Exam Flashcards
What should you always ask?
- eating/defecating make it better or worst
- last menstrual cycle
- what were you doing (trigger)
Most common surgical emergency of the abdomen**
acute appendicitis
r/o 1st!
acute appendicitis Sx
often inconsistent only 50% class RLQ pain, N/V Abdominal pain most common* (could be periumbilical/epigastric migrating to RLQ) Sx usu <48hrs N/V/D, constipation, anorexia vomit AFTER onset of pain*
what should you worry about if vomiting precedes abdominal pain?
intestinal obstruction
McBurney’s point
RLQ tenderness 96% in acute appendicitis
2/3 of way from umbilicus to ASIS
Physical exam special tests for acute appendicitis
McBurney’s point
Rebound tenderness (Blumberg sign)
Rovsing sign: RLQ pain w/LLQ palpation
Obturator sign: RLQ pain w/int/ext rot of flexed R. hip
Psoas sign: RLQ pain w/extension of R. hip or flex of R. hip against resistance
Acute appendicitis labs
leukocytosis w/left shift 80-85% (unreliable in infants/elderly/preg)
elevated CRP
imaging study to eval for acute appendicitis
CT Abd/Pel w/oral contrast
Acute appendicitis Tx
NPO, IVF, Pain control, Antibiotics, consult surgery
what should you worry w/”pain out of proportion to exam***
mesenteric infarction
bowel is dying, surgical emergency! need to re-vascularize
often w/A.fib/CHF
CTA, MRA
imaging of choice for suspected rupture abdominal aortic aneurysm
U/S standard (pt unstable)
CT/CTA confirm if pt stable
high pre-hospital mortality
Classic triad for ectopic pregnancy*
abdominal pain
amenorrhea
vaginal bleeding
Imaging/labs for suspected ectopic pregnancy
hCG
U/S
when do MIs most often occur?
early in the morning, may only present w/indigestion
most common Sx of GERD/Esophagitis
Burning pain, worse w/lying down
abrupt onset of abdominal pain in PUD is worrisome of?**
ulcer perforation
Sx: gnawing/burning epigastric pain
Test of choice to Dx PUD*
EGD (esophagogastroduodenoscopy)
Biggest causes of acute appendicitis**
alcohol
gallstones
(constant boring pain)
Acute pancreatitis signs
Cullen sign
Grey-Turner sign
what can acute pancreatitis be caused by in the elderly?
pancreatic tumor
Biliary colic
sudden constant pain, 1-5hrs, may radiate to R scapula
gallstone temp block cystic duct
N/V
can develop into acute cholecystitis if untreated
acute cholecystitis
inflammation of GB wall RUQ pain, radiate to R. scapula N/V, anorexia, fever Labs: leukocytosis, mild LFT elevation U/S Dx, May need surgery
Charcot’s Triad (Ascending Cholangitis)
Fever
RUQ pain
Jaundice
biliary dyskinesia
recurrent RUQ pain in absence of gallstones
pain typically 30-60min after eating (spicy, greasy), last 1-4hours
most common cause of small bowel obstruction
intra-abdominal adhesions
acute gastroenteritis
self limiting
eval for dehydration
typically fever, vomiting first then diarrhea, anorexia
supportive care, no abiotic
C. diff colitis Tx
metronidazole (PO, IV)
vancomycin (PO only! IV doesn’t penetrate gut)*
most common type of peritonitis
secondary, identify source
Late complication of PID
Tubo-ovarian abscess
can be fatal if ruptures –> endotoxic shock
PID Dx criteria
lower abd tenderness
cervical motion tenderness
adnexal tenderness
often vaginal discharge
what can be the only presenting Sx of ovarian torsion*
lower abd pain
may resolve spontaneously, if not, can infarct
most nutrients are absorbed in…*
small intestines
Hepatitis A mode of transmission*
Almost exclusively fecal-oral
person to person
Hep A virus type*
SS RNA
When is Hep A transmission highest*
anicteric prodrome
What can destroy Hep A virus?
boiling water, chlorine, iodine
Increasing age in Hep A results in*
increasing adverse events
Sx variable w/age
Hep A prognosis
usu mild, self-limited illness
Icteric phase of Hep A
dark urine first
some have pale stools
Jaundice in adults
Hepatomegaly
Treat Hep A in developing countries*
sugar canes
Hep A IgG*
past infection; patient IMMUNE
OR vaccinated*
Post exposure prophylaxis of Hep A
immune serum globulin (Gammaguard) w/in 2wks of exposure
Hep B virus type*
DNA virus
Incubation period of Hep B
1-6mon! (while Hep A is 2-6wks)
Estimated global prevalence of Hep B
Est 1/3 of global popu infected
How is Hep B transmitted?
bodily fluids (blood, semen, vaginal secretions) sexual, needles, PERINATAL,
Hep B Sx
acute phase: many asymp
viral prodrome w/icteric hepatitis (arthralgia, myalgia, transient skin rash, fatigue,)
jaundice last 1-3mon
anicteric hepatitis more to develop into chronic (more common)
Hep B core IgG
Past infection
NOT pos from vaccine
(Hep B Surface AB: HAD virus or vaccine)
Hep B E Ag
active viral replication, highly contagious
Heb B E AB
Carrier
Hep B Surface AB
HAD virus or vaccinated
Hep B: IF SURFACE ANTIBODY IS POS AND NOTHING ELSE*
VACCINATED FOR HEP B!!!* (immune)
Hep B: IF SURFACE AB IS POS AND CORE AB IS POS*
THEY HAD Hep B; BC DON’T GET POS CORE AB FROM VACCINE
Hep B Surface Ag
Acute or chronic (+6mon) infection
Hep B: Surface Ag Pos and E Ag pos*
Highly contagious infectious Hep B!
Hep B: Surface Ag Pos and E AB pos*
CHRONIC Hep B
What do all pts w/chronic Hep B (carrier or active) need?
screening regimen for hepatocellular carcinoma (HCC)
increased risk w/co-infection w/ Hep C or D
Hep B Tx
First line: pegylated interferon alpha, entecavir, tenofovir disoproxil fumarate (TDF)*
Goal: suppress viral load & boost patient’s immune response
Hep B lab values
ALT > AST
AlkPhos/GGT elevated (no more than 3x ULN)
What should you routinely screen for every women, every pregnancy, every time?*
Hep B surface antigen
Newborns born to mothers w/ chronic hepatitis B need…
hepatitis B immune globulin and hepatitis B vaccination within 12 hours of birth!
Hep C virus type
SS RNA
Most frequent cause for liver transplant in US
Hep C
Prognosis of Hep C
70-85% remain viremic –> can develop chronic Hep C –> fibrosis –> cirrhosis (25%) or hepatic carcinoma
Hep C transmission
needles (IVDU, tattoo), straw (intranasal cocaine), razor, blood infusion before 1990
sexual and maternal UNCOMMON
Dx Hep C
Check HCV PCR and HCV AB
Classic acute picture = HCV RNA positive but HCV AB negative (takes wks to mon to convert)
Hep C prognosis
good if treated
but incidence incr from opioid epidemic
Hep C Sx
most asymp, PE often normal, fatigue most common
Often not symp until advanced liver dz w/decompensation: mental status changes, edema, ascites, variceal bleeding
Is Hep C a protective AB?
NO! Can get Hep C again!
most common Hep C genotype
Genotype 1 (80% in US)
Hep C Tx Guidelines
Acute: just monitor for spontaneous clearing (min 6mon)
Chronic: depends on Genotype
WHO: TX ALL 12YO and older
Hep C Tx
protease inhibitor (eg sofosbuvir/simeprevir)
Hep D is only seen in…
Pts w/Hep B
worst prognosis, progresses to cirrhosis more rapidly, can lead to fulminant hepatic failure
Hep D Tx
supportive, Tx Hep B
Fatty Liver Dz types
alcoholic: reversible; any person who consumes >60g alcohol per day
non-alcoholic: commonly assoc w/metabolic syndrome
very common, 1/3 popu
fastest growing cause of liver disease in the Western world
Non-alcohol fatty liver dz
most common cause of chronic liver disease in US adults (followed by alcohol & hep C)
Non-alcoholic steatohepatitis
What is predicted to become leading cause of liver transplantation by 2030
NAFLD (no sepcific Tx: control diet, weight loss, alc abstinence)
Alcoholic liver disease stages
alcoholic fatty liver, alcoholic hepatitis, alcohol-related cirrhosis
Pathophysiology alcoholic liver dz
ETOH → activated Kuppfer cells → inflammation → fibrosis → cirrhosis
Alcoholic liver dz Lab values
AST>ALT (atleast 2x)
marked elevation of GGT (but not specific)
Most common autosomal recessive genetic disorder among Caucasians in the US
hemochromatosis
hemochromatosis
autosomal recessive, iron deposition in multiple organs, including the liver
75% asymp
test Transferrin
70-80% of those w/Autoimmune hepatitis are…
women
screen w/ANA
Tx: corticosteroids +/- azathioprine
What can you eval for in pts w/unexplained liver dz?
alpha 1 antitrypsin deficiency, even w/o resp Sx
Most common initial presentation of Wilson’s dz
cirrhosis
Wilson’s dz SxS
Kayser-Fleischer Rings
Chronic active hepatitis
Cirrhosis – most common initial presentation
Fulminant hepatic failure
Serum ceruloplasmin <20 mg/dL
Tx: Lifelong chelating agents (penicillamine)
Goblet cells
secretes mucus to protect mucosa from digestive enzymes and acid
Parietal cells
secrete HCl, intrinsic factor (absorbs B12 in sm int)
Chief cells
secrete pepsinogen (inactive form of pepsin - breaks down protein)
pernicious anemia
B12 deficiency
can result from gastric bypass surgery
Primary responsible agents for mucosal damage assoc w/PUD**
gastric acid and pepsin
Zollinger-Ellison syndrome
Rare: Caused by non-beta islet cell, gastrin-secreting tumor –> stimulates acid-secreting cells of the stomach –> gastric mucosal ulceration
primary tumor typ pancreas or duodenum
difference between stomach ulcer and erosion
ulcer is deeper, local inflammatory rxn, extends through muscularis mucosa
What doubles the risk of PUD?
H. pylori infection
Most cases of PUD are caused by**
H. pylori infection
NSAIDs (submucosal erosions, inhib cyclooxygenase, dec prostaglandins, and their protective effects)
H. pylori infection
produce urease to alkalize acidic stomach, colonization of stomach causes inflammation, impairs duodenal bicarb secretion, inc gastrin/pepsinogen production
promote gastric metaplasia in duodenum, increased susceptibility to acid injury, causing duodenal ulcers (can lead to gastric outlet obstruction)
most common symptoms of PUD
epigastric pain (gnawing, burning)
GASTRIC ulcers*
eating exacerbates the pain, little relief w/antacids
DUODENAL ulcers*
eating diminishes pain, relief w/antacids
nocturnal pain
Sudden onset of PUD Sx is worrisome for…
perforation
PUD Sx
MAY BE ASYMP Dyspepsia (belching, bloating, fatty food intolerance, distention) Chest discomfort Heartburn Hematemesis or melena if bleeding
Dx test for PUD
EGD (upper GI endoscopy)
if anemia in PUD…
alarm signal, endoscopy to rule out sources of chronic GI blood loss
H. pylori testing
Urea breath test
stool antigen test
What should you do after treating PUD?***
repeat endoscopy in 6-8wks to verify healing!
Non-healing ulcer is ca until proven otherwise***
Non-healing gastric ulcer is what until proven otherwise***
Gastric cancer
H. pylori Tx
1st line: Triple therapy regimen (10-14 days)
Clarithromycin: 500mg PO BID
Amoxicillin: 1g PO BID
Metronidazole: 500mg PO BID
PPI PO BID (eg esomeprazole, lansoprazole)
What is H. pylori infection associated with?
atrophic gastritis
MALT lymphoma
at risk for malignancy
PUD perforations can lead to…
fistulas
cause pancreatitis
need surgical eval
Best screening test for Zollinger-Ellison Syndrome*
fasting serum gastrin (pt ideally off PPI; serial measurements on diff days)
What can Zollinger-Ellison Syndrome be assoc w/?
multiple endocrine neoplasia - type 1
If pt has multiple ulcers or ulcers in weird places…
check gastrin level! (serial measurement on diff days)
Most common type of gastric cancer**
adenocarcinoma 90-95%*
What nodes are associated with gastric ca?
Sister Mary Joseph node (firm nodule in umbilicus) Irish node (enlarged L axillary LN)
Dx tests for gastric ca
EGD for Dx (depth)
EUS/CT for staging (mets)
Gastric ca prognosis
3rd most common cause of ca-related death
often found as advanced dz
early dz asymp or mimic PUD
What can be the 1st sign of gastric ca?
Virchow’s node (L supraclavicular lymphadenopathy)
Boerhaave’s syndrome
esophageal rupture
urgent surgical eval
Dx w/imaging
broad spectrum abiotics (rapid sepsis)
Mallory-Weiss Tear*
mucosal tear due to retching, non-bloody emesis followed by bloody emesis
Longitudinal mucosal laceration at the gastroesophageal junction or gastric cardia*
Mackler’s Triad for Boerhaave Syndrome
lower chest pain
vomiting
subQ emphysema
Gastroparesis
Delayed emptying of the stomach due to an issue with motility, NOT a mechanical obstruction
DM a common cause*
Gastroparesis Tx**
Metoclopramide (Reglan) – acts on dopamine receptors in stomach/intestines/brain
**watch for tardive dyskinesias (stop medication to prevent permanent Sx)
Ligament of Treitz*
Landmark that determines UGI vs LGI bleed (determines Tx)
located: 4th portion of duodenum*
most common site of GI bleeding*
Upper GI tract
Iron deficiency anemia, (+) hemoccult in the elderly is…**
CANCER until proven otherwise*
testing required after heme (+) stool
EGD
Colonoscopy
^neg then eval small bowels
1 cause of Upper GI bleed**
Ulcer disease, erosions (esophageal, stomach, duodenum)
What are Mallory-Weiss tears often assoc w/?
alcohol
Portal hypertension*
Shunting of hepatic blood away from liver due to increased resistance typically from CIRRHOSIS*.
Bleeding Varices
Usu sudden, overt , major bleeding
75% esophageal**
in 50% of cirrhosis pts (can be fatal)
How to eval for UGI Bleed?
stabilize pt then EGD** (Dx AND Tx)
AIMS65 Score*
determines risk of in-hospital mortality from upper GI bleeding: greater than 2, high risk Albumin <3 g/dl INR >1.5 Mental status altered SBP <90 Age >65yo
Where do diverticular bleeds most often occur?*
Right 50-90%
Ascending colon**
(not assoc w/diverticulitis, typically PAINLESS*)
Where does diverticulitis most commonly occur?*
primarily left colon
Most common source of lower GI bleed
Colon carcinoma (but often occult)
Most common source of OVERT lower GI bleed
Diverticular bleed
Most common LGIB in elderly
Diverticular bleed
Diverticular bleed prognosis
Many stop spontaneously (75%) Typically PAINLESS (diverticulitis painful)
Ischemic Colitis
Hematochezia (+) cramping abdominal pain
develops when blood flow to a part of your colon is reduced (predom NON-occlusive ischemia)
Tx: supportive, self-resolving
Angiodysplasia
ACQUIRED vascular ectasia, degenerative, possibly from chronic venous congestion of the intestine; mostly elderly
self-limiting
Where does angiodysplasia most commonly occur?
80% proximal colon
Bright red rectal bleeding
Maroon Stools
Irritable Bowel Dz
Which hemorrhoids are painful?*
External (distal to dentate line)
What lab should you also order w/hematochezia
BUN/CREAT
Pt. w/ h/o abdominal aortic graft who enter the ER with GIB must receive immediate surgical attention to r/o…
aortoenteric fistula (1%, rare, life-threatening)
“Herald” bleed
episode of acute hemorrhage that ceases spontaneously-
Postural hypotension in suspected GI bleed
(supine-to-upright fall in systolic BP of >10 mm Hg or increase in heart rate of >20 beats per minute) indicates moderate blood loss (10-20% of circulatory volume)
Supine hypotension in suspected GI bleed
suggests severe blood loss (usually >20% of circulatory volume)
Gold standard study for LGIB*
Colonoscopy
UGIB & Treatment of Varices*
EGD with therapeutic banding/clipping/cauterization
Tx for UGI bleeds secondary to esophageal varices
Intrahepatic Portosystemic Shunt (Reduces the pressure gradient between portal and systemic circulations)*
transjugular if also portal HTN
False diverticula
only involve mucosa and submucosa (true: all layers)
Diverticulosis
having non-inflamed diverticula
Diverticula
small pouches created by the herniation of the mucosa into the wall of the colon through intestinal layers and smooth muscle
Diverticulitis
inflammation of one or more diverticula
Where does diverticula most commonly occur?*
sigmoid colon (highest intraluminal pressure) (L more common in US but mostly false diverticula)
Most common Sx of diverticulitis
LLQ pain 70%
fecal matter in urine, think…
colovesicular fistula (could be a complication of diverticulitis)
Best imaging study to eval diverticulitis
CT abdomen/pelvis
Colonoscopy contraindicated during acute ep bc high risk for rupture; can be used after to r/o malignancy
What should you rule out w/diverticulitis?
Cancer
What medications should you avoid in treating diverticulitis
NSAIDs
Corticosteroids
greater risk of perforation
Meckel Diverticulum
Congenital abnormality that is a true diverticulum of the small bowel
Rules of 2s for Meckel Diverticulum (PIMP)
2% of the population, within 2 feet of the ileocecal valve, 2 inches in length, two types of heterotopic mucosa (gastric and pancreatic), and presentation before the age of two.
ALT correlates w/…
degree of abdominal adiposity
AST increases w/…
skeletal muscle injury
Is ALT or AST more specific for liver injury and death?
ALT (bc AST also found in mito of cardiac, skeletal muscle, blood cells)
(but normal ALT doesn’t mean no liver inflammation; damage reach certain point, stop leaking damaged enzymes)
Slight elevations of transaminases (50-200)
Low-grade inflammation
Huge elevations (+1,000) of transaminases
Acute liver injury/necrosis
Tests indicating liver “plumbing problems”
Bilirubin
Alk Phos: bile duct inflammation (obstruction, autoimmune, infection); high levels = inflammation; low = no dz or pancreatic ca
GGT
Specific to liver
Indirect Bilirubin
product of breakdown of heme, NOT water-soluble. Bound to albumin and sent to the liver (won’t cause dark urine but may cause jaundice if high)
Direct Bilirubin
conjugated in the liver → makes it water-soluble. Converted to urobilinogen (makes urine yellow)
Bilirubin levels in PRE hepatic jaundice
elevated UNconjugated Bili
Bilirubin levels in POST hepatic jaundice
elevated conjugated bili
Bilirubin levels in hepatic jaundice
BOTH conjugated and unconjugated may be elevated
Nutrition on LFTs
albumin low due to low nutrition status (but low albumin can also suggest chronic dz like ca, cirrhosis)
TYLENOL MAX DOSE IN 24HRS*
3 grams (those w/o liver dz) 2 gram (Liver dz)
alk phos elevated out of proportion to aminotransferases
Think obstruction (liver/bile ducts) - CHOLESTATIC
aminotransferases elevated out of proportion to alk phos
Think liver inflammation - hepatocellular
Isolated Hyperbilirubinemia - CONJUGATED**
think decreased excretion or leakage of pigment from hepatocytes
Dubin-Johnson Syndrome*
Rotor Syndrome*
Isolated Hyperbilirubinemia - UNCONJUGATED**
Gilbert’s Syndrome: Bili goes up in period of stress*
Crigler-Najjar Syndrome*
Most common cause of drug-induced liver injury**
Acetaminophen*
Augmentin (amoxicillin/clavulanate) induced liver injury pattern on LFT*
Cholestatic pattern
Ibuprofen induced liver injury pattern on LFT*
Mixed
Diarrhea
passage of frequent (3 or more a day), small volume loose stools; alteration in normal absorption
leading cause of malnutrition in children under five years old*
diarrhea
Osmotic diarrhea causes*
Celiac Sprue/disease
Lactose intolerance
what is not impaired in osmotic diarrhea?*
Electrolyte absorption is not impaired
1 cause of secretory diarrhea*
Infections (eg S. Aureus, E.Coli, Vibrio Cholerae)
Secretory Diarrhea
Diarrhea that occurs when excretion of water in the intestines exceeds absorption: low stool osmolality frequently electrolyte loss usually does not resolve if fasting often nocturnal
Functional Diarrhea
Improvement at night and with fasting
Cause: Irritable bowel disease*
1 parasitic cause of diarrhea in US and worldwide.
Giardia (NO fever usu)*
Dx and Tx: Giardia
Stool O&P: 3 samples
Tx: metronidazole
Entamoeba Histolytica
Parasitic infection - diarrhea
Common in tropical countries
Contaminated food or water
Cryptosporidiosis
Parasitic infection - diarrhea
One of the most common causes of waterborne disease
Can live in humans and animals and passed in stool
Has a shell that allows it to survive for long periods of time and protect from chlorine disinfectants
Could be cause of chronic diarrhea in HIV/immunocompromised
Tx Cryptosporidiosis
Nitazoxanide
2 Most common Viral Causes of acute gastroenteritis*
Norwalk Virus (“winter stomach flu”): Common cause of acute gastroenteritis in the US Rotavirus
Most common GI disease in children 6-24 months
Rotavirus
Fever absent bacterial infection
Staph
Clostridium perfringens
Most common cause of Travelers diarrhea**
Enterotoxigenic E. Coli: ETEC
Food or water contaminated with animal/human feces
Typhoid Fever
Severe form of salmonella (due to salmonella typhi)
life threatening
Common bacterial cause of diarrhea in the USA
Campylobacter Jejuni
(“rice water stool”)
Vibrio cholera (usu uncomplicated w/limited Sx)
What do you not give to Enterohemorrhagic E.Coli (Shiga Toxin Producing)
Antibiotics - increased risk of HUS
C. diff Tx
Metronidazole tx of choice for initial episodes and mild-moderate disease
Vancomycin or Fidaxomicin PO if severe or failure to Metronidazole
PO ONLY**
INR that does not correct with parenteral vitamin K is suspicious for
severe hepatocellular injury
1 clue to advanced liver disease that is missed by PCP*
the low platelet count (nl = 150K), esp if combined with prolonged INR!
pt has ADVANCED liver dz until proven otherwise
most sensitive indicator of how the liver is functioning***
INR
Acute Liver Failure
Acute hepatocellular injury + hepatic encephalopathy + prolonged PT (elevated INR)
LFTs are typically >10 x upper limits of normal
Endocrine cells of pancreas
Alpha cells - Glucagon
Beta cells – Insulin
Delta cells - Somatostatin (inhibit insulin and glucagon release)
PP cell: pancreatic polypeptide hormone
Causes of acute pancreatitis
Biliary tract stones Drugs ERCP Ethanol abuse* Metabolic Idiopathic Infections: viral, bac, fung Ischemia Parasites Postoperative Scorpion sting* Trauma
Causes of chronic pancreatitis
Autoimmune Duct obstruction Ethanol abuse*** (Most often the cause!) Hereditary Hypercalcemia* - 25% Hyperlipidemia Triglycerides* (play a big role in pancreatitis!) - 15% Idiopathic
most common cause of pancreatitis*
Gallstones
“Female, Fair, Fat, Fertile, 40 yo”
Gallstones (cholelithiasis)
second leading cause of pancreatitis**
ETOH
most common identifiable cause of acute pancreatitis in CHILDREN
TRAUMA
Pancreatitis - Presentation
Acute Onset of Abdominal Pain: Usually Mid-Epigastric Knife Like Radiates to back (~50%) May have lower chest pain (trouble taking a deep breath) May have had previous episodes Often assoc w/N/V Later: abd fullness, GI bleed (KEEP MI IN DDX)
Pancreatitis PE
Typically seen “writhing” in pain May not be able to find comfortable position: may have slight relief leaning forward Febrile Tachycardia Tachypnea Hypotension Abdominal distension/ascites
Signs of Pancreatitis
Cullen’s sign: periumbilical ecchymosis
Grey-Turner’s sign: flank bruising
What lab study is specific for pancreatic dz*
Lipase (order daily ASAP)
Amylase nonspecific
What electrolyte imbalance is present in 25% of pancreatitis*
hypocalcemia
Hypoalbuminemia in pancreatitis
poor prognosis bc pt malnourished (cant eat, digest, or only drinking ETOH)
(Elevated LDH also poor prognosis)
Daily Labs for pancreatitis
Amylase, Lipase
LDH
Ca
CBC
thought to be the most sensitive test for pancreatitis, particularly chronic pancreatitis
trypsin (breaks down protein)
but not widely available
Imaging studies for pancreatitis
abdominal U/S
Preferred: abd CT w/contrast
ERCP: for atyp causes
ERCP urgent interventions in pancreatitis
Biliary sepsis
Biliary obstruction and severe pancreatitis
Ascending cholangitis
Progressivejaundiceorhyperbilirubinemia
Pancreatitis Tx
DO NOT SEND PTS HOME (acute) Maintain pt NPO IV fluids* (helps) Pain control – meperidine standard but shifting now to dilaudid (concern that morphine and its derivatives can cause spasm at sphincter of Oddi and increased biliary pressure, can make ab pain/Sx worst) Anti-emetic – IV zofran, phenergan Parenteral antacid (H2 blocker or PPI)
1st line Tx of hypertriglyceridemia
Fibrates
Ranson’s Criteria
Acute PancreatitisClinical Course scoring sys
≤ 2, 0% mortality
3-4, 15 %
5-6, 50%
≥7, ~95%Leading cause of chronic pancreatitis*
70% ETOH
Most common type of pancreatic ca**
Ductal epithelium (adenocarcinoma)
Best imaging study for pancreatic ca*
helical CT
Pancreatic Cancer:Presentation
Unexplained weight loss (>5 pounds per month)
Biliary duct blockage (if head ofpancreasinvolved): Jaundice, Dark urine and light colored stool
Epigastric abdominal painradiating to back
Nauseaorvomiting
Anorexia
Weakness
(check Virchow’s node)
Painless jaundice**
Pancreatic ca until proven otherwise!!
Courvoisier’s Sign**
Non-tender, but distended, palpableGall Bladder
Associated withJaundice
Pancreatic ca usu found at*
head of pancreas
bile
produced by hepatocytes
bile acids, bilirubin, cholesterol, phospholipids, water, electrolytes
Emulsifies fats
CCK
stimulates GB to contract
secreted from duodenal mucosa when fatty chyme enters
Most common type of cholelithiasis*
cholesterol stones 80%
What happens to your biliary system when pts stop eating
decreased enteral stimulation of the gallbladder (no CCK release) with resultant biliary stasis and stone formation
Biliary colic
stones or sludge obstruct the cystic duct during GB contraction
Pain in epigastric/RUQ area with radiation to right scapula
Usually lasts 30-90 minutes, but up to 5hr
no fever or jaundice
Imaging test of choice for gallbladder or biliary disease*
U/S (good for stones >2mm)
but CT and MRI/MRCP – superior for CBD stones
Cholelithiasis Tx - symptomatic
cholecystectomy first-line
Asymptomatic stones – typically no intervention unless stones >2.5 cm or calcification of GB wall
Acute Cholecystitis
Inflammation of the GB due to a stone impacted in the cystic duct (prolonged)
Acute Cholecystitis PE
RUQ tenderness, fever, tachycardia, palpable GB/RUQ fullness (30-40%)
Murphy sign – tenderness and inspiratory pause with palpation of RUQ
Dx: U/S
Diffusely calcified GB (“porcelain GB”)*
malignancy until proven otherwise
Acute Cholecystitis Tx
Initial: bowel rest, IVF, analgesia, antibiotics, electrolyte correction
Antibiotics: piperacillin/tazobactam, ampicillin/sulbactam, or meropenem. If severe life-threatening cases, then imipenem/cilastatin; alt: 3rd gen ceph, Metronidazole
Laparoscopic cholecystectomy is standard of care for surgical treatment – early operation (within 72 hrs) is preferred (better outcomes)
Percutaneous drainage if surgery high risk
Acalculous Cholecystitis population
very sick patients, elderly men
Chronic Cholecystitis
repeated attacks of pain (biliary colic) that occur when gallstones periodically block the cystic duct.
GB can become thick-walled, scarred, and small
Tx: cholecystectomy
Acute Cholangitis
Bile duct obstruction allows bacteria from duodenum to ascend; usu gram neg
Tx: antibiotics FIRST, then relieve obstruction w/ERCP
Reynold’s pentad
Acute suppurative cholangitis:
Charcot’s triad plus confusion and hypotension
What is Primary Sclerosing Cholangitis strongly assoc w/?*
STRONG association with IBD, especially ulcerative colitis***
thought to be autoimmune; Can lead to cirrhosis and portal HTN
leading cause of chronic hepatitis and cirrhosis
Hep C
As hepatic fibrosis progresses, steatosis…
regresses (may make diagnosis of NAFLD as cause more difficult)
Medications that can cause chronic liver dz and cirrhosis**
Amiodarone
Methotrexate
If pt has gastroesophageal varices on EGD, by definition they have clinically significant*
portal HTN
Gastric varices*
less likely to bleed but if bleed then more severe - can be fatal
Esophageal varices Tx
Tx: non-selective BB or banding
serum-ascites albumin gradient (SAAG)**
Attribute ascites to peritoneal or non-peritoneal causes
SAAG = (albumin concentration of serum) – (albumin concentration of ascitic fluid)
Non-peritoneal SAAG
SAAG > 1.1 g/dL
portal HTN, hypoalbuminemia (nephrotic syndrome, malnutrition), malignancy, pancreatic ascites, biliary ascites, trauma, myxedema
Peritoneal SAAG
SAAG <1.1 g/dL malignancy ascites (peritoneal implants), TB peritonitis, sarcoidosis, FBs, vasculitis (SLE, HSP), endometriosis, fungal or parasitic infections
ascites Tx
Mild ascites: sodium restrictions, diuretics 1-2x/week
Moderate to severe ascites: aggressive diuretics, monitor electrolytes:
Spironolactone: K sparing
Furosemide
(often used in combo)
Spontaneous Bacterial Peritonitis
Caused by translocation of GI tract bacteria across gut wall or by hematogenous spread of bacteria
Spontaneous Bacterial Peritonitis Dx**
ascites: >250 PMNs per mm3 with positive culture (classic)
culture-negative neutrocytic ascites
still significant mortality (still need abiotics!)
Spontaneous Bacterial Peritonitis tx**
Cefotaxime x 5 days
repeat paracentesis in 48-72hrs
Hepatic Encephalopathy is assoc w/
elevated ammonia level (normally detoxified by liver), but not always!
Tx: Lactulose, Rifaximin
TIPS
Transjugular, intrahepatic, portosystemic shunt – connects portal vein to the hepatic vein, bypassing liver circulation
10-25% of pts with cirrhosis HAVE…
Hepatocellular carcinoma (HCC), esp w/Hep B, C, etoh
Crohn’s Disease*
Inflammation and ulceration of the GI tract that can involve the full thickness of the bowel* in a patchy, non-continuous distribution (skip lesions)**
(terminal ileum and colon most common)
chronic, recurrent condition
Rectum involvement in Crohn’s Dz
rectum itself is relatively spared compared to the rest of the colon
Complications of Crohn’s Dz
fistulae, abscesses, perianal disease, and strictures
Crohn’s Dz Etiology
strong genetic component*
defect in immune response
Common PE finding in Crohn’s Dz
FISTULAS* between colon/small bowel and other organs (bladder, vagina, rectum).
Bloody Diarrhea, keep what on your DDx?*
Crohn’s Dz, Ulcerative colitis
Sx of Crohn’s Dz
weight loss, lethargy, fever, and general malaise
N/V/D intermittent, could be bloody
pain usu RLQ, quality ranges
PYODERMA GANGRENOSUM
cutaneous ulcerations in Crohn’s Dz
When does Crohn’s Dz require urgent eval?**
High fever, severe abdominal pain, or symptoms of small bowel obstruction
Dx test of choice for Crohn’s*
colonoscopy, biopsy affected areas
String Sign on Small bowel series
Crohn’s Dz, colonoscopy
Cobblestoning of small bowel
Crohn’s Dz, patchy lesions (fissures, elcers), severe case
Dx w/colonoscopy
what test is 90% sensitive for detection of IBD
Fecal Lactoferrin
40% to 80% of patients with ulcerative colitis is positive for…
p-ANCA
ASCA
antibodies to baker’s yeast and brewer’s yeast found in up to 68% of patients with Crohn’s disease
What medication should you avoid in Crohn’s Dz
NSAIDs
Crohn’s Dz Tx
mild to mod: salicylate (5 ASA: 5 aminosalicylates), maintenance mesalamine
mod to sev: systemic corticosteroids (prednisone or Budesonide), consider immunosup maintenance (azathioprine)
Humira, Infliximab, methotrexate, tacrolimus f refractory
no immunosuppressants if infectious colitis on DDx
any pt w/anemia, weight loss, and fever of unknown origin, consider
Crohn’s Dz
where is the inflammation in ulcerative colitis?*
localized primarily in the mucosa and is uniform and continuous (not full thickness and patchy as in Crohn’s)*
Perirectal involvement is a typical feature of ulcerative colitis*
only colon and rectum involved
Hallmark feature of ulcerative colitis**
bloody diarrhea
assoc w/tenesmus
cigarette smoking in ulcerative colitis
protect against UC (but worsens in Crohn’s)
Examples of 5-ASA (5-aminosalicylates)
Rowasa, Pentasa, Asacol
1st step Tx in IBD
Anti-TNF’s
Remicade, Humira, Cimzia
block major step in inflammatory path, quick in IBD Tx but expensive
Acute Dysphagia
Typically foreign body impaction in esophagus, such as food bolus, inability to swallow saliva
Tx: remove FB during endoscopy
Causes of Chronic Dysphagia
Esophageal or Peptic Stricture Esophageal Cancer Eosinophilic Esophagitis Esophageal Webs and Rings Esophageal Motility Disorders Systemic Sclerosis Achalasia Erosive Esophagitis
dysphagia, dysphagia, dysphagia*
Esophageal Cancer: progressive dysphagia (solids to liquids)
Dx: endoscopy (Ct staging, PET distant mets)
When reflux symptoms do not improve with acid suppression, consider*
Eosinophilic esophagitis (EGD and biopsy: >15 eosinophils per hpf; ring formation)
Eosinophilic esophagitis tx
First line – inhaled corticosteroid (spray during breath hold then swallow) x 8 wks
Candida esophagitis – most common adverse reaction
Esophageal Web – most common in
cervical esophagus (typically anterior) --> narrowing post-cricoid area <2 mm thick tissue membrane protruding into lumen (esophageal ring most common in distal esophagus)
Plummer-Vinson Syndrome
(anemia + cervical esophageal web + dysphagia)
Zenker Diverticulum
Pulsion diverticulum of the hypopharynx – herniation of esophageal mucosa (false diverticulum)
Rare, typically elderly population
Dx: barium swallow
solids AND liquids dysphagia
Scleroderma
achalasia
Achalasia*
Inadequate peristalsis in lower esophagus with tight LES (doesn’t relax)
progressive dysphagia for solids AND liquids**
“bird beak” esophagus*
Esophageal Motility Disorders Tx
CCB or TCA (EG IMIPRAMINE)
Alarming Sx in GERD (or risk for Barret’s)
GIB, IDA, unexplained wt loss, anorexia, dysphagia/odynophagia, intractable vomiting, new onset dyspepsia ≥ 60 yrs
GERD Tx
H2 receptor antagonist: pepcid
then PPI instead
Barrett’s Esophagus**
Replacement of the stratified squamous epithelium in the distal esophagus with metaplastic columnar epithelium (Z line = junction between cell types) risk of esophageal ca >30fold Asymp, BUT many have GERD Tx: indefinite PPI for all pts
Celiac Disease
malabsorptive immune mediated disorder, triggered by environmental agent (gluten) in genetically predisposed individuals
- Specifically intolerance to gliadin (alcohol-soluble fraction of gluten)
- villous atrophy on sm int biopsy
- Assoc with HLA-DQ2 and HLA-DQ8 gene loci
What genetic disorders are assoc with Celiac Dz?*
Down syndrome, Turner’s syndrome and Type 1 Diabetes
Classic Sx of Celiac Dz
foul-smelling diarrhea with floating stools and steatorrhea, flatulence
weight loss or other evidence of malabsorption (vitamin or nutrient deficiency, osteopenia)
*but most don’t come classically…
Skin manifestation of Celiac Dz
dermatitis herpetiformis
When should testing be done on pt w/suspected celiac dz
while pt on gluten rich diet
serologic eval: anti-tTG and/or IgA; endoscopy if pos
How many specimens from duodenum to make Celiac Dz Dx?
6 biopsy specimens
Hydrogen Breath Test
Lactose tolerance testing
When is orthostatic BP suggestive of impending shock?
Decrease 10-20 mmHg systolic pressure with a reflex increase in pulse > 15 bpm
Most common condition causing acute episodes of vomiting
viral gastroenteritis
What can you assume w/pts on marijuana
Assume pt has some level of gastroparesis
Treatment: diet + promotility drugs (ex: Metoclopramide, Erythromycin) + glucose control
Most urgent DDx to consider w/vomiting
MI
CVA/cerebral hemorrhage
Mackler triad (Boerhaave’s syndrome)
chest pain
vomiting
subcutaneous emphysema due to esophageal rupture
What is Crohn’s Dz at risk for?
4 to 20 fold inc risk of colon ca
high risk genetic syndromes for Colorectal ca
Lynch Syndrome (HNPCC) Familial Adenomatous Polyposis (FAP): nearly 100% develop <50yo
USPTF screening guidelines Colon ca
50-75yo
Irritable bowel syndrome Sx
Abdominal pain, usually lower quadrant, relieved by defecation
Bloating / Distention
Mucus in stools
Constipation
Diarrhea
Abdominal discomfort after eating
*strongly influenced by emotional factors
Most common IBS subtype
IBS with predominant constipation (50%)
Functional, chronic constipation not explained by another disease
IBS Dx test
Fecal calprotectin or fecal lactoferrin
Meds that can cause constipation
Diuretics
Antacids
Antidepressants
75% of hepatic blood supply comes from*
portal vein (and 50% O2)
Functions of hepatocyte*
Glycogen storage Decomposition of Red Blood Cells Plasma Protein synthesis – albumin, alpha/beta globulins Production of Non-Essential amino acids Gluconeogenesis Hormone production Detoxification Bile production Urea production – from Ammonia and CO2 (thousands of enzymes)
KUPFFER CELL- FUNCTION
RBC Destruction – worn out cells (life span 100-120 days)
Aid in production of Antibodies/ plasma proteins and bile pigments
Phagocytic clearing of pathogens
Activation is responsible for early ETOH-induced liver injury
Where is RBC broken down?
spleen
Which form of bilirubin is water soluble?
conjugated bilirubin (direct bilirubin)
determining jaundice etiology through lab values
look at direct bili levels (total high, indirect high)
Prehepatic: normal
Intrahepatic: low
Posthepatic: high
acute onset of watery, nonbloody, voluminous diarrhea accompanied by nausea and vomiting
Enterotoxigenic Escherichia coli
A patient has had problems with prolonged diarrhea. Stool cultures grow out Cryptosporidium. It is important to?
Test the patient for HIV
treatment of choice for diarrhea caused by Giardia lamblia is?
Metronidazole
most common cause of traveler’s diarrhea is adults?
E. coli
Most commonly used NG tube for decompression
Salem Sump (dual lumen)
When are NG tubes indicated?
treatment of ileus or bowel obstruction (decompression)
administer medications
enteral nutrition
contraindications: esophageal stricture, basilar skull fracture, esophageal varices
not recommended for long term enteral nutrition
How to measure NG tube*
xyphoid to earlobe, then earlobe to nares
image w/XRay to confirm placement
tip of tube below diaphragm
Meissner’s plexus
nervous plexus of submucosa; glands and smooth muscles
Auerbach’s plexus
nervous plexus of muscularis externa; GI motility
Retroperitoneal organs
S = Suprarenal (adrenal) glands A = Aorta/Inferior Vena Cava D = Duodenum (second and third segments) P = Pancreas U = Ureters C = Colon (ascending and descending only) K = Kidneys E = Esophagus R = Rectum
What does the stomach absorb*
ETOH, Aspirin, NSAIDS
Marasmus
Protein and calorie deficiency
NO edema
Kwashiorkor
protein deficiency resulting in edema
“Bird beak sign” on film
achalasia
SENTINEL LOOP on film
short segment of adynamic ileus close to intra-abdominal inflammatory process (e.g., pancreatitis, appendicitis)
