GI-CM Flashcards Preview

Module 9: Mali: GI > GI-CM > Flashcards

Flashcards in GI-CM Deck (359):
1

what is included in the upper GI tract?

brief function?

mouth to stomach

"food intake"

2

what is included in the middle GI system?

brief function?

small intestine

-duodenum

-jejunum

-ileum

 

"digestion and absorption"

 

3

what is considered part of the lower GI?

function?

cecum to rectum

"storage channel for elimination of waste"

4

what are considered accessory organs to the GI tract? 3

salivary glands

liver

pancreas

 

5

what are the 5 functions of the mouth?

2 enzymes released here and their functions?

1. directs food

2. mastication

3. moistens/lubricates

4. initial digestion

5. receptacle for saliva

 

 

 amylase break down starches

6

function of the esophagus?

what does it do?

conduit

 

1. smooth muscle

2. mucosal and submucossal glands that protect and lubricated

7

explain the two spincters that are found in the esophagus and what their function is?

pharyngoesophageal

keeps air from entering the esopahgus while breathing

concious and unconcious

 

 

gastroesophageal

prevents gastric reflux

8

what is the function of the stomache? 

name the 6 parts?

mostly storage untl ready to head into the duodenum since very little digestions actually occurs here

 

1. cardiac region

2. fundus

3. pyloric region

4. antrum

5. pyloric canal

6. pyloric spincter

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9

what are the 3 segements of the SI? and major function?

whats one important thing that happens in teh first?

DIGESTION AND ABSORPTION

 

1. duodenum

a. contains opening for bile duct and main pancreatic duct

 

2.  jejunum

 

3.  ilieum

10

what does bile break down?

what does pancreatic juices break down?

bile:  lipids!!!

 

pancreatic juices:  lipids, carbs, proteins

11

what are the two main functions of the LI?

what are the 8 parts?

STORAGE and WATER ABSORPTION

 

1. cecum

2. colon

-ascending

-transverse

-descending

-sigmoid

3.rectum

4. anal canal

12

what are the four layers of the wall of the intestin and what are their functions?

4

1

2

1

 

1. mucosal layer

a. changes shape to increase SA

b. produce mucous to protect and lubricate the GI tract

c. digestion and absorption

d. protection barrier against pathogens

 

2. submucosal layer

vascular, lymphatics, nerves to supply tissue

 

3. muscularis externa

a. contains both circular and longitudal laters 

b. contracts to move food along GI tract

 

4. serosa

single layer of cells that makes the mesothelium

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13

what are the 2 different types of movement found in the GI system? characteristics?

2 each

 

1. rythmic

a. moves food forward and keeps GI contents mixed up "oscillations"

b. present from esophagus to SI

 

 

2. tonic

a. constant levels of contaction or tone without regular periods of relaxation

b. think always contracted like spincters and upper region of the stomact

14

what are the 2 types of cells of the GI tract?

characterstics?

1. unitary

cells are electrically coupled so that signals can move quickly initiating SM contractions

"many cells that function as 1"

this is how you get things moving in 1 direction and make a smooth rythmic motion

 

 

2. pacemaker

"slow waves" of interstitial cells

the resting waves are the pacemaker cells that keep the oscillations at slow waves and keep it primed

 

timulated by stretch, acetylcholine or parasympathetic then the AP is prompted and you get depolarization and contraction

 

don't cause any contractions but just keep the tissue primed for when stimulated

 

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15

enteric nervous system of the GI system

 

what is this and why is it unique?

2 divisions?

location of each?

functios of each?

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intrinsic nervous system

means it functions on its own without influence from the brain or higher systems

 

1. submucosal plexsus

a. controls the function of each section of the GI tract

b. takes in the signals from the mucosa in that specific region and adjust the motility, secretions, and absorption appropriately

between the mucosal and submucosal layers

 

 

2. myenteric plexsus

a. linear chair along the muscular externa all the way down the GI tract, causing motility along the entire aspect

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16

parasympathetic stimulation

 

what overall effect does this have?

what 2 nerves control this and what areas do they cover?

INCREASES FUNCTION!!

 

stomach-transverse colon= vagus nerve

 

transverse-rectum=pelvic nerve

17

sympathetic stimulation

overall effect?

 

 

inhibitory, slows it down

 

 

18

swallowing

voluntary/involuntary?

4 nerves that control the first

1 nerve control the second

whta are they?

VOLUNTARY MOST OF THE TIME BUT CAN BE INVOLVUNARY

 

 

ORAL AND PHARYNGEAL

TRIGEMINIAL 5

GLOSSPHARYNGEAL 9

VAGUS 10

HYPOGLOSSAL 12

 

ESOPHAGEAL PHASE

VAGUS 10

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19

ORAL PHASE OF SWALLOWING

 

VOLUNTARY OR NOT?

WHAT HAPPENS IN THIS?

STARTS VOLUNTARY

bolus of food is in the mouth until the posterior tongue lifts it to the posterior wall

20

pharyngeal phase of swallowing

 

voluntary/involuntary?

when does this occur?

4 things that happen?

INVOLUNTARY

**point  when food is at the posterior roof of mouth to esophagus**

 

1. respiration halts so you don't breath in food

2. pharyngeal spincter relaxes

3.larynx closed

4. soft palate closes of the nasopharyngeal folds so food doesn't go up into the nose

21

esophageal phase of swallowing

 

what are the two types?

where and when do they occur?

1. primary peristalsis

upper 1/3

begins when food enters the esophagus

 

2. secondary peristalsis

lower 2/3

 

where peristalsis realy occurs, occurs if primary peristalsis can't handle the load

 

as it comes down it triggers stretch receptors so the spincters relax and let the food enter the stomach

22

dysphagia

 

5 things that can contribute

1. lubrication loss-xerostomia

 

2. size of bolus, poor mastication

 

3. paralysis-stroke (aspiration)

 

4. strictures (scar tissue in esophagus)

 

5. cancer (obstruction)

23

gastric motility

 

function of peristalsis?

explain emptying process?when?

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1. peristalsis

a. used the make chyme

b. starts in the body and moves out to the antrum

c. as the chyme moves towards the antrum, the antrum contracts blocking the pyloric spincter so it doens't exit the stomach and continues to be churned

 

2. emptying

a. chyme is empyting into duodenum between antrum contractions because the spincter is relaxed during this time, lets SMALL amounts out at a time!

24

rate of gastric emptying

 

explain the neural and hormonal controls of this?

3

2

1. neural control

a. hypertonic solutions in duodenum: (indicates lots of particles already present, so digestion needs to occur first)

b. pH below 3.5 (indicates recent release of acidic stomach contents

c. presence of fatty acids, amino acids, and peptides (food)

 

 

2. hormonal control

a. cholecystokinin

b. glucose-dependent insulinotrophic peptides

**these are released in response to fats being released into the duodenum, so if these are elevated it means food as already been released from stomach so don’t want to release more**

25

explain two conditions that are cause the gastric emptying to be too slow?

4

 

3

1. hypertrophic pyloric stenosis

a. very young in life, babies

b. thick pylorus so don't get anything through

c. causes vomiting in the baby and can't keep anything down

d. "grape" in pylorus

 

2. gastric atony

a. no tone so no contraction

b. stomach just sits there and is a problem with the nerves

c. causes: stroke, diabetes, surgical complications

26

what is a condition that can cause the gastric emptying to occur too fast?

dumping syndrome

 

-no control over pyloric spincter

often complication from gastric surgery

 

 

leads to:

diarrhea

higher chance of getting ulcers in the duodenum since higher amount of acid!

27

what the two types of motility in the SI?

1. segmentation waves

2. peristaltic movements

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28

SI:

segmentation waves

'

 

what is this?

what happens in this?

what is the goal of this?

 local mixing!

exposes more chyme to more surface area

circular msucle occludes the lumen and drives some of the contents forward and some backwards

**imagine squeezin a long balloon**

 

**mixing it up in one spot allowing for digestion**

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29

SI:

peristaltic movements

what is this?

accomplished by?

goal?

stimulus?

contraction in proximal portion and subsequent relaxation in distal

accomplished by the myenteric plexus

 

goal: smooth muscle propel the chyme along the gut, moving it foward

 

 

stimulated by MORE CHYME! NEED TO MOVE IT ALONG!!!

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30

what are two probles that can occur with SI motility? what might you ifnd with each othese?

2

3

 

1. inflammation

a. increased motility

b. hyperacitve bowel sounds because the body wants to get it out

 

2. ileus

a. no motion or bowel movement

b. chyme just sitting there

c. see air fluid levels on xray (cmes from eating or bacteria)

31

colonic motility

what are the 2 types?

when does this occur?

what allows this to occur?

goals of each?

 

contracts longer here than in SI since more mass and less chyme ad this poinr and occurs 24-48 hours after ingestion

 

1. segemental

a. HAUSTRATIONS: produce digging like movements to insure fecal material is exposed to mucosa

b. e-segment allows this to occur

 

2. propulsive

propels contents forward using LARGE segments!! close to 20 cm contract at the same time as one segment since it is mass instead of chyme that needs to be pushed along

lasts 10-30 minutes a couple times a day

32

explain the differences between the internal and external spincters?

 

what type of muscle?

voluntary/involuntary?

control?

internal

SMOOTH MUSCLE

INVOLUNTARY

 

 

external

striated muscle

VOLUNTARY

pudenal nerve control

33

what are the 2 reflexes that influence defecation?

1. intrinsic myenteric reflex

stimulated by the local enteric nervous system from distention of the rectal wall with inititiartion of the preistaltic waves that push the fecal material into area

 

2. parasympathetic reflex

sacral cord level

when nerve endings in the rectum are stimulated its feedback increases the peristaltic movements and relaxes internal spincter

34

explain the difference of what happens when it is an appropriate time to defecate vs inappropriate time to defecate?

appropriate time

the external sphincter is under conscious control by the cortex

when the rectum is stimulated from distention it sends messages to the cortex to relax the sphincter

if appropriate, cortex sends message to relax this sphincter

 

 

inappropriate time

same process as above BUT

if inappropriate cortex sends impulses to constrict external sphincter and inhibit efferent parasympathetic activity

keeps butt hole clenched

eventually this feedback loop fatigues and the urge to defecate stops

 

35

gastric hormones:

gastrin

 

what is this released by?

what does it cause?

what stimulates it?

produced by G-cellsin antrum and prompts gastric acid secretion, HCL

 

stimulus: vagus nerve from presence of food

36

gastric hormones:

ghrelin

 

what is this produced by?

what does it stimulate to be released?

what does it cause?

what are two things that stimulate its release?

produced by endocrine cells in the fundus and stimulates the release of growth hormone and causes stimulatory effect on food intake and digestive function with decreased energy expenditure

 

stimulus:

1. nuitritional like fasting

2. hormonal, decreased GH

37

what are 3 hormones that are secreted by the intestines?

1. secretin

2. cholecystokinin 

3. incretin hormones (GIP, GLP-1)

38

intestinal hormones:

secretin

 

what cells is this release by and why?

what causes its release?

what does it inbit and stimulate?

overall effect?

secreted by S CELLS in the mucosa of the duodenum and jejunum in response to acidic PH of the chyme entering the duodenum from the stomach 

 

inhibits gastric secretion since this increases the HCL relase form the stomach

 

response:

prompts pancreas to release large quantities of fluid with high bicarbonate and low chloride to equalize the chyme (acid) that was released from the stomach

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39

gastric hormones:

cholecystokinin (CCK)

 

what is this secreted by?

this is a?

3 things that it stimulates?

2 things that stimulate its release?

secreted by I cells and is used as a neurotransmitted

 

 

stimulates:

1. pancreatic enzyme release (lipase-fats)

2. contraction of gall bladder

3. potentiates secretion of secretin to increase bicarbonate in repsonse to acidity of chyme in SI

 

Stimulated by:

chyme release into SI and products of protein digestion and long chain fatty acid

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40

intestinal secretions:

incretin hormones

what do these 2 hormoens do?

what are the two hormones?

what are they secreted by and where?

4

2

increase insulin release after an oral glucose load /carb load decreasing blod sugar levels

 

1. glucagon-like peptide (GLP-1)

secreted by L cells in the distal small bowel

supresses glucagon release

decreases gastric emptying

get cells to release insulin

 

2. glucose dependent insulinotrophic polypeptide (GIP)

k cells in jejunum

decrease blood glucose by increasing insulin

41

what are the 5 regulations of GI secretions?

1. pH

2. osmolarity

3. chyme

4. hormones

5. neuroregulation

42

salivary secretions

 

3 functions?

1 breakdown?

stimulated and inhibited by?

1. lubrication

2. antimicrobial-lysozyme

3. digestion-amylase break down starches

 

stimulated by parasympathetic

inhibited by sympathetic

43

parietal cells

 

2 things it secretes?

in stomach

secrete:

1. gastric acid HCL

2. intrinsic factor needed for Ca++ absorption

44

chief cells

 

2 things it secretes?

1. pepsin(ogen)

2. gastric lipase

45

D-cells

 

1 secretion?

somatostatin (inhibits acid)

46

G-cells

 

1 secretion

gastrin (stimulates acid)

47

gastric lining

 

what is this? junctions? balance? 3

what is one major component that creates this? 3 functions

mucosal barrier

impermeable  cell surface because of tight junctions

coupled secretions of H and HCO3, remains balanced

PROTECTIVE LAYER!!

 

prostaglandins

improve blood flow

decrease acid secretion

increase mucous protection

provides protection

48

what are 3 things that disrupt the gastric mucosal lining? how?

1. ASA

penetrates the lipid layer and can damage the endothelium

2. ETOH

lipid soluble so may disrupt mucosal barrier

3. bile acids

job is to break down lipis so this breaks down the wall

 

 

**ALL OF THESE INHIBIT PROSTAGLANDINS WHICH HAVE A GASTRIC PROTECTIVE EFFECT SO THIS IS WHY YOU GET STOMACHE UPSET becuase H+ ions move into the cells an cause

-ischemia

-vscular stasis

-hypoxia

-necrosis**

49

what are the 3 things that stimulate the release of HCL and intrinsic factor from the parietal cells?

1. gastrin from G-cells

2. acteylcholine

3. histamine

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50

intestinal secretions:

Brunner glands

 

location?

funciton?

location: where the contents of the stomach and secretions from the liver ender the duodenum

 

function: secrete large amounts of alkaline mucous to neutralize the acid content from the stomach

51

intestinal secretions:

serious fluids

 

where do they come from? what is it? 3 functions?

secreted from crypts of lieberkuhn

 

secrere isotonic alkaline solution that acts as a vechicle for absorption

 

function:

1. protection

2. replaced erpithelial cells that have sloughed off

3. antibacterial

52

what is the function of the surface enzymes in the SI?

aid in absorption, 

secrete pesidases that split sugars

53

what are the 3 functions of the intestinal flora?

1. metabolic-absorb nuitrients and help with energy

2. trophic-growth and regeneration

3.protection against foreign bugs

54

what are the 4 functions of the large intestine?

2 for the last

1. anaerobes

2. metabolic

3. vitamin synthesis/absorption K, Mg

4. protetion

a. mucous secretion

-protects linin and facilitates compaction of feces

 

b. bicarbonate secretion

-attaches to mucous and coats stool so the acid by products of bacteria in feces don't damage the intestine

55

what are the 3 ways that digestions occurs in the SI? what are each of these?

1. hydrolysis

breakdown of one compound that involves a chemical reaciton with water

 

2. enzyme cleavage

requires enzymes to cut down substances into smaller pieces and is accomplished by 

brush border enzymes

 

3. fat emulsification

breakdown of large globules of fat into smaller pieces

56

what are 3 things that contribute to the power of the SI to be good at absorption?

1. large surface area with vili

 

2. brush border enzymes

secrete enzymes that digest proteins and carbohydrates

 

3. goblet cells

secrete mucous

57

intestinal absorption:

carbohydrates

 

what must they be broken down to before they can be absorbed?

expain this process? 5

must be monosacchrides before they can be absorbed in the small intestine

 

process:

1. mouth: starch starts being broken down in the mouth by amylase

2. pancreatic secretions also contain amylase

3. amylase breaks down starches (carbs) to disaccarides 

4. dissacchrides are broken down into monosacchrides by brush border enzymes

5. absorption in SI

58

what are the 3 common dissarcharides that must be broken down by brush border enzymes before being absorbed in the SI? what are they broken down into?

1. sucrose: glucose and fructose

 

2. lactose: glucose and galactose

 

3. maltose: glucose and glucose

59

intestinal absorption:

fats

 

explain three main steps of this and what is included in each step?

1. emulsification

breaks down large globules triglycerides into smaller particles so that digestive enzymes can break down

stomach to duodenum

 

2. pancreatic lipase

released in duodenum cleaves triglyceriddes  into fatty acids and monglycerides

 

3. micelles

made from bile salts and monoglycerides and transport products to brush borden enzymes to be absorbed, they are then transformed into chylomicrons that are triglyercerides and sent to the lymphatic system

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60

protein digestion/absorption

explain where things occur

 

2

 

1. pepsinogen

released y chief cells in the stomache in response to food, which ins then activated by the low pH to PEPSIN, then becomes inactivated in the duodenum from alkaline pH

 

2. pancreatic enzymes trypsin

chymotrypsin

carboxypeptidase

elastase

 

 

61

malabsorption syndrome

get osmotic diarreah with fatty stool "steatorrhea"

 

sxs

muscle wasting

weight loss

failure to thirve

62

what are 6 things that can influence annorexia?

influences on appetite

hunger

hypothalamus

smell

emotional factors

drugs and disease

63

vomiting

 

5 ways this system can be triggered?

3 things these triggers stimulate?

limits the possibility of damage from ingested noixious agents by emptying contents of the stomach and portion of SI

 

triggers:

1. GI tract/organs

2. CNS system respinding to sights, sounds, or emotions

3. vestibular apparatus-mostion sickness

4. chemoreceptors-drugs or toxins

5. hypoxia

 

stimulates:

1. salivary centers

2. respiratory center

-stops breathing

3. abdominal muscles

-contraction/increased pressure

-LES relazation

64

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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65

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**

66

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

67

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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68

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

69

why is it important to treat GERD?

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

70

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

1. benadryl

2. lidocaine

3. maalox

71

in child with asthma, what is one thing you want to look for? why?

look for GERD! asthma and GERD coexist in 50% of children with asthma dx

72

what is the most common cause of esophagitits?

GERD, 50% of patients with GERD have esophagitits

73

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

 

74

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!!!

75

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!!!!

76

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

77

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!!

78

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

79

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

80

achalasia

 

what is this?

what is it caused by?

3 things you are at greater risk for?

4 sxs?

loss of peristalsis in distal esophagus and failure of the LES to relax (LES tone increased) caused by dennervation to LES

 

obstruction of esophagus from LES relaxtion failure from failed stretch receptors or nerves

 

 

increased risk for:

1. aspiration

2. irritation

3. cancers

 

sxs:

dysphagia is most common

substernal cp

regurgitation

difficulty belching

 

81

achalasia

 

4 dx? 1 key word

4 tx options?

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DX: 

1. CXR

2. Barrium swallow showing BIRD BEAK APPEARANCE!!!

3. manometry

4. endoscopy

 

 

TX:

1. nitrates/CCBs

2. botulinum toxin

3. pneumonic dilation with balloon procedure

4. myotomy

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82

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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83

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**

84

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

85

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

86

esophageal cancer:

adenocarcinoma

 

where do you find this?

4 most important RF?

2 protective

Q image thumb

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)

87

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***

88

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***

89

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

when the lumen is less than 13 mm

90

esophageal cancer

 

2 DX

2 STAGE

dx:

1. barium studies

2. endoscopy

 

Staging:

1. CT OF CHEST AND UPPER ABDOMENT

2. PET SCAN

91

of the esophageal cancers, which is dxed more?

adenocarcinoma and squamous cell carcinoma are both dxed with equal amouth these days

92

what is the 5 year survival rate if dxed with esophageal cancer?

10-13% :-/

93

is smoking a RF for developing esophageal cancer?

yep! just like everything else!!!

94

where are adenocarcinomas and squamous cell esophageal cancers found?

adenocarcinoma: lower 1/3

 

squamous: middle esophagus

95

esophageal varices

 

what is this?

what causes this?

mortaltiy rate? 

MOST COMMON CAUSE?

Q image thumb

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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96

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

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

97

what is a random syndrome that can cause portal HTN?

budd chiari syndrome

98

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

99

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

100

esophageal varices

 

long term tx considerations

5

1. abx

2. decrease portal HTN BB/nirates

3. shunts

4. liver transplant

5. STOP ETOH

101

what is boerrhave syndrome

esophageal rupture

102

oropharyngeal dysphagia

 

what is this?

what does it ususally come from?

diffiiculty inititating the swalling reflex 

 

usually comes from neuromuscla disorders that cause weakness or lack of coorindatio of the muscles involved in swallowing

 

 

Ex: CVA, parkinsons

103

esophageal dysphagia

 

what is this?

where?

arises within the body of the esophagus, LED, or cardia most commonly from mechanical or motility disturnances

 

ex: stricuture, radiation

104

odynophagia

 

what dioes this present as?

reflect what?

substernal sharp pain on swalloing

 

usually reflects SEVERE erosive disease

105

esophageal spasm

 

what is this?

what is a specific subset of this? qualification?

2 tx options

motiltiy disorder usually associated with CP or dysphagia

 

NUTCRACKER ESOPHAGUS: increased pressure over 180 during peristalsis which creates the dysphagia

 

DX:

mamometry

 

TX:

1. nitrates (relaxes)

2. CCB diltiazem (relaxes)

 

106

esophageal manometry

 

what is this test and what are 2 things it is helpful in dxing?

measures the pressure in the esophagus, signifying the effectiveness of peristalsis

 

used frequently for achalsaia (NO PERISTALSIS) and NUTCRACKER ESOPHAGUS (hyper peristalsis/contractions)

107

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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108

esophageal web

 

what is this?

where?

1 simple example of this?

1 dx?

1 tx?

mid to upper esophagus

membranes of squmous mucosa that causes intermittent dysphagia with solid food

 

plummer vinson syndrome-WEB WITH IRON DEFICIENT ANEMIA AND GLOTTITIS

 

DX:

barium esophagram

 

Tx:

mechanical dilation with balloon

109

pearl: in eldery patient esp after a stroke who is getting reccurent pnuemonia, what should you always check?

modified barium swallow

110

nissen fundoplication

 

what is this procedure used to tx?

how does it work?

laproscopic procedure used to treat GERD or hiatial hernia

 

1. gastric fundus is wrapped around the lower end of the esophagus

2. stablaizes this area  and spincter and prevents hernia and GERD

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111

hiatial hernia

 

what is this?

what are the sxs?

tx?

occurs at the LES where the upper part of the stomach moves into the upper chest and through the small opening in the diaphram

 

the diaphragmatic hiatus acts as an additional spincter around the lower end of the esophagus

 

SXS:

produces symptoms of GERD or dysphagia

 

TX:

surgical

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112

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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113

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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114

what do you need to avoid in schleroderma pts because it can cause a RENAL CRISIS?

high dose corticosteroids.

 

don't do it!

115

gastritis

 

what is this?

5 causes?

2 sxs

dx

Q image thumb

inflammation or irritation of the gastric lining

 

causes:

ETOH

H. pylori

NSAIDS

STRESS

autoimmune

 

 

SXS:

often asymptomatic

initial presentation may be GI blleeding

"coffee ground, melena, emesis

 

 

DX:

endoscopy

differentiates from PUD

 

116

gastritis-ETOH

 

 

how do you tx this?

nausea, dyspepsia, hematemesis

 

 

TX:

H2, PPI, or sucralfate

4 week tx

117

gastritis-H. pylori

 

 

how presents?

2 things associated with?

usually symptomatic

 

cofactor for PUD

 

two things associated with:

1. gastric adenocarcinoma

2. B-cell gastritis-mucosal associated lymphoid tissue (MALT)

118

NSAID gastritis

 

common?

recognized early?

2 tx? (how)

VERY COMMON 25-50%

MOST GO UNREGOGNIZED BECAUSE OF NO SXS

 

 

TX:

1. D/C NSAIDS

2. TX EMPIRICALLY IF ON NSAIDS

3. PPI 2-4 WEEKS

119

stress gastritis

 

who do you find this in?

because?

3 causes?

1 tx?

prophylaxsis

common in ICU patients

 

develop quickly in this population

caused by decreased mucosal flow

 

Seen in:

1. trauma

2. respiration failure/mechanical ventilation

3. coagulation problems

 

 

prophylaxisis in high risk: PPI oral or NG tube to decrease bleeding

 

tx: PPI

 

120

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

121

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

122

Peptic ulcer disease

 

 

what this this?

2 causes?

1

3

size?

Q image thumb

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

 

 

123

what are the 5 common causes of PUD?

1. NSAIDS

2. H. pylori

3. idiopathic

4. hypersecretory states

5. smoking

124

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

125

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

 

126

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!!!!!**

127

what is a RF for all ulcers?

smoking!

128

explain the patho for duodenal ulcer with h. pylori?

6 steps

1. H. pylori infection increases acid production

2. causes gastric metaplasia in duodenal bulb

3. H. pylori infection

4. causes duogenitis

5. causes mucosal breakdown

6. causes duodenal ulcer from breakdown

129

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

130

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!

131

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

132

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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133

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 

134

in reccurent ulcers what must you do!?

rule out H. pylori and NSAID use

135

peptic ulcer disease:

complication!

bleeding ulcers

what percent of people?

times increase in mortality?

2 sxs?

2 dx?

4 tx? but keep in mind?

Q image thumb

occur in 10-20% of pts with PUD

**may be the first sign of an ulcer**

REBLEEDING INCREASES MORTALITY 10X

 

SXS:

hematemensis

melena

 

DX:

endoscopy!  

predicts liklihood of rebleeding

HgB, Hct

 

TX:

80% OF THESE STOP BLEEDING SPONTANEOUSLY

1. isotonic fluids to replace volume

2. endoscopy can help stop bleeding

3. HIGH DOSE PPI to decrease bleeding

4. surgery in extere

 

 

136

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

137

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

138

gastroparesis

 

what is this? 

issue with what?

5 causes?

2 sxs?

3 dx?

3 tx?

delayed stomach emptying caused by partial paralysis of the stomach, so food remains in the stomache for abnormally long time

 

vagus nerve issue

 

causes:

1. DM

2. bulemia

3. parkinsons

4. abdominal surgery

5. cigarettes

 

SXS:

1. chronic nausea

2. fullness after just a few bites

3. vomiting

 

 

DX:

1. xray

2. mamometry

3. gastric emptying scans

 

TX:

1. dietary changes, lowe fiber, low residue diets

2. SMALLER MEALS

3. antidepressant mirtazapine

 

139

pyloric stenosis

 

 

who do you find it in?

m/f?

caused by?

2 main sxs?

2 dx?

1 tx? 

*2 key buzz words**

children 4-6 weeks old

more comme males

 

gastric outlet is blocked by pyloric hypertrophy

 

SXS:

1. progressive projectile vomiting in child who remains hungry

2. oval shaped mass right of the umbilicus, esp right after eating!!

 

DX:

US

barium swallow with "STRING SIGN"

 

 

TX:

SURGERY!!!!!

140

zollinger-ellison syndrome

 

what is this?

by the time of dx...?

rate?

what can it cause?

3 locations?

met site?

gastrinoma that secretes large amounts of gastrin so causes recurrent and refractory gastric ulcers, 1/3 have mets by dx

 

SLOW GROWTH

 

the increase in gastrin increases the osmoliarty of the lumen so it draws water out and can cause diarreah

 

locations:

1. pancreas

2. duodenum

3. lymph nodes

metastasizes to liver

141

zollinger-ellison syndrome

 

what are the 3 sxs?

3 dx options?

2 tx depending if isolated or mets?

SXS:

GERD

diarrhea

malabsorption weight loss

 

DX:

1. serum gastrin over 500

2. pH less than 3

3. somatostatin receptor scintigraphy endoscop US

finds primary tumor and mets

 

 

tx:

isolated primary tumor: PPI and resection

mets: PPI high dose 

142

what percent of gastinomas are malignant?

2/3

143

gallbladder

 

2 functions

when is it filled?

when is it released?

Q image thumb

1. STORES BLADDER

2. CONCENTRATES BILE

 

 

filled when the spincter of oddi is closed

 

contracts in response to cholecystokinin to release bile into the duodenum

 

144

bile

 

 

what does it do?

3 things it is made of?

Q image thumb

digests fats in SI, terminal ileum, and recycled to liver for reexcretion

 

CONTENTS

1. bile salts (from cholesterol)

2. bilirubin (waste product RBC)

3.alkaline fluids

145

 cholecystic

referring to gallbladder

146

cholecystitis

inflammation (chronic or acute)

147

cholithiasis

stones in GB

148

choledocholithiasis

stone in the bile duct

149

cholecystectomy

surgical removal of GB

150

pancreas 

exocrine portion

 

2 cell types?

which more common?

things it secretes?

3

1

Q image thumb

ducts enter the duodenum

 

ENCOMPASSES:

1. acinar cells-95% of pancreas

1. secrete proteolytic enzymes including trysinogen, chymotrypsinogen, procarboxypeptidases for protein digestion

2. amylase for carb digestion

3. lipase-fat digestion

 

 

2. ductal epithelial cells

a. alkaline secretion to decrease the acidic pH of the duodenal contents

151

cholecystalgia

pain (aka billiary colic)

152

pancreas

 

 

3 location descriptors

during development

2 things contains

in retroperitoneum

head near duodenum

tail posterior to stomach

 

during development two pancreat buds come together to fuse

 

 

CONTAINS:

exocrine portion

endocrine portion

153

what are the most common cells in the pancreas?

acrinar cells

154

pancreas:

endocrine portion

 

where do secretions go?

what are the cells made into?

what are the 3 cell types??

secretion into the blood stream

 

1. islets of langerhans

"islands of endocrine cells" 1-2% of pancreas

 

beta-cells: insulin synthesis/secretion

alpha cells: glucagon

deta cells: somatostatin, inhibits GH and TSH

155

tumor markers:

ca 19-9

pancreas

156

tumor markers

ca-125

ovarian cancer

157

tumor markers

AFP

liver cancer

158

tumor markers

CEA

colon cancer

159

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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160

tumor markers

PSA

prostate

161

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

 

162

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**

163

when dxing pancreatitis and looking at labwork, what test is most effective?

lipase

 

(this is better than amylase)

164

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

165

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

166

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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167

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

168

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

169

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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170

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

 

 

171

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

172

what are 4 things that that increase persons chance of bad outcome/mortality with pancreatitis?

1. organ failure

2. pancreatic necrosis

3. obesity

4. old age

173

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!!!

174

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

175

pancreatic cancer

 

4 sxs?

toc? 1

Q image thumb

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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176

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

177

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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178

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

179

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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180

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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181

explain 3 pathphys concepts of cholelithiasis?

 

one population more at risk 

1. cholesterol supersaturation of bile

2. nucleation

cholesterol comes together and crystalizes, propogates

3. GB hypermotility

slower emptying=more time for stones for form 

THINK PREGNANT WOMAN!!!

182

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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183

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

184

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 $$$

185

acute ascending cholangitis

 

what is this?

why is it important?

sxs? KEY

infection and inflammation of the billiary tract COMMON BILE DUCT

obstruction then infection

 

potentially life threatening

CAN LEAD TO SEPSIS OR SHOCK!!!!

 

 

sxs:

charcots triad

1. abdominal pain

2. jaundice

3. fever

*KNOW IT*

 

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186

acute ascending cholangitis

 

what are the 3 things seen on labs?

what must you make sure to do?

2 tx options?

LABS:

1. leukocytosis

2. hyperbilirubinemia

3. alkaline phosphatase increasing

******MAKE SURE TO ORDER BLOOD CULTURES X2**

 

 

TX:

1. ABX TO COVER GRAM NEGATIVE ANAEROBES, ENTEROCOCCI

penicillin

aminoglycoside

2. REMOVAL OF OBSTRUCTED STONES ERCP

 

187

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

188

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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189

niacin

2 functions

4 sources

1 presentation

FUNCTION:

1. energy

2. fat metabolism

 

 

Soucres:

1. tuna/ salmon

2. chicken/beef

 

 

Presentation:

FLUSHING

190

thiamine

 

4 sources

2 functions

4 presentations

SOURCES

1. pork

2. grains

3. dried beans

4. peas

 

FUNCTION:

carbohydrate metabolism

nerve function

 

PRESENTATION

berberi

nervous tingling

poor coordination

edema

cardia dysfrunction

191

vitamin A

 

4 sources

2 presentations

3 toxicities

SOUCRES

1. liver

2. fish oils

3. fortified milk 

4. eggs

 

CLINICAL PRESENATION

night blindness

dry skin

 

TOXICITY

1. skin disorders

2. hair loss

3. teratogenicity

192

riboflavin

4 sources

1 function

2 presentations

sources:

1. milk

2. spinach

3. liver

4. grains

 

functions

ENERGY

 

presentation

oral inflammation

eye disorders

193

vitamin C

 

4 sources

3 functions

3 presentations?

SOURCES

1. citrus berries

2. starberies

4. broccoli

4. greens

 

functions:

1. collagen synthesis

2. hormone function

3. neurotrasmitter synthesis

 

PRESENTATION!

scurvy

poor would healing

petechiae

bleeding gums

194

what does the toxicity of vitamin C cause?

diaareah

195

vitamin D

 

1 source

2 functions

2 at risk

source

FORTIFIED MILK

 

functions

CALCIUM REGULATION

CELL DIFFERENTIATION

 

at risk:

elderly

and those without sun exposure

196

vitamin D

 

2 preseentations

3 toxicitiy

rickets

osteomalacia

 

toxicity;

1. hypercalemia

2. kidney stones

3. soft tissue deposits

197

vitamin K

 

4 sources

1 function

1 presentation

2 toxicity

sources:

1. liver

2. green leafy veggies

3. broccoli

4. peas

5. green beans

 

functions

clotting

 

presentation:

 bleeding

 

toxitiy presents as:

1. anemia

2. juandice

198

folate

 

4 sources

1 function

4 presentations of deficiency

sources

1. green leafy veggies

2. organe juice

3. grains

4 organ meats

 

RF: 

PREGNANCY!!!!!

 

presentation:

1. megaloblastic anemia

2. sore tongue

3. diarreah

4. mental disorder

199

appendicitis

 

what is this?

MC cause?

2 risks?

3 presentations?

inflammation of the appendix causing leakage of cecum contents and blockage MC common due to fecalith

 

RISK OF SEPSIS AND DEATH IF RUPTURES

 

SXS:

1. sudden onset of abdominal pain

2. umbilicus progresses to RLQ pain

3. pain to palpation

 

 

200

appendicitis

 

5 physical tests to do to confirm?

2 tests to do to confirm suspicion?

TESTS:

1. rovsings sign

2. obturatory sign

3. psoas sign

4. mcburneys

5.rebound tenderness

6. CT-inflammation

7. surgical consult

201

appendicitis

 

what is the tx for this?

what is the controversy concerning this?

surgical tx is standard of care

 

*****abx in recent studies conclude that 80% could be txed IV but 25% required emergency removal of appendix within first year post op....SO NOT IDEAL***

202

constapation

 

what is the qualification for this classification?

what are the 7 causes?

difficult passing stool 

 

qualification:

difficulty in over 25% of attempts for over 3 months with NO obstructive or peristalsis disorder

 

 

causes:

 

nervous system disorders

neural transmitter malfunction

hormone malfunction

heighten immune response

poor diet

poor activity

mediation Se

 

203

constapation

 

what must you rule out?

2 DX options?

3 tx options?

 

 

must r/o obstruction, impaction

 

DX:

1. DRE (r/o obstruction/impaction)

2. xray for bowel gas pattern

 

TX:

1. diet

2. increase fluid intake

3. activity

4. medication evaluation

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constapation

 

what are the 3 classes of drugs you can use to tx this?

what is the function of each?

**add the drugs from table**

1. bulk forming laxatives

-absorbs water and increases fecal mass

-Fiber

 

2. ostmotic laxatives

causes H2O retnetion in the stool (pull water into the stool)

-PEG

 

 

3. stimulant laxatives

increase acteylcholine regulated GI motility peristalsis

-senna

205

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"

206

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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celiac disease in children

 

when does this start?

4 causes in children

2 things at increased risk for

 

GI issues start when there is gluten introduced to the diet

 

irritablitly

anxious

distention

abdominal pain

 

high risk for:

1. dehydration

2. hypokalemia due to increased fluid loss

 

208

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***

 

209

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**

210

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

211

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

212

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

213

who is diverticulosa most common in?

 

2 percents?

western/industerialized societies

 

30% by 60

65% have by age 85

 

214

what are 3 RF for diverticulosa?

1. connective tissue disorders

2. low fiber diet

3. too little exercise

215

what are the two conditions that make up inflammatory bowel disease?

1. crohns disease

2. ulcerative colitis

216

crohns disease

 

3 populations common in

1. common in 15-35

2. jewish population

3. increased risk with family hx

217

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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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

219

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**

 

220

which is more common crohns or ulcercerative colitis?

ulcerative colits 3x more likely

221

what groups of people does ulcerative colitis effecT?

1. ages 20-30

2. caucasions and jewish descent

3. family hx is strongest RF

222

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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223

what do you use to dx ulcerative collitis?

colonoscopy

224

what are the 3 tx options for ulcerative collitis?

1. 5-ASA

-sulfasalzine

-mesalamine

2. corticosteroids

3. colonectomy CURE best choice

removal of colon

225

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

 

 

 

226

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

227

mesenteric ischemia

 

 

what are the two categories? sxs associated with

2

1

what are 5 causes?

Acute (embolus)

SUDDEN SEVERE ABDOMINAL PAIN

FEVER

 

or chronic (athlerosclerosis)

ABDOMINAL PAIN POST EATING

 

causes:

1. CVD impacting flow

2. trauma

3. neoplasm

4. physical obstruction

5. systemic illness-DM, sickle cell, PVD, even dehydration

 

 

228

mesenteric ischmia

 

2 dx methods?

1 tx

DX: 

1. mesenteric angiogram TOC

2. CT or abdomen with contrast-bowel wall edema

 

Tx:

SURGERY with stent or emboli removal

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229

ischemic colitis

 

what is this?

who get its?

inflammation and injury to the large intestine resulting in decreased BF

 

most common in elderly patients

230

small intesine neoplasms

when are these found?

common?

4 types?

dx? 2 

NOT TYPICALLY DETECTED TILL LATE STAGES!!!

*rare.*

 

98% of adenocarcinomas, carcinoids, sarcomas, and lymphomas

 

often not dxed until metastisized to other parts of the body!!

sxs vague and non specific

 

DX:

1. colonoscopy with bx TOC!!

2. CT

231

what is the most common GI  cancer? in US?

COLORECTAL MOST COMMON GI CANCER!!! 3rd most common in US for males and females!!

232

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*

233

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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234

what does colonrectal cancer come from?

the progression of adenomatous polyp into malgnancy

235

obstruction

 

5 causes

explain last 3

4 sxs

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1. tumor

2. foreign body

3. paralytic ileus-trauma, surgery, infection, metbaolic disease with DM

4. volvulus-twisting of intesinte

5. intusssception-telescoping of intestine

 

 

sxs;

1. severe abdominal cramping

2. inability to pass stool

3. increased bowel sounds first, then decreased

4. abdominal swelling, distention

 

236

obstruction

 

3 dx

3 tx

1. abdominal xray

2. CT

3. barium enema

 

tx:

1. NG tube (relieve pressure)

2. relieve obstruction

3. surgery often needed

237

what are four complications from obstruction?

tissue death

perforation

sepsis

death

238

intussusception

 

what is this?

who most common in?

2 causes? 

3 sxs? 

2 dx children and adult

1 tx? 

telescoping of the intestines

MC in children, but also in adults with obstruction or neoplasms

 

1. currant jelly stools

2. sausage like mass felt on abdominal palpation

3. coliky pain

DX:

children: barium enema

adult: CT is best

 

 

TX: SURGERY

239

toxic megacolon

 

what is this?

typically caused by? and 3 others?

what are 2 risks worry about?

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acute toxic colitis that causes dilation of the colon

 

typically complication of inflammatory disease most commonly 

1. ulcerative colitis

2. infectious causes

3. ischemia

4. pseudomembraneous causes

 

 

**risk is sepsis and death**

 

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240

what are the requirements to dx toxic megacolon?

4

4

must contain 3 of 4 of these

temp over 101.5

HR over 120

leukocytosis over 10.5

anemia

 

and 1 of these

dehydration

altered mental status

electrolyte abnormality

hypotension

241

toxic megacolon

 

5 sxs

dx, and finding?

SXS:

1. abdominal pain

2. bloating 

3. fever

4. tachycardia

 

5.  LOSS OF BOWEL SOUNDS

 

 

DX:

xray, dilation of colon over 6 cm in transverse colon

242

toxic megacolon

 

4 tx options?

1. decompress bowel immediately

2. if not successful, colectomy

3. abx and steroids

4. tx fluid and electrolyte imbalances

243

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

244

lactose intolerance

 

1 dx?

1 tx?

dx:

hydrogen breath test

 

tx:

dietary avoidance

245

angiodysplasia

 

what is this?

why does it happen

3 sxs? 

Q image thumb

swollen fragile blood vessels in the colon so considered vascular lesions

 

patho:

aging and degen of the structure of blood vessels causes formation of arteriovenous malformation

often the cause of GI bleed in elderly  not attributed to other causes

 

 

1. maroon/melena colored stool

2. pallor

3. SOB from anemia

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246

angiodysplasia

 

3 dx?

3 tx options?

DX

1. colonscopy

2. CT scan

3. angiography

 

 

TX:

1. majority stop bleeding without intervention

IF NOT

2. cautery via colonscope

3. clotting through angiography

247

what is the dentate line? 

senstion?

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divides the rectal mucosa from the squamous epithelium in the canal

 

above in anorectal canal: INSENSATE (no pain)

 

below in andoderm:  SENSATE AND PAINFUL!!

248

what does the dentate line divide?

3

1. nervous system

2. vascular supply

3. nervous system

**most important, divides where a patient can feel and where they can't so important when determine sxs!!**

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249

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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250

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!!

251

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**

252

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**

 

 

253

rectal abcess

 

where do these most commonly occur?

where does it come from?

4 causes?

most in posterior rectal wall, originate in the crpyts with gland obstruction

 

s. aureus

bacteroides

proteus

strep

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254

rectal abcess

 

2 causes

3 steps

1. crypt gland obstruction

2. increased muscle tone causing obstruction

 

STEPS

1. stasis

2. dilation

3. infection

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255

once a anal abcess in a crypt has formed...where can go if infection spreads? 4

most common?

1. superficially to external spincter to make perianal abcess most common

 

2. deep through the external spincter into fat of ischioretal fossa

3.  deep into supralevator space

4. interspincteric

256

who are rectal abcess most common in? 

 

how do they present?

5 (3 key)

 

MEN!!!!!!!!!!!

 

1. sever pain while sitting

2. drainage on PE

3. palpable fluctuant mass

4.worse with coughing, sitting, defectatin

5.really really painful DRE

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257

rectal abscess

 

how to dx? 1

how to tx? 2

outcomes?

DX

1. CT-size and location, fistula presence

 

 

TX:

1. surgical drainage if not fistula

2. post op sitz bath

50% will be cured

50% will have fistula formation

258

fistula in ano

"rectal fistula"

 

6 associations?

1. crohns

2. GC procitis

3. carcinomas

4. hodgkins lymphoma

5. radiation fibrosis

6. immunocomprimised states

259

what do you need to remember if someone has an abcess or resctal fistula?

DO NOT DO DRE!

260

anorectal fistulas

Goodalls rule

 

what does it tell you?

2 rules?

**used to determine the location of the internal opening of the fistula**

 

anterior external opening

goes to interally via straight line

 

posterior exernal opening, tracts internally via curved line

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261

anorectal fistulas

 

2 sxs patient presents with

1 tx?healing?

*be careful of**

1. embaressing persistent discharge

2. not painful but itchy

 

TX:

1. fistulotomy (opening tract)

healed by secondary intention with granulation tissue

left open to heal on its own

***watch out for spincter!! must preserve its function**

 

262

fecal impaction

 

 

what is this and when typcailly does it occur?

2 key sxs?

PE? 1 

TX 3

large mass of dried hard stool typically after chronic constapation

 

 

SXS:

1. sudden watery diarreah in patient that has had cronic constapation

2. straining with passage of liquid or small stool

 

PE:

DRE shows hard mass or dry stool in vault

 

 

TX:

1. removal manually

2. prevention with stool softeners, colase, bulk (fiber) and H20

3. high fiber diet

 

263

what is the most common anorectal complain in adults over 50?

hemmoroids

264

what percent of people over 50 have hemmoroids?

50%`

265

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

266

what are 6 RF for hemmoroids?

constapation

straining at stool

pregnancy

obesity

chronic liver disease

portal HTN

267

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

268

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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269

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

270

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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271

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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272

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

 

 

273

what is the least common but the most prognostic for cancer of the adenoma polyps?

vilous adenoma

*think vilian=evil*

274

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)

275

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

276

when should you screening african americans for colorectal cancer?

45 rather than 50 according to the college of gastroenterology

277

what are the sxs associated with polyps/colorectal cancer?

they might bleed

 

more important to think about family hx

278

pilonidal cyst/disease

 

what is this?

what does it look like?

location?

who is it in? age? KEY!!!!!!

common, congenital abnormality

"opening of a sinus tract that may conttain a tuft of hair"

 

location:

midline, post sacral intergluttal fold superoir to anus

 

ALMOST ALWAYS MEN 20-30, always under 40

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pilonidal cyst/disease

 

4 key sxs?

1 tx otpion? why?

 

1. fluctuant mass with erytmatous "halo"

2. purluent d/c

3. NO ANAL PAIN OR DEFECATION ISSUES

4. painful but in gluteal area

 

Tx:

1. MOST LIKELY SURGERY with secondary closure (leaving open) vs ID with abx

HIGH RATE OF RECURRANCE SO SURGERY IS BETTER OPTION TO GET DEEPER TRACTS!!!

280

incisional hernia

 

associated with vertical incisions esp in pts with wound infection or obesity

 

tx: surgery!

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inguinal hernia

 

3 types?

where are they?

which is most common?

1. direct

passage of intesine through external inguinal ring at hesselbachs triangle

 

2. indirect 

MOST COMMON

passage through inguinal canal INTO SCROTOM, often

 

3 femoral

less common through femoral ring

 

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umbical hernia

 

when do they get it?

how is it txed?

congenital and appears at birth

most resolve on their own

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283

vental hernias

when does this occur?

occur when weakening in the anterior abdominal walla and can be either incisional or unilical

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284

portal vein

 

lacks what?

internal pressure?

supplies what percent of blood

formed from? 

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valvless

pressure 3-5 mmHg

75% of the livers total blood supply by volume

formed by the superior mesenteric artery

285

hepatic vein

 

where does it go?

structure?

2

3

2

 

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venous drainage of liver through 3 valveless hepatic veins into inferior vena cava

 

right: 5, 8

middle: 4, 5, 8

left: 2, 3

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286

neural innervation of the liver

2

1. parasympathetic of vagus nerve

2. parasympathetic from the celiac plexsus

287

explain the 2 cels in the liver and when you see them?

parenchyma is made up of actively diviiding hepatocytes

 

in damaged tissue this becomes fibrotic and you will see oval cels indicating damage

288

what are the 3 main functions of the liver? subgroups?

3

4

1

1. metabolic and catabolic

a. glucogenesis

b. synthesis of phospholipids and cholesterol

c. detoxification of meds and alchohol

 

2. storage

glycogen

protein

iron

vitamins

 

3. excretory functions

synthesis and secretion of bile

289

what are 6 synthetic functions of the liver that occur in the hepatocytes?

1. coagulation factors: PT/INR, PTT

2. plasma proteins: albumin

3. acute phase proteins

4. carbohydrate metabolism

5. lipid metabolism

6. bilirubin metabolism: bile excretion

290

what are the two tests that suggest hepatocellular damage/inflammation?

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1. AST

2. ALT

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291

what 3 LFTs suggest obstructive disease?

1. bilirubin

direct=conjucated

indirect=unconjugated

2. ALP/alkaline phosphatase

3. GGTP/gamma-glutamyl transferase *ordered sepereately

292

conjugated bilirubin=

direct bilirubin

293

unconjugated bilirubin=

indirect bilirubin

294

asartate aminotransferase

(AST)

 

elevated in?

specific?

 

elevated in acute conditions

 

found in the muscle, kidney, and heart so low specificity for liver damage since mreasures more than just the liver

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295

alanine aminotransferase

(ALT)

 

elevated in?

specific?

elevated in chronic conditions

 

primarily found in the liver so more specific than AST

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296

if the ration of AST:ALT is greater than 2:1 ration, what should you think of?

alcoholism or drug toxicity

297

unconjugated (indirect) bilirubin

 

what is this?

if increased indicates? 3

broken down RBC in speel bind to albumin and go to hepatocytes

 

if increased indicates:

PREHEPATIC PROBLEM

1. hemolysis of RBC

2. imparied hepatocyte function

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direct bilirubin (conguated)

 

what happens to this?

where does it usually go?

if increased indicates 2 things?

enzymatically conjugation occurs with glucuronic acid...goes into bile...into small intestine where aprox 95% is reabsorbed

 

if increased:

INDICATEDS POSTHEPATIC PROBLEM

1. obstruction of biilary system=CHOLESTASIS

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is bilirubin in the urine common?

no, it should not be present in the urine!!

300

alkaline phosphatase

 

where is this found?

found in the liver, intestine, kidney, and placenta

 

therefore, not specific to the liver

301

gamma-glutamyltransferase

 

what does this indicate?

what does this help rule in/out?

liver specific

**helps differentiate if the liver is the problem if the alkalne phosphatase is increased**

302

if you have increased alk phos and increased GGTP....what should this make you think?

OBSTRUCTION

303

what are the first and second most common causes of chronic liver disease?

1. hep C

2. alcohol

304

gilberts disease

 

what is this?

why does it happen?

2 key sxs?

most common hereditiary cause of increased bilirubin

 

impaired enzymatic conjugation of Indirect bilirubin

 

sxs:

1. jaudice at birth

2. icteric sclera

305

gilberts disease

 

what are the 3 tests done to dx?

1 tx option?

DX:

1. elevated INDIRECT bilirubin

2. normal direct bilirubin

normal US

 

 

tx

only in infancy with "bili lights" to prevent liver failure

306

nonalcoholic fatty liver disease

(NASH)

6 causes

1. certrain drugs

2. obesity

3. starnation

4. diabetes melltius

5. high blood tryglicerides

6. alcohol

307

nonalchoholic liver disease

(NASH)

 

what are the sxs?

3 dx findings? 1 key

what should you consider if more than more one abnormal finding?

sxs

NON UNLESS CIRROSIS

 

 

DX

1. increased echotecture at times HSM on US

2. AST/SLT increased sometimes alk phos

2. ALT more than AST 

(opposit of ETOH)

**CONSIDER BX IF MORE THAN ONE POTENTIAL CAUSE OF ABNORMAL LFTS**

 

 

 

308

non alcoholic fatty liver dxs

 

5 tx options?

TX

 

1. lifestyle: weightloss, lowfat diet

2. management of high triglycerides, BS

3. decrease ETOH

4.  meds/supplements

-vitamine E, 

-ursodiol

309

hemochromatosis

 

what is this?

who does it present in?

sxs? 4

3 important labs for dx

 

autosomal recessive causing iron deposition in orgams

OVER 50 years

 

often asymptomatic

can include:

arthalagias

hepatomegaly

gray skin

DM

 

Labs

1. high ferritin and iron % saturation

2. HFE gene analysis

3. liver bx with iron stain

 

 

310

what is the tx for hemochromatosis?

phlebotamy, remove the iron

311

wilson's disease

what is this?

 

what happens in this?

3 things it causes?

2 labs must check

 

rare autosomal recessive disorders

 

liver unable to exrete copper, so get copper overload in brain, bone, kidney, cornea

 

1. basal ganglia sxs (parkinson like)

2. liver disease

3. kayser-fleicher rings 

brown on green pigment in cornea

 

Labs.

1. LOW CERULOPLASMIN

2. 24 hour urine copper

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wilsons disease

 

what are 2 key sxs?

1 tx option?

sxs:

1. visual disturbances

from the kayser fleischer rings get brown ring causing visual disturbances

 

2. neurologic/psychiatric changes

 

 

TX:

1. copper chelators like zinc

313

alpha 1 antitrypsin deficiency

 

what is this?

what 2 organs does it effect?

2 effects?

tx?

 

genetic condition effecting lung and liver

 

alpha-1 antitrypsin (A1A) synthesized in liver resulting in reduced circulating levels

 

increase in A1A in liver=obstruction

 

decrease A1A circulation=obstructive lung disease

 

 

tx: 

replace A1A

314

alchoholic hepatitis

 

what is this?

what is the ratio you see? 

2 labs might see?

most common cause of cirrohosis

 

AST>ALT 2:1 rarely over 300

labs:

1. vitamin and calorie deficiency

2. megaloblastic anemia (folate, B1, B6)

 

315

what is the ration associated with alcoholic hepatitis?

AST greater than ALT 2:1 rarely over 300

316

acute phase alcholic hepatitis

 

associated with what?

how serious?

3 sxs of this?

what must you calculate?

typically with heavy use or binge

 

can be fatal, pts often encephalopathic

 

sxs:

1. HEPATOSPLENOMEGALY

2. ASCITIES

3. JAUNDICE

 

**calculate discriminant function***

over 31=poor 1 month prognosis

317

what is consider tylenol OD?

 

what precent of acute hepatitis?

serious?

tx?

single or total dose exceeding 10 grams

 

accounts for 45% of cases of acute hepatitis

 

fatal if untreated

 

 

tx:

1. N-acetylcysteine

use this if  hepatoxicity or ingestion time unknown

318

autoimmune hepatitis

 

who is this common in?

2 labs to check?

2 biomarkers to check? 

1 test needed to dx?

2 tx options!

most common in females 14-50 WHO MOST LIKELY HAVE ANOTHER AUTOIMMUNE CONDITION

 

LABS:

1. elevated enzymes

2. elevated alk phos

 

BIOmarkers:

1.  ANA

2. anti-smooth muscle

 

 

Dx: 

need bx to make dx

 

tx:

prednisone and imuran

319

primary biliary cirrhosis

 

what is this strongly associated with?

what is key finding on testing?

test?

2 tx options?

75% cases are patients with ulcerative colitis, males

 

"beading" of bile ducts on MRCP (MRI)

 

Tx:

1. ursodiol

2. transplant cure!

320

if person has family hx of colorectal cancer, when do you start screening?

start 10 years prior to the dx of your 1st degree relative and do every 5 years from there with colonoscopy

321

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

 

322

viral infections account for what percent of hepatitis?

50% of all cases

hep a b  c d e account for 95% of thse

323

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

324

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

 

325

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

326

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

327

who gets vaccinated for hep A? 4

Harvix

 

travelers

miliary personnel

lab workers

immunocomprimised

328

when you think of raw shellfish think..

hep A!

329

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!!!!*****

330

what type of hepatitis can lead to hepatocellular carcinoma?

HEPATITIS B!! vaccines for this mandated

331

what are the categories of hepatitis B?

3

immunity

-vaccination

-natural infection

 

actue infection

 

chronic infection

-active

-chronic

332

***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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333

surface=

core=

envelope=

surface=immunity (vaccine or exposure)

core=exposed to virus

envelope=present infection with active replication

334

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

335

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

 

336

hepatitis prevention and vaccination

2

1. recombinant hepatitis vaccine

2. hep B immune globulin (exposued)

337

what is key to know about hepatitis D?

transmission?

RNA coinfection with HEP BE IS REQUIRED!!!

HBsAg

 

transmission: sexual contact

338

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

339

**what important people do you need to test for hepatitis C?**

test everyone born between 1945 to 1965

 

340

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

341

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

342

what do you want to check when txing someone for hep C?

viral load after 12 weeks to confirm cure

 

 

343

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!!!

344

what is interesting about hep G?

if coinfected with HIV, helps reduce the HIV replication

345

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

346

cirrhosis

 

what is this?

2 classifications?

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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

347

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

348

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

349

cirrhosis

5 tx

1. alcohol abstinence

2. vitamin supp

3. nuitrional supp

4.BB for portal HTN

5. CURE IS TRANSPLANT!!!

350

what MUST you do for someone with cirrhosis?

*****must screen for alpha fetal protein and imaging ever 6 months***

351

what is used to stage liver disease?

what does it determine?

MELD SCORE

 

**determines prognosis of patient in order to determeine priorty of patient for transplant**

352

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

 

353

hepatocellular carcinoma

 

4 tx

1. surgical ressection

2. chemo

3. portal vein embolizations

4. transplant if small and localized

354

metastatic liver lesions

 

what is this?

3 ways it gets there?

3 dx methods?

3 tx options

MOST COMMON NEOPLASM OF THE LIVER!!!

 

1. portal venous circulation

2. direct extension

3. lymphatic spread

 

DX

1. triple phase CT or MRI

2. Percutaneous bx of lesions

3. PETS scan and tumor markers for primary tumor

 

TX:

1. ressection

2. chemo

3. not option for transplant

 

355

hepatic ressection

 

how much can you take?

can remove up to 80% because it regenerates!! woah!

 

regains albumin ability by 3rd week

356

portal HTN

what are the 3 classifications of this?

5 things it can cause?

1. presinusoidal: slpenic or protal vein

2. sinusoidal: cirrhosis

3. postsinusoidal: hepatic veins, ouflow problem

 

CAN CAUSE:

1. esophageal varices

2. ascites

3. encephalopathy

4. splenomegaly

5. hepatorenal syndrome

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what are the most common PORTAL HTN locations?

presinusoidal and sinusoidal

358

what is basically the only cause of postsinusoidal portal HTN?

budd-chiari syndrome

359

portal HTN

 

5 tx options depending on cause

1. nonselective BB

2. banding for varices

3. diuretics for ascites

4. lactulose and xifaxan for encephalopathy

5. surgical if meds fail

TIPS-transjugular intrahepatic portosystemic shunt

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