GI Portion Flashcards

(145 cards)

1
Q

gastroesophageal reflux disease

what is this?

population common in?

percent in US?

5 complications it can lead to

A

most common dxs of esophagous 15-20% US, common in pregnancy

transient relaxation of lower esophageal spincter LES leading to gastric acid reflux that causees damange to esophagus and spincter and can lead to:

1. esphagitits- 50% will get this!!!

2. esophageal stricutre

3. barrettes esophagous

4. esophageal adenocarcinoma

  1. hiatial hernia

-

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3
Q

GERD

what are 6 sxs?

1 thing to keep in mind about sxs?

A
  1. heartburn, restrosternal and postprandial

substernal pain/discomfort most commong 30-60 minutes after a meal

worsens when laying down or recumbant

  1. regurgitation (vomit burp)

spontaneous reflux of sour bitter gastric contents in mouth

  1. dysphagia (discomfort)

cough at night from acid asipiraiton

  1. reccurent pneumonia
  2. sxs temp relieved with antacids
  3. can radiate to arm/jaw

***keep in mind sxs don’t correlate with dxs progression so can’t tell how much damage has been done**

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4
Q

what is the pathway for txing GERD?

6

A
  1. lifestyle adjustments
  2. OTC antacids-2 weeks
  3. H2 receptor antagonists
  4. Proton pump inhibitors

**if these fail EDG**

  1. prokinetics
  2. surgical
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5
Q

GERD

3 dx options

6 reasons of when it is not appopropriate to use the first line dx

A
  1. empirically first line unless (below)
  2. esphagogastroduodenoscopy(EGD) if high risk or tx has failed
    a. over 50
    b. weight loss
    c. melena
    d. odynophagia pain with eating
    e. heavy alcohol or tabacco
    f. non repsonsive to tx
  3. modified/full barium swallow
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7
Q

what are the lifestyle changes a patient should make to relieve sxs of GERD?

5

A
  1. avoid eating 2-3 hours before bed

2. elevate head of bed

3. loose weight

  1. avoid acidic food, chocolate, peppermint, ETOH, coffee
  2. stop smoking
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8
Q

why is it important to treat GERD?

A

prevent cancer aka barrette esophagus because the damange from acid makes this more likely to occur

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9
Q

what is the emergency cocktail you give someone in the ED for heart burn?

A
  1. benadryl
  2. lidocaine
  3. maalox
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10
Q

what is the most common cause of esophagitits?

A

GERD, 50% of patients with GERD have esophagitits

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11
Q

esophagitits

what is this?

5 general causes?

4 sxs

A

inflammation of the esophagus, esp in immunocomprimised

  1. viral
  2. bacterial
  3. paraistic
  4. abx induced
  5. radiation or chest cancers

sxs;

  1. odyniaphagia
  2. dysphagia
  3. substernal chest pain
  4. oral thursh
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12
Q

esophagitis

herpes liabilis (HSV)

3 SXS?

2 DX?

1 TX

A

N/V/ chills

herpetic vesicles on nose/lips

dx:

1. endoscopy showing small vesicles or superficial lesions

2. culture esophageal lesions

TX:

ACYCLOVIR 7-21 DAYS!!!

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13
Q

ESOPHAGITIS

VARICELLA-ZOSTER

1 dx?

tx?

A

N/V fever chils

DX:

endoscopy: vesicles or confluent ulcers

Tx:

  1. usually resolve spontaneously but can cause necrotizing esophagitits
  2. ACYCLOVIR!!!!
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14
Q

esophagitis

CMV

who does this occur in?

characteristics of ulcer? 2

3 sxs?

1 tx?

A

only occurs in immunocomprimised patients

CREEPING ULCER or can be GIANT ULCER

sxs:

odyniaphagia

persistent CP

hematememis

Tx:

IV GANCICLOVIR

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15
Q

esophagitis

candidia

who does it occur in?

3 complications?

1 dx?

1 tx?

A

occurs in immunocomprimised host

can cause complications:

  1. bleeding
  2. perforation
  3. stricture

dx:

endoscopy: small yellowwhite raised plaques

tx:

oral or IV fluconazole!!

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16
Q

barrett’s esophagus

how does this occur? what hcanges?

what are they at increased risk for? how much?

A

metaplastic changes in which the stratified squamous** is replaced by the **columnar epithelium that is typically found in the duodenum….extens poximally from LES from repeated exposure to acid esp with GERD (thats why the cells change to this type because its the same exposure the duodenum gets)

increases risk for adenocarcinoma 5-10%

this change increases risk for neoplastic changes/cancer 40-100 times greater than general public

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17
Q

barettes esophagus

2 dx rules?

3 tx?

A

DX:

EDG every 2 years with bx to check for neoplastic changes

if there is high risk dysplasia, consider surgrical resection

TX:

**more txing symtpoms unless surgical intervention**

  1. antacids
  2. H2 blockers OTCs
  3. PPIs
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18
Q

esophageal cancer

what are the two types?

frequency?

prognisis?

who is more common?

A

types:

  1. adenocarcinoma
  2. squamous cell carcinoma

prognosis typicaly poor, 5 year survival 10-13%

both appeare with equal frequency

males more common than females

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19
Q

esophageal cancer:

adenocarcinoma

where do you find this?

4 most important RF?

2 protective

A

distal esophagus

RF:

  1. reflux over 20 years
  2. Barrettes esophagus-almost all cases
  3. obesisty
  4. caucasion males
  5. smoking increases risk (not main)

Protective effects:

  1. fiber
  2. NSAIDS (seems counterintuitive)
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21
Q

esophageal cancer:

squamous cell carcinoma

prevalence?

location?

4 RF?

key point to remember?

A

prevalence is decreasing

middle esophagus

RF:

  1. smoking
  2. alchohol
  3. diet low in fruits and veggies
  4. achalasia increases risk 16 x

*** accounts for 90% of all squamous carcinoma in US***

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22
Q

esophageal cancers

sxs

1 early

3 late

A

SXS:

early:

1. transient “sticking” of food that turns to PROGRESSIVE DYSPHAGIA

later:

  1. retrosternal pain/burning

2.iron deficient anemia -loss from chronic cancer, but not enough to notice hememensis or occult

3. tracheobronchial fistula

late complication where the esophageal wall infilates the stem bronchus causeing intractable coughing with frequent pneumonia

_***if this occurs person has less than four weeks to live***_

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23
Q

in esophageal cancer, when would you expect to see the weight loss and dysphagia?

A

when the lumen is less than 13 mm

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24
Q

esophageal cancer

2 DX

2 STAGE

A

dx:

  1. barium studies
  2. endoscopy

Staging:

  1. CT OF CHEST AND UPPER ABDOMENT

2. PET SCAN

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25
Q

where are adenocarcinomas and squamous cell esophageal cancers found?

A

adenocarcinoma: lower 1/3

squamous: middle esophagus

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26
Q

esophageal varices

what is this?

what causes this?

mortaltiy rate?

MOST COMMON CAUSE?

A

emergency!!!

dilation of the submucosal veins that develop in pts with portal HTN

patho: blood flow through the liver is diminished causing blood flow increase through the microscopic bood vessesl within the esophageal wall and the vessels dilate profoundly, and then continue to dilate until they are large enough to rupture

patient acutely ill, mortality rate 40-70%

MOST COMMON CAUSE OR PORTAL HTN IS CIRROSIS that causes this

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28
Q

where is the most common stie for esophageal varices? why?

A

distal esophagus at gastroesophageal junction because veins are most superficial here!!

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29
esophageal varices ## Footnote 6 sxs 3 dx
sxs: **_1. hematemesis!!! over 50% stop bleeding spontaneously_** 2. melena 3. tachycardia 4. hypotension 5. syncope 6. jaundice DX: **1. emergent endoscopy** CBC BUN/creatine type and cross
30
esophageal varices ## Footnote 4 immediate tx options
1. immediate tx-stop bleeding because mortaltiy approaches 75% 2. visceral ligation- rubber band 3. sclerotherapy 4. balllon tamponade
31
mallory-weiss tear ## Footnote what is this? what does it occur from? who commonly seen in? MC location? 3 RF? 2 sxs?
linear mucosal tear in the distal esophagus or gastric cardia from forceful _vomiting_ or retching, causing _hematemesis_ commonly seen in _alcoholics_ ## Footnote **most common location: gastroesophageal junction** **RF:** **alcholic** **hiatial hernia** **eating disorder BULEMIA** **SXS:** 1. multiple bouts of vomiting and retching followed by **_PAINLESS HEMATEMESIS_** 2. abdominal pain \*\*\*keep in mind the bleeding usually stops spointaneously as teh condition is usually benign\*\*
33
mallory weiss tear ## Footnote 1 dx? 2 tx?
DX: ENDOSCOPY TX: 1. **stabliazation** - transfusion/gastric lavage if needed 2. **control bleeding via endoscopy** \*\*keep in mind most bleeding stops spontaneously and condition is usually benign\*\*
34
esophageal ring ## Footnote what is this? sxs? dx? 1 tx?
ring of tissue located at the _gastroesophageal_ junction called **_schatzkis ring_** sxs: 1. dysphagia with **_foods, but not typically liquds_** DX: barium esophagram TX: mechanical dilation with balloon
35
in mallory weise syndrome what is somethign you want to do before releasing someone from hospital?
obtain occult negative stool to insure not bleeding still or hemmoraging
36
systemic scleroderma ## Footnote what is this? what are the **5 common presentations**? what is the **#1 think you worry about in this?** what test do you do in the lab? what are the treatments?
thickening and harderning of the skin **via collagen deposition** 1. raynauds (75%) 2. vascular changes in nail bed 3. GI dysmotility "watermelon stomache" 4. puffy hands 5. fixed face \*\*\*\*\*WORRY ABOUT PULMONARY FIBROSIS AND ACUTE RENAL FAILURE\*\*\*\*\*\*\* DX: ANA-SPECKLED Tx: treat system effected renal-ACE inhibitors raynauds-calcium channel blockers Gi: promotility lungs: cyclophosphamide
37
CREST Syndrome what is the pneumonic to remember the symptoms and what do you need to monitor annually in these patients?
LIMITED SCLERODERMA **C- calcinosis** of joints leading to puffy hands **R- raynauds** **E-Esophageal dysmotility** **S-sclerodactyly** of _MCPs_ **T: telangiectasis** \*\*complication=pulmonary hypertension so need to get _annual PFT/DLCO to make sure no lung fibrosis_\*\* Tx: symptoms
40
stomach neoplasms ## Footnote where do these occur? appearance? 4 sxs? 3 dx? 1 tx
occur in antrum, MC in lesser curvature **_bulky, irregularly shaped_** **_firm, jagged edges_** usually asymptomatic till late disease early detection is therefore difficult DX: 1. barium swallow xray 2. endoscopic studies with bx 3. cytologic (screening in atrophic gastritis/polyps) TX: **_surgery-radical subtotal gastrectomy TOC_**
41
what are 6 RF for stomach neoplasms?
1. genetic predisposition 2. carcinogenic diet _smoked food/perserved food_ 3. autoimmune gastritis _increased inflammation_ 4. gastric adenomas 5. polyps 6. h. pylori, cofactor for some
42
Peptic ulcer disease ## Footnote what this this? 2 causes? 1 3 size?
**break in the gastric or duodenal mucosa that _extends through the muscularis mucosa_ that comes from** **1. _impaired normal mucosal defense factors_** NSAIDS **_2. defense factors overwhelmed by aggressive luminal factors_** acid pepsin infection greater than 5 mm in diameter
44
what are the 5 common causes of PUD?
1. NSAIDS 2. H. pylori 3. idiopathic 4. hypersecretory states 5. smoking
45
3 locations of PUD? which one is most common? how long do they take to heel? what do you need to keep in mind that is very important depending on location?
1. duodenal ## Footnote a. **_MOST COMMON LOCATION!!_** b. 90% heal in 4 weeks 2. pylorus 3. gastric \*\*CAN BE MALIGNANT\*\* \*\*must get bx at endoscopy time\*\* a. take longer to heal 8 weeks! b. increased length of tx
46
peptic ulcer disease NSAIDS cause? why? 4 RF? 2 tx? length of time?
caused by long term NSAID use esp nonselective COX1 and COX2 blockers _COX1 decreases prostaglandins_ which have a _protective effect on gastric mucosa_, it the lack of this **_impairs gastric mucous and HCO3 secretion_** \*\*this is why COX2 selective are better option since decrease risk of bleeding\*\* RF: 1. ASA 2. corticosteroids 3. over 60 TX: **_1. PPI_** or H2 \*\*\*4 weeks duodenal\*\*\* \*\*\*8 weeks gastric\*\*\* **_2. D/C NSAID_**
47
peptic ulcer disease: h. pylori KEY? characteristic? acute/chronic characteristics? what is key about this?!
**_nesscary cofactor for 75-90% of duodenal/gastric ulcers_** characteristics: PRODUCE UREASE ACUTE: a. infectious "gastroenteritis" CHRONIC: a. **_ASYMPTOMATIC_** b. DIFFUSE SUPERFICIAL MUCOSAL INFLMMATION WITH POLYPS \*\*ERRADIACATION IS ESSENTIAL OTHERWISE _85% WILL RECURR!!!!!\*\*_
48
what is a RF for all ulcers?
smoking!
49
explain te patho of stomach ulcers caused by h. pylori?
1. infection in body​ 2. causes **gastritis and chronic inflamation that overwhelms immune system** 3. causes **mucosal breakdown** 4. creates gastric ulcer
50
PEPTIC ULCER DISEASE ## Footnote 2 sxs 3 dx when do you use each? 1 think must do?
SXS 1. _epigastric like pain "hunger like" in 80-90%_ 2. _50% have relief by eating antacids within 2-4 hours_ \*\*physical exam is often unremarkable so need to watch for changes in pattern, indicating perforation or penetration\*\* DX: 1. endoscopy EDG TOC! allow so for visulaization and also bx!! 2. fecal antigen test (noninvasive) 3. c-urear breath test (noninvasive) \*\*\*\*OPTIONS 2 AND THREE AT THE TOC FOR ACTIVE PUD AND PROOF OF ERADICATION\*\*\* _MUST D/C PPI 7-14 DAYS PRIOR OR MAY GET FALSE POSITIVIVE!_
51
peptic ulcer disease: ## Footnote Treatment for H. pylori what is the tx regimen? what must you do after tx and when?
2/3 abx, PPI, +/- bismuth ## Footnote **_1. amoxicillin_** 1 g BID **_2. clarithromycin_** 500 mg BID **_3. HIGH DOSE 40 mg PPI_** BID \*\*\*no reason shouldn't use quadrople therapy see in this pic\*\* KNOW BOTH \*\*must confirm eradication with C-urea breath test or fecal antigen test 4 weeks post abx 2 weeks post PPI\*\*\*
52
peptic ulcer disease tx without h. pylori 2 3 for first 1 second
1. _antisecretory agents_ A.**_PPIs_** 1st DOC-inhibit 90% acid secretion **_ompreazole_** **_lansoprazole_** B. H2-inhibit histamine mediated secertion C. OTC anti-secretory 2. _mucosal defense agents_ 2nd line can be used as adjunct for _symptom relief_ **sacralfate, busmuth**
54
peptic ulcer disease: post H. pylori tx tx 2 considerations
**DUODENAL f still large or bleeding post tx:** _continue PPI for 2-4 weeks_ **GASTRIC if large ot blleding post tx:** _continue PPI for 4-6 weeks_
55
in reccurent ulcers what must you do!?
rule out H. pylori and NSAID use
56
peptic ulcer disease: ## Footnote COMPLICATIONS PENETRATION/PERFORATION results in? 2 sxs? tx?
results in chemical peritonitis a. severe generalized abdominal pain b. _rigid abdominal rebound_ _TX:_ _1. laproscopic perforation closure_ _2. increased RX TX_
57
peptic ulcer disease: refractory ulcers what is this caused by? 3 contributing factors
uncommon, contributed to non compliance with medication Contirbutory factors: 1. cigs 2. NSAIDS 3. failutre to eradicate H. pylori! MUST DO THIS
58
explain the pathophys of pacreatitis? what are 2 theories that cause this?
1. inflammation of the pancreas causes damage to the **_acrinar cells_** 2. the inactive proenzymes like _trysinogen_ are activated early while still in the pancreas 3. early activated _lipases_ disolve the fat 4. so the _pancreatic enzymes_ start to DIGEST THE PANCREASE "EATS ITSELF" theories: 1. obstruction of the pancreatic duct due to stones 2. failure of the two parts of the pacreas to fully join during development _pancreatic divism_
59
acute pancreatitis ## Footnote what are 2 MC causes? account for what? 6 others?
causes: 1. gallstones 45%-**MC** 2. alcohol 35% \*\*these two are most common and make up 80% of cases\*\* other causes: trauma drugs (iatrogenic) obstruction (tumors) infections (mumps) metabolic (hyperlipidemia) toxins (methyl alcohol, scorpion stings) \*\*MOST RECOVER AND HAVE NORMAL FUNCTING PANCREASE\*\*
60
when dxing pancreatitis and looking at labwork, what test is most effective?
lipase (this is better than amylase)
61
acute pancreatitis ## Footnote 5 labs tests? TOC for dx?
LAB TESTS: **_elevated cbc_** (infection) **_elevated lipase_** (pancreas) **_elevated LFT_** **_elevated glucose_** **_decreased calcium_** TEST OF CHOICE FOR DX: **_CT SCAN!!!_** scored A-E, A is good, E is bad
62
acute pancreatitis ## Footnote 6 sxs where is pain? severity? what makes worse/better? pain with...? two key signs you dont want to miss?
1. **_epigastric radiates to back_** 2. **_billiary colic PERSISTS DOESN"T GO AWAY_** 3. **_worse SUPINE, BETTER LEANING FORWARD_** 4. **_PAINFUL INSPIRATION, SHALLOW BREATHS_** 5. _TACHYCARDIA_ **_6. hemmoragic pancreatitis_** _cullens sign_: periumbical ecchymosis _grey tuner's sign:_ flank eccymosis
64
acute pancreatitis ## Footnote 5 labs tests? TOC for dx?
LAB TESTS: **_elevated cbc_** (infection) **_elevated lipase_** (pancreas) **_elevated LFT_** **_elevated glucose_** **_decreased calcium_** TEST OF CHOICE FOR DX: **_CT SCAN!!!_** scored A-E, A is good, E is bad
65
chronic pancreatitis pathophysiology ## Footnote what is this? what should you think about when thinking of this? what happens?
inflammatory disease of the pancreas **_irreversible**_ _**changes occur_** **_can lead to permanent loss of function_** HINT: think necrosis fibrosis theory of alcoholic pancreatitis alcohol to tissue damage to fibrosis to partial obstruction
66
chronic pancreatitis ## Footnote what is the MC cause of this? 3 others? NOT CAUSED BY WHAT? what can this lead to?
1. alcohol cause #1!! \*\*\*THIS IS **_NOT_** CAUSED BY GALLSTONES LIKE ACUTE\*\* 2. **_obstructive causes of spincter of oddi by neoplasms_** 3. **_malnuitirion_** 4. metabolic chronic pain leads to opoid addiction! keep this in mind
67
chronic pancreatitis 4 sxs?
sxs: 1. **_epigastric abdominal pain_** that radiates to the **_LEFT_** 2. insufficiency of pancreatic function leads to **_a. steatorhhea_** damages decreases lipase **_b. diabetes_** once islets damaged **3. asymptomatic and found incidently**
68
chronic pancreatitis ## Footnote 5 tx options most important!! 2 drugs?
1. _stop the alcoho_l!! 2. controls sxs a. **pain control** **b. prancreatic enzyme supplements _viokase and pancrease_** 3. endoscopic duct decompression 4. surgical draingage of duct 5. celiac plexsus nerve block
69
acute pancreatitis ## Footnote 6 tx options? what is the process dependent on?
mostly supportive ## Footnote a. NPO 48-72 hours **_NO ALCOHOL_** **_b. ERCP if presense of stone**_ _**on CT scan_** b. maintain hydration c. pain control d. NG tube in extreme e. abx if infectious f. incision and drainage if infected/necrosis
70
chronic pancreatitis ## Footnote 4 dx options fat stranding
1. amylase/lipase **_NORMAL_** ## Footnote body gets used to working under these circumstances 2. _secretin stimulation test "gold standard" for **early** chronic pancreatitis dx_ 3. plain xray films QUICK AND CHEAP-see calcifications 4. CT SCAN-better at seeing calcifications but $$/rad _"arrowhead and fat stranding"_
71
what are the two criteria used to identify the mortality with pancreatitis?
1. Ranson's criteria ## Footnote _Take home: higher numbers means more severe disease and increased risk of death_ -measured at time of admission and during first 48 hours **6+=50% mortality** 2. APACHE II score \*\*typically impatient ICU use\*\* over **_8_** is severe!!!
72
pancreatic cancer ## Footnote what are thet wo tumor markers? survival? 1 RF?
tumor markers: 1. CA19-9 85% 2. CEA 40-45% 5 year survival is only 4% _really bad_ only RF: _chronic pancreatitis_
73
pancreatic cancer ## Footnote what two lab findings supposrt this? 3 tx options?
LABS: **_1. elevated direct bilirubin_** **_2. elevated alkaline phosphatase_** (significantly elevated in cancer) **_TX:_** **_1. chemo_**-poor respinse only reduces size to buy little time 2. _whipple surgery_-only at cancer specialties 3. **_pallaitive care_**
74
acute cholecystitis ## Footnote 2 dx tests? when to use? 2 labs?
TOC #1: **_US_** ## Footnote find gallstones and _wall thickening over **3 mm**_ TOC #2: **_HIDA nuclear med scan_** (cholescintigraphy) GOLD STANDARD and _BEST TEST_ \*\*\*\*not usually used since it is $$$$$$$, so US becomes TOC\*\*\*\*\*\* Two elevated labs: **_elevated gamma-glutamyl transpeptidase_** **_elevated bilirubin_**
75
what are the four RF for cholithiasis?
1. over 40 2. obesity (or rapid weight loss) 3. female/pregnant 4. native american **"FEMALE, FAT, FORTY, FERTIL" 4, F's**
76
choledocholithiasis ## Footnote where is the stone? where does it come from? where is pt? sxs? 4
stone in the **_COMMON BILE DUCT_** usually migrate from the gallbladder patient very sick and likely in ICU!! compared to cholelithiasis sxs: asymptomatic in 30-40% **_BILLARY COLIC_** **_jaundice, pancreatitis_**
77
acute cholelithiasis ## Footnote what are you 3 tx options and who are they appropriate for?
1. cholecystectomy-MOST COMMON "it hurts ## Footnote 2. leave in if doesn't hurt _UNLESS_ high risk to keep in a. diabetics b. sickle cell c. Native americans with _calfieiced "porcelain" stone_ 3. dissolve cholesterol stones with _actigal, urodeoxycholic acid_ but $$$
78
pancreatic cancer ## Footnote 4 sxs? toc? 1
sxs: 1. _painless **jaundice** is PC until prove otherwise_ 2. **_virchows node_-**supraclavicular node 3. **_trouseaus signs- recurring superficial thrombophlebitis_**can be anywhere 4. weight loss TOC: _CT scan dual phase helical_
79
acute cholecystitis ## Footnote what happens in this? what is most likely to cause this? leads to 3 things? possible worst case? 2 _key_ sxs?
the **_cystic duct**_ becomes blocked _**most commonly from gallstone!_** less common: cancer, sludge, infection blockage causes distention and edema that cauess _ischemia, necrosis, perforation_ and possible _generalized sepsis_ SXS 1. RUQ/epigastric pain _radiate to shoulder/scapula_ 2. _murphys sign_ (tenderness and pt stops inspiration on palpation)
80
acute cholycystitis ## Footnote TXOC? 3 others?
TreatOT: TAKE IT OUT!! MOST COMMON!! via _laproscopic cholecystectomy_ 2. leave in if very mild 3. drain it if patient too sick 4. abx if elevated WBC
81
cholelithiasis two types of stones? percentage? what do they look like?
**1. cholesterol stones** MC-75% of stones!! don't show up on xray 2. **calcium bilirubinate/ca salts** 25% of stones pigmented black/brown sludge stones
82
acute cholithiasis ## Footnote what do you need to keep in mind about sxs? how do they present? 3 dx TOC? what do you need to keep in mind?
_asymptomatic in 50-60%_ ## Footnote symptomatic patients: **biliary collic with _RUQ pain/epigastric areas_** **_refers to back, scapula or R shoulder_** DX: TOC: transabdominal US **_shows stone without wall thickening_** \*\*_keep in mind not great for stones in common bile duct\*\*_
83
choledolithiasis ## Footnote what are the two dx/tx options? what must you keep in mind?
1. MRCP magnetic resonance cholangiopacreatogprahy ONLY DX ## Footnote 2. ERCP-endoscopic retrograde cholangioancreatography DX **_AND TX so GOLD STANDARD!!_** \*\*\*\*keep in mind contraindicated in pancreatitis/cholecystomy\*\*\*
84
celiac disease ## Footnote what type of condition is this? what is the patho of this and the specific component? nickname?
autoimmune dx of _SI_ ## Footnote introlerance to **_gluten and the alpha-gliadin_** gluten triggers immune response in turn causing damage to the small intestine causes _nuitritional deficits secondary to absorption issues_ "celiac sprue"
85
celiac disease ## Footnote what are 6 sxs that come with this? explaination of the last?
1. unintended weight loss ## Footnote 2. persistently underweight 3. sxs of poor nuitrition 4. "failure to thrive in child" 5. diarreah 6. _dermatitis herpetiformis_ a. ***intense itching*** ***b. blisterning rashes*** ***c. 10-15% of patients***
87
celiac disease ## Footnote what are the 3 dx options of this? key thing to remeber?
1. anti-tissue transglutaminase antibodies OR anti-endomysium IgA antibodies ## Footnote 2. _bx if small intestine_ and blood + for antibody \*\*\*\*if they have dermatitis herpetiform with + antibody skin bx, THEN NO NEED FOR INTESTINAL BX\*\*\*
88
celiac disease ## Footnote what are the 2 tx for this? what about screening?
1. gluten free diet ## Footnote - wheat - rye - barley 2. abx for dermatitis herpetiformis \*\*\*make sure to screen if family hx using blood test for autoantibodies\*\*
89
diverticula ## Footnote what are these? how are they formed?
sac-like protrusions in the colonic wall **blood vessels penetrate the mucosal wall** **internal layers penetrate through weak areas creating diverticula**
90
diverticulosis ## Footnote what is this? where does it most commonly occur? what is important to know about this? presentation? 2 things to avoid?
condition of having divericula typically asymptomatic MC in SIGMOID COLON, _account for 50% of all lower GI bleeds, bright red blood in rectum earliest finding MOST COMMON_ diet restricted in seeds, strawberries
91
diverticulitis ## Footnote what is this? 3 sxs? 2 tests?
inflammation of the pocuhes 1. severe **_LLQ_** pain 2. change in bowel habit 3. constapation Tests: 1. **_CT TOC with IV and oral contrast_** 2. WBCs 3. barium enema 4. colonoscopy
92
who is diverticulosa most common in? ## Footnote 2 percents?
western/industerialized societies ## Footnote 30% by 60 65% have by age 85
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what are 3 RF for diverticulosa?
1. connective tissue disorders 2. low fiber diet 3. too little exercise
94
Inflammatory bowel disease crohns disease where are the lesions? how deep are lesions? where is the pain? 3 things that can occur as complications? 4 things that are common? 3 other things it can effect? bowel appearance?
1. legions mouth to anus; spread out with healthy tissue between _2. transmural_ **_3. RLQ pain MC_** 4. fistulas, abscesses, fibrotic stricutres 5. bleeding common 6. weight loss common 7. obstruction common 8. perianal disease common 8. can effect skin eyes joints liver 9. _large volume_ diarreah and mucous (trash bag)
95
what are the two conditions that make up inflammatory bowel disease?
1. crohns disease 2. ulcerative colitis
97
what 2 are tests you want to do to look for crohns?
1. anti-saccharomyces cervisial (ASCA)- 44% of crohns are pos ## Footnote 2. _colonoscopy TOC_
98
what are the 4 tx options for crohns?
1. 5-aminosalcyclics (5-ASA) ## Footnote **-mesalamine** **-sulfasalazine** 2. corticosteroids 3. cimzia-certolizumab 4. humira-adalmumab \*\*surgery doesn't work since it involves the entire GI tract\*\*
99
which is more common crohns or ulcercerative colitis?
ulcerative colits 3x more likely
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ulcerative colitis ## Footnote where is this? pain presents? what is most common and worse? what does person have increased? what might they develop? describe lesions and how deep? what does the colon look like on colonscopy? what are 3 things aren't present?
1. primarily localized in _colon_ **_2. LLQ_** 3**_. bleeding from rectum_** **_is most common_** 3. _urgency need of BM_ _4. potenital anemia due to blood loss_ 4. lesions are continuous starting at the rectum and in mucosa only 5. _colon wall thin with continuous inflammation_ 6. no granulomas (weight loss/obstruction very rare with this)
102
what do you use to dx ulcerative collitis?
colonoscopy
103
what are the 3 tx options for ulcerative collitis?
1. 5-ASA - sulfasalzine - mesalamine 2. corticosteroids 3. **_colonectomy CURE best choice_** removal of colon
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irritable bowel syndrome ## Footnote what is this? who most common in? age? pathogenIsis? 3 **causes**
**_dx of exclusion, no other cause_** FUNCTIONAL BOWEL WITH MUCOSAL INFLAMMATION women more than men presents before age **_45_** **_1. abnormal motiltiy_** _2. **visceral hypersensitivity**_ lower visceral pain threshold **_3. psychosocial interaction_**-emotional stress
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irritable bowel syndrome ## Footnote 3 tx options? 4 medications tx options
1. pt education and behavior/ emotional support ## Footnote 2. dietary therapy 3. pharm a. antispasmotics b. antidiarreals c. psychotropic d. serotonin receptor agonists
106
colorectal cancer ## Footnote what are 3 risk factors?
1. genetic predisposition 2. presence of _adenomatous polyps)_ _3. diets high in fats and refined carbs that are low in plant fiber \*industerialized world\*_
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colonrectal cancer ## Footnote 4 sxs 2 key dx 3 others
sxs: 1. **_colic type pain_** **_2. anorexia_** **_3. thin appeareance_** **_4. pallior/anemia_** dx: 1. xray: _classic apple core/npaking ring appearance_ 2. endoscopy with bx 3. iron deficient anemia 4. hypoalbuminemia 5. occult blood in stool
109
rectal polyps what are these? why is it improtant to know type? 1 type concerned about? why? 2 shapes?
small outcropping that grows in the rectum or colon \*\*need to deterine the type since some are associated with carcinoma\*\* _adenomas_ **_PREMALIGNANT POLYP_** **_PRECURSOR TO COLORECTAL CANCER_** **_sessile_**: flat and intimately attacted to mucosa **_peduclated_**: round and attached be stalk
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what does colonrectal cancer come from?
the progression of adenomatous polyp into malgnancy
112
what are the 3 types of adenoma polys? which is most common? which has higest risk of cancer? risk of cancer and prevalance for each?
1. tubular adenoma ## Footnote **_MOST COMMON TYPE 65-80%_** pedunculated, little cancer risk 2. tubulovillous adenoma 10-25% of adenomas 22% risk of cancer 3. **_vilous adenomas_** **_40% RISK OF CANCER_** only 5-10% so least common but most deadly
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what is the least common but the most prognostic for cancer of the adenoma polyps?
vilous adenoma \*think vilian=evil\*
114
what are the two tests that are reccomended annually to screen for colorectal cancer?
1. guiac fecal occult blood test (gFOBT) ## Footnote 2. immunochemical-based fecal occult blood test (iFBT)
115
what are the 3 screening tests that are reccomended for colorectal cancer? which is most reccomended? what age do you start?
age 50 to less than 10 years life expectancy ## Footnote 1. **_optical colonscopy_**-10 years 2. flexible sigmoidoscopy-5 years 3. CT colonography-10 years
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lactose intolerance ## Footnote what is this? 4 populations common in? 5 sxs? key 1?
**_difficulty digesting lactose from lack of lactulase_** MOST COMMON IN: 1. AFRICAN AMERICANS 2. HISPANIC/LATINO 3. ASIAN AMERICANS 4. NATIVE AMERICANS SXS: 1. bloating 2. pain 3. increase passage of gas 4. diarrhea and nausea **_5. 2 hours post consumption of milk or dairy_**
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lactose intolerance ## Footnote 1 dx? 1 tx?
dx: ## Footnote hydrogen breath test tx: dietary avoidance
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what is the dentate line? ## Footnote senstion?
divides the rectal mucosa from the squamous epithelium in the canal ## Footnote above in anorectal canal: INSENSATE (no pain) below in _andoderm_: _SENSATE AND PAINFUL!!_
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anal fissure ## Footnote what is this? where do these occur? signicant stat? 2 causes?
**Tear in the andoderm of rectal canal** 90% are posterior along midline **_most common cause of painful rectal bleeding_** causes: 1. passage or hard stool 2. prolonged diarreah
122
a kid with tearing pain with bowel movements and bright red blood when he or she whipes with toitlet paper shuld mak eyou think of...
ANAL FISSURE!!
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anal fissure ## Footnote 3 sxs? what not to do?
sxs: 1. "tearing" pain with BM since below dentate line 2. hematochezia during BM 3. SPREAD BUTTOCKS to examine \*\*NEVER DO RECTAL EXAM, TOO PAINFUL!..and cruel\*\*
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anal fissure ## Footnote 2 tx categories 4 1 (also, who not to do in)
1. 90% heal without tx ## Footnote a. bulk agents b. stool softeners c. sitz baths d. hydrocortizone ointment Anusol 2. _surgical-lateral internal anal spincterotomy GOLD STANDARD if failure conservative_ \*\*can't do if patient incontinent\*\*
125
internal hemmoroids ## Footnote 4 key sxs with these!
above the denate line!! veins surrounded by mucosa 1. **_PAINLESS, above denate_** **_2. bright red bleeding with defecation_** **_3. may prolapse and be palpable on DRE_** **_4. bleed_**
126
what are the stages used to define internal hemmoroids?
**_first_**-bleed **_second-_**bleed and prolapsed, spontanously reduce **_third_**-bleed, prolapse, and require manual reduction **_fourth degree_**-bleed/incarcerate
127
explain the pathophysiology of hemmoroids? 5
1. anal canal is lined with "cushions" that are **_vascualr and connective tissue and make the hemmorrhoidal plexsus_** 2. exist in 3 columns 3. **_cushions encorge during defecation_** to profect the anal canal from abrasion 4. when venous engorgement is increased with conditions like pregnancy, straining, and increased abdominal pressure it **prompts production of abnormal hemorrhoidal tissue** which can be symptomatic
128
external hemmoroids ## Footnote whe do they occur/what are they covered in? 3 sxs dx method? 1 tx?
below the dentate line and covered with andoderm 1. usually don't **_bleed_** 2. may **_thrombose_** which is VERY painful 3. cause **_pain, discomfort and most severe at time of defecation_** dx "either present or not" tx: 1. excision of outside of the mucotaneous junction leaving wound open **_hemroidectomy_**
129
what are 6 RF for hemmoroids?
constapation straining at stool pregnancy obesity chronic liver disease portal HTN
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Internal hemmoroid tx categories ## Footnote 5 2
1-2 degree: ## Footnote a. fiber b. water c. stool softner d. anusol hydrocortisone e. numbing agent nupercainal ointment 3-4 degree: a. SURGICAL b. EXCESIONALHEMMOIROIDECTOMY
133
acute hepatitis ## Footnote what is the mortalty? 3 most common causes? what are 4 sxs associated with this? **_KEY!!_**
**mortality 40-80%** sudden onset deterioration of hepatocyte function causing coagulopathy 1. tylenol 45% of cases 2. alcohol and drugs 3. heptitis A and B sxs: **_1. jaundice_** **_2. elevated transmidates AST/ALT_** **_3. coagulopathy INR over 1.5_** **_4. encepalopathy-alteration in mental status due to evelated ammonia_**
134
viral infections account for what percent of hepatitis?
50% of all cases hep a b c d e account for 95% of thse
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hepatitis A ## Footnote precentage? virus type? incubation? transmission route? (3)
**65% of all cases** **RNA**occurs exclusively in liver cells **incubates 2-6 wks** transmission **_FECAL ORAL_** 1. travel 2. contanimated food and water 3. close contact with infected individuals
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hepatitis A ## Footnote sxs? 1 (time) 7 after sxs
SXS 1. prodrome, flu like _most infectious here 12-21 days_ _2. icteric phase_ **1. dark urine appeares first (bilrubinuria)** **2. pale stool follows** **3. jaundice 70-85%** **4. abdominal RUQ pain 40%** **5. _prurits, indicates bilirubin_** 6. arthralgias 7. hepatomegally
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hepatitis A ## Footnote 3 dx findings tx
DX: 1. anti-hep A IGM and IGG 2. LFTS - increase AST/ALT over 1000 - increased bilirubin 5-10 x TX: selflimiting supportive
138
what are 5 prevention methods for hepatitis A?
improvement in hygiene and sanitation cooking food avoidance of water foods and endemic areas avoidance of raw shellfish immunization
139
who gets vaccinated for hep A? 4
Harvix **travelers** **miliary personnel** **lab workers** **immunocomprimised**
140
when you think of raw shellfish think..
hep A!
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hepatitis B ## Footnote what type of virus? what percent of people have it and who? 3 transmission pathways? **_KEEY THING TO KNOW ABOUT THIS_**
DNA virus 1/3 of population infected, majority immigrants or 1st gen transmission: 1. perianatal 2. sexual 3. blood containing med equiment **_\*\*\*\*\*\*\*causes 80% of hepatocellular carcinoma=fatal!!!!\*\*\*\*\*_**
142
what type of hepatitis can lead to hepatocellular carcinoma?
HEPATITIS B!! vaccines for this mandated
143
what are the categories of hepatitis B? 3
**immunity** - vaccination - natural infection **actue infection** **chronic infection** - active - chronic
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\*\*\*what are the **_2_** test results you want to keep in mind when looking at hepatits infection\*\*\*
**_hepatitis B surface antibody (HBsAB)=_**IMMUNITY--ONLY PRESENT IN VACCINATED PEOPLE ## Footnote **_hepatitis B envelope antigen (HBeAg)_**: NEEDS TREATMENT, current infection
146
surface= core= envelope=
surface=**immunity (vaccine or exposure)** core=**exposed to virus** envelope=**present infection with active replication**
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acute hepatitis B ## Footnote what is the breadown for how they present? (%) 1 key dx? 2 supportive? tx2? why?
70% are subclinical (no jaundice or aniteric) 30% get icteric hepatitis dx **_1. HBcIGM for dx_** 2. elevated AST/ALT 3. elevated bilirubin TX: 1. supportive \*\*many will seroconvert to HBsAB and HBeAB meaning they develop immunity on their own!!\*\* 2. high calorie diet
148
chronic hepatitis B ## Footnote three phases of this? 3 tx options and length of time?
initial phase: **positive HBeAG** immune clearance phase **HBsAg, HBeAG** **elevated ALT** **inflammation on liver bx** inactive carrier tx: 1. tenofovir DOC 2. entecavir DOC \*\*\*both of these are lifelong drugs!!!\*\*\* 3. interferone alpha 6 months
149
hepatitis prevention and vaccination ## Footnote 2
1. recombinant hepatitis vaccine 2. hep B immune globulin (exposued)
150
what is key to know about _hepatitis D_? transmission?
RNA coinfection with **_HEP BE IS REQUIRED!!!_** **_HBsAg_** transmission: sexual contact
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hepatitis C ## Footnote what is this? 3 RF/transmission? virus type? age?
**_most common chronic blood borne infection in the US_** ## Footnote 1. injection drug use/cocaine 2. sexual contact 3. transfusion RNA virus, 30-49 y/o
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\*\*what important people do you need to test for hepatitis C?\*\*
**_test everyone born between 1945 to 1965_**
153
what percent of people proceed to the chronic state? what are two things you are at increased risk for?
80% proceed to the chronic state HIGH RISK OF CIRRHOSIS AND HEPATOCELLULAR CARCINOMA
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hepatitis C ## Footnote 3 tx options? when do you start tx? 2 main options? how long is the tx?
1. supportive first since can clear on their own 2. avoid hepatotoxic drugs 3. \*\*most wait **_6 months_** for posisble clearance before starting antiviral therapy\*\* - harvoni (sofosbuvir/ledipasvir) - daklinza (daclatasvir) \*\*12-24 weeks tx depending tx naive and if cirrhosis\*\* \*\*some regimens still include ribaviran, but not all of them\*\* NO INTERFERON
155
what do you want to check when txing someone for hep C?
viral load after **_12 weeks_** to confirm cure
156
what is cool about treating hep C?
IT IS CURABLE!!! nearly 100!!!!! there is no vaccine and no post exposure immunoglobulin **_THEREFORE YOU WANT TO SCREEEN!!!_**
157
what is interesting about hep G?
if coinfected with HIV, helps reduce the HIV replication
158
cirrhosis ## Footnote what is this? 2 classifications?
**chronic end stage dxs of the liver marked by _degeneration of cells_ from inflammation resulting in _fibrous thickening of tissue_** 4 stages of fibrosis and cirrhosis is the last **_compensated_**: although fibrotic can still preform functions **_decompensated_**: fibrotic with loss of essential function
159
HEP E ## Footnote 2 places you find this? transmition _AT RISK POP?_
North Africa South Asian fecal oral self-limiting ***issues in pregnacy!!! EXTREMELY SEVERE!!!! esp in third trimester 20% mortality!!!!!! KEY***
161
cirrohosis ## Footnote 4 sxs of compensated? 7 sxs of decompensated?
_compensated sxs:_ ammenorreah impotence gynecomastica **_hematemesis as present features in 15-25% (esophageal varices)_** _decompenstated_: **1. spider angiomas** **2. muscle wasting** **3. palmar erythema** **4. dilated superficial veins of abdomen** **5. ascities** **6. portal HTN** **7. encepalopathy**
162
cirrohsis 5 labs 3 tests
LABS: low platelets **_prolonged PT_** moderate elevations enzymes **_elevated bilirubin_** **_low serum albumin_** **_1. abdominal US WITH DOPPLER_** - nodular appearing liver +/- hepatosplenomegaly 2. LIVER BX! TOC to confirm, determine staging
163
cirrhosis ## Footnote 5 tx
1. alcohol abstinence 2. vitamin supp 3. nuitrional supp 4. BB for portal HTN 5. _CURE IS TRANSPLANT_!!!
164
what MUST you do for someone with cirrhosis?
_**\*\*\*\*\*must screen for alpha fetal protein and imaging ever 6 months\*\*\***_
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hepatocellular carcinoma (HCC) ## Footnote what is this strongly associated with? 5 year survival? 3 sxs? 1 key 3 dx methods **one key think you want to order**
associated with **_cirrhosis_** ## Footnote 4-6 months from time of dx 5 year survival is 25% SXS: 1. _painless jaundice_ 2. weight loss 3. hepatomegaly dx 1. triple phase CT or MRI 2. **_percutaneous bx of lesions!!! TOC_** **_3. Alpha fetoprotein tumor marker is PATHOPNEUMONIC_**
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hepatocellular carcinoma ## Footnote 4 tx
1. surgical ressection 2. chemo 3. portal vein embolizations 4. _transplant_ if small and localized