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GI Flashcards

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1
Q

Define dyspepsia

A

Pain or discomfort centered in the upper abdomen associated with fullness,early satiety, bloating or nausea.
intermittent or continuous, (+/-) meal related

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2
Q

If you are concerned about duodenal ulcers, what additional history do you want to know?

A
  • characterization of pain (burning)
  • relation to food (worse 2-5 hrs after meal)
  • do you wake up from sleep (around 1am)
  • relief with antacids
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3
Q

What are “alarm features” with dyspepsia?

A 
weight loss
recurrent vomiting
dysphagia
evidence of bleeding
anemia
***refer for endoscopy
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4
Q

How can H.pylori be diagnosed?

A
  • urea breath test (current infection)
  • H.pylori ab test (any previous infection)
  • biopsy with endoscopy
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5
Q

How do NSAIDs increase risk of ulcers?

A

NSAIDs inhibit gastroduodenal prostaglandin synthesis:

1) reduced secretion of mucus and bicarbonate
2) reduced mucosal blood flow

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6
Q

What is Zollinger-Ellison syndrome?

A

gastrin-producing tumor (usually pancreatic) that causes acid hypersecretion, peptic ulcers and diarrhea
***suspect if PUD w/o NSAID use or H.pylori

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7
Q

How can you diagnose Zollinger-Ellison syndrome?

A

serum gastrin levels: markedly elevated (>1000)

CT to localize tumor

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8
Q

What are some complications of PUD?

A

1) hemorrhage: hematemesis, melena
2) perforation: sudden onset pain, peritonitis, poss. pancreatitis*
3) gastric outlet obstruction: persistent vomiting and weight loss w/o abd distension*
* ** require surgery

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9
Q

What diseases are associated with H.pylori infection?

A

1) duodenal/gastric ulcers
2) chronic active gastritis
3) gastric adenocarcinoma
4) gastric mucosa-associated lymphoid tissue lymphoma (gastric MALToma)

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10
Q

What is Plummer-Vinson syndrome?

A

Upper esophageal webs with:

1) microcytic hypochromic (iron deficiency) anemia
2) atrophic glossitis
3) spoon shaped fingernails (koilonychia)

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11
Q

What is the molecular pathogenesis of colorectal cancer?

2 pathways

A

1) Microsatellite instability pathway: (~15%)
DNA mismatch repair –> sporadic and HNPCC syndrome

2) Chromosomal instability (~85%)
loss of APC gene –> K-RAS mutation –> loss of tumor suppressor genes (p53, DCC)

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12
Q

What does cholecystokinin do?

A

**works on neural muscarinic pathways to cause pancreatic secretion in response to fatty acids and amino acids

increases:
- pancreatic secretion
- gallbladder contraction
- sphincter of Oddi relaxation
decreases:
- gastric emptying
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13
Q

Where is cholecystokinin come from?

A 
I cells
(duodenum, jejunum)
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14
Q

Where is gastrin come from?

A

G cells

antrum of stomach

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15
Q

What does gastrin do?

A

increases:

  • gastric H+ secretion
  • growth of gastric mucosa
  • gastric motility
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16
Q

What affects gastrin secretion?

A

Increases production:

  • stomach distension
  • alkalinization (chronic PPI use)
  • amino acids (Tryptophan, Phenylalanine)
  • peptides
  • vagal stimulation
  • *Zollinger-Ellison syndrome has very high gastrin levels

Decreases production:
- stomach pH <1.5

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17
Q

What is Zollinger-Ellison syndrome?

A

Gastrin secreting tumor of pancreas or duodenum
Causes ulcers in distal duodenum and jejunum
- abd pain
- diarrhea/malabsorption
May be associated with MEN1

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18
Q

What is MEN1?

A

3 P’s: (Wermer syndrome)

1) Parathyroid tumors
2) Pituitary tumors (prolactin or GH)
3) Pancreatic endocrine tumors (Zollinger-Ellison, insulinomas, VIPomas, or glucagonomas)
* **often presents with kidney stones and stomach ulcers

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19
Q

What is MEN2A?

A

2 P’s: (Sipple syndrome)

1) Medullary thyroid carcinoma (secretes calcitonin)
2) Pheochromocytoma
3) Parathyroid hyperplasia
* *Associated with ret gene mutation

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20
Q

What is MEN2B?

A

1 P:

1) Medullary thyroid carcinoma (secretes calcitonin)
2) Pheochromocytoma
3) Oral/intestinal ganglioneuromatosis (mucosal neuromas)
* **Associated with marfanoid habituss
* *Associated with ret gene mutation

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21
Q

What does GIP do?

A

Gastric inhibitory peptide
Exocrine: decrease gastric H+ secretion
Endocrine: increase insulin release
*** Increased by fatty acids, amino acids and oral glucose

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22
Q

Where does GIP come from?

A 
K cells
(duodenum, jejunum)
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23
Q

What does motilin do?

A

Produces migrating motor complexes (MMCs)

increased in fasting state

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24
Q

Where does motilin come from?

A

small intestine

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25
What does secretin do?
Increases pancreatic bicarbonate secretion (neutralizes gastric acid in duodenum for pancreatic enzymes to work) Decreases gastric acid secretion Increases bile secretion
26
Where does secretin come from?
``` S cells (duodenum) ```
27
What does somatostatin do?
Decreases: - gastric acid and pepsinogen secretion - pancreatic and small intestine fluid secretion - gallbladder contraction - insulin and glucagon release * ***increased secretion when acid increased * ***decreased secretion with vagal stimulation
28
Where does somatostatin come from?
D cells | pancreatic islets, GI mucosa
29
What does nitric oxide do?
Relaxes smooth muscle including LES | if no NO then no opening of LES --> achalasia
30
What does VIP do?
Vasoactive intestinal polypeptide - increases intestinal water and electrolyte secretion - relaxes intestinal smooth muscle and sphincters
31
What does VIP do?
Vasoactive intestinal polypeptide increases intestinal water and electrolyte secretion relaxes intestinal smooth muscle and sphincters
32
What does VIP do?
Vasoactive intestinal polypeptide increases intestinal water and electrolyte secretion relaxes intestinal smooth muscle and sphincters
33
What affects VIP secretion?
Increases with distention and vagal stimulation | Decreases with adrenergic input
34
What is a VIPoma?
``` non alpha, non beta pancreatic tumor that secretes VIP Causes: - copious watery diarrhea - hypokalemia - achlorhydria ```
35
What are some clinical features of portal hypertension?
ascites peripheral edema splenomegaly varices (esophageal, gastric, hemorrhoids)
36
What are the two main stigmata of cirrhosis
1) portal HTN | 2) hepatocellular dysfunction
37
What happens with hepatocellular dysfunctoin?
Decreased albumin production | Decreased clotting factor production
38
How is cirrhosis classified?
Child's classification A: no ascites, bili 3.5 B: controlled ascites, bili 2.0-2.5, minimal encephalopathy, good nutrition, albumin 3.0-3.5 C:uncontrolled ascites, bili >3.0, severe encephalopathy, poor nutrition, albumin >3.0
39
What are causes of cirrhosis?
1. alcoholic liver disease 2. chronic hepatitis (B&C) 3. drugs (tylenol, mtx) 4. autoimmune hepatitis 5. primary biliary cirrhosis 6. inheritied metabolic disease (hemochromatosis, Wilson disease) 7. hepatic congestion from HFrEF, constrictive pericarditis 8. alpha1 anti-trypsin deficiency 9. hepatic veno-occlusive disease 10. NASH
40
What are signs of chronic liver disease?
``` ascites varices gynecomastia/testicular atrophy palmar erythema spider angiomas on skin hemorrhoids caput medusae ```
41
What is the biochemical cause of ascites?
- increased hydrostatic pressure (Portal HTN) | - reduced oncotic pressure (hypoalbuminemia)
42
What are the complications of liver failure?
``` AC,9H Ascites Coagulopathy Hypoalbuminemia portal HTN hyperammonemia Hepatic encephalopathy Hepatorenal syndrome Hypoglycemia Hyperbilirubinemia/jaundice Hyperestrinism Hepatocellular carcinoma ```
43
What is hepatorenal syndrome
renal failure due to advanced liver disease that causes renal hypoperfusion from vasoconstriction of renal vessels
44
What are some clinical features of hepatorenal sydrome?
``` azotemia oliguria hyponatremia hypotension low urine Na (<10mEq/L) ```
45
What do you find on LFTs for a cholestatic pattern? | What diseases do you think of?
``` Elevated AST and ALT Elevated T bili Elevated Alk Phos - gall stones/blockage - Med-induced blockage (MTX) - NASH ```
46
What do you find on LFTs for a hepatocellular pattern? | What diseases do you think of?
Very highly elevated AST/ALT - acute hepatitis (A usually) - acute autoimmune hepatitis (AMSA+, PSC, PBC) - shock liver - alcohol/toxin (tylenol) - NASH - Infiltrate: Wilsons/hemochromatosis
47
What do you find on LFTs for an isolated bilirubin pattern? | What diseases do you think of?
Elevated indirect bili - hemolysis of RBCs Elevated direct bili - congenital diseases: Gilbert, Criegler-Najjar, Roter, Dubin-Johnson
48
What is the Charcot Triad? | What is disease does it indicate?
1. RUQ pain 2. Jaundice 3. Fever * **Cholangitis
49
What are the main functions of the liver? (6)
1. Make bile 2. Make proteins (albumin and clotting factors) 3. Toxin metabolism 4. Drug metabolism 5. Lipid metabolism 6. Gluconeogenesis
50
What is in the hepatic triad?
1. Hepatic artery 2. Portal vein 3. bile duct
51
What are indications that diarrhea is inflammatory?
- blood - mucus - small volume * **IBD (UC, Crohns), infection, malignancy
52
What are indications that diarrhea is osmotic/secretory?
- watery - large volume * **Carbohydrate metabolism, VIPoma, carcinoid, laxatives, DM neuropathy, Meds, GI bypass, gastroporesis
53
What are indications that diarrhea is malabsorptive?
- fatty/floats - foul-smelling - bloating * **mucosal (Celiac) or maldigestive (Pancreatic insufficiency)
54
What are risk factors for colorectal cancer?
1. age 2. adenomatous polyps 3. hx of cancer/adenomatous polyps 4. IBD (UC > Crohns) 5. family hx (esp. if age s, Peutz-Jeghers, FJPC, HNC)
55
What is Familial adenomatous polyposis
AD disease with hundres of adenomatous polyps in the colon and usually duodenum (sometimes jejunum, ileum, and stomach) Will get CRC by age 40 Treat with prophylactic colectomy
56
What is Gardner's syndrome?
Polyps with osteomas, dental abnomalities, benign soft tissue tumors, desmoid tumors, sebaceous cysts Will get CRC by age 40
57
What is Turcot's syndrome?
AR | plyps plus cerebellar medulloblastoma or glioblastoma multiforme
58
What is Peutz-Jeghers disease?
Single or multiple hamartomas scattered through GI tract (small bowel > colon > stomach) Associated with pigment spots around lips, oral mucosa, genitals, palmar surfaces May have intussusseption or GI bleeding but low risk for CRC
59
What is Reynold's pentad? | What disease does it make you think of?
- Fever - Jaundice - RUQ pain - Septic shock - altered mental status (CNS depression) (Charcot's triat + septic shock and CNS depression) ***Severe Cholangitis
60
What is Mallory-Weiss syndrome?
mucosal tear at GE junction from forecul vomiting or retching - associated with binge drinking in alcoholics - hematemesis (slight streaking to bright red blood)
61
What is a Schatzki's Ring?
Distal esophageal web: circumferential ring in lower esophagus with sliding hiatal hernia - usually due to ingestion of substance in a suicide attempt (bleach, detergent, alkali, acids)
62
Where is a Zenker diverticulum located?
Upper 1/3 of esophagus
63
What is the Rome III criteria for IBS?
1. recurrent abd pain/discomfort and changed bowel habits for >6mo 2. sypmtoms atleast 3 days/mo for 3 months 3. two or more of: - pain releived by bowel movement - onset of pain is related to a change in frequency of stool - onset of pain is related to a change in stool appearance * **recommend high fiber diet
64
What are some symptoms of C.diff infection?
- diarrhea (10-15 per day) - lower abd pain/tenderness - cramping - fever - leukocytosis * *high suspicion if previou Abx use
65
What are symptoms of Crohn disease
Symptoms over a period of months or years: - abd pain - diarrhea - wt loss
66
What are symptoms of diverticulitis?
-abd pain - fever - LLQ tenderness - leukocytosis - diverticula of the colon **associated with age NO PAIN OR DIARRHEA
67
What are symptoms of ischemic colitis?
Self-limited symptoms: (usually within 48hrs) - LLQ pain - bloody diarrhea

Internal Med (6 decks)

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