DSA Clinical Correlations _ES Flashcards
acholic
absence of secretion of bile [acholic stools are white clay colored stools in cholilithiasis
anorexia
lack of appetite
acute abdomen
any serious acute intraabdominal condition (example: appendicitis) attended by pain, tenderness, and muscular rigidity and for which emergency surgery must be considered
borborygmi
a rumbling noise caused by propulsion of gas through the intestines
cachexia
a profound and marked state of constitutional disorder; general ill health and malnutrition
cholestasis
stoppage or suppression of bile flow, due to factors within (intrahepatic cholestasis) or outside the liver (extrahepatic cholestasis)
coffee-ground emesis
denotes blood congealed and separated within gastric contents that takes the form of coffee grounds when in contact with acidic environment
colic
acute paroxysmal abdominal pain
Courvoisier’s sign
enlarged nontender gallbladder secondary to pancreatic disease or cancer
Cullen’s sign
ecchymosis around the umbilicus (periumbilical) secondary to hemorrhage
curling ulcer
“stress ulcer” - a peptic ulcer of the duodenum in a patient with extensive superficial burns
cushing ulcer
“stress ulcer” - a peptic ulcer occurring from severe head injury or with other lesions of the CNS
dyspepsia
postprandial epigastric discomfort
dysphagia
difficulty swallowing
dysplasia
abnormal tissue development, alteration in size, shape, and organization of cells
edentulous
having no teeth
esophagitis
inflammation of the esophagus
ERCP
endoscopic retrograde cholangiopancreatography
eructation
expulsion of swallowed air
AKA burping
EUS
endoscopic ultrasound
flatus
gas or air in the GI tract expelled through the anus
gastritis
inflammation of the stomach with distinctive histologic and endoscopic features
gastropathy
gastric conditions where there is epithelial or endothelial damage without inflammation
GGT
gamma-glutamyl transferase, used to determine the cause of elevated alkaline phosphatase
GGT and ALP both elevated
liver disease
ALP elevated, GGT normal
other (usually bone) cause of elevated ALP
NOT LIVER DISEASE
Grey Turner Sign
flank ecchymosis secondary to hemorrhage
globus pharyngeus
previously labeled “globus hystericus”
foreign body sensation localized in the neck that does not interfere with swallowing and sometimes is relieved by swallowing
-often occurs in the setting of anxiety or OCD
-clinical experience teaches that it is often attributable to GERD
guarding
protective response in muscle resulting from pain or fear of movement, voluntary vs involuntary
heel strike
pt supine. doc strikes patient’s heel. pain upon striking could indicate appendicitis (peritonitis)
hematemesis
vomiting blood
hematochezia
passage of bright red blood or maroon stools
icterus
jaundice
yellowish staining of the integument, sclera, and deeper tissues and of the excretions with bile pigments, which are increased in plasma
iliopsoas muscle test
have the pt flex their hip against your resistance - increased abdominal pain is a positive test. this suggests irritation of the psoas muscle from inflammation of the appendix.
KUB Xray
plain abdominal x-ray of the Kidney Ureters and Bladder
LGIB
lower gastrointestinal bleeding
Lloyd punch/Kidney punch/CVA tenderness
gently tapping the area of the back overlying the kidney (costovertebral angles) produces pain. this suggests an infection around the kidney or renal stone.
McBurney’s point
rebound tenderness or pain 1/3 of the distance from the ASIS to the umbilicus may suggest appendicitis/peritoneal irritation
melena
dark colored stool consistent with broken down hemosiderin in bowel; typically malodorous, sticky, thick like paste, “tarry”
“melenic stool”
Mittelschmerz
lower abdominal pain in the middle of the menstrual cycle (feel ovulation) doesn’t cause rebound tenderness
MRCP
magnetic resonance cholangiopancreatography
murphy sign
palpate deeply under right costal margin during inspiration and observe for pain and/or sudden stop in inspiratory effort. tests for acute cholecystitis or cholelithiasis.
nausea
subjective sensation of impending urge to vomit
obstipation
severe intractable constipation caused by intestinal obstruction
obturator muscle test
flex the patient’s right thigh at the hip, with knee bent, and rotate the leg internally at the hip. right hypogastric pain is + test. this suggests irritation of the obturator muscle from an inflammed appendix.
odynophagia
painful swallowing
pneumobilia
abnormal presence of gas in the biliary system/bile ducts
pneumomediastinum
abnormal presence of air or gas in the mediastinum, may interfere with respiration and circulation, may lead to pneumothorax or pneumopericardium, occur spontaneously or as a result of trauma or pathology or after diagnostic procedure.
psoas sign
associated with retrocecal appendix. manifested by RLQ pain with passive right hip extension.
pyrosis
substernal burning sensation AKA heartburn
rebound tenderness
pain upon removal of pressure, rather than the application of pressure to the abdomen. tests for peritoneal inflammation/acute abdomen.
regurgitation
effortless reflux of liquid or gastric or esophageal food contents in the absence of N/V. The spontaneous reflux of sour or bitter gastric contents into the mouth.
retching
peristalsis of stomach and esophagus conducted with a closed glottis
rigidity
like it sounds, abdomen is hard, involuntary reflex contraction of abdominal wall
Rovsing’s sign
pain in the RLQ during left-sided pressure - referred rebound tenderness seen in appendicitis
steatorrhea
fatty, greasy, stools
tenesmus
ineffectual and painful straining at stool (or urination)
UGIB
upper gastrointestinal bleeding
ulcer
local defect, or excavation, of the surface of an organ or tissue that is produced by the sloughing (shedding) of inflamed necrotic tissue
ureterolithiasis
stone from kidney making its way through ureter to bladder, urine analysis will show hematuria
virchow’s node
palpable mass, lymph node, in the left supraclavicular/sternoclavicular fossa
vomiting/emesis
queasiness –> retching, forceful ejection of upper gut contents from the mouth
causes of nausea and vomiting
Visceral afferent stimulation
- infections
- mechanical obstruction
- dysmotility
- peeritoneal irritation
- hepatobiliary or pancreatic disorders
- topical GI irritants
- cardiac disease
- urologic disease
Vestibular disorders
CNS disorders
- increased intracranial pressure
- migraine
- infection
- psychogenic
Irritation of chemoreceptor trigger zone
- antitumor chemotherapy
- medications and drugs
- radiation therapy
- systemic disorders
causes of oropharyngeal dysphagia
neurologic disorders
- brainstem cerebrovascular accident, mass, lesion
- amyotrophic lateral sclerosis, MS, psuedobulbar palsy, post-polio syndrome, Guillian-Barre syndrome
- parkinson disease, huntington disease, dementia
- tardive dyskinesia
muscular and rheumatologic disorders
- myopathies, polymyositis
- Sjoren syndrome
metabolic disorders
- amyloidosis
- Cushing disease
- Wilson disease
- medication side effects
Infectious disease
-polio, diphtheria, botulism, Lyme disease, syphilis, mucositis
Structural
- Zenker diverticulum
- Cervical osteophytes
- cricopharyngeal bar
- proximal esophageal webs
- oropharyngeal tumors
- post surgical radiation changes
- pill induced injury
Motility disorder
-upper esophageal sphincter dysfunction
Questions to ask about esophageal dysphagia
- Solids vs liquids vs both?
- worsening (progressive) vs staying the same (not progressive)
- constant vs intermittent
causes of esophageal dysphagia
mechanical
- Schatzki ring = intermittent, not progressive
- Peptic stricture =heartburn+ progressive
- esophageal cancer = progressive, >50 yo, smoking and drinking
- eosinophilic esophagitis = young adults; small caliber lumen; proximal stricture, rings, or white papules
motility
- achalasia = progressive
- diffuse esophageal spasm = intermittent, not progressive, may have CP
- scleroderma = chronic heartburn, Raynaud phenomenon
- ineffective esophageal motility = intermittent, not progressive, commonly associated with GERD
Achalasia
- type of disorder
- etiology
motility disorder
LES cannot relax
abnormal peristalsis
-loss of nitric oxide-producing inhibitory neurons in the myenteric plexus
Achalasia symptoms
- gradual
- progressive dysphagia of solids and liquids
- regurgitation of undigested food (nocturnal regurgitation can provoke cough or aspiration)
- substernal discomfort or fullness after eating
- adaptive: eat slowly or lifting neck or throwing shoulders back to enhance esophageal emptying
- weight loss
Achalasia diagnosis
- barium esophagogram with “bird’s beak” distal esophagus
- smooth symmetric tapering of the distal esophagus
- after barium esophagram (EGD) is always performed
- esophageal manometry confirms diagnosis = complete absence of normal peristalsis and incomplete LES relaxation with swallowing
- “sigmoid esophagus” without treatment
Achalasia treatment
- botulism toxin injection
- dilation
- surgery
Secondary Achalasia
- cause
- symptoms
-Chagas disease
-esophageal dysfunction same as primary, different cause
-Mexico, Central, South America; becoming more common in southern US
-caused by parasite = Trypanosoma cruzi
Symptoms
-megaoesophagus = “bird beak” sign
-megacolon
-cardiomyopathy
-Romana’s sign (swollen eye)
-Chagoma
How’s the physiology of the esophagus affected in achalasia?
- impaired peristalsis
- incomplete LES relaxation during swallowing
- elevation of LES resting pressure
Red Flag Symptoms
- dysphagia
- odynophagia = painful swallowing
- hematemesis
- melena
- unintentional weight loss
- persistent vomiting
- constant/severe pain
- unexplained iron deficiency anemia
- palpable mass (in sternoclavicular fossa)
- lymphadenopathy
- family history of uppergastrointestinal cancer
How’s the physiology of the esophagus affected in GERD?
changes in the barrier between the esophagus and stomach (LES relaxes abnormally or weakens)
peptic ulcer disease (PUD)
- types
- definition
- gastric or duodenal (50% of UGIB)
- ulcers extend through the muscularis mucosae and are usually over 5 mm in diameter
peptic ulcer disease (PUD)
- symptoms
- signs
- PE findings
symptoms
- gnawing, dull, sharp, burning, aching, or “hunger-like” epigastric pain
- last several weeks with intervals of months to years where they are pain free (periodicity)
signs
-“coffee grounds” emesis, hematemesis, melena, hematochezia
PE findings
- often normal in uncomplicated PUD
- mild, localized epigastric tenderness to deep palpation may be present
Helicobacter pylori
-describe the organism
bacteria
- flagellated
- motile
- microaerophilic
- spiral (curved or helix)
- gram negative rod (bacilli)
- urease-producing organism
- colonizes gastric antral mucosa
Helicobacter pylori
-associated with
- most prevalent chronic bacterial disease
- associated with PUD, chronic gastritis, gastric adenocarcinoma, gastric mucosa associated lymphoid tissue (MALT) lymphoma
Helicobacter pylori
-risk factors
- poverty
- overcrowding
- limited education
- ethnicity
- rural
- birth outside US
Helicobacter pylori
-transmission
- person to person (fecal oral)
- exact mode unknown
Helicobacter pylori
-detection
- urea breath test: first line; used to confirm eradication
- fecal antigen test: first line; sensitive, specific, inexpensive; confirm eradication
- antibodies in serum: inexpensive;+ 1-2 years after treatment
- Upper endoscopy with gastric biopsy: rapid urease testing of antrum CLO; Warthin-Starry’s silver stian and immunohistochemistry stain
**Have pt stop PPI x 14 days before fecal and breath tests or high chance of false negative
How does Helicobacter pylori damage the gastric mucosa?
- releases cytotoxins that breakdown the mucosal barrier and underlying cells
- the enzyme urease allows the bacteria to colonize the gastric mucosa
What does urease do?
converts urea to NH3, which alkalinizes the local environment
Which is more common: gastric or duodenal ulcer?
duodenal
gastric vs duodenal ulcer
- risk factor/associated with
- location
gastric ulcer
- NSAIDs risk factor for mucosal damage
- lesser curvature of the antrum of stomach
duodenal ulcer
- H Pylori
- anterior wall lining of proximal duodenum
- multiple ulcers or ulcers distal to 2nd portion of duodenum think ZES
gastric vs duodenal ulcer
-pathophysiology
gastric
- infection in gastric body –> lower acid secretion
- loss of protective mucosal barier = aggressive factors (gastric acid, pepsin) overwhelm defensive factors (gastric mucus, bicarb, microcirculation, prostaglandins, mucosal “barrier”)
duodenal
- infection in gastric antrum –> increase gastric secretion
- H+ secretion higher
- H Pylori + stress + smoking = increased risk
gastric vs duodenal ulcer
-symptoms
gastric
- sharp and burning epigastric pain
- worsens within 30 min-1.5 hours after inciting event (eating)
duodenal
- gnawing epigastric pain
- worsens 3-5 hours after inciting event (eating)
- may be temporarily relieved by food/eating
gastric vs duodenal ulcer
-diagnosis
BOTH
- EGD
- check for H pylori
gastric vs duodenal ulcer
-treatment
gastric
-may be malignant ulcer, so need follow up to ensure it has completely resolved
BOTH
-H2 blocker, PPI, eradicate H Pylori, stop smoking
Other causes of gastrointestinal ulcers
- NSAIDs: COX1 and COX2, prostaglandins, NO; lead to decreased protective effects for gastric and duodenal mucosa; damage is within epithelial layers with resorption effects
- ZES - Gastrinoma: gastrin producing tumor that causes intractable peptic ulcers; rare
- Cushing ulcer: secondary to intracranial lesion, injury
- Curling ulcer: secondary to severe burns
When should you consider Zollinger-Ellison Syndrome (ZES) - Gastrinoma?
- intractable ulcer/recurrent ulcer disease/severe ulcer disease
- associated with ulcers in atypical locations
- enlarged gastric folds
- ulcer associated with: diarrhea (watery, large amounts, secretory), steatorrhea, weight loss, N/V, significantly elevated fasting gastrin level and + secretin stimulation test, epigastric pain/GERD, hematemesis/hematochezia, melena
Describe ZES tumors
- slow growing
- sometimes pancreatic (primary gastrinoma 25%)
- most commonly in duodenum (primary gastrinoma 45%) (submucosal, often small)
- occasionally in lymph nodes (priamry gastrinoma 5-15%)
- > 60% malignant and >1/3 have already metastasized to liver - 30% have 10 yr survival rate
- 25% associated with Multiple Endocrine Neoplasia
ZES diagnosis
suggestive
-large mucosal folds on endocopy or upper GI imaging
confirmatory
- serum gastrin >1000 ng/L
- secretin stimulation test (+): negative in other causes of hypergastrinemia
- CT and MRI for large hepatic metastases and primary lesions, but low sensitivity for small lesions
DDx of epigastric pain (dyspepsia)
- PUD
- functional dyspepsia: no organic explanation
- atypical GERD
- gastric cancer
- food poisoning
- viral gastroenteritis
- biliary tract disease
DDx of severe epigastric pain
- atypical PUD: unless complicated by a perforation or penetration
- acute pancreatitis
- acute cholecystitis
- acute cholelithiasis
- esophageal rupture
- gastric volvulus
- gastric or intestinal ischemia
- ruptured aortic aneurysm
- MI
DDx for UGIB
- PUD
- erosive gastritis
- arteriovenous malformations/angioectasias
- Mallory-Weiss tear
- esophageal varices
esophagoduodenoscopy (EGD)
-study of choice
- evaluating persistent heartburn
- dysphagia
- odynophagia
- structural abnormalities detected on barium esophagography
esophagoduodenoscopy (EGD)
-diagnostic or therapeutic
BOTH
- direct visualization
- allows biopsy of mucosal abnormalities and of normal appearing mucosa
- allows for dilation of strictures
colonoscopy
- prep
- pt sedated
barium XR
- AKA barium swallow
- dysphagia
- mechanical vs motility
- Zenker’s diverticulum
- achalasia
- proximal esophageal lesions
pH testing
- pH within the esophageal lumen may be monitored continuously for 24-48 hrs.
- pH only recording provide information about the amount of esophageal reflux but not nonacid reflux
- techniques using combined pH and multichannel intraluminal impedance allow assessment of acid and nonacid liquid reflux
esophageal manometry
- assesses esophageal motility
- determine the location of the LES to allow precise placement of a conventional electrode pH probe
- establish the etiology of dysphagia in patients in whom a mechanical obstruction cannot be found (especially if a diagnosis of achalasia is suspected by endoscopy or barium study)
plain film XR
- KUB XR: porceelain gallbladder from chronic cholecystitis; emphysematous cholecystitis
- free air: perforated hollow organ EMERGENCY
- constipation
- scoliosis
- small bowel obstruction
CT
-gastric ulcer: detection of subphrenic and other collections that may occur after perforation of a gastric ulcer
HIDA: hydroxy iminodiacetic acid scan
- nuclear scan with radiolabeled isotopes taken up by biliary tree
- cholecystitis or stone obstruction: gallbladder will NOT show up
- HIDA + CCK gives ejection fraction
-Normal if gallbladder is seen
ultrasound
- low radiation
- performed and tolerated easily
- gallbladder wall thickening
- gall stones
endoscopic ultrasound (EUS)
- upper endoscope
- similar to EGD scope
- diagnostic and therapeutic functions
- visualize pancreas through lining of stomach
ERCP (endoscopic retrograde cholangiopancreatography)
- invasive way to visualize the hepatobiliary and pancreatic ducts
- diagnostic and therapeutic
- catheter can be inserted into sphincter of Oddi to inject dye
- pancreatitis is a possible and somewhat common complication of ERCP
- remove gall stones
MRCP (magnetic resonance cholangiopancreatography)
- non-invasive way to visualize hepatobiliary and pancreatic ducts
- cannot provide intervention
liver function tests “LFT’s”
PT/INR
albumin
cholesterol
liver chemistry tests
AST/ALT (transaminases)
ALP (alkaline phosphatase)
LDH
GGT
What is the difference between CBC and CBC with differential?
CBC with differential shows percentage and absolute differential counts (PMN, lymph, baso, Eos, Mono)
What is the difference between BMP and CMP?
CMP includes:
- albumin:globulin ration (A:G)
- albumin
- alkaline phosphatase
- aspartate aminotransferase (AST/SGOT)
- alanine aminotransferase (ALT/SGPT)
- bilirubin, total
Labs for pancreatitis
- lipase
- amylase
labs for liver
- GGT
- fractionate bilirubin
- PT/INR
ZES - gastrinoma labs
- fasting gastin
- secretin stimulation test
