Part 22 Flashcards
1
Q
Complications of vomiting (2)
A
- ruptured esophagus (boerhaave’s syndrome)
- mallory weiss tear
2
Q
Chief cells
A
Cells of the stomach that secrete pepsinogen that will be cleaved into pepsin for breaking down protein
3
Q
Non urgent (hemodynamically stable) peptic ulcer dz treatment options (4)
A
- treat underlying cause
- limit risk factors
- add anti-secretory agent
- repeat endoscopy in 6-8 weeks to verify healing
4
Q
Current literature and infants introduction of gluten
A
Recommended to eat less than 5g of gluten containing food on average per day from 4-6 months continuing until age 2
5
Q
Classic signs and symptoms in celiac disease patients (6)
A
- foul smelling diarrhea
- excess flatulence
- growth failure in children
- iron deficient anemia
- dermatitis herpetiformis (maculopapular on the extensor suraces)
- concomitant lactose intolerance
6
Q
Diagnostic testing for celiac disease (5)
A
- all testing should be done while patient is ON a gluten rich diet except genetic testing***
- serologic eval IgA tissue transglutaminase and/or IgA endomysial antibody
- total IgA (in case IgA deficient)
- genetic testing (patient might still have gluten sensitivity but not celiac)
- modified gluten challenge and small bowel biopsy (at least 6 specimen) (confirmatory)
7
Q
Upon biopsy for celiac testing, any patient with ____ would benefit from a gluten free diet
A
villous atrophy
8
Q
Nasogastric (NG) tubes
A
PVC, polyurethane, or silicone flexible tube inserted thru the nose with the end terminating at the stomach, a salem sump tube is most commonly used for decompression (additional lumen tube for decompression of the stomach or blowing off the wall)
9
Q
NG tube indications (2)
A
- treat ileus or small bowel obstruction with decompression (removal of contents of GI which is a good measure of how severe a small bowel obstruction is)
- enteral nutrition and administer medications short term in patients who cannot swallow
10
Q
NG tube contraindications (5)
A
- esophageal stricture
- esophageal varices or diverticuli
- basilar skull fracture
- prophylactic placement is NOT done (such as after bariatric surgery)
- long term enteral nutrition
11
Q
Placement of an NG tube steps
A
- gather supplies
- measure estimated length based on zyphoid to earlobe and earlobe to nares
- have patient positioned sitting up chin to chest
- insert tube horizontally
- have patient sip on water as NG tube is advanced
- ensure patient can speak
- tape in place
- connect to suction
- confirm placement thru aspiration of contents/simultaneous auscultation or abdominal x ray
12
Q
NG tube complications (4)
A
- coiling
- reflux
- cribiform plate perforation
- pneumonia or tracheal perforation
13
Q
When is a post pyloric feeding tube utilized? What 2 complications occur with it?
A
-When there is concern for aspiration (A simple NG tube can cause reflux into the esophagus), concerns over difficulty in placement and causing “dumping syndrome”
14
Q
Long term enteric feeding options
A
If greater than 2 weeks, may refer to
-Percuaneous endoscopi gastrostomy/jejunostomy (PEG/PEJ) or a PEG-J which is both
15
Q
Venting PEGs
A
Indications for a PEG tube in palliative care where a patient who has a distal obstruction and is terminal can continue to eat and suck out the contents as needed
16
Q
Open drain (penrose)
A
A type of drain that is open type with passive pressure simply to keep the skin open, drainage usually occurs around the tube not necessarily thru it
17
Q
What to do if a long term enteric feeding tube is clogged?
A
Flush it, sometimes with coca cola and if that doesn’t work then x ray
18
Q
Closed drain
A
Can utilize active or passive pressure
19
Q
Diverticula
A
Small pouches created by herniation of the mucosa into the wall of the colon thru intestinal layers and smooth muscles, can be true (contain all layers thru the adventitia) or false (only involving mucosa or submucosa)
20
Q
Where are diverticula most common?
A
Sigmoid colon (high intraluminal pressure)
21
Q
Diverticulitis complications
A
- peritonitis due to perforation
- fistula (often colovesicular - fecaluria)
22
Q
Lab tests for suspected diverticulitis (4)
A
- CBC (will see left shift and maybe anemia)
- electrolytes (if N/V/D)
- urine culture
- pregnancy test
23
Q
Best imaging study for suspected diverticulitis and one that is contraindicated
A
- CT of abdomen and pelvis with contrast ideally
- colonoscopy
24
Q
Mild diverticulitis treatment (2)
A
- clear liquid diet with advancement as tolerated
- oral broad spectrum (7-10 day course) of ciprofloxacin/metronidazole or augmentin
25
Severe diverticulitis treatment (5)
- if comorbidities then admission
- NPO with IVF hydration
- broad spectrum IV antibiotics
- morphine (avoid NSAIDS/steroids as that worsens colonic perforation)
- surgery if free air perforation or fistula
26
Long term management of diverticulitis (3)
- initial low fiber diet for 1 month followed by high fiber diet
- NO recommendation to avoid nuts and seeds
- colonoscopy 4-6 weeks later
27
Diverticular bleed
A common cause of lower GI bleeding typically painless hematochezia with massive bright red bleed, usually self limiting, aspirin and NSAIDS increase risk
28
Meckel diverticulum and the rule of 2's
Congenital abnormality that causes true diverticulum of the small bowel, most commonly incidental finding but can develop complications, surgical resection if complications occur
2% of population, within 2 feet of ileocecal valve, 2 inches in length, types of heterotopic mucosa, and present before the age of 2
29
Retching
Vomiting but with absence of expulsion fo gastric content (dry heaving)
30
Regurgitation and rumination
Gentle return of small amounts of food or secretions from the esophagus to the pharynx or the stomach into the hypopharynx respectively
31
4 afferent pathways of vomiting
- CNS
- chemoreceptor trigger zone
- vestibular system
- visceral nervous system
32
3 Phases of vomiting
1) nausea, sweating, salivation (parasympathetic and sympathetic)
2) retching (motor system deep breath/breath hold to block the glottis, reverse peristalsis begins from the mid intestines)
3) posturing, contraction of abdominal muscles, and ejection
33
Approach to a patient with nausea and vomiting (PE and potential labs) (6)
- what is their hydration status (orthostatic VS)
- neuro exam
- EKG and troponin
- CBC
- BUN and creatinine
- pregnancy test
34
Most common cause of acute episodes of vomiting and treatment (1)
Viral gastroenteritis, supportive care and hydration
35
Common nausea medications and their classes (4)
Transdermal scopolamine (anticholinergic)
Promethazine (H1 antihistamine)
Metoclopramide (dopamine receptor antagonist)
ondansetron/zofran (5HT3-antagonist)
36
Pregnancy induced nausea treatment options (2)
- doxylamine
- ondansetron
37
Functional chronic nausea and vomiting and treatment (1)
Unexplained vomiting at least once a week that is NOT cyclical, treated often with low dose tricyclic antidepressants
38
Gastroparesis (diabetic, post viral or idiopathic) and treatment (3)
Symptoms suggestive of obstruction (food not moving thru intestine or emptying of stomach within an hour), treated with dietary modification and metoclopramide or erythromycin
39
Cyclic vomiting syndrome
Stereotypical incapacitating attacks often with specific triggers, have prodromal phase with distinct aura then associated with severe abdominal pain, pallor, excess salivation and intense thirst
40
Cannabinoid hyperemesis syndrome
Condition where severe bouts of nausea and vomiting occur mainly in daily long term users of marijuana due to effect it has on intestinal receptors (which opposes the brain effect), begins with prodromal phase (early morning nausea and abdominal pain) then hyperemetic phase (hot showers ease!!!) and recovery phase (goes away), treated with cessation
41
Complications of vomiting (6)
- dehydration
- hypokalemia
- metabolic acidosis
- aspiration
- mallory weiss tear
- ruptured esophagus (boerhaave's syndrome)
42
Mackler's triad for boerhaave syndrome
- chest pain
- vomiting
- subcutaneous emphysema due to rupture
43
Essential nutrients
Those that the body cannot make in sufficient quantities to meet physiologic needs
44
Carb/protein/fat kcals per gram
4/4/9
45
Nutrient transport in the GI system upon absorption
- Water soluble enter the blood stream
- fat soluble vitamins and other fats form chylomicrons and are released into the lymphatic system
46
Secretin
Hormone in small intestine that is released upon chyme entering the duodenum which stimulates pancreatic release of bicarb juices into duodenum
47
Cholecystokinin
Hormone triggered when fat enters small intestines that stiulates gallbladder to release bile for fat emulsification
48
Clinical assessment of malnutrition (4)
- muscle wasting (temporalis muscle)
- fat wasting (hollow sunken in eyes)
- edema and ascites
- alopecia
49
Marasmus
Protein and calorie deficiency resulting in wasting but NO edema
50
Kwashiorkor
Protein deficiency but not caloric deficiency resulting in extreme edema
51
Thiamine B1 deficiency common groups and clinical manifestations and treatment
- alcoholism, poverty, crohns, GI surgery
- beriberi (wet cardiovascular heart failure, late stage dry beriberi neurologic wernicke and korsakoff syndrome)
- IV then oral thiamine
52
Riboflavin B2 deficiency common groups and clinical manifestations and treatment
- Undeveloped countries, malabsorption or malnutrition
- cheilosis/angular stomatitis, glossitis (swollen shiny tongue), corneal vascularization
- IV then oral riboflavin
53
Niacin B3 deficiency common groups and clnical manifestations and treatment
- alcoholism, poverty, PPD rxn
- pellagra (dermatitis, diarrhea, and dementia)
- oral supplementation
54
Vit A deficiency common groups and clinical manifestations and treatment
- children, elderly, poor
- night blindness, bitot spot, xerosis (dry skin)
- oral supplementation and refer to opthalmology
55
Vit C deficiency common groups and clinical manifestations and treatment
- those without access to fresh fruits and veggies
- scurvy (poor wound healing), petechiae (small red spots), splinter hemorrhage
- oral supplementation
56
Vit D deficiency common groups and clinical manifestations and treatment
- inadequate sunlight, inadequate dietary intake
- rickets (kids) and osteomalacia (adults)
- sun exposure or oral supplementation
57
Vit E deficiency common groups and clinical manifestations and treatment
- those on anticoagulants or malnutrition
- excess bleeding
- oral/im/subQ supplementation
58
Phenylketonuria (PKU) and treatment
Autosomal recessive disorder where a pt is unable to metabolize phenylalanine tested at newborn screening as delay in diagnosis will lead to potential brain injury, treated with low phenylalanine diet and tyrosine supplementation, strict protein control for life
59
Benefits of enteral nutrition (3)
- more physiologic with preservation of gut mucosa
- fewer complications
- cheaper
60
Peripheral parenteral nutrition
Short term use of nutrition admission thru a peripheral vein that can supplement those with low intake despite being unable to meet caloric needs on own
61
Total parenteral nutrition
Use for patients who require extended period of tie (>7 days) using the superior vena cava to meet high calorie requirements
62
Fecal occult blood test (guaiac)
Noninvasive cheap test to annually perform where a sample of stool is placed on a card that is then sent to a lab for screening, requires 3 samples, cessation of certain meds, but minimal bowel prep
63
Fecal immunochemical test (FIT)
More expensive version of the yearly guaiac that has less false positives, can be done with a single sample, doesn't require cessation of meds or bowel prep
64
Cologard (FIT-DNA)
Stool DNA analysis of hemoglobin in abnormal cells shed by polyps or cancer, requires full stool sample once every 3 years that detects morecancer than the guaiac
65
Flex sigmoidoscopy
Procedure to view the rectum and sigmoid colon that can be performed by physicians who are not gastroenterologists, minimal prep, usually minimal sedation and time, can do every 5 years recommended to be combined with FIT or guaiac if a patient is refusing a colonscopy
66
CT colonography
Alternative procedure that requires aggressive bowel prep, no sedation or risk of perforation but positives require colonoscopy and repeat exposures to radiation, done every 5 years
67
Factors that impact gastric acid secretion (4)
- gastrin binding to receptors on parietal cell
- H2 binding to receptors on parietal cell
- Ach binding to parietal cell
- proton pump
68
Defensive factors that prevent peptic ulcers
- mucus
- bicarb
- blood flow
- prostaglandins
69
Aggressive factors that cause peptic ulcers
- gastric acid
- pepsin
- pathogen such as helicobacter pylori
- NSAID use
70
Nondrug therapy to prevent ulceration of GI (2)
- diet plays no role
- alcohol and cigarettes
71
Histamine 2 receptor antagonist mech of action
-Because parietal cells have receptors for histamine to promote gastric secretions when released from mast cells thruout gastric mucosa, these antagonists prevent secretion
72
Cimetidine (tagamet) drug class, ADR's (2)
- prototype H2 blocker
- antiandrogenic effects causing gynecomastia, reduced libido, impotence, CNS effects
73
Ranitidine (zantac) differs from cimetidine in 3 ways
- more potent
- fewer ADR's (no antiandrogen effects)
- fewer interaactions
74
Sucralfatte (carafate) drug class and mech of action
- aluminum hydroxide complex of sucrose
- Promotes ulcer healing by creating protective barrier against acid and pepsin, forms a viscous and sticky substance that covers ulcer crater for 6 hours
75
Proton pump inhibitor mech of action
-binds to proton pump of parietal cell causing irreversible inhibition of enzyme that generates gastric acid at the final step, inhibiting up to 90% of 24 hr acid secretion without tolerance in only one a day dosing
76
Proton pump inhibitor therapeutic uses (4) and ADR's (6)
- GERD
- peptic ulcer disease
- long term therapy of hypersecretory conditions
- no impact on warfarin
- headache, NVD
- pneumonia
- fractures increased risk of osteoperosis (use lowest dose and maintain Ca2+ and vit D)
- rebound acid hypersecretion when discontinued
- hypomagnesemia
- C diff infection in long term
77
Misoprostol drug class and therapeutic use
Synthetic analogue of prostaglandin E1 used for prevention of gastric ulcers caused by long term NSAID therapy
78
Misoprostol ADR's (2)
- NVD
- Pregnancy category X
79
Antacids mech of action
-Alkaline compounds that neutralize gastric acid reducing descrution of gut wall
80
Antacids ADR's (3)
- constipation and diarrhea depending on aluminum or magnesium (many preps balance these out)
- Na+ loading increasing hypertension
- acid rebound
81
Antacids drug interactions (3)
-can influence dissolution of many drugs (cimetidine and ranitidine) and chelate drugs in stomach preventing absorption (fluorquinolones or tetracyclines)
82
Bismuth subsalicylate (pepto) function
Promote ulcer healing by forming protective coating over ulcer, promotes secretion of bicarb and prostaglandins, suppresses growth of H pylori, as well as assist in diarrhea treatment, and can be prophylaxis against travelers diarrhea
83
Bisthmus subsalicylate (pepto bismol) ADR's (2)
- harmless stool color change
- long term risk of neurologic injury
| - long term risk of neurologic injury
84
Bisthmuth based quadruple therapy
First line treatment for H pylori including pepto, metronidazole, tetracycline, and standard dose PPI
85
Clarithromycin based quadruple therapy
First line treatment for h pylori including amoxicilin, clarithromycin, metronidazole, and PPI for 14 days
86
Alginic acid and example
Acts as a barrier to reflux and coats the esophagus when reflux occurs (gavison – sodium bicarb + alginic acid)
87
Metoclopramide (reglan) mech of action
Inhibition of inhibitory D2 receptors in gut with subsequent release of Ach into myenteric plexus causing peristalsis, increases lower esophageal sphincter tone
88
Metoclopramide indications (2) and ADR’s (3)
- GERD
- diabetic gastroparesis
-diarrhea, gynecomastia, tardive dyskinesia
89
copolamine (hyoscine, transderm-scop) drug class, mech of action, ADR’s (3)
- anticholinergic muscarinic antagonist
- most effective drug for prophylaxis and treatment of motion sickness by depressing the neuronal activity in the pathwaybetween vestibular system and vomiting system
- Dry mouth, blurred vision, urinary retention
90
Antihistamine use for motion sickness and examples (3)
- Less effective than scopolamine for motion sickness but the sedation makes them less desirable
- dimehydrinate (Dramamine), meclizine (Antivert), diphenhydramine (Benadryl)
91
Diphenoxylate drug class, function, administration
- opioid
- indicated for diarrhea only
- PO only dispensed with combo with atropine (Lomotil) – prevents abuse
92
Loperamide (immodium) drug class, function
- opioid
- OTC used to treat diarrhea by suppressing bowel motility (including IBS), does not cross BBB leaving CNS effects not noticeable
93
Polyethylene glycol (Miralax) function
Can increase frequency of bowel movements in patients with IBS-C, well tolerated and safe for long term use
94
Bile acid metabolic function
Coats products of lipid breakdown to form micelles to help with fat absorption thru this intestinal epithelium
95
Conjugated bilirubin is not reabsorbed. It enters the colon and is converted to....
....urobilinogen by bacteria, from there some is reabsorbed and secreted into urine (yellow color), most exit colon via conversion to urobilin and sterobilin (brown color)
96
Clinical presentation of cholelithiasis
Often asymptomatic for decades and don't require treatment, eventually begin to demonstrate biliary colic (patternless epigastric pain usually 30-90 min right upper quadrant random times) alongside n/v, diaphoresis, but no fever, jaundice, or peritoneal signs
97
Porcelain gallbladder
Findings of calcification of the gall bladder wall that is cancer until proven otherwise
98
Acute cholecystitis
Complication of cholelithiasis in long term, inflammation of the GB, in 20% of pts with biliary colic, have colicky pain that becomes constant and may radiate as well as associated N/V and FEVER*** as well as positive murphy's sign
99
Risk factors for cholecystitis
- rapid weight loss
- increasing age
- medications (including hormone therapy)
100
Choledocholithias
Stone within the common bile duct originating from the gall bladder resulting in a colicky pattern and posing risk for cholangitis with obstruction
101
Acute cholangitis and treatment options (2)q
Bile duct obstruction (stone, scarring, tumor) causing bacteria from duodenum to ascend into the common bile duct resulting in the charcot triad of presentation (abodminal pain, jaundice, fever) requiring antibiotics and relief of obstruction for treatment
102
Charcot triad and Reynold's pentad
Seen in presentation of acute cholangitis involving abdominal pain, jaundice, and feve for charcot triad and additional confusion and hypotension in reynold's pentad
103
Primary sclerosing cholangitis has strong association with...
...ulcerative colitis
104
Primary sclerosing cholangitis
Chronic liver disease with progressive cholestasis and inflammation and fibrosis of intrahepatic and extrahepatic ducts, thought to be autoimmune
105
Primary sclerosing cholangitis lab findings (2) and treatment (2)
- LFT cholestatic pattern
- MRCP beaded appearance
- steroids
- liver transplant
106
Crohn's disease mild moderate and severe management
Mild - budoesonide (corticosteroid)
Moderate to severe - azathioprine or methotrexate
107
Sulfasalazine (azulfidine) drug class, function, indication (1), ADR (1)
5-ASA (metabolized into this)
suppresses prostoglandin synthesis decreasing inflammatory response
-acute treatment of mild to moderate ulcerative colitis
-Hematologic disorders
108
Azathioprine (imuran) drug class and function
Thiopurine immunosuppressant, take 3-6 months to reach use effective for long term treatment and not for acute suppression of inflammation associated with ulcerative colitis and crohns
109
Cirrhosis definition
Chronic IRREVERSIBLE disease of the liver marked by degeneration of the cells, inflammation, and fibrous thickening of the tissue
110
Cirrhosis presentation (6)
- may be asymptomatic other than fatigue
- may be severe symptoms related to functions affected
- weight loss or weight gain
- jaundice
- asterixis
- caput medusa and hepatomegaly
111
Muehrke's lines
PE finding sometimes related to cirrhosis or nephrotic syndrome or albumin deficiency involving double white lines that run across the fingernails horizontally
112
Terry's nails
PE finding where nails are entirely white except for the tips which remain pink, often indicative of cirrhosis
113
Spider angioma
A physical exam finding on the skin of an erythemous spider web shaped lesion indicative of cirrhosis in a patient
114
Pre vs intra vs post hepatic causes of portal hypertension
- splenic vein thrombosis
- cirrhosis
- chronic right heart failure
115
Gastroesophageal varicies on EGD are diagnostic for clinically signficant...
....portal hypertension
116
2 prophylactic treatments against esophageal varices
- banding
- nonselective B blocker
117
Mild ascites treatment options (2)
- sodium restriction
- diuretics 1-2x a week
118
Goal value for moderate to severe ascites treatment per day
.5-1kg per day
119
Spontaneous bacterial peritonitis
Very highly recurring common reason for patients with previously managed ascites to tip caused by translocations of GI tract bacteria across gut wall
120
Spontaneous bacterial peritonitis diagnostic study (1)
-Diagnostic paracentesis with eval of ascitic fluid >250 PMN's/mm with pos culture****
121
Hepatic encephalopathy treatment (2)
- lactulose (stimulates passage of ammonia but causes loose stool)
- rifaximin
122
TIPS procedure
Transjugular intrahepatic portosystemic shunt that connects portal vein to hepatic vein bypassing liver circulation indicated for management of variceal bleeding or of refractory ascites, but can induce or worsen underlying hepatic encephalopathy due to lack of blood filtering
123
Hepatorenal syndrome
Caused by vasoconstriciton of large and small renal arteries resulting in impaired renal perfusion and continuum of renal dysfunction, seen in patients with combo of cirrhosis and ascites, either type I (rapid progressive liver failure) or type II (slow and better prognosis)
124
Hepatorenal syndrome diagnosis (1)
Creatinine clearence <40ml/min not explained by pre-existing renal disease, nephrotoxins or diuretic use
125
Model for end stage liver disease (MELD) score
Liver transplant program scoring system for cirrhosis to assess severity of condition, recipient >25 may not be candidate
