GI Re-Up #3 Flashcards
Pathophysiology of GERD
What are some complications of GERD?
-Incompetent LES. Transient relaxation of LES –> gastric acid reflux –> esophageal mucosal injury
Complications: Esophagitis (from acid), Stricture (narrowing from acidic damage), Barrett’s Esophagus, Esophageal adenocarcinoma
Symptoms of GERD
-What are atypical symptoms?
-What are alarm symptoms?
-Heartburn (pyrosis) increased with supine position. Sour taste in mouth, cough, sore throat.
-Atypical: hoarseness, aspiration PNA, wheezing, CP
-Alarm: dysphagia, odynophagia, weight loss, bleeding
Although typical GERD is a clinical diagnosis based on history and symptoms, what diagnostics CAN you do? What is the GOLD standard for typical GERD?
-Esophageal Manometry: decreased LES pressure
-24 hour ambulatory pH monitoring: GOLD
If persistent symptoms or alarm symptoms with GERD, what diagnostic should you do?
Endoscopy
Management for GERD, initial, medical, and surgical
-Lifestyle modifications: elevated head of bed, avoid laying down for 3 hours after eating, avoid spicy or fatty food, no chocolate or alcohol, smoking cessation, weight loss.
-< 2 episodes/week: Antacids and H2 blockers (Famotidine, Cimetidine, Ranitidine)
- 2 or more episodes/week: PPI’s (Omeprazole, Pantoprazole)
-Nissen fundoplication in refractory patients
Explain the pathophysiology of Barrett’s Esophagus
-Esophageal squamous epithelium is replaced by precancerous metaplastic columnar cells from cardia of stomach (precursor to esophageal adenocarcinoma)
-Complication of long-standing GERD
What diagnostic is done to diagnose Barrett’s Esophagus?
-How often should this be repeated if:
–Barrett’s Esophagus only (metaplasia)
–Low grade dysplasia
–High grade dysplagia
-Upper endoscopy with biopsy
-Metaplasia: PPI and rescope every 3-5 years
-Low grade Hyperplasia: PPI and rescope every 6-12 months
-High grade Hyperplasia: ablation with endoscopy, photodynamic therapy, radio frequency ablation
There are three components to pathophysiology of IBS. Explain them.
What are some symptoms of IBS.
-Abnormal motility (chemical imbalance in intestine of serotonin and acetylcholine).
-Visceral hypersensivity (lowered pain thresholds to distention)
-Psychosocial interactions (altered CNS processing)
-Symptoms: abdominal pain associated with altered defecation/bowel habits, diarrhea, constipation, alternations between the two. Pain often relieved with defecation.
Explain what some “alarm symptoms” of IBS are
-Evidence of GI bleed: ocular blood in stool, anemia
-Anorexia, weight loss, fever, family history of GI cancer
-Persistent diarrhea causing dehydration, Onset > 45 years old, fecal impaction
To diagnose IBS, you use the Rome IV Criteria. What are the components of this?
What is the first line management for IBS?
-Rome IV Criteria: recurrent abdominal pain on average at least 1 day/week in last 3 months with 2 of the following 3: related to defecation, change in stool frequency, change in stool form/appearance
Lifestyle and dietary changes: low fat, high fiber, and unprocessed food diet. Avoid gas producing foods (beans, apples, raisins). Sleep, smoking cessation, exercise.
For constipation in IBS, what are some treatment options?
How about diarrhea symptoms?
-Constipation: fiber, psyllium. Polyethylene glycol.
-Diarrhea: Loperamide, Dicyclomine, Hyoscyamine.
Acute mesenteric ischemia is abrupt onset of small intestinal hypo perfusion. What is the MC etiology of this condition? How about some other etiologies?
-MC etiology: acute arterial occlusion (embolism from A-fib). Superior mesenteric artery occlusion MC.
-Hypoperfusion due to shock, vasopressors, cocaine.
-Obstruction of intestinal venous outflow.
Symptoms of acute mesenteric ischemia
-Severe abdominal pain out of proportion to physical findings. Pain poorly localized.
-Nausea, vomiting, diarrhea
-Peritonitis if advanced disease
What is the initial diagnostic done to assess for acute mesenteric ischemia?
What is definitive?
CT angiography initially
Conventional arteriography is definitive
Management for acute mesenteric ischemia
-Surgical revascularization: embolectomy if due to embolism, angioplasty with stenting or bypass to treat thrombosis.
-Surgical resection if bowel not salvageable.
On the other hand, chronic mesenteric ischemia is….
Most patients with this condition have what other condition?
-Ischemic bowel disease due to mesenteric atherosclerosis (decreased supply during increased demand; eating)
Most patients have atherosclerotic disease (history of MI for example)
Symptoms of chronic mesenteric ischemia
What is the definitive diagnostic test (same as acute)?
-Chronic dull abdominal pain worse after meals (intestinal angina)
-Anorexia (aversion to eating)
-Leads to weight loss
Angiography is the definitive diagnostic test
Definitive management for chronic mesenteric ischemia
-Revascularization (angioplasty with stenting or bypass for example)
Acute gastritis is superficial inflammation or irritation of the stomach mucosa with mucosal injury. What is the pathophysiology of this?
-Imbalance between protective and aggressive mechanisms of the gastric mucosa
Etiologies of gastritis
-What is the MCC?
-What are others?
Symptoms are similar to that of _______. However, most are asymptomatic.
What is the diagnostic of choice for this condition?
MCC: H. Pylori
-Others: NSAIDs, Aspirin, acute stress in ill patients, heavy ETOH, radiation, trauma, corrosives, portal hypertension
Similar to that of PUD: dyspepsia, nausea, vomiting
Upper endoscopy with biopsy
But you should also do H. Pylori testing
Treatment for gastritis?
-Similar to PUD (H. Pylori eradication, H2, PPI’s, stop offending agents)
Autoimmune Metaplastic Atrophic Gastritis is a form of chronic gastritis associated with chronic inflammation, gland atrophy, and epithelial metaplasia. What’s the pathophysiology of this?
Where does it MC occur?
-Auto antibodies against intrinsic factor and parietal cells. This can lead to B12 deficiency (pernicious anemia)
-Gastric fundus and body (spares the antrum)
Autoimmune hepatitis, which is idiopathic chronic inflammation of the liver due to circulating autoantibodies, is MC in ___________.
Although physical exam may be normal, what CAN be there?
-MC in young women
-Hepatomegaly, splenomegaly, jaundice
What diagnostic is specific for autoimmune hepatitis?
What is the treatment?
-Positive ANA, smooth muscle antibodies
Corticosteroids + Azathioprine
Acute Viral Hepatitis has three phases. Explain and describe symptoms for each.
What labs are shown in acute viral hepatitis?
Prodromal Phase: malaise, fatigue, URI, anorexia, decreased desire to smoke, nausea, vomiting, abdominal pain, spiking fever (in Hep A)
Icteric Phase: jaundice
Fulminant: encephalopathy, coagulopathy, hepatomegaly, jaundice, edema, ascites, asterixis, hyperreflexia
Labs: Increased ALT and AST
Fulminant Hepatitis is acute hepatic failure in patients with Hepatitis. What are some common etiologies of this condition?
Symptoms?
-Acetominophen toxicity MCC in US
-Viral hepatitis, sepsis
-Reye Syndrome: children given Aspirin after viral infection
-Symptoms: Encephalopathy, asterixis, increased ICP, coagulopathy (increased PT, INR, PTT), hepatomegaly, jaundice, Reye Syndrome (rash on hands and feet), liver damage, vomiting, dilated pupils with minimal response to light
What is seen on labs with fulminant hepatitis?
-Abnormal LFT’s
-Increased INR 1.5 or greater
-Hypoglycemia
-Increased ammonia
Treatment for fulminant hepatitis
-Supportive: IVF, Mannitol for ICP elevation, PPI for stress ulcer prophylaxis, blood products if coagulopathy
-Liver transplant definitive
How is Hepatitis A transmitted?
Symptoms of Hepatitis A?
How can you prevent this?
-Fecal- Oral: contaminated food and water, especially with international travel, day care workers, MSM, homeless, shellfish, illicit drug use
-Symptoms: Asymptomatic MC, spiking fever, malaise, anorexia, vomiting, abdominal pain, jaundice, hepatomegaly
-Handwashing and improved sanitation, food safety, immunization
Labs shown for Hepatitis A
-Think about acute and past exposure differences
-Acute: IgM anti-HAV
-Past Exposure: IgG HAV Ab with negative IgM
-LFT: Elevated ASL, AST, bilirubin
No treatment is needed for Hepatitis A and it is rarely associated with fulminant or chronic hepatitis. What is given as a pre-exposure prophylaxis?
How about post-exposure prophylaxis?
-healthy person 1-40 years old:
-healthy person > 40 years old:
-immunocompromised or liver disease:
HAV vaccination for travelers 6 months of age or older
-HAV vaccine for 1-40 years old
-HAV vaccine with or without immunoglobulin
-HAV vaccine + HAV immunoglobulin
Hepatitis E is transmitted similar to that of Hepatitis A. Explain.
There is increased risk of fulminant hepatitis with Hepatitis E in what populations?
What will be seen on labs?
-Fecal-oral route
Pregnant women, malnourished, pre-existing liver disease
IgM anti-HEV
No treatment is needed for Hepatitis E and it is not associated with a chronic state. Which population has the highest mortality with this condition?
Pregnancy, especially during third trimester
Hepatitis D Virus (HDV) is a defective virus that requires _______ to cause co- or superimposed infection.
How is this transmitted?
Hepatitis B virus
Parenteral (exposure to blood or blood products)
What is seen on labs for Hepatitis D infection?
What is also performed?
Total anti-HDV. PCR assays for HDV RNA serum.
Hepatitis B serologies
How can you prevent Hepatitis D?
What is the treatment?
Hepatitis B vaccination
No FDA approved management at this time. Liver transplant definitive.
Hepatitis C, 85% of patients with this will develop _______.
What’s the MC route of transmission in the US?
Chronic infection
Parenteral IV drug use MC in the US
What is seen on labs for Hepatitis C?
-Screening
-Confirmatory
-Screening: HCV antibodies. Increased LFT’s
-Confirmatory: HCV RNA (more sensitive than antibodies)
These treatments are available options for Hepatitis C. Just look at them, don’t memorize.
-Ledipasvir-Sofosbuvir
-Elbasvir-Grazoprevir
-Etc.
:)
True or False: Hepatitis C is the MC infectious cause of chronic liver disease, cirrhosis, and liver transplantation in the US?
True
Transmission routes of Hepatitis B (there are four)
The symptoms of acute hepatitis are the same in all types.
-Percutaneous, sexual, parenteral, perinatal
What is the treatment for acute HBV?
Supportive mainstay (majority won’t progress to chronic infection)
Treatment for chronic HBV
When can the treatment stop?
-Antiviral therapy if persistent, severe symptoms, marked jaundice, increased ALT
–Entecavir, Tenofovir
Treatment can stop after confirmation (two tests four weeks apart) that the patient has cleared HBsAG
What is the Hep B vaccine schedule in
-Infant:
-Adults (no prior vaccination)
What is one contraindication to this vaccine?
-Infant: birth, 1-2 months, 6-18 months of age
-Adult: 3 doses at 0, 1, and 6 months
Do not give if allergic to Baker’s Yeast
HBV Antibody interpretation
-Positive HB surface Ag (HBsAg)
-Positive HB surface Ab (anti-HBs)
-HB core Ab IgM (anti-HBc)
-HB core Ab IgG (anti-HBc)
HBsAg: acute or chronic. First positive serologic marker in acute. Core antibody determines if acute or chronic.
anti-HBs: either recovery or vaccination
anti-Hbc (IgM): window period or acute hepatitis
anti-Hbc (IgG): resolved infection or chronic hepatitis
What is the stepwise list you should do in reading Hep B serologies?
1) Look at Surface antigen (HBsAg): if positive, acute or chronic
2) If HBsAg positive, look at Core Antibody (anti-Hbc). If IgM = acute. If IgG = chronic
3) Only need this step if HBsAg was negative. Look at Surface antibody (anti-Hbs). If positive, either vaccination or recovery
4) If surface antibody was the only thing positive, this means vaccination
-If core IgG antibody positive, this mens recovery/distant infection
What does the envelope antigen (HBeAg) tell you?
-If positive in either acute or chronic, this tells you it is highly replicating (if positive) or not (if negative)
Therefore, what labs are seen in
-Acute Hepatitis
-Chronic Hepatitis
-Successful Vaccination
-Distant resolved infection (recovery)
-Acute: + HbsAg, + anti-Hbc IgM
-Chronic: + HbsAg, + anti-Hbc IgG
-Vaccination: + anti-Hbs
-Distant Recovery: + anti-Hbs, + anti-Hbc IgG
