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Rotation 2: IM Outpatient > GI Portion > Flashcards

Flashcards in GI Portion Deck (145):
1

gastroesophageal reflux disease

 

what is this?

population common in?

percent in US?

5 complications it can lead to

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

5. hiatial hernia

 

-

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3

GERD

what are 6 sxs?

1 thing to keep in mind about sxs?

1. heartburn, restrosternal and postprandial

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

worsens when laying down or recumbant

 

2. regurgitation (vomit burp)

spontaneous reflux of sour bitter gastric contents in mouth

3. dysphagia (discomfort)

cough at night from acid asipiraiton

4. reccurent pneumonia

5. sxs temp relieved with antacids

6. 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**

4

what is the pathway for txing GERD?

6

1. lifestyle adjustments

2. OTC antacids-2 weeks

3. H2 receptor antagonists

4. Proton pump inhibitors

**if these fail EDG**

5. prokinetics

6. surgical

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5

GERD

3 dx options

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

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

7

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

5

1. avoid eating 2-3 hours before bed

2. elevate head of bed

3. loose weight

4. avoid acidic food, chocolate, peppermint, ETOH, coffee

5. stop smoking

8

why is it important to treat GERD?

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

9

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

1. benadryl

2. lidocaine

3. maalox

10

what is the most common cause of esophagitits?

GERD, 50% of patients with GERD have esophagitits

11

esophagitits

 

what is this?

5 general causes?

4 sxs

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

 

12

esophagitis

herpes liabilis (HSV)

 

3 SXS?

2 DX? 

1 TX

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!!!

13

ESOPHAGITIS

VARICELLA-ZOSTER

 

 1 dx?

tx?

N/V fever chils

 

 

DX:

endoscopy: vesicles or confluent ulcers

 

Tx:

1. usually resolve spontaneously but can cause necrotizing esophagitits

2. ACYCLOVIR!!!!

14

esophagitis

CMV

 

who does this occur in?

characteristics of ulcer? 2

3 sxs? 

1 tx?

only occurs in immunocomprimised patients

 

CREEPING ULCER or can be GIANT ULCER

 

 

sxs:

odyniaphagia

persistent CP

hematememis

 

 

Tx:

IV GANCICLOVIR

15

esophagitis

candidia

 

who does it occur in?

3 complications?

1 dx?

1 tx?

occurs in immunocomprimised host

 

can cause complications:

1. bleeding

2. perforation

3. stricture

 

dx:

endoscopy: small yellowwhite raised plaques

 

tx: 

oral or IV fluconazole!!

16

barrett's esophagus

 

how does this occur? what hcanges?

what are they at increased risk for? how much?

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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

17

barettes esophagus

 

2 dx rules?

3 tx?

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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

18

esophageal cancer

 

what are the two types?

frequency?

prognisis?

who is more common?

 

 

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

19

esophageal cancer:

adenocarcinoma

 

where do you find this?

4 most important RF?

2 protective

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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)

21

esophageal cancer:

squamous cell carcinoma

 

 

prevalence?

location?

4 RF?

key point to remember?

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***

22

esophageal cancers

 

sxs

1 early

3 late

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***

23

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

when the lumen is less than 13 mm

24

esophageal cancer

 

2 DX

2 STAGE

dx:

1. barium studies

2. endoscopy

 

Staging:

1. CT OF CHEST AND UPPER ABDOMENT

2. PET SCAN

25

where are adenocarcinomas and squamous cell esophageal cancers found?

adenocarcinoma: lower 1/3

 

squamous: middle esophagus

26

esophageal varices

 

what is this?

what causes this?

mortaltiy rate? 

MOST COMMON CAUSE?

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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

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

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

29

esophageal varices

 

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

 

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

 

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

 

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**

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33

mallory weiss tear

 

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

 

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

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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

 

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

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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

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40

stomach neoplasms

 

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

 

 

what this this?

2 causes?

1

3

size?

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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

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

 

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:

Treatment for H. pylori 

what is the tx regimen? 

what must you do after tx and when?

2/3 abx, PPI, +/- bismuth

 

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***

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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:

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

 

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 

 

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

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

 

 

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64

acute pancreatitis 

 

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

 

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

 

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

 

5 tx options

most important!!

2 drugs?

1. stop the alcohol!!

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

 

6 tx options?

what is the process dependent on?

mostly supportive

 

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

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70

chronic pancreatitis

 

4 dx options

fat stranding

1. amylase/lipase NORMAL

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"

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71

what are the two criteria used to identify the mortality with pancreatitis?

1. Ranson's criteria

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

 

 

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

 

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

 

2 dx tests? when to use?

2 labs?

TOC #1: US 

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

 

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

 

what are you 3 tx options and who are they appropriate for?

1. cholecystectomy-MOST COMMON "it hurts

 

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

 

4 sxs?

toc? 1

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sxs:

1. painless jaundice is PC until prove otherwise

2. virchows node-supraclavicular node

3. trouseaus signs- recurring superficial thrombophlebitiscan be anywhere

4. weight loss

 

 

TOC:  CT scan dual phase helical

 

 

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79

acute cholecystitis

 

what happens in this?

what is most likely to cause this?

leads to 3 things? possible worst case?

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)

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80

acute cholycystitis

 

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

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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

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82

acute cholithiasis

 

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%

 

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**

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83

choledolithiasis

 

what are the two dx/tx options?

what must you keep in mind?

1. MRCP magnetic resonance cholangiopacreatogprahy ONLY DX

 

2. ERCP-endoscopic retrograde cholangioancreatography DX AND TX so GOLD STANDARD!!

****keep in mind contraindicated in pancreatitis/cholecystomy***

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84

celiac disease

 

what type of condition is this?

what is the patho of this and the specific component?

nickname?

autoimmune dx of SI

 

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

 

what are 6 sxs that come with this? 

explaination of the last?

1. unintended weight loss

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

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87

celiac disease

 

what are the 3 dx options of this? 

key thing to remeber?

1. anti-tissue transglutaminase antibodies OR anti-endomysium IgA antibodies

 

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

 

what are the 2 tx for this?

what about screening?

1. gluten free diet

-wheat

-rye

-barley

2. abx for dermatitis herpetiformis

 

 

***make sure to screen if family hx using blood test for autoantibodies**

89

diverticula

 

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

 

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

 

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?

 

2 percents?

western/industerialized societies

 

30% by 60

65% have by age 85

 

93

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)

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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

 

2. colonoscopy TOC

98

what are the 4 tx options for crohns?

1. 5-aminosalcyclics (5-ASA)

-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

100

ulcerative colitis

 

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)

 

 

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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

104

irritable bowel syndrome

 

 

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

 

 

 

105

irritable bowel syndrome

 

3 tx options?

4 medications tx options

1. pt education and behavior/ emotional support

2. dietary therapy

3. pharm

a. antispasmotics

b. antidiarreals

c. psychotropic

d. serotonin receptor agonists

106

colorectal cancer

 

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*

107

colonrectal cancer

 

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

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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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110

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

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

 

 

113

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)

 

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

 

1. optical colonscopy-10 years

2. flexible sigmoidoscopy-5 years

3.CT colonography-10 years

116

lactose intolerance

 

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

117

lactose intolerance

 

1 dx?

1 tx?

dx:

hydrogen breath test

 

tx:

dietary avoidance

118

what is the dentate line? 

senstion?

Q image thumb

divides the rectal mucosa from the squamous epithelium in the canal

 

above in anorectal canal: INSENSATE (no pain)

 

below in andoderm:  SENSATE AND PAINFUL!!

119

anal fissure

 

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

 

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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!!

123

anal fissure

 

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**

124

anal fissure

 

2 tx categories

4

1 (also, who not to do in)

1. 90% heal without tx

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

 

4 key sxs with these!

Q image thumb

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

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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

 

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

 

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129

what are 6 RF for hemmoroids?

constapation

straining at stool

pregnancy

obesity

chronic liver disease

portal HTN

132

Internal hemmoroid tx categories

5

2

 

1-2 degree:

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

 

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

135

hepatitis A

 

 

precentage?

virus type?

incubation?

transmission route? (3)

65% of all cases

RNAoccurs exclusively in liver cells

incubates 2-6 wks

 

transmission FECAL ORAL

1. travel

2. contanimated food and water

3. close contact with infected individuals

136

hepatitis A

 

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

 

137

hepatitis A

 

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!

141

hepatitis B

 

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

144

***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

 

 

hepatitis B envelope antigen (HBeAg): NEEDS TREATMENT, current infection

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146

surface=

core=

envelope=

surface=immunity (vaccine or exposure)

core=exposed to virus

envelope=present infection with active replication

147

acute hepatitis B

 

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

 

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

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

151

hepatitis C

 

what is this?

3 RF/transmission?

virus  type?

age?

 

most common chronic blood borne infection in the US

 

1. injection drug use/cocaine

2. sexual contact

3. transfusion

 

RNA virus, 30-49 y/o

152

**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

154

hepatitis C

 

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

 

what is this?

2 classifications?

Q image thumb

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

 

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

 

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

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***

165

hepatocellular carcinoma (HCC)

 

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

 

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

 

166

hepatocellular carcinoma

 

4 tx

1. surgical ressection

2. chemo

3. portal vein embolizations

4. transplant if small and localized