney function ⇢ poor K excretion S/SXS: often asymptomatic until arrhythmias (K >7.0) EKGΔ *NOTE ⇢ poor correlation between K & EKGΔ •Magnesium sulfate if digitalis toxicity
•CKD (uncommon until GFR <15) •arrythmias (e.g., AV blocks, VFIB, arrest), N/V/D •peaked T waves ⇢ ST depression ⇢ QRS widening •hemodialysis for refractory
•hypoaldosteronism (Addison Disease) •muscle weakness, flaccid paralysis, paresthesias, ⇣ DTRs •QRS widening ⇢ sine waves ⇢ VFIB/asystole
CALCIUM About Diagnostics Management
Hypocalcemia •serum Ca <8.5mg/dL, normal 8.5-10.2mg/dL •ionized calcium most accurate measure of serum Ca Findings in Hypocalcemia (⇣ Ca) Severe, Symptomatic (tetany, arrythmias):
•MCC of ⇣ total calcium ⇢ hypoalbuminemia •true hypocalcemia = ⇣ ionized Ca, implies insufficient PTH: Other Labs: Conditions: •IV calcium gluconate + continuous Ca infusion
•MCC of ⇣ ionized Ca (ref. 4.4-5.2mg/dL) ⇢ CKD action of PTH or active vitamin D ⇣ ⇡ PO4 hypoparathyroidism •usually added to D5W
ENDOCRINE: INCREASED LOSS: alcoholism, diuretics, CKD ⇡ ⇣/nml PO4 vitamin D deficiency •monitor calcium level q4-6h to maintain level
•hypoparathyroidism (including ⇡/⇣ Mg) DECREASED INTAKE/ABSORPTION: vitamin D deficit ⇣ vitamin D at 7-8.5mg/dL
•calcitonin secretion (medullary thyroid cancer) DISEASES: pancreatitis, rhabdomyolysis, septic shock ⇡ ⇡ PO4 hyperphosphatemia
PHYSIOLOGIC: ⇣ albumin (ionized Ca normal), loops, ⇡ ⇡ PO4 CKD Asymptomatic:
S/SXS: tetany** •carpopedal spasm, cramps hyperphosphatemia, aminoglycoside abx, foscarnet ⇡ creatinine •PO calcium (calcium carbonate) & vitamin D
•perioral paresthesias ⇡ ⇣ Mg malabsorption or
PE: maneuvers to elicit latent tetany alcoholism •Mg supplementation if also low
•Chvostek sign: tapping facial nerve (below/in front ear) causes twitching of facial muscles *low calcium associated w/ ⇣ albumin does not
•Trousseau sign: ipsilateral carpopedal spasm when upper arm compressed w/ BP cuff EKGΔ: prolonged QT require replacement therapy
Hypercalcemia •serum Ca >10.5mg/dL, ionized Ca >5.2mg/dL •malignancy associated w/ Ca >14mg/dL Primary Hyperparathyroidism: ⇡ PTH, ⇡ Ca, ⇣ PO4 Symptomatic, >14mg/dL:
•Hyperparathyroidism & malignancy MCC (90%) •if PTH normal/mildly ⇡ get 24h urine Ca excretion •IV NS until euvolemia achieved
ENDOCRINE: hyperparathyroidism, acromegaly, INCREASED INTAKE/ABSORPTION: vitamin D excess, ▪24h urine Ca >200mg ⇢ primary hyperparathyroidism
adrenal insufficiency, pheochromocytoma, vitamin A excess, milk-alkali syndrome •hemodialysis for refractory
thyrotoxicosis MISC: granulomatous (sarcoidosis, tuberculosis), •PTH <20pg/mL: get PTHrP & vitamin D/metabolites
NEOPLASTIC: tumors producing PTHrP, lymphoma, thiazides, Paget disease, hypophosphatemia, lithium ▪⇡ 25(OH)D ⇢ vitamin D intoxication •Cinacalcet: suppresses PTH secretion
plasma cell myeloma ▪⇡ calcitriol ⇢ granulomatous or lymphoma •bisphosphonates, Denosumab
▪⇡ PTHrP ⇢ solid tumor malignancy •SQ/IM calcitonin enhances renal excretion,
S/SXS: <12mg/dL often asymptomatic ⇢ “stones, bones, abdominal groans, psychiatric moans” ▪ALL LOW ⇢ plasma cell myeloma, ⇡ vitamin A but use limited to 48h (tachyphylaxis)
•nephrolithiasis (Ca oxalate > Ca phosphate) •bone pain, osteopenia/osteoporosis thyrotoxicosis
•anorexia, N/V, constipation •anxiety, lethargy, cognitive changes EKGΔ: shortened QT •granulomatous ⇢ prednisone

MAGNESIUM About Diagnostics Management

Hypomagnesemia •serum Mg <1.8mg/dL DIMINISHED ABSORPTION/INTAKE: chronic diarrhea, PPIs, •normal Mg 1.8-3.0mg/dL Symptomatic:
•only 1% of total body Mg extracellular alcoholism, small bowel bypass, malnutrition •associated ⇣ Ca & hypocalciuria, ⇣ PTH, ⇣ K •IV magnesium sulfate in D5W or NS
•⇣ Mg causes ⇣ K & ⇣ Ca INCREASED RENAL LOSS: thiazides/loops, hypercalcemia,
S/SXS: tremors, cramps, confusion, hyperaldosteronism, hyperparathyroidism, hyperthyroidism, EKGΔ: wide QRS, prolonged PR, ventricular arrhythmias, Chronic: PO magnesium oxide
⇡ DTRs, Chvostek/Trousseau signs, drugs (e.g., aminoglycosides, cisplatin, amphoB, cetuximab) torsades
weakness, HTN, tachycardia, torsades OTHER: diabetes, respiratory alkalosis, parathyroidectomy
Hypermagnesemia •serum Mg >2.6mg/dL •normal Mg 1.8-3.0mg/dL •DC exogenous sources of Mg
•almost ALWAYS d/t advanced CKD & chronic intake of Mg-containing drugs (e.g., antacids, laxatives) •CKD: ⇡ BUN, ⇡ Cr, ⇡ K, ⇡ PO4, ⇡ uric acid, calcium often ⇣ •calcium chloride (antagonizes Mg)
S/SXS: muscle weakness, ⇣ DTRs, confusion, flaccid paralysis, ileus, hypotension, respiratory muscle •hemodialysis may be necessary, especially
paralysis, complete heart block, cardiac arrest EKGΔ: wide QRS, prolonged PR, prolonged QT in patients w/ severe CKD
PHOSPHATE About Diagnostics Management
Hypophosphatemia •serum PO4 <2.5mg/dL DECREASED ABSORPTION: malnutrition, phosphate-binding •normal PO4 2.5-4.5mg/dL >1mg/dL, asymptomatic:
antacids, alcoholics, vitamin D deficiency •normal 24h urine PO4 <100mg/d, FEPO4 <5% •PO phosphate
S/SXS: rare until PO4 <1mg/dL INCREASED RENAL EXCRETION: hyperparathyroidism, ▪renal wasting MC in hyperparathyroidism & Fanconi
•weakness, paresthesias FGF23 mutation rickets, acetazolamide, Fanconi syndrome <1mg/dL, symptomatic:
•encephalopathy (irritability, confusion, TRANSCELLULAR SHIFT: refeeding, respiratory alkalosis, Fanconi: metabolic acidosis, glucosuria, aminoaciduria •IV phosphate replacement
seizures, dysarthria), ⇣ contractility hungry bone syndrome, OCPs, β-agonists, salicylate poison
•respiratory failure, bone pain OTHER: ⇡ Ca, ⇣ Mg, metabolic alkalosis XR (chronic): changes resembling osteomalacia •treat ⇣ Mg if low
Hyperphosphatemia •serum PO4 >4.5mg/dL EXTRACELLULAR PO4 LOAD: rhabdomyolysis, tumor lysis •normal PO4 2.5-4.5mg/dL Symptomatic hypocalcemia/EKG changes:
•advanced CKD MCC by chemo, metabolic acidosis (lactic/ketoacidosis), •IV calcium gluconate
respiratory acidosis •other abnormalities d/t underlying disease •hemodialysis may be needed in CKD
S/SXS: generally asymptomatic DECREASED RENAL EXCRETION: AKI/CKD, acromegaly, Chronic:
•manifestations of underlying disorder hypoparathyroidism EKGΔ: QT prolongation •calcium acetate/carbonate ⇣ absorption
 Acid/Base Disorders
Characterized by changes in concentration of H+ ions in the body Primary Acid-Base Disorders: secondary to changes in either serum bicarbonate (primary acid buffer) or PCO2
•⇡ H+ = ⇣ pH (acidemia) •⇣ H+ = ⇡ pH (alkalemia) •Kidneys compensate for respiratory acid-base disorders, lungs compensate for metabolic acid-base disorders
Reference Ranges: •PCO2 40mmHg (35-45mmHg) •pH 7.4 (7.35-7.45) •If expected compensatory response differs from lab findings ⇢ mixed acid-base disorder
•HCO3 24mEq/L (22-28mEq/L) •anion gap 6-12mEq/L ▪Primary Metabolic Disturbance ⇢ Measured PCO2 > expected PCO2 ⇢ 1° metabolic + respiratory acidosis
Measured PCO2 < expected PCO2 ⇢ 1° metabolic + respiratory alkalosis
▪Primary Respiratory Disturbance ⇢ Measured HCO3 > expected HCO3 ⇢ 1° respiratory + metabolic alkalosis
Measured HCO3 < expected HCO3 ⇢ 1° respiratory + metabolic acidosis

Metabolic Acidosis
High-Anion Gap ⇢ MUKPILES #MCC + ingestions Non-Gap (hyperchloremic) ⇢ GI loss or RTA Primary Disturbance: ⇣ pH (<7.4), ⇣ HCO3 (<24) Respiratory Compensation: ⇡ RR ⇢ hyperventilation = ⇣ PCO2 (<40)
M: methanol (formic acid) ➀ GI HCO3 loss (diarrhea): ⊖UAG *loss of bicarb or gain of H+ Expected PCO2: ⇣ [PCO2] 1.3mmHg per 1mEq/L ⇣ [HCO3]
U: uremia (AKI/CKD, rhabdomyolysis)# ➁ Renal Tubular Acidosis (RTA): ⊕UAG *full compensation expected within 12-24h
K: ketoacidosis (diabetic, alcoholic, starvation)# •Distal (I): inability to excrete H+ @DCT Calculate anion gap: [Na] – [Cl + HCO3]
P: propylene glycol ▪⇣ urinary ammonium excretion •high-anion gap (>12mEq/L) ⇢ “MUKPILES” ⇢ DX: ketones, lactate, BUN/creatinine +/- tox screen
I: iron/isoniazid •Proximal (II): inability to reabsorb HCO3 @PCT •normal (6-12mEq/L) ⇢ calculate UAG TX: directed at underlying cause (lactic acidosis, ketoacidosis, etc.)
L: lactic acidosis# ▪no impairment of distal H+ secretion •renal failure: give alkali (NaHCO3, sodium citrate) +/- dialysis
E: ethylene glycol (oxalic acid) •Hyperkalemic (IV): ⇡ K secondary to ⇣ aldosterone •ethylene glycol/methanol OD: fomepizole + HD
S: salicylates (e.g., ASA) ▪⇣ aldosterone inhibits ammonium production UAG: [urine Na] + [urine K] – [urine Cl]
•⊖UAG ⇢ GI HCO3 loss (diarrhea) ⇢ TX: Na, K, & HCO3 repletion PRN
Lactic Acidosis: •⊕UAG ⇢ RTA (⇣ renal acid excretion) ⇢ TX: correct metabolic abnormalities to prevent nephrocalcinosis/CKD
•Type A: related to hypoxia (e.g., septic or hypovolemic shock, hypoxemia, carbon monoxide poisoning) •Distal: NaHCO3, often requires K supplementation
•Type B: not related to hypoxia (e.g., liver failure, seizures, ETOH/methanol intoxication, isoniazid) •Proximal: NaHCO3 or KHCO3 (more needed), thiazide diuretic
•⇡⇡ K: fludrocortisone, restrict dietary K, furosemide, NaHCO3
Metabolic Alkalosis
*volume depletion & hypokalemia are MC stimuli for ⇡ HCO3 reabsorption Primary Disturbance: ⇡ pH (>7.4), ⇡ HCO3 (>24) Respiratory Compensation: ⇣ RR ⇢ hypoventilation = ⇡ PCO2 (>40)
Chloride Responsive (urine Cl <20mEq/L): chloride/ECFV loss, Cl repletion = correction *loss of H+ or gain of bicarb Expected PCO2: ⇡ [PCO2] 0.7mmHg per 1mEq/L ⇡ [HCO3]
•Contraction alkalosis: ▪loop/thiazide diuretics, sweat loss in cystic fibrosis *full compensation expected within 12-24h
▪vomiting/NG suction (HCl loss), congenital chloride diarrhea
•Renal H+ loss: ▪post-hypercapnia Urinary Cl <20mEq/L ⇢ chloride responsive ⇢ TX: IV 0.9% NaCl (NS), treat underlying cause
Urinary Cl >20mEq/L ⇢ chloride unresponsive ⇢ TX: patients w/ severe alkalosis (pH >7.6) sometimes require more
Chloride Unresponsive (urine Cl >20mEq/L): severe K/Mg ⇣ or mineralocorticoid ⇡⇡, Cl repletion ≠ correction •Urinary K <30mEq/L ⇢ laxative abuse, severe ⇣ K urgent correct of blood pH
•Mineralocorticoid excess: ▪1°/2° aldosteronism, congenital adrenal hyperplasia, hyperreninism •Urinary K >30mEq/L ⇢ look at BP •hemodialysis an option if volume overloaded + renal dysfunction
⊕HTN ▪CHF, cirrhosis w/ ascites, nephrotic syndrome ⊘HTN: Bartter, Gitelman •Acetazolamide 250-375mg ⇡ HCO3 excretion but may also
▪Liddle’s: pseudohypoaldosteronism (epithelial Na channel defect) ⊕HTN: consider mineralocorticoid excess accelerate urinary losses of potassium & phosphate
▪glycyrrhizic acid (licorice) ingestion (mimics mineralocorticoid excess)
•Genetic ion transport d/o: ▪Bartter ⇢ NaCl reabsorption defect in loop of Henle (mimics loops)
⊘HTN (normo/hypo) ▪Gitelman ⇢ NaCl reabsorption defect in DCT (mimics thiazides)
Respiratory Acidosis (hypercapnia)
ACUTE: Primary Disturbance: ⇣ pH (<7.4), ⇡ PCO2 (>40) Metabolic Compensation: ⇡ HCO3 reabsorption (>24)
•acute lung disease (e.g., pneumonia, pulmonary edema), acute COPD/asthma exacerbation *hypoventilation (retain CO2) Expected HCO3, Acute: ⇡ [HCO3] 1mEq/L per 10mmHg ⇡ [PCO2]
•CNS depression d/t head trauma, postictal state, drugs (e.g., opiates, BDZs), OSA Expected HCO3, Chronic: ⇡ [HCO3] 3.5mEq/L per 10mmHg ⇡ [PCO2]
S/SXS: HA, confusion, anxiety, drowsiness, tremor, blunted DTRs, myoclonic jerks, asterixis +/- papilledema *full compensation expected within 3-5d

CHRONIC: ACUTE TX: CHRONIC TX:

•airway obstruction (e.g., COPD/asthma) •noninvasive ventilation (BiPAP) to blow off CO2 •directed at underlying cause
•respiratory muscle weakness (e.g., Myasthenia gravis, ALS, Guillain-Barre, Multiple Sclerosis) •invasive ventilation (trach) sometimes needed •chronic hypercapnia must be corrected slowly (i.e., over hours to
S/SXS: may be well tolerated, but may have memory loss, sleep disturbances, excessive daytime sleepiness, •Naloxone for opioid OD minutes) because lowering PCO2 too rapidly can cause post-
personality changes hypercapnic “overshoot” alkalosis ⇢ seizures, death
Respiratory Alkalosis (hypocapnia)
ACUTE: **think ⇢ pain, anxiety, or hypoxemia (e.g., high altitude, pneumonia, PE, ARDS) Primary Disturbance: ⇡ pH (>7.4), ⇣ PCO2 (<40) Metabolic Compensation: ⇣ HCO3 reabsorption (<24)
•fever, sepsis, stroke, seizures (postictal) *hyperventilation (blow off CO2) Expected HCO3, Acute: ⇣ [HCO3] 2mEq/L per 10mmHg ⇣ [PCO2]
•mechanical overventilation, drugs (e.g., salicylates, theophylline, progesterone) Expected HCO3, Chronic: ⇣ [HCO3] 5mEq/L per 10mmHg ⇣ [PCO2]
S/SXS: lightheadedness, confusion, peripheral/circumoral paresthesias, cramps, syncope *full compensation expected within 3-5d
•hypocalcemia ⇢ carpopedal spasms TX: directed at underlying cause
CHRONIC: PE during pregnancy, liver failure, hyperthyroidism, brainstem tumor •not life-threatening, pH lowering interventions not needed
S/SXS: asymptomatic, no specific signs •DISCOURAGE paper bag breathing ⇢ doesn’t fix PCO2 & may ⇣ PO2
 About Clinical Manifestations
Deep (DVT) S/SXS: LE swelling (unilateral), pain, warmth, & erythema
•isolated distal DVT: symptoms confined to calf
•proximal DVT: calf or whole leg symptoms
*Homans’ sign (calf pain on passive foot dorsiflexion) is
UNRELIABLE for presence of DVT
Diagnostics Management
D-dimer (✓sensitivity, ✗specificity) *useful to r/o DVT
•high ⊖predictive value for low/moderate PTP
DVT unlikely (low/moderate PTP) ⇢ D-dimer
⊖ = <500ng/mL ⇢ DVT ruled out, no further testing
⊕ = ≥500ng/mL ⇢ compression U/S w/ Doppler

DVT likely (high PTP) ⇢ compression U/S w/ Doppler

MC Prothrombotic States:
•Factor V Leiden mutation
•Prothrombin gene mutation
Risk Factors:
•hx of immobilization (e.g., travel)
•recent surgery/trauma (~12wks)
•previous VTE, family history of VTE
•obesity, >65yo, malignancy, smoker
•pregnancy, postpartum, OCPs, HRT
•heart failure, IBD
Provoked DVT: ⊕identifiable RF
Unprovoked DVT: ⊖identifiable RF
*NO D-DIMER FIRST
Compression U/S w/ Doppler:
⊖ = full compressibility of all imaged veins
⊕ = non-compressibility of imaged vein w/ pressure
Ascending contrast venography
*CT/MR venography previously gold standard, now
rarely used
Phlegmasia Cerulea Dolens (PCD) *painful blue leg (rare)
•massive iliofemoral VTE occludes deep + superficial veins
•total loss of venous outflow ⇈ compartment pressures
•acute edema + ischemic pain + cyanosis
Initial Management (diagnosis ⇢ 3wks)
➀ home tx preferred IF: hemodynamic stable, low
bleeding risk, ⊖comorbidities, ⊕home support,
⊖history of noncompliance
➁ AC choice ⇢ DOACs *avoid use if CrCl ≤30
➂ Proximal DVT ⇢ AC alone > thrombolytic + AC
➃ IVC filter only recommended if CI to AC
*if IVC required, retrievable IVC recommended
Primary Treatment (at least 3mo)
➀ Provoked by transient/chronic RF, unprovoked
⇢ shorter AC course (3-6mo) recommended
Secondary Prevention (after primary treatment)
➀ DC anticoagulation vs continue indefinitely
▫ Provoked, transient RF ⇢ DC after primary tx
▫ Provoked, chronic RF ⇢ indefinite AC
Unprovoked
➁ Choice of agent for secondary tx
▫ AC w/ DOAC recommended over ASA
▫ If using Warfarin (VKA) ⇢ INR 2.0-3.0

Recurrent DVT
➀ DC AC following primary tx ONLY if previous DVT
was provoked by a transient RF
➁ Hx of DVT unprovoked/provoked by chronic RF
⇢ indefinite AC

About Clinical Manifestations Diagnostics Management

Compartment Muscle & nerve ischemia (decreased tissue perfusion)
Syndrome when the closed muscle compartment pressure >
perfusion pressure
Etiologies: trauma MC after fracture of the long
bones, esp. involving the lower extremities, crush
injuries, constriction (tight casts, splints,
circumferential burns)
•pain out of proportion to injury most specific
•pain & paresthesia
PE:
•pain w/ passive stretching of the affected muscles
(most sensitive/earliest sign)
•tense compartment (firm or “wood-like” feeling)
•pulselessness, pallor, decreased sensation & paresis
(late finding); capillary refill usually preserved
•increased intracompartmental pressure >30mmHg
•Delta pressure <20-30mmHg
•↑ creatinine kinase & myoglobin
Prompt decompression: emergency
fasciotomy
While awaiting decompression:
•place limb at level of heart w/ elevation
•supportive – removal of constrictive
dressings, IV fluids, oxygen
Complications About Diagnostics Management
Postoperative •MC pulmonary complication, usually within 48h •Affects 25% of patients who have abdominal surgery CXR: Largely preventable:
Atelectasis •smokers, elderly, obese, respiratory disease •opacification, loss of lung volume •early mobilization, frequent position changes
Postoperative Atelectasis: collapse of lung tissue w/ loss of volume •ipsilateral diaphragmatic elevation •encouragement to cough, incentive spirometer
Obstructive: mucous, misplaced ET tube S/SXS: fever, tachypnea, tachycardia
•immediate effect: ⇣ oxygenation of blood Exam: diaphragm elevation, scattered rales, ⇣ breath TX: clearing airway
•minimal perfusion ⇢ V/Q mismatch sounds; possible tracheal deviation towards affected side •chest percussion, coughing, deep suctioning
Nonobstructive: respiratory suppression d/t anesthesia, pain •bronchodilators/mucolytics may help COPD patients
•⇡ risk for infection in parts of lung remaining atelectatic >72h •obstructive ⇢ intrabronchial suction via endoscope
Wounds SEROMA: localized serious fluid collection not containing pus or blood, delay healing & ⇡ risk of wound infection LABS: CBC ⇢ leukocytosis Superficial:
HEMATOMA: collection of blood & clot caused by unsuccessful hemostasis or coagulation •suture removal, I&D, thorough irrigation, debridement
•blood/wound cultures •pack wound, +/-ABX
Surgical Site Infection (SSI): incisional skin/soft tissue or organ/space infection at recent surgery site, MC within 5-10d •subsequent routine wound care
Classification: Onset: Tissue Involvement: Clinical Features: +/- imaging to assess for deep
Superficial Incisional ≤30d ▪skin & SQ tissue ▪purulent discharge from incision, +/- fever tissue or organ/space infection Deep, Organ/Space:
▪localized tenderness, warmth, erythema, swelling •OR ⇢ exploration, washout, drainage, debridement
Deep Incisional 30-90d ▪deeper soft tissue ▪purulent discharge from deep within incision, ⊕fever •ABX required, pack wound
(i.e., fascia, muscle layers) ▪tenderness, wound dehiscence
▪necrotizing fasciitis: cloudy gray discharge, +/- crepitus *DELAYED CLOSURE, left to heal by secondary intention
Organ/Space 30-90d ▪any part deeper than fascia or ▪purulent discharge from a drain in organ/space, abscess
muscle layers opened in surgery ▪⊕fever, additional features depend on organs affected Procedure: ABX:
MC Pathogens: Risk Factors: NOT genital/GI tract ▪Cefazolin or Oxacillin
▪S. aureus ▪CoNS (S. epidermidis MC) •patient-related: ▪steroids, smoking, diabetes, >age ▪Vancomycin or Linezolid (MRSA)
▪E. coli ▪Enterococcus spp. ▪coexisting infection at another site Perineum, axilla, ▪Ceftriaxone + Metronidazole
▪HIV/AIDS, prolonged hospital stay GI, or GU
Pathogens causing necrotizing fasciitis: first 24h postop •procedure-related: ▪suboptimal prep, OR venting
▪GAS (e.g., S. pyogenes), Clostridium spp. (e.g., C. perfringens) ▪ABX prophylaxis, long surgery
 Cardiovascular 9%
About Clinical Manifestations Diagnostics Management
Abdominal Aortic Focal aortic dilation >1.5 normal (>3.0 Most pts are asymptomatic – may be found CT w/ contrast: best initial test in Symptomatic or ruptured:
Aneurysm (AAA) considered aneurysmal) – infrarenal incidentally on imaging or in pts w/ an symptomatic, hemodynamically stable •IMMEDIATE SURGICAL REPAIR
MC site abdominal bruit or a palpable abdominal pts to deter presence, size, & extent -endovascular stent graft
mass -open repair
PATHO: proteolytic degeneration of Focused bedside U/S: may be initial •BBs reduce shearing forces, decreases expansion & rupture risk
aortic wall & connective tissue Symptomatic (unruptured): study of choice in hemodynamically
inflammation •abdominal, flank, or back pain unstable pts w/ suspected AAA AAA Screening: one-time screening via abdominal U/S in men 65-75yrs
•on exam, an abdominal bruit may be who ever smoked
Risk Factors: auscultated & a palpable abdominal mass Pts w/ known AAA who present w/
•smoking (main modifiable), >60yrs, may be palpated classic sxs or signs of rupture can be
Caucasians, males taken to the operative room for surgical
•hyperlipidemia, atherosclerosis, Symptomatic (ruptured): repair w/o preoperative imaging
connective tissue disorder (Marfan), •abdominal, flank, or back pain
syphilis, HTN •abdominal bruit Asymptomatic w/ suspected AAA:
•Protective Factors: female, DM, non- •pulsatile mass •abdominal U/S: initial test in
Caucasian, moderate alcohol •hypotension or syncope asymptomatic pts & to monitor
consumption •flank ecchymosis progression

Aortoenteric fistula: presents as acute GI

bleed in pts who underwent prior aortic
grafting
Aortic Dissection Tear through the innermost layer of Chest pain: sudden onset severe, tearing
the aorta (intima) due to cystic medial (ripping, knife-like) chest/upper back pain;
necrosis may radiate between the scapulae
•ascending: anterior chest pain
Ascending MC near the aortic arch or •aortic arch: neck/jaw pain
left subclavian •descending: interscapular pain
•descending
•aortic arch Unequal BP in both arms
CT angiogram, MR angiogram, TEE
CXR: widened mediastinum
Acute proximal: surgical
- preoperative BP control
Descending/distal: medical
- non-selective BBs (labetalol)
+/- sodium nitroprusside
- SBP rapidly lowered to a goal of 100-120 within 20min

Risk Factors:
•HTN (most important)
•age >50yrs
•men, vasculitis, trauma, family hx
•Turner’s syndrome
•collagen d/o (Marfan, Ehlers-Danlos),
pregnancy
 About
Peripheral Arterial Atherosclerotic disease of the
Disease arteries of the lower extremities
L-A-teral ulcers ⇢ Arterial
Acute Arterial Acute limb ischemia – rapidly
Occlusion developing or sudden decrease in
limb perfusion
VASCULAR Etiologies: thrombotic occlusion
EMERGENCY MC (w/ preexisting peripheral
arterial disease) – MC in the
superficial femoral or popliteal
artery
Clinical Manifestations Diagnostics Management
Intermittent claudication – MC sxs (lower extremity pain w/ ambulation) ABI: most useful screening test Supportive: first line therapy – exercise (fixed
•+ PAD if <0.90 (0.50 is severe); rest pain distance walking), decreasing RF (smoking
Aortic bifurcation/common iliac; buttock, hip, groin (25-30%) if <0.4 (normal is 1-1.2) cessation associated w/ greatest benefit,
Femoral artery or branches; thigh, upper calf (80-90%) •>1.2 à possible noncompressible hyperlipidemia, DM), foot care
Popliteal artery; lower calf, ankle/foot (80-90%) (calcified) vessels – may lead to a false
Tibial & peroneal arteries; foot (40-50%) reading Platelet inhibitors: cilostazol most effective
medical therapy; aspirin, clopidogrel,
*Leriche’s Syndrome: triad of buttock/thigh claudication + impotence + Arteriography: gold standard – usually pentoxifylline
↓ femoral pulses only performed if revascularization is
planned Revascularization: percutaneous transluminal
Ischemic rest pain: in advanced disease; MC at night & relieved w/ foot angioplasty (first line revascularization
dependency procedure) bypass grafts, endarterectomy (last
line)
PE:
•pulses: decreased or absent; bruits (>50% occlusion), decreased
capillary refill
•skin: atrophic changes – muscle atrophy, thin/shiny skin, hair loss,
thickened nails cool limbs, areas of necrosis; usually no edema
LATERAL MALLEOLUS ULCERS
•color: pale on elevation, dependent rubor (dusky red w/ dependency)
6 Ps: paresthesias (often early), pain, pallor, pulselessness, Bedside arterial doppler to assess for Reperfusion mainstay of tx – surgical bypass,
poikilothermia, paralysis (late finding associated w/ a worse prognosis); pulses surgical or catheter based
sxs usually distal to the occlusion thromboembolectomy, endarterectomy;
CT angiography or catheter angiography thrombolytic therapy or percutaneous
Decreased capillary refill, decreased or absent pulses, cool temperature angioplasty
An immediately threatened limb may
undergo further evaluation & treatment Supportive: pain control, fluid resuscitation, UFH
in a surgical suite

About Clinical Manifestations Management

Varicose Veins Dilation of superficial veins due to failure of the
venous valves in the saphenous veins, leading to
retrograde flow, venous stasis, & pooling of blood
Risk Factors: family hx, female, increased age,
standing for long periods, obesity, increased
estrogen (OCP, pregnancy), chronic venous
insufficiency
Chronic Venous Changes due to venous HTN of the lower
Insufficiency extremities as a result of venous valvular
incompetency
Most are asymptomatic but may present due to cosmetic issues Conservative: compression stockings, leg
elevation, pain control
Dull ache or pressure sensation; pain is worse w/ prolonged standing or sitting w/ the leg dependent &
is relieved w/ elevation Ablation: catheter-based endovenous thermal
ablation (laser or radiofrequency)
PE: dilated visible veins, telangiectasias, swelling, discoloration, venous stasis ulcers: severe varicosities
resulting in skin ulcerations; +/- mild ankle edema Ligation & stripping, sclerotherapy
Leg pain worsened w/ prolonged standing, prolonged sitting w/ the feet dependent Conservative: initial management of choice – leg
elevation, compression stockings, exercise,
Leg pain improved w/ ambulation & leg elevation weight management

MC occurs after superficial thrombophlebitis, after
DVT or trauma to the affected leg
Pain classically described as a burning, aching, throbbing, cramping, or “heavy leg” Treat the underlying cause – surgical
intervention usually reserved for pts not
PE: responsive to conservative therapy
•stasis dermatitis: itchy eczematous rash (inflammatory papules, crusts, or scales), excoriations,
weeping erosions & brownish or dark purple hyperpigmentation of the skin (hemosiderin deposition) Ulcer management: compression bandaging
•venous stasis ulcers systems (e.g., zinc impregnated gauze), wound
MEDIAL MALLEOLUS ULCERS debridement if needed, ASA (accelerates
•dependent pitting leg edema, increased leg circumference, varicosities & erythema w/ normal pulse healing)
& temperature
•atrophic blanche: atrophic, hypopigmented areas w/ telangiectasias & punctate red dots
 About Clinical Manifestations
Stable •manifestation of stable atherosclerotic CAD HX: man >50y or woman >60y; complains of
Angina episodic chest discomfort – heaviness, pressure,
Pectoris Myocardial ischemia: myocardial oxygen demand exceeds squeezing, smothering, choking (not sharp)
oxygen supply •pt often localizes pain over sternum
•typically lasts 2-30min
•results when a fixed coronary plaque prevents sufficient •may radiate to arms, back, jaw/neck, shoulders
blood supply through a coronary artery at times of increased
O2 demand, resulting in predictable chest discomfort during Episodes caused by exertion/emotional upset &
times of physical or emotional stress relieved by rest/NTG
Atypical angina, “anginal equivalents”
•dyspnea, N/V, fatigue, diaphoresis, faintness
•women, diabetics, elderly
Chest pain classification:
EKG Ischemia Findings: •substernal
•T wave flattening, hyperacute T waves (peaked) •provoked by exertion/emotional stress
•T wave inversions (TWI) •relieved w/ rest/NTG
•ST depressions 3/3 = typical angina (definite)
2/3 = atypical angina (probable)
0-1/3 = noncardiac chest pain
Diagnostics
LABS: to evaluate for risk factors
•total cholesterol, LDL, HDL, triglycerides,
glucose (A1C), creatinine, hematocrit
UA: examine for DM & renal disease (including
microalbuminuria)
CBC: anemia can aggravate angina
TFTs: hyperthyroidism can aggravate angina,
hypothyroidism can lead to atherosclerosis
CRP >3mg/L is an independent risk factor for
myocardial ischemia
EKG: +/- ST depressions, T wave inversions;
normal in absence of symptoms
⊖ serum markers
Stress testing: nuclear perfusion imaging, ECHO
Gold standard: cardiac catheterization,
coronary CT angiography
Management
Acute TX: sublingual nitroglycerin q5min up to 3x
RF TX: hyperlipidemia, HTN, DM, smoking cessation
Prevention Therapy:
1) beta blockers, first-line therapy
2) nitrates, take ~5min before activity
3) aspirin 75-325mg/d
4) high-intensity statin regardless of baseline LDL
ACEI/ARBs: known benefit for pts w/ HTN, diabetes,
↓ LVEF <40%, chronic kidney disease
CCBs: indicated if beta blockers are contraindicated,
poorly tolerated, or ineffective
Ranolazine: anti-anginal medication, useful for pts
w/ chronic angina despite standard medical therapy
Indications for Revascularization w/ CABG:
•chronic stable angina w/ 3-vessel disease
•2-vessel disease w/ prominent LAD involvement
•1/2-vessel disease w/ high-risk features
– LV dysfunction
•>50% stenosis of left artery
•refractory symptoms, chronic angina

Coronary Vasospasm About Clinical Manifestations Diagnostics Management

Vasospastic Angina PATHO: focal or diffuse spasm of epicardial
(Prinzmetal or coronary artery resulting in dynamic high-grade
Variant Angina) obstruction
•vascular smooth muscle hyperreactivity
Risk Factors: female, <50yo, smokers, hx of other
vasospastic d/o (e.g., Raynaud phenomenon,
migraine)
Cocaine: can induce ischemia & infarction by
causing coronary artery vasoconstriction via
alpha-1 receptor activation
Chest pain/angina characteristics: COVADIS Diagnostic Criteria: •sublingual NTG
•CP indistinguishable from obstructive CAD 1) nitrate-responsive angina •smoking cessation
•occurs predominantly at rest, often 12am to early morning 2) transient ischemic EKG changes •ASCVD risk factor modification
•lasts 5-15 minutes, responds rapidly to NTG 3) angiographic evidence of coronary artery spasm
– defined as >90% constriction CCBs: diltiazem, amlodipine, etc.
Possible triggers: •prevent vasoconstriction & promote
•changes in autonomic activity (↑ vagal tone) EKG: normal between episodes vasodilation in coronary vasculature
•cocaine, amphetamines, marijuana, alcohol •transient ST-elevation/depression
•ephedrine-based products, triptans, 5-FU, ergonovine If ⊕ EKG findings à cardiac troponins to r/o MI AVOID:
•Mg deficiency, hyperventilation, allergic reactions •troponins ⊖ in vasospastic angina •nonselective beta blockers
•exposure to extreme cold – e.g., propranolol
Exercise stress test, ambulatory EKG monitoring – can exacerbate vasospasm
PE: +/- tachycardia, HTN, diaphoresis, S4 gallop
ANTIANGINAL RX About
Beta Blockers β1-Selective: MOA: beta-1 receptor antagonism; ↓ myocardial oxygen demand ADRs: bradycardia, hypotension, fatigue, dizziness, depression
Bisoprolol Metoprolol •↓ HR (⊖chronotropy), ↓ contractility (⊖inotropy), ↓ LV wall tension (↓ preload) Warning: can mask signs of hypoglycemia in pts w/ diabetes
Betaxolol Acebutolol
Atenolol Indications: chronic stable angina, unstable angina; *mortality benefit (1st-line agents) BOXED WARNING: do not stop BB therapy abruptly = rebound angina
Contraindications: vasospastic (variant) angina, acute HF, 2nd/3rd degree heart block
Nitrates Short-acting: Long-acting topical: MOA: nitrates release nitric oxide (NO) within smooth muscle cells which causes ↑ cGMP, leading Contraindications: use w/ PDE-5 inhibitors
(Vasodilators) NTG SL tablet NTG ointment 2% to relaxation of vessels – sildenafil (Viagra), tadalafil, vardenafil, avanafil
NTG SL powder NTG TD patch •↓ myocardial O2 demand: ↓ venous return (↓ preload) which ↓ LV wall tension
NTG TL spray Long-acting PO: •↑ myocardial O2 supply: ↑ blood flow through collateral arteries (non-atherosclerotic arteries) ADRs: dizziness/lightheadedness, flushing, syncope
ISMN Indications (short-acting): recommended for all patients w/ angina for immediate relief Warnings: hypotension, HA
ISDN Indications (long-acting): used when beta blockers are contraindicated or as add-on therapy – long-acting formulation à tolerance (tachyphylaxis)
Calcium DHPs: Non-DHPs: MOA: inhibit calcium entry/release into myocardial cell, ↓ cardiac workload & O2 demand Non-DHPs
Channel Nifedipine Verapamil •↑ myocardial blood supply Indications: unstable angina (Verapamil), stable angina, Prinzmetal
Blockers Amlodipine Diltiazem DHPs Contraindications: SBP <90, cardiogenic shock, 2nd/3rd degree AV block,
(CCBs) Indications: stable angina, Prinzmetal; preferred over non-DHP when used in combo w/ BB acute MI, pulmonary congestion
ADRs: flushing, HA, peripheral edema, reflexive tachycardia, gingival hyperplasia ADRs: edema, HA, dizziness, constipation (verapamil), gingival
Warnings: excess hypotension, worsening angina or MI d/t reflexive tachycardia, HF (exacerbate hyperplasia
edema), hepatic function Warnings: sinus bradycardia, AV nodal block, hypotension, HF, ↑ LFTs
Ranolazine MOA: may ↓ myocardial O2 demand by ↓ late phase Na current which facilitates Ca entry via the Contraindications: liver cirrhosis, use w/ strong 3A4 inhibitors
(Ranexa) Na-Ca exchanger
•↓ ventricular tension, ↓ cardiac contractility, improved blood flow ADRs: constipation, nausea, dizziness, HA
Indications: option for patients who are intolerance to BB or need additional symptom relief, *no Warnings: prolongs QT interval in pts w/ CAD, can lead to torsades &
mortality benefit death – do NOT use if someone has prolonged QT
 About
Acute ACS is spectrum of unstable cardiac ischemia
Coronary •UA ↔ NSTEMI ↔ STEMI
Syndrome
(ACS) Unstable Angina (UA):
•ischemia w/o necrosis, partial obstruction
•+/- EKG findings, ⊖biomarkers
Non-ST Elevation Myocardial Infarction (NSTEMI):
•ischemia w/ necrosis, partial obstruction
•+/- EKG findings, ⊕biomarkers
ST-Elevation Myocardial Infarction (STEMI):
•ischemia w/ necrosis, complete obstruction
•⊕EKG findings, ⊕biomarkers
PATHO: insufficient O2 supply to cardiac muscle demands
•progressive growth of atherosclerotic lesions within the
coronary arteries à decreased luminal diameter &
coronary blood flow
•acute coronary plaque disruption à exposed
thrombogenic endothelium à platelet aggregation &
thrombus formation
Universal MI Classification:
•Type 1: spontaneous MI
•Type 2: secondary to ischemic imbalance (excluding CAD)
•Type 3: MI resulting in death w/o biomarkers
•Type 4: MI related to PCI
•Type 5: Mi related to CABG
Early Complications of MI:
•heart failure, cardiogenic shock, bradyarrhythmias, AV
block, tachyarrhythmias
•LV free wall rupture, interventricular septum rupture,
papillary muscle rupture
Late Complications of MI:
•LV thrombus, LV aneurysm
•Pleuropericarditis (Dressler Syndrome)
– 2-10wk post-MI fever, leukocytosis, friction rub
– pericardial or pleural effusion
Clinical Manifestations
UA: new-onset angina, angina w/
increasing frequency or duration, angina
w/ minimal exertion or at rest
MC: substernal chest tightness/pressure
•radiates to L arm, neck/jaw, epigastrium
•occurs at rest, lasts >30min
Levine sign: clenched fist over chest
Associated S/SXS:
•dyspnea, diaphoresis, nausea
•sense of impending doom
Atypical, “silent” presentation: dyspnea,
weakness, sweating, N/V, epigastric pain,
palpitations, dizziness, fatigue
*women, elderly, diabetics
PE: often nonspecific
•pallor, diaphoresis, tachypnea
Cardiogenic Shock: hypotension,
tachycardia, confusion, diaphoresis, pallor
Heart Failure: JVD, pulmonary crackles,
S3/S4 gallop, MR murmur
RV Infarction:
➀ hypotension ➁ JVD ➂ clear lung fields
plus ⇨ evidence of inferior MI on EKG
Diagnostics
EKG within 10mins of arrival, 1st often not diagnostic
*repeat q15-30mins until definitive diagnosis made
Classic Evolution of STEMI:
STEMI EKG Findings:
•ST elevations ≥1mm in 2 contiguous leads
•new LBBB, new Q waves
UA/NSTEMI EKG Findings:
•normal, T wave inversions, ST depressions
⊕EKG changes in inferior leads à think RV infarction!!
– get R-sided EKG
– ⊕RV infarction (RCA) = ST elevation in V4R
ST depression* in V1 & V2 = posterior infarction
Cardiac enzymes: initial, 3-6h later
•high sensitivity cardiac troponins I & T preferred
– hs-cTnI, hs-cTnT; ⊕ = >99%ile of ULN
– rise within 2-3h, peak 12-24h, normalize in 7-10d
•CK-MB
– rise within 3-4h, peak 12-24h, normalize in 1-2d
•myoglobin
– rise within 1-2h, peak 4-6h, normalize in 24h
STEMI/NSTEMI = ⊕biomarkers, UA = ⊖biomarkers
Management
AMI protocol: EKG within 10min, door to PCI within
90min (120min w/ travel to PCI facility)
IMMEDIATE MEASURES FOR ALL PTS: ANOM
•aspirin 162-325mg chewed (non-enteric-coated)
•0.4mg SL NTG q5min x3 dose MAX
*AVOID in inferior, PDE-5 inhibitor in last 24h
•O2 (if SpO2 <90%), morphine (if refractory to NTG)
Initiate within first 24h:
•beta blocker
*AVOID in RVMI, acute HF, bradycardia, AV block
•ACEI/ARB
•high-intensity statin
ADDITIONAL THERAPIES FOR ALL ACS:
•antiplatelet drug (P2Y12) + AC (UFH, LMWH)
*GP IIb/IIIa antagonists not routinely used
STEMI: reperfusion therapy, PCI preferred
– placement of drug-eluting stent (DES) MC
*fibrinolysis only recommended if PCI unavailable
within 120min
UA/NSTEMI: TIMI score to assess need for PCI
*fibrinolysis NOT useful in UA/NSTEMI
Score ≥3 = benefit to early revascularization (PCI)
Conservative TX: medical therapy + risk
stratification w/ noninvasive assessment of LV
function & stress testing
•if recurrent angina, ↓ LV function, or evidence of
significant ischemia à angiography indicated
DISHCARGE MEDS FOR ALL PTS:
•DAPT (ASA 81mg + P2Y12) continued ≥1y
– ASA 81mg indefinitely even after P2Y12 DC’d
•beta blocker + ACEI + statin continued indefinitely
ANTIPLATELET RX About
Aspirin (ASA) MOA: irreversibly binds to/inhibits COX-1/COX-2 enzymes, dose-related effects Contraindications: NSAID/salicylate allergy, asthma, rhinitis, nasal
•COX-1 inhibition = TXA2 inhibition = ↓ platelet activation/aggregation, ↓ vasodilation polyps, children w/ viral infection (Reyes)
– cardioprotective effects 75-160mg ADRs: *bleeding, dyspepsia, heartburn, nausea
Indications: ACS (chewed), secondary prevention of CV death, MI, & stroke *mortality benefit Warnings: tinnitus, severe skin rash (rare)
ADP Receptor Irreversible: Reversible: MOA: bind ADP P2Y12 platelet receptor, inhibiting ADP-induced platelet aggregation Contraindications: serious active bleed
Antagonists (P2Y12 Clopidogrel Ticagrelor (Brilinta) Indications: ACS ADRs: bleeding
Inhibitors) Prasugrel Cangrelor – Clopidogrel: ACS, secondary prevention of MI, stroke, & PAD Warnings: stop 7d before elective CABG
ANTICOAGULANT RX About
Indirect Thrombin UFH LMWH: MOA: bind to antithrombin III to accelerate its activity which enhances inactivation of Contraindications: hx of HIT, active bleed, severe thrombocytopenia
Inhibitors Enoxaparin (Lovenox) thrombin & factor Xa, prevents new clot formation ADRs: bleeding, thrombocytopenia, HIT
Fondaparinux Dalteparin Indications: ACS, VTE
Direct Thrombin Bivalirudin MOA: reversibly binds to both circulating & clot-bound thrombin, inhibiting fibrin activation Contraindications: active major bleeding
Inhibitor Indications: pts undergoing PCI as an alternative to heparin ADRs: bleeding, anemia, hematoma
Monitor: activated clotting time (ACT), aPTT, PT/INR
ADJUNCT TX RX About
Beta Blockers β1-Selective: ⍺ + β blockers: MOA: block sympathetic stimulation, ↓ myocardial oxygen demand by ↓ HR/BP & ↓ Contraindications: RV MI, active HF (pulmonary edema), 2nd/3rd
Bisoprolol Carvedilol contractility; ↓ risk of VFIB, improve LV function degree block, asthma, hypotensive, bradycardia, prolonged PR >0.30s
Metoprolol Indications: ALL ACS pts should have BB initiated within first 24h & continued indefinitely *if s/sxs of active HF, delay initiation until HF under control
Atenolol *mortality benefit ADRs: sexual dysfunction, sedation, fatigue, depression
Warnings: do not stop BB abruptly (rebound angina), may mask s/sxs of hypoglycemia
Statins Simvastatin Atorvastatin MOA: inhibit the rate-limiting step in hepatic cholesterol synthesis via inhibition HMG-CoA Contraindications: active hepatic disease, persistent elevated LFTs,
Pravastatin Rosuvastatin reductase; increase LDL receptors, promoting LDL clearance; reduce triglycerides pregnancy/breastfeeding
Lovastatin Indications: best drug to decrease LDL; have been shown to decrease cardiovascular ARDs: muscle damage (myositis, rhabdomyolysis), ↑ LFTs, hepatitis,
complications GI sxs, DM
FIBRINOLYSIS RX About
Tissue Plasminogen Alteplase (tPA) MOA: activate plasminogen to plasmin which degrades fibrin ADRs: bleeding, hypotension
Activators Reteplase (rPA) Indications: STEMI ONLY, alternative if PCI unavailable within 120min & sxs onset ≤12h, less Monitoring: BP q30-60min, EKG for arrhythmias/ST changes,
Tenecteplase (TKA) evidence if sxs onset 12-24h cTnI/cTnT q4h x24h
Absolute Contraindications: active internal bleed, any hx of ICH, CVA in past 1y, known
intracranial neoplasm, suspected aortic dissection or pericarditis Discharge: continue DAPT ≥1y

Dyspnea on Exertion
Arrhythmia: AFIB, inappropriate sinus tachycardia, sick sinus syndrome/bradycardia
•HX: palpitations, syncope
•PE: irregular rhythm, pauses
•DX: EKG, event recorder, Holter monitor, stress testing

Myocardial: cardiomyopathies, coronary ischemia

•HX: DOE, PND, orthopnea, chest pain or tightness, prior coronary artery disease or AFIB
•PE: edema, JVD, S3, displaced cardiac apical impulse, hepatojugular reflux, murmur, crackles, wheezing, tachycardia, S4
•DX: EKG, BNP, echo, stress testing, coronary angiography

Restrictive: constrictive pericarditis, pericardial effusion/tamponade

•HX: chest pain, dyspnea
•PE: paradoxical pulse (exaggerated variation in BP w/ respiration)
•DX: EKG showing low voltage QRS w/ electric alternans; echo w/ increased pericardial fluid; radiograph: water bottle heart

Valvular: aortic insufficiency/stenosis, congenital heart disease, mitral valve insufficiency/stenosis

•HX: DOE
•PE: murmur, JVD
•DX: echo
 About
Dilated Systolic dysfunction, leading to a dilated, weak heart
Cardiomyopathy
Risk Factors: MC 20-60yrs, men
(MC!!)
Etiologies:
•idiopathic MCC
•enterovirus – Coxsackievirus B
•toxic: alcohol abuse, cocaine, doxorubicin
•metabolic: vitamin B1 (thiamine) deficiency
Hypertrophic •Autosomal dominant genetic disorder of
Cardiomyopathy inappropriate LV &/or RV hypertrophy w/ diastolic
dysfunction
•Subaortic outflow obstruction due to asymmetrical
septal hypertrophy & systolic anterior motion of the
mitral valve
The obstruction worsens w/:
•↑ contractility (exercise, Digoxin, beta agonists)
•↓ LV volume (dehydration, decreased venous return,
Valsalva maneuver)
Restrictive Diastolic dysfunction in a non-dilated ventricle, which
Cardiomyopathy impedes ventricular filling (decreased compliance); the
stiff ventricle fills w/ great effort
Etiologies:
•infiltrative diseases: amyloidosis MC, sarcoidosis,
hemochromatosis
Stress Transient regional systolic dysfunction of the LV that
(Takotsubo) can imitate MI but is associated w/ absence of
Cardiomyopathy significant obstructive coronary artery disease or
evidence of plaque rupture
Risk Factors: postmenopausal women exposed to
physical or emotional stress
PATHO: thought to be multifactorial, including
catecholamine surge during physical or emotional
stress, microvascular dysfunction, & coronary artery
spasm
Clinical Manifestations
Systolic heart failure
•L-sided failure: dyspnea, fatigue
•R-sided failure: peripheral edema, JVD,
hepatomegaly, GI sxs
•embolic events, arrhythmias
PE:
•S3 gallop hallmark
•mitral or tricuspid regurgitation
•dyspnea MC symptom
•fatigue, angina, syncope, dizziness, arrhythmias
•sudden cardiac death, esp. in adolescent or
preadolescent children esp. during times of
extreme exertion usually due to VFIB
PE: harsh systolic murmur best heart at LLSB
↑ intensity:
•↓ venous return (Valsalva, standing)
•amyl nitrate (decreased afterload)
↓ intensity:
•↑ venous return (squatting, supine, leg raise)
•handgrip (increased afterload)
•may have loud S4, mitral regurgitation, or pulsus
biferiens
R-sided HF > L-sided HF
•R-sided failure: peripheral edema, JVD,
hepatomegaly, ascites, GI sxs
•L-sided failure: dyspnea, fatigue
•Kussmaul’s sign: increased in JVP w/ inspiration
Similar to ACS
•substernal chest pain
•dyspnea, syncope
Diagnostics
Echo:
•left ventricular dilation, thin ventricular walls
•decreased EF, ventricular hypokinesis
Chest x-ray: cardiomegaly, pulmonary edema,
pleural effusion
EKG: may show sinus tachycardia or arrhythmias
Echo
•asymmetric ventricular wall thickness
(especially septal)
•systolic anterior motion of the mitral valve
•small LV chamber size
EKG:
•LVH
Echo:
•non-dilated ventricles w/ normal thickness
•diastolic dysfunction
•marked dilation of both atria
EKG: ST elevations (esp. in anterior leads); may
have ST depressions
Cardiac enzymes: often +
Coronary angiography: absence of acute plaque
rupture or obstructive coronary disease
Echo: transient regional left ventricular systolic
dysfunction, esp. apical left ventricular
ballooning; usually performed after ACS has
been r/o
Management
•ACEI, BB
•diuretics
•automated implantable
cardioverter/defibrillator if EF <35-30%
•BBs, CCBs, disopyramide
•myomectomy, alcohol septal ablation
*pts should avoid dehydration, extreme
exertion, & exercise; cautious use of digoxin,
nitrates, & diuretics
Treat the underlying disorder
Initial:
- ASA, NTG, BB, heparin, coronary angiography
Short-term: conservative & supportive
- BBs
- ACEI for 3-6mo
- serial imaging to assess for improvement
- anticoagulation in some w/ severe LV
dysfunction or if thrombus present
 About Clinical Manifestations Diagnostics Management
Pericarditis Inflammation of the pericardium, the outer layer of Chest pain: sudden onset EKG: diffuse ST elevations in the precordial leads Anti-inflammatory meds: NSAIDs or ASA x7-14d
the heart •pleuritic (sharp, worse w/ inspiration) w/ associated PR depressions in those leads - colchicine second line
Fibrinous or serofibrinous: e.g., post-MI, infectious •persistent
•postural (worse when supine & improved w/ Dressler Syndrome: ASA or colchicine
Etiologies: sitting forward) - avoid NSAIDs because they can interfere w/
•2 MCC – idiopathic, viral (Coxsackievirus & •pain may radiate to back, shoulder, neck, arm, or myocardial scar formation
echovirus) epigastric area
•Dressler syndrome (post MI pericarditis + fever +
pleural effusion) Pericardial friction rub: best heard at end
expiration while upright & leaning forward
Pericardial Accumulation of fluid in the pericardial space •chest pain (if associated w/ acute pericarditis) Echo: test of choice – increased fluid in Treat the underlying cause (acute pericarditis)
Effusion Normally, about 5-15ml of fluid is in the pericardial •dyspnea, fatigue pericardial space Serial echo if needed
space EKG: electrical alternans (alternating amplitudes
Etiologies: viral, idiopathic, immune, malignancy – lung PE: decreased (muffled) heart sounds (due to of the QRS complexes); low QRS voltage Large effusions may need pericardiocentesis for
cancer MC, breast second MC, aortic dissection, fluid) CXR: “water bottle” heart symptomatic relief
uremia
Cardiac Pericardial effusion causing significant pressure on Beck’s triad: distant (muffled) heart sounds + ↑ Echo: pericardial effusion + diastolic collapse of IMMEDIATE PERICARDIOCENTESIS to remove
Tamponade the heart, impeding cardiac filling, leading to JVP + systemic hypotension cardiac chambers the pressure
decreased CO & shock - volume resuscitation & pressor support if
EMERGENCY Pulsus paradoxus: exaggerated (>10mmHg) ↓ in EKG: low voltage QRS complexes, electrical needed
Etiologies: complication of acute pericarditis or systolic pressure w/ inspiration alternans - pericardial window drainage if recurrent
trauma; malignancy MC non-traumatic cause
Dyspnea, fatigue, peripheral edema, shock, reflex CXR: may show enlarged cardiac silhouette
tachycardia, cool extremities
Right heart catheterization: equalization of
pressures in diastole
Constrictive Loss of pericardial elasticity (thickening, fibrosis, •dyspnea (MC), fatigue, orthopnea CXR: pericardial calcification may be seen esp. on Diuretics for symptom relief as well as
Pericarditis calcification) leading to restriction of ventricular lateral view, clear lung fields reduction of edema & venous pressure
diastolic filling Right-sided HF signs: •normal or slightly increased heart size
•↑ JVD, peripheral edema, N/V •square root sign on cardiac catheterization Definitive: pericardiectomy
PATHO: fibrosis limits ventricular filling, decreased •↑ hepatojugular reflex
stroke volume & cardiac output •Kussmaul’s sign (the lack of an inspiratory Echo: pericardial thickening &/or calcification
decline or an ↑ in jugular vein pressure w/ (also used to r/o restrictive cardiomyopathy)
Etiologies: any cause of acute pericarditis inspiration) •”square root” sign – early diastolic dip followed
•US – idiopathic & viral MCC by a plateau if diastasis
•worldwide – TB MCC Pericardial knock: high pitched diastolic sound
similar to S3 (sudden cessation of ventricular CT scan/MRI: pericardial thickening or
filling) calcification
Valvular Disorders About
Aortic Stenosis PATHO: LV outflow obstruction leads to a
(AS) fixed CO, ↑ afterload, LVH, & eventually
lV failure
SYSTOLIC
MC VALVULAR DISEASE – sxs usually occur
when Aov <1cm2
Etiologies:
•degenerative: calcification, wear & tear,
>70
•congenital & bicuspid valve (pts <70)
•Rheumatic Heart Disease: +/- aortic
regurg.
Aortic Incomplete aortic valve closure leads to
Regurgitation LV volume overload w/ eventual LV
(AR) dilation & HF
DIASTOLIC Etiologies:
•acute: acute MI, aortic dissection,
endocarditis; can lead to pulmonary
edema
•chronic: aortic dilation – Marfan
syndrome, inflammatory disorders,
rheumatic fever, syphilis, HTN
Mitral PATHO: abnormal, retrograde blood flow
Regurgitation from the LV into the LA, leading to LA
(MR) dilation & increased pulmonary pressure
SYSTOLIC Etiologies:
•leaflet abnormalities: MVP MCC in US,
rheumatic fever MCC in developing
countries
-endocarditis, valvulitis, LV dilation
-Marfan syndrome
•papillary muscle dysfunction: myocardial
ischemia or infarction, cardiomyopathy
•ruptured chordae tendinae: collagen
vascular disease, dilated cardiomyopathy
Mitral Stenosis PATHO:
(MS) •obstruction of flow from LA to LV
secondary to narrowed mitral orifice à
DIASTOLIC blood backs up into the left atrium
•↑ L-atrial pressure/volume overload à
pulmonary congestion à pulmonary HTN
à CHF
Etiologies:
•rheumatic heart disease almost always
the cause – MC in 3rd/4th decade
•congenital, left atrial myxoma,
thrombus, valvulitis (SLE, amyloid,
carcinoid)
S/Sxs Murmur
Once symptomatic, lifespan is Systolic crescendo-decrescendo murmur
dramatically reduced •location: RUSB, radiates to carotid artery
•dyspnea ↑ intensity:
•angina •sitting while leaning forward
•syncope •↑ venous return (squatting, supine, leg raise)
•CHF •expiration
↓ intensity:
•↓ venous return (Valsalva, standing)
•inspiration
•handgrip (d/t ↓ ejection of blood)
•weak, delayed carotid pulse (pulsus parvus et
tardus), narrow pulse pressure
Signs of widened pulse pressure Diastolic blowing decrescendo murmur
(seen in chronic) •location: LUSB
Water Hammer pulse: swift
upstroke & rapid fall of radial ↑ intensity:
pulse accentuated w/ wrist •sitting while leaning forward
elevation •↑ venous return (squatting, supine, leg raise)
•expiration, handgrip
Corrigan’s pulse (carotid)
↓ intensity:
Hill’s sign (most sensitive) •↓ venous return (Valsalva, standing)
•popliteal > brachial BP by •inspiration, amyl nitrate
60mmHg
Austin-Flint Murmur: mid-late diastolic rumble
•bounding pulses, pulsus @ apex secondary to retrograde regurgitant jet
bisferiens competing w/ antegrade flow from LA into LV
Chronic: Blowing holosystolic murmur
•HF sxs – dyspnea, fatigue •location: apex, radiates to axilla
•AFIB
•hemoptysis, HTN ↑ intensity:
•left lateral decubitus, expiration, exercise
Acute: •↑ venous return (squatting, supine, leg raise)
•pulmonary edema •handgrip
•hypotension
↓ intensity:
•↓ venous return (Valsalva, standing)
•inspiration, amyl nitrate
•dyspnea, hemoptysis Low-pitched, mid-diastolic rumbling murmur
•pulm. HTN •location: apex
•AFIB *enlarged atria •prominent S1, opening snap
•right-sided HF
↑ intensity:
Mitral facies = flushed cheeks •left lateral decubitus, expiration, exercise
w/ facial pallor •↑ venous return (squatting, supine, leg raise)
Ortner’s Syndrome: laryngeal ↓ intensity:
nerve compression à hoarse •↓ venous return (Valsalva, standing)
•inspiration
Diagnostics
Echo:
•small aortic orifice
•LVH
•calcified aortic valve
EKG: LVH
•left atrial enlargement, AFIB
CXR: nonspecific
•postaortic dilation
•aortic valve calcification
•pulmonary congestion
Cardiac catheterization: definitive
Echo: regurgitant jet
Cardiac catheterization: definitive
Echo:
•hyperdynamic LV, regurgitant jet
EKG: nonspecific
•left atrial enlargement, LVH
•AFIB
CXR: nonspecific
•left atrial enlargement, LVH
•pulmonary edema
EKG:
•left atrial enlargement
•AFIB
•pulmonary HTN
Echo
CXR: left atrial enlargement
Cardiac catheterization
Management
Surgical therapy: replacement only
effective treatment
•indications: symptomatic, ↓ EF, or area
<0.6cm2)
-mechanical: long-term anticoag.
-bioprosthetic
Percutaneous aortic valvuloplasty (PAV)
•used as a bridge to AVR, if not a
surgical candidate, or in peds
Intraaortic balloon pump: *bridge to
AVR
Severe AS prior to surgery:
•avoid PA/vasodilators (nitrates)
•avoid (-) inotropes (CCBs, BBs)
Medical therapy: afterload reduction
•ACEI, ARBs, nifedipine, hydralazine
Surgical: definitive
•indications: acute or symptomatic,
asymptomatic w/ LV decompensation
(EF <55%)
Medical: sxs control w/ afterload
reducers or diuretics
•ACEI, ARBs, hydralazine, nitrates
Surgical: repair > replacement
•indications: EF ≤60%, refractory to
medical therapy
Percutaneous balloon valvuloplasty:
•best tx for symptomatic MS in younger
pts w/ noncalcified valves or if refractory
to medical therapy
Mitral valve replacement: reserved if
mitral valvuloplasty is contraindicated or
w/ unfavorable valve morphology
Medical:
•diuretics & sodium restriction for
edema & volume overload
•rate control of AFIB w/ BBs, CCBs, or
digoxin (anticoag. for AFIB – warfarin)
 Endocrinology 8%
Thyroid About Clinical Manifestations Diagnostics Management
Hyperthyroidism Causes: Clinical hyperthyroidism – diffuse, enlarged thyroid TFTs: Grave’s:
•Grave’s Disease (MC) •↑ metabolic rate (except menstrual flow which ↓) •Grave’s, TMG/TA: ↑ FT4/FT3, ↓ TSH - radioactive iodine (MC therapy)
•toxic multinodular goiter (Plummer’s Disease) •heat intolerance •TSH secreting pituitary adenoma: ↑ FT4/FT3, ↑ TSH - methimazole or PTU
•toxic adenoma •weight loss (despite ↑ appetite) •PTU preferred in pregnancy
•TSH secreting pituitary adenoma •skin warm, moist, soft RAIU: - BBs (propranolol) for sxs relief
•amiodarone •fine hair, alopecia, easy bruising •Grave’s: ↑ diffuse uptake - thyroidectomy
•hyperactivity: anxiety, tremors, nervousness, fatigue, •TMG: patchy areas of both ↑ & ↓ uptake - ophthalmopathy: glucocorticoids
Grave’s: autoimmune – TSH receptor antibodies weakness, increased sympathetic •TA: ↑ local uptake (hot nodule)
cause ↑ thyroid hormone synthesis, release, & •diarrhea, hyperdefecation •TSH secreting pituitary adenoma: ↑ diffuse uptake
thyroid gland growth worse w/ stress •tachycardia, palpitations TMG/TA:
(pregnancy, illness) •high-output heart failure Grave’s: + TSH-receptor Ab (hallmark) - radioactive iodine (MC therapy)
+/- thyroid peroxidase, anti-TG Ab - subtotal thyroidectomy
Thyrotoxic Crisis (Thyroid Storm): potentially Grave’s: - methimazole or PTU
fatal complication of untreated thyrotoxicosis •ophthalmopathy: lid lag, exophthalmos/proptosis - BBs for sxs of thyrotoxicosis
usually after a precipitating event •pretibial myxedema: nonpitting, edematous, pink-brown TSH secreting pituitary adenoma:
plaques/nodules on skin •pituitary MRI: adenoma TSH secreting pituitary adenoma:
*Pemberton’s sign •thyroid bruits - transsphenoidal surgery to remove

TMG/TA: Thyroid Storm:

•no skin/eye changes - IV fluids
•compressive sxs: dyspnea, dysphagia, stridor, hoarseness - propranolol
-due to laryngeal compression - PTU; 1hr later à IV sodium iodide
- IV glucocorticoids
TSH secreting pituitary adenoma: - antipyretics (AVOID ASPIRIN)
•bitemporal hemianopsia
-due to compression of optic chiasm
•HA, mental disturbances

Thyroid Storm:
•hyperthyroid sxs (exaggerated) & hypermetabolic state
-high fever (104-106F)
-CV dysfunction (palpitations, AFIB, CHF)
-CNS dysfunction (delirium, psychosis, coma)
Hypothyroidism Causes: Clinical hypothyroidism – painless, enlarged thyroid TFTs: ↓ FT4/FT3, ↑ TSH Hashimoto:
•Hashimoto (Chronic Lymphocytic) – MC •↓ metabolic rate (except menstrual flow which ↑) - levothyroxine
•medications: amiodarone, lithium, alpha •cold intolerance Hashimoto: •monitor TSH @ 6wk intervals
interferon •weight gain (despite ↓ appetite) •(+) anti-thyroid peroxidase &/or anti-TG Ab •ADRs: adverse CV effects, osteoporosis
•dry, thick roughened skin •bx: lymphocytes, germinal follicles, Hurthle
Hashimoto: autoimmune thyroid cell destruction •loss of outer 1/3 eyebrow Medication-Induced:
by anti-thyroid peroxidase & anti-thyroglobulin •hypoactivity: fatigue, sluggishness, memory loss, - often returns to euthyroid when D/C
antibodies depression, ↓ DTR - corticosteroids
•hoarseness of voice
Myxedema Coma: extreme form of •constipation, anorexia Myxedema Coma:
hypothyroidism usually d/t an acute •bradycardia, decreased CO - IV levothyroxine
precipitating factor – MC seen in elderly women •pericardial effusion - supportive: warming, IV fluids
in winter - IV glucocorticoids
Hashimoto:
•myxedema: nonpitting (periorbital, peripheral)

Medication-induced:
•thyrotoxicosis à hypothyroid (depends when they
present)

Myxedema Coma: exaggerated hypothyroidism

•bradycardia
•hypothermia
•hypotension
Thyroid Carcinoma Papillary Thyroid Carcinoma Follicular Thyroid Carcinoma Medullary Thyroid Carcinoma Anaplastic Thyroid Carcinoma
MC thyroid cancer 2nd MC type of thyroid cancer Derived from calcitonin-synthesizing Rare; MC seen in elderly >65yrs
- least aggressive, best prognosis - slow growing parafollicular C cells - most aggressive
- MC 40-60yrs - 90% sporadic - poor prognosis
Risk Factors: - 10% associated w/ MEN IIa or IIb
•MC after radiation exposure of head/neck Risk Factors: Presentation: rapid growth, compressive sxs
•↑ incidence w/ iodine deficiency Labs:
Presentation: painless thyroid nodule •METS: distant METS MC than local (lung MC) •↑ calcitonin PE: “rock” hard thyroid mass
“Follicular goes Far”
Workup: Management: Management:
•FNA Workup: - total thyroidectomy - most not amenable to surgical resection
•TFTs usually normal •FNA cannot distinguish from follicular adenoma - external beam radiation, chemo
•definitive: post-op histologic testing Monitoring: - palliative tracheostomy to maintain airway
Management: - calcitonin to monitor for recurrence or residual
- thyroidectomy (total or near total) Management:
- post-op levothyroxine - thyroidectomy (total or near total)
- post-op levothyroxine
Post-Op Monitoring:
- thyroglobulin Post-Op Monitoring:
- TSH - thyroglobulin
- neck U/S - TSH
- neck U/S

Thyroid Nodule About Clinical Manifestations Diagnostics Management

>90% benign
Risk Factors: extremes of age, hx of
head/neck radiation
Benign:
•follicular adenoma (colloid) MC nodule
•adenomas, cysts, localized thyroiditis
Most are asymptomatic TFTs – initial test Surgical excision if thyroid cancer is
Compressive sxs: difficulty swallowing or breathing, •TSH subnormal/low à RAIU suspected
hoarseness •TSH normal/high à FNA w/ bx
Functional nodules: rare – presents w/ thyrotoxicosis Observation + follow-up U/S every 6-12mo
Thyroid U/S
PE: •suspicious: irregular margins, hypoechoic, central vascularity,
•benign: varied presentation documented nodule growth
•malignant: rapid growth, fixed, no movement w/
swallowing FNA: best to evaluate etiology
•performed in nodules >1.5cm w/ normal TSH or highly
suspicious

RAIU:
•cold nodule (no/low uptake) à bx to r/o malignancy
 Adrenal Gland: GFR, ACE – glomerulosa (aldosterone), fasciculata (cortisol), reticularis (estrogens/androgens), medulla (epi/norepinephrine)
Adrenal About
Carcinoma Rare disease that can also be functional but
should be considered on the differential of
“Adrenal any adrenal mass, esp. tumors >4cm
Cortical Cancer •less common benign masses include
(ACC)” myelolipoma/lipoma, ganglioneuroma,
epithelial cyst, & pseudocyst
Nearly 4% of abdominal CT scans obtained for
another indication demonstrate an incidental
adrenal mass
•adrenal tumors can also be detected
clinically due to manifestations of tumor
hormone production
•of all adrenal masses, 80% are nonfunctional
adenomas, while 15% are functional w/
laboratory evidence of hormonal production
Functional tumors include:
•pheochromocytomas
•aldosteronoma
•cortisol-producing adenomas
Diagnostics Management
Virilizing features, mixed cortisol & aldosterone hypersecretion, heterogenous or large adrenal tumors (>4cm) Adrenalectomy
should raise suspicion of ACC or those w/ imaging characteristics outlined below should be considered high risk
for ACC
Labs:
•plasma fractionated metanephrines – must r/o pheochromocytoma for any adrenal mass
•serum potassium & aldosterone & plasma renin
•24hr urinary-free cortisol or dexamethasone suppression test
•DHEA-S
CT scan:
Adrenal cortical cancer typical characteristics:
•size >4cm
•high attenuation (>10 Hounsfield units)
•enhancement on contrast-enhanced phase
•delayed contrast washout (<50% washout at 10min post-contrast)
•calcifications
•irregular shape
•central necrosis
Adenoma typical characteristics:
•low attenuation (<10 Hounsfield units)
•rapid washout (>60% washout at 15min post-contrast)
•smooth borders

MRI
•adenoma: lipid-rich – signal intensity loss on out-of-phase sequences
•pheochromocytoma: high intensity on T2 images
•ACC: central necrosis, hemorrhage, calcification, local invasion, IVC tumor thrombus

PDG-PET: pheochromocytoma & ACC are FDG-avid (adrenal to liver max SUV ratio >1.45)

Pheochromocytoma About Clinical Manifestations Diagnostics Management

•catecholamine-secreting adrenal tumor (chromaffin HTN most consistent finding – may be temporary or Biochemical testing: plasma Complete adrenalectomy after at least 1-2wks
cells) sustained fractionated metanephrines confirmed of medical therapy
•rare (causes 0.1-0.5% HTN) but MC adrenal tumor in by 24hr urinary fractionated
adults PHE: catecholamines including metabolites Medical therapy:
•may be associated w/ MEN II, neurofibromatosis type I, •Palpitations •↑ metanephrines •nonselective alpha blockade:
& von Hippel-Lindau disease •Headache •↑ vanillylmandelic acid phenoxybenzamine or phentolamine 1-2wks à
•Excessive sweating BB/CCBs to control BP prior to surgery
90% benign; rule of 10s – 10% malignant, 10% bilateral, MRI or CT of abdomen & pelvis
10% seen in children, 10% extra-adrenal (paraganglioma) •chest or abdominal pain, weakness, fatigue, Do NOT initiate therapy w/ beta-blockade to
weight loss (despite appetite), & pallor MIBG scanning: nuclear isotope that can prevent unopposed alpha constriction during
PATHO: detect tumors outside of the adrenal catecholamine release triggered by surgery or
•secretes norepinephrine, epinephrine, & dopamine gland if CT or MRI is negative spontaneously, which could lead to life-
autonomously & intermittently – triggers include surgery, threatening HTN crisis
exercise, pregnancy, meds (TCAs, opiates,
metoclopramide, glucagon, histamine)
 Fatigue
6-12wks of fatigue is not unusual during recovery from even minor surgery
•meds commonly associated w/ fatigue: sedative-hypnotics, antidepressants, muscle relaxants, opioids, antihypertensives, antihistamines, & many type of abx
DDX: endocrine/metabolic causes of fatigue
•hypothyroidism
•diabetes mellitus
•pituitary insufficiency
•hypercalcemia
•adrenal insufficiency
•chronic renal failure
•hepatic failure
Laboratory testing:
•CBC – anemia
•ESR
•chemistry panel – liver disease, renal failure, protein malnutrition
•TFTs – hypothyroidism
•HIV antibodies – if not previously tested
•pregnancy test

Hyperparathyroidism About Clinical Manifestations Diagnostics Management

Excess PTH Signs of hypercalcemia: “stones, bones, Triad: hypercalcemia + ↑ PTH + ↓ phosphate Parathyroidectomy
abdominal groans, psychiatric moans”
Etiologies: •nephrolithiasis •↑ 24hr urine calcium excretion, ↑ vitamin D •Cinacalcet if not surgical candidate
•parathyroid adenoma MCC; parathyroid hyperplasia or •painful bones, fractures
enlargement •ileus, constipation, N/V Ancillary: may have osteopenia on bone scan; imaging Very high calcium:
•lithium •weakness, ↓ DTRs studies to detect parathyroid adenoma (U/S or nuclear •IV fluids, furosemide, calcitonin
•MEN I & IIa scanning)

Palpitations
DDX: anxiety, electrolyte abnormalities (hypokalemia, hypomagnesemia), exercise, hyperthyroidism, ischemic heart disease, ingestion of stimulant drugs (cocaine, amphetamines, caffeine), medications (digoxin, beta-
blockers, hydralazine, diuretics, minoxidil), pheochromocytoma, hypoglycemia in DM1, mitral valve prolapse, AFIB, WPW, sick sinus syndrome
DX: Structural heart disease (CAD, cardiomyopathy, valve disease)
•ECG, echo, exercise stress test
•Labs: CMP, CBC, TSH, urine toxicology
Tx based on diagnosis

Tremors
RESTING: Parkinson’s, Wilson’s
POSTURAL and ACTION (Terminal): physiologic tremor, stress, fatigue, anxiety, emotion
•Endocrine: hypoglycemia, thyrotoxicosis, pheochromocytoma, adrenocorticosteroids
•Drugs/toxins: b-agonists, dopamine agonists, amphetamines, lithium, TCAs, neuroleptics, theophylline, caffeine,
•valproic acid, alcohol withdrawal, mercury, lead, arsenic, others
•Charcot-marie tooth syndrome
•Cerebellar tumor
Kinetic (intention) tremor: disease of cerebellar outflow, MS, trauma, tumor, vascular dz, Wilson’s, drugs, toxins
Misc. rhythmical movement disorders: psychogenic tremor, orthostatic tremor, rhythmical movements in dystonia, asterixis, clonus, nystagmus
ESSENTIAL:
•HX/PE: postural tremor of hands, head, voice; family hx; action tremor; aggravated by stress and worse w/ intentional movement; alleviated by relaxation and EtOH;
-Legs usually spared
-WORSENED by psych distress
Tx - BB propranolol, Barbs - primidone, Benzos, deep brain stim
Diabetes About Clinical Manifestations Diagnostics Management
Insipidus •inability of the kidney to concentrate urine, leading to •polyuria + polydipsia •increased serum osmolarity Central:
production of large amounts of dilute urine •high-volume nocturia •decreased urine osmolality & specific gravity •desmopressin (DDAVP) first line
•increased urine volume •carbamazepine second line
2 TYPES: Neurologic sxs of hypernatremia
Central: no production of ADH (MC) •confusion, lethargy, disorientation Fluid deprivation test: *establishes dx Nephrogenic:
•idiopathic MCC, destruction of posterior pituitary, head •seizures, coma •continued production of large amounts of dilute urine •correct underlying cause
trauma, CNS tumor, infection (low urine osmolality) •hydrochlorothiazide, indomethacin, or
PE: amiloride is sxs persist
Nephrogenic: partial or complete renal insensitivity to •dehydration, hypotension, rapid vascular collapse ADH stimulation test: *distinguishes central v. nephro •sodium & protein restriction
ADH •central: responds to ADH
•lithium, amphotericin B, hypokalemia, hypercalcemia, •nephrogenic: continued production of large amounts
acute tubular necrosis, hyperparathyroidism of dilute urine (no response to ADH)

Essential About Clinical Manifestations Diagnostics Management

Familial Tremor Autosomal dominant inherited d/o of Intentional tremor: postural bilateral action tremor MC affecting the upper Dx of exclusion based on Treatment usually not needed
unknown etiology extremities & head (hands, forearms, head, neck, or voice) hx, family hx, & physical
•worsened w/ intentional movement & adrenergic activity (emotional stress, anxiety) after r/o other causes Propranolol may help if severe or situational
Incidence increases w/ age •improved w/ ETOH; slight improvement w/ rest
Second line: primidone
PE: Third line: alprazolam
•on finger to nose testing, tremor increase at the end of approaching the target or
holding a position against gravity Refractory: thalamotomy
•no other significant neurological findings (cogwheel phenomenon may be seen in
some)
 Dermatology 5%
About Management
Burns •Thermal: scalding, contact w/ hot surface, fires ▪Complications: bacterial superinfection, sepsis, respiratory damage, multiorgan failure Immediate measures ⇢ ABC’s
•Non-Thermal: radiation, chemical burns, electrical burns •airway: intubation indicated for known/suspected
inhalation injury or >30-40% TBSA, DO NOT DELAY!!
Classification: Affected tissue layers: Appearance: Blanching: Sensation: Healing: •obtain vascular access
Superficial ▪epidermis ▪“sunburn” ⇢ dry, red ⊕ w/ pressure ▪painful ▪3-6d
(1st degree) ▪⊘blisters ▪⊖scarring Initial fluid resuscitation:
•indicated for any patient w/ >15% TBSA
Superficial partial ▪epidermis + superficial (papillary) dermis ▪Moist, red, weeping ⊕ w/ pressure ▪painful to temp., ▪7-21d •fluid requirement during initial 24h
thickness (2nd) ▪⊕blisters air, & touch ▪⊖scarring, +/- pigment Δ ▪Parkland formula ⇢ 4mL x %TBSA x weight(kg)
▪first half in first 8h, second half in remaining 16h
Deep partial ▪epidermis + deeper (reticular) dermis ▪mottled, cheesy white to red ⊖ or sluggish ▪painful to pressure ▪2-9wks w/o grafting ▪Lactated Ringer’s typically
thickness (2nd) ▪damage hair follicles & glandular tissue ▪wet or waxy dry only ▪⊕hypertrophic scarring •modify fluids to maintain urine output 0.5mL/kg/h
▪⊕blisters (easily unroof)
Immediate burn care:
Full thickness ▪epidermis + dermis + SQ tissue ▪waxy white to leather gray ⊖ ▪deep pressure only ▪healing w/o surgery not •remove any burnt clothing/jewelry/obvious debris
(3rd degree) to charred & black possible •cool burns w/ cool water or saline-soaked gauze
▪dry & inelastic, ⊘blisters ▪⊕severe scarring, contractures *NEVER ICE
•maintain body temperate ≥95°F (35°C)
Deeper injury ▪epidermis + dermis + SQ + deep ▪black, charred, dry, dull ⊖ ▪minimal perception ▪life & limb threatening
(4th degree) structures (muscles, fat, fascia, bones) ▪⊘blisters of deep pressure Pain management: IV morphine
LABS: CBC, electrolytes, BUN & creatinine, glucose,
Criteria for Minor Burns: *pts meeting ALL criteria may be treated outpatient Burn Center Referral Criteria: VBG, carboxyhemoglobin
▪partial-thickness burns <10% TBSA in patients 10-50yo ▪partial-thickness burns >10% TBSA
▪partial-thickness burns <5% TBSA in patients <10yo or >50yo ▪third-degree burns in any age group Prophylaxis: tetanus update if indicated, topical
▪full-thickness burns <2% TBSA in any patient w/o other injury ▪burns of face, hands, feet, genitalia, perineum, or major joint antibiotics to all nonsuperficial burns
▪isolated injury (i.e., no suspicion of inhalation or high-voltage injury) ▪electrical burns (including lightning) ▪silver sulfadiazine (SSD), mafenide acetate
▪does not involve face, hands, feet, or perineum ▪chemical burns
▪does not cross major joints ▪inhalation injury Superficial & superficial partial-thickness:
▪is not circumferential ▪burns in pts w/ medical conditions that could complicate •irrigation, topical moisturizers
management, prolong recovery, or affect mortality ▪calamine lotion, aloe vera gel
Estimating %TBSA (adults): •topical antibiotics
Rule of 9s ⇢ superficial (1st degree) NOT included Palmar Method ⇢ uses PATIENT’S palm ▪triple ointment ⇢ bacitracin, neomycin, polymyxin B
▪entire head/neck = 9% ▪entire palm including fingers = 1% •daily cleansing & debridement
▪each arm = 9%, each leg = 18% ▪entire palm excluding fingers = 0.5%
▪anterior trunk = 18%, posterior trunk = 18% Deep partial-thickness, 3rd/4th degree:
▪genitalia = 1% •early debridement of burnt, necrotic tissue
•escharotomy &/or fasciotomy if indicated
▪impending vascular or respiratory compromise
•skin grafts, topical antibiotics
Skin Cancer About Management
Basal Cell •MC form of skin cancer, slow growing, locally invasive, METS rare Etiology: intense or chronic UV light exposure High risk features ⇢ lesions of ANY size on head/neck, hands, feet, genitalia, pretibial
Carcinoma •occurs on sun-exposed skin in fair-skinned individuals •PTCH1 gene mutation, chronic arsenic exposure area OR lesions ≥20mm at any site
(BCC) •70% occur on face, 15% on trunk
First-line therapies:
•3 main subtypes: nodular, superficial, morpheaform/infiltrative Other Subtypes: •standard surgical excision, 4-5mm margins
Nodular (80%) ▪Basosquamous: rare, aggressive subtype ▪primary nodular or superficial BCC <20mm on trunk & extremities
▪typically presents on face as a pink or flesh-colored papule ▪Nodular/superficial BCCs can product melanocytes, referred ▪recurrence rates <5%
▪translucent, pearly quality w/ telangiectasia & rolled borders to as pigmented BCCs •curettage & electrodesiccation (C&E)
▪will often bleed & ulcerate (“rodent ulcer”) ▪alternative first line for superficial, low-risk BCC
Superficial (15%) ⇢ chronic area of “eczema” DX: shave or punch biopsy ▪not recommended for BCC on terminal hair-bearing skin (risk of follicular extension)
▪typically presents on trunk as erythematous scaling plaque ▪nodules/strands of atypical basaloid cells w/ Second-line therapies:
▪may be rimmed w/ fine translucent (pearly) papules hyperchromatic nuclei & peripheral palisading •Imiquimod 5% cream: immune response modifier, applied QHS 5d/wk x6wks
Morpheaform/Infiltrative (5-10%) Dermoscopic features (cannot confirm BCC): •Fluorouracil 5% cream: inhibits DNA synthesis/cell proliferation, applied BID x4-6wks
▪scar-like appearance, flesh-colored/very light pink, undefined borders ▪lack of pigmented network + ≥1 characteristic finding:
⇢ arborizing vessels, blue-gray ovoid nests, & ulceration High risk features ⇢ Mohs micrographic surgery (MMS)
Cutaneous •2nd MC form of skin cancer, tumors of epidermal keratinocytes Etiology: UV exposure MCC, actinic keratosis often precursor High-risk cSCC ⇢ lesions of ANY size on head/neck, hands/feet, pretibial, anogenital
Squamous •locally invasive, 2% metastasis rate, regional LN MC site •Other RF: HPV, ionizing radiation, arsenic, tobacco use area OR lesions ≥2cm at any site
Cell Clinical Features:
Carcinoma •MC located on face & neck, also lower lip, ears, & hands Bowen’s Disease: cSCC in situ (full thickness of epidermis) First-line therapies:
(cSCC) ▪lightly pigmented skin ⇢ MC on sun-exposed areas ▪erythematous, well-demarcated, scaly patch or plaque •standard surgical excision, 4-6mm margins to depth of mid/deep SQ adipose tissue
▪darkly pigmented skin ⇢ MC on non-sun-exposed areas ▪located in sun-exposed areas e.g., head & neck ▪recurrence rates 0-15%
•associated w/ areas of chronic inflammation or scarring ▪slow-growing, usually asymptomatic •Mohs surgery (particularly when tissue-sparing is desired)
•classic presentation ⇢ painless, nonhealing, bleeding ulcer ▪BX: pleomorphic keratinocytes w/ hyperchromatic nuclei
*NO infiltration into dermis Second-line therapies (non-surgical candidates):
•Invasive Cutaneous SCC: Some Clinical Variants: •curettage & electrodesiccation (C&E) ⇢ Contraindicated:
▪well-differentiated lesions: erythematous, hyperkeratotic ▪Verrucous Carcinoma (rare): cauliflower-like, wart ▪recurrent, high-risk, invasion into/past SQ
plaque or nodule, +/- ulceration ▪Cutaneous SCC of the lip: primarily, lower lip ▪cSCC in terminal hair-bearing areas
▪poorly-differentiated lesions: fleshy, granulomatous papules or ▪Marjolin’s Ulcer: rare form of cSCC, typically aggressive •cryotherapy (small, low-risk cSCC)
nodules, ⊖hyperkeratosis, +/- ulceration, hemorrhage, necrosis » develops from burns, scars, poorly healing wounds
High-risk ⇢ Mohs micrographic surgery (MMS)
DX: shave, punch, or excisional biopsy, should extend at least into mid-reticular dermis for suspicious lesions
▪atypical keratinocytes, full thickness of epidermis + extension into dermis or deeper tissues Bowen’s Disease: surgical excision, C&E, cryotherapy, topical fluorouracil or imiquimod
▪keratin pearls: mixture of pleomorphic epithelioid cells w/ central keratinization
Melanoma •most serious form of skin cancer, 5th MC in men & women Etiology: melanocytes, atypical nevi often precursor TX: wide excision
•RF: UV radiation, light skin, xeroderma pigmentosa, family hx •BRAF gene mutations, CDKN2A gene mutations ▪Breslow thickness (tumor depth) & presence/absence of ulceration guides excision
⇢ only ~30% arise from preexisting nevi ▪MC sites: ♂ ⇢ trunk, esp. upper back; ♀ ⇢ legs margins & whether to perform sentinel lymph node biopsy (SLNB)
▪Radial growth phase (RGP) ⇢ confined to epidermis Breslow Depth: Margins: Therapy for Metastatic Melanoma:
▪Vertical growth phase (VGP) ⇢ infiltrate dermis *potential for METS In situ 0.5-1.0cm ▪BRAF inhibitors: dabrafenib, vemurafenib
Melanoma Subtypes: Characteristics: Growth: Appearance: ≤1.0mm 1.0cm ▪Immunotherapy: ipilimumab, nivolumab
Superficial Spreading ▪sun-exposed skin ▪prolonged RGP ▪variably pigmented, irregular borders 1.01-2.0mm 1-2cm
(MC, ~70%) ▪upper back ♂, LE ♀ ▪delayed VGP ▪brown, red, blue, black, gray, white 2.01-4.0mm 2.0cm
≥4.01mm 2.0cm
Nodular ▪middle-aged whites ▪⊖RGP, immediate VGP ▪darkly pigmented, smooth nodule
(2nd MC, 15-30%) ▪upper back ♂, LE ♀ ▪fast growth in depth ▪often ulcerated w/ bleeding SLNB Indications:
▪melanoma ≥0.8mm
Lentigo Maligna ▪sun-exposed skin ▪SLOW transformation ▪begins as tan/brown macule, gradually enlarges ▪melanoma <0.8mm w/ ⊕ulceration
(3rd MC, 10-15%) ▪face MC, older adults ▪RGP lasts years ▪may develop darker, asymmetric foci, color Δ

Acral Lentiginous ▪Asians, darker skin tones ▪prolonged RGP ▪dark brown/black irregularly pigmented macule
(<5%) ▪palms, soles, subungual ▪Hutchinson’s sign: dark long band in nail

Clinical Diagnosis Rules: DX: excisional/complete biopsy, full thickness, 1-3mm margins
➀ ABCDE criteria ▪immunohistochemistry: ⊕S-100
➁ The “ugly duckling” criteria Dermoscopic features ⇢ atypical pigment network
▪1 nevi looks obviously different from the others
Cellulitis About Clinical Manifestations Diagnostics Management
Acute spreading infection of the deeper dermis & Localized macular Clinical Oral abx: cephalexin, dicloxacillin, amoxicillin
subcutaneous tissues erythema (flat margins IV abx: cefazolin
not sharply SIRS Criteria (at least 2): Cat bite: Augmentin
Bacteria entry usually occurs after a break in the skin, demarcated), swelling, •temp >100.4F or <96.8F Dog or human bite: Augmentin
such as underlying skin problems, trauma, surgical warmth, tenderness •HR >90bpm
wounds •RR >20 breaths/min MRSA:
Systemic sxs not •WBC >12,000, <4,000, or >10% bands PO: clindamycin, doxycycline, TMP-SMX
Etiologies: common IV: vancomycin
•MC caused by group A strep
•staph aureus Lymphangitis
(streaking)

Pressure Injury About Stages Management

(Decubitus Ulcer) Ulcers resulting from vertical pressure
Commonly seen on bony prominences (sacrum, calcaneus,
ischium)
Risk Factors: elderly, immobilization, incontinence
PATHO: pressure impairs delivery of oxygen & nutrients &
waste removal from the affected area; moisture causes skin
macerations, leading to skin breakdown
Stage I Superficial, nonblanchable redness that does not dissipate Wound care w/ moist wound environment; pain control (opioids if
after pressure is relieved severe)
Stage II Epidermal damage extending into the dermis; resembles a
blister or abrasion Debridement if necrotic tissue is present; negative pressure wound
Stage III Full thickness of the skin & may extend into the therapy
subcutaneous layer Optimize nutrition (protein & caloric intake, esp. stages 3/4)
Stage IV Deepest; extends beyond the fascia, extending into the
muscle, tendon, or bone Pressure redistribution: position & re-position & using support
If slough or eschar obscures the extend of tissue loss, this is an surfaces (air-fluidized beds, powered mattresses)
unstageable ulcer
Stage 1: transparent film for protection
Stage 2: dressing that maintain a moist wound environment –
transparent films or occlusive dressings (hydrocolloids or hydrogels) if
there is no infection present
Stage 3/4: debridement of necrotic tissue (mechanical, surgical,
enzymatic); surgical debridement for thick eschars or extensive tissue
necrosis

Discharge
Breast/nipple discharge: mastitis/breast abscess, breast cancer, gynecomastia, inflammatory breast cancer, hypogonadism
GI: vaginal infections (e.g., yeast, BV, trichomoniasis, HPV, herpes), cervicitis, foreign body (e.g., tampon), chlamydia/gonorrhea, menpause

Urticaria (Hives) About Clinical Manifestations Diagnostics Management

Edema of the superficial layers of the skin due histamine-
related increased vascular permeability
Type I (IgE) immediate, hypersensitivity reaction leading
to superficial localized edema & erythema of the dermis,
mucous membranes, & subcutaneous tissues
PATHO: release of vasodilators (histamine, bradykinin,
kallikrein, PGs) form mast cells & basophils of the skin
Triggers: foods, meds, heat or cold, stress, insect bites, Antihistamines (H1 blockers) initial
environmental, & infection - second gen: cetirizine, loratadine, fexofenadine
- chronic (>6wks) - first gen: diphenhydramine, hydroxyzine, chlorpheniramine
Sudden onset of circumscribed hives or wheals H2 blockers (ranitidine) may be added if no response to H1
(blanchable, raised, erythematous areas on the skin blockers
or mucous membranes) that may coalesce
•intense pruritis Severe, recurrent, persistent: steroids
•usually transient (often disappearing within 24hrs)
Desquamation About
Erythema Type IV hypersensitivity reaction of the skin
Multiforme often following infections or medication
exposure – MC in young adults 20-40yrs
Etiology:
Infections: HSV MCC; M. pneumoniae, VZV,
EBV, CMV, coxsackie, parvovirus B19, M.
tuberculosis, Salmonella, HIV
Medications: NSAIDs, sulfonamides,
anticonvulsants, antibiotics
Clinical Manifestations Diagnostics Management
Target lesions – MC on extremities (hands/feet) Clinical SELF-LIMITED!!
•dusky, violaceous macule or blister
•intermediate surrounding ring of pallor Bx if dx not clear Symptomatic TX: bland emollients or topical abx
•peripheral erythematous ring applied to eroded areas, IVF for pts w/ mucositis
NON-PRURITIC, blanches & poor PO intake, antihistamines if pruritic
NEGATIVE Nikolsky sign (no epidermal detachment) HSV: acyclovir
Mucositis: typically mild & limited to one mucous membrane If ophthalmic involvement à REFERRAL
(usually oral); conjunctival/urogenital involvement rare

CLASSIC target lesions: THREE zones, well
defined borders
SJS & TEN Rare hypersensitivity reactions affecting the
skin & mucosal membranes
Etiology: predominantly drug-related
(penicillin, sulfonamides, allopurinol,
NSAIDs, anticonvulsants)
•other: infections (M. pneumoniae,
influenza)
SJS: <10% BSA
SJS/TEN Overlap: 10-30% BSA
TEN: >30% BSA
ATYPICAL target lesions: TWO zones or
poorly defined border
*Generally develops within 2mo of drug
initiation, & often within first 1-4wks
Minor: EM w/o or w/ only mild mucosal dz; NO systemic sxs
Major: EM w/ severe mucosal involvement + systemic sxs
(fever, arthralgias)
Prodrome: fever, malaise, pharyngitis, eye pain
Cutaneous: typically begin on torso & face; rapidly generalizes
SJS: atypical targetoid lesions, often violaceous &/or blistered;
lesions may coalesce, particularly on face & torso
TEN: tender, erythematous patches & plaques that develop
large bullae that coalesce & rapidly slough, leaving large,
denuded areas of skin
(+) Nikolsky sign: applied lateral pressure to blister causes
extension of separation from dermis
Mucositis: oropharyngeal, conjunctival, urethral, genital,
perirectal; often causes pain, poor PO intake, dehydration
Ocular manifestations: conjunctivitis, eyelid edema,
blepharitis, corneal erosions, symblepharon, corneal scarring
Clinical PROMP DC OF ALL POSSIBLE INCITING MEDS!!!
•if underlying infectious etiology à treat
Bx: full thickness skin necrosis
Supportive: pain management, nutritional
Consider: bacterial cultures, M. pneumoniae support, maintain normal body temperature,
PCR maintain hydration & electrolyte balance
•hypo-Na/K/phos common
Wound care: leave bullae intact, avoid
aggressive debridement, petroleum gauze,
topical antibiotics, minimize pressure, frequent
application of bland emollients/lubricating
ointments to involved mucosa, +/- PO
disinfectant rinse (chlorhexidine)
IVIG: may be effective at arresting progression
*CLOSE MONITORING FOR SEPSIS

Rash
Difficult to diagnose, esp if generalized
DDX:
o Abx side effects – fever, skin rashes, AMS
o zinc deficiency – perioral pustular rash
o paget disease: pruritus, well-demarcated, erythematous, eczematous rash
o herpes zoster: classic vesicular lesions; dermatomal distribution
o herpes simples: clear vesicles on erythematous base, crusting
o systemic rheumatoid disease (still’s): multiple (>5) joint involvement, fever, LAD, hepatosplenomegaly, rash, subcutaneous nodules, pericarditis
o fat emboli from long bone fracture: respiratory insufficiency, coagulopathy, encephalopathy, upper body petechial rash
TX: observe / treat empirically, diagnostic testing, refer to dermatology for workup

Redness/Erythema
Causes: infection, massage, electrical treatment, acne medication, allergies, exercise, solar radiation (sunburn), photosensitization, cutaneous radiation syndrome, mercury toxicity, blister agents, niacin administration,
waxing/tweezing, radiotherapy treatment
DDX: ulcer, eczema, stasis / contact dermatitis, drug allergy, cellulitis / MRSA, chemical burns, angioedema / urticaria, venous insufficiency, herpes zoster, scarlet fever, tinea infections, psoriasis, acne, polycythemia vera,
paronychia, osteomyelitis, abscess, autonomic hyperreflexia, lymphadenitis, carbuncle, furuncle, neutropenia.
 Neurology 5%
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

About Clinical Manifestations Diagnostics Management

Epidural Location: arterial bleed MC between skull & dura Brief LOC à lucid interval à coma CT: convex (lens-shaped) bleed +/- herniate if not evacuated early
Hematoma *does NOT cross suture lines
(Hemorrhage) Mechanism: MC after temporal bone fracture à HA, N/V, focal neuro sxs, rhinorrhea (CSF fluid) Observation if small
middle meningeal arterial disruption
CN III palsy if tentorial herniation If ↑ ICP: mannitol, hyperventilation, head
elevation, +/- shunt

Subdural Location: venous bleed MC Varies, may have focal neuro CT: concave (crescent-shaped) bleed Hematoma evacuation vs. supportive
Hematoma - between dura & arachnoid d/t tearing of cortical sxs *bleeding CAN cross suture lines
(Hemorrhage) bridging veins Evacuation if massive or ≥5mm midline shift
Chronic:
MC in elderly •insidious onset of HA
•cognitive impairment
Mechanism: MC blunt trauma (“contre-coup”), •somnolence
venous bleed •occasional seizures
CT à HYPOdense
Intracerebral •bleeding within the brain parenchyma Neurologic sxs usually increase within min-hrs CT w/o contrast Supportive: gradual BP reduction
Hemorrhage •may compress the brain, ventricles, & sulci •HA, N/V
•syncope Prevention of increased intracranial pressure
Risk Factors: •focal neuro sxs (hemiplegia, hemiparesis, seizures) •raising head of the bed 30 degrees
•HTN MCC of spontaneous ICH •altered mental status •limiting IV fluids
•cerebral amyloid angiopathy MCC of nontraumatic •BP management
ICH in the elderly PE: •analgesia, sedation
•arteriovenous malformation MCC in children •may have focal motor & sensory defects
•trauma, older age, high ETOH intake, coagulopathy Reduction of intracranial pressure: IV mannitol

Subarachnoid Bleeding between the arachnoid membranes & the •sudden, intense thunderclap HA (unilateral, CT scan w/o contrast Supportive: bed red, stool softeners, lower
Hemorrhage pia mater occipital area) intracranial pressure
Etiologies: “worse HA of my life” LP à performed if CT (-) •Nimodipine reduces cerebral vasospasms,
•MC due to a ruptured berry aneurysm at the •N/V, meningeal sxs (photophobia, neck stiffness, •xanthochromia improving neurologic outcomes
anterior communicating artery fever)
•AVM, stroke, trauma •LOC 4-vessel angiography Hydrocephalus à ventriculostomy
PE: •usually performed after confirmed SAH to
Risk Factors: •meningeal signs: nuchal rigidity, + Brudzinski, + identify source of bleeding & other aneurysms Prevention of rebleeding:
•smoking, HTN Kernig •endovascular coiling or surgical clipping of
•PCKD, atherosclerotic disease, ETOH, Ehlers-Danlos •CN III palsy – fixed, dilated, “blown” pupil aneurysm or AVM used to prevent rebleeding
syndrome, Marfan syndrome, family hx •Terson Syndrome: retinal hemorrhages Coiling > clipping
 Change in Speech
Aphasia is an inability to comprehend or formulate language because of damage to specific brain regions
o postoperative cerebral vascular accident (stroke) – trouble speaking, along w/ having a numb or drooping face & feeling weak in one arm, is one of the 3 major signs of
stroke
o multiple sclerosis – lesions in areas of the brain responsible for speech can have speech issues that range from mild to severe
o intracerebral hemorrhage
o migraine HA may cause transient aphasia
o carotid disease
o recurrent laryngeal nerve injury (thyroidectomy)
o apraxia of speech
Dysarthria is a motor speech disorder resulting from neurological injury of the motor component of the motor speech system
o degenerative diseases: Parkinson’s, ALS, MS, Huntington’s, Neimann-Pick, Friedreich’s ataxia
o toxic & metabolic conditions: Wilson’s, hypoxic encephalopathy (drowning), central pontine myelinolysis
o brain tumor, cerebral palsy, GB syndrome, hypothermia, Lyme disease, stroke, intracranial HTN (pseudotumor cerebri), Tay-Sachs

About Clinical Manifestations Diagnostics Management

Central Retinal Artery Retinal artery thrombus or embolus Acute, sudden painless monocular vision Fundoscopy: retinal ischemia Initial – CO2 rebreathing, 100% oxygen, ocular
Occlusion loss – may be preceded by amaurosis fugax - pale retina w/ cherry-red macula massage, decompression of anterior chamber,
MC 50-80yrs, hx of atherosclerotic disease - boxcar appearance of retinal vessels ophthalmology consult, fibrinolysis
OPHTHALMOLOGIC +/- ipsilateral carotid bruit (segmentation of blood flow)
EMERGENCY Etiologies: - emboli may be seen Reduction of IOP:
•emboli from carotid artery atherosclerosis MC •timolol
•cardiogenic emboli – 2nd MC cause overall but MC •acetazolamide
cause in young pts/pts w/o atherosclerosis
•vasculitis

Retinal Detachment About Clinical Manifestations Diagnostics Management

Separation of the retina from the underlying retinal Photopsia (flashing lights) w/ detachment followed Fundoscopy: retinal tear (detached OPHTHALMOLOGIC EMERGENCY – keep pt
pigment epithelium by floaters (spots in the visual fields) followed by tissue “flapping” in the vitreous humor) supine while awaiting consult w/ head turned
progressive unilateral peripheral vision loss: •asymmetric red reflex toward the side of detachment
Risk Factors: myopia, previous cataract surgery, shadow or “curtain coming down” in the periphery •+ Shafer’s sign: clumping of brown-
advancing age, trauma initially followed by loss of central visual field colored pigment vitreous cells in the Do not use miotic drops
anterior vitreous humor resembling
Types: NO ocular pain or redness “tobacco dust” Laser, cryotherapy, or ocular surgery
•rhegmatogenous (MC): full-thickness retinal tear
causes the retinal inner sensory layer detachment from
the choroid plexus
•tractional: adhesions separate the retina from its base
(proliferative diabetes retinopathy, sick cell disease,
trauma)
•exudative (serous): fluid accumulates beneath the
retina causing detachment (HTN, CRVO, papilledema)
 About
Corneal Abrasion
Acute Narrow Angle- Increased intraocular pressure leading to
Closure Glaucoma damage of the optic nerve
Risk Factors:
•pts w/ preexisting narrow angle or large lens
•age >60yrs, far-sighted, Asians, females
OPHTHALAMOLOGIC
EMERGENCY PATHO:
- decreased drainage of aqueous humor via
trabecular meshwork & canal of Schlemm
- precipitants: mydriasis further closes the
angle (dim lights, sympathomimetics,
anticholinergics)
Giant Cell Arteritis •large & medium vessel granulomatous
vasculitis of the extracranial branches of the
carotid artery (temporal artery, occipital artery,
ophthalmic artery, posterior ciliary artery)
Clinical Manifestations Diagnostics Management
FB sensation, tearing, red & painful eye, photophobia, Check visual acuity first Abx drops: erythromycin
blepharospasms (hard to open the eye) Contact lens: ciprofloxacin, ofloxacin
Fluorescein stain: “ice rink”/linear abrasions
Patching for abrasions >5mm (not to exceed
24hrs)
24hr ophthalmology follow up
Sudden onset of severe, unilateral ocular pain Tonometry: ↑ IOP (>21mmHg) Timolol + apraclonidine + pilocarpine + PO
•halos around lights, loss of peripheral vision (tunnel acetazolamide
vision) Fundoscopy: optic disc blurring or “cupping” •timolol – topical BB
of optic nerve (thinning of the outer rim of the •apraclonidine – topical alpha-2 agonist
N/V, HA topic nerve head) •pilocarpine – topical miotic/cholinergic
PE: Definitive: iridotomy – laser preferred
•conjunctival erythema, cloudy “steamy” cornea
•mid-dilated fixed pupil (reacts poorly to light)
•eye hard on palpation
•HA, jaw claudication w/ mastication, visual changes •increased ESR/CRP •high-dose corticosteroids to prevent
•scalp tenderness •temporal bx blindness
•fever, fatigue, weight loss, night sweats, malaise

Risk Factors: women, >50yrs, Northeastern

Europeans

Optic Neuritis About Clinical Manifestations Diagnostics Management

(Optic •acute inflammatory demyelination of the optic nerve •painful loss of vision Fundoscopy: optic disc swelling/blurring •IV methylprednisolone à oral steroids
Nerve/CN II •decrease in color vision (desaturation) (papillitis)
Inflammation) Risk Factors: MC in women & young pts 20-40yrs •visual field defects (scotoma – blind spot) over hrs-days *vision usually returns w/ treatment
*unilateral MRI (confirms when MS suspected)
Etiologies: MS, autoimmune, medications (ethambutol)
PE:
•ocular pain worse w/ eye movement
•Marcus-Gunn pupil: eye dilates when light enters

Idiopathic About Clinical Manifestations Diagnostics Management

Intracranial HTN Idiopathic increased intracranial (CSF) s/sxs of increased ICP: CT scan: performed prior Acetazolamide first line (decreases CSF
(Pseudotumor pressure w/ no clear cause evident on •HA: pulsatile, worse w/ straining or changes in posture to LP to r/o intracranial production) & weight loss recommended
Cerebri) neuroimaging (CT/MRI) •retrobulbar pain that may be worse w/ eye movements mass - furosemide may be adjunct
Pseudotumor Cerebri: mimics a brain tumor w/ •N/V, tinnitus - topiramate when HA prominent/obese pts
N/V, visual disturbances •visual changes – may lead to blindness if not treated LP: ↑ CSF pressure
(≥250mmH2O) + Short course of systemic steroids may be
Risk Factors: Ocular Exam: otherwise normal CSF indicated if acute visual loss as a temporizing
- obese women of childbearing age •fundoscopy: papilledema (usually bilateral, symmetric) measure prior to surgical intervention
- meds: steroid withdrawal, GH, thyroid •may have visual field loss MRI w/ MR venography
replacement, OCPs, long-term tetracycline use, •may have diplopia due to a cranial nerve V1 (abducens) palsy Repeat LP reduces intracranial pressure
vitamin A toxicity
- venous sinus thrombosis Refractory: ventriculoperitoneal shunt or optic
nerve sheath fenestration
CVA About
Transient Transient episodes of neurologic deficits caused by
Ischemic Attack focal brain, spinal cord, or retinal ischemia w/o acute
infarction
3 main types:
- embolic: AFIB, left ventricular thrombus
- lacunar: penetrating small vessels
- large artery: ischemia due to atherosclerosis
Lacunar Small vessel disease of the penetrating branches of
Infarcts cerebral arteries in the pons & basal ganglia
Risk Factors: 80% have hx of HTN, DM
Dx: CT scan – small punched-out hypodense areas
(lacunar infarcts) usually in central & noncortical
areas (e.g., basal ganglia)
Ischemic Acute onset of neurological deficits due to death of
Strokes brain tissue from ischemia
MC type of stroke
Causes:
•thrombotic: MC (2/3)
•embolic: (1/3) commonly come from heart, aortic
arch, or large cerebral arteries – sources: AFIB,
valvular disease, patent foramen ovale
Risk Factors: HTN most significant & modifiable RF
- dyslipidemia, DM, AFIB, smoking
- nonmodifiable: male, ↑ age, ethnicity, family hx
Clinical Manifestations
Neurologic deficits lasting <24hrs – most last for a
few minutes w/ complete resolution in 1hr
Amaurosis fugax: transient monocular vision loss
“temporary shade down on one eye”
PE: carotid bruits may be heard
5 classic presentations:
Pure Motor (MC): hemiparesis or hemiplegia in the
absence of sensory or “cortical” signs (aphasia,
agnosia, neglect, apraxia, hemianopsia)
Ataxic Hemiparesis: ipsilateral weakness &
clumsiness
Pure Sensory Deficits: numbness, paresthesias of
arm, face, leg on one side of the body in the absence
of sensory or “cortical” signs
Carotid/Ophthalmic – amaurosis fugax (monocular
blind)
MCA – aphasia, neglect, hemiparesis, gaze
preference, homonymous hemianopsia
ACA – leg paresis, hemiplegia, urinary incontinence
PCA – homonymous hemianopsia
Basilary Artery – coma, cranial nerve palsies, apnea,
drop attack, vertigo
Diagnostics
Neuroimaging + neurovascular imaging + r/o
cardioembolic source
•neuroimaging: CT initial, MRI more sensitive
•neurovascular: CT/MR angiography, carotid
Doppler
Conventional angiography: definitive (invasive)
Ancillary testing: r/o cardioembolic source (EKG,
telemetry, echocardiogram), r/o metabolic or
hematologic source (hypoglycemia, CBC)
Sensorimotor: weakness & numbness of the face,
arm, leg on one side of the body in the absence of
“cortical” signs
Dysarthria (Clumsy Hand Syndrome): dysarthria,
facial weakness, dysphagia, & slight weakness &
clumsiness of one hand in the absence of
“cortical” signs
CT head w/o contrast – best initial to r/o
hemorrhagic stroke; may be normal in first 6-
24hrs
Ancillary testing:
- neurovascular: CT/MR angiography
- carotid Doppler U/S
- EKG
- echocardiography
- cardiac monitoring
Management
Place pt in supine position to increase cerebral
perfusion, avoid lowering BP unless >220/120
- thrombolytics contraindicated
Noncardiogenic TIA:
- antiplatelet therapy: aspirin, clopidogrel
ABCD2 score 0-3: aspirin alone
ABCD2 score ≥4: aspirin + clopidogrel
- carotid endarterectomy recommended if
internal carotid artery stenosis 50-99% w/ a life
expectancy of at least 5yrs
- long term: reduce modifiable RF (DM,
hyperlipidemia, HTN control), exercise
Cardiogenic TIA (AFIB): oral anticoagulation
Aspirin, control RF (HTN, DM)
Immediate management:
- within 3hrs of sxs onset: alteplase
(thrombolytic) if no contraindications (BP
>185/110, recent/bleeding d/o, recent
trauma)
- >3-4.5hrs: aspirin
- BP control IF ≥185/110
Long-term management:
- antiplatelet therapy: aspirin, clopidogrel,
dipyridamole
- anticoagulation ONLY if cardioembolic (AFIB)
- statin (regardless of LDL level)
 Motor &/or Sensory Loss
SCI ANTERIOR CORD CENTRAL CORD POSTERIOR CORD BROWN SEQUARD
Mechanism of Injury •MC after blowout vertebral body burst fractures •hyperextension injuries (50% occur w/ MVA), •rare •unilateral hemisection of the spinal cord
(flexion) falls in elderly, gunshot wounds, tumors, cervical •damage to posterior cord or posterior spinal •MC after penetrating trauma (tumors may
•anterior spinal artery injury or occlusion spinal stenosis, syringomyelia stenosis cause it)
•direct anterior cord compression •MC incomplete cord syndrome •rare injury
•aortic dissection, SLE, AIDS •it affects primarily the central gray matter
(including the spinothalamic tracts)
Deficits Motor deficit: Motor deficit: •LOSS OF PROPRIOCEPTION/VIBRATORY SENSE Ipsilateral deficits:
•lower extremity > upper extremity* •upper extremity > lower extremity*; the distal ONLY •motor (lateral corticospinal tract)
(corticospinal) portion of the upper extremity more severe •vibration/proprioception (dorsal column)
involvement (e.g., hands) from corticospinal
Sensory deficit: involvement Contralateral deficits:
•pain, temperature (spinothalamic tract) •pain/temperature (lateral spinothalamic tract)
•light touch Sensory deficit: usually 2 levels below the injury (where
•may develop bladder dysfunction (retention, •pain/temp (spinothalamic tract) deficit greater spinothalamic tract crosses at the spinal cord
incontinence) in upper extremity; sometimes described as a level)
“shawl” distribution
Preservation •proprioception, vibration, pressure (dorsal •proprioception, vibration, pressure (dorsal •pain & light touch
column spared) column spared) •NO motor deficits
Vascular About Clinical Manifestations Diagnostics Management
Disorders (Carotid Carotid artery narrowing, or stenosis, caused by If symptomatic, usually presents as TIA or stroke Duplex doppler U/S •smoking cessation
Disease) atherosclerotic plaque •transient visual disturbance (amaurosis fugax) •>50% moderate
M>F •unilateral muscle weakness or paresthesia •>70% severe Antiplatelet therapy for symptomatic pts
•dizziness •clopidogrel
Risk Factors: family hx, hyperlipidemia, smoking, HTN, •tinnitus Angiography •ASA + dipyridamole
diabetes, older age •aphasia
•statins for all pts
Associated conditions: PE:
•peripheral artery disease •carotid bruit (if 60-70% stenosis) Operative: carotid artery revascularization
•coronary artery disease •motor or sensory deficits •stenosis >70%
•post-TIA or stroke
-carotid endarterectomy (CEA)
-carotid artery stenting (unable to tol. CEA)

Wernicke’s About Clinical Manifestations Diagnostics Management

Syndrome Risk Factors: chronic ETOH use Encephalopathy
*results in thiamine deficiency •disorientation, confusion
•indifference, inattentiveness
Ocular motor dysfunction
•nystagmus, lateral rectus palsy
•conjugate gaze palsies
Ataxia Workup: CBC, CMP, UA, toxicology IV thiamine infusion
•gait, stance
Heat CT à exclude intracranial bleeding, *do NOT give glucose before thiamine – can
strokes, & space-occupying lesions worsen sxs
MRI: signal abnormality within the
mamillary bodies

Urology/Renal 5%
About Clinical Manifestations Diagnostics Management
Acute Cystitis PATHO: usually an ascending infection of the lower Irritative sxs: dysuria (burning), frequency, urgency UA: pyuria (>10WBCs/hpf), hematuria, - nitrofurantoin or TMP-SMX
urinary tract from the urethra •hematuria, suprapubic pain & tenderness leukocytes esterase, nitrites, cloudy urine, - FQs second line (“floxacin”)
“bladder bacteriuria - phenazopyridine (analgesic)
infection” Etiologies: •turns urine orange
•E. coli MC Urine culture: definitive
“UTI” •staph saprophyticus 2nd MC in sexually active •epithelial (squamous cells) = contamination

Risk Factors: female, pregnancy, elderly, DM,

infants
Acute Infection of the upper GU tract (kidney parenchyma Upper tract sxs: fever, chills, back/flank pain; N/V UA: Outpatient: FQs first line (“floxacin”)
Pyelonephritis & renal pelvis) •pyuria (>10WBCs/hpf)
PATHO: usually an ascending infection of the lower Lower tract sxs: dysuria, urgency, frequency •leukocyte esterase Inpatient: cephalosporins, FQs, aminoglycosides,
“kidney urinary tract •nitrites penicillins
infection” PE: •hematuria, cloudy urine
Etiologies: E. coli MC + CVA tenderness •WBC casts – HALLMARK ADMIT: older age, signs of obstruction, comorbid
Risk Factors: DM, hx of recurrent UTIs or kidney Fever, tachycardia conditions, inability to tolerate PO abx
stones, pregnancy, congenital urinary tract CBC: leukocytosis w/ left shift
malformations Urine culture: definitive Pregnancy: IV ceftriaxone

Urethritis About Clinical Manifestations Diagnostics Management

Non-gonococcal urethritis (NGU): chlamydia Urethral discharge & penile or vaginal pruritis NAAT Gonorrhea: ceftriaxone 250mg IM x1 plus
trachomatis azithromycin 1g x1
Dysuria Gram stain:
Gonococcal urethritis: abrupt onset of sxs •no organisms = NGU Chlamydia: doxycycline 100mg BID x10d or
•opaque, yellow, white, or clear thick discharge Abdominal pain or abnormal vaginal bleeding •gram (-) diplococci: gonorrhea azithromycin 1g PO
•pruritis
 About Clinical Manifestations Diagnostics Management
Epididymitis Epididymal pain & swelling thought to be secondary to Gradual onset (over a few hours to days) of localized Scrotal U/S – enlarged epididymis, Scrotal elevation, NSAIDs, cool compresses
retrograde infection or reflux of urine – bacterial infection MC testicular pain & swelling (usually unilateral) increased testicular blood flow
•groin, flank, or abdominal pain <35yrs: doxycycline (100mg BID x10d) +
Etiologies: UA: pyuria (↑ WBCs) or bacteriuria ceftriaxone (250mg IM x1)
•males 14-35: chlamydia trachomatis (MC), Neisseria +/- fever, chills, irritative sxs (urgency, frequency,
gonorrhea dysuria) NAAT for gonorrhea & chlamydia >35yrs: FQs (ciprofloxacin, ofloxacin,
•men >35: E. coli MC levofloxacin)
PE:
•scrotal swelling & tenderness; epididymal Bacterial in children: cephalexin or amoxicillin
tenderness & induration
•(+) Prehn sign: relief of pain w/ scrotal elevation
•(+) cremasteric reflex: elevation of the testicle after
stroking the inner thigh
Prostatitis Prostate gland inflammation secondary to an ascending Irritative voiding sxs: frequency, urgency, dysuria UA & urine culture: Acute:
infection •acute: pyuria & bacteriuria >35: FQs or TMP-SMX x4-6wks
Obstructive sxs: hesitancy, poor or interrupted •chronic: + after massage! <35: ceftriaxone + doxycycline
Acute: stream, straining to void, incomplete emptying
•>35yrs: E. coli MC AVOID prostatic massage in acute (may Chronic: FQs or TMP-SMX x6-12wks
•<35yrs: gonorrhea & chlamydia Acute: exquisitely tender prostate cause bacteremia) •tamsulosin can help w/ chronic pain
•fever, chills, perineal pain
Chronic: Refractory (chronic): TURP
•E. coli MC Chronic: nontender (or minimally tender) prostate
•proteus •usually presents as recurrent UTIs or intermittent
dysfunction

PE: boggy prostate!!!!!

Testicular About Major Types

Cancer MC solid tumor in young men 15-35yrs (average age 32) Germinal Cell Tumors: (MC) – nonseminomas & seminomas Non-Germinal Cell Tumors:
•Nonseminomas: ↑ alpha-fetoprotein & beta-hCG; •Leydig cell tumors: may secrete androgens or estrogens which
Risk Factors: resistance to radiation may à precocious puberty
•cryptorchidism (most significant) •Seminomas: 4 S’s •Sertoli cell tumors: may secrete hormones
•Caucasians, Klinefelter’s syndrome, hypospadias -simple (lacks tumor marker alpha-fetoprotein) •Gonadoblastoma, testicular lymphoma
-sensitive (to radiation)
-slower growing
-stepwise spread
Clinical Manifestations Diagnostics Management
Painless testicular mass MC presentation Scrotal U/S: Low-grade nonseminoma: radical orchiectomy w/
•seminoma: hypoechoic mass retroperitoneal lymph node dissection
PE: firm, hard, fixed mass that does not transilluminate •nonseminoma: cystic, nonhomogeneous mass
Low-grade seminoma: radical orchiectomy; +/- radiation, chemo
Tumor markers:
•nonseminomas: ↑ alpha-fetoprotein & beta-hCG High-grade seminoma: debulking chemo + orchiectomy &
radiation
Staging: CT of abdomen, pelvis, & chest

Bladder About Clinical Manifestations Diagnostics Management

Carcinoma Transitional cell carcinoma MC type Painless hematuria in a smoker Cystoscopy w/ bx: gold standard Endoscopic resection w/ cystoscopy every 3mo
•recurrent or multiple lesions can be treated w/
3x MC in men than women intravesical chemotherapy

Risk Factors: smoking

Chronic Kidney About
Disease & ESKD Normal GFR in young adults ~125mL/min/1.73m2
Etiologies: diabetes MCC of ESKD, HTN 2nd MCC
RF: DM, HTN, family hx, ≥60yo, AA, Hispanic,
Asian/Pacific Islander, American Indian, NSAIDs,
AKI hx
Cardiovascular disease is the leading cause of
morbidity/mortality in CKD
•Kidney Failure: end stage of CKD, defined as
severely ↓ kidney function OR dialysis treatment
•ESKD/ESRD (GFR <15): chronic kidney failure
treated w/ either dialysis or transplantation
CKD Definition: presence of either kidney damage
or ↓ kidney function for ≥3mo
Types of Structural/Functional Abnormalities:
Pathologic Abnormalities:
•Glomerular diseases (diabetes, autoimmune
disease, systemic infections, drugs, neoplasia)
•Vascular diseases (atherosclerosis, HTN,
ischemia, vasculitis, thrombotic microangiopathy)
•Tubulointerstitial diseases (UTI, stones,
obstruction)
•Cystic disease (polycystic kidney disease, “PKD”)
History of transplant:
•Chronic allograft nephropathy (non-specific
findings of tubular atrophy, interstitial fibrosis,
vascular & glomerular sclerosis)
•Rejection, drug toxicity, BK virus nephropathy
•Recurrent disease (glomerular disease, oxalosis,
Fabry disease)
Urinary sediment abnormalities:
•RBC casts, proliferative glomerulonephritis
•WBC casts, pyelonephritis or interstitial nephritis
•Oval fat bodies or fatty casts, diseases w/
proteinuria
•Granular casts & renal tubular epithelial cells in
many parenchymal diseases (non-specific)
Imagining abnormalities: polycystic kidneys,
hydronephrosis, cortical scarring, renal masses,
enlarged kidneys d/t infiltrative diseases, RAD,
small/echogenic kidneys
Drugs to Consider: NSAIDs, COX-2 inhibitors,
antimicrobials, chemo agents, antiretroviral drugs,
PPIs, lithium
Clinical Manifestations Diagnostics/Staging Management
CKD stages 1-4 are asymptomatic Initial workup: CBC, CMP, urine dipstick & microscopy, •dietary modifications
•when GFR falls to ~10-15, nonspecific s/sxs begin to ACR & PCR on random urine sample •treat reversible causes
appear (e.g., malaise, weakness, insomnia, inability to •slow progression
concentrate, N/V) •treat complications of kidney failure
•oliguria/anuria rare in CKD alone, almost always indicates •identify patients that will require
at least some component of AKI kidney replacement therapy
Cardiovascular Manifestations: Dietary Modifications:
•volume overload, edema, systemic HTN* •protein 0.8-1.0g/kg/d
•ischemic heart disease (d/t accelerated atherosclerosis) •fiber 20-25g/d
•LVH, HF, rhythm disturbances •sodium <2g/d
•uremic pericarditis (pleuritic chest pain) •potassium 40-70meq/d, avoid NSAIDs
•↑ BUN (ref. range 7-20mg/dL) •phosphorous 600-800mg/d
Skin Manifestations: •↑ creatinine •calcium 1400-1600mg/d
•pale (anemia), hyperpigmented (↑ β-MSH production) (ref. range 0.6-1.2mg/dL, female) •iron ≥10-18mg/d
•pruritis +/- scratching lesions (ref. range 0.5-1.1mg/dL, male)
•ecchymoses & hematomas (d/t bleeding diathesis) Albumin is the main protein lost through urine in CKD BP Control: ACEI/ARBs, diuretics
•uremic frost (i.e., crystallization of urea), uncommon •Proteinuria is best marker of progression •goal 125-130/<80
•skin necrosis (calciphylaxis) & bullous lesions (rare) Proteinuria: ACEI/ARBs, SGLT2s
Glucose Control: SGLT2s, GLP-1s
Gastrointestinal Manifestations: HLD: statins
•anorexia & N/V (typical of advanced kidney failure) •TC goal <200mg/dL
•malnutrition •LDL goal <100mg/dL
•uremic fetor (i.e., urinelike breath odor d/t urea + saliva
forming ammonia), often associated w/ metallic taste Volume overload:
•inflammatory/ulcerative lesions & GI bleeding •salt restriction + diuretic therapy
Metabolic acidosis:
Neurologic Manifestations: •bicarbonate supplement
•CVAs (d/t accelerated atherosclerosis) Hyperphosphatemia:
•anemia (↓ H/H)
•uremic encephalopathy (progressive cognitive •Non-calcium PO phosphate binders
•hyperphosphatemia
impairment leading to seizures & coma if untreated) (sevelamer, lanthanum)
•hypocalcemia
•uremic neuropathy (i.e., central, peripheral, & autonomic Anemia: ESAs
•hyperkalemia
neuropathy), RLS or burning feet syndrome •erythropoietin, darbepoetin alfa
•metabolic acidosis
•hypermagnesemia
Hematologic Manifestations: Indications for Nephrologist Referral:
•hyperuricemia
•normocytic, normochromic anemia (primarily d/t •GFR <30, ACR ≥300, PCR ≥500
insufficient EPO production) •abnormal urine microscopy (cellular
Urinary sediment: +/- broad waxy casts
•abnormal leukocyte/immune system functions (more casts, non-urologic hematuria, sterile
•result of dilated, hypertrophic nephrons
frequent & severe infections) pyuria)
•platelet dysfunction (bleeding, bruising) •difficult to manage lab abnormalities
Evaluation of Metabolic Bone Disease: •resistant HTN
Endocrine & Metabolic Manifestations: •serum calcium, phosphorus, vitamin D, PTH •inability to identify a cause
•impotence, infertility, ↓ libido (d/t hypogonadism)
Other levels to evaluate: Hgb, iron, vitamin B12,
•amenorrhea & galactorrhea (d/t hyperprolactinemia)
folate
•insulin resistance + glucose intolerance (azotemic
pseudodiabetes), hyperlipidemia
IMAGING:
Renal U/S: most useful imaging study, initial TOC
CKD-Mineral & Bone Disorders (CKD-MBD)
•BL small (<10cm), echogenic kidneys suggest chronic
Mineral Abnormalities: hyperphosphatemia +
hypocalcemia + low vitamin D (calcidiol & calcitriol) lead to scarring of advanced CKD
•normal/enlarged kidneys can be seen w/ PKD,
secondary hyperparathyroidism (i.e., ↑ bone turnover)
diabetic nephropathy, HIV-associated nephropathy,
Bone Manifestations (renal osteodystrophy): *all
plasma cell myeloma, amyloidosis, obstructive
characterized by bone pain & easy fractures
uropathy
•osteitis fibrosa cystica (brown tumors)
•adynamic bone disease (calcifications), *MC in dialysis pts
Doppler ultrasonography: useful if renovascular
•osteomalacia, “soft bones” (growth retardation)
ischemic disease suspected
 HEMODIALYSIS PERITONEAL DIALYSIS
Dialysis •blood cycles through a dialyzer that removes waste & toxins, then returns to your body •peritoneal cavity filled w/ cleansing dialysis fluid then drained
•requires an access portal •cleans blood through internal walls of abdomen
•3-5x/wk •QD, can be done at home

Access Type: peritoneal catheter

•high risk of clotting & infection

3 Types of Access:
•AV Fistula (a): artery & vein surgically connected
▪⇡ blood flow causes vein to enlarge & strengthen
▪considered gold standard, low complication rate, longer life-span
•AV Graft (b): length of artificial tubing surgically connected to vein & artery, similar function to fistula
▪second-line ⇢ doesn’t last as long as fistula, prone to clotting
•Central Venous Catheter (CVC) (c): inserted into a large vein, internal end rests in top heart chamber
▪not intended for permanent access d/t higher complication rates, least desirable

Edema
Peripheral edema: lower legs or hands
Abdomen: ascites
Chest: pulmonary edema (lungs) & pleural effusion (space surrounding the lungs)
MCC chronic venous insufficiency, also a common complication of DVT
o lymphedema: surgical removal of lymph nodes for the tx of cancer (MC breast cancer) can cause swelling of a limb or limbs w/ thickening of the skin on the side of the surgery
o angioedema: reactions to some medications & some inherited disorders can cause fluid to leak out of the blood vessels into surrounding tissues
o drugs: oral diabetes meds, high BP meds, non-prescription pain relievers (ibuprofen), estrogens
o infection: peritonitis
o hypernatremia
o kidney disease: can cause swelling in lower legs & around the eyes
o heart failure: can cause swelling in the legs, abdomen, & lungs à SOB
o cirrhosis: can obstruction blood flow through the liver à swelling in the abdomen (ascites) or lower legs (peripheral edema)
S/SX: “heavy legs”, itching, pain, hyperpigmentation, thick, brawny skin, stasis dermatitis, atrophie, ascites, difficulty breathing
DX: D-dimer (low suspicion), color duplex U/S, ABI, urine dipstick (r/o nephrotic syndrome)
TX: compression stockings, elevating the legs, sodium restriction

Nephrolithiasis About Clinical Manifestations Diagnostics Management

Types: Renal colic: sudden, constant upper lateral back or UA: <5mm:
•calcium oxalate (MC), calcium phosphate flank pain over the CVA radiating to the groin or •hematuria - 80% chance of spontaneous passage
•uric acid: high protein foods, gout, chemo anteriorly; difficult to find a comfortable position •pH <5.0: uric acid, cystine - IV fluids, analgesics, antiemetics
•struvite: magnesium ammonium phosphate •pH 5.5-6.8: calcium oxalate - tamsulosin
•cystine: congenital defect in reabsorption N/V, frequency, urgency, hematuria •pH >7.2: struvite
•pH >7.5: calcium phosphate 5-10mm:
PE: CVA tenderness - 20% chance of spontaneous passage
Non-contrast CT abdomen/pelvis - extracorporeal shock wave lithotripsy
- ureteroscopy w/ or w/o stent: immediate
KUB x-ray: calcium & struvite stones are relief of obstruction
radiopaque - percutaneous nephrolithotomy: stones
>10mm
Orthostatic About Clinical Manifestations Diagnostics Management
Hypotension Orthostatic hypotension à postural hypotension – excessive Drop of >20mmHg systolic, >10mmHg BP & HR measures after 5min supine & at 1 & 3min after Physical measures to reduce venous
fall in BP when an upright position is assumed diastolic, or both 2-5min after changing standing pooling, increased Na intake, +/-
from supine to standing •<10beats/min increase in HR suggests autonomic impairment fludrocortisone or midodrine
Etiologies: •>30beats/min increase in HR suggests hypovolemia
•autonomic dysfunction (DM, age): no increased in HR
•medications EKG, serum electrolytes, glucose
•postprandial
•vagal or carotid sinus hypersensitivity Tilt table testing (when autonomic dysfunction is suspected)
•hypovolemia
•adrenal insufficiency

Drugs: alcohol, alpha-blockers, antidepressants,

antihypertensives, antiparkinsonism, antipsychotics, beta-
blockers, diuretics, muscle relaxants, narcotic analgesics,
phosphodiesterase inhibitors, sedatives/hypnotics,
vasodilators

Renal Cell About Clinical Manifestations Diagnostics Management

Carcinoma Tumor of the proximal convoluted renal tubule cells (they Triad: CT (initial) Stage I-III: radical nephrectomy
are very metabolically active cells so they are the most •hematuria •immune-mediated therapy (e.g., interleukin-2
prone to dysplasia) •flank or abdominal pain Renal U/S, MRI & monoclonal antibody molecular targeted
•palpable abdominal mass treatment) – usually resistant to
95% of primary tumors originating in the kidney Erythrocytosis often present radiation/chemo
•Clear Cell Carcinoma MC •HTN & hypercalcemia
Bilateral involvement of solitary kidney:
Characterized by lack of warning signs, variable Tumors blocks left testicular vein drainage à left- •partial nephrectomy
presentations, & resistance to chemo/radiation sided varicocele
Advanced disease:
Risk Factors: smoking, HTN, obesity, men, dialysis, •malaise, weight loss •molecularly targeted agents
cadmium or industrial exposure •debulking nephrectomy
METS: cannon ball METS to lungs (MC site); bone
Renal Artery HTN secondary to renal artery stenosis of 1 or both kidneys •HA •CT angiography Definitive à revascularization
Stenosis *MCC of secondary HTN •<20yrs or >50yrs w/ HTN •MR angiography •angioplasty w/ stent
•severe HTN •duplex doppler U/S •bypass
PATHO: decreased renal blood flow leads to activation of •HTN resistant to 3 or more drugs
RAAS Renal catheter arteriography à GOLD Medical: ACEI/ARBs *CI if bilateral stenosis
PE: STANDARD* •thiazide diuretics
Etiologies: •abdominal bruit •long-acting CCB
•atherosclerosis MC in the elderly •mineralocorticoid receptor antagonist
•fibromuscular dysplasia MC in women <50yrs ACEI à acute kidney injury!!!!!
Urinary Postoperative Urinary Retention (POUR)
Retention Common complication of both spinal & epidural
anesthesia
PATHO: prolonged blockade of parasympathetic
fibers that innervate the bladder w/ resultant
urinary retention
•Obstructive causes: urethral stricture, bladder
calculi or neoplasm, FB
•Neurogenic causes: MS, Parkinson’s, CVA, POUR
•Traumatic causes: urethral, bladder, or spinal cord
injury
•Extraurinary: fecal impaction, AAA, rectal or
retroperitoneal mass
•Infectious: local abscess, cystitis, genital herpes,
zoster
Acute Urinary Retention
Inability to void in the presence of a full bladder
Risk Factors: male, prostatic enlargement, epidural,
spinal, or prolonged anesthesia, antihistamine &
narcotic use, pelvic & peritoneal procedures
S/SX: suprapubic discomfort w/ urgency & inability
to void, unable to void within 8hr after surgery /
catheter removal, painful, vomiting, palpable
bladder, hypotension, bradycardia, cardiac
dysrhythmias
Complications: infection, ischemia, long-term
bladder dysfunction
DX: bladder U/S 500mL of urine, postvoid residual
>500mL, urine culture, CBC if infection suspected
Chronic Urinary Retention
S/SX: painless, develops gradually, suprapubic
dullness, rounded midline mass, frequent urination
of small amounts or overflow incontinence:
sensation of fullness
DX: postvoid residual by catheterization or U/S,
abdominal CT or U/S to identify suspected masses,
stones, or hydronephrosis
TX: immediate sterile catheterization
Detrusor Sphincter Dyssynergia
Consequence of neurologic pathology: SCI or MS
PATHO: urethral sphincter muscle dyssynergically
contracts during voiding causing the flow to be
interrupted & bladder pressure to arise
S/SX: daytime & nighttime wetting, hx of UTI /
bladder infections
Associated: constipation & encopresis
DX: postvoid residual >150mL
TX: botulinum A toxin injections, surgical incision of
the bladder neck (can result in incontinence)

TX: immediate sterile catheterization

Wilms Tumor About Clinical Manifestations Diagnostics Management

(Nephroblastoma) MC seen in children within the first 5yrs of life Palpable abdominal mass Abdominal U/S Total nephrectomy followed by chemo
*does NOT cross midline
Risk Factors: *lung MC site for METS so chest imaging
•family hx, horseshoe kidney •hematuria, constipation, abdominal pain, N/V, HTN, often indicated
anemia, anorexia, fever
WAGR:
•Wilms tumor
•Aniridia
•GU malformations
•mental Retardation
 Hematology 3%
HEME About
Iron Deficiency MC cause of anemia
Anemia
Microcytic anemia w/ ↓ reticulocyte count & ↑
Microcytic RDW due to a deficiency of iron
Etiologies:
•chronic blood loss (MC in US): excessive
menstruation, GI blood loss (colon cancer)
•decreased absorption: diet (MC worldwide), celiac,
bariatric surgery, H. pylori
PATHO: decreased RBC production due to lack of iron
& decreased iron stores (decreased ferritin);
normally, iron is stored in ferritin in bone marrow,
liver, & spleen
Alpha (-a/aa): silent carrier; clinically normal
Thalassemia Trans (-a/-a) or cis (--/aa): trait; trans common in pts
of African descent
Microcytic (-a/--): HbH disease; Heinz bodies
(--/--): hydrops fetalis; stillbirth or death shortly after
•Hgb Barts: gamma tetramers (γγγγ)
MC in SE Asians
Beta β,β – normal
Thalassemia β,βo or β,β+ – MC; minor; trait; heterozygous, mild
reduction in beta-chain synthesis w/ a resultant mild
Microcytic microcytic anemia
β+,β+ or β0,β+ – intermedia (mild); homozygous,
markedly reduced beta-chain synthesis & moderate
anemia that will occasionally require transfusion
β+,β+ or β0,β0 – major (Cooley’s Anemia);
homozygous, no detectable to severely reduced
beta-chain production, severe microcytic
hypochromic anemia that requires lifelong RBC
transfusions
MC in Mediterranean
Clinical Manifestations
Classic sxs of anemia: fatigue, SOB, HA
CNS: irritability, difficulty sleeping
Pagophagia: craving for ice
Pica: craving for non-food substances
PE:
•koilonychia: spooning of the nails
•angular cheilitis: inflammation of one or both corners
of the mouth
•tachycardia, glossitis (smooth tongue)
•signs of anemia (pallor)
*hx of drinking >24oz of cow’s milk a day or transition
to cow’s milk <12mo old is common
Trait: mild microcytic anemia, asymptomatic
HbH: moderate hemolytic anemia, jaundice,
hepatosplenomegaly, gallstones, occasional need for
transfusion during illness
Trait: mild microcytic anemia, asymptomatic
Intermedia (β+,β+ or β0,β+): moderate hemolytic
anemia (Hgb >7g/dL)
•splenomegaly, intermittent transfusion requirement
Major (β+,β+ or β0,β0):
•massive hepatosplenomegaly, growth retardation
•bony deformities – frontal bossing, maxillary
prominence from extramedullary hematopoiesis (all
preventable w/ aggressive transfusion therapy)
*if iron overload from chronic transfusions is not
adequately treated w/ chelation therapy, pts can
develop cirrhosis, endocrine abnormalities, cardiac
dysfunction, & skin hyperpigmentation
Diagnostics Management
CBC: Iron replacement: Ferrous sulfate – 4-6mg/kg/d
•microcytic hypochromic anemia divided in 2-3 doses
•↑ RDW
•anisocytosis Take w/ vitamin C, w/ water or orange juice, &
•↓ reticulocytes on an empty stomach for ↑ absorption
•may have thrombocytosis & poikilocytosis ADRs: GI (N/V/D/C, flatulence, dark stool)
Smear: hypochromic microcytic RBC w/ pencil •continue 8-12wks after Hgb has normalized
forms (total of 3-4mo of replacement)
•limit milk to ≤8oz/d
Iron studies:
↑ TIBC Severe, life-threatening anemia: RBC transfusion
↓ ferritin, transferrin saturation, serum iron
Bone marrow: absent iron stores
Trait: mild microcytic anemia Trait: no intervention
•normal levels of HbA, HbA2, & HbF
•+Hb Barts (gamma-chain tetramer) on HbH: folic acid supplementation
newborn screen
Stem cell transplant: curative
HbH: moderate hypochromic, microcytic
anemia (Hgb 7-10g/dL)
•variation in RBC shape/size on peripheral
blood smear & other findings of chronic
hemolysis
•reticulocytosis
•HbH on electrophoresis
•newborn screen >25% Hb Barts
Trait: mild microcytic anemia Trait: no intervention
•HbA2 level 3.5-8%
•HbF level 1-5% Major: chronic transfusion therapy may be
*significant variability depending on type of required as early as 2mo, but necessary by 2y
mutation; may not be detected on newborn •10-15mL/kg of PRBCs required q3-4wks
screen •goal pretransfusion Hgb 9-10g/dL
Chelation therapy for chronically transfused pts
Intermedia: clinical designation based on w/ iron overload – PO/SC/IV chelators available
having a moderate microcytic anemia (Hgb & necessary 5-7d/wk
>7g/dL) – only necessitates transfusion w/
normal growth In pts receiving chronic transfusion, ferritin
levels should be monitored to screen for iron
Major (Cooley’s): clinical designation w/ a overload, but annual MRI should be used to
resultant severe anemia (Hgb 3-7g/dL) more accurately assess cardiac/liver iron
•reticulocytosis concentrations & guide chelation therapy
•HbF 30-100%, HbA2 2-7%
•MCV 50-60fL Stem cell transplant: curative
*NB screen will demonstrate only HbF in pts
w/o any beta-chain production
Anemia About Clinical Manifestations Diagnostics Management
B12 Sources: meats, eggs, dairy Hematologic: fatigue, exercise intolerance, pallor CBC w/ peripheral smear: IM B12 – IM cyanocobalamin
Deficiency Absorption: combines w/ intrinsic factor, absorbed •megaloblastic anemia: hypersegmented - weekly until corrected à monthly
mainly in distal ileum Epithelial: glossitis, diarrhea, malabsorption neutrophils, macro-ovalocytes, mild - can switch to PO once resolution of sxs
Macrocytic leukopenia &/or thrombocytopenia - pts w/ pernicious anemia need lifelong monthly
MCV >100 PATHO: deficiency causes abnormal DNA synthesis Neuro sxs: •low reticulocytes injections
•symmetric paresthesias MC initial symptom
Etiologies: •lateral & posterior spinal cord demyelination & ↓ B12, ↑ LDH, ↑ homocysteine
•decreased absorption: pernicious anemia, Crohn degeneration: ataxia, weakness, vibratory, sensory, &
disease, chronic ETOH use, H2 blockers/PPIs, metformin proprioception deficits, ↓ DTRs ↑ methylmalonic acid (distinguishes from
•decreased intake: vegans folate deficiency)
Folate PATHO: deficiency causes abnormal DNA synthesis NO NEURO SXS! CBC w/ peripheral smear: PO folic acid
Deficiency •megaloblastic anemia (hypersegmented
Etiologies: Hematologic: fatigue, exercise intolerance, pallor, neutrophils, macro-ovalocytes)
Macrocytic •inadequate intake (MC): alcoholics, unbalanced diet chlorosis (pale, faintly green complexion – extremely •low reticulocytes
MCV >100 •increased requirements: pregnancy rare)
•impaired absorption ↓ B12, ↑ LDH, ↑ homocysteine
•impaired metabolism: methotrexate, trimethoprim Epithelial: glossitis, aphthous ulcers, diarrhea,
•loss: dialysis malabsorption NORMAL methylmalonic acid (distinguishes
from B12 deficiency)

Anemia About Clinical Manifestations Diagnostics Management

Anemia of Anemia due to decreased RBC production in the setting PATHO: 3 main factors decrease serum iron CBC: Treat the underlying disease
Chronic of chronic disease •↑ hepcidin: blocks release of iron from •mild normocytic normochromic anemia
Disease macrophages & reduces GI absorption •↓ reticulocytes, normal/↑ RDW Erythropoietin-alpha if renal disease or low EPO
Etiologies: chronic inflammatory conditions – chronic •↑ ferritin: sequesters iron into storage Iron studies: levels
Normocytic infection, inflammation, autoimmune disorders, •erythropoietin inhibition •normal/↑ ferritin
malignancy •↓ TIBC, ↓ serum iron
Hemolytic Anemias About
Sickle Cell Anemia SCD – group of inherited hemoglobinopathies
secondary to the production of abnormal Hgb
Normocytic complicated w/ an associated hemolytic
anemia & vaso-occlusion
Genetic mutation in both beta-globulin genes,
w/ at least 1 mutation resulting in HbS –
homozygous SS MC form & most severe (MC
in AA)
Other forms: compound heterozygous states
where HbS is combined w/ another abnormal
Hgb or a beta-thalassemia mutation – HbC,
HbE, beta-plus thalassemia, beta-zero
thalassemia
G6PD Deficiency x-linked recessive enzymatic disorder of RBCs
that may cause episodic hemolytic anemia
Normocytic
Risk Factors: males, AA males
PATHO: decreased G6PD activity during
oxidative stress results in an oxidative form of
Hb (methemoglobin); the denatured
hemoglobin precipitates as Heinz bodies
Exacerbating factors:
•infection MC cause, fava beans
•dapsone, methylene blue, primaquine,
nitrofurantoin, phenazopyridine
Clinical Manifestations
Painful episodes: vaso-occlusive event resulting in acute
onset of severe pain commonly in back, check, &
extremities
•swelling of hands/feet in infants (dactylitis)
Fever (>38.5C): more susceptible to bacterial infections
because of functional asplenia; highest risk for sepsis
from encapsulated organisms such as S. penumoniae,
N. meningitidis, & Salmonella
Splenic sequestration: intrasplenic trapping of RBCs &
platelets – decrease in Hgb & often platelets w/ an
acute enlargement of spleen that can lead to life-
threatening anemia (often associated w/ acute
viral/bacterial illnesses)
Acute chest syndrome: fever, respiratory sxs, new
pulmonary infiltrate on CXR
•causes: bacterial (M. pneumoniae, C. pneumoniae, S.
aureus, S. pneumoniae, H. flu), viral, fat emboli, in situ
vaso-occlusion, pulmonary edema, thromboembolism
Aplastic crisis: marked anemia w/ reticulocytopenia,
frequently secondary to parvovirus infection that
causes a maturation arrest of RBC production in bone
marrow for 1-2wks
•increased fatigue, pallor, fever
•reticulocytopenia begins ~5d after exposure & lasts 7-
10d
Stroke: SCD-SS & Sβ0-thalassemia have 10% risk of
stroke by 20yo; predominant etiology is large-vessel
vasculopathy w/ proliferative intimal hyperplasia
•hemiparesis, facial droop, aphasia, generalized sxs
(AMS, stupor, seizures)
•neonatal jaundice
For milder forms pts are clinically & hematologically
normal until they have an “oxidative challenge”
Severe forms can have a baseline hemolytic anemia
6-24h after exposure to oxidative agent: dark urine,
jaundice, pallor, tachycardia, nausea, abdominal pain
24-48h: low-grade fever, irritability, listlessness,
splenomegaly, hepatomegaly
Diagnostics
Peripheral smear:
•target cells, sickled erythrocytes, ↓ H/H
•Howell-jolly bodies indicates functional asplenia
Hgb electrophoresis: 90% HbS, 8% HbF
Fever: all pts w/ SCD + fever need urgent
evaluation w/ PE, blood culture, CBC w/ diff,
reticulocyte count; consider urine culture, CXR
Stroke: head MRI, CBC w/ reticulocyte count, Hgb
electrophoresis for HbS %, type & screen
•prevention: routine transcranial Doppler
*hemolytic anemia pattern
⇡ indirect bilirubin, reticulocytes, LDH
⇣ haptoglobin
Peripheral smear:
•normocytic hemolytic anemia only during crises
•schistocytes (“bite” cells), anisocytosis, blister
cells
•(+) Heinz bodies hallmark
Hemolytic anemia:
↑ reticulocytes, indirect bilirubin
↓ haptoglobin
DAT (-)
Enzyme assay for G6PD: fluorescent spot test;
DNA testing; usually performed after episodes
Management
Painful episodes:
•outpatient: PO meds (anti-inflammatories w/
or w/o opioid) & hydration
•inpatient: combo of ibuprofen or ketorolac
w/ an opioid & IV hydration
Fever: ceftriaxone or high-dose ampicillin +
observation
Splenic sequestration: follow Hgb & spleen size
closely; fluid admin in stable pts w/ mild
decrease in Hgb
•hypoxia, tachypnea, tachycardia: transfuse 5-
10mL/kg RBCs, then reassess
Acute chest syndrome: ampicillin or 3rd gen
cephalosporin (cefotaxime, ceftriaxone) +
macrolide (erythromycin, azithromycin,
clarithromycin) + oxygen if hypoxic; pain
control; incentive spirometry
•respiratory/hemodynamic instability requires
RBC transfusion
Aplastic crisis: PRBC transfusion if pt is
symptomatic
Stroke: exchange transfusion to decrease HbS
%; long-term – placed on chronic RBC
transfusion protocol to minimize risk for further
strokes
Preventative Management:
•Penicillin prophylaxis, folic acid
supplementation, hydroxyurea for pts >9mo
Usually self-limited; avoid offending foods &
drugs
•Hgb returns to normal within 3-6wks
Hgb >7mg/dL + clinically stable + no
hemoglobinuria: observe for 24-48h
Hgb <7mg/dL or Hgb 7-9mg/dL w/ continued
brisk hemolysis (persistent hemoglobinuria):
consider PRBC transfusion
Neonatal jaundice: phototherapy
 About Clinical Manifestations Diagnostics Management
Hereditary Autosomal dominant hereditary intrinsic Recurrent episodes of hemolysis: anemia, jaundice, Peripheral smear: - folic acid
Spherocytosis (HS) hemolytic anemia splenomegaly •hyperchromic microcytosis, 80% spherocytes - splenectomy
•↑ MCHC •delayed until at least 4yo
Autoimmune PATHO: deficiency in RBC membrane & Pigmented gallstones •pneumococcal vaccine prior
cytoskeleton (spectrin), leading to increased •EMA binding
RBC fragility & sphere-shaped RBCs •(+) osmotic fragility, (-) Coombs
Autoimmune Acquired hemolytic anemia due to Anemia: pallor, fatigue, weakness, dyspnea CBC + peripheral smear: Warm:
Hemolytic Anemia autoantibody production against RBCs Hemolysis: hemoglobinuria, jaundice, splenomegaly •microspherocytosis (esp. warm) - first line: steroids; transfusion if severe
(AIHA) •polychromasia - second line: splenectomy, rituximab
PATHO: Cold-induced vascular phenomenon: Hemolysis:
Autoimmune •warm: IgG antibodies •acrocyanosis: numbness or mottling of the fingers, •↓ haptoglobin Cold:
•cold: IgM antibodies toes, nose, ears that resolves w/ warming up of the •↑ reticulocyte count - avoidance of cold temperatures
body parts •↑ indirect bilirubin - transfusions, plasmapheresis, IVIG
Etiologies: •↑ LDH
•warm: penicillin, cephalosporins, SLE
•cold: M. pneumoniae, EBV (+) Coombs
Paroxysmal Rare, acquired stem cell mutation – RBCs Triad: hemolytic anemia (hemoglobinuria) + Hemolysis: Complement inhibitors:
Nocturnal become deficient in GPI anchor surface pancytopenia + unexplained thrombosis in atypical •↓ haptoglobin - eculizumab
Hemoglobinuria proteins veins •↑ reticulocyte count
•dark, cola-colored urine during the night or early •↑ indirect bilirubin - folic acid
PATHO: deficiency in CD55 & CD59 lead to morning •↑ LDH - allogenic hematopoietic cell transplant
increased complement activation & only potential for cure
intravascular RBC destruction Flow cytometry test: CD55/CD59-deficienct RBCs

About Clinical Manifestations Diagnostics Management

Hemophilia x-linked recessive disorder occurring almost
exclusively in males
•A = factor VIII deficiency (MC)
•B = factor IX deficiency *Christmas disease
•C = factor XI deficiency *Ashkenazi jews
Von Willebrand Autosomal dominant disorder associated w/
Disease ineffective platelet adhesion due to deficient
or defective vWF
Hemarthrosis: delayed bleeding or swelling in weight- •prolonged aPTT - A: factor VIII infusion; desmopressin (DDVAP)
bearing joints (MC ankles) - B: factor IX infusion
Mixing studies: PTT corrects w/ mixing studies - C: factor XI infusion
Excessive hemorrhage due to trauma & surgery or
incisional bleeding A = low factor VIII
•epistaxis, bruising, GI or urinary tract hemorrhage B = low factor IX
C = low factor XI
Mucocutaneous bleeding: epistaxis, bleeding gums, •prolonged PTT & bleeding time (worse w/ aspirin) - DDVAP
petechiae, purpura, bruising, menorrhagia, prolonged - factor VIII concentrates
bleeding time after minor cuts Ristocetin-induced platelet aggregation (gold standard) - VWF-containing products

MC hereditary bleeding disorder

HEME About Clinical Manifestations Diagnostics Management
Immune PATHO: autoimmune-antibody reactions vs. platelets w/ Often asymptomatic Isolated thrombocytopenia Children: observation; 80% resolve w/o
Thrombocytopenic splenic platelet destruction à consumptive tx within 6mo
Purpura (ITP) thrombocytopenia Mucocutaneous bleeding: petechiae, bruising, Normal coagulation tests - +/- IVIG
purpura, bullae, bleeding of tooth/gums,
Incidence: menorrhagia Adults:
•young children 2-4yrs; often 1-3wks following acute viral - steroids
infection (often self-limited) *no splenomegaly - IVIG
•adults: young women <40; idiopathic, often recurrent - splenectomy (refractory)
Thrombotic PATHO: auto-ab vs. ADAMTS13 (vWF-cleaving protease) PENTAD: “FAT RN” Thrombocytopenia - plasmapheresis: removes Ab & adds
Thrombocytopenic à unusual large vWF multimers à micro thrombosis of •fever ADAMTS13
Purpura (TTP) small vessels à thrombocytopenia (consumptive) & •anemia: microangiopathic hemolytic anemia Hemolytic anemia:
hemolytic anemia *jaundice •peripheral smear: ↑ reticulocytes, schistocytes - immunosuppression: steroids,
•thrombocytopenia: bruising, purpura, bleeding (bite or fragmented cells) cyclophosphamides
Incidence: •renal failure/uremia •LFTs: ↑ indirect bilirubin, ↓ haptoglobin
•young adults 20-50yrs •neuro sxs: HA, CVA, AMS
•MC women Normal coagulation tests
Hemolytic Uremic PATHO: exotoxins (shiga-like & shiga toxins) damages TRIAD: “RAT” Thrombocytopenia - observation in most children (usually
Syndrome (HUS) vascular endothelium, activating platelets à •renal failure/uremia (predominant symptom) self-limited)
microthrombosis of small vessels à consumptive •anemia: microangiopathic hemolytic anemia Hemolytic anemia:
thrombocytopenia & hemolytic anemia *jaundice •peripheral smear: ↑ reticulocytes, schistocytes - plasmapheresis
•ADAMTS13 normal •thrombocytopenia: bruising, purpura, bleeding (bite or fragmented cells) - +/- FFP if severe
•LFTs: ↑ indirect bilirubin, ↓ haptoglobin
Incidence: *NO ABX – may worsen the disease
•predominantly seen in children w/ diarrhea prodrome: ↑ BUN/creatinine
Enterohem. E coli O157:H7 (80%), Shigella, Salmonella
•adults: seen w/ HIV, SLE, & antiphospholipid syndrome Normal coagulation tests
Disseminated PATHO: pathologic clotting cascade activation à Diffuse hemorrhage: venipuncture sites, mouth, Hemolytic anemia: Reversal of the underlying cause
Intravascular widespread thrombi à consumption of platelets à nose; extensive bruising •peripheral smear: ↑ reticulocytes, schistocytes mainstay of tx
Coagulation (DIC) diffuse bleeding (bite or fragmented cells)
Thrombosis: renal failure, gangrene (as clots block •LFTs: ↑ indirect bilirubin, ↓ haptoglobin - +/- platelet transfusion (if <20,000)
Incidence: circulation) - +/- FFP
•MC in young or elderly *abnormal coagulation tests
•MC gram negative species Pts usually acutely ill ↓ fibrinogen - +/- heparin in select cases
•OB emergencies, malignancy, massive tissue trauma ↑ D-dimer, PT, & PTT
Severe thrombocytopenia
Heparin Induced Acquired thrombocytopenia esp. within the first 5-10d of Thrombocytopenia – bleeding •thrombocytopenia Immediate D/C of all heparin +
Thrombocytopenia the initiation of heparin •timing of platelet drop (>50%) initiation of non-heparin anticoagulants
(HIT) Thrombosis – venous thrombosis, gangrene, organ •thrombosis •direct thrombin inhibitors (argatroban,
Risk Factors: infarction, skin necrosis lepirudin)
•UFH > LMWF, surgical > medical, F > M Gold standard: 14-C-serotonin release assay •fondaparinux
•DOAC (apixaban, edoxaban,
PATHO: autoantibody formation to the hapten of heparin rivaroxaban)
+ platelet factor 4 causes platelet activation &
consumption, leading to thrombocytopenia & thrombosis
ONC About Clinical Manifestations Diagnostics Management
Hodgkin Germinal or pregerminal B-cell malignancy originating in the Painless LAD (cervical, supraclavicular) Excisional whole lymph node bx: Early-stage disease:
Lymphoma lymphatic system •ETOH may induce lymph node pain •Reed-Sternburg cell (“owl eye” - chemo + radiation
Bimodal: 15-35, >60 appearance)
Risk Factors: EBV, immunosuppression, smoking Upper body lymph nodes: neck MC, axilla, shoulder, Advanced stage: combo chemo “ABVD”
mediastinum CXR: mediastinal mass (adenopathy) - Adriamycin
4 main types: - Bleomycin
•Nodular sclerosing: MC type; female predominance Mediastinal LAD or mass: 2nd MC presentation CBC normal, elevated ESR - Vinblastine
•Mixed cellularity: associated w/ EBV - Dacarbazine
•Lymphocyte rich/predominant: best prognosis •hepatomegaly, splenomegaly CT – staging
•Lymphocyte depleted: worst prognosis
Systemic “B” sxs: fever/chills, night sweats, weight
loss, Pel-Ebstein fever (cyclical x1-2wks)
•associated w/ a poorer prognosis
Non-Hodgkin Major Types: Local: painless LAD Burkitt: starry sky appearance on Asymptomatic: no tx
Lymphoma DIFFUSE LARGE B-CELL: MC MARGINAL ZONE: *immunocompromised pt (HIV) w/ GI sxs & painless microscopy
•fast-growing, aggressive •extranodal MALT: H. pylori peripheral LAD Stage I: radiation, chemo
NO Reed-Sternberg cells
FOLLICULAR: BURKITT: associated w/ EBV Extranodal involvement: High-grade (aggressive): R-CHOP
•indolent, chromosomal •Endemic (Africa): jaw/face •GI: bowel obstruction CT: help establish stage based on extent - Rituximab
translocation •Sporadic: GI/paraaortic •bone marrow: fatigue, easy bruising, recurrent of nodal & extranodal involvement - Cyclophosphamide
•Immunodeficient: HIV infections - Hydrochloride
MANTLE CELL •spinal cord: loss of sensation Lymph node biopsy - Oncovorin
SMALL LYMPHOCYTIC: lymph - Prednisolone
Risk Factors: ↑ age, HIV, EBV, nodes & spleen Systemic “B” sxs less common
HHV-8, H. pylori, autoimmune d/o
Spread: non-contiguously to extranodal sites à skin,
GI tract, brain
ONC About
Acute Myelogenous MC acute form of leukemia in adults
Leukemia (AML) Median onset 65yrs; 20% of cases of childhood
leukemia
3 Major Subtypes:
Acute Promyelocytic Leukemia (APL or M3)
•t(15; 17) associated w/ DIC, Auer rods, &
myeloperoxidase activity
Acute Megakaryocytic Leukemia
•MC in children <5yrs w/ Down Syndrome
Acute Monocytic Leukemia
•associated w/ infiltration of the gums (gingival
hyperplasia)
Chronic Myelogenous Older males
Leukemia (CML)
PATHO: fusion of 2 genes: BCR (chromosome 22)
& ABL1 (chromosome 9), resulting in the BCR-
ABL1 fusion gene. Translocation between
chromosomes 9 & 22 = Philadelphia
chromosome (abnormal chromosome 22 which
harbors the BCR-ABL1 gene)
Acute Lymphocytic •malignancy arising from immature lymphoid
Leukemia (ALL) stem cells in the bone marrow
•B cell (MC!), T cell, or null type (non B or T cell)
MC childhood malignancy – peak 2-5yrs
•boys > girls, Down Syndrome
PATHO: overpopulation of immature WBCs
(blasts) overtake normal hematopoiesis resulting
in pancytopenia
Chronic Lymphocytic MC leukemia in adults
Leukemia (CLL)
Mature B cell clonal malignancy
Risk Factors: increasing age (70yrs median age),
men
Clinical Manifestations Diagnostics Management
Pancytopenia: lethargy, malaise, anorexia >20% blasts (immature WBCs) Chemo + bone marrow transplant
•thrombocytopenia: mucocutaneous bleeding •Promyelocytic
•neutropenia: increased infections & fever -(+) auer rods Tumor Lysis Syndrome: w/ chemo tx
-sudan black & myeloperoxidase (+) ↑ K, ↓ Ca, ↑ phos, hyperuricemia, renal
25% of children develop bone pain or arthralgia d/t •Acute monocytic failure
leukemic infiltration of perichondral bone or -gingival infiltration/hyperplasia TX: allopurinol, IV fluids
leukemic expansion of marrow cavity •Megakaryocytic: ↑ down syndrome
May develop soft-tissue tumor called chloroma in Normochromic, normocytic anemia
spinal cord or skin; greenish hue Thrombocytopenia, low reticulocyte count
Progressive bone marrow failure leads to pallor, Bone marrow examination FNA & bx – confirmatory
ecchymoses or petechiae, & fever
DDX: aplastic anemia, IPT, EBV
Fatigue, night sweats, malaise, weight loss, fever •Philadelphia chromosome PO chemo
•striking ↑ WBC: >100,000 - hydroxyurea
Splenomegaly •LAP score ↓ - imatinib
Pruritis after hot baths/showers Chronic: <5% blasts Imatinib: BRC-ABL tyrosine kinase inhibitor
Accelerated: 5-30% blasts - Philadelphia (+)
Acute: >30% blasts
Pancytopenia: >20% blasts; PAS (+) PO chemo in Philadelphia (+)
•fever & infections (leukopenia) •precursor B-cell ALL (85%): CNS sxs - induction: kills detectable disease for
•bleeding from thrombocytopenia (petechiae, •precursor T cell MC associated w/ adolescents w/ complete remission
purpura) mediastinal mass & CNS sxs - consolidation: short term intensive
•anemia (pallor, fatigue) therapy to sustain remission
ANC <1000 - maintenance: low dose to eradicate any
CNS sxs: remaining undetectable cells
•HA, stiff neck, visual changes, vomiting
Stem cell transplant for relapse
PE:
•hepatomegaly or splenomegaly MC
-anorexia, weight loss, abd. pain/distention
•lymphadenopathy
CHILD + LAD + BONE PAIN + bleeding + fever
Pancytopenia: fatigue MC symptom •smudge (smear) cells Indolent: observation
•thrombocytopenia: mucocutaneous bleeding •well-differentiated lymphocytes; >5,000/µL
•neutropenia: increased infections & fever Symptomatic or progressive:
ZAP-70 (+) à 8yrs survival - chemo
PE: LAD MC, splenomegaly 2nd MC ZAP-70 (-) à >25yrs
Allogenic stem cell transplant is curative
 Pulmonary 3%
LUNG CANCER About DX
Bronchogenic MCC of cancer-related deaths in the US Types ⇢ ➀ Small Cell Lung Cancer (SCLC) – 15% First ⇢ CXR Central: transbronchial biopsy
Carcinoma Risk Factors: smoking, asbestos ➁ Non-Small Cell Lung Cancer (NSCLC) – 85% Then ⇢ CT w/ contrast •Carcinoid: pink/purple, well-vascularized
•Adenocarcinoma (MC) Histopathology:
S/SXS: cough, SOB, fever, weight loss, fatigue *Bronchoalveolar Carcinoma (adeno in situ) Adenocarcinoma: ▪neoplastic gland formation, pneumocyte marker expression (TTF-1), or
•Squamous Cell Carcinoma intracytoplasmic mucin
•Large Cell Carcinoma Squamous: ▪keratin production by tumor cells &/or intracellular desmosomes
Small Cell Lung Cancer (SCLC): •Carcinoid Tumors Large Cell: ▪sheets of round/polygonal cells w/ prominent nucleoli & abundant pale
•central, aggressive, often METS at presentation staining cytoplasm w/o differentiating features
•Paraneoplastic: Cushing’s, SIADH, SVC syndrome (face/neck swelling), Lambert-Eaton (proximal muscle
weakness, dry mouth, hyporeflexia) Immunohistochemistry:
▪SCLC ⊕ TTF-1, high proliferation rate (Ki-67, MIB-1)
Adenocarcinoma: *asbestos exposure Large Cell Carcinoma: ▪Adenocarcinoma ⊕ TTF-1, napsin A, CK 7, mucicarmine, PAS-D
•peripheral, slow growing, MC seen in non-smokers •central or peripheral, rare ⊖ thyroglobulin
•Paraneoplastic: thrombophlebitis •large peripheral mass w/ prominent necrosis MC ▪Squamous ⊕ p40, p63, CK 5/6, desmoglein
•Paraneoplastic: gynecomastia ⊖ CK 7 (usually)
Squamous Cell Carcinoma: Management
•central, often associated w/ hemoptysis NSCLC: surgical excision, radiation + chemo
•hypercalcemia, +/- elevated PTHrp SCLC: chemo + radiation, no surgery!
Pancoast syndrome: shooting arm pain/weakness, Horner’s (ipsilateral miosis, ptosis, anhidrosis)
Screening: USPSTF recommends ANNUAL low-dose CT screening for those 55-80 who have no sxs of lung
Carcinoid Tumors ⇢ excess secretion of serotonin, histamine, bradykinin cancer + a 30PPY smoking hx who currently smoke or have quit within 15yrs
•central, GI tract MC site, lung 2nd MC
S/SXS: hemoptysis, focal wheezing, recurrent pneumonia
•Carcinoid syndrome: flushing, diarrhea, hypotension

LUNG CANCER About Diagnostics Management

Mesothelioma ▪malignant tumor that develops from mesothelial cells ▪♂ > ♀ 3:1, ages ~40-70y CXR/CT w/ contrast: unilateral pleural thickening w/ pleural effusion TX: surgery + chemo + radiation therapy

Localization ⇢ ▪Pleural mesothelioma (MC, 80%) ▪MCC ⇢ asbestos exposure** Thoracentesis: bloody, exudative Surgery: pleurectomy/decortication or radical
▪Peritoneal mesothelioma (rare) extrapleural pneumonectomy
▪Pericardial mesothelioma (very rare) Confirm ⇢ biopsy + immunohistochemistry
Chemo: cisplatin + pemetrexed
Pleural Mesothelioma: BX (epithelioid): polygonal, oval, or cuboidal cells arranged in various
▪3 histologic subtypes ⇢ epithelioid (MC), sarcomatoid, biphasic (mixed) growth patterns including papillary, tubular/acinar (glandular), Non-surgical candidates:
adenomatoid, etc. +/- psammoma bodies & necrosis ▪systemic chemotherapy
S/SXS: dyspnea, CP, cough, night sweats, weight loss, fatigue, pleural effusion ▪management of pleural effusion
Immunohistochemistry: used to distinguish from adenocarcinoma ▪pleurodesis, tunneled catheters, VATS
▪mesothelioma markers ⇢ ⊕calretinin, CK5/6, WT-1, D2-40 ▪palliative RT
▪adenocarcinoma markers ⇢ ⊕CEA, BerEP4, MOC-31, claudin-4, B72.3
PULM About
Pneumonia Community-Acquired Pneumonia (CAP)
•outside hospital or within 48h of admission
RF: older age, tobacco use, excessive ETOH use,
comorbid medical condition (esp. COPD), recent viral
URI, immunosuppression
Viral Pathogens (“Atypical” Presentation):
•RSV, influenza, parainfluenza
•CMV, adenovirus, SARS-CoV-2
Nosocomial Pneumonia
– Hospital-Acquired Pneumonia (HAP)
•acquired >48h after admission
– Ventilator-Associated Pneumonia (VAP)
•acquired >48h after endotracheal intubation
Pathogens:
•Pseudomonas aeruginosa (cystic fibrosis)
•Enterobacter spp.
•Acinetobacter spp.
•S. aureus (esp. MRSA)
RF: recent abx use, prolonged hospitalization (≥5d)
Clinical Manifestations Diagnostics
CAP: acute onset fever, cough (+/- sputum), dyspnea LABS: CBC, CMP, CPR, procalcitonin
EXAM: tachycardia, tachypnea, crackles (rales), rhonchi •leukocytosis w/ left shift
– tactile fremitus, egophony, dullness to percussion •procalcitonin
<0.25ng/dL suggests viral
*no clinical features reliably distinguish between different ≥0.25ng/dL suggests bacteria
pathogens, but certain features can raise the index of suspicion
for certain microbes CXR: AP + lateral views
Legionella: GI (N/V/D), hyponatremia, elevated liver •lobar consolidations
transaminases, CPR >100mg/L •interstitial infiltrates
•cavitations
Mycoplasma *MC in ambulatory setting
S/SXS: gradual onset HA, malaise, low-grade fever +/- sore throat VIRAL: bilateral, multifocal, patchy or
– cough (+/- sputum) follows, may have pleuritic CP/SOB ground-glass opacities
*chest soreness from persistent coughing common complaint *dense consolidations, pleural
– ⊕URI SXS (rhinorrhea, otitis media, sinusitis, cervical LAD) effusion & abscess should be
Non-Respiratory Associated Disease: absent
•autoimmune hemolysis (cold agglutinin disease), usually mild BACTERIAL: dense lobar or alveolar
•mucocutaneous disease consolidations
– erythema multiforme, SJS, other skin rashes, mucositis
•mild hepatic transaminase elevations CURB-65 Assessment (1pt each)
•arthralgias & myalgias C – confusion
U – BUN >19mg/dL (>7mmol/L urea)
Nosocomial: new lung infiltrate + ≥2 clinical features of infection R – respiratory rate ≥30
S/SXS: new-onset fever, leukocytosis or leukopenia, purulent B – SBP <90mmHg or DBP ≤60mmHg
sputum, decline in oxygenation 65 – age ≥65yo
0-1: outpatient
Pseudomonas: IV antibiotics within past 90d, structural lung 2: admission
disease (e.g., cystic fibrosis, bronchiectasis) ≥3: assess for ICU care (esp. if 4-5)
Microbiology (only need if inpatient)
•blood culture x2
•sputum gram stain + culture
•S. pneumoniae urine antigen
•PCR for Legionella
•PCR for pneumonia (BioFire PN)
Management
CAP, outpatient:
•Amoxicillin + macrolide (preferred)
– Doxycycline is macrolide alternative
⊕heart, lung, liver, or kidney disease, diabetes,
alcoholism, malignancy, asplenia,
immunosuppression, or use of abx in last 3mo:
•Augmentin + macrolide (preferred)
– Doxycycline is macrolide alternative
•FQ monotherapy (alternative)
CAP, inpatient, non-ICU:
•antipneumococcal beta lactam + macrolide
•FQ monotherapy
CAP, inpatient, ICU:
•antipneumococcal beta lactam + Azithromycin
*preferred
•antipneumococcal beta lactam + FQ
– Suspect MRSA: ⊕Vancomycin or Linezolid
– Suspect Pseudomonas:
•beta lactam + FQ
*both w/ antipseudomonal coverage
ABX REVIEW
Anti-MRSA: Vancomycin, Linezolid
Respiratory FQ
– Levofloxacin, Moxifloxacin, Gemifloxacin (PO)
Antipseudomonal FQ: Ciprofloxacin, Levofloxacin
Antipneumococcal Beta Lactam:
– Augmentin, Ampicillin-Sulbactam (Unasyn)
– Ceftriaxone, Cefotaxime, Ertapenem
Antipneumo + Antipseudomonal Beta Lactam:
– Piperacillin-Tazobactam (Zosyn), Imipenem
– Meropenem, Cefepime, Ceftazidime
Macrolides: Azithromycin, Clarithromycin
Nosocomial (Pseudomonas coverage):
•Zosyn or Cefepime
– Risk of MRSA: ⊕Vancomycin or Linezolid
PULM About
Pneumothorax PTX: a collection of air within the pleural space between the lung (visceral pleura) & the chest wall (parietal Traumatic PTX: a type of PTX caused by trauma (e.g., penetrating injury, iatrogenic trauma)
(PTX) pleura) that can lead to parietal or complete pulmonary collapse ▪blunt trauma (e.g., MVC in which thorax hits steering wheel or rib fracture occurs)
PATHO: ⇡ intrapleural pressure ⇢ alveolar collapse ⇢ decreased V/Q ratio & ⇡ right-to-left shunting ▪penetrating injury (e.g., gunshot or stab wound)
▪Iatrogenic PTX ⇢ mechanical ventilation w/ high PEEP (barotrauma), thoracentesis, CVC
Primary Spontaneous PTX (PSP): occurs in patients w/o clinically apparent underlying lung disease placement, bronchoscopy, lung biopsy (usually closed PTX)
▪caused by ruptured subpleural apical blebs RF: smoking (90%) ⇢ up to 20-fold ⇡ in risk (risk ⇡ w/ PATHO: ▪Closed: air enters through a hole in the lung (e.g., d/t blunt trauma)
▪MC affects tall, thin males, ♂ > ♀ ~6:1 cumulative # of cigarettes smoked) ▪Open: air enters through a lesion in the chest wall (e.g., d/t penetrating trauma)
▪peak incidence 16-25yo ▪family hx, male, young, homocystinuria, tall/slim

Secondary Spontaneous PTX (SSP): occurs as a complication of underlying lung disease Tension PTX (TPTX): a life-threatening variant of PTX characterized by progressively ⇡ pressure within the
▪♂ > ♀ ~3:1, peak incidence 60-65yo ▪Marfan syndrome, malignancy chest & cardiorespiratory compromise
▪COPD (smoking): rupture of bullae in emphysema ▪infections: TB, PCP (alveolitis, rupture of a cavity) PATHO: ➀ disrupted visceral pleura, parietal pleura, or tracheobronchial tree
▪Catamenial PTX ⇢ thoracic endometriosis (rare) ▪CF: bronchiectasis w/ obstructive emphysema & bleb ➁ 1-way valve mechanism ⇢ air enters the pleural space on inspiration but cannot exit
or cyst rupture ➂ progressive accumulation of air in pleural space & ⇡ ⊕pressure within the chest
Recurrent PTX: a second episode of spontaneous PTX, either ipsilateral or unilateral ➃ collapse of ipsilateral lung, compression of contralateral lung, trachea, heart, & SVC;
angulation of IVC
PSP/SSP ⇢ PATHO: rupture of blebs/bullae ⇢ air moves into pleural space w/ ⇡ ⊕pressure ⇢ ipsilateral ➄ impaired respiratory function, ⇣ venous return to the heart ⇢ reduced CO ⇢ hypoxia
lung is compressed & collapses & hemodynamic instability
Clinical Manifestations/DX Management
S/SXS: sudden, severe &/or stabbing ipsilateral pleuritic CP & dyspnea TX: assess stability ⇢ requires ALL of the following to be considered stable:
PE: ⇣/absent breath sounds, hyperresonance to percussion, ⇣ fremitus on the ipsilateral side ➀ RR <24 breath/min ➃ normal BP
➁ SpO2 >90% on RA ➄ able to speak in whole sentences
⊕subcutaneous emphysema: infiltration of air under the dermal layers of the skin ➂ HR 60-120bpm
▪distention/bloating of chest, neck, face
▪palpation ⇢ crackling sensation (crepitus) Primary Spontaneous PTX (PSP):
▪stable, small (≤3cm) PSP ⇢ usually resolves spontaneously within ~10d
Tension PTX: ▪severe acute respiratory distress: cyanosis, restlessness, diaphoresis ▪observation +/- supplemental O2 (6L/min x6h to target SpO2 >96%)
▪reduced chest expansion on the ipsilateral side, distended neck veins ▪repeat CXR after 3-6h
▪hemodynamic instability (e.g., tachycardia, hypotension, pulsus paradoxus) » stable or improving ⇢ DC home w/ outpatient f/u CXR in 24h
» enlarging ⇢ chest tube
ABG indications: tachypnea, accessory muscle use, SpO2 <92%, hx of hypercapnia ▪stable, large (>3cm) PSP ⇢ chest tube preferred over needle/catheter aspiration
▪possible findings ⇢ hypoxemia & respiratory alkalosis
Secondary Spontaneous PTX (SSP):
DX: CXR ▪stable, small (<2cm) SSP ⇢ admit + chest tube (⇡ risk of developing TPTX d/t underlying lung disease)
▪ipsilateral pleural line + absence of bronchovascular markings past the pleural line ▪if asymptomatic, observation &/or needle aspiration can be considered
▪⊕deep sulcus sign: abnormally deepened costophrenic angle on ipsilateral side **SUPINE film ▪stable, large (≥2cm) SSP ⇢ admit + chest tube

Size assessment cut-off ⇢ cm between pleural line & chest wall at level of the apex Traumatic/tension PTX, bilateral PTX, or unstable:
▪PSP: 3cm ▪emergency chest tube thoracostomy ⇢ admit
▪SSP: 2cm ▪if chest tube is delayed, perform needle decompression

Tension PTX: clinical DX based on S/SXS of tachycardia, Chest tube placement: superior rib margin, anterior to midaxillary line in 5th ICS (nipple line)
hypotension, & severe dyspnea Needle/catheter aspiration: superior rib margin in 2nd ICS, midclavicular line
▪supportive CXR findings:
•tracheal shift to contralateral side Definitive TX: surgical pleurodesis ⇢ VATS (preferred), medical thoracoscopy
•rib splaying, flattening of the ipsilateral diaphragm ▪indications: prolonged air leak >5d, recurrent PTX, bilateral PTX, high-risk of recurrence

Hemoptysis
Coughing up of blood or blood-stained mucus from the bronchi, larynx, trachea, or lungs
MCC include:
o bronchitis (50%): hemoptysis, dry cough, cough w/ phlegm
o tumor mass (20%): hemoptysis, chest pain, rib pain, tobacco hx, weight loss, clubbing
o tuberculosis (8%): hemoptysis, chest pain, sweating
o bronchiectasis, pulmonary catheters, trauma, pulmonary hemorrhage
TX: treat the underlying cause
PULM About Diagnostics Management
Pleural ▪fluid between pleural layers impairs lung expansion ▪normal pleural fluid volume 10-20mL CXR: blunting of costophrenic angle ⇢ meniscus sign TX: therapeutic thoracentesis
Effusion ▪lateral XR, posterior CP∠ (A): ▪treat underlying cause
Transudative: ⇡ hydrostatic pressure + ⇣ plasma oncotic pressure Exudative: ⇡ capillary permeability » ~75mL fluid needed to blunt CP∠
▪CHF (MCC): 81% bilateral ▪pneumonia (parapneumonic effusion), TB, pancreatitis ▪frontal XR, lateral CP∠ (B): Parapneumonic: ABX
▪cirrhosis w/ ascites (hepatic hydrothorax): 70% right sided ▪pulmonary embolism: ⊕effusion in 30%, exudative ~80% » ~200mL fluid needed to blunt CP∠
▪nephrotic syndrome: usually bilateral, subpulmonic ▪cancer: lung, breast, or lymphoma MC Empyema:
▪hypoalbuminemia: uncommon, >90% bilateral ▪autoimmune (e.g., SLE, RA, sarcoidosis, vasculitis) DX ⇢ thoracentesis ▪ABX, chest tube drainage
▪atelectasis: ⇡ intrapleural ⊖pressure Yellow Nail Syndrome: ➀ chronic exudative effusions Light’s criteria: 1+ of the 3 ⇢ exudative ▪VATS debridement
➁ lymphedema ➀ pleural fluid LDH >2/3 ULN serum LDH
Chylothorax: milky white effusion high in TGs caused by trauma ➂ dystrophic yellow nails ➁ pleural fluid protein/serum protein >0.5 Hemothorax:
or neoplastic (MC lymphomatous) damage to thoracic duct ➂ pleural fluid LDH/serum LDH >0.6 ▪fluid resuscitation, PRBCs
▪small pleural effusion (<300mL) often asymptomatic ▪chest tube +/- open thoracotomy
Hemothorax: bloody fluid (pleural Hct >50% peripheral Hct) d/t S/SXS: dyspnea, pleuritic CP (retrosternal), dry cough Additional PF markers: Exudative:
trauma, spontaneous PTX, coagulopathy, etc. ⇣ tactile fremitus, ⇣ breath sounds, dullness to percussion ▪PF cholesterol >55mg/dL Malignant:
» pleural friction rub (uncommon) ▪PF LDH >200U/L ▪therapeutic thoracentesis
Empyema: pus in the pleural space; can occur as complication ▪PF protein >3.0g/dL ▪indwelling pleural catheter
to pneumonia, abscess, etc. ▪PF glucose <60mg/dL ▪chemical pleurodesis
▪PF cholesterol/serum cholesterol >0.3
Trapped Lung: encasement w/ fibrous peel ⇡ ⊖intrapleural pressure caused by empyema or tumor ⇢ transudation of fluid ▪Albumin gradient (serum-PF) <1.2g/dL
from parietal pleural capillaries; borderline between transudative/exudative ▪Protein gradient (serum-PF) <3.1g/dL

ILDs About Diagnostics Management

Sarcoidosis ▪multisystem inflammatory disorder characterized by noncaseating granulomas in 1+ organs/tissues, ♀ > ♂ 2:1 LABS: hypercalciuria, ⇡ ACE, hypergammaglobulinemia, ⇡ ESR Treatment indications:
▪average onset 30-55yo, highest prevalence in Black Americans & northern Europeans, esp. Scandinavian PFTs: typically restrictive pattern, ⇣ DLCO ▪symptomatic progressive disease
▪lungs MC affected organ (90%), lymph nodes MC extrapulmonary site (70-90%) ▪persistent pulmonary infiltration
CXR: bilateral hilar LAD (BHL) +/- pulmonary infiltrates (i.e., ▪progressive ⇣ lung function
PATHO: unknown antigen triggers cell-mediated immune response characterized by accumulation of T cells & macrophages, reticular &/or ground glass opacities)
release of cytokines & chemokines, & organization of responding cells into granulomas TX: glucocorticoids +/- DMARDs
S/SXS: often asymptomatic in early stages Pulmonary: cough, dyspnea, CP + fatigue, malaise, fever, weight loss Stage: BHL: Pulmonary infiltrates:
0 (normal) ⊘ ⊘ Glucocorticoids: prednisone
Hepatic: LFT abnormalities, hypolucent lesions on CT Lymphadenopathy: hilar/paratracheal mediastinal adenopathy I ⊕ ⊘ If no response ⇢ DMARDs
Neuro: cranial neuropathy ⇢ facial nerve palsy (VII), II ⊕ ⊕ ▪MTX (preferred), azathioprine
hearing loss (VIII) Cutaneous: papular, nodular, or plaque-like lesions III ⊘ ⊕ ▪HCQ, biologics (e.g., anti-TNFs)
Cardio: heart block, arrhythmias, HF, infarction, ▪erythema nodosum ⇢ painful nodules on anterior LE IV ⇢ diffuse pulmonary fibrosis (irreversible ⇣ lung function)
pericardial disease, sudden death ▪lupus pernio ⇢ violaceous lesions on nose, cheeks, chin, & ears ▪often associated w/ fibrotic-appearing conglomerate
Renal: hypercalciuria (MC), hypercalcemia, stones masses, traction bronchiectasis, & traction cysts
MSK: arthritis (ankles MC), myopathy, lytic lesions Ocular: uveitis (MC) ⇢ blurred vision, photophobia, tearing
Confirmatory ⇢ BX: noncaseating granulomas
Lofgren Syndrome: ➀ acute migratory polyarthritis Heerfordt Syndrome (Uveoparotid Fever):
➁ erythema nodosum ➀ parotid swelling ➂ anterior uveitis
➂ hilar adenopathy ➁ fever ➃ facial nerve palsy
PULM About Diagnostics
Pulmonary PE: luminal obstruction of ≥1 pulmonary arteries, typically CBC/CMP: +/- leukocytosis, ⇡ ESR, ⇡ serum lactate, ⇡ LDH, ⇡ AST
Embolism d/t blood thrombi from DVT
ABG: +/- hypoxemia, ⇡ A-a O2 gradient, respiratory alkalosis,
MCC ⇢ DVT hypocapnia
Non-thrombotic: fat, air, bacterial
EKG ⇢ nonspecific: tachycardia, nonspecific ST/T changes
PATHO: thrombus formation ⇢ DVT (MC iliac vein) ⇢ embolize
to pulmonary arteries via IVC ⇢ partial/complete obstruction CXR ⇢ nonspecific abnormalities common: atelectasis, effusion
Saddle Thrombus: blood clot that lodges at the bifurcation of the The following signs are rare, but should raise suspicion for PE:
pulmonary trunk as it splits into the R/L pulmonary arteries ▪Hampton’s hump: shallow, hump-shaped opacity in the
▪can obstruct flow through the pulmonary arteries & lead to R heart strain, hemodynamic instability, periphery of the lung w/ its base against the pleural surface
&/or death ▪Westermark’s sign: sharp cutoff of pulmonary vessels w/ distal
hypoperfusion
S/SXS: acute onset dyspnea (MC), pleuritic CP, cough +/- features of DVT (e.g., unilateral leg swelling) ▪Palla’s sign: enlarged descending pulmonary artery w/ a
▪hemoptysis is unusual presenting symptom (13%) “sausage” appearance
PE: tachypnea, rales, tachycardia, ⇣ breath sounds MASSIVE: arrythmias (e.g., AFIB), presyncope, PE suspected ⇢ calculate PTP using Wells score
▪accentuated pulmonic component of S2 syncope, hemodynamic collapse (<10%) ➀ Wells <2: low PTP ⇢ PERC to determine if D-dimer indicated
▪all 8 criteria fulfilled = no further testing indicated
▪all 8 criteria not fulfilled ⇢ D-dimer
Pretest Probability (PTP) ⇢ Wells score, PERC ➁ Wells 2-6: intermediate PTP ⇢ D-dimer
➂ Wells >6: high PTP ⇢ CT pulmonary angiography (CTPA)
▪D-dimer not needed
D-dimer ⇢ <500ng/mL = ⊖/normal
≥500ng/mL = ⊕ ⇢ get CTPA
▪for patients >50yo, age-adjusted cutoff value (ng/mL) = age x 10 embolectomy
» ex. 65yo patient ⇢ <650ng/mL as cutoff value for ⊖D-dimer
CTPA w/ contrast: intraluminal filling defects of pulmonary
arteries
V/Q scanning ⇢ alternative if CTPA contraindicated
Management
▪supplemental O2 to target SpO2 ≥90%
▪IV fluids for hypotensive patients
Initial Anticoagulation (first 5-10d):
▪SQ LMWH or fondaparinux
Long-term AC (minimum of 3mo): DOACs
▪thrombin inhibitor: dabigatran
▪factor Xa inhibitors: rivaroxaban (Xarelto),
apixaban (Eliquis), edoxaban
Indications for AC >3mo:
▪unprovoked PE w/ low/moderate bleeding risk
▪provoked PE secondary to chronic RF
▪active cancer w/ any bleeding risk
Contraindications to AC: significant active bleed,
recent high-risk bleed (e.g., ICH), recent major
surgery, severe thrombocytopenia
IVC filter: AC is contraindicated or risk of bleeding
is unacceptably high
Hemodynamically unstable ⇢ reperfusion
▪tPA (e.g., alteplase, reteplase, tenecteplase)
▪DC anticoagulation before tPA, resume after
Alternatives: catheter-directed thrombolysis,
Absolute contraindications to thrombolysis:
▪active bleeding
▪prior ICH
▪ischemic stroke ≤3mo ago
▪structural intracranial disease (AVM, neoplasm)
▪bleeding diathesis
 Obstetrics/Gynecology (no % given)
About
Breast Abscess Localized collection of pus in breast tissue
Rare complication of acute mastitis
*smoking significantly associated w/ recurrence
MC in lactating women secondary to nipple
trauma (esp. primigravida)
Etiology: Staph aureus MC
•Others: streptococcus, candida albicans
Breast Benign solid tumor composed of glandular &
Fibroadenoma fibrous tissue
2nd MC benign breast mass (after fibrocystic dz)
& MC best tumor in women <30yrs
Increased incidence in African Americans
Fibrocystic Noncancerous, fluid-filled breast cysts due to
Disease exaggerated response to hormones
Also known as glandular hyperplasia – duct
dilation, breast cysts, & stromal fibrosis
MC benign breast disorder in reproductive age
women (esp. 30-50yrs)
Often regress after menopause
Adenopathy
Enlargement of lymph nodes due to gynecologic infections, malignancy, or inflammation
•MC seen in breast disease is axillary adenopathy
•others: internal mammary, parasternal, supraclavicular
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
Clinical Manifestations
•unilateral breast pain (esp. one quadrant) w/ tenderness,
warmth, swelling, fever
•cracked nipples or visible fissure + induration and
fluctuance (due to pus)
•may have purulent nipple discharge
•breast mass – usually nontender but may become tender
prior to menstruation
•gradually grows over time but may enlarge in pregnancy
•does NOT change significantly in size w/ menstrual cycle
PE: firm, nontender, solitary, smooth, well-circumscribed,
freely mobile, rubbery lump in the breast
•usually 2-3cm & no axillary involvement
•multiple, painful or painless breast masses that may ↑ or
↓ in size w/ menstrual hormonal changes (often worse
prior to menstruation)
PE:
•multiple, painful, nodular, mobile, smooth round or
ovoid lumps in both breasts of varying sizes
•often bilateral & usually NOT associated w/ axillary lymph
node involvement
•MC found in upper outer sections of the breast
Diagnostics
Clinical based on PE
U/S – if question of cellulitis vs.
abscess; ill-defined mass w/
septations if abscess
Aspirated fluid cultures – staph
aureus presents as gram + cocci in
clusters
Clinical
U/S – solid, well-circumscribed,
avascular mass
Fine needle aspiration – definitive dx
•fibrous tissue & collagen arranged in
a “swirl”
U/S – test of choice; dense,
prominent, fibroglandular tissue w/
cysts but no discernable mass
FNA: straw-colored or green fluid (no
blood); not usually performed
•suspicious findings: dry aspirate,
blood aspirate, persistent/recurrent
mass after aspirate – any of these
findings à core needle bx
Treatment
Drainage via needle aspiration (lactational abscess) or I&D
+ abx
•dicloxacillin, cephalexin, clindamycin
•MRSA à TMP-SMX or clindamycin
*not a contraindication to breast feeding – milk drainage is
important to facilitate resolution of infection
Conservative: observation, reassurance & follow up –
most small tumors resorb w/ time
*can repeat U/S in 3-6mo
Excision: may be needed if enlarging after repeat U/S or
for large masses
Cryoablation: alternative to surgery if <4cm
Supportive management: observation, supportive bra,
low fat diet, reduce caffeine & chocolate intake,
warm/cool compress, analgesics, evening primrose oil or
vitamin E
OCPs can reduce sxs
FNA removal or fluid is diagnostic & therapeutic in complex
cases
More severe sxs: tamoxifen, danazol
NEOPLASMS About Types Clinical Manifestations Diagnostics
BREAST MC non-skin malignancy in women Ductal Carcinoma in Situ (DCIS): non- Painless, hard fixed immobile lump MC presentation Combination of PE, mammography, & FNA or core bx
CANCER invasive, has not spread outside milk ducts •may be mobile early on, may be painful in <10% is highly accurate – U/S sometimes used to see if
1/8 lifetime prevalence •may complain of unilateral discharge (may be bloody) mass is cystic
Invasive Ductal Carcinoma (IDC): MC (70-
*Second MCC of cancer death in women 80%), spread beyond ducts into other parts *Mass MC in the upper outer quadrant Mammography: initial modality to evaluate breast
(after lung) of breast tissue, associated w/ lymphatic masses in women >40yrs
metastases (esp. axillary) Skin changes: asymmetric erythema, discoloration, ulceration, •microcalcifications, spiculated masses – highly
Risk Factors: skin retraction (dimpling if Cooper’s ligament involved), changes suspicious for malignancy
•Genetics – BRCA 1 & BRCA 2, first degree Lobular Carcinoma in Situ (LCIS): non- in breast size & contour, nipple inversion, skin thickening
relative invasive, has not spread outside lobules of U/S: recommended initial modality to evaluate breast
•Increasing age – >50% occur in >60yo breast (milk glands) Locally advanced disease à axillary LAD masses in women <40yrs
•Increased number of menstrual cycles –
nulliparity, later first full-term pregnancy Invasive Lobular Carcinoma (ILC): 2nd MC Metastatic disease à MC sites are: (“2Bs, 2Ls”) FNA: removes least amount of tissue, doesn’t allow
>35yrs, early onset of menarche (<12yr), (10%), spread from lobules into surrounding •bone (vertebrae, ribs, pelvis, femur) for receptor testing if positive, 10% false negative rate
late menopause, never having breastfed normal tissue, often bilateral •brain Large needle (core biopsy): PREFERRED, allows for
•Increased estrogen exposure – •lungs (dyspnea, cough) receptor testing if positive, can leave great deformity
postmenopausal HRT, prolonged Paget Disease of the Breast: ductal •liver (abdominal pain, nausea, jaundice) & needle may miss lesion
unopposed estrogen therapy, obesity, carcinoma presenting as an eczematous Open biopsy: most accurate
alcohol use nipple lesion +/- bloody discharge from the Paget Disease of the Breast: chronic eczematous itchy scaly rash
*endometrial cancer increases risk for nipple on the nipples & areola (may ooze); lump often present Biomarkers & Gene Proliferating:
breast cancer and vice versa •ER/PR(-) OR HER2(+) OR “triple negative” à higher
Inflammatory Breast Cancer (IBC): Inflammatory Breast Cancer: red, swollen, warm, itchy breast risk of recurrence
Strongest RFs: female gender, age aggressive, fast-growing, infiltration of skin & •often w/ nipple retraction ER+ = better prognosis
lymph vessels, NO LUMP •peau d’orange = skin changes that looks like the peel of an HER2/neu+ = more aggressive
Other factors – alcohol, weight, exercise, orange due to lymphatic obstruction – associated w/ poorer •Oncotype dx, mammaprint – categorizes risk of
diet (red meat) Triple Negative: HER2/neu(-), ER(-), PR(-) prognosis recurrence score
2-5yrs after dx à MC time for recurrence
Management Screening Prevention
Know goal of therapy à curative or palliative (curative for stages I-III) Mammogram – best screening in women >40yrs SERM – tamoxifen & raloxifene
Tx based on TMN staging •detects breast cancer as early as 2yrs before a mass can •can be used for breast cancer prevention in high-risk individuals
be palpated clinically •can be used in postmenopausal women or women >35 w/ high-risk
Early stage: breast conservation therapy (lumpectomy) + sentinel node •tx usually used for 5yrs
biopsy + f/u radiation Brest self-examination has NOT been shown to reduce •Tamoxifen preferred – more effective but associated w/ endometrial cancer
ER+ long-term overall mortality & increased risk of DVT
•premenopausal: tamoxifen
•postmenopausal: aromatase inhibitors (letrozole, anastrozole, Average Risk: USPTF guidelines recommends Tamoxifen:
exemestane) mammogram every 2yrs beginning at 50yrs until 74yrs •estrogen agonist: endometrium, bone, liver, coagulation system
HER2/neu+: trastuzumab (ADR: cardiotoxicity) (women over 74 can be offered screening every 2yrs if •estrogen antagonist: breast
their life expectancy is at least 10yrs) •indications: adjuvant tx in ER/PR+, prevention, osteoporosis prevention in
Radiation therapy: usually done after lumpectomy or post mastectomy to postmenopausal women
destroy residual tumor cells (external beam radiation or brachytherapy) Moderate Risk (e.g., pts w/ first-degree relative w/ breast •ADRs: hot flashes (induces menopause), ocular toxicity
cancer): screening at 50yrs every 2yrs OR 10yrs prior to BB WARNING: endometrial cancer, venous thromboembolism
Adjuvant chemotherapy: used to treat and residual disease the age the first-degree relative was diagnosed
•Indications: lesions >1cm, +axillary LAD, stages II-IV, inoperable disease (whichever is earlier) Raloxifene:
(esp. ER- disease) •estrogen agonist: bone
•doxorubicin, cyclophosphamide, fluorouracil, docetaxel Women w/ breast implants should undergo the same •estrogen antagonist: breast, endometrium
screening schedule as women w/o implants •indications: prevention in high-risk pts, osteoporosis prevention in
NONINVASIVE: postmenopausal women
•treat the breast à simple mastectomy or lumpectomy/radiation Clinical Breast Exam: at least every 3yrs in women 20- •ADRs: weight gain, thromboembolic events (less than tamoxifen), hot flashes
•NO CHEMO 39yrs (annually after age 40)
Aromatase inhibitors – alternative to SERMs
INVASIVE: •letrozole, anastrozole, exemestane
•treat the breast à mastectomy or lumpectomy/radiation ADRs: osteoporosis
•Evaluate the axilla: complete axillary dissection or sentinel node biopsy
•SYSTEMIC CHEMOTHERAPY
•HORMONES – Tamoxifen, AI, Herceptin