23. Clinical Correlations DSA Flashcards
Absence of secretion of bile leading to white clay colored stools in conditions like cholelithiasis
Acholic
Lack of appetite
Anorexia
Any serious acute intra-abdominal condition (like appendicitis) attended by pain, tenderness, muscular rigidity, etc. for which emergency surgery must be considered
Acute abdomen
Rumbling noise made by propulsion of gas through intestines
Borborygmi
A profound and marked state of constitutional disorder; general ill health and malnutrition
Cachexia
Stoppage or suppression of bile flow, due to factors within or outside the liver
Cholestasis
Symptom denoting blood congealed and separated within gastric contents that takes its form when in contact with acidic environment
Coffee-ground emesis
Acute paroxysmal abdominal pain
Colic
Indicator of enlarged, nontender gallbladder secondary to pancreatic disease or cancer
Courvoisier’s sign
Indicated by ecchymosis around the umbilicus (periumbilical) secondary to hemorrhage
Cullen sign
A peptic ulcer of the duodenum in a patient with extensive superficial burns
Curling ulcer (“stress ulcer”)
Peptic ulcer occurring from severe head injury or with other lesions of the CNS
Cushing ulcer
Postprandial epigastric discomfort
Dyspepsia
Difficulty swallowing
Dysphagia
Abnormal tissue development, alteration in size, shape, and organization of cells
Dysplasia
Edentulous
Having no teeth
ERCP
Endoscopic retrograde cholangiopancreatography
Eructation
Expulsion of swallowed air; aka burping
EUS
Endoscopic ultrasound
Gas or air in the GI tract expelled through the anus
Flatus
Inflammation in the stomach with distinctive histologic and endoscopic features
Gastritis
Gastric conditions where there is epithelial or endothelial damage without inflammation
Gastropathy
GGT
Gamma-glutamyl transferase, used to determine the cause of elevated alkaline phosphatase (ALP)
What is indicated by elevation in both GGT and ALP?
Liver disease
What is indicated by an elevated ALP with a normal GGT?
Not liver disease, usually bone
Flank ecchymosis secondary to hemorrhage
Grey Turner Sign
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. Often attributable to GERD
Globus pharyngeus
Protective response in muscle resulting from pain or fear of movement, voluntary vs involuntary
Guarding
Hematemesis
Vomiting blood
Passage of bright red blood or marron stools
Hematochezia
Icterus
Aka jaundice; yellowing of integument, sclera, and deeper tissues and excretions with bile pigments that have increased in plasma
KUB X-ray
Plain film of kidney, ureters, and bladder
LGIB
Lower GI bleeding
Dark colored stool consistent with broken down hemosiderin in bowel; typically malodorous, sticky, thick paste “tarry”
Melena
[described as melenic stools, NOT melanotic]
Lower abdominal pain in the middle of the menstrual cycle (feel ovulation), doesn’t cause rebound tenderness
Mittleschmerz
MRCP
Magnetic resonance cholangiopancreatography
Detected by palpating deeply under right costal margin during inspiration, and observing for pain and/or sudden stop in respiratory effort; tests for acute cholecystitis or cholelithiasis
Murphy sign
Subjective sensation of impending urge to vomit
Nausea
Severe intractable constipation caused by intestinal obstruction
Obstipation
Painful swallowing
Odynophagia
Abnormal presence of gas in the biliary system/bile ducts
Pneumobilia
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 path or after diagnostic procedure
Pneumomediastinum
Abnormal presence of air or gas in peritoneal cavity
Pneumoperitoneum
Sign associated with retrocecal appendix, manifested by RLQ pain with passive right hip extension
Psoas sign
Substernal burning sensation, aka heartburn
Pyrosis
Pain upon removal of pressure, rather than the application of pressure to the abdomen. Tests for peritoneal inflammation/acute abdomen
Rebound tenderness
Effortless reflux of liquid or gastric or esophageal food contents in the absence of N/V. The spontenous reflux of sour or bitter gastric contents into the mouth
Regurgitation
Peristalsis of the stomach and esophagus conducted with a closed glottis
Retching
Involuntary reflexive contraction of abdominal wall; abdomen feels hard
Rigidity
Pain in RLQ during left sided pressure, referred rebound tenderness seen in appendicitis
Rosving’s sign
Fatty, greasy, stools
Steatorrhea
Ineffectual and painful straining at stool or urination
Tenesmus
UGIB
Upper GI bleeding
Local defect, or excavation of the surface of an organ or tissue that is produced by the sloughing/shedding of inflamed necrotic tissue
Ulcer
Stone from kidney making its way through ureter to bladder, urine analysis will show hematuria
Ureterolithiasis
Palpable mass that is a LN in the left supraclavicular/sternoclavicular fossa
Virchow’s node
Queasiness, retching, and forceful ejection of upper gut contents from the mouth
Vomiting/emesis
T/f: causes of vomiting are isolated to the GI system
False
Causes of vomiting involved in visceral afferent stimulation
Infections Mechanical obstruction Dysmotility Peritoneal irritation Hepatobiliary or pancreatic disorders Topical GI irritants Postoperative Cardiac disease Urologic disease
What are some vestibular disorders that can cause vomiting?
Labyrinthitis
Meniere syndrome
Motion sickness
CNS disorders that can cause vomiting
Increased intracranial pressure
Migraines
Infections like meningitis or encephalitis
Psychogenic disoders like anorexia or bulemia
Irriation of chemoreceptor trigger zones can cause vomiting, including antitumor chemotherapy, medications/drugs, radiation, and systemic disorders
What are some medications that cause vomiting?
Opioids Anticonvulsants Antiparkinsonism drugs Beta blockers, digoxin Nicotine Oral contraceptives Cholinesterase inhibitors Diabetic meds
Irriation of chemoreceptor trigger zones can cause vomiting, including antitumor chemotherapy, medications/drugs, radiation, and systemic disorders
What are some systemic disorders that cause vomiting?
Diabetic ketoacidosis Uremia Adrenocortical crisis Parathyroid disease Hypothyroid Pregnancy Paraneoplastic syndrome
Oropharyngeal dysphagia
Trouble initiating swallowing
Causes of oropharyngeal dysphagia
Neurologic disorders (MS, GB) Muscular and rheumatologic disorders Metabolic disorders (cushings, thyrotoxicosis) Infectious disease (polio, diphtheria, syphilis) Structural disorders (zenker diverticulum, tumors) Motility disorders (UES dysfunction)
Causes of esophageal dysphagia
Mechanical obstruction - solid foods worse than liquids = Schatzki ring, peptic stricture, esophageal cancer, eosinophilic esophagitis
Motility disorder - solid AND liquid foods = achalasia, diffuse esophaeal spasm, scleroderma, ineffective motility
Condition caused by loss of peristalsis in the distal 2/3 smooth muscle of esophagus resulting in impaired relaxation of LES
Achalasia
Achalasia results from denervation of the esophagus, resulting primarily from what?
Loss of NO producing inhibitory neurons in the myenteric plexus
Symptoms of achalasia
Gradual, progressive dysphagia for solids and liquids, resulting in regurgitation of undigested food
substernal discomfort
Weight loss
2 primary diagnostic techniques for achalasia
Barium esophagogram - shows birds beak sign in distal esophagus. EGD endoscopy is performed to r/o mechanical obstruction
Esophageal manometry confirms diagnosis d/t complete absence of normal peristalsis and incomplete LES relaxation with swallowing
What disease is known as “secondary achalasia”?
Chagas disease
How is the esophageal dysfunction distinguished in primary vs. secondary achalasia?
They are indistinguishable! Important to consider chagas disease in patients from endemic regions like mexico, central, and south america
Chagas patients may exhibit other systemic signs such as chagomas or romana’s sign at the portal of entry
How is the physiology of the esophagus affected in achalasia in terms of peristalsis, esophageal sphincter funciton, and resting pressure at those sphincters?
Impaired peristalsis
Incomplete LES relaxation during swallowing (stays closed during swallowing resulting in the backup of food)
Elevation of LES resting pressure
What are some “red flags” to watch for when a patient presents with dyspepsia and epigastric pain?
Dysphagia (especially progressive) Odynophagia Hematemesis Melena Unintentional weight loss Persistent vomiting Constant/severe pain Unexplained iron deficiency anemia Palpable mass LAD Family hx of upper GI cancer
How is the physiology of the esophagus affected in GERD?
LES relaxes abnormally or weakens, allowing reflux to occur
What condition accounts for 50% of upper GI bleeding?
Gastric or duodenal PUD
When is the presence of an ulcer considered PUD?
When ulcer extends through muscularis mucosae and is over 5 mm in diameter
Symptoms of PUD
Epigastric pain described as gnawing, dull, sharp, burning, aching, or hunger-like
Most patients have periodic episodes
Signs of gastrointestinal bleeding
Coffee grounds emesis, hematemesis, melena, or hematochezia
T/F: PE is often normal in uncomplicated PUD
True; may find mild, local epigastric tenderness to deep palpation though
Describe characteristics of H pylori bacteria
Flagella Motile Microaerophilic Spiral (curved, helix) Gram negative bacilli Urease producing Colonizes gastric antral mucosa
What conditions are associated with H pylori?
PUD (usually duodenal)
Chronic gastritis
Gastric adenocarcinoma
MALT lymphoma
What strain of H pylori significantly increases risk of ulcer?
Cag-A toxin positive strain
How is chronic gastritis due to H pylori distinguished from Zollinger Ellison when they both elevate gastrin levels?
ZE will elevate above 1000, chronic gastritis typically does not go that high
Risk factors for H pylori
Poverty Overcrowding Limited education Ethnicity Rural Birth outside US
Transmission of H pylori
Likely Person to person via fecal oral route
Although exact mode is not known
Methods of detection of H pylori and the important consideration prior to running these tests
Best:
Urea breath test
Fecal Ag test
Other:
Serum Ab test
Upper endoscopy with gastric biopsy
**need to have patient stop PPI x14 days prior to fecal and breath tests or high chance of false negative
How does H pylori damage gastric mucosa?
Releases cytotoxins that breakdown mucosal barrier and underlying cells
Urease allows bacteria to colonize gastric mucosa, converts urea to NH3 which alkalinizes the local environment
Which is more common, gastric or duodenal ulcers?
Duodenal
How does location of ulcer differ in PUD associated with gastric vs. duodenal ulcers?
Gastric: typically in lesser curvature of antrum
Duodenal: anterior wall lining of proximal duodenum; multiple ulcers distal to second portion of duodenum
How does the pathology of PUD distinguish gastric vs. duodenal ulcers in terms of gastric acid production?
Gastric ulcers result in decreased acid secretion
Duodenal ulcers result in increased acid secretion
How does symptom description change in gastric ulcers vs. duodenal ulcers?
Gastric: sharp, burning, epigastric pain that worsens 30 min-1.5 hours after eating
Duodenal: gnawing epigastric pain that worsens 3-5 hours after eating, may be temporarily relieved by food/eating
How does NSAID use lead to risk of upper GI ulcers?
MOA ultimately inhibits COX1 and 2, prostaglandins, and NO which leads to decreased protection of gastric and duodenal mucosa
Damage is within epithelial layers with resorption effects, or macroscopically with actual tissue damage
Possible etiologic factors for apparently H pylori and NSAID-negative ulcers
Smoking history Comorbid disease H pylori that has escaped detection Surreptitious NSAID use Neoplasia, infection, infiltrative disease Acid hypersecretion Ischemic mechanisms
What condition should be considered in the following presentation:
Intractable/recurrent/severe ulcer disease associated with ulcers in atypical locations, enlarged gastric folds
Ulcer is associated with secretory diarrhea, steatorrhea, weight loss, N/V, significantly elevated fasting gastrin levels and positive secretin stimulation test, epigastric pain/GERD, and hematemesis/hematochezia/melena
Zollinger-Ellison Syndrome-Gastrinoma
Describe tumor characteristics of gastrinoma
Slow growing
Sometimes pancreatic
Most commonly in duodenum
Occasionally in LNs
> 60% malignant, >1/3 have already metastasized to liver
You evaluate a patient and diagnose them with a ZES gastrinoma, hyperparathyroidism based on increased calcium levels, and pituitary neoplasm. What condition do they have, which has a 25% association rate with ZES gastrinomas?
Multiple Endocrine Neoplasia type 1 (MEN 1)
Diagnosis of ZE-gastrinomas are suggested first by large mucosal folds on endoscopy or upper GI imaging. What typically confirms the diagnosis?
Serum gastrin >1000 ng/L (fasting, w/o PPI)
+secretin stimulation test (would be negative in other causes of hypergastrinemia)
CT and MRI to look for large hepatic metastasis and other primary lesions
How does ZES lead to steatorrhea?
Gastrin secreting tumor leads to increased H+ secretion by parietal cells, which overwhelms buffer capacity of HCO3 in duodenum
Low duodenal pH inactivates pancreatic lipases, leading to fatty stools
Differential diagnosis of epigastic pain (dyspepsia)
PUD Functional dyspepsia (no explanation) Atypical gastroesoph. reflux Gastric cancer Food poisoning Viral gastroenteritis Biliary tract disease
Severe epigastric pain is atypical for PUD unless complicated by a perforation
What are other causes of severe epigastric pain?
Acute pancreatitis Acute cholecystitis/cholelithiasis Esophageal rupture Gastric volvulus Gastric/intestinal ischemia Ruptured AAA Myocardial ischemia
Differential dx of upper GI bleed
PUD Erosive gastritis Arteriovenous malformations/angioectasis Mallory-weiss tear Esophageal varices
What is the diagnostic study of choice for evaluating PERSISTENT heartburn, dysphagia, odynophagia, or structural abnormalities detected on barium esophagography?
Upper endoscopy
[aka esophagogastroduodenoscopy = EGD]
How is an EGD both diagnostic and therapeutic?
Gives direct visualization and allows biopsy of mucosal abnormalities and of normal appearing mucosa
Allows for dilation of strictures
What diagnostic test is used to differentiate between mechanical lesions and motility disorders?
Barium esophagography
[aka barium swallow xray/barium esophagram]
A barium study is more sensitive for detecting esophageal narrowing d/t what types of conditions?
Rings
Achalasia
Proximal esophageal lesions
What is esophageal pH recording and impedance testing?
Techniques using combined pH and multichannel intraluminal impedance allow assessment of acid and nonacid liquid reflux
What is the purpose of esophageal manometry?
Assesses esophageal motility
Determines the location of the LES to allow precise placement of a conventional electrode pH probe
Establishes etiology of dysphagia in patients in whom mechanical obstruction cannot be found, especially if achalasia is suspected by endoscopy or barium study
What is suspected if free air is seen under the right side of the diaphragm on an upright CXR?
Perforated hollow organ
SURGICAL EMERGENCY
CT has no part in the primary detection of gastric ulcers, when is CT used for ulcers?
Detection of subphrenic and other collections that may occur after a perforation of a gastric ulcer
What is HIDA scan? What is an abnormal finding?
Hydroxy iminodiacetic acid scan
Abnormal = gallbladder does not show up
HIDA + CCK checks gallbladder ejection fraction; if low (<38%), then biliary dyskinesia is suspected
What type of ultrasound can detect tumors in the pancreas and other organs surrounding the GI tract?
Endoscopic ultrasound (EUS)
What is ERCP - Endoscopic Retrograde Cholangiopancreatography - used for?
To visualize hepatobiliary and pancreatic ducts, can also provide therapeutic intervention
What is MRCP - Magnetic Resonance Cholangiopancreatography - used for? How does it differ from ERCP?
Does the same thing as ERCP - visualizes hepatobiliary and pancreatic ducts - but it is NONINVASIVE and CANNOT provide intervention (opposite ERCP)
Most people refer to LFTs as AST/ALT transaminases, alkaline phosphatase (ALP), and bilirubin, (LDH and GGT). Why is LFT a misnomer in these cases?
These can come from other sources, and if they do come from the liver they indicate liver damage moreso than function
Most people refer to LFTs as AST/ALT transaminases, alkaline phosphatase (ALP), and bilirubin, (LDH and GGT). This is a misnomer.
What are examples of TRUE LFT’s?
PT/INR
Albumin
Cholesterol
What is in a CBC?
WBC Hgb Hct MCH MCHC MCV RDW RBC count Platelet count
What is in a CBC with differential?
Same stuff as a CBC, with percentage and absolute differential counts (PMN, lymph, baso, eos, mono)
MCV
Mean corpuscular volume
MCH
Mean corpuscular hemoglobin
MCHC
Mean corpuscular hemoglobin concentration
RDW
Red cell distribution width
What is included in a BMP?
BUN BUN:Cr ratio Ca CO2 Cl Creatinine eGFR Glucose Potassium Sodium
A comprehensive metabolic panel includes the same things as a BMP, with what additions?
Albumin:Globulin ratio Albumin ALP AST/SGOT ALT/SGPT Total bilirubin Total globulin Total protein
Mild elevations in serum aminotransferases where ALT is predominant may indicate what conditions?
Chronic hepatitis B, C, and D Acute viral hepatitis Steatosis/steatohepatitis Hemochromotosis Medications/toxins Autoimmune hepatitis Alpha-1 antitrypsin deficiency Wilson disease Celiac disease Glycogenic hepatopathy
Mild elevations in serum aminotransferases where AST is predominant may indicate what conditions?
Alcohol related liver injury
Cirrhosis
Mild elevations in serum aminotransferases coming from non-hepatic sources may indicate what conditions?
Strenuous exercise Hemolysis Myopathy Thyroid disease Macro-AST
Severe elevations in serum aminotransferases greater than 15x normal may indicate what conditions?
Acute viral hepatitis (A-E, herpes) Medications/toxins Ischemic hepatitis Autoimmune hepatitis Wilson disease Acute bile duct obstruction Acute budd-chiari syndrome Hepatic artery ligation
Lipase and amylase labs may be considered when looking for signs of ______
Pancreatitis
GGT, fractionate bilirubin, and PT/INR are labs to consider when assessing the _____
Liver
Osteopathic considerations of the GI system include parasympathetics which supply the upper GI tract (esophagus thru transverse colon) via the _____, _____ vertebral levels and _____ nerve
As well as the lower portion of the GI tract (descending colon, sigmoid, and rectum) via the _____ vertebral levels and _______ nerves
OA, AA, Vagus
S2-S4; pelvic splanchnic
Sympathetic levels of viscerosomatics corresponding to the:
Appendix
Esophagus
Stomach
Appendix = T12
Esophagus = T2-8
Stomach = T5-9
Sympathetic levels of viscerosomatics corresponding to the:
Liver
Gallbladder
Small intestine
Liver = T6-9
Gallbladder = T6-9
Small intestine = T5-9, T9-12
Sympathetic levels of viscerosomatics corresponding to the:
Colon
Pancreas
Colon = T9-L2
Pancreas = T5-11
What type of ulcer requires follow up to make sure it has completely resolved because it can be a sign of malignancy?
Gastric ulcer
How does ZES lead to its characteristic finding of enlarged gastric folds?
The gastrinoma secretes large quantities of gastrin, leading to increased H+ secretion by parietal cells which exerts a trophic effect, leading to increased parietal cell mass and enlarged gastric folds
What parasite causes secondary achalasia?
Trypanosoma cruzi
[causes chagas disease]
Differentiating upper vs. lower GI bleeding is often characterized based on whether it is proximal or distal to what landmark?
Ligament of treitz
You diagnose your patient with MALT lymphoma associated with an active H. pylori infection. You first administer antibiotics to get rid of the H. pylori infection. What effect does this have on the cancer?
Cures it!
Not all infections with H. pylori lead to ulcers. What component of H. pylori makes the development of an ulcer far more likely?
Exotoxin (vacuolating toxin that causes gastric mucosal injury)
