Clinical Approach to GI Patient: DSA 2 Flashcards

1
Q

What hormone is positive in a pregnancy test?

A

Beta-Hcg

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2
Q

Gastroparesis often occurs from what condition?

A

Diabetes melitus

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3
Q

Gastroparesis presents with chronic or intermittent symptoms of?

A

Postprandial fullness

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4
Q

What diagnostic tool is used for gastroparesis?

A

Gastric scintigraphy (Gastric emptying study)

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5
Q

In the treatment of gastroparesis, what agents should be avoided in diabetic patients?

Why should glucose levels be maintained below 200 mg/dL?

A

1) Agents that reduce GI motility such as opioids and anticholinergics
2) Because hyperglycemia may slow gastric emptying

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6
Q

What effects do metoclopramide and erythromycin have on gastroparesis?

A

Treat it by enhancing gastric emptying

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7
Q

Loss of peristalsis in the intestine in the absence of any mechanical obstruction is termed?

A

Acute Paralytic ileus

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8
Q

Acute paralytic ileus is most commonly seen in hospitalized patients as a result of?

A

1) Surgery
2) Electrolyte abnormalities
3) Severe medical illness

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9
Q

What would indicate acute paralytic ileus from a plain abdominal radiography or CT?

A

Gas and fluid distention in small and large bowel

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10
Q

Severe or prolonged paralytic ileus requires parenteral administration of fluids and electrolytes along with?

A

Nasogastric suction

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11
Q

What is postoperative ileus reduced by?

A

Avoidance of iv opioids as well as early ambulation, gum chewing, and initiation of a clear liquid diet

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12
Q

What is acute small bowel obstruction (SBO) most commonly caused by?

A

Adhesions

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13
Q

What are common symptoms seen with SBO?

A

1) N/V that can be feculent
2) Obstipation (no BM or flatus)
3) Decreased normal bowel sounds with instead high pitched tinkling bowel sounds

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14
Q

How is SBO diagnosed on Plain abdominal radiography (KUB X-ray/Abdominal series X-ray) or CT scan?

A

1) Dilated loops of small bowel

2) Air fluid levels

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15
Q

How is SBO treated?

A

Nasogastric tube (NGT) suction

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16
Q

Menetrier disease is an idiopathic condition characterized by?

What is lossed and what does this lead to?

What is not a common presentation seen with this condition?

What does it increase the risk for?

A

1) Giant thickened gastric folds
2) Chronic protein loss leading to anasarca
3) GI bleed
4) Gastric adenocarcinoma

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17
Q

Alcohol, NSAIDs/steroids, cocaine, ischemia, H pylori, stress (shock), radiation, and allergy can all lead to?

How is this treated?

A

1) Acute gastritis

2) Treat/avoid underlying cause

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18
Q

What is type B gastritis (Antral-type) caused by?

A

H pylori leading to B12 deficiency

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19
Q

With type B gastritis, the eradication of H. pylori is not routinely recommended unless the patient also has either?

A

1) PUD

2) Maltoma

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20
Q

What are potential complications of type B gastritis?

A

1) B12 deficiency
2) Gastric adenocarcinoma
3) Gastric B cell lymphomas

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21
Q

What is seen with type A gastritis (Fundic-type)?

What autoimmune mechanism is seen with this?

A

1) Loss of rugal folds

2) Abs to parietal cells or anti-intrinsic factor Abs

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22
Q

Type A gastritis may present with symptoms of?

How is it treated?

A

1) Carcinoid or of Vitamin B12 deficiency

2) Parenteral B12 (cyanocobalamin) supplementation

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23
Q

What is type A gastritis assocaited with?

A

1) Hypergastrinemia that can develop carcinoid tumors

2) Pernicious anemia that can develop megaloblastic anemia and gastric adenocarcinoma

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24
Q

Which ulcer involves hypersecretion of gastrin?

Which is relieved by food and Gnawing epigastric pain doesn’t occur until 60 min to 3 hours after meals?

Which is worse by food within 30 minutes of eating causing food aversion?

Which do you need to perform endoscopy with biopsy to rule out malignancy?

A

1) Duodenal
2) Duodenal
3) Gastric
4) Gastric

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25
Q

What is the shape of H. pylori?

What is its staining?

What is its interaction with O2?

What enzyme does it produce?

What toxin is it positive for?

A

1) Spiral (curved) bacilli with flagella
2) Gram-negative
3) Microaerophilic
4) Urease
5) Cag-A

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26
Q

What is the treatment for maltoma?

A

Treat the H. pylori infection

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27
Q

What needs to be done after completion of H. pylori eradication therapy?

A

Confirm it with urea breath test, fecal antigen test, or endoscopy with biopsy

28
Q

What can happen in PUD with hollow organs such as the esophagus, stomach, and intestine?

What is the treatment?

How is it diagnosed?

A

1) Perforated viscus
2) Emergency surgery
3) Free air under diaphragm or air in mediastinum

29
Q

What is a peptic ulcer [in particular of the duodenum] in a patient with extensive burns?

What is a peptic ulcer occurring from severe head (brain) injury or with other lesions of the CNS?

What patients are more prone to stress ulcers?

A

1) Curling ulcer
2) Cushing’s ulcer
3) ICU patients

30
Q

What should your differential be for a patient presenting with dyspepsia?

A

1) GERD
2) Gastritis
3) PUD
4) Stress ulcers

31
Q

What is diagnostic and may be therapeutic for an upper GI bleed?

What structure demarcates UGIB from LGIB?

What direction to this structure indicates UGIB?

A

1) Endoscopy
2) Ligament of Treitz
3) Proximal to it indicates UGIB

32
Q

Orthostatic dizziness, confusion, angina, tachycardia, syncope, weakness, SOB, severe palpitations, and cold/clammy extremities indicate?

A

UGIB

33
Q

What are some comorbidities that can cause UGIB?

A

1) Aortic stenosis, renal disease
2) Smoking
3) Alcohol use

34
Q

What should be of importance in obtaining during history taking for UGIB?

A

Thorough medication history

35
Q

During a PE for UGIB, what are some signs of hypovolemia?

A

1) Resting tachycardia
2) Orthostatic hypotension
3) Supine hypotension
4) Acute abdomen

36
Q

What is the treatment/management for UGIB?

A

1) Stabilize
2) 2 large bore IVs
3) Fluid bolus if signs of shock
4) Blood Transfusion if indicated

37
Q

What effect should packed red blood cells have on hemoglobin?

A

Hb should rise 1 g/dL for each unit of transfused PRBCs

38
Q

What should all patients with upper tract bleeding undergo within 24 hours of arriving in the emergency department?

A

Upper endoscopy

39
Q

What are some pharmacologic therapies for UGIB?

A

IV or oral PPI

40
Q

What are some differential Dx considerations for UGIB?

A

1) PUD/stress ulcer
2) Esophageal varices
3) Hemorrhagic gastritis
4) Mallory-Weiss tear/Boerhaave syndrome
5) Dieulafoy lesion
6) GAVE syndrome

41
Q

Esophageal varices most commonly develop secondary to?

A

Portal hypertension (cirrhosis)

42
Q

What are some symptoms of esophageal varices?

A

1) Acute GI hemorrhage (melena, hematochezia, hematemesis)

2) Hypovolemia manifested by postural vital signs/shock

43
Q

What increases the risk of esophageal varices to bleed?

A

1) Size of varices
2) Red wale markings
3) Severity of liver dz
4) Active alcohol abuse

44
Q

What should be administered to treat esophageal varices that are bleeding?

A

1) Fresh frozen plasma or platelets
2) Vitamin K
3) Emergent upper endoscopy with variceal banding

45
Q

How are esophageal varices prevented?

A

1) Nonselective beta-adrenergic blockers

2) Long term treatment with band ligation

46
Q

What are alcoholics at an increased risk for due to portal HTN?

A

Hemorrhagic gastropathy

47
Q

What is the most common clinical manifestation of erosive gastritis?

A

UGIB that presents as coffee ground emesis

48
Q

Why is hemodynamically significant bleeding rare with erosive hemorrhagic gastritis?

A

It is superficial

49
Q

How is hemorrhagic gastritis diagnosed?

A

Upper endoscopy with biopsy

50
Q

What is a primary gastrinoma that is most likely in the proximal duodenum?

A

Zollinger Ellison syndrome

51
Q

25% of ZE syndrome are associated with what autosomal dominant familial syndrome?

A

MEN 1 (multiple endocrine neoplasia type 1 )

52
Q

How do ZE syndrome patients with MEN 1 present?

A

1) Pancreatic gastrinoma
2) Hyperparathyroidism
3) Pituitary neoplasm

53
Q

How does ZE syndrome present?

A

PUD that isn’t responding to tx, is severe, atypical, recurrent

54
Q

What is seen on EGD for ZE syndrome?

What confirms it?

A

1) Large mucosal folds (hypertrophic gastric mucosa)

2) Serum (fasting) gastrin greater than 1000

55
Q

In all patients with Zollinger-Ellison syndrome you want to draw levels (to exclude MEN 1) for?

A

1) PTH
2) Prolactin
3) LH/FSH
4) GH

56
Q

What is the pharm Tx for ZE syndrome?

A

PPI

57
Q

What condition is characterized by a superficial/non-transmural tear at the GE junction?

A

Mallory Weiss tear

58
Q

How do Mallory Weiss tear present?

How are the vital signs and PE?

A

1) Nausea, hematemesis

2) Normal

59
Q

How are Mallory Weiss tear diagnosed?

A

Upper endoscopy

60
Q

What condition is characterized by a spontaneous transmural rupture at GE junction?

It correlates with a history of?

A

1) Boerhaave syndrome

2) Alcohol use

61
Q

How does Boerhaave syndrome present?

A

1) Life-threatening so most patients are in distress
2) Hematemesis
3) Pneumomediastinum or Subcutaneous emphysema

62
Q

How do patients with Gastric Antral Vascular Ectasia (GAVE) syndrome aka as watermelon stomach present?

A

1) Nondescript abdominal pain

2) Occult GI bleed leading to iron deficiency anemia

63
Q

How is GAVE syndrome differentiated from portal HTN gastropathy?

A

Changes are in fundus not antrum

64
Q

What is one of the causes of obscure gastrointestinal bleeding found in the stomach that could result in treacherous and life-threatening gastrointestinal hemorrhage?

A

Dieulafoy lesion

65
Q

How does Dieulafoy lesion present?

A

1) Hematemesis
2) Obscure GI bleeding
3) Occult GI bleed leading to iron deficiency anemia