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