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

GI-CM Flashcards

1
Q

what is included in the upper GI tract?

brief function?

A

mouth to stomach

“food intake”

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2
Q

what is included in the middle GI system?

brief function?

A

small intestine

  • duodenum
  • jejunum
  • ileum

“digestion and absorption”

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3
Q

what is considered part of the lower GI?

function?

A

cecum to rectum

“storage channel for elimination of waste”

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4
Q

what are considered accessory organs to the GI tract? 3

A

salivary glands

liver

pancreas

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5
Q

what are the 5 functions of the mouth?

2 enzymes released here and their functions?

A
  1. directs food
  2. mastication
  3. moistens/lubricates
  4. initial digestion
  5. receptacle for saliva

amylase break down starches

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6
Q

function of the esophagus?

what does it do?

A

conduit

  1. smooth muscle
  2. mucosal and submucossal glands that protect and lubricated
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7
Q

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

A

pharyngoesophageal

keeps air from entering the esopahgus while breathing

concious and unconcious

gastroesophageal

prevents gastric reflux

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8
Q

what is the function of the stomache?

name the 6 parts?

A

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
Q

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

whats one important thing that happens in teh first?

A

DIGESTION AND ABSORPTION

  1. duodenum
    a. contains opening for bile duct and main pancreatic duct
  2. jejunum
  3. ilieum
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10
Q

what does bile break down?

what does pancreatic juices break down?

A

bile: lipids!!!

pancreatic juices: lipids, carbs, proteins

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11
Q

what are the two main functions of the LI?

what are the 8 parts?

A

STORAGE and WATER ABSORPTION

  1. cecum
  2. colon
    - ascending
    - transverse
    - descending
    - sigmoid
  3. rectum
  4. anal canal
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12
Q

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

4

1

2

1

A
  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

  1. submucosal layer

vascular, lymphatics, nerves to supply tissue

  1. muscularis externa

a. contains both circular and longitudal laters

b. contracts to move food along GI tract

  1. serosa

single layer of cells that makes the mesothelium

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13
Q

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

2 each

A
  1. rythmic

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

b. present from esophagus to SI

  1. 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

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14
Q

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

characterstics?

A
  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

  1. 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
Q

enteric nervous system of the GI system

what is this and why is it unique?

2 divisions?

location of each?

functios of each?

A

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

  1. 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
Q

parasympathetic stimulation

what overall effect does this have?

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

A

INCREASES FUNCTION!!

stomach-transverse colon= vagus nerve

transverse-rectum=pelvic nerve

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17
Q

sympathetic stimulation

overall effect?

A

inhibitory, slows it down

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18
Q

swallowing

voluntary/involuntary?

4 nerves that control the first

1 nerve control the second

whta are they?

A

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
Q

ORAL PHASE OF SWALLOWING

VOLUNTARY OR NOT?

WHAT HAPPENS IN THIS?

A

STARTS VOLUNTARY

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

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20
Q

pharyngeal phase of swallowing

voluntary/involuntary?

when does this occur?

4 things that happen?

A

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
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21
Q

esophageal phase of swallowing

what are the two types?

where and when do they occur?

A
  1. primary peristalsis

upper 1/3

begins when food enters the esophagus

  1. 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

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22
Q

dysphagia

5 things that can contribute

A
  1. lubrication loss-xerostomia

  1. size of bolus, poor mastication
  2. paralysis-stroke (aspiration)
  3. strictures (scar tissue in esophagus)
  4. cancer (obstruction)
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23
Q

gastric motility

function of peristalsis?

explain emptying process?when?

A
  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!

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24
Q

rate of gastric emptying

explain the neural and hormonal controls of this?

3

2

A
  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**

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25
Q

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

4

3

A
  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

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26
Q

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

A

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!

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27
Q

what the two types of motility in the SI?

A
  1. segmentation waves
  2. peristaltic movements
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28
Q

SI:

segmentation waves

’

what is this?

what happens in this?

what is the goal of this?

A

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
Q

SI:

peristaltic movements

what is this?

accomplished by?

goal?

stimulus?

A

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
Q

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

2

3

A
  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)

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31
Q

colonic motility

what are the 2 types?

when does this occur?

what allows this to occur?

goals of each?

A

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

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32
Q

explain the differences between the internal and external spincters?

what type of muscle?

voluntary/involuntary?

control?

A

internal

SMOOTH MUSCLE

INVOLUNTARY

external

striated muscle

VOLUNTARY

pudenal nerve control

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33
Q

what are the 2 reflexes that influence defecation?

A
  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

  1. parasympathetic reflex

sacral cord level

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

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34
Q

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

A

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

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35
Q

gastric hormones:

gastrin

what is this released by?

what does it cause?

what stimulates it?

A

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

stimulus: vagus nerve from presence of food

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36
Q

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?

A

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
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37
Q

what are 3 hormones that are secreted by the intestines?

A
  1. secretin
  2. cholecystokinin
  3. incretin hormones (GIP, GLP-1)
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38
Q

intestinal hormones:

secretin

what cells is this release by and why?

what causes its release?

what does it inbit and stimulate?

overall effect?

A

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
Q

gastric hormones:

cholecystokinin (CCK)

what is this secreted by?

this is a?

3 things that it stimulates?

2 things that stimulate its release?

A

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
Q

intestinal secretions:

incretin hormones

what do these 2 hormoens do?

what are the two hormones?

what are they secreted by and where?

4

2

A

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

  1. glucose dependent insulinotrophic polypeptide (GIP)

k cells in jejunum

decrease blood glucose by increasing insulin

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41
Q

what are the 5 regulations of GI secretions?

A
  1. pH
  2. osmolarity
  3. chyme
  4. hormones
  5. neuroregulation
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42
Q

salivary secretions

3 functions?

1 breakdown?

stimulated and inhibited by?

A
  1. lubrication
  2. antimicrobial-lysozyme
  3. digestion-amylase break down starches

stimulated by parasympathetic

inhibited by sympathetic

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43
Q

parietal cells

2 things it secretes?

A

in stomach

secrete:

  1. gastric acid HCL
  2. intrinsic factor needed for Ca++ absorption
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44
Q

chief cells

2 things it secretes?

A
  1. pepsin(ogen)
  2. gastric lipase
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45
Q

D-cells

1 secretion?

A

somatostatin (inhibits acid)

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46
Q

G-cells

1 secretion

A

gastrin (stimulates acid)

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47
Q

gastric lining

what is this? junctions? balance? 3

what is one major component that creates this? 3 functions

A

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

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48
Q

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

A
  1. ASA

penetrates the lipid layer and can damage the endothelium

  1. ETOH

lipid soluble so may disrupt mucosal barrier

  1. 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**
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49
Q

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

A
  1. gastrin from G-cells
  2. acteylcholine
  3. histamine
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50
Q

intestinal secretions:

Brunner glands

location?

funciton?

A

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

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51
Q

intestinal secretions:

serious fluids

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

A

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
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52
Q

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

A

aid in absorption,

secrete pesidases that split sugars

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53
Q

what are the 3 functions of the intestinal flora?

A
  1. metabolic-absorb nuitrients and help with energy
  2. trophic-growth and regeneration
  3. protection against foreign bugs
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54
Q

what are the 4 functions of the large intestine?

2 for the last

A
  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

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55
Q

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

A

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

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56
Q

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

A

1. large surface area with vili

  1. brush border enzymes

secrete enzymes that digest proteins and carbohydrates

3. goblet cells

secrete mucous

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57
Q

intestinal absorption:

carbohydrates

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

expain this process? 5

A

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
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58
Q

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?

A

1. sucrose: glucose and fructose

2. lactose: glucose and galactose

3. maltose: glucose and glucose

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59
Q

intestinal absorption:

fats

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

A
  1. emulsification

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

stomach to duodenum

  1. pancreatic lipase

released in duodenum cleaves triglyceriddes into fatty acids and monglycerides

  1. 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
Q

protein digestion/absorption

explain where things occur

2

A
  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

  1. pancreatic enzymes trypsin

chymotrypsin

carboxypeptidase

elastase

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61
Q

malabsorption syndrome

A

get osmotic diarreah** with **fatty stool “steatorrhea”

sxs

muscle wasting

weight loss

failure to thirve

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62
Q

what are 6 things that can influence annorexia?

A

influences on appetite

hunger

hypothalamus

smell

emotional factors

drugs and disease

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63
Q

vomiting

5 ways this system can be triggered?

3 things these triggers stimulate?

A

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
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64
Q

gastroesophageal reflux disease

what is this?

population common in?

percent in US?

5 complications it can lead to

A

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

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

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

2. esophageal stricutre

3. barrettes esophagous

4. esophageal adenocarcinoma

  1. hiatial hernia

-

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65
Q

GERD

what are 6 sxs?

1 thing to keep in mind about sxs?

A
  1. heartburn, restrosternal and postprandial

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

worsens when laying down or recumbant

  1. regurgitation (vomit burp)

spontaneous reflux of sour bitter gastric contents in mouth

  1. dysphagia (discomfort)

cough at night from acid asipiraiton

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

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

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66
Q

GERD

3 dx options

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

A
  1. empirically first line unless (below)
  2. esphagogastroduodenoscopy(EGD) if high risk or tx has failed
    a. over 50
    b. weight loss
    c. melena
    d. odynophagia pain with eating
    e. heavy alcohol or tabacco
    f. non repsonsive to tx
  3. modified/full barium swallow
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67
Q

what is the pathway for txing GERD?

6

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

**if these fail EDG**

  1. prokinetics
  2. surgical
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68
Q

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

5

A
  1. avoid eating 2-3 hours before bed

2. elevate head of bed

3. loose weight

  1. avoid acidic food, chocolate, peppermint, ETOH, coffee
  2. stop smoking
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69
Q

why is it important to treat GERD?

A

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

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70
Q

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

A
  1. benadryl
  2. lidocaine
  3. maalox
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71
Q

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

A

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

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72
Q

what is the most common cause of esophagitits?

A

GERD, 50% of patients with GERD have esophagitits

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73
Q

esophagitits

what is this?

5 general causes?

4 sxs

A

inflammation of the esophagus, esp in immunocomprimised

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

sxs;

  1. odyniaphagia
  2. dysphagia
  3. substernal chest pain
  4. oral thursh
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74
Q

esophagitis

herpes liabilis (HSV)

3 SXS?

2 DX?

1 TX

A

N/V/ chills

herpetic vesicles on nose/lips

dx:

1. endoscopy showing small vesicles or superficial lesions

2. culture esophageal lesions

TX:

ACYCLOVIR 7-21 DAYS!!!

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75
Q

ESOPHAGITIS

VARICELLA-ZOSTER

1 dx?

tx?

A

N/V fever chils

DX:

endoscopy: vesicles or confluent ulcers

Tx:

  1. usually resolve spontaneously but can cause necrotizing esophagitits
  2. ACYCLOVIR!!!!
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76
Q

esophagitis

CMV

who does this occur in?

characteristics of ulcer? 2

3 sxs?

1 tx?

A

only occurs in immunocomprimised patients

CREEPING ULCER or can be GIANT ULCER

sxs:

odyniaphagia

persistent CP

hematememis

Tx:

IV GANCICLOVIR

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77
Q

esophagitis

candidia

who does it occur in?

3 complications?

1 dx?

1 tx?

A

occurs in immunocomprimised host

can cause complications:

  1. bleeding
  2. perforation
  3. stricture

dx:

endoscopy: small yellowwhite raised plaques

tx:

oral or IV fluconazole!!

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78
Q

barrett’s esophagus

how does this occur? what hcanges?

what are they at increased risk for? how much?

A

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

increases risk for adenocarcinoma 5-10%

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

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79
Q

barettes esophagus

2 dx rules?

3 tx?

A

DX:

EDG every 2 years with bx to check for neoplastic changes

if there is high risk dysplasia, consider surgrical resection

TX:

**more txing symtpoms unless surgical intervention**

  1. antacids
  2. H2 blockers OTCs
  3. PPIs
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80
Q

achalasia

what is this?

what is it caused by?

3 things you are at greater risk for?

4 sxs?

A

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

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81
Q

achalasia

4 dx? 1 key word

4 tx options?

A

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
Q

mallory-weiss tear

what is this?

what does it occur from?

who commonly seen in?

MC location?

3 RF?

2 sxs?

A

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
Q

mallory weiss tear

1 dx?

2 tx?

A

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**

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84
Q

in mallory weise syndrome what is somethign you want to do before releasing someone from hospital?

A

obtain occult negative stool to insure not bleeding still or hemmoraging

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85
Q

esophageal cancer

what are the two types?

frequency?

prognisis?

who is more common?

A

types:

  1. adenocarcinoma
  2. squamous cell carcinoma

prognosis typicaly poor, 5 year survival 10-13%

both appeare with equal frequency

males more common than females

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86
Q

esophageal cancer:

adenocarcinoma

where do you find this?

4 most important RF?

2 protective

A

distal esophagus

RF:

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

Protective effects:

  1. fiber
  2. NSAIDS (seems counterintuitive)
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87
Q

esophageal cancer:

squamous cell carcinoma

prevalence?

location?

4 RF?

key point to remember?

A

prevalence is decreasing

middle esophagus

RF:

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

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

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88
Q

esophageal cancers

sxs

1 early

3 late

A

SXS:

early:

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

later:

  1. retrosternal pain/burning

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

3. tracheobronchial fistula

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

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

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89
Q

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

A

when the lumen is less than 13 mm

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90
Q

esophageal cancer

2 DX

2 STAGE

A

dx:

  1. barium studies
  2. endoscopy

Staging:

  1. CT OF CHEST AND UPPER ABDOMENT

2. PET SCAN

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91
Q

of the esophageal cancers, which is dxed more?

A

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

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92
Q

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

A

10-13% :-/

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93
Q

is smoking a RF for developing esophageal cancer?

A

yep! just like everything else!!!

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94
Q

where are adenocarcinomas and squamous cell esophageal cancers found?

A

adenocarcinoma: lower 1/3

squamous: middle esophagus

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95
Q

esophageal varices

what is this?

what causes this?

mortaltiy rate?

MOST COMMON CAUSE?

A

emergency!!!

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

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

patient acutely ill, mortality rate 40-70%

MOST COMMON CAUSE OR PORTAL HTN IS CIRROSIS that causes this

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96
Q

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

A

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

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97
Q

what is a random syndrome that can cause portal HTN?

A

budd chiari syndrome

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98
Q

esophageal varices

6 sxs

3 dx

A

sxs:

1. hematemesis!!! over 50% stop bleeding spontaneously

  1. melena
  2. tachycardia
  3. hypotension
  4. syncope
  5. jaundice

DX:

1. emergent endoscopy

CBC

BUN/creatine

type and cross

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99
Q

esophageal varices

4 immediate tx options

A
  1. immediate tx-stop bleeding because mortaltiy approaches 75%
  2. visceral ligation- rubber band
  3. sclerotherapy
  4. balllon tamponade
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100
Q

esophageal varices

long term tx considerations

5

A
  1. abx
  2. decrease portal HTN BB/nirates
  3. shunts
  4. liver transplant
  5. STOP ETOH
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101
Q

what is boerrhave syndrome

A

esophageal rupture

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102
Q

oropharyngeal dysphagia

what is this?

what does it ususally come from?

A

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

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103
Q

esophageal dysphagia

what is this?

where?

A

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

ex: stricuture, radiation

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104
Q

odynophagia

what dioes this present as?

reflect what?

A

substernal sharp pain on swalloing

usually reflects SEVERE erosive disease

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105
Q

esophageal spasm

what is this?

what is a specific subset of this? qualification?

2 tx options

A

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)
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106
Q

esophageal manometry

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

A

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

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

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107
Q

esophageal ring

what is this?

sxs?

dx?

1 tx?

A

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
Q

esophageal web

what is this?

where?

1 simple example of this?

1 dx?

1 tx?

A

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

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109
Q

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

A

modified barium swallow

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110
Q

nissen fundoplication

what is this procedure used to tx?

how does it work?

A

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
Q

hiatial hernia

what is this?

what are the sxs?

tx?

A

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
Q

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?

A

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
Q

CREST Syndrome

what is the pneumonic to remember the symptoms and what do you need to monitor annually in these patients?

A

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
Q

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

A

high dose corticosteroids.

don’t do it!

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115
Q

gastritis

what is this?

5 causes?

2 sxs

dx

A

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

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116
Q

gastritis-ETOH

how do you tx this?

A

nausea, dyspepsia, hematemesis

TX:

H2, PPI, or sucralfate

4 week tx

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117
Q

gastritis-H. pylori

how presents?

2 things associated with?

A

usually symptomatic

cofactor for PUD

two things associated with:

1. gastric adenocarcinoma

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

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118
Q

NSAID gastritis

common?

recognized early?

2 tx? (how)

A

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

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119
Q

stress gastritis

who do you find this in?

because?

3 causes?

1 tx?

prophylaxsis

A

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

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120
Q

stomach neoplasms

where do these occur?

appearance? 4

sxs?

3 dx?

1 tx

A

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

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121
Q

what are 6 RF for stomach neoplasms?

A
  1. genetic predisposition
  2. carcinogenic diet

smoked food/perserved food

  1. autoimmune gastritis

increased inflammation

  1. gastric adenomas
  2. polyps
  3. h. pylori, cofactor for some
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122
Q

Peptic ulcer disease

what this this?

2 causes?

1

3

size?

A

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

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123
Q

what are the 5 common causes of PUD?

A
  1. NSAIDS
  2. H. pylori
  3. idiopathic
  4. hypersecretory states
  5. smoking
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124
Q

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?

A
  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

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125
Q

peptic ulcer disease

NSAIDS

cause?

why?

4 RF?

2 tx? length of time?

A

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

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126
Q

peptic ulcer disease:

h. pylori

KEY?

characteristic?

acute/chronic characteristics?

what is key about this?!

A

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!!!!!**

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127
Q

what is a RF for all ulcers?

A

smoking!

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128
Q

explain the patho for duodenal ulcer with h. pylori?

6 steps

A
  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
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129
Q

explain te patho of stomach ulcers caused by h. pylori?

A
  1. infection in body​
  2. causes gastritis and chronic inflamation that overwhelms immune system
  3. causes mucosal breakdown
  4. creates gastric ulcer
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130
Q

PEPTIC ULCER DISEASE

2 sxs

3 dx

when do you use each?

1 think must do?

A

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!!

  1. fecal antigen test (noninvasive)
  2. 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!

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131
Q

peptic ulcer disease

tx without h. pylori

2

3 for first

1 second

A
  1. antisecretory agents

A.PPIs 1st DOC-inhibit 90% acid secretion

ompreazole

lansoprazole

B. H2-inhibit histamine mediated secertion

C. OTC anti-secretory

  1. mucosal defense agents

2nd line can be used as adjunct for symptom relief

sacralfate, busmuth

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132
Q

peptic ulcer disease:

Treatment for H. pylori

what is the tx regimen?

what must you do after tx and when?

A

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
Q

peptic ulcer disease:

post H. pylori tx tx

2 considerations

A

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

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134
Q

in reccurent ulcers what must you do!?

A

rule out H. pylori and NSAID use

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135
Q

peptic ulcer disease:

complication!

bleeding ulcers

what percent of people?

times increase in mortality?

2 sxs?

2 dx?

4 tx? but keep in mind?

A

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
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136
Q

peptic ulcer disease:

COMPLICATIONS

PENETRATION/PERFORATION

results in?

2 sxs?

tx?

A

results in chemical peritonitis

a. severe generalized abdominal pain
b. rigid abdominal rebound

TX:

1. laproscopic perforation closure

2. increased RX TX

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137
Q

peptic ulcer disease:

refractory ulcers

what is this caused by?

3 contributing factors

A

uncommon, contributed to non compliance with medication

Contirbutory factors:

  1. cigs
  2. NSAIDS
  3. failutre to eradicate H. pylori! MUST DO THIS
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138
Q

gastroparesis

what is this?

issue with what?

5 causes?

2 sxs?

3 dx?

3 tx?

A

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

  1. vomiting

DX:

  1. xray
  2. mamometry
  3. gastric emptying scans

TX:

1. dietary changes, lowe fiber, low residue diets

2. SMALLER MEALS

  1. antidepressant mirtazapine
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139
Q

pyloric stenosis

who do you find it in?

m/f?

caused by?

2 main sxs?

2 dx?

1 tx?

*2 key buzz words**

A

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

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

DX:

US

barium swallow with “STRING SIGN”

TX:

SURGERY!!!!!

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140
Q

zollinger-ellison syndrome

what is this?

by the time of dx…?

rate?

what can it cause?

3 locations?

met site?

A

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

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141
Q

zollinger-ellison syndrome

what are the 3 sxs?

3 dx options?

2 tx depending if isolated or mets?

A

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

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142
Q

what percent of gastinomas are malignant?

A

2/3

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143
Q

gallbladder

2 functions

when is it filled?

when is it released?

A
  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

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144
Q

bile

what does it do?

3 things it is made of?

A

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
Q

cholecystic

A

referring to gallbladder

146
Q

cholecystitis

A

inflammation (chronic or acute)

147
Q

cholithiasis

A

stones in GB

148
Q

choledocholithiasis

A

stone in the bile duct

149
Q

cholecystectomy

A

surgical removal of GB

150
Q

pancreas

exocrine portion

2 cell types?

which more common?

things it secretes?

3

1

A

ducts enter the duodenum

ENCOMPASSES:

  1. acinar cells-95% of pancreas

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

  1. amylase for carb digestion
  2. lipase-fat digestion
  3. ductal epithelial cells
    a. alkaline secretion to decrease the acidic pH of the duodenal contents
151
Q

cholecystalgia

A

pain (aka billiary colic)

152
Q

pancreas

3 location descriptors

during development

2 things contains

A

in retroperitoneum

head near duodenum

tail posterior to stomach

during development two pancreat buds come together to fuse

CONTAINS:

exocrine portion

endocrine portion

153
Q

what are the most common cells in the pancreas?

A

acrinar cells

154
Q

pancreas:

endocrine portion

where do secretions go?

what are the cells made into?

what are the 3 cell types??

A

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
Q

tumor markers:

ca 19-9

156
Q

tumor markers

ca-125

A

ovarian cancer

157
Q

tumor markers

AFP

A

liver cancer

158
Q

tumor markers

CEA

A

colon cancer

159
Q

acute pancreatitis

6 sxs

where is pain?

severity?

what makes worse/better?

pain with…?

two key signs you dont want to miss?

A
  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

160
Q

tumor markers

PSA

161
Q

explain the pathophys of pacreatitis?

what are 2 theories that cause this?

A
  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
Q

acute pancreatitis

what are 2 MC causes? account for what? 6 others?

A

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
Q

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

A

lipase

(this is better than amylase)

164
Q

acute pancreatitis

5 labs tests?

TOC for dx?

A

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
Q

acute pancreatitis

5 labs tests?

TOC for dx?

A

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
Q

acute pancreatitis

6 tx options?

what is the process dependent on?

A

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

167
Q

chronic pancreatitis pathophysiology

what is this?

what should you think about when thinking of this?

what happens?

A

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
Q

chronic pancreatitis

what is the MC cause of this?

3 others?

NOT CAUSED BY WHAT?

what can this lead to?

A
  1. alcohol cause #1!!

***THIS IS NOT CAUSED BY GALLSTONES LIKE ACUTE**

  1. obstructive causes of spincter of oddi by neoplasms
  2. malnuitirion
  3. metabolic

chronic pain leads to opoid addiction! keep this in mind

169
Q

chronic pancreatitis

4 dx options

fat stranding

A
  1. amylase/lipase NORMAL

body gets used to working under these circumstances

  1. secretin stimulation test “gold standard” for early chronic pancreatitis dx
  2. plain xray films QUICK AND CHEAP-see calcifications
  3. CT SCAN-better at seeing calcifications but $$/rad

“arrowhead and fat stranding”

170
Q

chronic pancreatitis

4 sxs?

A

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
Q

chronic pancreatitis

5 tx options

most important!!

2 drugs?

A
  1. _stop the alcoho_l!!
  2. controls sxs
    a. pain control

b. prancreatic enzyme supplements viokase and pancrease

  1. endoscopic duct decompression
  2. surgical draingage of duct
  3. celiac plexsus nerve block
172
Q

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

A
  1. organ failure
  2. pancreatic necrosis
  3. obesity
  4. old age
173
Q

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

A
  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

  1. APACHE II score

**typically impatient ICU use**

over 8 is severe!!!

174
Q

pancreatic cancer

what are thet wo tumor markers?

survival?

1 RF?

A

tumor markers:

  1. CA19-9 85%
  2. CEA 40-45%

5 year survival is only 4% really bad

only RF: chronic pancreatitis

175
Q

pancreatic cancer

4 sxs?

toc? 1

A

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

176
Q

pancreatic cancer

what two lab findings supposrt this?

3 tx options?

A

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

  1. whipple surgery-only at cancer specialties
  2. pallaitive care
177
Q

acute cholecystitis

what happens in this?

what is most likely to cause this?

leads to 3 things? possible worst case?

2 key sxs?

A

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)
178
Q

acute cholecystitis

2 dx tests? when to use?

2 labs?

A

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
Q

acute cholycystitis

TXOC?

3 others?

A

TreatOT: TAKE IT OUT!! MOST COMMON!! via laproscopic cholecystectomy

  1. leave in if very mild
  2. drain it if patient too sick
  3. abx if elevated WBC
180
Q

cholelithiasis

two types of stones?

percentage?

what do they look like?

A

1. cholesterol stones

MC-75% of stones!!

don’t show up on xray

  1. calcium bilirubinate/ca salts

25% of stones

pigmented black/brown sludge stones

181
Q

explain 3 pathphys concepts of cholelithiasis?

one population more at risk

A
  1. cholesterol supersaturation of bile
  2. nucleation

cholesterol comes together and crystalizes, propogates

  1. GB hypermotility

slower emptying=more time for stones for form

THINK PREGNANT WOMAN!!!

182
Q

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?

A

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**

183
Q

what are the four RF for cholithiasis?

A
  1. over 40
  2. obesity (or rapid weight loss)
  3. female/pregnant
  4. native american

“FEMALE, FAT, FORTY, FERTIL” 4, F’s

184
Q

acute cholelithiasis

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

A
  1. cholecystectomy-MOST COMMON “it hurts

  1. leave in if doesn’t hurt UNLESS high risk to keep in
    a. diabetics
    b. sickle cell
    c. Native americans with calfieiced “porcelain” stone
  2. dissolve cholesterol stones with actigal, urodeoxycholic acid but $$$
185
Q

acute ascending cholangitis

what is this?

why is it important?

sxs? KEY

A

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*

186
Q

acute ascending cholangitis

what are the 3 things seen on labs?

what must you make sure to do?

2 tx options?

A

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
Q

choledocholithiasis

where is the stone?

where does it come from?

where is pt?

sxs? 4

A

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
Q

choledolithiasis

what are the two dx/tx options?

what must you keep in mind?

A
  1. MRCP magnetic resonance cholangiopacreatogprahy ONLY DX

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

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

189
Q

niacin

2 functions

4 sources

1 presentation

A

FUNCTION:

  1. energy
  2. fat metabolism

Soucres:

  1. tuna/ salmon
  2. chicken/beef

Presentation:

FLUSHING

190
Q

thiamine

4 sources

2 functions

4 presentations

A

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
Q

vitamin A

4 sources

2 presentations

3 toxicities

A

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
Q

riboflavin

4 sources

1 function

2 presentations

A

sources:

  1. milk
  2. spinach
  3. liver
  4. grains

functions

ENERGY

presentation

oral inflammation

eye disorders

193
Q

vitamin C

4 sources

3 functions

3 presentations?

A

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
Q

what does the toxicity of vitamin C cause?

195
Q

vitamin D

1 source

2 functions

2 at risk

A

source

FORTIFIED MILK

functions

CALCIUM REGULATION

CELL DIFFERENTIATION

at risk:

elderly

and those without sun exposure

196
Q

vitamin D

2 preseentations

3 toxicitiy

A

rickets

osteomalacia

toxicity;

  1. hypercalemia
  2. kidney stones
  3. soft tissue deposits
197
Q

vitamin K

4 sources

1 function

1 presentation

2 toxicity

A

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
Q

folate

4 sources

1 function

4 presentations of deficiency

A

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
Q

appendicitis

what is this?

MC cause?

2 risks?

3 presentations?

A

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

  1. umbilicus progresses to RLQ pain
  2. pain to palpation
200
Q

appendicitis

5 physical tests to do to confirm?

2 tests to do to confirm suspicion?

A

TESTS:

  1. rovsings sign
  2. obturatory sign
  3. psoas sign
  4. mcburneys
  5. rebound tenderness
  6. CT-inflammation
  7. surgical consult
201
Q

appendicitis

what is the tx for this?

what is the controversy concerning this?

A

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
Q

constapation

what is the qualification for this classification?

what are the 7 causes?

A

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
Q

constapation

what must you rule out?

2 DX options?

3 tx options?

A

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
204
Q

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**

A
  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
Q

celiac disease

what type of condition is this?

what is the patho of this and the specific component?

nickname?

A

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
Q

celiac disease

what are 6 sxs that come with this?

explaination of the last?

A
  1. unintended weight loss

  1. persistently underweight
  2. sxs of poor nuitrition
  3. “failure to thrive in child”
  4. diarreah
  5. dermatitis herpetiformis
    a. intense itching

b. blisterning rashes

c. 10-15% of patients

207
Q

celiac disease in children

when does this start?

4 causes in children

2 things at increased risk for

A

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
Q

celiac disease

what are the 3 dx options of this?

key thing to remeber?

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

  1. bx if small intestine and blood + for antibody

****if they have dermatitis herpetiform with + antibody skin bx, THEN NO NEED FOR INTESTINAL BX***

209
Q

celiac disease

what are the 2 tx for this?

what about screening?

A
  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
Q

diverticula

what are these?

how are they formed?

A

sac-like protrusions in the colonic wall

blood vessels penetrate the mucosal wall

internal layers penetrate through weak areas creating diverticula

211
Q

diverticulosis

what is this?

where does it most commonly occur?

what is important to know about this?

presentation?

2 things to avoid?

A

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
Q

diverticulitis

what is this?

3 sxs?

2 tests?

A

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
Q

who is diverticulosa most common in?

2 percents?

A

western/industerialized societies

30% by 60

65% have by age 85

214
Q

what are 3 RF for diverticulosa?

A
  1. connective tissue disorders
  2. low fiber diet
  3. too little exercise
215
Q

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

A
  1. crohns disease
  2. ulcerative colitis
216
Q

crohns disease

3 populations common in

A
  1. common in 15-35
  2. jewish population
  3. increased risk with family hx
217
Q

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?

A
  1. legions mouth to anus; spread out with healthy tissue between

2. transmural

3. RLQ pain MC

  1. fistulas, abscesses, fibrotic stricutres
  2. bleeding common
  3. weight loss common
  4. obstruction common
  5. perianal disease common
  6. can effect skin eyes joints liver
  7. large volume diarreah and mucous (trash bag)
218
Q

what 2 are tests you want to do to look for crohns?

A
  1. anti-saccharomyces cervisial (ASCA)- 44% of crohns are pos

  1. colonoscopy TOC
219
Q

what are the 4 tx options for crohns?

A
  1. 5-aminosalcyclics (5-ASA)

-mesalamine

-sulfasalazine

  1. corticosteroids
  2. cimzia-certolizumab
  3. humira-adalmumab

**surgery doesn’t work since it involves the entire GI tract**

220
Q

which is more common crohns or ulcercerative colitis?

A

ulcerative colits 3x more likely

221
Q

what groups of people does ulcerative colitis effecT?

A
  1. ages 20-30
  2. caucasions and jewish descent
  3. family hx is strongest RF
222
Q

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?

A
  1. primarily localized in colon

2. LLQ

3. bleeding from rectum is most common

  1. urgency need of BM

4. potenital anemia due to blood loss

  1. lesions are continuous starting at the rectum and in mucosa only
  2. colon wall thin with continuous inflammation
  3. no granulomas

(weight loss/obstruction very rare with this)

223
Q

what do you use to dx ulcerative collitis?

A

colonoscopy

224
Q

what are the 3 tx options for ulcerative collitis?

A
  1. 5-ASA
    - sulfasalzine
    - mesalamine
  2. corticosteroids
  3. colonectomy CURE best choice

removal of colon

225
Q

irritable bowel syndrome

what is this?

who most common in?

age?

pathogenIsis? 3 causes

A

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
Q

irritable bowel syndrome

3 tx options?

4 medications tx options

A
  1. pt education and behavior/ emotional support

  1. dietary therapy
  2. pharm
    a. antispasmotics
    b. antidiarreals
    c. psychotropic
    d. serotonin receptor agonists
227
Q

mesenteric ischemia

what are the two categories? sxs associated with

2

1

what are 5 causes?

A

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
Q

mesenteric ischmia

2 dx methods?

1 tx

A

DX:

  1. mesenteric angiogram TOC
  2. CT or abdomen with contrast-bowel wall edema

Tx:

SURGERY with stent or emboli removal

229
Q

ischemic colitis

what is this?

who get its?

A

inflammation and injury to the large intestine resulting in decreased BF

most common in elderly patients

230
Q

small intesine neoplasms

when are these found?

common?

4 types?

dx? 2

A

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
Q

what is the most common GI cancer? in US?

A

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

232
Q

colorectal cancer

what are 3 risk factors?

A
  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
Q

colonrectal cancer

4 sxs

2 key dx

3 others

A

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
234
Q

what does colonrectal cancer come from?

A

the progression of adenomatous polyp into malgnancy

235
Q

obstruction

5 causes

explain last 3

4 sxs

A
  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
Q

obstruction

3 dx

3 tx

A
  1. abdominal xray
  2. CT
  3. barium enema

tx:

  1. NG tube (relieve pressure)
  2. relieve obstruction
  3. surgery often needed
237
Q

what are four complications from obstruction?

A

tissue death

perforation

sepsis

death

238
Q

intussusception

what is this?

who most common in?

2 causes?

3 sxs?

2 dx children and adult

1 tx?

A

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
Q

toxic megacolon

what is this?

typically caused by? and 3 others?

what are 2 risks worry about?

A

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**

240
Q

what are the requirements to dx toxic megacolon?

4

4

A

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
Q

toxic megacolon

5 sxs

dx, and finding?

A

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
Q

toxic megacolon

4 tx options?

A
  1. decompress bowel immediately
  2. if not successful, colectomy
  3. abx and steroids
  4. tx fluid and electrolyte imbalances
243
Q

lactose intolerance

what is this?

4 populations common in?

5 sxs? key 1?

A

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
Q

lactose intolerance

1 dx?

1 tx?

A

dx:

hydrogen breath test

tx:

dietary avoidance

245
Q

angiodysplasia

what is this?

why does it happen

3 sxs?

A

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

  1. pallor
  2. SOB from anemia
246
Q

angiodysplasia

3 dx?

3 tx options?

A

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
Q

what is the dentate line?

senstion?

A

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
Q

what does the dentate line divide?

3

A
  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!!**

249
Q

anal fissure

what is this?

where do these occur?

signicant stat?

2 causes?

A

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
250
Q

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…

A

ANAL FISSURE!!

251
Q

anal fissure

3 sxs?

what not to do?

A

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
Q

anal fissure

2 tx categories

4

1 (also, who not to do in)

A
  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
Q

rectal abcess

where do these most commonly occur?

where does it come from?

4 causes?

A

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

s. aureus

bacteroides

proteus

strep

254
Q

rectal abcess

2 causes

3 steps

A
  1. crypt gland obstruction
  2. increased muscle tone causing obstruction

STEPS

  1. stasis
  2. dilation
  3. infection
255
Q

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

most common?

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

  1. deep through the external spincter into fat of ischioretal fossa
  2. deep into supralevator space
  3. interspincteric
256
Q

who are rectal abcess most common in?

how do they present?

5 (3 key)

A

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
257
Q

rectal abscess

how to dx? 1

how to tx? 2

outcomes?

A

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
Q

fistula in ano

“rectal fistula”

6 associations?

A
  1. crohns
  2. GC procitis
  3. carcinomas
  4. hodgkins lymphoma
  5. radiation fibrosis
  6. immunocomprimised states
259
Q

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

A

DO NOT DO DRE!

260
Q

anorectal fistulas

Goodalls rule

what does it tell you?

2 rules?

A

**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

261
Q

anorectal fistulas

2 sxs patient presents with

1 tx?healing?

*be careful of**

A
  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
Q

fecal impaction

what is this and when typcailly does it occur?

2 key sxs?

PE? 1

TX 3

A

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
Q

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

A

hemmoroids

264
Q

what percent of people over 50 have hemmoroids?

265
Q

explain the pathophysiology of hemmoroids?

5

A
  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
Q

what are 6 RF for hemmoroids?

A

constapation

straining at stool

pregnancy

obesity

chronic liver disease

portal HTN

267
Q

internal hemmoroids

4 key sxs with these!

A

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
Q

what are the stages used to define internal hemmoroids?

A

first-bleed

second-bleed and prolapsed, spontanously reduce

third-bleed, prolapse, and require manual reduction

fourth degree-bleed/incarcerate

269
Q

Internal hemmoroid tx categories

5

2

A

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
Q

external hemmoroids

whe do they occur/what are they covered in?

3 sxs

dx method?

1 tx?

A

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
271
Q

rectal polyps

what are these?

why is it improtant to know type?

1 type concerned about?

why?

2 shapes?

A

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

272
Q

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?

A
  1. tubular adenoma

MOST COMMON TYPE 65-80%

pedunculated, little cancer risk

  1. tubulovillous adenoma

10-25% of adenomas

22% risk of cancer

  1. vilous adenomas

40% RISK OF CANCER

only 5-10% so least common but most deadly

273
Q

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

A

vilous adenoma

*think vilian=evil*

274
Q

what are the two tests that are reccomended annually to screen for colorectal cancer?

A
  1. guiac fecal occult blood test (gFOBT)

  1. immunochemical-based fecal occult blood test (iFBT)
275
Q

what are the 3 screening tests that are reccomended for colorectal cancer? which is most reccomended? what age do you start?

A

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
Q

when should you screening african americans for colorectal cancer?

A

45 rather than 50 according to the college of gastroenterology

277
Q

what are the sxs associated with polyps/colorectal cancer?

A

they might bleed

more important to think about family hx

278
Q

pilonidal cyst/disease

what is this?

what does it look like?

location?

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

A

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

279
Q

pilonidal cyst/disease

4 key sxs?

1 tx otpion? why?

A
  1. fluctuant mass with erytmatous “halo”
  2. purluent d/c

3. NO ANAL PAIN OR DEFECATION ISSUES

  1. 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
Q

incisional hernia

A

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

tx: surgery!

281
Q

inguinal hernia

3 types?

where are they?

which is most common?

A
  1. direct

passage of intesine through external inguinal ring at hesselbachs triangle

  1. indirect

MOST COMMON

passage through inguinal canal INTO SCROTOM, often

3 femoral

less common through femoral ring

282
Q

umbical hernia

when do they get it?

how is it txed?

A

congenital and appears at birth

most resolve on their own

283
Q

vental hernias

when does this occur?

A

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

284
Q

portal vein

lacks what?

internal pressure?

supplies what percent of blood

formed from?

A

valvless

pressure 3-5 mmHg

75% of the livers total blood supply by volume

formed by the superior mesenteric artery

285
Q

hepatic vein

where does it go?

structure?

2

3

2

A

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

right: 5, 8
middle: 4, 5, 8
left: 2, 3

286
Q

neural innervation of the liver

2

A
  1. parasympathetic of vagus nerve
  2. parasympathetic from the celiac plexsus
287
Q

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

A

parenchyma is made up of actively diviiding hepatocytes

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

288
Q

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

3

4

1

A
  1. metabolic and catabolic

a. glucogenesis

b. synthesis of phospholipids and cholesterol

c. detoxification of meds and alchohol

  1. storage

glycogen

protein

iron

vitamins

  1. excretory functions

synthesis and secretion of bile

289
Q

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

A
  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
Q

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

291
Q

what 3 LFTs suggest obstructive disease?

A
  1. bilirubin

direct=conjucated

indirect=unconjugated

  1. ALP/alkaline phosphatase
  2. GGTP/gamma-glutamyl transferase *ordered sepereately
292
Q

conjugated bilirubin=

A

direct bilirubin

293
Q

unconjugated bilirubin=

A

indirect bilirubin

294
Q

asartate aminotransferase

(AST)

elevated in?

specific?

A

elevated in acute conditions

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

295
Q

alanine aminotransferase

(ALT)

elevated in?

specific?

A

elevated in chronic conditions

primarily found in the liver so more specific than AST

296
Q

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

A

alcoholism or drug toxicity

297
Q

unconjugated (indirect) bilirubin

what is this?

if increased indicates? 3

A

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

298
Q

direct bilirubin (conguated)

what happens to this?

where does it usually go?

if increased indicates 2 things?

A

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

299
Q

is bilirubin in the urine common?

A

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

300
Q

alkaline phosphatase

where is this found?

A

found in the liver, intestine, kidney, and placenta

therefore, not specific to the liver

301
Q

gamma-glutamyltransferase

what does this indicate?

what does this help rule in/out?

A

liver specific

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

302
Q

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

A

OBSTRUCTION

303
Q

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

A
  1. hep C
  2. alcohol
304
Q

gilberts disease

what is this?

why does it happen?

2 key sxs?

A

most common hereditiary cause of increased bilirubin

impaired enzymatic conjugation of Indirect bilirubin

sxs:

  1. jaudice at birth
  2. icteric sclera
305
Q

gilberts disease

what are the 3 tests done to dx?

1 tx option?

A

DX:

  1. elevated INDIRECT bilirubin

2. normal direct bilirubin

normal US

tx

only in infancy with “bili lights” to prevent liver failure

306
Q

nonalcoholic fatty liver disease

(NASH)

6 causes

A
  1. certrain drugs
  2. obesity
  3. starnation
  4. diabetes melltius
  5. high blood tryglicerides
  6. alcohol
307
Q

nonalchoholic liver disease

(NASH)

what are the sxs?

3 dx findings? 1 key

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

A

sxs

NON UNLESS CIRROSIS

DX

1. increased echotecture at times HSM on US

2. AST/SLT increased sometimes alk phos

  1. ALT more than AST

(opposit of ETOH)

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

308
Q

non alcoholic fatty liver dxs

5 tx options?

A

TX

  1. lifestyle: weightloss, lowfat diet
  2. management of high triglycerides, BS
  3. decrease ETOH
  4. meds/supplements
    - vitamine E,
    - ursodiol
309
Q

hemochromatosis

what is this?

who does it present in?

sxs? 4

3 important labs for dx

A

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
Q

what is the tx for hemochromatosis?

A

phlebotamy, remove the iron

311
Q

wilson’s disease

what is this?

what happens in this?

3 things it causes?

2 labs must check

A

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

312
Q

wilsons disease

what are 2 key sxs?

1 tx option?

A

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
Q

alpha 1 antitrypsin deficiency

what is this?

what 2 organs does it effect?

2 effects?

tx?

A

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
Q

alchoholic hepatitis

what is this?

what is the ratio you see?

2 labs might see?

A

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
Q

what is the ration associated with alcoholic hepatitis?

A

AST greater than ALT 2:1 rarely over 300

316
Q

acute phase alcholic hepatitis

associated with what?

how serious?

3 sxs of this?

what must you calculate?

A

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
Q

what is consider tylenol OD?

what precent of acute hepatitis?

serious?

tx?

A

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
Q

autoimmune hepatitis

who is this common in?

2 labs to check?

2 biomarkers to check?

1 test needed to dx?

2 tx options!

A

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
Q

primary biliary cirrhosis

what is this strongly associated with?

what is key finding on testing?

test?

2 tx options?

A

75% cases are patients with ulcerative colitis, males

“beading” of bile ducts on MRCP (MRI)

Tx:

1. ursodiol

2. transplant cure!

320
Q

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

A

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

321
Q

acute hepatitis

what is the mortalty?

3 most common causes?

what are 4 sxs associated with this? KEY!!

A

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
Q

viral infections account for what percent of hepatitis?

A

50% of all cases

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

323
Q

hepatitis A

precentage?

virus type?

incubation?

transmission route? (3)

A

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
Q

hepatitis A

sxs?

1 (time)

7 after sxs

A

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

  1. arthralgias
  2. hepatomegally
325
Q

hepatitis A

3 dx findings

tx

A

DX:

  1. anti-hep A IGM and IGG
  2. LFTS
    - increase AST/ALT over 1000
    - increased bilirubin 5-10 x

TX: selflimiting supportive

326
Q

what are 5 prevention methods for hepatitis A?

A

improvement in hygiene and sanitation

cooking food

avoidance of water foods and endemic areas

avoidance of raw shellfish

immunization

327
Q

who gets vaccinated for hep A? 4

A

Harvix

travelers

miliary personnel

lab workers

immunocomprimised

328
Q

when you think of raw shellfish think..

329
Q

hepatitis B

what type of virus?

what percent of people have it and who?

3 transmission pathways?

KEEY THING TO KNOW ABOUT THIS

A

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
Q

what type of hepatitis can lead to hepatocellular carcinoma?

A

HEPATITIS B!! vaccines for this mandated

331
Q

what are the categories of hepatitis B?

3

A

immunity

  • vaccination
  • natural infection

actue infection

chronic infection

  • active
  • chronic
332
Q

***what are the 2 test results you want to keep in mind when looking at hepatits infection***

A

hepatitis B surface antibody (HBsAB)=IMMUNITY–ONLY PRESENT IN VACCINATED PEOPLE

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

333
Q

surface=

core=

envelope=

A

surface=immunity (vaccine or exposure)

core=exposed to virus

envelope=present infection with active replication

334
Q

acute hepatitis B

what is the breadown for how they present? (%)

1 key dx? 2 supportive?

tx2? why?

A

70% are subclinical (no jaundice or aniteric)

30% get icteric hepatitis

dx

1. HBcIGM for dx

  1. elevated AST/ALT
  2. elevated bilirubin

TX:

  1. supportive

**many will seroconvert to HBsAB and HBeAB meaning they develop immunity on their own!!**

  1. high calorie diet
335
Q

chronic hepatitis B

three phases of this?

3 tx options and length of time?

A

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!!!***

  1. interferone alpha 6 months
336
Q

hepatitis prevention and vaccination

2

A
  1. recombinant hepatitis vaccine
  2. hep B immune globulin (exposued)
337
Q

what is key to know about hepatitis D?

transmission?

A

RNA coinfection with HEP BE IS REQUIRED!!!

HBsAg

transmission: sexual contact

338
Q

hepatitis C

what is this?

3 RF/transmission?

virus type?

age?

A

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
Q

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

A

test everyone born between 1945 to 1965

340
Q

what percent of people proceed to the chronic state? what are two things you are at increased risk for?

A

80% proceed to the chronic state

HIGH RISK OF CIRRHOSIS AND HEPATOCELLULAR CARCINOMA

341
Q

hepatitis C

3 tx options?

when do you start tx?

2 main options?

how long is the tx?

A
  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
Q

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

A

viral load after 12 weeks to confirm cure

343
Q

what is cool about treating hep C?

A

IT IS CURABLE!!! nearly 100!!!!!

there is no vaccine and no post exposure immunoglobulin THEREFORE YOU WANT TO SCREEEN!!!

344
Q

what is interesting about hep G?

A

if coinfected with HIV, helps reduce the HIV replication

345
Q

HEP E

2 places you find this?

transmition

AT RISK POP?

A

North Africa

South Asian

fecal oral

self-limiting

issues in pregnacy!!! EXTREMELY SEVERE!!!! esp in third trimester 20% mortality!!!!!! KEY

346
Q

cirrhosis

what is this?

2 classifications?

A

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
Q

cirrohosis

4 sxs of compensated?

7 sxs of decompensated?

A

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
Q

cirrohsis

5 labs

3 tests

A

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
Q

cirrhosis

5 tx

A
  1. alcohol abstinence
  2. vitamin supp
  3. nuitrional supp
  4. BB for portal HTN
  5. CURE IS TRANSPLANT!!!
350
Q

what MUST you do for someone with cirrhosis?

A

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

351
Q

what is used to stage liver disease?

what does it determine?

A

MELD SCORE

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

352
Q

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

A

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
Q

hepatocellular carcinoma

4 tx

A
  1. surgical ressection
  2. chemo
  3. portal vein embolizations
  4. transplant if small and localized
354
Q

metastatic liver lesions

what is this?

3 ways it gets there?

3 dx methods?

3 tx options

A

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
Q

hepatic ressection

how much can you take?

A

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

regains albumin ability by 3rd week

356
Q

portal HTN

what are the 3 classifications of this?

5 things it can cause?

A
  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
357
Q

what are the most common PORTAL HTN locations?

A

presinusoidal and sinusoidal

358
Q

what is basically the only cause of postsinusoidal portal HTN?

A

budd-chiari syndrome

359
Q

portal HTN

5 tx options depending on cause

A
  1. nonselective BB

  1. banding for varices
  2. diuretics for ascites
  3. lactulose and xifaxan for encephalopathy
  4. surgical if meds fail

TIPS-transjugular intrahepatic portosystemic shunt

Module 9: Mali: GI (6 decks)

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