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IPAP 21-2 Soph Semester > GI Block > Flashcards

GI Block Flashcards

1
Q

The largest membrane in the body is what… and what kind of cells is it made up off

A

The peritoneum

And a layer of simple squamous cells

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2
Q

What organs are retroperitoneal

A

Kidneys, ascending and descending colon
Duodenum
And Head/ Body of pancreas ( not the tail)

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3
Q

What are the layers of the esophagus

A

Adventitia, Muscualris and mucosa

Muscularis is 1/3 skeletal muscle, 1/3 mixed, and 1/3 smooth muscle for superior to interior

Mucosa: smooth muscle, lamina propia, and Nonkeratinized Stratified squamous

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4
Q

Note the difference between the UES and the LES

A

UES: upper esophageal sphincter is skeletal muscle
LES: lower sphincter is smooth muscle

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5
Q

What is the 1st part of the small intestine

A

Duodenum

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6
Q

What are the 4 main regions of the stomach

A

Cardia, Fundus, Body, Pylorus

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7
Q

What are the cells in the gastric pit

A

Surface mucous cell, Mucous neck cells, Parietal cells (HCL and IF) , Chief cells (Pepsinogen, Gastric lipase) , G cells (Gastrin)

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8
Q

In the presence of histamine how do ACh and Gastrin react

A

They are secreted more, making histamine a synergistic component (hence H2 blockers)

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9
Q

What are the ducts of the pancreas

A

Pancreatic duct ( Duct of Wirsung): connects to the common bile duct and enters the duodenum and the “AMPULA of VATER” controlled by the sphincter of oddi

Duct of Santorini (accessory duct): connects to the duodenum superior to the ampulla of Vater

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10
Q

What are the cell types of the pancreas

A

Clusters of glandular Epithelial cells call acini

And pancreatic islets (langerhaans)

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11
Q

Start at the left hepatic duct and trace your way to the duodenum

A

Left hepatic combines with right hepatic to form the common hepatic which joins with the cystic duct to make the common bile duct with connects to the duct of Wirsung (pancreatic duct) to make the ampulla of Vater, that passes through the sphincter of oddi into the duodenum

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12
Q

Ph of pancreatic juices

A

7-8

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13
Q

What stops the action of Pepsid from the stomach

A

Pancreatic juices (pH)

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14
Q

What enzyme digests starch

A

Pancreatic amylase

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15
Q

What enzyme breaks down proteins

A

Trypsin, Chymotrypsin, Carboxypeptidase, Elastase

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16
Q

What is the principle enzyme that breaks down triglycerides

A

Pancreatic lipase

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17
Q

What divides the two lobes of the liver

A

Falciform ligament

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18
Q

What connects the falciform ligament to the umbilicus

A

Ligamentum teres

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19
Q

Where does the liver receive blood from

A

Hepatic artery 25% (O2)

Portal Vein 75%

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20
Q

What is the blood flow through the liver

A 
Hepatic artery+portal vein
Hepatic sinusoids 
Central vein 
Hepatic vein 
I. VC 
Right atrium
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21
Q

Where does bile come from

A

Hepatic lobules to bile canaliculi to bile ducts

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22
Q

What makes up the portal tríad

A

Bile duct, portal venue, portal artriole

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23
Q

What are the general functions of the liver

A

Carb and lipid and protein metabolism, synthesis of bile salts, activation of vitamin D, Metz of drugs and hormones, excretion of bilirubin
Storage of glycogen and fat vitamins, as well as copper and iron,

Phagocytosis

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24
Q

PH of Bile

A

7.6-8.6

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25
Q

What is the longest and shortest portion of the small intestine

A

Longest: ileum (6 ft)
Shortest: duodenum ( 10 inches)

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26
Q

What vitamins are produced in the large intestine

A

Vitamin K and biotin

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27
Q

What are the 4 regions of the large intestine

A

Cecum, colon, rectum, and anal canal

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28
Q

What is the pectinate line of the anal canal

A

Inferior most portion of the anal columns

Above this line is visceral innervation (sensitive to only stretch)
Below this line somatic innervation, sens. To pai, temp and touch

Important to hemorrhoid location

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29
Q

What is the definition of dyspepsia

A

Acute, chronic, or recurrent pain located in the upper abdomen
Clinically relevant > 1 month

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30
Q

What are the associated s/s of dyspepsia

A 
Postprandial fullness
Early satiation
Anorexia
Belching
Nausea/vomiting
Bloating
Heartburn
Regurgitation
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31
Q

Does dyspepsia= heartburn

A

No

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32
Q

What are the 2 types of dyspepsia

A

Organic: GI tract dysfunction, mediations, Pancreatic/biliary DOs, systemic conditions, PUD and GERD

Functional

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33
Q

What is the most common cause of chronic dyspepsia

A

Functional dyspepsia

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34
Q

What is the DO criteria for functional dyspepsia

A

Postprandial fullnes, early fullness, Epi gastric pain or burning

With no evidence of structural dz

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35
Q

What are the alarm features of dyspepsia

A 
Unintentional weight loss
New-onset dyspepsia after age 55 years
Dysphagia
Persistent vomiting
Any overt gastrointestinal bleeding, hematemesis, or melena
Family history of esophageal or gastric cancer
Iron deficiency anemia
Palpable abdominal mass or lymph node
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36
Q

What labs should be ordered in dyspepsia

A

H pylori
CBC
CMP
Thyroid panel

Others:
Celiac disease test
Stool for ova and parasites, guardia, fecal fat, or elastase

Ultrasound or CT ( pancreatic, biliary, Volvulus, or vascular dz)

Gastric emptying studies

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37
Q

What is the investigation of choice for dyspepsia

A

Upper endoscopy

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38
Q

What patients get an upper endoscopy

A

All patients over 60 with new onset of dyspepsia

All pts with alarm features

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39
Q

What is the most important risk factor for gastric cancer

A

H pylori

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40
Q

What are the 4 tests for H pylori

A

Invasive: Gastric mucosal biopsies

Non invasive: Fecal Antigen, Urea breath test, serology

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41
Q

What test is the initial DO for H pylori and to confirm eradication

A

Fecal antigen test

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42
Q

What is the Tx for H pylori

A

high resistance: PPI, Bismuth, Tetra, and metro

Low resistance: PPI, Clarytho, Amoxicilin, metro

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43
Q

What is the managment of function dyspepisa

A

Lifestyle changes ( smaller meals, food diary, quit smoking)

Antisecratory Tx x 4 weeks
Antidepressants
Metocloprimide

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44
Q

What is the brain stem vomiting center

A

Área póstrema, nucleus tractus solitarios, and central pattern generator

All within the medulla

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45
Q

Acute onset of nausea without Ab pain what is the DDx

A

Food poisoning, acute gastroenteritis, systemic illness

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46
Q

Acute onset of N/V with Ab pain, DDx?

A

Peritoneal irritation, acute gastric or intestinal obstruction, or pancreaticobiliary disease

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47
Q

Persistent N/V, DDx ?

A

Pregnancy, gastric outlet obstruction, gastroparesis, intestinal dysmotility, psychogenic disorders, and central nervous system or systemic disorders.

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48
Q

Vomitting immediately after meals, DDx?

A

Bulimia or psychogenic

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49
Q

What is the criteria for orthostatic HOTN

A

Orthostatic hypotension - the presence of at least one of the following within 3 min of standing:

Decrease in systolic blood pressure by ≥20 mm Hg
or
Decrease in diastolic blood pressure by ≥10 mm Hg

A HR increase of ≥30 bpm may suggest hypovolemia, independent of whether the patient meets criteria for orthostatic hypotension

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50
Q

What is Ondansetron

A

Seretonin 5-HT3 antagonists

ANTIEMETIC

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51
Q

What are promethazine and prochloperazine

A

Dopamine antagonists

ANITEMETICS

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52
Q

What are meclizine, dimenhydrinate, scopalamine, and diphenhydramine

A

Antihistamines

ANTIEMETICS

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53
Q

What is singultus

A

Hiccups

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54
Q

Causes of hiccups

A 
Sudden excitement, emotion
Gastric distention
Esophageal obstruction
Alcohol ingestion
Sudden change in temperature
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55
Q

Persistent hiccups are a clue to

A

Persistent hiccups may be a sign of serious underlying pathology.

CNS – neoplasm, infection, trauma

Metabolic – uremia, hypocapnia

Chronic irritation of the vagus or phrenic nerve

Postoperative

Psychogenic

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56
Q

What is the managment of hiccups

A 
Physical maneuvers:
Teaspoon of dry sugar
Holding breath/Valsalva
Rebreathing
Scaring

Consider medications if persistent >48 hrs

  • PPI if GERD is present
  • Baclofen, gabapentin, or metoclopramide

Surgical referral for ablation/stimulation of the phrenic nerve for refractory

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57
Q

What is eructation

A

Belching, burping

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58
Q

What is FODMAPs

A

Causes of flatus

Fermentable 
Oligosacharides 
Disaccharides 
Monosaccharides 
Polyps
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59
Q

What are the drugs to tx flatus

A

Alpha-d-galactosidase enzyme (Beano®)
Simethicone (Gas-X®)
Lactase enzyme (Lactaid®)

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60
Q

What is the definition of constipation

A

Decreased stool frequency
(fewer than three bowel movements [BM] per week)

with complaints of excessive straining, lower abdominal fullness, hard stools, feeling of incomplete evacuation, commonly associated with hardened feces or another underlying disorder.

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61
Q

Common causes of constipation

A

Dehydration, poor diet, poor habits, DM, hypothyroid, Cancer, Drugs, IBS

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62
Q

What is the constipation W-Up

A

Dullness to percussion in the lower quadrants (left)
DRE- obstruction and hard stool in rectal vault

CBC
CMP
Thyroid Panel
FOBT

Radiographs 
Endoscopy (colonoscopy or sigmoidoscopy)
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63
Q

What is the pharm managment of constipation

A

Pharmacotherapy:

Osmotic Laxative:

  • Magnesium hydroxide (Milk of Magnesia, Epsom Salts)
  • Polyethelyne glycol 3350 (Miralax)
  • *Polyethelyne glycol (GoLYTELY)
  • *Magnesium citrate
Stimulant Laxative:
-Bisacodyl (Dulcolax)
-Senna (ExLax)
Stool Surfactants:
-Docusate Sodium (Colace)

Enema:
Tap water
Saline (Fleet)

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64
Q

What is the managment to fecal Impaction

A

Initial treatment is directed at relieving the impaction with enemas (saline, mineral oil, or diatrizoate) or digital disruption of the impacted fecal material.

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65
Q

When should pts get referrals for constipation

A 
Symptoms are refractory to treatments
Patient has structural abnormality
Evidence of obstruction
Over age 50 or Alarm symptoms
Referral for scope
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66
Q

What is the definition of diarrhea

A

Increased stool frequency (>3 BMs/day)

and/or

Loose/liquid stools

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67
Q

What is often the cause of non inflammatory diarrhea

A

Virus, sometime bacteria and rarely parasites

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68
Q

What is the time frame for acute vs chronic diarrhea

A

Acute is less than 2 weeks

Chronic is longer than 4 weeks

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69
Q

What is the criteria for persistent diarrhea

A

Lasting 2-4 weeks

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70
Q

What is the essential DO for acute non inflammatory diarrhea

A

Less than 2 weeks
Non bloody
Mild and self limited
Caused by a virus or non invasive bacteria

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71
Q

When should evaluation for Diarhea be performed

A

For severe cases or lasting longer than 7 days

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72
Q

What are the agents that can cause non inflammatory acute diarrhea

A

Viral (most common):

  • Norovirus (50%)
  • Rotavirus (children, older adults)
  • Cytomegalovirus (AIDS)

Bacterial (less common):

  • Clostridum perfringens, Bacillus cereus, Staphylococcus aureus
  • Shiga toxin–producingEscherichia coli
  • Vibrio choleraetoxin (causes the small intestinal cells to secrete, rather than absorb, fluid and electrolytes)

Parasites:
-Giardia, Cryptosporidium, Cyclospora, Cystoisospora belli

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73
Q

What is essential to DO acute inflamatory diarrhea

A

Less than 2 weeks
Bloody
Pus
Fever

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74
Q

What is the evaluation W-up for acute inflammatory diarrhea

A

Routine stool cultures ( e.coli 0h157)

C. Diff testing, ova and parasites

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75
Q

What is tenesmus

A

Rectal cramping seen in acute inflammatory diarrhea

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76
Q

What are the agents that curse acute inflammatory diarrhea

A 
Salmonella (most common)
Campylobacter
Shigella
Shiga toxin–producing Escherichia coli
Enteroinvasive Escherichia coli
Clostridium difficile (recent antibiotics)
Nosocomial origin
Yersinia 
Entamoeba histolytica
 (bloody diarrhea in patients who recently traveled to a developing country)
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77
Q

When is prompt eval of diarrhea warranted

A

Signs of inflammatory diarrhea:

  • Fever
  • WBC 15,000/mcL or more
  • Bloody diarrhea
  • Severe abdominal pain
  • Profuse watery diarrhea and dehydration
  • Frail older patients or nursing home residents
  • Immunocompromised patients
  • Exposure to antibiotics
  • Hospital-acquired diarrhea (onset following at least 3 days of hospitalization)
  • Systemic illness
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78
Q

How will fecal leukocytes be in non inflamatory diarrhea

A

Negative

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79
Q

How many samples are needed in ova and parasite testing

A

3

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80
Q

What is the test that is a marker of intestinal inflammation

A

Fecal lactoferrin

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81
Q

What are the anti motility agents used to tx acute diarrhea

A

Loperamide

Bismuth (good for travelers diarrhea)

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82
Q

When should ABX be used in the Tx of diarrhea

A

Patients with fever, abdominal pain, bloody diarrhea, or dysentery presumed due to Shigella

Patients who have recently traveled internationally with body temperatures 38.5 °C or higher and/or signs of sepsis

Immunocompromised patients with severe illness and bloody diarrhea

Patients with severe diarrhea in the context of hospitalization or antibiotic therapy (C dif)

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83
Q

What are the DOC for empiric diarrhea ABX Tx

A

Fluoroquinolones – drugs of choice:

  • Ciprofloxacin 500 mg BID for 5-7 days
  • Ofloxacin 400 mg BID for 5-7 days
  • Levofloxacin 500 mg QD for 5-7 days
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84
Q

What are the drugs that are used to Tx travelers Diarhhea

A

Fluoroquinolones – 3 day courses
Not useful for travel to Southeast Asia

Azithromycin – 1000mg single dose

Rifaximin 200 mg TID x 3 days

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85
Q

ABX in diarrhea should only be used to Tx which agents

A 
Shigellosis
Cholera
Extraintestinal salmonellosis
Listeriosis
Traveler’s diarrhea
C difficile
Giardiasis
Amebiasis
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86
Q

When should a pt be admitted with diarrhea

A

Severe dehydration for intravenous fluids

Bloody diarrhea that is severe or worsening

Severe abdominal pain, worrisome for toxic colitis, inflammatory bowel disease, intestinal ischemia, or surgical abdomen.

Signs of severe infection or sepsis (temperature higher than 39.5°C, leukocytosis, rash).

Severe or worsening diarrhea in patients who are older than 70 years or immunocompromised.

Signs of hemolytic-uremic syndrome (acute kidney injury, thrombocytopenia, hemolytic anemia).

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87
Q

What is the first step in evaluating a pt with chronic diarrhea

A

Review their med list

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88
Q

What should be considered in all pts with chronic postprandial diarrhea

A

Carb malabsorption

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89
Q

How will fasting effect osmotic diarrhea?

Secretory diarrhea?

A

Osmotic : Stool volume decreases with fasting
Increased stool osmotic gap

Secretory: Increased intestinal secretion or decreased absorption
High volume, watery stool
Little to no change with fasting
Normal stool osmotic gap

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90
Q

What can cause secretory chronic diarrhea

A

Laxative abuse
Endocrine tumors
Bile salt malabsorption

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91
Q

What are the causes of chronic inflammatory diarrhea

A

Inflammatory Bowel Disease

  • Crohn Disease
  • Ulcerative Colitis

Microscopic Colitis

Malignancy

Radiation

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92
Q

A young adult with lower Ab pain and altered bowel habits, with out wt loss, nocural diarrhea, anemia or GI bleeding think?

A

IBS

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93
Q

What are the causes of chronic infectious diarrhea

A

Parasitic infections

Giardia, E histolytica, and Cyclospora

Intestinal nematodes

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94
Q

What is the W-up to chronic diarrhea

A

First exclude most common causes:

Medications, IBS, lactose intolerance

Evaluation directed at most likely etiology based on symptoms and history

Lab Tests:
CBC, Chem 17, LFT, Thyroid studies, ESR, CRP
Stool studies

Culture, Leukocytes, Lactoferrin, Occult blood, O&P, electrolytes

Colonoscopy ( r/o IBD and neoplasm)

24 hr stool collection

Referral to gastro

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95
Q

What is the anatomic landmark that separates upper and lower GI

A

Ligament of trietz

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96
Q

What defines Acute upper GI bleeding

A

Essentials of Diagnosis
-Hematemesis

-Varying degrees of hypovolemia

+/- Melena (may be hematochezia in massive bleed)

-Bleeding proximal to the Ligament of Treitz

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97
Q

What are the general causes of acute upper GI bleeding

A 
PUD 
Portal Hypertension (esophageal varices) 
Mallory Weiss tears (alcohol abuse)
Angioectasis 
Telangiectasis 
Neoplasms 
Erosive gastritis/ esophagitits

Boerhaave syndrome (rupture of esophagus)

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98
Q

What is the 1st and most important step in the managment of an acute upper GU bleed

A

Stable or unstable?

Unstable: SBP< 100
HR>100

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99
Q

What is the managment of unstable upper GI bleed

A

Start IV

  • CBC, PT/INR, CMP, type and screen
  • Fluid or Blood Replacement
  • Start isotonic fluids
  • 2-4 units PRBC
  • NG Tube

May be helpful in initial assessment, aspiration of blood or coffee grounds confirmatory

Consider octreotide if patient has liver disease or portal hypertension

Reduces splanchnic blood flow and portal BP

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100
Q

What are the high risk factors for rebleeding in acute upper GI bleeds

A

Age > 60

Comorbid illnesses

SBP < 100 mmHg

Pulse > 100 bpm

Bright red blood in NG aspirate or upon rectal examination

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101
Q

Where do high risk pts with upper GI bleeds get sent to

A

ICU

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102
Q

What do all pts with acute upper GI bleeds get

A

EGD (endoscopy)

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103
Q

What is the pharm approach to acute upper GI bleed

A

PPI
Octreotide ( reduces portal BP and lowers rebleed RSK)

D/c NSAIDS
ABX if H. Pylori

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104
Q

What are the causes of lower GI bleeding

A 
Anorectal Disease (MC mild)	
-Hemorrhoids, fissures, ulcers

Diverticulosis (MC severe)
-Painless, bright red blood, “large” volume

Inflammatory Bowel Disease
-Ulcerative Colitis, Crohn Disease

Infectious Colitis

Neoplasm

Angioectasias
-Commonly in older patients (> 70 yrs)

Ischemic Colitis

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105
Q

What is the causes of lower GI bleeds in pts less than 50

A

Anorectal Disease
Inflammatory Bowel Disease
Infectious Colitis

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106
Q

What are the likely causes of lower GI bleed in pts over 50

A

Diverticulosis

Malignancy

Angioectasias

Ischemic Colitis

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107
Q

What is the DDI with painful defecation

A

External hemorrhoids or anal fissures

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108
Q

What is the DDx with abdominal pain/ .cramps

A

IBD or colitis

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109
Q

What is the DDx with pts with lower GI bleeds yet painless

A

Internal hemorrhoids or diverticular bleeding

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110
Q

If the lower GI bleeding is a large volume thing

A

Diverticular bleeding

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111
Q

If the lower GI bleeding is low volume think

A

IBD, or hemorrhoids

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112
Q

What is an ominous sign in LGIB

A

Anemia- particularly If suspecting a neoplasm

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113
Q

What is the W- up/ .testing of LGIB

A

Exclude upper source ( NGT, EGD)

Colonoscopy- if large volume or older than 45
(Within 24 hrs if active bleed)

Anoscopy or sigmoidoscopy - if small volume or younger than 45

Technetium scal and angiography- if continued unstable or hematochezia

Capsule endoscopy

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114
Q

What is the Tx approach to Large volume LGIB

A

Therapeutic colonoscopy
-Vasoconstrictive injection, cautery, clips/bands

Intra-arterial embolization

Surgery

  • Last resort
  • Indicated if patient requires > 6 units of PRBC in 24 hrs or more than 10 units total
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115
Q

Where is obscure bleeding in the GI tract usually from

A

Small intestine

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116
Q

What is occult blood in the GI tract from

A

(positive result of fecal occult blood testing, usually in the setting of iron deficiency anemia)

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117
Q

What type of bleeding does a fecal immuniochemical test detect

A

Only LGIB

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118
Q

The presence of unexplained anemia or abnormal CBC think

A

Occult bleeding

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119
Q

If there is an occult GIB, you must investigate for a..

A

Neoplasm

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120
Q

Asymptomatic pt with incidental FOBT w/out anemia, gets what test

A

Colonoscopy

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121
Q

Symptomatic pt with +FOBT and or unexaplined anemia should get..

A

Upper Endoscopy AND Colonoscopy

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122
Q

IF the GI bleeding is bright red, what is the likely source

A

Left colon

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123
Q

If the GI bleeding is brown with streaks of red, what is the likely source

A

Rectosigmoid or anus

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124
Q

If the GI bleeding is maroon, what is the likely source

A

Small intestine ro right colon

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125
Q

If the GI bleeding is Black what is the likely source? N

A

Upper GI

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126
Q

What is the definition of ascites

A

The pathologic accumulation of fluid in the peritoneal cavity

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127
Q

What is the normal amount of fluid in the peritoneum

A

Men: none

Women -/+ 20 ml ( menestral dependent)

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128
Q

What is the most common cause of ascites

A

Portal hypertension

  • hepatic congestion (CHF)
  • liver dz (80%)
  • hepatitis

Others: Hypoalbunima and Nephrotic syndrome
Chylous, pancreatic DO, bile ascites

Infections or Cancer

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129
Q

What two veins lead to the hepatic portal vein

A

Splenic and Superior Mesenteric

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130
Q

What is portal HTN

A

Pressure gradient between the portal vein and the IVC > 10 mmHg

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131
Q

What is the pt hz relevant to ascites

A

Alcohol, hepatic, and cancer

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132
Q

Fever with ascites suggests

A

Bacterial peritonitis

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133
Q

What are the prominent physical exam findings in Ascites

A

Hepatic enlargement, elevated JVP, and large adominal wall veins

W/ liver dz: muscle wasting and malnourishment

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134
Q

What is the physical exam test for ascites

A

Shifting Dulles test

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135
Q

What are the lab tests / W-up for ascites

A

Abdominal paracentesis
White cell count
Albumin and Total Protein
Culture and Gram stain

136
Q

What does a cloud paracentisis of the abdomin tell you

137
Q

What does a milky paracentises of the abdomin tell you

138
Q

What is the ranges for a serum-ascites albumin gradient (SAAG)

A

Serum albumin - ascetic fluid albumin

> 1.1 = portal HTN
< 1.1= non portal HTN causes

139
Q

What are the common pathogens in Spontaneous bacterial peritonitis

A

E. coli

Klebsiella pneumonia

Streptococcus pneumonia

viridans streptococci

Enterococcus species

140
Q

What is the definition of spontaneous Bacterial peritonitis

A

Infection of ascitic fluid in the absence of an intra-abdominal source of infection

*Must be distinguished from secondary bacterial peritonitis (ie, intra-abdominal infection)

141
Q

What is spontaneous bacterial peritonitis typically caused from

A

Ascites as a result of chronic liver dz

142
Q

What are the S/s of spont. Bacterial peritonitis

A

Ascites
FEver
Abdominal pain without focal TTP

143
Q

What is the most important lab test in the evaluation of ascetic fluid

A

Grain stain and culture with Cell count + differential

Paracentesis

144
Q

If a secondary bacterial peritonitis is suspected what should you order

A

get abdominal CT to discover source of infection.

145
Q

What is the Tx approach for Spont. Bacterial Peritonitis

A

ADMIT

Empiric: 3rd gen cephalosporin ( cefotaxime or Ceftriaxone)
Comb9ined with a betalactam agent ( ampicillin/ Sulbactam)

146
Q

What is the prophylactic Tx for patients with spontaneous Bacterial peritonitis

A

~70% of patients who survive an episode of spontaneous bacterial peritonitis will have another episode within 1 year

Once-daily oral antibiotic (ciprofloxacin or TMP-SMX DS)

Reduces rate of recurrence to < 20%

147
Q

What is chylous ascites

A

Accumulation of lipid-rich lymph (chyle) in the peritoneal cavity

Milky white in appearance

Due to lymphatic obstruction (lymphoma)

148
Q

What is pancreatic ascites

A

intraperitoneal accumulation of massive amounts of pancreatic secretions

Due to disruption of pancreatic duct

Seen in chronic pancreatitis

149
Q

What is the cause of bile ascites

A

Due to complications from biliary tract surgery, or percutaneous liver biopsy, or abdominal trauma

150
Q

What is the cause of Heart burn ( pyrosis )

A

Reflux of material into the esophagus

151
Q

What is the cause of dysphasia

A

Aka Difficulty swallowing

Mechanical obstruction or motility DO

152
Q

What is odynophagia

A

Painful swallowing

Usually erosive DO
Or can be infectious from Candida, HSV, or CMV

Or caustic ingestion of pill induced ulcers

153
Q

What is the study of choice for Esophageal DO

A

EGD ( Upper Endoscopy)

154
Q

How are barium esophagographys used in esophageal DO/ managment

A

Performed first to differentiate b/w structural and motility abnormalities

More sensitive for detecting subtle esophageal narrowing due to rings, achalasia, and proximal esophageal lesions.

155
Q

What is a test that determines the function of the LES

A

Esophageal manometry

156
Q

What are the 4 causes of GERD

A

Dysfunction of the LES

Hiatal Hernia

Abnormal esophageal clearance

Delayed gastric emptying

157
Q

What is the clinical presentation of GERD

A

Heartburn
Regurgitation
Dyspepsia

158
Q

What is the DDx for GERD

A 
Esophageal motility DO 
Peptic Ulcer 
Angina Pectoris 
Functional DO 
Eosinophil esophagits
159
Q

What are the alarm features of GERD

A 
Troublesome dysphagia
Odynophagia
Weight loss
Iron deficiency anemia
Fever, chills, night sweats
160
Q

PTs that continue to show S/s despite anti acid TX with GERD require..

A

EGD (upper Endoscopy)

161
Q

What is the Test of Choice for GERD pts

A

EGD ( upper endoscopy)

162
Q

What effect does smoking/ nicotine have on the LES

A

Relaxes it, increases RSK for GERD

163
Q

What is the managment approach for mild GERD with intermittent S/s

A

PRN OTC antacids or H2 blockers

164
Q

What is the Tx approach to patients with GERD and have troublesome S/s

A

Once daily PPI

165
Q

What is the Tx approach to managing a pt with S/s of GERD that persist beyond 4 weeks

166
Q

What are Cimetidine, Ranitidine, and Famotidine

A

H2 blockers

Onset w/in 30 min and duration 8 hours

167
Q

What are omeprazole, Rabeprazole, Lasoprazole, Esomeprazole, Pantoprazole

A

PPI

Take 30 minutes borre 1st meal

168
Q

Any pt with alarm S/s should get l

A

Immediate referral for EGD ( upper endoscopy)

169
Q

When can pts D/c PPI use

A

Patients may discontinue PPI after 8-12 weeks if symptomatic relief has been achieved

Most will relapse and require continuous therapy with lowest dose that controls symptoms

170
Q

What is the surgical option for GERD

A

Nissen Fundoplication

fundus of the stomach is wrapped around the esophagus and sewn into place so that the lower portion of the esophagus passes through a small tunnel of stomach muscle
Acts as a reinforcement for the LES

For patients who are refractory to medical treatment or have severe disease

171
Q

What is Barrett’s esophagus

A

Squamous epithelium of the esophagus is replaced by metaplastic columnar epithelium containing goblet and columnar cells

Result of prolonged exposure to caustic gastric contents

Development may actually reduce the symptoms of GERD

11-fold increased risk of esophageal adenocarcinoma

172
Q

What is the Tx for Barrett’s esophagus

A

PPI therapy

Endoscopy w/ biospsies q 3-5 years

173
Q

What is a peptic stricture

A

Narrowing of the esophageal lumen at the GEJ

Progressive solid food dysphagia

Treated with endoscopic dilation

174
Q

What are the agents of infections esophagitis

A

Candida
CMV
HSV

175
Q

Infectious Esophagitis occurs most commonly in what pts

A 
AIDS 
Transplants 
Immuno comp 
Cancer pts 
Chronic immuno suppressive drugs ( Steriods, RA, IBD)
176
Q

How do immuno comp pts present with Infectious esophagus and what is the emperic Tx

A

Immunosuppressed patient presents with dysphagia and odynophagia, +/- chest pain

Diagnosis and specific etiology determined via EGD with biopsy

Treatment directed at specific etiology
May try empiric anti-fungal
Fluconazole (Diflucan), if no response in 5 days= EGD

177
Q

What are the common offfending agents for Pill induced esophatitis

A 
NSAIDs
potassium chloride pills
Quinidine
Zalcitabine
Zidovudine
Alendronate
Risedronate
emepronium bromide
Iron
vitamin C
antibiotics (doxycycline, tetracycline, clindamycin, trimethoprim-sulfamethoxazole)

Injury is most likely to occur if pills are swallowed without water or while supine

178
Q

What is eosinophilic esophagitis

A

Inflammatory response of the esophagus to allergen
(food or environmental)

Infiltration of eosinophils

Inflammation leads to progressive dysphagia

Narrowing of the esophageal lumen

179
Q

What is the W- up for eosinophilic esophagitis

A

Ask about history of asthma, allergies, atopic dermatitis (eczema).

Clinical Findings:
Dysphagia to solid foods
Heartburn

EGD with mucosal biopsy required for diagnosis

Specimens show eosinophilic infiltrates

180
Q

What is the Tx approach for eosinophilic esophagus

A

Empiric trial of PPI first

BID dosing for 2 months

Referral to allergist

Topical corticosteroids
-Swallowed fluticasone (from inhaler)

181
Q

What are esophageal webs

A

Esophageal Webs – thin membranes of squamous epithelium

Mid to upper esophagus

Most are asymptomatic

May cause intermittent dysphagia or GERD like symptoms

182
Q

What are esophageal rings

A

(“Schatzki Rings”)
Circumferential mucosal structure in the distal esophagus

Similar symptoms as webs

Strong association with hiatal hernia

183
Q

What are schatzki rings strongly associated with

A

Hiatal hernias

184
Q

What is the DO test for Webs and RIngs of the esophagus and what is the Tx if symptomatic

A

Diagnostic test-
Barium swallow

Treatment-
Endoscopic dilation if symptomatic

185
Q

What is sender diverticulum

A

Pharyngoesophageal diverticulum
-‘pharyngeal pouch’

Symptoms

  • Progressive dysphagia
  • Sensation of food ‘sticking’ in the throat
  • Halitosis
  • Regurgitation of undigested food, pills

Use - Barium Swallow to diagnose

186
Q

What is achalasia

A

Esophageal motility disorder

Loss of normal peristalsis in the distal 2/3 of the esophagus

Impaired relaxation of the LES

ETIOLOGY-
Idiopathic
(autoimmune, viral, or primary neurodegenerative processes suspected)

187
Q

What are the S/s of achalasia

A

Progressive dysphagia to solids and liquids

Regurgitation of undigested food

Substernal discomfort after eating

Adoption of ‘maneuvers’ to enhance emptying

Weight loss

188
Q

What are the DO and presentation of Achalasia

A

Barium Swallow - “Bird’s Beak Deformity”

Tapering of the distal portion of the esophagus

EGD and esophageal manometry to confirm

189
Q

What is the DDx of achalasia

A

Chagas Dz from T. Cruzi (Mexico and Central/ South America)

But has a more rapid onset

190
Q

What is the Tx f or achalasia

A

Refer patients to GI for evaluation and management

  • Botulinum Toxin into the LES – 85% effective, 50% relapse, preferred for poor surgical candidates
  • Pneumatic dilation – preferred, 90% effective
  • Surgery - 95% effective
191
Q

What is the perferred Tx for achalasia

A

Pneumatic dilation

192
Q

What is the cause of esophageal Varices

A

Dilated submucosal veins due to portal hypertension

Can cause severe upper GI bleeds with a high mortality rate

193
Q

What is the Tx approach to esophageal Varicies

A

Emergent Treatment:

  • Hemostasis
  • Stabilization of the patient

Follow-on Treatment:

  • Reduction of portal hypertension
  • Beta blockade (propranolol)
  • Variceal band ligation
194
Q

What is Mallory Weiss syndrome

A

Mucosal tear at the GEJ

  • Sudden increase in abdominal pressure
  • Retching or vomiting
  • Strong association with alcoholism

Causes acute upper GI bleed
Patient presents with hematemesis

195
Q

What is the Tx approach to a Mallory Weiss tear

A

Stabilize the pt
Then upper endoscopy

Epinephrine
Cautery or endoclip

196
Q

What is Boerhaave syndrome

A

Complete rupture of the esophagus

Shock, pneumomediastinum, general badness

197
Q

What are the S/s of Esophageal Carcinoma

A

Progressive solid food dysphagia
Odynophagia
Significant, unexplained weight loss
May be body aches or pains associated with metastasis

198
Q

What is a type I hiatal hernia

A

Sliding hernia

Displacement of the gastroesophageal junction above the diaphragm.

The stomach remains in its usual longitudinal alignment and the fundus remains below the GE junction

199
Q

What are Type II, III, and IV hiatal hernias

A

True hernia with a hernia sac

Upward dislocation of the gastric fundus through a defect in the phrenoesophageal membrane

200
Q

What is the DO test for hiatal hernia

A

Barium swallow study

201
Q

What is the Tx approach to hiatal hernia

A

Small hernias =GERD management

Larger hernias = surgical repair

202
Q

What is the dif between gastropathy and gastritis

A

Gastropathy – mucosal damage without inflammation

Gastritis – mucosal damage WITH inflammation

203
Q

What is gastritis commonly secondary to

A

infectious or autoimmune etiologies

204
Q

What is gastropathy commonly secondary to

A

endogenous or exogenous irritants

  • Alcohol
  • NSAIDS
  • Physical stress
205
Q

How does a pt with gastropathy typically present

A

Anorexia and Epigastic pain

Most common clinical manifesting is UGIB

206
Q

What is a prostaglandin

A

Lipids derived from arachidonic acid

Generated by the action of cyclooxygenase (COX) isoenzymes

207
Q

What do prostaglandins do

A

Play a key role in the generation of the inflammatory response

Inflammation is the immune system’s response to infection and injury

Stimulate epithelial cells to release more bicarbonate and mucus

Reduces the permeability of gastric epithelium

Reduces acid back-diffusion

Act as potent vasodilators

Increase gastric mucosal blood flow

Increases resistance to injury

Prostaglandins that contribute to gastroprotection are derived principally from COX-1

208
Q

What are Asprin, Ibuprofen, Naproxen, Indomethacin, Piroxicam, Diclofenac

A

COX-1 inhibitors

Can causes NSAD Gastropathy

209
Q

What is the most common complaint of NSAID gastropathy

210
Q

What is the Tx approach to Gastropathy

A

Discontinuation of NSAID
Reduction to lowest effective dose
Switch to COX-2

211
Q

What is the Tx approach to Alcoholic gastropathy

A

Dyspepsia, nausea, vomiting with minor hematemesis

Treatment with discontinuation of alcohol

H2 or PPI for 2-4 weeks.

212
Q

Stress-related mucosal erosions and subepithelial hemorrhages may develop within ___ hours in critically ill (bedridden) patients.

How is this prevented

A

72 hours

Prophylactic H2-receptor antagonists (intravenous) or proton pump inhibitors (oral or intravenous )

213
Q

Pts with stress gastropathy and __________ are at the highest risk for significant bleeding

A

Coagulopathy

Or

Respiratory failure w/ mechanical ventilation

214
Q

What is the Tx approach to portal HTN gastropathy

A

Beta blockers to lower portal pressure

215
Q

Prior to testing for H pylori what must pts do

A

Patients should discontinue anti-secretory therapy for 2 weeks prior to testing

216
Q

When can tests of cure be done for H pylori

A

4 weeks after completion of Tx

217
Q

What is standard triple therapy, and when is it used

A

PPI< Clarithromycin and amoxicillin

Used with clarithromycin resistnence is less tha 15 percent

218
Q

What is the cause of pernicious anemia gastritis

A

V b12 def.

219
Q

What are the S/s of eosinophilic gastritis

A

Abdominal pain, rarely fullness and postprandial Vomitting

220
Q

What is the presentation of Menetrier Dz

A

Idiopathic hypertrophic gastropathy

Nausea, epigastric pain, weight loss, diarrhea

221
Q

What is the age difference of a duodenal vs gastric ulcer

A

Duodenal ulcers
More common in younger patients (30-55)

Gastric Ulcer
More common in older patients (55-70)

222
Q

What are the causes of PUD

A

NSAIDS
H pylori infection

All others: 
Hypersecretory conditions
CMV (transplant patients)
Chronic disease states 
Crohn Disease
Lymphoma
223
Q

What is the most common S/s of PUD

A

Dyspepsia ( epigastric pain)

224
Q

How do pts present with gastric vs duodenal ulcers

A

Shortly after eating with gastric ulcers

2-4 hours after eating for duodenal ulcers

225
Q

What is the W-up for PUD

A

EGD establishes the diagnosis

Refer suspected PUD patients for endoscopy

Labs:
CBC – check for anemia
FOBT – eval for occult bleeding

H pylori
If PUD is found on endoscopy, biopsy will be taken

226
Q

What is the 1st line Tx for PUD

227
Q

How is sucralfate used in PUD

A

Sucralfate (Carafate) – forms viscous protective coating at sites of ulceration

Mucosal defense

228
Q

How is misoprostol used in PUD

A

Misoprostol (Cytotec) – prostaglandin analog

Often given as prophylaxis for long term NSAID patients

Downside – administered 4x/day and causes diarrhea in 10-20%

229
Q

A pt presents with sudden severe abdominal pain, and rigid abdomen, and reduced bowel sounds, and rebound TTP
On radiographs there is air under the Diaphram

A

Ulcer perforation

230
Q

What is the Tx approach for a ulcer perforation

A

Fluids
NG suction
IV PPI
ABX

Surgical repair

231
Q

What is Zollinger Ellison Syndrome

A

Gastrin-secreting neuroendocrine tumor

Results in hypergastrinemia and gastric acid hypersecretion

80% within the “gastrinoma triangle”
Porta hepatis -pancreatic neck - 3rd portion of duodenum

232
Q

What are the three most common gastrónoma locations

A

Pancreas
Duodenal wall
Lymph nodes

Common in pts with MEN-1

233
Q

When should pts be screened for ZES

A

Screen with fasting gastrin levels

In patients with refractory ulcers or in patients with PUD and family history of MEN1

In patients with PUD who are not taking NSAIDS and are H pylori negative

234
Q

What is gastroparesis

A

Delayed gastric emptying in the absence of a mechanical obstruction

235
Q

What is the most common associated systemic dz with gastroparesis

236
Q

What are the S/s of gastroparesis

A 
Nausea
Vomiting
Early satiety
Bloating and/or upper abdominal pain
Weight loss in severe cases
237
Q

What must be ruled out with gastroparesis

A

Mechanical obstruction

238
Q

What is the Tx approach for Gastroparesis

A

Acute exacerbations require NG decompression and IV fluid & electrolyte replacement

General treatment measures:
Dietary modification
Small frequent meals
Avoid high fat foods
Avoid carbonated beverages, alcohol, smoking

Optimize glycemic control in diabetics

Prokinetic medications:
Metoclopramide (Reglan)
Domperidone
Erythromycin

239
Q

What are the clincal signs of metastatic disease

A

Sister Mary Joseph nodule

Virchow nodes

240
Q

What is teh W- up for gastric Adenocarcinoma

A

Labs:

  • CBC often shows anemia
  • LFTs may be elevated

Endoscopy:
-Confirms diagnosis

Other radiographs:
CT, PET once cancer is confirmed to find mets.

241
Q

Primary Lymphomas arise from

Secondary lymphomas arise from

A

Secondary tumors from spread of non-Hodgkin lymphoma

Primary tumors arise from MALT:
Mucosa-associated Lymphoid Tissue
Associated with chronic H pylori infection

242
Q

What is a carcinoid tumor and carcinoid syndrome

A

Carcinoid tumor - neuroendocrine tumors originating in the digestive tract or lungs

Carcinoid Syndrome - constellation of symptoms mediated by various humoral factors that are elaborated by some carcinoid tumors

243
Q

Describe carcinoid syndrome

A

Cutaneous flushing
Begins suddenly
Lasts up to 30 min
Involves face, neck, upper chest

Associated with mild burning sensation

Venous telangiectasias

Diarrhea
Watery, non-bloody, with abdominal cramping

244
Q

What is the classical presentation for Infantile Hypertrophic Pyloric Stenosis

A

3-6 week old child

Immediate postprandial projectile vomiting

Fussy and hungry immediately after meals

Constipation, dehydration

245
Q

How does a hypertrophic pylorus present in neonates on physical exam

A

“Olive” like mass in the RUQ

246
Q

What is a pyloromytomy

A

Surgical correction of the pyloric sphincter

247
Q

What does the duodenum absorb

A

IRON, calcium, phosphorus, magnesium, copper, thiamin, riboflavin

248
Q

What does the jejunum absorb

A

Vitamins A, D, E, K, FOLATE

249
Q

What does the ileum absorb

A

Vitamin B12, Bile salts/acids

250
Q

How do malabsorption pts present

A

Steatorrhea (fecal fat), Anemia’s, Diary intolerant

251
Q

What is celiac dz

A

Celiac Sprue; Gluten sensitive enteropathy

Immunologic response to gluten:
diffuse damage to the proximal small intestinal mucosa

252
Q

What are the S/s of celiacs

A 
Dyspepsia
Diarrhea
Steatorrhea
Weight loss
Flatulence
Abdominal distension/bloating
Borborygmi
Weakness, muscle wasting only if severely malnourished
Extraintestinal manifestations
Fatigue
Depression
Iron deficiency anemia
Amenorrhea
Transaminitis 
Dermatitis herpetiformis
253
Q

What is the cutaneous manifestation of Celiac

A

Dermatitis herpetiformis

Pruritic papules and vesicles (herpes-like)
Extensor surfaces of extremities
Trunk, scalp, neck

254
Q

What is the test of choice in celiac Dz

A

IgA tissue transglutaminase (IgA tTG) antibody
-Test of choice
-if negative, but there is still a strong clinical suspicion for Celiac then draw serum IgA levels

Uncovers potentially undiagnosed IgA deficiency

IgG-deamidated gliadin peptides (DGPs)
For patients with identified IgA deficiency

255
Q

What is the test in celiacs that is for pts with ID’d IgA deficiency

A

IgG deamidated gliadin peptides

256
Q

What is the most abundant Ig in the body

257
Q

What is the confirmatory test in celiacs dz

A

Mucosal biopsy in pts with postive serology

Histology examination reveals blunting and/or atrophy of the intestinal villi

258
Q

What dz is villous atrophy seen in

A

Celiacs dz

259
Q

What is the DO approach to celiacs

A 
HPE
Serologic testing
Trial of gluten free diet
Mucosal biopsy
For those with positive serology or those with high clinical suspicion
260
Q

What is Whipple Dz

A

Rare multisystem illness caused by infection with the bacillus Tropheryma whippelii

Most common in white males, ages 30-50

No human-human spread

Seen mostly in farm or sewage workers
Contact with sewage/waste water

Fatal if untreated

261
Q

Classic presentation of Whipple Dz

A

Migratory Arthralgias (first symptom)

Large joint involvement

Diarrhea
With flatulence, steatorrhea

Abdominal Pain

Weight Loss

Fever of unknown origin

262
Q

How is the DO of Whipple Dz established

A

Mucosal biopsies

“Foamy Macrophages”

263
Q

What is the Tx for Whipple Dz

A

IV ceftriaxone x 2 weeks

TMP-SMX DS – 1 tab po BID x 12 months

264
Q

What is Tropical sprue

A

Chronic diarrheal disease, possibly of infectious origin
Often seen following acute diarrheal disease

Involves the entire small intestine

Characterized by malabsorption of nutrients
especially folic acid and vitamin B12

265
Q

What are the S/s of Tropical sprue

A 
Chronic diarrhea
Steatorrhea
Weight loss
Anorexia
Malaise
B12 and Folate deficiency
Glossitis & chelitis

Inflamed mouth

266
Q

How does tropical sprue present on CBC

A

Megaloblastic anemia

267
Q

How does tropical sprue present of Endoscopy

A

Gross findings
flattening of duodenal folds

Microscopic findings
shortened, blunted villi and elongated crypts with increased inflammatory cells

268
Q

What is the Tx and prevention of Tropical Sprue

A

Prevention
Boil/bottled water
Peel fruits before eating

Treatment
TMP-SMX x 6 months
Folate, B12 supplementation

269
Q

What is lactase

A

Lactase - brush border enzyme that hydrolyzes lactose into glucose and galactose

270
Q

What is the Tx and approach to lactose intolerance

A

Presumptive diagnosis : try 2-3 weeks of lactose free diet
Observe for symptomatic improvement

Diagnostic test (for confirmation)
Hydrogen breath test

Treatment with reduced lactose diet
Titrate to patient symptoms
Also consider dietary consultation

271
Q

What patients are at risk for GI bacterial overgrowth

A

Consider in patients who:
Are on chronic PPI therapy
Due to gastric achlorhydria

Have an anatomic abnormality of the small intestine

Suffer from a small intestine motility disorder

May have a gastrocolic or coloenteric fistula

Crohn disease, malignancy, surgical resection

272
Q

What are the S/s of Bacterial GI overgrowth

A 
Flatulence
Weight loss
Abdominal pain
Diarrhea
Steatorrhea
Macrocytic anemia
273
Q

What is the empiric TX for bacterial GI overgrowth

A

Ciprofloxacin
Amoxicillin-clavulanate
Rifaximin

274
Q

What is short bowel syndrome

A

Due to the removal of significant segments of the small intestine

Type and degree of malabsorption depend on:
Length of the resection
Site of the resection
Degree of adaptation of the remaining bowel

275
Q

Acute paralytic ileus in most often seen in what pts

A

Most commonly observed in hospitalized patients due to:
Abdominal surgery
Severe illness
Respiratory failure, sepsis, uremia
Medications that affect intestinal motility
Opioids, anticholinergics

276
Q

What are the S/s of acute paralytic ileus

A 
Diffuse, constant abdominal pain
Nausea and vomiting
Abdominal distension
Lack of abdominal TTP
No signs of peritoneal irritation
Diminished or absent bowel sounds
277
Q

What does paralytic ileus look like of radiographs

A

Plain abdominal x-ray shows distended gas-filled loops of small and large bowel

278
Q

What is the Tx approach to ileus

A

Generally supportive in nature

Treatment of underlying illness
Pain management
Fluid maintenance & electrolyte replacement
Bowel rest
Nasogastric decompression
For patients with significant distension or severe vomiting

279
Q

What is chronic intestinal psuedo obstruction

A

Intermittent signs of obstruction in the absence of a physical obstruction

Small bowel involvement results in:

  • Abdominal distension
  • Vomiting
  • Diarrhea
  • Varying degrees of malnutrition
280
Q

What is the Tx for acute exacerbations of intestinal psuedo obstruction

A

Acute exacerbations require NG decompression and IV fluid & electrolyte replacement

281
Q

What is the most common cause of small bowel obstruction

A

Post op adhesions or hernias

282
Q

List of things that can cause small bowel obstruction

A 
Neoplasms
Strictures
Foreign body
Intussusception 
Gallstones (Gallstone ileus)
Post op 
Hernias
283
Q

What are the prominent risk factors for small bowel obstruction

A 
Prior abdominal or pelvic surgery
Abdominal wall or groin hernia
Intestinal inflammation
History of, or increased risk for neoplasm
Prior irradiation
History of foreign body ingestion
284
Q

Clinical presentation, physical exam and lab tests for small bowel obstruction

A 
Clinical Presentation:
Abrupt onset of:
Colicky abdominal pain
Nausea
Profuse vomiting
Obstipation
Inability to pass flatus or stool
Physical exam:
Abdominal distension
Tympany on percussion
Hyperactive bowel sounds early
Hypoactive later on
Signs of dehydration
Lab Tests
CBC
CMP
Urinalysis
Type and crossmatch
If surgery may be indicated
285
Q

What are the signs of strangulated small bowel obstruction and what is the Tx

A

fever, tachycardia, localized abdominal pain, and/or leukocytosis

CT scan To diagnose strangulated obstruction

286
Q

What is string of pearls sign

A

Air fluid levels on x ray in the small bowel that high light obstruction

287
Q

Acute Tx for SBO

A 
Fluid resuscitation
Bowel decompression (NG)
Pain control
Anti-emetic medications
Early surgical consultation
Admission
288
Q

What is the cause of gallstone ileus

A

Complication of cholelithiasis.

Due to impaction of a ≥2cm gallstone in the ileum after being passed through a biliary-enteric fistula

Much more common in female patients and older patients

289
Q

What pts is intussesception most common in

A

Children less than 1 yr old

290
Q

A child presenting with vomiting abdominal pain, AMS, abdominal mass, and rectal bleeding

A

Intussusception

291
Q

What is the 1st line Tx of intussusception in children and adults

A

Pneumatic reduction with air under fluoroscopic guidance or hydrostatic reduction with saline under ultrasonographic or fluoroscopic guidance preferred first line therapeutic intervention for uncomplicated children.

Surgery if complicated or adult.

292
Q

Neoplasm of the small bowel often causes

A

Intussusception or obstruction

293
Q

Where is the most common place for adenocarcinomas in the bowel

A

Most commonly in duodenum or proximal jejunum

Present with symptoms of obstruction, chronic GI bleed or weight loss

294
Q

What pts are at increased RSK of lymphomas

A

Increased incidence with AIDS, chronic immunosuppressive therapy, Crohn disease

295
Q

What is protein losing enteropathy and what is the approach to tx

A

Condition that results in excessive loss of serum protein into the GI tract
Results in hypoalbuminemia

Treatment aimed at underlying disorder
Low fat and high-protein diet
Surgical resection of affected bowel

296
Q

What is the presentation and approach to Mesenteric ischemia

A

Physical exam:
Classically- “pain out of proportion with physical exam”

Diagnostic test:
CT angiography

Treatment:
Admission
Papaverine – smooth muscle relaxant
Thrombolytics
Surgical referral
297
Q

What is the most common congenital abnormality of the GI tract

A

Meckels Diverticulum

Typically less than 10 yo
Ave age 2.5 years

298
Q

What is the rule of 2s for Meckels Diverticulum

A

Occurs in 2% of the population

2:1 Male-Female ratio

Located within 2 feet of ileocecal valve

2 cm in length

2 types of mucosa:
-Native intestinal mucosa and heterotopic mucosa (most commonly gastric or pancreatic)

Symptoms commonly occur before age 2

299
Q

A child less than 10 yo with painless lower GI bleeding without S/s of gastroenteritis or IBD

300
Q

A 40 yo with GI bleeding with no source ID’d of standard endo

301
Q

How do you DO and Tx meckels

A

Capsule endoscopy and meckels scan ( 99 technetium)

Tx: Surgical referral
Asymptomatic patient - no treatment is typically needed 
Symptomatic Patient:
Stabilize if GI bleed present
Surgical removal of diverticulum
Correct intussusception, etc if present
302
Q

What are the 5 normal positions of the appendix

A 
Retrocecal 
Subcecal
Preileal
Postielal
Pelvic
303
Q

What is the presentation of appendicitis

A

Early - Vague, colicky periumbilical pain

Later (within 12 hrs) – pain migrates to RLQ
McBurney’s Point

Pain is sharp and increased with peritoneal irritation
Coughing, jumping, “bumpy ride”

Patient will be lying still

Low grade fever

304
Q

What are the 5 PE test to locate appendicitis

A 
TTP at McBurney’s point 
Heel Tap 
Psoas Sign 
Obturator sign 
Rovsings Sign
305
Q

What is the Lab Tests results and Tx for appendicitis

A

CBC will show moderate leukocytosis with nuetrophillia

TX:

Surgical appendectomy
-Consult early

Antibiotics:

  • Pre-op
  • Conservative (non-surgical) management (20-35% recurrence w/in 1 yr)

Broad spectrum with gram-negative and anaerobic coverage
Cefoxitin or cefotetan
Ampicillin-Sulbactam
Ertapenem

306
Q

where are internal hemorrhoids located

A

Internal hemorrhoids are located proximal to the dentate line

Arise from the superior hemorrhoidal veins

307
Q

Internal hemorrhoids come from what vein

A

Superior hemorrhoidal veins

308
Q

Where are external hemorrhoids located

A

External hemorrhoids are located distal to the dentate line
Arise from the inferior hemorrhoidal veins

Covered with squamous epithelium of the anal canal or perianal region

contains numerous somatic pain receptors

309
Q

S/s of hemorrhoids

A

Most often presenting complaint is bright red rectal bleeding

Streaks on the stool or on the paper
bright red blood dripping into the toilet

Other symptoms

  • Perianal itching
  • Mucoid discharge with stool
  • Pain w/ external hemorrhoids
310
Q

What is the cause of internal hemorrhoids pruritus

A

They are Covered with columnar epithelium leading to mucous deposition on the perianal skin that can cause pruritus

Prolapse may permit leakage of rectal contents

Patients with leakage may clean aggressively, irritating the perineum and also allowing contact of fecal material with denuded skin

311
Q

What is a grade I hemorrhoid

A

Bleeding only, no prolapse

312
Q

What is a grade II hemorrhoid

A

Prolapse with defecation,

Spontaneously reduces

313
Q

What is a grade III hemorrhoid

A

Prolapse with defecation, must be manually reduced

314
Q

What is a grade IV hemorrhoid

A

Prolapsed, Incarcerated, cannot be manually reduced

315
Q

Thrombosis of an extrenal hemorrhoid plexus results in…

A

Perianal hematoma,

Acute onset, exquisitely painful

Tense and bluish perianal nodule covered with skin

Symptoms last 2-3 days, relieved w/warm sitz bath, analgesics, and ointments

Clot excision (clinic) may provide relief if performed w/in 48 hrs

316
Q

What is the medical treatment for hemorrhoids

A

Topical Astringents
-Witch hazel pads (Tucks)

Topical Hydrocortisone
-Cream or foam (Proctofoam)

Topical anesthetics
-Pramoxine or dibucaine

Hydrocortisone suppositories (Preparation H)

Further Treatment (internal hemorrhoids)

  • Rubber band ligation
  • Sclerotherapy
  • Electrocoagulation

Surgical Treatment
-Surgical excision (hemorrhoidectomy) when conservative measures fail (Stage I, II, or III) or Stage IV

Acute thrombosed Stage IV

Complications of hemorrhoidectomy include postoperative pain (which may persist for 2–4 weeks) and impaired continence

317
Q

What are the complications associated with hemorrhoidectomy

A

Complications of hemorrhoidectomy include postoperative pain (which may persist for 2–4 weeks) and impaired continence

318
Q

What is an anal fissure

A

Anal fissure - a tear in the anoderm distal to the dentate line

319
Q

What causes chronic anal fissures

A

Chronic fissure develops due to spasm of the internal sphincter

impaired healing

320
Q

What is a primary anal fissure

A

Posterior (90%) or anterior midline location (25% postpartum women)

Usually single fissure

Rarely located off midline

321
Q

What is a secondary anal fissure

A

Lateral or atypical position off midline location (<1%)

Multiple fissures may be present

Associated with chronic IBD, HIV, syphilis, malignancy, granulomatous disease, psoriasis, previous surgery

322
Q

What is the Tx for anal fissures

A

Sitz Baths

Increase fiber and fluid intake

Stool softeners – docusate sodium

Topical anesthetic – lidocaine jelly

Chronic fissures:
Topical vasodilators
-Nifedipine, nitroglycerin, or diltiazem

Botulinum toxin injection

Surgical treatment:
Fissurectomy
Lateral internal sphincerotomy

323
Q

What do anorectal abscesses usually arise from

A

Obstructed or infected anal crypt gland

324
Q

What are the three locations for perianal abscess formations

A

Supralevator space
Intersphincteric space
Ischioanal space

325
Q

Clinical presentation of perianal abscess

A

Severe pain in the anorectal region

Constant and not directly associated with defecation

Fever and malaise are common

326
Q

TX for perianal abscess

A

Simple (perianal)
I&D in clinic

Complex (perirectal)
I&D in OR

Oral antibiotics - may reduce the rate of fistula formation

Sitz bath

Pain management

327
Q

What is the complication of a perianal abscess

A

Fistula formation (fistula in ano)

An epithelialized track can form connecting the abscess in the anus or rectum with the perirectal skin

Leads to chronic purulent drainage, pruritus, pain

Requires surgical excision

328
Q

What is the etiology and S/s of infectious proctitis

A

Etiology usually STI

  • Gonorrhea
  • Syphilis
  • Chlamydia
  • Herpes

Symptoms include:

  • Anorectal discomfort
  • Tenesmus
  • Constipation
  • Mucus or bloody discharge
329
Q

How does anal syphillis present

330
Q

Presentation of anal herpes

A

Grouped vesicles

331
Q

Presentation of anal gonorrhea

A

Mucopurulent DC

332
Q

Presentation anal chlamydia

A

Slight DC may be asymptomatic

333
Q

What must you R/o with condylomata acuminata

anal warts

A

Must r/o cancer

334
Q

What are the majority of cancer types of the anus

A

Squamous cell cancers are the majority

335
Q

Who is at high RSK of anal cancer

A

People who have anal sex or who have anal warts

336
Q

What are carcinoma of the anus often confused with

A

Hemorrhoids,

Have similar S/s
Bleeding, pain, local mass,

Use a CT or MRI to DO

IPAP 21-2 Soph Semester (20 decks)

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