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Pance Re-Up > GI Re-Up #3 > Flashcards

GI Re-Up #3 Flashcards

1
Q

Pathophysiology of GERD

What are some complications of GERD?

A

-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

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2
Q

Symptoms of GERD
-What are atypical symptoms?
-What are alarm symptoms?

A

-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

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3
Q

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?

A

-Esophageal Manometry: decreased LES pressure

-24 hour ambulatory pH monitoring: GOLD

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4
Q

If persistent symptoms or alarm symptoms with GERD, what diagnostic should you do?

A

Endoscopy

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5
Q

Management for GERD, initial, medical, and surgical

A

-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

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6
Q

Explain the pathophysiology of Barrett’s Esophagus

A

-Esophageal squamous epithelium is replaced by precancerous metaplastic columnar cells from cardia of stomach (precursor to esophageal adenocarcinoma)
-Complication of long-standing GERD

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7
Q

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

A

-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

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8
Q

There are three components to pathophysiology of IBS. Explain them.

What are some symptoms of IBS.

A

-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.

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9
Q

Explain what some “alarm symptoms” of IBS are

A

-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

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10
Q

To diagnose IBS, you use the Rome IV Criteria. What are the components of this?

What is the first line management for IBS?

A

-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.

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11
Q

For constipation in IBS, what are some treatment options?

How about diarrhea symptoms?

A

-Constipation: fiber, psyllium. Polyethylene glycol.

-Diarrhea: Loperamide, Dicyclomine, Hyoscyamine.

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12
Q

Acute mesenteric ischemia is abrupt onset of small intestinal hypo perfusion. What is the MC etiology of this condition? How about some other etiologies?

A

-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.

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13
Q

Symptoms of acute mesenteric ischemia

A

-Severe abdominal pain out of proportion to physical findings. Pain poorly localized.
-Nausea, vomiting, diarrhea
-Peritonitis if advanced disease

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14
Q

What is the initial diagnostic done to assess for acute mesenteric ischemia?

What is definitive?

A

CT angiography initially

Conventional arteriography is definitive

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15
Q

Management for acute mesenteric ischemia

A

-Surgical revascularization: embolectomy if due to embolism, angioplasty with stenting or bypass to treat thrombosis.
-Surgical resection if bowel not salvageable.

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16
Q

On the other hand, chronic mesenteric ischemia is….

Most patients with this condition have what other condition?

A

-Ischemic bowel disease due to mesenteric atherosclerosis (decreased supply during increased demand; eating)

Most patients have atherosclerotic disease (history of MI for example)

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17
Q

Symptoms of chronic mesenteric ischemia

What is the definitive diagnostic test (same as acute)?

A

-Chronic dull abdominal pain worse after meals (intestinal angina)
-Anorexia (aversion to eating)
-Leads to weight loss

Angiography is the definitive diagnostic test

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18
Q

Definitive management for chronic mesenteric ischemia

A

-Revascularization (angioplasty with stenting or bypass for example)

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19
Q

Acute gastritis is superficial inflammation or irritation of the stomach mucosa with mucosal injury. What is the pathophysiology of this?

A

-Imbalance between protective and aggressive mechanisms of the gastric mucosa

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20
Q

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?

A

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

21
Q

Treatment for gastritis?

A

-Similar to PUD (H. Pylori eradication, H2, PPI’s, stop offending agents)

22
Q

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?

A

-Auto antibodies against intrinsic factor and parietal cells. This can lead to B12 deficiency (pernicious anemia)

-Gastric fundus and body (spares the antrum)

23
Q

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?

A

-MC in young women

-Hepatomegaly, splenomegaly, jaundice

24
Q

What diagnostic is specific for autoimmune hepatitis?

What is the treatment?

A

-Positive ANA, smooth muscle antibodies

Corticosteroids + Azathioprine

25
Q

Acute Viral Hepatitis has three phases. Explain and describe symptoms for each.

What labs are shown in acute viral hepatitis?

A

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

26
Q

Fulminant Hepatitis is acute hepatic failure in patients with Hepatitis. What are some common etiologies of this condition?

Symptoms?

A

-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

27
Q

What is seen on labs with fulminant hepatitis?

A

-Abnormal LFT’s
-Increased INR 1.5 or greater
-Hypoglycemia
-Increased ammonia

28
Q

Treatment for fulminant hepatitis

A

-Supportive: IVF, Mannitol for ICP elevation, PPI for stress ulcer prophylaxis, blood products if coagulopathy
-Liver transplant definitive

29
Q

How is Hepatitis A transmitted?

Symptoms of Hepatitis A?

How can you prevent this?

A

-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

30
Q

Labs shown for Hepatitis A
-Think about acute and past exposure differences

A

-Acute: IgM anti-HAV
-Past Exposure: IgG HAV Ab with negative IgM
-LFT: Elevated ASL, AST, bilirubin

31
Q

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:

A

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

32
Q

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?

A

-Fecal-oral route

Pregnant women, malnourished, pre-existing liver disease

IgM anti-HEV

33
Q

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?

A

Pregnancy, especially during third trimester

34
Q

Hepatitis D Virus (HDV) is a defective virus that requires _______ to cause co- or superimposed infection.

How is this transmitted?

A

Hepatitis B virus

Parenteral (exposure to blood or blood products)

35
Q

What is seen on labs for Hepatitis D infection?

What is also performed?

A

Total anti-HDV. PCR assays for HDV RNA serum.

Hepatitis B serologies

36
Q

How can you prevent Hepatitis D?

What is the treatment?

A

Hepatitis B vaccination

No FDA approved management at this time. Liver transplant definitive.

37
Q

Hepatitis C, 85% of patients with this will develop _______.

What’s the MC route of transmission in the US?

A

Chronic infection

Parenteral IV drug use MC in the US

38
Q

What is seen on labs for Hepatitis C?
-Screening
-Confirmatory

A

-Screening: HCV antibodies. Increased LFT’s
-Confirmatory: HCV RNA (more sensitive than antibodies)

39
Q

These treatments are available options for Hepatitis C. Just look at them, don’t memorize.
-Ledipasvir-Sofosbuvir
-Elbasvir-Grazoprevir
-Etc.

A

:)

40
Q

True or False: Hepatitis C is the MC infectious cause of chronic liver disease, cirrhosis, and liver transplantation in the US?

A

True

41
Q

Transmission routes of Hepatitis B (there are four)

The symptoms of acute hepatitis are the same in all types.

A

-Percutaneous, sexual, parenteral, perinatal

42
Q

What is the treatment for acute HBV?

A

Supportive mainstay (majority won’t progress to chronic infection)

43
Q

Treatment for chronic HBV

When can the treatment stop?

A

-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

44
Q

What is the Hep B vaccine schedule in
-Infant:
-Adults (no prior vaccination)

What is one contraindication to this vaccine?

A

-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

45
Q

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)

A

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

46
Q

What is the stepwise list you should do in reading Hep B serologies?

A

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

47
Q

What does the envelope antigen (HBeAg) tell you?

A

-If positive in either acute or chronic, this tells you it is highly replicating (if positive) or not (if negative)

48
Q

Therefore, what labs are seen in
-Acute Hepatitis
-Chronic Hepatitis
-Successful Vaccination
-Distant resolved infection (recovery)

A

-Acute: + HbsAg, + anti-Hbc IgM
-Chronic: + HbsAg, + anti-Hbc IgG
-Vaccination: + anti-Hbs
-Distant Recovery: + anti-Hbs, + anti-Hbc IgG

Pance Re-Up (76 decks)

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