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IPAP Class 21-2 > GI Block One > Flashcards

GI Block One Flashcards

1
Q

What does food equal

A

Chemical energy

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2
Q

What type of system is the GI system

A

Tubular, with close association to cardio

  • Alimentary Nourishment Canal *
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3
Q

Length of GI when alive vs when cadaver

A

16-23 feet

23-29 feet
due to loss of muscular tone

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4
Q

Muscular alimentary canal main organs (5)

A 
Esophagus 
Stomach
Small Instestine 
Large Instestine
Anus
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5
Q

Accessory digestive organs

A

Gallbladder
Liver
Pancreas

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6
Q

Six processes of digestion

A

Ingestion

Secretion

Mixing Propulsion

Digestion

Absorption

Defection

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7
Q

Largest serous membrane in the body and contents

A

Peritoneum

Simple squamous epithelium with parietal and visceral peritoneum

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8
Q

Organs retroperitoneal

A 
Kidneys 
Ascending colon
Descending colon 
Duodenum 
Pancreas
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9
Q

Where does the esophagus begin and end

A

Laryngopharynx to esophageal hiatus before the stomach

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10
Q

Muscular contents of the esophagus

A

Superior 1/3 = skeletal ; think UPPER ESOPHAGEAL SPHNICTER

Middle 1/3 = skeletal; and smooth

Inferior 1/3 = smooth ; think LOWER ESOPHAGEAL SPHINCTER

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11
Q

What is the esophageal ole in digestive enzyme production and reabsorption

A

It has NONE

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12
Q

serves as a mixing chamber and holding reservoir

A

Stomach

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13
Q

What do parietal cells secrete

A

Hydrochloric acid and Intrinsic Factor

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14
Q

What do chief cells secrete

A

Pepsinogen and gastric lipase

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15
Q

How often are peristaltic waves

A

15-20 seconds

  • approximately 3mL of chyme is ejected into the duodenum each wave*
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16
Q

What are the parietal cells role in digestion?

A

Proton pumps (powered by H+/K+ ATPases) actively transport a H+ into lumen while bringing a K+ into the cell

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17
Q

What does the enzyme carbonic anhydride catalyze?

A

Formation of carbonic acid from water and co2

Providing a H+ source for proton pumps and bicarbonate

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18
Q

How can HCL be signaled to release from parietal cells (3)

A

Acetylcholine (ACh) released by parasympathetic neurons

Gastrin being secreted by G Cells

Histamine- paracrine substance released by local mast cells in lamina propria

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19
Q

Pancreatic duct (Duct of Wirsung) does what?

A

Joins common bile duct from liver and gallbladder then enters duodenum as the hepatopancreatic ampulla (also known as the ampulla of Vater)

Ampulla of Vater is regulated by the sphincter of Oddi

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20
Q

What do acini clusters secrete

A

Pancreatic juice

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21
Q

How much pancreatic juice is secreted daily

A

1200-1500mL

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22
Q

Contents of pancreatic juice

A

Sodium bicarbonate, water, salts, enzymes

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23
Q

What do pancreatic amylase secrete/trypsin?

A

PA = Starch digestion

Trypsin =Protein digestion

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24
Q

What are the active enzymes vs inactive

A

Active
Trypsin
Chymotrypsin
CArboxypeptidase

Inactive 
Trypsinogen 
Chymotryipsinogen 
Procarboxypepetidase 
Proelastase
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25
Q

Where does the falciform ligament extend

A

extends from undersurface of the diaphragm between the two lobes to the superior surface of the liver

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26
Q

Where does the ligamentum teres extend

A

extends from falciform ligament to umbilicus

remnant of umbilical vein of fetus

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27
Q

What tow sources feed the liver blood

A

Hepatic Artery (25%) - 02

Portal Vein (75%) - deoxygenated blood and nutrients

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28
Q

How does blood transfer in the liver

A

Sinusoids —> Central Vein —> Hepatic Vein —> IVC —> Right atrium of the heart

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29
Q

Hepatocytes grouped together form complex three-dimensional arrangements (wall/slice)

A

Hepatic Laminae

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30
Q

Liver major functional unit

A

Hepatic lobules

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31
Q

Four types of metabolism of the liver

A

Carbohydrate - blood glucose mx

Lipid - fat stores

Protein - ATP production

Drugs and Hormones

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32
Q

Phagocytes of the liver

A

Kupffer cells

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33
Q

pH of Bile

A

7.6 - 8.6

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34
Q

Stores and concentrates bile made by the liver (up to 10x’s more concentrated)
Water and ions are reabsorbed by the gallbladder walls
Between meals, bile is made and released by liver into common hepatic duct and down into common bile duct

A

Gallbladder

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35
Q

Three regions of the small Instestines

A

Duodenum - shortest region ; retroperitoneal

Jejunum - 3 ft long

Ileum - longest region 6 feet long ; goes to ileocecal sphincter

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36
Q

Methods of absorb toon of the small Intestine

A

Diffusion
Facilitated diffusion
Osmosis
Active Transport

  • 90% of all absorption occurs in the small intestines
    (remainder in stomach and large intestines)*
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37
Q

Four regions of large intestine

A

Cecum
Colon
Rectum
Anal Canal

~5 ft. long, ~2.5inches in diameter

Attached to the posterior abdominal wall by its mesocolon

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38
Q

Opening from the terminal ileum to the large intestine

Allows materials to be passed from small intestine into the large intestine

A

Ileocecal sphincter

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39
Q

What is the significance of the pectinate line

A

Above it = innervated by inferior hypogastic plexus; sensitive to stretch ONLY

Below it = innervated by rectal nerves; sensitive to pain temperature and touch

important for hemorrhoids

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40
Q

What is dypepsia and when is it clinically relevant

A

Acute, chronic, or recurrent pain predominantly located in the upper abdomen (epigastric)

Clinically relevant ≥ 1 month

heartburn

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41
Q

Difference between organic and functional dyspepsia

A

Organic is associated with a disease and functional is defined as a metabolic process disorder

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42
Q

4 organic causes of dyspepsia

A

Luminal GI Tract Dysfunction
Medications
Pancreaticobiliary Disorders
Systemic Conditions

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43
Q

Most prevalent cause of dyspepsia

A

GERD (~20%)

PUD (5–15%)

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44
Q

Investigation of choice for dyspepsia

A

Upper endoscopy

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45
Q

Causes of indigestion commonly (4)

A

Overeating, eating too quickly,
High-fat foods,
Stress
Alcohol/Caffeine

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46
Q

What drugs can typically be a cause for organic dyspepsia

A

Aspirin and NSAIDS

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47
Q

Explain pancreaticobilalry disorders and what should this be distinguished from?

A

Abrupt onset of epigastric or right upper quadrant pain

Acute/Chronic pancreatitis or neoplasms

Causes due to cholelithiasis or choledocholithiasis should be readily distinguished from dyspepsia

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48
Q

Common systematic conditions for organic dyspepsia

A

Diabetes mellitus and MI

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49
Q

Most common cause of chronic dyspepsia is functional or organic

A

Functional

enteric infection

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50
Q

Functional dyspepsia can be one of which things and what other criteria?

A

Bothersome postpraindal fullness
Early satiation
Epigastric pain/ burning

AND

No evidence of structural dz

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51
Q

Alarm features of dyspepsia (8)

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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52
Q

Lab testing for dyspepsia includes findings of what?

A

H pylori testing (urea breath test, fecal antigen test)

CBC
Electrolytes, liver enzymes, calcium (CMP)
Thyroid Panel

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53
Q

When is abdominal imaging performed

A

When pancreatic, biliary tract, vascular disease, or volvulus is suspected.

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54
Q

When do we perform gastric emptying studies?

A

Patients with recurrent nausea and vomiting who have not responded to empiric therapies.

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55
Q

Most important risk factor for gastric cancer

A

H. pylori

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56
Q

Where does H Pylori reside

A

adjacent to epithelial cells at the mucosal surface and in gastric pits

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57
Q

Invasive H Pylori testing

A

Gastric mucosal biopsies

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58
Q

Noninvasive H pylori testing

A

Fecal antigen [PRIMARY]

Urea breathe test

Serology

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59
Q

First line quadruple therapy

A

PPI, clarithromycin, amoxicillin, and metronidazole for 10 to 14 days.

In areas of high clarithromycin resistance and/or in patients with penicillin allergy.

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60
Q

Bismuth quadruple therapy

A

PPI, bismuth subsalicylate (Pepto-Bismol), tetracycline, and metronidazole for 10 to 14 days.

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61
Q

What does Metoclopramide do

A

decreases gastric emptying time

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62
Q

What is rumination

A

the chewing and swallowing of volitionally regurgitated food

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63
Q

4 causes for vomiting

A

Afferent canal fibers from the GI viscera

Stimulation of fibers of the vestibular system

Higher central nervous system centers (amygdala)

The chemoreceptor trigger zone

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64
Q

What type of receptors are in the fibers of the GI viscera

A

Serotonin

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65
Q

Acute onset of nausea without abdominal pain could be?

A

Food poisoning
Acute gastroenteritis
Systemic illness

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66
Q

Acute onset of nausea with abdominal pain could be?

A

Peritoneal irritation
Acute gastric obstruction
Pancreaticobilliary dz

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67
Q

Constipation is associated with what?

A

Hardened feces or underlying disorder

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68
Q

2 top common causes of constipation

A

Inadequate fiber

Poor hydration

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69
Q

What type of meds cause constipation most

A

Opioids

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70
Q

Constipation PE finding

A

Dullness to percussion in left quad

DRE

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71
Q

Who qualifies for A FULL work up for constipation symptoms.

A

50 years old

Severe constipation

Signs of an organic disorder

Alarm symptoms

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72
Q

What are constipation alarm symptoms

A

hematochezia, weight loss, positive FOBT

family history of colon cancer or inflammatory bowel disease

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73
Q

What are the lab studies for consitpation

A

Complete blood count
Serum electrolytes (CMP)
Thyroid panel
Fecal occult blood test

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74
Q

What do radiographs show in a constipation work up

A

Abdominal non specific bowel gas pattern

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75
Q

Two types of endoscopy for constipation

A

Colonoscopy or flexible sigmoidoscopy

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76
Q

ConstipationTxM

A

Dietary fiber

Water

Probiotics

Toilet habits

Regular exercise

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77
Q

What are the osmotic laxatives

A

Magnesium hydroxide (Milk of Magnesia, Epsom Salts)

Polyethelyne glycol 3350 (Miralax)

**Polyethelyne glycol (GoLYTELY)

**Magnesium citrate

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78
Q

What are the stimulant laxatives

A

Bisacodyl (Dulcolax)

Senna (ExLax)

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79
Q

What are the stool surfactants

A

Docusate sodium (Colace)

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80
Q

What is fecal impaction

A

paradoxical “diarrhea”

Passage of liquid stool around the impacted feces

**can use enemas or DRE to BREAK IT UP*

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81
Q

Long term straining at the stool may result in chronic dilation of the veins of the rectum.
Also known as….?

A

Hemorrhoids

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82
Q

Acute diarrhea in adults is characterized by 1 of the following occurring in 1 day:

A

loose or watery stools 3 or more times,

the passage of greater than 200 g of stool,

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83
Q

Most often caused by viruses, but may be caused by bacteria and parasites (to a lesser degree)
Results in milder disease

A

Non inflammatory diarrhea

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84
Q

Caused by bacteria (invasive and/or toxin producing)
More severe disease; likely to disrupt mucosal integrity
Bloody diarrhea alone or dysentery (ie, bloody diarrhea with fever, abdominal pain, and rectal tenesmus) may be present

A

Inflammatory Diarrhea

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85
Q

Acute vs chronic

Inflammatory vs non inflammatory

A

Acute – Less than two weeks
Chronic – Longer than four weeks

Bloody vs Non bloody

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86
Q

Diarrhea between 2 and 4 weeks

A

Persistent

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87
Q

Things to ask about acute diarrhea

A 
Bloody vs. watery (non-bloody)
Recent travel
Diet changes (new restaurant)
Recent antibiotic use
Sick contacts
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88
Q

What are signs of dehydration

A

Dizziness, light-headedness, orthostatic hypotension

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89
Q

Most common viral causes of inflamm diarrhea

A

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

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90
Q

Less common bacterial causes of inflamm diarrhea

A

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)

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91
Q

Parasites than can cause inflamm diarrhea

A

Giardia, Cryptosporidium, Cyclospora, Cystoisospora belli

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92
Q

How do drugs cause inflamm diarrhea

A

Drugs can disrupt the mechanisms of mucosal permeability, transport, motility, and gut metabolism

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93
Q

Essentials of diagnosis for acute inflamm diarrhea

A

Drugs can disrupt the mechanisms of mucosal permeability, transport, motility, and gut metabolism

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94
Q

Diagnostic veal of acute inflamm diarrhea

A

Routine stool bacterial cultures (including E coli O157:H7)

Testing as clinically indicated for Clostridium difficile toxin, and ova and parasites.

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95
Q

Symptoms of acute inflamm diarrhea

A 
Loose, bloody stools
Lower in volume
Fever
Severe abdominal cramps (LLQ)
Urgency
Tenesmus
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96
Q

Differential diagnosis for infectious acute inflamm most common

A

Salmonella

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97
Q

When do you get labs for non inflamm diarrhea

A

If persist longer than 7 days

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98
Q

What WBC count is concerned for acute diarrhea

A

15,000/mcL or more

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99
Q

What are the fecal leukocytes likely in non inflamm diarrhea

A

Negative

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100
Q

How many samples do you need for ova and parasites

A

3

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101
Q

What is a marker of intestinal inflammation

A

Fecal Lactoferrin

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102
Q

General diet strategies for diarrhea Txm

A 
BRAT diet (soft, easy to digest foods)
Avoid high-fiber foods, fats, dairy, caffeine

Rehydration
Oral Rehydration Salts (ORS)
IV for severe cases

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103
Q

Antimotility agents

A

Loperamide (Immodium)
Do not prescribe for bacterial or inflammatory diarrhea with blood in stool, or for febrile patients

Bismuth subsalicylate (Pepto-Bismol) 
Good for traveler’s diarrhea by virtue of its anti-inflammatory and antibacterial properties.
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104
Q

When should you GIVE ABX for acute diarrhea Txm

A

Shigella infxn

Recent travel pts with 38.5 degrees or higher

Immunocomp’s

Severe hospitalized diarrhea (C diff)

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105
Q

Drug of choice for diarrhea

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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106
Q

Other meds for acute diarrhea Txm

A

trimethoprim-sulfamethoxazole 160/800 mg BID

doxycycline 100 mg BID

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107
Q

Define travelers diarrhea

A

Diarrhea that develops during travel or within 10 days of return

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108
Q

Meds for travelers diarrhea

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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109
Q

ABX is rec for what specific types of diarrhea

A 
Shigellosis
Cholera
Extraintestinal salmonellosis
Listeriosis
Traveler’s diarrhea
C difficile
Giardiasis
Amebiasis
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110
Q

What are signs of severe infection or sepsis

A

temperature higher than 39.5°C, leukocytosis, rash

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111
Q

What are signs of hemolytic uremic syndrome

A

acute kidney injury, thrombocytopenia, hemolytic anemia

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112
Q

Osmotic diarrhea

A

Stool volume decreases with fasting
Increased stool osmotic gap

  • consider carb malabsorption*
  • Consider factitious diarrhea(laxative antacid)*
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113
Q

What is a secretory condition in chronic diarrhea

A

Increased intestinal secretion or decreased absorption

High volume, watery stool

Little to no change with fasting

Normal stool osmotic gap

**consider factious diarrhea, endocrine tumors, bile salt malabsorption*

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114
Q

Chronic diarrhea inflammatory conditions

A

Fever, hematochezia, abdominal pain

Consider IBS ; crohns and ulcerative colitis

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115
Q

Examples of motility disorders in chronic diarrhea

A

Postsurgical
Systemic disorders (eg, DM, hyperthyroidism)
Irritable bowel syndrome
Young adults

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116
Q

Chronic infections that can cause chronic diarrhea

A

Parasitic infx

Giardia, E histolytica, and Cyclospora
Intestinal nematodes

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117
Q

Systemic conditions that can cause chronic diarrhea

A

Thyroid disease

Diabetes

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118
Q

Chronic diarrhea most common causes

A

Meds, IBS, lactose intolerance

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119
Q

Lab tests and stool studies for chronic diarrhea

A

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

Stool studies:
Culture, Leukocytes, Lactoferrin, Occult blood, O&P, electrolytes

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120
Q

What type of colonoscopy is recommended for chronic diarrhea in severe cases

A

Colonoscopy with biopsy

To exclude IBD and neoplasm

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121
Q

Overt bleeding from where = GI hemorrhage

A

Upper GI tract (esophagus, stomach, and duodenum)
Lower GI tract (colon)
Obscure locations (small intestine)
Occult bleeding

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122
Q

widens the angle of the duodenojejunal flexure, allowing movement of intestinal contents

A

The ligament of Trietz

Suspension muscle of duodenum

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123
Q

Ways to describe upper GI bleed

A

Hematemesis
Varying degrees of hypovolemia
+/- Melena (may be hematochezia in massive bleed)

Bleeding proximal to the Ligament of Treitz

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124
Q

Most common cause of upper GI bleed

A

Peptic Ulcer Disease (PUD) – 40%

Portal Hypertension – 10-20%

Esophageal Varices – high mortality rate

Mallory-Weiss Tear
Longitudinal tears in the mucosa of the esophagus
Typically due to forceful retching or vomiting
Strong association with alcohol abuse

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125
Q

Rupture of the esophagus due to forceful retching

Also associated with alcohol abuse

A

Boerhaave syndrome

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126
Q

what vascular anomalies are associated with upper GI bleeds

A

Angioectasias

Telangiectasias

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127
Q

First and most important step for assessment and stabilization of hemodynamic status

A

Stable or Unstable

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128
Q

What is octreotide, when is it indicated?

A

Consider octreotide if patient has liver disease or portal hypertension
Reduces splanchnic blood flow and portal BP

Unstable Upper GI bleed

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129
Q

What are high risks for 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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130
Q

Pharmaco recommendations for acute management of upper GI bleed

A

PPI = DOC

Octreotide

Stop NSAIDs
ABX for H. Pylori

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131
Q

Arterial bleed non bleeding visible vessel or clot ; combo endoscopic hemostasis gets what Txm?

A

IV bonus and infusion PPI for 72 hours

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132
Q

Oozing without other stigma; hemoclip or thermal coat hemostasis gets what Txm?

A

Oral PPI twice daily

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133
Q

Flat spot or clean base ulcer gets what Txm?

A

Oral PPI and early discharge

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134
Q

Bleeding distal to the Ligament of Treitz

Majority of lower GI bleeding from the colon

Typically lower risk of serious blood loss than in upper GI bleeding

A

Lower GI bleed

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135
Q

Most common mild and severe etiology for acute lower GI bleed

A

Mild = Anorectal Dz ; hemorrhoids, fissures, ulcers

Severe = painless bright red blood ‘’large’’ volume

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136
Q

What etiology is common in patients over 70 years old for acute lower GI bleed

A

Angioectasis

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137
Q

Most likely causes of lower GI bleed form pts less than 50

A

Anorectal Disease
Inflammatory Bowel Disease
Infectious Colitis

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138
Q

Most likely causes of lower GI bleed form pts older than 50

A

Diverticulosis
Malignancy
Angioectasias
Ischemic Colitis

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139
Q

Abdominal pain and cramps is usually due to

A

IBD

Colitis

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140
Q

Large volume blood loss is commonly what type of bleed

A

Diverticular

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141
Q

What is an ominous lab finding where Val lower GI bleed

A

Anemia

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142
Q

First thing to exclude in diagnostic bleeding testing

A

UPPER GI SOURCE

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143
Q

Large volume w/in 24 hours if active bleed, 24-36 hrs if stable no active bleed; what test is warranted?

A

Colonoscopy

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144
Q

Small volume diagnostic test

A

Anoscopy and sigmoidoscopy

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145
Q

Hemodynamically unstable and hmatochezia diagnostic test

A

Technetium scan and angiography

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146
Q

Txm for large volume bleed

A

Therapeutic colonoscopy
Intra-arterial embolization
Surgery

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147
Q

persistent or recurrent bleeding, despite negative initial GI evaluation, unknown origin but commonly from small intestine

A

Obscure GI bleed

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148
Q

Overt GI bleed

A

melena, maroon stool, or hematochezia

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149
Q

Occult GI bleed

A

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

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150
Q

How do you ID occult GI bleeding

A

Fecal Occult Blood Test
Fecal Immunochemical Test
More accurate, but only detects lower GI bleed
Presence of unexplained anemia on CBC

ID FOR NEOPLASM

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151
Q

Asymptomatic w/ incidental +FOBT/FIT but no anemia =

A

colonoscopy

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152
Q

Symptomatic w/ either +FOBT/FIT or unexplained anemia =

A

upper endoscopy and colonoscopy

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153
Q

When do you get a capsule endoscopy

A

Occult bleeding or iron def

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154
Q

Bright red blood is what source

A

Left colonic source

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155
Q

Brown stools mixed or streaked with bright red

A

Rectosigmoid or anus

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156
Q

Maroon stool source

A

Small Instestine or right colonic source

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157
Q

Black (Melina) blood source

A

Upper GI

158
Q

Largest serous membrane in the body

A

Peritoneum

159
Q

What type of tissue is the peritoneum

A

Consists of a layer of simple squamous epithelium (mesothelium) with underlying layer of areolar connective tissue

160
Q

Common causes of ascites

A

Liver dz = 80%

Hepatic congestion

Hypualbuminemia

161
Q

Functions of the hepatic portal system

A

supplies the liver with metabolites

ensures that ingested substances are processed in the liver before reaching the systemic circulation

162
Q

What is defined as pathological increase in portal pressure

A

Pressure gradient increase in portal pressure between portal vein and IVC > 10 mmHg

163
Q

How can liver dz lead to ascites?

A

Cirrhosis —> increased intrahepatic vascular resistance ————->increased capillary pressure —->increased hepatic lymph formation —->ascites

164
Q

What can lead to ascites

A

Alcohol abuse
Risk factors for Hepatitis
History of malignancy (cancer)

165
Q

Signs of portal HTN and liver dz

A 
Hepatic enlargement (+/- tenderness)
Elevated JVP
Large abdominal wall veins

Liver dz
Muscle wasting
Malnourishment

W/ FEVER = BACTERIAL PERITONITIS

166
Q

Shifting dullness test

A

a change in the location of dullness to percussion when the patient is turned due to movement of the ascites

167
Q

Lab tests and what studies are collected

A

Abdominal paracentesis

Inspection
Cloudy  infection; Milky  chyle; Bloody  traumatic/malignant

Studies
White cell count
Albumin and total protein* (SAAG)
Culture and Gram stain

168
Q

Formula for serum-ascites albumin gradient

A

(serum albumin) – (ascitic fluid albumin) = SAAG

≥1.1 g/dL = portal hypertension

<1.1 g/dL = non-portal hypertension cause

169
Q

Good imaging studies for ascites

A

US and CT

170
Q

What must you distinguish ascites from?

A

Inter abdominal infx from secondary bacterial peritonitis

171
Q

Spontaneous bacterial peritonitis common path’s (5)

A 
E coli
Klebsiella pneumonia
Streptococcus pneumonia
viridans streptococci
Enterococcus species
172
Q

What is the TTP associated with spontaneous bacterial peritonitis

A

Abdominal pain WITHOUT focal tenderness to palpation

173
Q

MOST. Important lab test eval of ascetic fluid via paracentesis (2)

And if you suspect secondary bacterial peritonitis

A

Gram stain and culture
Cell count with differential

Abdominal CT

174
Q

Empiric TXM for spontaneous bacterial peritonitis

A

IV 3rd generation cephalosporin (eg, cefotaxime or ceftriaxone)

Combination beta-lactam/beta-lactamase agent (eg, ampicillin/sulbactam

175
Q

What is good prophylaxis for pts who survive an episode of sponataneous bacterial peritonitis

A

Once daily oral ABX

176
Q

Define malignant ascites

A

Due to carcinoma of a peritoneal organ

Blocked lymphatic channels as a result of malignancy
direct production of fluid into the peritoneal cavity by highly active cancers

177
Q

Chylous ascites

A

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

Milky white in appearance

Due to lymphatic obstruction (lymphoma)

178
Q

Pancreatic ascites

A

intraperitoneal accumulation of massive amounts of pancreatic secretions
Due to disruption of pancreatic duct
Seen in chronic pancreatitis

179
Q

Bile ascites

A

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

180
Q

TB peritonitis

A

Rare in the US – may encounter during deployment

Active TB infection with peritoneal involvement

181
Q

General signs and symptoms of esophageal dz

A

Heartburn (pyrosis)

Dysphasia (can’t swallow)

Odynophagia (painful swallow)

182
Q

Study of choice for esophageal dz

A

Upper Endoscopy (EGD)

183
Q

When do we perform barium esophagograpahy

A

To differentiate b/w structural and motility issues

184
Q

What tests function of lower esophageal sphincter

A

Manometry

185
Q

GERD is a disfx of what?

A

LOWER esophageal sphincter

186
Q

What it’s the squamous columnar junction

A

Lower Esophagus and stomach meeting point

187
Q

What it’s the correlation of severity and tissue damage

A

THERE ISNT ONE

188
Q

ALARM FEATURES of GERD

A 
Troublesome dysphagia
Odynophagia
Weight loss
Iron deficiency anemia
Fever, chills, night sweats
189
Q

What can be visualized with the EGD

A

Esophagus, stomach, duodenum

190
Q

What type of foods precipitate reflux

A

Fatty foods, chocolate, peppermint, alcohol

191
Q

Mild GERD Txm

A

PRN OTC antacids or H2

192
Q

Troublesome symptoms TXM of GERD

A

PPI daily

193
Q

If symptoms persists more than 4 weeks on daily PPI

A

Switch to BID dose

194
Q

Characteristics of OTC Antacids

A

Rapid relief, short duration of action

195
Q

H2 Receptor antagonists and pharmacotherapy

A

-tidine
Cimetidine (Tagamet), Ranitidine (Zantac), Famotidine (Pepcid)

Onset of action is 30 minutes, duration is 8 hours
Can be taken before meals to prevent onset of symptoms

196
Q

PPI’s dosing and efficacy to H2

A 
-prazole 
Omeprazole (Prilosec) 20 mg
Rabeprazole (Aciphex) 20 mg 
Lansoprazole (Prevacid) 30 mg
Esomeprazole (Nexium) 40 mg
Pantoprazole (Protonix) 40 mg

Once daily dosing; 30 mins before breakfast

Superior to H2’s

197
Q

When can you discontinue PPI’s

A

8-12 weeks

most will need continued therapy

198
Q

Nissan Fundoplication Surgical Summary

A

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

REINFORCES THE LES

199
Q

Squamous epithelium of the esophagus is replaced by metaplastic columnar epithelium containing goblet and columnar cells
Result of prolonged exposure to caustic gastric contents

A

BARRETT Esophagus

200
Q

What can Barrett esophagus do to symptoms of GERD

A

Reduce

201
Q

Association between GERD and esophageal adenocarcinoma

A

11-fold increased risk of esophageal adenocarcinoma
PPI therapy
surveillance endoscopy w/ biopsies every 3–5 years

202
Q

Narrowing of the esophageal lumen at the GEJ
Progressive solid food dysphagia
Treated with endoscopic dilation

A

Peptic stricture

203
Q

What are the diff types of esophagitis

A

Infectious
Pill-induced
Eosinophilic

204
Q

What empiric antigunfal can be used for infxn esophagitis

A

Fluconazole (Diflucan)  if no response in 5 days  EGD

205
Q

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

A

Eosinophilic esophagitis

Leads to progressive dysphagia

206
Q

What history should you ask about for EO EOsophagitis

A

Asthma
Allergies
Atopic Dermatitis

207
Q

Clinical findings of EO Esophagitis

A

Dysphagia to solid foods

Heartburn

208
Q

Txm of EO Eosinophilic esophagitis

A 
Empiric trial of PPI first
BID dosing for 2 months
Referral to allergist
Topical corticosteroids
Swallowed fluticasone (from inhaler)
209
Q

Esophageal webs

A

Thin mucous membrane of squamous epithelium

Mid to upper esophagus
Most are asymptomatic
May cause intermittent dysphagia or GERD like symptoms

210
Q

Esophageal rings (Schwarzkopf Rings)

A

Circumferential mucosal structure in the distal esophagus
Similar symptoms as webs
Strong association with hiatal hernia

211
Q

Diagnostic test and Txm of esophageal webs and rings

A

Diagnostic test
Barium swallow

Treatment
Endoscopic dilation if symptomatic

212
Q

Zenker diverticulum and symptoms?

A

Pharyngoesophageal diverticulum
‘pharyngeal pouch’

Symptoms
Progressive dysphagia
Sensation of food ‘sticking’ in the throat
Halitosis
Regurgitation of undigested food, pills
213
Q

How do you diagnose zenker

A

Barium swallow

214
Q

Achalasia and etiology

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)
215
Q

Main symptom of Achalasia

A

Progressive dysphagia to solids and liquids

216
Q

What deformity is associated with Achalasia

A

Birds beak

217
Q

Chagas

A

parasitic disease caused by Trypanosoma cruzi

Endemic to Mexico and South & Central America
Inquire about travel history

similar to Achalasia

218
Q

Txm of Achalasia

A

Botulinum Toxin into the LES – 85% effective, 50% relapse, preferred for poor surgical candidates

Pneumatic dilation – preferred, 90% effective

Surgery - 95% effective

219
Q

Dilated submucosal veins due to portal hypertension
Over 50% with cirrhosis

Cause severe upper GI bleeding
High mortality rate

A

Esophageal varices

220
Q

Follow on Txm of esophageal varices

A

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

221
Q

Mucosal tear at the GEJ

A

Mallory-Weiss Syndrome
Sudden increase in abdominal pressure
Retching or vomiting
Strong association with alcoholism

Pt presents with hematemesis

222
Q

TxM of Mallor-Eiss Syndrome

A 
Endoscopic hemostatic agents
Vasoconstrictive agents (epinephrine)
Cautery
Endoclip
223
Q

Complete rupture of the esophagus

A

BOERHAAVE SYND

224
Q

Rare form of cancer

3:1 male to female ratio
May be squamous cell or adenocarcinoma

A

Esophageal carcinoma

225
Q

S and S of esophageal carcinoma

A

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

226
Q

What establishes diagnosis of esophageal carcinoma

A

EGD

227
Q

Type I: Sliding hernia:

A

Displacement of the gastroesophageal junction above the diaphragm.
The stomach remains in its usual longitudinal alignment and the fundus remains below the GE junction

228
Q

Type II, III, IV: Paraesophageal hernias:

A

True hernia with a hernia sac

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

229
Q

Diagnosis and TXM of Hiatal Hernia

A

Diagnosis
Barium swallow

Treatment
Small hernias  GERD management
Larger hernias  surgical repair

230
Q

Gastropathy vs Gastritis

A

Gastropathy – mucosal damage without inflammation

Gastritis – mucosal damage with inflammation

231
Q

What irritants are assoc with gastropathy

A

Alcohol
NSAIDS

Need mucosal biopsy for diagnosis

232
Q

Less common etiologies of Erosive Hemorrhagic gastropathy

A

Physical stress

Portal HTN

233
Q

S and S of Erosive and Hemorrhagic Gastropathy

A

General Symptoms and Signs

Patient may be asymptomatic
When symptomatic:
Anorexia
Epigastric pain

234
Q

Most common clinical manifestations of Erosive and Hemorrhagic Gastropathy

A

Upper GI bleed

235
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

236
Q

Describe gastric prostaglandins

A

Stimulate epithelial cells to release more bicarbonate and mucus

Act as potent vasodilators

237
Q

NSAID gastropathy most common s and s and Treatment

A

Dyspepsia

TXM = stop NSAID

238
Q

If you have to continue NSAID Txm what should you due to decrease risk of NSAID gastropathy

A

Ensure medication taken with milk or meals

Add daily PPI

239
Q

How does alcoholic gastropathy occur

A

Ethanol has direct toxic effect on gastric mucosa

It also impairs gastric motility and leads to delayed gastric emptying

240
Q

Txm of alcoholic gastropathy

A

Treatment with discontinuation of alcohol and

H2 or PPI for 2-4 weeks.

241
Q

What prophylaxis can be given for stress gastropathy

A

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

242
Q

Stress gastropathy is associated with bleed if what else is present

A

Coagulopathy

Respiratory failure w/ mechanical ventilation

243
Q

Txm of portal HTN gastropathy

A

beta blockade to

lower portal pressure.

244
Q

What type of inflitrtation happens with H pylori gastritis

A

Neutrophilic and lymphocytic infiltration

245
Q

When do we test for H. Pylori

A

dyspeptic patients
chronic GERD patients
suspected or confirmed PUD patients.

246
Q

What do use to test post treatment eradication

A

Fecal antigen

247
Q

What should be discontinued before H. Pylori testing

A

anti-secretory therapy for 2 weeks prior to testing

248
Q

When do we perform H pylor test of cure

A

4 weeks post TXM

249
Q

Standard Bismuth Quad therapy

A

PPI PO twice daily
Bismuth subsalicylate 262mg - two tablets PO four times daily
Tetracycline 500mg PO four times daily
Metronidazole 500mg PO three times daily

250
Q

Standard Non bismuth Quad Therapy

A

PPI PO twice daily
Amoxicillin 1000mg PO twice daily
Metronidazole 500mg PO twice daily
Clarithromycin 500mg PO twice daily

251
Q

Standard Triple Therapy (in lower than 15 % resistance)

A

PPI PO twice daily
Clarithromycin 500 mg PO twice daily
Amoxicillin 1 g orally PO twice daily
(or metronidazole 500 mg PO BID, if PCN allergic)

252
Q

Menetrier Dz

A

Idiopathic hypertrophic gastropathy

Nausea, epigastric pain, weight loss, diarrhea

253
Q

Peptic Ulcer

A

A break in the gastric or duodenal mucosa

Due to impaired mucosal defense mechanisms

254
Q

Types of ulcers associated with age

A

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

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

255
Q

Difference between s and s of gastric vs duodenal ulcers

A

Shortly after eating with gastric ulcers

2-4 hours after eating for duodenal ulcers

256
Q

Pain with eating gastric duodenal

A

Gastric - Increase

Duodenal - Decrease

257
Q

Work 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
258
Q

Txm goals of PUD (4)

A

Relieve dyspepsia
Promote ulcer healing
Eradicate H pylori infection, if present
Prevent recurrence

259
Q

PUD Txm NSAID

A

Discontinue if possible
Titrate to lowest effective dose
Switch to COX-2

260
Q

Treatment of PUD first line

A

PPI’s

261
Q

Mucosal defense adjunct treatment meds (2)

A

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

Misoprostol (Cytotec) – prostaglandin analog
Often given as prophylaxis for long term NSAID patients
Downside – administered 4x/day and causes diarrhea in 10-20%

262
Q

Common complication of PUD

A

Acute upper GI hemorrhage

Ulcer perforation

263
Q

S and s of ulcer perforation

A

Sudden, severe abdominal pain
Rigid abdomen, reduced bowel sounds, + rebound ttp
Pneumoperitoneum
(Air under the diaphragm)

264
Q

Surgical repair of ulcer perforation if

A

Evidence of free abdominal air or peritonitis

Deterioration of patient while admitted

265
Q

Ulcer penetration

A

Penetration of the ulcer through the bowel wall without free perforation or leakage of luminal contents into the peritoneal cavity

266
Q

Common places that ulcers penetrate

A

Pancreas, liver, biliary tree

267
Q

What symptom change is key for ulcer penetration diagnosis

A

Change in dyspepsia = increased

Lack of relief with foods or antacids

268
Q

Gastric outlet obstruction

A

Chronic edema of pylorus or doudenal bulb

269
Q

Symptoms of gastric outlet obstruction

A

Early satiety
Postprandial vomiting (undigested food contents)
Weight loss

270
Q

Treatment for gastric outlet obstruction

A

Correct electrolyte embalance
High dose PPI
Endoscopic dilation

271
Q

Gastrin-secreting neuroendocrine tumore

A

Gastrinoma (Zollinger Ellison)

272
Q

What is the gatrinoma triangle

A

Junction of common and cystic duct
Pancreatic neck
3rd portion of the duodenum

273
Q

Commonalities of Zollinger Ellison syndrome gastrinoma

A

G locations
Pancreas
Duodenal wall
Lymph nodes

common in patients with MEN-1

274
Q

What do Zollinger Ellison syndrome pts develop 90% of the time

A

PUD

275
Q

When do you screen for Gastrin levels

A

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

276
Q

Gastroparesis.

A

Delayed gastric emptying in the absence of a mechanical obstruction

277
Q

Most common associated dz cause of gastroparesis

A

Diabetes Mellitus

278
Q

Cardinal symptoms of gstroparesis

A 
Nausea
Vomiting
Early satiety
Bloating and/or upper abdominal pain
Weight loss in severe cases
279
Q

What type of gastroparesis reps NG decompression and IV fluid/ electrolyte replacement

A

Acute exacerbations

280
Q

General Txm of gastroparesis

A

Diet changes

Glycemic control in DM pts

Prkineteic Meds = Metoclopramide (Reglan)
Domperidone
Erythromycin

281
Q

Classic signs of metastatic gastric adenocarcinoma

A

Sister Mary Joseph Nodule

Virchow node

282
Q

Diagnostic studies of Gastric Adenomcarcinoma

A

Labs
CBC often shows anemia
LFTs may be elevated

Endoscopy
Confirms diagnosis

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

283
Q

Secondary tumor from spread of non Hodgkin lymphoma

A

Gastric lymphoma

284
Q

What type of tissue arises from MALT

A

Mucosa associated lymphoid tissue

Chronic H pylori

285
Q

Carcinoid tumor vs 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

286
Q

3 symptoms of carcinoid syndrome

A

Cutaneous flush
Venous telangiectasis
Diarrhea (watery no blood, abdominal cramps)

287
Q

Classic child pyloric stenosis

A

3-6 week old child
Immediate postprandial projectile vomiting
Fussy and hungry immediately after meals
Constipation, dehydration

288
Q

Where do you palpate the infantile hypertrophic pylori stenosis

A

Palpation of “olive” in the right upper quadrant

Hypertrophic pylorus

289
Q

Signs and symptoms of malabsorption disorders

A

Steatorrhea = bulky greasy stools that FLOAT

Microcytic/Macrocytic anemia = iron b12 folate malabsorption

Diary intolerance = lactase deficiency

290
Q

What is celiac dz

A

Gluten sensitive enteropathy
Immune response
=diffuse damage to proximal small intestinal mucosa

291
Q

S and s of celiac disease (4)

A

Dyspepsia
Diarrhea
Steatorrhea
Borborygmi (loud stomach sounds)

292
Q

Extra instinct manifestations (4)

A

Fatigue
Depression
Transaminitis
Dermatitis herpetoformis

293
Q

Dermatitis herpetiformis

A

Prurience Papuans nad vesicles of extensor surfaces; trunk scalp, neck.

294
Q

Lab testing for celiac

A

CBC
CMP
UA
Specific celiac serology (IgA and IgG)

295
Q

What is IGA tissue transglutaminase antibody

A

IgA tTG

Test of choice in Celiac ID

Serum IgA levels can reveal undiagnosed IgA deficiency

296
Q

IgG-deamidated gliadin peptides (DGPs)

A

ID’s patients with IgA deficiency

297
Q

IgA

A

Most abundant antibody protects mucosal tissues form microbial invasion and maintains homeostasis

298
Q

What is the confirmatory test for celiac dz diagnosis

A

Mucosal biopsy of proximal and distal duodenum
W/ Histological blunting and/or atrophy of the intestinal villi

(Villous Atrophy)

299
Q

Can you eat oats with celiac disease

A

NO!

300
Q

What do celiac patients have a SLIGHT increased risk for?

A

Lymphoma and adenocarcinoma

301
Q

Whipped disease

A

Rare multisystem illness caused by infection with the Bacillus Tropheryma whippelii

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

302
Q

Classic presentation of whipple dz

A 
Migratory arthralgias (Large joint involvement) 
Diarrhea
Abdominal pain 
Weight loss
Fever
303
Q

What are less common signs of whipple dz (4)

A

Skin hyperpigmentation
Generalized lymphadenopathy
Ophthalmoplegia
Nystagmus

304
Q

How do you diagnose whipple dz

A

Evidence of bacterium in mucosal biopsy sample

“Foamy macrophages”

305
Q

Treatment of whipple dz

A

IV ceftriaxone x 2 weeks

TMP-SMX DS – 1 tab po BID x 12 months

306
Q

Tropical spruce

A

Environmental enteropathy; tropical malabsorption

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

Entire small Instestine involvement

Malabsorption of folic acid and B12

307
Q

S and s of tropical spue

A

“Inflammation of the Mouth”

Chronic diarrhea
Steatorrhea
Weight loss
Anorexia
Malaise
B12 and Folate deficiency
Glossitis & chelitis
308
Q

Findings of endoscopy in tropical sprue

A

Gross findings
flattening of duodenal folds

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

309
Q

How do you prevent and treat tropical sprue

A

Prevention
Boil/bottled water
Peel fruits before eating

Treatment
TMP-SMX x 6 months
Folate, B12 supplementation

310
Q

Explain lactase deficiency

A

Lactase = brush borer enzyme that hydrolysis lactose into glucose and galactose

Malbosrbed lactose is fermented by intestinal bacteria = gas and organic acids

311
Q

S and s of lactase deficiency

A

“Dose dependent”

Small intake —>may be asymptomatic
Moderate intake —> bloating, abdominal cramps, and flatulence
Large intake —> osmotic diarrhea

312
Q

Diagnostic test of lactase deficiency

A

Hydrogen breath test

313
Q

What patients should you be concerned with bacterial overgrowth

A

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

314
Q

Bacterial overgrowth main symptoms

A

Steatorrhea

Macrocytic anemia

315
Q

Treatment of bacterial overgrowth

A

Ciprofloxacin
Amoxicillin-clavulanate
Rifaximin

316
Q

Short bowel syndrome

A

Removal of significant segments of the small intestine

317
Q

Acute paralytic ileus

A

A dynamic = post op

Failure of peristalsis

Hospitalized patients due to
surgery
severe illness
meds of motility = opioids, anticholinergics

318
Q

Main symptoms of acute paralytic ileus (4)

A

Diffuse constant abdominal pain
Lack of abdominal TTP
Absent/Low bowel sounds
Abdominal distention

319
Q

Diagnostic testing

A

Non specific electrolytes and X-ray ID

320
Q

Txm of acute paralytic ileus

A

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

321
Q

Chronic intestinal pseudo obstruction

A

Similar to Gastroparesis

Signs of obstruction without actual obstruction

322
Q

Work up for chronic intestinal pseudo obstruction

A

CT or endoscopy

NG decompression and IV fluid/electrolyte replacement

323
Q

What is small bowel obstruction most commonly attributed to

A

postoperative adhesions or hernias

324
Q

Clinical presentation of small bowel obstruction

A 
Colicky abdominal pain
Nausea
Profuse vomiting
Obstipation
Inability to pass flatus or stool
325
Q

Small bowel obstruction physical exam

A

Abdominal distension
Tympany on percussion

Hyperactive bowel sounds early
Hypoactive later on

Signs of dehydration

326
Q

Lab test for small bowel obstruction

A 
CBC
CMP
Urinalysis
Type and crossmatch
If surgery may be indicated
327
Q

Radiographs of small bowel obstruction show what

A

Plain abdominal films

Both upright and supine
Dilated loops of small bowel with air-fluid levels

328
Q

What does a CT scan ID in small bowel obstruction

A

strangulated obstruction

329
Q

Small bowel obstruction treatment - ACUTE (6)

A 
Fluid resuscitation
Bowel decompression (NG)
Pain control
Anti-emetic medications
Early surgical consultation
Admission
330
Q

What is the precession of strangulated bowel obstruction

A

Dilation —> Compromise of the intramural vessels of the small intestine —>Ischemia —>Necrosis —>Bowel perforation —>Sepsis

331
Q

Gallstone ileus

A

Complication of cholelithiasis.

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

332
Q

What dz can cause intussusception

A

Mencken diverticulum

333
Q

Triad of intussusception classic symptoms

A

colicky abdominal pain, vomiting, “currant jelly stools

334
Q

Txm of intussusception

A

Pneumatic Reduction of air with flouroscope

Hydrostatic reduction with saline with US or flour

Surgery

335
Q

Neoplasm of the small bowel may cause

A

Intussusception and obstruction

336
Q

Small intestinal neoplasms (4)

A

Adenocarcinoma

Lymphomas

Intestinal carcinoid

Sarcoma

337
Q

Protein losing enteropathy

A

Excessive loss of serum protein in the GI tract
=hypoalbuminemia

Established GI disorder

338
Q

Mesenteric ischemia

A

Interruption of blood flow to the bowel

  • arterial occlusion
  • venous thrombosis
  • non-occlusive (vasospasm, low cardiac output)
339
Q

PE finding common with mesenteric ischemia

A

Classically = “pain out of proportion with physical exam”

340
Q

Diagnostic test of mesenteric ischemia

A

CT angiography

341
Q

TxM of Mesenteric Ischemia

A

Papaverine – smooth muscle relaxant
Thrombolytics
Surgical referral

342
Q

Rule of twos for meckels (6)

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
343
Q

Clinical presentation of meckels

A

GI Bleeding – due to heterotopic gastric mucosa (acid-producing tissue - may lead to ulcers and bleeding)

Abdominal Pain – most common anatomic location may present similarly to acute appendicitis

344
Q

Diagnosis of meckels

A

Capsule Endoscopy

Meckel’s Scan:
nuclear medicine study using 99m technetium pertechnetate, which has an affinity for gastric mucosa

345
Q

TxM of meckels

A

Surgery Referral

Asx = no treatment

Sx = stabilize the bleed, surgical removal, correct intussusception if present

346
Q

True diverticulum of the cecum

A

Appendix

Attachment at the base of Cecum

347
Q

Appendix locations

A 
Retrocecal 
Subcecal
Preileal
Postielal
Pelvic
348
Q

Pathogenesis of appendicitis

A

Obstruction —>increased pressure —>venous congestion ——->infection —>necrosis

349
Q

Fecalith

A

Hard stony mass of feces

350
Q

How long until untreated necrotic appendix leads to sepsis?

A

36 hours

351
Q

Clinical 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

352
Q

Where can the migration of cecum during pregnancy cause pain in appendicitis

A

Right flank

Right subcostal

353
Q

Physical exam findings of appendicitis

A

TTP at Mcburneys Point
Direct AND Rebound tenderness
Guarding
Rigidity

354
Q

Signs of peritoneal irritation

A

Heel tap (pain worsened by walking or coughing)

Psoas sign (pain on passive extension of right hip)

Obturator sign (pain with passive flexion and internal rotation of the right hip)

Rovsing’s Sign (palpation of LLQ elicits pain in the RLQ

355
Q

What is the CBC finding of appendicitis

A

Moderate leuoko’s and neutrophilia

356
Q

ABX Txm for Appendicitis

A

Cefoxitin or cefotetan

Ampicillin-Sulbactam

Ertapenem

357
Q

Normal vascular structures (cushions) in the anal canal, arising from a channel of arteriovenous connective tissues that drains into the superior and inferior hemorrhoidal veins

A

Hemorrhoids

358
Q

Internal hemorrhoids

A

are located proximal to the dentate line

Arise from the superior hemorrhoidal veins

359
Q

External hemorrhoids

A

are located distal to the dentate line

Arise from the inferior hemorrhoidal veins

Covered with squamous epithelium of the anal canal or perianal region

360
Q

Main patio of hemorrhoids

A

Increased venous pressure

361
Q

Clinical presentation 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 —> external hemorrhoids

362
Q

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

A

Internal hemorrhoids

363
Q

Skin tags associated with may be difficult to clean, resulting in prolonged contact of fecal material with the perianal skin and local irritation

A

External hemorrhoids

364
Q

What do you inspect for on PE with suspect hemorrhoids

A

Skin tags, fissures, fistula, condyloma, dermatitis

Anoscopic exam = visualize internal hemorrhoids

365
Q

Bleeding only no prolapse; GRADE

A

1

366
Q

Prolapse with defecation; spontaneous reduction; GRADE

A

2

367
Q

Prolapse with defecation: must be manually reduced; GRADE

A

3

368
Q

Prolapse with defecation: must be manually reduced; GRADE

A

3

369
Q

Prolapsed, incarcerated: cannot be manually reduced; GRADE

A

4

370
Q

Thrombosis of the external hemorrhoidal plexus results in

A

Perianal hematoma

371
Q

Thrombosed hemorrhoids acute onset =

A

exquisitely painful

Thrombosis of the external hemorrhoidal plexus results in 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

372
Q

TxM of Hemorrhoids

A

High fiber diet + increased fluid intake
Avoid straining
Limit sitting time on toilet <5 min

Avoid aggressive wiping
Sitz baths

373
Q

Med TxM of hemorrhoids

A

Topical Astringents

Witch hazel pads (Tucks)

Topical Hydrocortisone

Cream or foam (Proctofoam)

Topical anesthetics

Pramoxine or dibucaine

Hydrocortisone suppositories (Preparation H)

374
Q

Further Txm ; internal hemorrhoids

A

Rubber band ligation
Sclerotherapy
Electrocoagulation

375
Q

A tear in the anoderm distal to the dentate line

A

Anal fissure ; due to trauma of anal canal

376
Q

Why do chronic anal fissures develop

A

Spasm of the internal sphincter, with impaired healing

377
Q

Anal fissures

A

Examination of the anus reveals small tear in the epithelium

Spreading buttocks may be acutely painful to the patient

Avoid digital rectal examination - pain

May observe “sentinel pile”
(Skin tag at the outermost edge of the fissure)

378
Q

Primary anal fissure

A

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

Usually single fissure

Rarely located off midline

379
Q

Secondary anal fissure

A

Lateral or atypical position offmidline location

Multiple fissures

Chronic IBD, HIV, syphilis, malignancy, granulomatous disease, psoriasis, previous surgery [associations]

380
Q

Chronic fissure Txm

A

Topical vasodilators
Nifedipine, nitroglycerin, or diltiazem

Botulinum toxin injection

Surgical TxM
Fissure to my
Lateral internal sphincerotomy

381
Q

Anorectal infxn

A

Anorectal abscess typically originates from an obstructed and infected anal crypt gland

382
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

383
Q

What do you find on PE of perianal abscess

A

Digital Rectal Exam!!
Rectal abscesses
Fistulas

384
Q

Perianal =

Perirectal =

A

Simple ; ID in clinic

Complex ; ID in OR

385
Q

What can reduce the rate of fistula formation in perianal abscess?

A

Oral antibiotics

386
Q

Fistula formation

A

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

387
Q

What is the usual etiology of infectious proctitis

A

Etiology usually STI

Gonorrhea
Syphilis
Chlamydia
Herpes

388
Q

Condylomata acuminata

A

Anal warts

May c/o itching, bleeding or pain

May coalesce and obscure the anal opening (usually in immunosuppressed patients)

Must distinguish from cancer

389
Q

Most common symptoms of carcinoma of the anus

A

Bleeding, pain, local mass

390
Q

What study is used to ID carcinoma of the anus and distinguish b/w hemorrhoids

A

CT or MRI to diagnose

IPAP Class 21-2 (12 decks)

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