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135 Cards in this Set

  • Front
  • Back
Rapidly conducting fibers meditate sharp, sudden, well-localized pain.
A-delta fibers: skin and muscle
Slow conducting fibers mediate dull, burning, poorly localized pain that is more gradual in onset and longer in duration.
Primary type of nociception for the abdominal viscera
C-fibers: muscle, periostium, mesentery, peritoneum, and viscera
Nociceptors (pain receptors) are located within:
Mucosa and muscularis of hollow viscera

Serosal surface of the peritoneum and mesentary
First-order neurons innervating the viscera carry information to the thoracolumbar sympathetic nervous system and synapse at the dorsal horn of the spinal cord.
Second-order neurons cross and ascend via the _____________ and ______________ tracts to synapse at the thalamus and proceed to the limbic and somatosensory area.
First-order neurons innervating the viscera carry information to the thoracolumbar sympathetic nervous system and synapse at the dorsal horn of the spinal cord.
Second-order neurons cross and ascend via the spinothalamic and spinoreticular tracts to synapse at the thalamus and proceed to the limbic and somatosensory area.
Visceral “Vague” Pain?
Dull, poorly localizing to the midline as organs transmit sensory afferents to both sides of the spinal cord.

Described as cramping, burning, gnawing.

Secondary autonomic effects lead to sweating, restlessness, nausea, vomiting.
Somatic “Sharp” (Somatoparietal) Pain
?
Irritation of the parietal peritoneum- more intense and more precisely localized than visceral pain.
e.g. early vague visceral periumbilical pain in acute appendicitis localizes to McBurney’s point with increased peritoneal irritation.

Generally worsened with movement or coughing.
Referred Pain?
Due to convergence of visceral afferent neurons with somatic afferent neurons from different anatomic regions on second-order neurons in the spinal cord at the same spinal segment
primary stim of visceral pain is what?
Primary stimulus is stretch!


Cutting, tearing, crushing does NOT cause pain
Accumulation of nocireactive substances change the microenvironment of the injured tissue to ______ the pain threshold.
Accumulation of nocireactive substances change the microenvironment of the injured tissue to reduce the pain threshold.
Colicky is seen with what maladies?
(e.g., intestinal, renal, biliary colic)
Progressive pain is seen with what maladies?
(e.g., appendicitis, diverticulitis)
Pain Spontaneously resolves with what malady?
(e.g., gastroenteritis)
Catastrophic onset of pain happens with what GI malady?
(e.g., ruptured AAA).
Changes in location may represent progression from visceral to ________ irritation (i.e. appendicitis) or development of diffuse peritoneal irritation (i.e. perforated _____).
Changes in location may represent progression from visceral to parietal irritation (i.e. appendicitis) or development of diffuse peritoneal irritation (i.e. perforated ulcer).
Renal colic - patients are _______ and writhe.
listless
Duodenal ulcer - pain alleviated by _________
meals
Peritonitis - patients often lie ______.
motionless
Gastric ulcer / chronic mesenteric ischemia – exacerbation with ______.
eating
Bowel sounds
Hyperactive- obstruction
Hypoactive- ______
Bowel sounds
Hyperactive- obstruction
Hypoactive- ileus
___ preferred initial imaging test for hepatobiliary system, kidneys, pelvic organs.
U/S preferred initial imaging test for hepatobiliary system, kidneys, pelvic organs.
Look at chart showing perforated peptic ulcer, mesenteric ishmia/infarction, and ruptured AAA
-
Common GI Symptoms - name some
Dysphagia and Odynophagia

Globus Sensation

Noncardiac Chest Pain

Dyspepsia

Nausea and Vomiting
Motor cranial nerves in swallowing
5, 7, 9, 10, 12
sensory cranial nerves in swallowing
5, 9, 10
Esophageal transit time for food boluses generally __ seconds
Esophageal transit time for food boluses generally 10 seconds
Hoarseness may result from __________________ nerve dysfunction or intrinsic muscle disease leading to ineffective vocal cord movements.
recurrent laryngeal
Weakness of the soft palate or pharyngeal muscles causes dysarthria, nasal speech, pharyngonasal __________
regurgitation
Esophageal Dysphagia:

3 crucial questions
Three crucial questions…
What type of food causes symptoms?
Is the dysphagia intermittent or progressive?
Does the patient have heartburn?
Dysphagia to BOTH solids and liquids suggest an esophageal __________ disorder.
dysmotility
Dysphagia to SOLIDS ONLY suggests a ________ obstruction
mechanical
Causes of Dysphagia to BOTH solids and liquids
Achalasia is characterized by generally painless regurgitation of undigested foods, frequently at night and weight loss.

Spastic motility disorders are characterized by chest pain with cold or hot liquid sensitivities.

Scleroderma is accompanied by severe GERD and dysphagia is generally related to peptic strictures.
First episode of dysphagia?
First episode often occurs during hurried meal ± alcohol (“Steakhouse Syndrome”)
Benign (Peptic) strictures:

Weight loss?
Weight loss is rare as patients maintain good appetite and convert their diet to soft foods and liquids.
Causes of motility disorders (3)
Achalasia
Spastic motility disorders
Scleroderma
Mechanical obstructions (2)
Webs and rings (Schatzki)
What pills cause pill-induced esophagitis
Antibiotics (especially doxycycline)
Feeling of lump or tightness in the throat unrelated to swallowing
Globus Sensation

Most common in middle aged women (“globus hystericus”).
Described as an intermittent anterior chest discomfort, often indistinguishable from cardiac CP.
Noncardiac Chest Pain
Dyspepsia
Disturbed digestion; indigestion.
Symptoms of dyspepsia
Constellation of symptoms different in all patients.
Pain or discomfort centered in the upper abdomen and associated symptoms may include:
Bloating
Heartburn
Early satiety
Postprandial fullness
Nausea
Anorexia
Regurgitation
Burping and belching
General causes of dyspepsia
Organic cause found in only 40% of cases
GERD, PUD, gastric cancer

Greater than 50% have no cause identified and are labeled:
Idiopathic or functional dyspepsia
major drug causes of dyspepsia
Ethanol
Aspirin/NSAIDs
Antibiotics (macrolides, sulfonamides, metronidazole)
Alarm symptoms of GERD and dyspepsia
weight loss, bleeding, anemia, dysphagia


suspect malignancy (especially if >45 years old).
Biliary Colic”
?
Discrete episodes of acute, severe upper/ RUQ pain that progressively increases to crescendo.
Lasts one hour (or more) then slowly decreases.
Pain may radiate to back or scapula.
Acute vs chronic pancreatic symptoms
Acute pancreatitis usually presents with severe pain with nausea and vomiting.
Chronic pancreatitis presents with dull, steady upper abdominal pressure aggravated with meals.
Symptoms of pancreatic cancer
Pancreatic or ampullary cancer may present with vague, low-grade, nonspecific upper abdominal symptoms
Associated with weight loss, jaundice, anorexia
Most common cause of dyspepsia!
50-70% of chronic dyspepsia have no organic abnormality identified.
Results in heightened sensitivity to normal physiologic events or otherwise minor noxious stimuli.
Visceral Hypersensitivity

Key component of IBS
Does Helicobacter pylori cause functional dyspepsia???
One of the most hotly debated topics over the past decade!

Acute infection causes transient nausea, vomiting and dyspepsia.

Chronic infection leads to PUD with concomitant dyspepsia in up to 15 % of patients.

High prevalence of infection in general population (20-30%) in Western countries.
T or F

Prevalence of H. pylori in patients with functional dyspepsia is similar to that of the general population.
T
H. pylori and dyspepsia:

no strong association although a _____ association cannot be excluded.
weak
Chronic nausea and vomiting may be due to:
Partial mechanical obstruction of the gastrointestinal tract
Intracranial pathology (e.g., brain tumor)
Motility disturbance (e.g., gastroparesis
Metabolic or endocrine etiology
Psychogenic disturbance
Acute nausea and vomiting may be due to:
Acute GI infection
Ingestion of toxins (food poisoning) or a new medication
Pregnancy
Head trauma
Visceral pain (secondary to acute gastrointestinal obstruction, inflammation, or ischemia).
Immediate postprandial vomiting suggests:
Psychogenic vomiting
Peptic ulcer near the pyloric channel, presumably because of pyloric irritability, edema, and spasm.
Delayed vomiting (more than 1 hour after eating) suggests:
Gastric outlet obstruction
Motility disorder of the stomach (e. g., diabetic or post-vagotomy gastroparesis).
What pain is not releieved by vomiting
Not pain caused by pancreatitis or biliary tract disease.
MOST IMPORTANT FACTOR in reflux events
tLESRs

transient lower esophageal sphincter relaxations
GER can occur with either by stress reflux or free reflux:

what are those terms
Stress reflux occurs when a hypotensive LES is overcome and "blown open" by an abrupt increase of intra-abdominal pressure.

Free reflux occurs without an identifiable change in either intragastric or LES pressure.
Classic Symptoms of GERD
Regurgitation of bitter acidic fluid into the mouth in the absence of nausea, retching, and abdominal contractions.

Retrosternal burning sensation typically starting inferiorly and radiates upward towards the neck, back and rarely arms.
GERD and Hoarseness

Direct Injury by Microaspiration of Acid.

Prevalence __% of all cases of GERD.

Associated with laryngeal ______.

Confirmed by Esophageal __ Study.

High Dose Acid Suppression Needed.
GERD and Hoarseness

Direct Injury by Microaspiration of Acid.

Prevalence 10% of all cases of GERD.

Associated with laryngeal cancer.

Confirmed by Esophageal pH Study.

High Dose Acid Suppression Needed.
Adequate response to ______ therapy is a crucial predictor of successful response to surgical treatment.
medical
GERD surgery that wraps the stomach around itself is called what?
Laparoscopic Nissen Fundoplication
What is this?

Creates a plication by intraluminally suturing distal esophagus
Endocinch
What is this GERD therapy?

Delivers radiofrequency energy to create lesion; heals and results in LES stenosis
May also interfere with neural mechanism of tLESRs
1600 cases performed thus far (2 deaths, 4 perforations)
Stretta
Reflux Esophagitis- Savary-Miller classification
Grade 1
Non-confluent reddish spots

Grade 2
Confluent, but not circumferential

Grade 3
Circumferentiaerosions

Grade 4
Chronic complications with deep ulcers, stenosis and Barrett’s metaplasia
Cameron’s Erosions

?
?
Maloney-Hurst Bougie Dilators?
Mercury-filled rubber bougies, first used by Hurst in 1915, have a blunt tip.

Hurst developed the tapered tip- may be useful for Schatzki’s ring dilations.

Generally “old-school” now! Not my preference!
Wire-guided Savary Dilators?
a flexible, tapered polyvinyl dilator with a hollow central core that permitted direct passage of the dilator over a guide wire.

Often performed under fluoroscopy for complex strictures.

Currently my dilator of choice for high cervical strictures.
TTS Balloon Dilators?
Dilation to 18 mm (54 French) allows intake of a regular diet.

Patients with an esophageal lumen less than 13 mm (39 French) will usually experience solid food dysphagia.
Maloney-Hurst Bougie Dilators?
Mercury-filled rubber bougies, first used by Hurst in 1915, have a blunt tip.

Hurst developed the tapered tip- may be useful for Schatzki’s ring dilations.

Generally “old-school” now! Not my preference!
Three patterns of Barrett's
Long segment Barrett’s metaplasia extends at least 3 cm proximally from the GE junction.

Short segment Barrett’s metaplasia projects less than 3 cm from the GE junction

Gastric cardia intestinal metaplasia, in which no metaplastic tongues are evident projecting from the GE junction, but biopsy specimens taken distal to the squamocolumnar junction still demonstrate specialized intestinal metaplasia.
Probably has LEAST MALIGNANT RISK!
Wire-guided Savary Dilators?
a flexible, tapered polyvinyl dilator with a hollow central core that permitted direct passage of the dilator over a guide wire.

Often performed under fluoroscopy for complex strictures.

Currently my dilator of choice for high cervical strictures.
Risk factorss of sq CA vs AdenoCA of the esophagus
--
TTS Balloon Dilators?
Dilation to 18 mm (54 French) allows intake of a regular diet.

Patients with an esophageal lumen less than 13 mm (39 French) will usually experience solid food dysphagia.
Three patterns of Barrett's
Long segment Barrett’s metaplasia extends at least 3 cm proximally from the GE junction.

Short segment Barrett’s metaplasia projects less than 3 cm from the GE junction

Gastric cardia intestinal metaplasia, in which no metaplastic tongues are evident projecting from the GE junction, but biopsy specimens taken distal to the squamocolumnar junction still demonstrate specialized intestinal metaplasia.
Probably has LEAST MALIGNANT RISK!
Risk factorss of sq CA vs AdenoCA of the esophagus
--
The only true esophageal dysmotility disorder
achalasia
Achalasia - Substantially increased risk for developing _________ cell esophageal cancer.
squamous
Pathophys of achalasia:

Preferentially involves the ______ ______-producing, inhibitory neurons that effect the relaxation of esophageal smooth muscle.

Degenerative changes in vagal fibers supplying the esophagus.
Pathophys of achalasia:

Preferentially involves the nitric oxide-producing, inhibitory neurons that effect the relaxation of esophageal smooth muscle.

Degenerative changes in vagal fibers supplying the esophagus.
Pseudoachalasia?
Malignancy, especially gastric carcinoma of the cardia
Chagas' disease
Amyloidosis
Sarcoidosis
Neurofibromatosis
Eosinophilic gastroenteritis
Multiple endocrine neoplasia, type 2B
Juvenile Sjögren's syndrome with achalasia and gastric hypersecretion
Chronic idiopathic intestinal pseudo-obstruction
Anderson-Fabry's disease
What is the name of this?:
Simultaneous contractions (>20 percent wet swallows)

Intermittent peristalsis

Repetitive contractions ( 3 peaks)

Prolonged duration contractions (>6 sec)
Diffuse Esophageal Spasm (“Corkscrew Esophagus”)
Treatment of Spastic Esophageal Disorders
Treat Reflux aggressively as this may be primary cause.

Often the only factor that can be modified!!!
Drugs for esophageal spasms
CCBs
antidepressants
Scleroderma?
Loss of distal (smooth muscle) peristalsis.

Hypotensive LES (<10 mmHg).

Normal proximal esophagus and UES (striated muscle).

Leads to variety of GI complications.
What is it?


Herniation through Killian's triangle, an area of muscular weakness between the horizontal and oblique fibers of the inferior constrictor muscle in the hypopharynx.

This likely occurs in the setting of inadequate relaxation of the UES.

Best seen on a barium swallow, the barium spills into the diverticulum through the opening filling the diverticulum which can later spill and cause aspiration.
Zenker's diverticulum
___ is the rate limiting step in the production of prostaglandins (PGs).
cyclooxygenase
Types of Cyclooxygenase affecting GI
COX-1
Risk Factors for PUD

Prior history of an adverse GI event (ulcer, hemorrhage) increases risk four to fivefold.

Age >__ increases risk five- to sixfold.

High (more than twice normal) dosage of a NSAID increases risk 10-fold.

Concurrent use of _____________ increases risk four to fivefold.
Steroids are not ulcerogenic by themselves!

Concurrent use of anticoagulants increases risk 10- to 15-fold.
Risk Factors for PUD

Prior history of an adverse GI event (ulcer, hemorrhage) increases risk four to fivefold.

Age >60 increases risk five- to sixfold.

High (more than twice normal) dosage of a NSAID increases risk 10-fold.

Concurrent use of glucocorticoids increases risk four to fivefold.
Steroids are not ulcerogenic by themselves!

Concurrent use of anticoagulants increases risk 10- to 15-fold.
Concurrent use of "____ aspirin” with COX-2 selective inhibitors will negate any potential benefit over a non-selective COX inhibitor.
Concurrent use of “Baby aspirin” with COX-2 selective inhibitors will negate any potential benefit over a non-selective COX inhibitor.
Duodenal Ulcer:
Initially ________ by eating.
Postprandial abdominal pain 2-5 hours after meals or on empty stomach.
Between 11pm- 2 am.

Gastric Ulcer:
Severe pain occurring immediately after meals and less frequently improved by ___.
Duodenal Ulcer:
Initially improved by eating.
Postprandial abdominal pain 2-5 hours after meals or on empty stomach.
Between 11pm- 2 am.

Gastric Ulcer:
Severe pain occurring immediately after meals and less frequently improved by food.
Upper GI Bleeding caused by what mostly
PUD – (55%)
Gold standard in diagnosing PUD
EGD
Indications for EGD
Acute GI Hemorrhage
Dysphagia or odynophagia
“Warning Signs” of GERD
Suspected esophagitis
Cancer surveillance
Abnormal Barium study
Dilation of stricture
Contraindications of EGD
Unable to cooperate with exam
Suspected perforated viscous
Hemodynamic instability
What do you do if you see Moderately-Low Rebleeding Risk Clean Based Cratered Ulcers
Biopsy for H. pylori and stop NSAIDS
Generally safe to discharge home immediately after EGD
What do yo udo with a The adherent clot seen with endo
Endoscopic therapy with injection therapy and/or electrocautery

Biopsy for H. pylori and stop NSAIDS

Observe in hospital 48 hours.
What do you do for a pt with Moderately High Rebleeding Risk GU with visible vessel…
Biopsy for H. pylori and stop NSAIDS
Endoscopic therapy indicated
Admit to IMC/ICU for 48-72 hours
Sites of Porto-systemic Collaterals
Esophageal varices-
caput medusae
Rectal varices-
Splenorenal shunts
Treatment of esophageal varices
Primary prophylaxis with nonselective beta blockers.

Secondary prophylaxis with banding and/or sclerotherapy.

Octreotide infusion used to decrease splanchnic blood flow in the treatment of acute variceal bleeding.
What is this?:

Increased risk of bleeding after treatment of esophageal varicies.

“Snakeskin” appearance, most evident in fundus and body.
Portal Hypertensive Gastropathy
AVMs:

Increased incidence in renal failure, ____________ disease and aortic stenosis
Von Willebrand's
What's this:

Watermelon Stomach”
Stripes represent ectatic and sacculated mucosal vessels.

Most common in elderly females with severe iron-deficiency anemia, slow GI bleed in absence of cirrhosis.

Treat with endoscopic coagulation with heater probe, Gold probe, APC or YAG laser.
Gastric Antral Vascular Ectasia (GAVE)
What is this?:

Dilated aberrant submucosal vessel which erodes the overlying epithelium in the absence of a primary ulcer.

Usually located in upper stomach along the high lesser curvature.
Dieulafoy's Lesions
What is this:

Bleeding from pancreatic duct.

Due to chronic pancreatitis, pancreatic pseudocysts, pseudoaneurysm or malignancy, or after therapeutic ERCP.
Hemosuccus Pancreaticus
What is this:

Direct communication between aorta and GI tract.

Presents with herald bleed manifested by hematemesis/ hematochezia followed by massive bleeding and exsanguination
Aortoenteric Fistulas
What type of gastric cancer?

Resembles colorectal cancer- distinct glands comprised of well differentiated columnar epithelial cells with a well developed brush border.

Predominate high-risk populations

More common in men and older patients

Associated with a better prognosis

Often preceded by a prolonged precancerous state.
Intestinal (expanding) type of Gastric Cancer
What type of cancer?

Poorly organized clusters or solitary mucin-rich (signet ring) cells and a diffusely infiltrating growth pattern.

Predominates in women and younger patients

Carries a poorer prognosis.

Not preceded by a known precancerous lesion.
Diffuse (infiltrative) type of Gastric Cancer
What type of gaastric cancr?

Linitis plastica of the stomach-
Diffuse (infiltrative) type
Diagnosis of Gastric Cancers
Endoscopy is gold standard!
Any suspicious gastric ulcers must be extensively biopsied.

Generally repeat EGD 3 months after treatment to confirm healing.
Persistence is worrisome for malignancy.

UGI Series compliments diagnosis
Water flask (“linitis plastica”) often difficult to detect on EGD.
Imaging used to stage gastric CA
Staging performed by CT and EUS.
HLA of deliac disease
Association with HLA-DQ2 and/ or DQ8 gene locus.
Presence of Ig_-antibodies against endomysium (a structure of smooth muscle connective tissue) and its target autoantigen (______ ________________- tTG) are pathognomonic for celiac disease.
Presence of IgA-antibodies against endomysium (a structure of smooth muscle connective tissue) and its target autoantigen (tissue transglutaminase- tTG) are pathognomonic for celiac disease.
___ is a ubiquitous intracellular enzyme released by inflammatory and endothelial cells and fibroblasts in response to mechanical inflammation or irritation.
tTG is a ubiquitous intracellular enzyme released by inflammatory and endothelial cells and fibroblasts in response to mechanical inflammation or irritation.
Four serologic markers used:
for Celiac Disease
IgA endomysial antibody (IgA EMA)
IgA tissue transglutaminase antibody (IgA tTG)
IgA antigliadin antibody (IgA AGA)
IgG antigliadin antibody (IgG AGA)
Endoscopic Appearance of Celiac disease
Scalloped appearance of the duodenal mucosa may correspond to villous atrophy.
What is cancer risk assoc with celiac disease
Increased risk for lymphoma most commonly described.

Higher incidence of esophageal squamous cell, small intestinal, colorectal and hepatocellular cancers also noted.
What is the following (assoc with celiac disease)

Pruritic, papulovesicles over the external surface of the extremities and on the trunk.

Granular deposits of IgA along nonaffected subepidermal basement membrane.
Dermatitis herpetiformis
Treatment of Celiac disease
Consultation with a skilled dietitian

Education about the disease

Lifelong adherence to a gluten-free diet

Identification and treatment of nutritional deficiencies including iron, calcium, phosphorus, folate, B12, and fat-soluble vitamins. Patients should also undergo screening for osteoporosis.

Access to an advocacy group

Continuous long-term follow-up by a multidisciplinary team.
most common site of adenoca in the SB
Most commonly located within duodenum
65% are periampullary
What type of tumor?

Well-circumscribed intraluminal mass with normal overlying mucosa and a central umbilication.

On cut section, the tumor showed a pale-yellow meaty appearance.
Carcinoid Tumors
symptoms of Carcinoid Syndrome
Watery diarrhea
Flushing
Sweating
Wheezing
Dyspnea
Abdominal pain
Hypotension and/or right heart failure due to tricuspid regurgitation or pulmonic stenosis caused by endocardial fibrosis
triggers for carcinoid syndrome
alcohol, blue cheese, chocolate, red wine, and exercise.
Diagnosis of carcinoid syndrome
24-hour urinary excretion of 5-HIAA- the end product of serotonin metabolism
urinary 5-HIAA excretion
> 100 mg/day positive.

Indium-111 octreotide scans are useful to localize carcinoids as tumor cells almost always contain somatostatin receptors.
MALT tumors occur most often in the ____
stomach
Mantle cell lymphoma has a predilection for the ____
colon and small intestine
SB is most common site of GI metastasis of ______.
melanoma
Cancers in SB that spread Hematogenously
Breast
Lung
Kidney
Cancers in SB that spread by Direct Extension:
Cervical
Ovarian
Colon cancer
Benign SB Adenomas
Villous- carry a significant potential for malignant transformation.

Tubular- lower malignant potential.

Brunner's gland adenomas- rare.
_____ - single, firm, well-defined masses that arise in the submucosal layer of the wall of the small intestine
Leiomyomas
Nutrient malabsorption associated with an increased number and/or type of bacteria in the upper gastrointestinal (GI) tract.
Small Bowel Bacterial Overgrowth (SBBO)
Normal bacterial concentration within the GI tract increases distally:
Stomach and proximal SB (___ organisms/ ml)
Terminal ileum (___ organisms/ ml)
Colon (___ organisms/ ml)
Stomach and proximal SB (10^4 organisms/ ml)
Terminal ileum (10^9 organisms/ ml)
Colon (10^12 organisms/ ml)
Gold standard to diagnose SBBO
Jejunal Aspirate – Gold Standard.
>105 organisms/ mL required.
Rarely performed due to technical difficulty.
Other method for diagnosis of SBBO
[14C]-d-xylose breath test-
Radiolabeled xylose is ingested.
GN Aerobes (present as part of SBBO) cleave [14CO2] which is then absorbed and detected in exhaled breath samples.
Not recommended for children or fertile women due to minor radiation exposure.
Not widely available therefore rarely used in clinical practice.
Treatment of SBBO
Treatment of the underlying cause:
Surgical correction if often NOT an option.
Prokinetics with Zelnorm, Octreotide may be helpful.

Treatment of the bacterial overgrowth:
Adequate antimicrobial coverage can be achieved with the following combinations:
Amoxicillin-clavulanate + Metronidazole.
A combination of a cephalosporin, such as cephalexin or triemthoprim-sulfamethoxazole.
Norfloxacin
Oral gentamicin and metronidazole.
Rifaimin (400 mg BID x 10-14 days)

Provide nutritional support:
Correct electrolyte and mineral imbalances.