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# US GI2 Test 1 > Stomach pain, Heartburn, Ingestion, NV, Hematemesis > Flashcards

Stomach pain, Heartburn, Ingestion, NV, Hematemesis Flashcards

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1
Q

Where are the following located/what is their secretion?

a. Parietal cells
b. Chief cells
c. G cells
d. Mucous cells

A
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2
Q

What may cause vomiting in the morning? after a meal?

A

a. pregnancy, uremia, alcoholic gastritis
b. PUD, psychogenic cause

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3
Q

What are complications of vomiting?

A
  • Rupture of the esophagus (Boerhaave’s syndrome)
  • Hematemesis from a mucosal tear (Mallory-Weiss syndrome)
  • Dehydration, malnutrition, dental caries and erosions
  • Metabolic alkalosis and hypokalemia
  • Aspiration pneumonitis
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4
Q

How do you treat N/V due to inner ear dysfunction? motion sickness? gastroparesis? chemotherapy?

A
  1. antihistamines (meclizine)
  2. anticholinergics (scopolamine)
  3. metoclopramide, erythromycin
  4. ondanestron, serotonin receptor blockers, glucocorticoids
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5
Q

Projectile vomiting can suggest what?

A

increased ICP

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6
Q

What are the possible etiologies of gastroparesis?

A
  • Endocrine disorders (DM, Hypothyroidism)
  • Postsurgical conditions (vagotomy, partial gastric resection, fundoplication, gastric bypass, Whipple procedure),
  • Neurologic conditions (PD, MS, Postpolio syndrome, Porphyria)
  • Rheumatologic syndromes
  • Infections (postviral, Chagas disease)
  • Amyloidosis
  • Paraneoplastic syndromes
  • Medications
  • Eating disorders (anorexia)

*cause may not always be identified

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7
Q

What tx options are available for gastroparesis?

A
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8
Q

We often see acute paralytic ileus in what pts?

A

hospitalized - due to surgery, peritonitis, electrolyte abnormalities, medications, severe medical illness

*Sx: N/V, obstipation, distention, minimal abdominal tenderness, decreased or absent bowel sounds

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9
Q

What is the pathophysiology in acute paralytic ileus?

A

Neurogenic failure or loss of peristalsis in the intestine in the absence of any mechanical obstruction

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10
Q

What is unique about the vomit in acute small bowel obstruction? how do we dx?

A
  • can be feculent
  • plan abd radiogrpahy (KUB/Abdominal series) or CT scan
    • shows dilated loops of small bowel, air fluid levels

*tx: nasogastric tube to suction, supportive, sometimes surgery

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11
Q

What is functional dyspepsia?

A

>3 months of dyspepsia without an organic cause

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12
Q

What situations promote GERD?

A

• increased gastric contents (a large meal, gastric stasis, or acid hypersecretion)

  • physical factors (lying down, bending over)
  • increased pressure on the stomach (tight clothes, obesity, ascites, pregnancy)
  • intermittent loss of lower esophageal sphincter tone (scleroderma, smoking, anticholinergics, calcium antagonists)

• hiatal hernia (promotes acid flow into the esophagus)

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13
Q

What are the sx of GERD/heartburn/indigestion?

A
  • epigastric abdominal pain, abdominal fullness, N/V, dysphagia, “waterbrash”, “heartburn”
  • sx occur 30-60 minutes after a meal
  • sx worse with reclining

*waterbrash: bad taste in mouth from refluxed acid

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14
Q

What are some extraesophageal manifestations of GERD?

A

asthma

laryngitis

chronic cough

aspiration pneumonitis

chronic bronchitis

sleep apnea

dental caries

halitosis

hiccups

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15
Q

When do you get an EGD or Abd imaging with a GERD pt?

A

when alarm features are present, >60, persistent sx despite tx

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16
Q

How do we tx GERD?

A
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17
Q
A
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18
Q

What is the cause of Type B Gastritis?

A

H. pylori

“antral type”

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19
Q

What is the cause of Type A Gastritis?

A

AI

“fundic type”

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20
Q

What are the risk factors of PUD?

A
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21
Q

Compare and Contrast DU and GU

A
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22
Q

Which ulcer type is mainly caused by H. pylori (90-95%)?

A

DU

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23
Q

Which ulcer type has normal or reduced acid secretion rates? exaggerated? affects of eating?

A

a. GU - worse by food within 30 min; food aversion
b. DU - gnawing pain 1-3 hrs after meal; can be relieved by food

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24
Q

What are the features of a perforated viscus?

A
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25
Q

What type of ulcers do burn pts get? head injury/CNS lesion pts?

A

a. Curling (duodenum)
b. Cushing’s

*both are stress ulcers

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26
Q

What are the characteristics of H. pylori?

A

Spiral, gram-negative, microaerophilic, urease-producing rods with flagella

27
Q

The prevalence of H. pylori is higher in…

A

 Non-whites

 Immigrants from developing countries

 Poverty/Low socioeconomic status

 Overcrowding

 Rural

 Limited education

 Increases with age

28
Q

Why is Cag-A + toxin with H. pylori important?

A

associated with increased risk of ulcer and gastric cancer

29
Q

What highlighted medications are used to eradicate H. pylori?

A
30
Q

What are some common risk factors of gastric adenocarcinoma?

A
  • Dietary factors:
    • Smoked fish and meats
    • Pickled vegetables
    • Nitrosamines
    • Benzpyrene
    • Reduced intake of fruits and veggies
  • H. Pylori
  • Smoking
  • Blood type A
  • Ménétrier’s disease
31
Q

Cholelithiasis: dx, sx, diagnositcs, complications, ddx

A
32
Q

What are the risk factors for gall stones? protective factors?

A
33
Q

Acute Cholecystitis

A
34
Q

Chronic Cholecystitis

A
35
Q

What is the pathophysiology behind acute pancreatitis? etiology?

A

a. cellular injury from activation of protein kinases, inflammatory mediators, activation of digestive enzymes; saponification
b. gall stones _<_5mm, heavy alcohol use, trauma, meds, AI, infections, congenital, neoplasm…

36
Q

What do you see on PE of acute pancreatitis?

A
37
Q

To dx acute pancreatitis, you need…

A

at least two of the three:

epigastric pain

lipase (and amylase) 3x the ULN

CT changes consistent with pancreatitis

38
Q

What diagnostic tools can you use in acute pancreatitis?

A
  • X-ray
  • US
  • Unenhanced CT
  • Rapid-bolus intravenous contrast-enhanced CT
  • MRI
  • Perfusion CT (PCT)
39
Q

How do you tx mild acute pancreatitis? severe?

A
  1. pancreas rest, fluid resuscitation (lots!!), pain control
  2. surgical consult, hemodynamic monitoring, calcium gluconate IV, FFP, serum albumin infusions, within 48 hrs of admission start enteral feeding with nasogastric tube
40
Q

What are some big complications of acute pancreatitis?

A
  • intravascular volume depletion - third spacing, pre-renal azotemia
  • fluid collections - pleural effusions
  • necrosis - infection
  • pseudocysts - can become infected
  • ARDS
  • pancreatic ascites
41
Q

Define the following:

Hematemesis

Melena

Hematochezia

A
  • Hematemesis: vomit bright red blood or “coffee grounds”
  • Melena: develops after as little as 50-100 mL blood loss in most cases
  • Hematochezia: (bright red blood per rectum) in massive UGIB (1000 mL or more of blood loss)

*source is proximal to Ligament of Treitz in UGIB

42
Q

What is a good to use to determine blood loss?

A

volume status

hematocrit is a poor early indication

43
Q

What clinical features are associated with increased risk of re-bleeding and death?

A

60 years or older

comorbid illness

systolic BP less than 90

pulse greater than 90

bright red blood in nasogastric aspirate or rectal exam

44
Q

What is the initial step in UGIB assessment?

A

assessment of hemodynamic status

Signs of shock:

  • Hypotension
  • Tachycardia
  • Oliguria
  • Altered mental status
  • Tachypnea
  • Cool, clammy, cyanotic skin
  • Metabolic acidosis
  • Elevated serum lactic acid (lactate)
45
Q

In an UGIB, what should be placed prior to further work up?

A

two large bore “18 gauge or larger” intravenous lines

46
Q

In unstable pts, what do you give?

A

IV fluids - .9% NaCl (aka NS normal saline) or LR

47
Q

What should all pts get within 24hrs if they present with UGIB?

A

upper endoscopy

Benefits:

  1. To identify the source of bleeding
  2. To determine the risk of rebleeding and guide triage
  3. To render endoscopic therapy
48
Q

Esophageal causes of hematemesis

A
49
Q

What are the five listed causes of UGIB? What pt background is associated with them?

A
  1. PUD/Stress ulcers
  2. Eosphageal varices - portal HTN
  3. Hemorrhagic gastropathy/gastritis - alcohol, aspirin, NSAIDs, critically ill, zollinger ellison syndrome,
  4. Mallory-Weiss Tear, Boerhaave Syndrome
  5. Erosive/hemorrhagic eosphagitis
50
Q

What do you see on hx/PE of UGIB?

A
  • sx of anemia/hypovolemia
  • hematemesis, melena, hemotochezia
  • smoker, liver dx, alcohol abuse, certain meds…
51
Q

What are PRBCs?

A

Packed RBCs

  • given to increase oxygen carrying capacity of blood
  • 1 unit of PRBCs raises HGB in adults by 1 g/dl
52
Q

What is FFP?

A

fresh frozen plasma

  • obtained after separating whole blood from RBCs and platelets
  • contains all coagulation factors
53
Q

6 units of platelets can increase the platelet count by how much?

A

50,000 per cubic mm

54
Q

Esophageal Varices: define, sx, risk of bleed, dx, tx, prevention of re-bleed

A
55
Q

What can cause hemorrhagic (erosive) gastropathy/gastritis?

A
  • aspirin, NSAIDs
  • alcoholic
  • severe stress/critically ill
    • burns
    • trauma
    • surgery
    • liver failure
    • shock
    • sepsis
    • …
56
Q

What are vital signs like in hemorrhagic gastropathy?

A

normal

57
Q

How do you dx hemorrhagic gastropathy?

A
  • upper endoscopy (EGD)
  • CBC

*tx: remove offending agent, maintenance of O2/blood volume; beta blocker, prevent stress ulcer (H2 blocker or PPI, enteral nutrition)

58
Q

What is the etiology of Zollinger Ellison Syndrome?

A
  • Primary Gastrinoma - Non-beta islet cell – gastrin secreting tumor
  • Pancreas (25%)
  • Proximal duodenum (45%)
  • Lymph nodes (5-15%)
  • 2/3 are malignant
  • 1/3 have already metastasized to the liver at presentation
  • Slow growing
  • associated with MEN 1
  • multiple endocrine neoplasia type 1
  • Pancreatic gastrinoma (or insulinoma),
  • hyperparathyroidism (↑Calcium)
  • pituitary neoplasm (gigantism)
59
Q

If PUD is not responding to tx, is very severe, atypical, and recurrent, you should think?

A

Zollinger Ellison Syndrome

dx: confirmed by >1000 ng/L serum gastrin

60
Q

What disease is characterized by thickened gastric folds involving the body of the stomach?

A

Menetrier Disease (idiopathic) - chronic protein loss

*GIB is not a common presentation

*tx: cetuximab, gastric resection (severe cases)

*risk of gastric adenocarcinoma

61
Q

What is a Mallory Weiss Tear?

A
  • superficial/non-transmural tear at GE junction
  • precipitated by V, retching, or vigorous coughing
  • vital signs are normal
62
Q

What is Boerhaave Syndrome?

A
  • spontaneous transmural rupture at GE junction
  • tx: NPO, parenteral ABs, surgery, enoscopic stenting
63
Q

Mallory Weiss Syndrome vs. Boerhaave’s Syndrome

A
64
Q
A

# US GI2 Test 1 (25 decks)

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