GI-CM Flashcards
1
Q
what is included in the upper GI tract?
brief function?
A
mouth to stomach
“food intake”
2
Q
what is included in the middle GI system?
brief function?
A
small intestine
- duodenum
- jejunum
- ileum
“digestion and absorption”
3
Q
what is considered part of the lower GI?
function?
A
cecum to rectum
“storage channel for elimination of waste”
4
Q
what are considered accessory organs to the GI tract? 3
A
salivary glands
liver
pancreas
5
Q
what are the 5 functions of the mouth?
2 enzymes released here and their functions?
A
- directs food
- mastication
- moistens/lubricates
- initial digestion
- receptacle for saliva
amylase break down starches
6
Q
function of the esophagus?
what does it do?
A
conduit
- smooth muscle
- mucosal and submucossal glands that protect and lubricated
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
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
- cardiac region
- fundus
- pyloric region
- antrum
- pyloric canal
- pyloric spincter
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
-
duodenum
a. contains opening for bile duct and main pancreatic duct - jejunum
- ilieum
10
Q
what does bile break down?
what does pancreatic juices break down?
A
bile: lipids!!!
pancreatic juices: lipids, carbs, proteins
11
Q
what are the two main functions of the LI?
what are the 8 parts?
A
STORAGE and WATER ABSORPTION
- cecum
- colon
- ascending
- transverse
- descending
- sigmoid - rectum
- anal canal
12
Q
what are the four layers of the wall of the intestin and what are their functions?
4
1
2
1
A
- 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
- submucosal layer
vascular, lymphatics, nerves to supply tissue
- muscularis externa
a. contains both circular and longitudal laters
b. contracts to move food along GI tract
- serosa
single layer of cells that makes the mesothelium
13
Q
what are the 2 different types of movement found in the GI system? characteristics?
2 each
A
- rythmic
a. moves food forward and keeps GI contents mixed up “oscillations”
b. present from esophagus to SI
- tonic
a. constant levels of contaction or tone without regular periods of relaxation
b. think always contracted like spincters and upper region of the stomact
14
Q
what are the 2 types of cells of the GI tract?
characterstics?
A
- 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
- 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
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
- 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
- myenteric plexsus
a. linear chair along the muscular externa all the way down the GI tract, causing motility along the entire aspect
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
17
Q
sympathetic stimulation
overall effect?
A
inhibitory, slows it down
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
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
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**
- respiration halts so you don’t breath in food
- pharyngeal spincter relaxes
- larynx closed
- soft palate closes of the nasopharyngeal folds so food doesn’t go up into the nose
21
Q
esophageal phase of swallowing
what are the two types?
where and when do they occur?
A
- primary peristalsis
upper 1/3
begins when food enters the esophagus
- secondary peristalsis
lower 2/3
where peristalsis realy occurs, occurs if primary peristalsis can’t handle the load
as it comes down it triggers stretch receptors so the spincters relax and let the food enter the stomach
22
Q
dysphagia
5 things that can contribute
A
- lubrication loss-xerostomia
- size of bolus, poor mastication
- paralysis-stroke (aspiration)
- strictures (scar tissue in esophagus)
- cancer (obstruction)
23
Q
gastric motility
function of peristalsis?
explain emptying process?when?
A
- peristalsis
a. used the make chyme
b. starts in the body and moves out to the antrum
c. as the chyme moves towards the antrum, the antrum contracts blocking the pyloric spincter so it doens’t exit the stomach and continues to be churned
2. emptying
a. chyme is empyting into duodenum between antrum contractions because the spincter is relaxed during this time, lets SMALL amounts out at a time!
24
Q
rate of gastric emptying
explain the neural and hormonal controls of this?
3
2
A
- neural control
a. hypertonic solutions in duodenum: (indicates lots of particles already present, so digestion needs to occur first)
b. pH below 3.5 (indicates recent release of acidic stomach contents
c. presence of fatty acids, amino acids, and peptides (food)
2. hormonal control
a. cholecystokinin
b. glucose-dependent insulinotrophic peptides
**these are released in response to fats being released into the duodenum, so if these are elevated it means food as already been released from stomach so don’t want to release more**
25
explain two conditions that are cause the gastric emptying to be too slow?
4
3
1. hypertrophic pyloric stenosis
## Footnote
a. very young in life, babies
b. **_thick pylorus so don't get anything through_**
c. **_causes vomiting in the baby and can't keep anything down_**
d. "_grape" in pylorus_
2. gastric atony
a. no tone so **_no contraction_**
**_b. stomach just sits there and is a problem with the nerves_**
**_c. causes: stroke, diabetes, surgical complications_**
26
what is a condition that can cause the gastric emptying to occur too fast?
dumping syndrome
## Footnote
-**_no control over pyloric spincter_**
**_often complication from gastric surgery_**
leads to:
diarrhea
higher chance of getting ulcers in the duodenum since higher amount of acid!
27
what the two types of motility in the SI?
1. segmentation waves
2. peristaltic movements
28
SI:
segmentation waves
'
what is this?
what happens in this?
what is the goal of this?
**_local mixing!_**
exposes more chyme to more surface area
**_circular msucle occludes the lumen and drives some of the contents forward and some backwards_**
\*\*imagine squeezin a long balloon\*\*
\*\*mixing it up in one spot allowing for digestion\*\*
29
SI:
peristaltic movements
what is this?
accomplished by?
goal?
stimulus?
contraction in proximal portion and subsequent relaxation in distal
accomplished by the _myenteric plexus_
goal: **_smooth muscle**_ _**propel the chyme along the gut, moving it foward_**
stimulated by MORE CHYME! NEED TO MOVE IT ALONG!!!
30
what are two probles that can occur with SI motility? what might you ifnd with each othese?
2
3
1. inflammation
## Footnote
a. increased motility
b. hyperacitve bowel sounds because the body wants to get it out
2. ileus
a. no motion or bowel movement
b. **_chyme just sitting there_**
c. see air fluid levels on xray (cmes from eating or bacteria)
31
colonic motility
what are the 2 types?
when does this occur?
what allows this to occur?
goals of each?
contracts longer here than in SI since more mass and less chyme ad this poinr and occurs **_24-48 hours after ingestion_**
1. segemental
a. **_HAUSTRATIONS_**: produce digging like movements to insure fecal material is exposed to mucosa
b. e-segment allows this to occur
2. propulsive
**_propels contents forward using LARGE segments!!_** close to 20 cm contract at the same time as one segment since it is mass instead of chyme that needs to be pushed along
lasts **_10-30 minutes a couple times a day_**
32
explain the differences between the internal and external spincters?
## Footnote
what type of muscle?
voluntary/involuntary?
control?
internal
## Footnote
**_SMOOTH MUSCLE_**
**_INVOLUNTARY_**
external
**_striated muscle_**
**_VOLUNTARY_**
**_pudenal nerve control_**
33
what are the 2 reflexes that influence defecation?
1. intrinsic myenteric reflex
## Footnote
stimulated by the local enteric nervous system from **_distention of the rectal wall with inititiartion of the preistaltic waves that push the fecal material into area_**
2. parasympathetic reflex
**_sacral cord level_**
when nerve endings in the rectum are stimulated its feedback increases the peristaltic movements and relaxes internal spincter
34
explain the difference of what happens when it is an appropriate time to defecate vs inappropriate time to defecate?
appropriate time
## Footnote
the external sphincter is under conscious control by the cortex
when the rectum is stimulated from distention it sends messages to the cortex to **_relax the sphincter_**
if appropriate, cortex sends message to relax this sphincter
inappropriate time
same process as above BUT
if inappropriate cortex sends impulses to constrict external sphincter and **_inhibit efferent parasympathetic activity_**
keeps butt hole clenched
eventually this feedback loop **_fatigues_** and the urge to defecate stops
35
gastric hormones:
gastrin
what is this released by?
what does it cause?
what stimulates it?
produced by _G-cellsin antrum_ and prompts _gastric acid secretion, HCL_
## Footnote
stimulus: vagus nerve from presence of food
36
gastric hormones:
ghrelin
what is this produced by?
what does it stimulate to be released?
what does it cause?
what are two things that stimulate its release?
produced by _endocrine cells in the fundus_ and stimulates the release of _growth hormone_ and causes _stimulatory effect on food intake and digestive function with decreased energy expenditure_
## Footnote
stimulus:
1. nuitritional like fasting
2. hormonal, decreased GH
37
what are 3 hormones that are secreted by the intestines?
1. secretin
2. cholecystokinin
3. incretin hormones (GIP, GLP-1)
38
intestinal hormones:
secretin
what cells is this release by and why?
what causes its release?
what does it inbit and stimulate?
overall effect?
secreted by **_S CELLS**_ in the mucosa of the _**duodenum and jejunum in response to acidic PH of the chyme entering the duodenum from the stomach_**
**_inhibits gastric secretion_** since this increases the HCL relase form the stomach
response:
**_prompts**_ _**pancreas**_ _**to release large quantities of fluid with high bicarbonate and low chloride to equalize the chyme (acid) that was released from the stomach_**
39
gastric hormones:
cholecystokinin (CCK)
what is this secreted by?
this is a?
3 things that it stimulates?
2 things that stimulate its release?
secreted by **_I cells_** and is used as a **_neurotransmitted_**
stimulates:
1. pancreatic enzyme release (lipase-fats)
2. contraction of gall bladder
3. potentiates secretion of secretin to increase bicarbonate in repsonse to acidity of chyme in SI
Stimulated by:
chyme release into SI and products of protein digestion and long chain fatty acid
40
intestinal secretions:
## Footnote
incretin hormones
what do these 2 hormoens do?
what are the two hormones?
what are they secreted by and where?
4
2
**_increase insulin release after an oral glucose load /carb load decreasing blod sugar levels_**
1. glucagon-like peptide (GLP-1)
**_secreted by L cells**_ in the _**distal small bowel_**
**_supresses glucagon release_**
decreases gastric emptying
get cells to release insulin
2. glucose dependent insulinotrophic polypeptide (GIP)
**_k cells in jejunum_**
decrease blood glucose by increasing insulin
41
what are the 5 regulations of GI secretions?
1. pH
2. osmolarity
3. chyme
4. hormones
5. neuroregulation
42
salivary secretions
## Footnote
3 functions?
1 breakdown?
stimulated and inhibited by?
1. lubrication
2. antimicrobial-lysozyme
3. digestion-amylase break down starches
stimulated by parasympathetic
inhibited by sympathetic
43
parietal cells
## Footnote
2 things it secretes?
in stomach
secrete:
1. gastric acid HCL
2. intrinsic factor needed for Ca++ absorption
44
chief cells
## Footnote
2 things it secretes?
1. pepsin(ogen)
2. gastric lipase
45
D-cells
## Footnote
1 secretion?
somatostatin (inhibits acid)
46
G-cells
## Footnote
1 secretion
gastrin (stimulates acid)
47
gastric lining
## Footnote
what is this? junctions? balance? 3
what is one major component that creates this? 3 functions
mucosal barrier
## Footnote
impermeable cell surface because of tight junctions
coupled secretions of H and HCO3, remains balanced
PROTECTIVE LAYER!!
prostaglandins
**_improve blood flow_**
**_decrease acid secretion_**
**_increase mucous protection_**
**_provides protection_**
48
what are 3 things that disrupt the gastric mucosal lining? how?
1. ASA
## Footnote
penetrates the lipid layer and can damage the endothelium
2. ETOH
lipid soluble so may disrupt mucosal barrier
3. bile acids
job is to break down lipis so this breaks down the wall
\*\*ALL OF THESE INHIBIT PROSTAGLANDINS WHICH HAVE A GASTRIC PROTECTIVE EFFECT SO THIS IS WHY YOU GET STOMACHE UPSET becuase H+ ions move into the cells an cause
- ischemia
- vscular stasis
- hypoxia
- necrosis\*\*
49
what are the 3 things that stimulate the release of HCL and intrinsic factor from the parietal cells?
1. gastrin from G-cells
2. acteylcholine
3. histamine
50
intestinal secretions:
Brunner glands
location?
funciton?
location: where the contents of the stomach and secretions from the liver ender the duodenum
function: secrete large amounts of alkaline mucous to neutralize the acid content from the stomach
51
intestinal secretions:
serious fluids
where do they come from? what is it? 3 functions?
secreted from crypts of lieberkuhn
## Footnote
secrere isotonic alkaline solution that acts as a vechicle for absorption
function:
1. protection
2. replaced erpithelial cells that have sloughed off
3. antibacterial
52
what is the function of the surface enzymes in the SI?
aid in absorption,
secrete pesidases that split sugars
53
what are the 3 functions of the intestinal flora?
1. metabolic-absorb nuitrients and help with energy
2. trophic-growth and regeneration
3. protection against foreign bugs
54
what are the 4 functions of the large intestine?
## Footnote
2 for the last
1. anaerobes
2. metabolic
3. vitamin synthesis/absorption K, Mg
4. protetion
a. **_mucous secretion_**
- protects linin and facilitates compaction of feces
**_b. bicarbonate secretion_**
-attaches to mucous and coats stool so the acid by products of bacteria in feces don't damage the intestine
55
what are the 3 ways that digestions occurs in the SI? what are each of these?
**_1. hydrolysis_**
breakdown of one compound that involves a chemical reaciton with water
**_2. enzyme cleavage_**
requires enzymes to cut down substances into smaller pieces and is accomplished by
_brush border enzymes_
**_3. fat emulsification_**
breakdown of large globules of fat into smaller pieces
56
what are 3 things that contribute to the power of the SI to be good at absorption?
**_1. large surface area with vili_**
2. **_brush border enzymes_**
secrete enzymes that digest _proteins and carbohydrates_
**_3. goblet cells_**
secrete mucous
57
intestinal absorption:
carbohydrates
what must they be broken down to before they can be absorbed?
expain this process? 5
must be **_monosacchrides before they can be absorbed in the small intestine_**
process:
1. **_mouth_**: **_starch_** starts being broken down in the mouth by **_amylase_**
2. pancreatic secretions also contain amylase
3. amylase breaks down starches (carbs) to **_disaccarides_**
4. dissacchrides are broken down into **_monosacchrides by brush border enzymes_**
5. absorption in SI
58
what are the 3 common dissarcharides that must be broken down by brush border enzymes before being absorbed in the SI? what are they broken down into?
**_1. sucrose_**: glucose and fructose
**_2. lactose_**: glucose and galactose
**_3. maltose_**: glucose and glucose
59
intestinal absorption:
fats
explain three main steps of this and what is included in each step?
1. emulsification
## Footnote
breaks down large globules triglycerides into smaller particles so that digestive enzymes can break down
_stomach to duodenum_
2. _pancreatic lipase_
released in duodenum cleaves triglyceriddes into fatty acids and monglycerides
3. micelles
made from _bile salts_ and monoglycerides and transport products to **_brush borden enzymes_** to be absorbed, they are then transformed into **_chylomicrons that are triglyercerides and sent to the lymphatic system_**
60
protein digestion/absorption
## Footnote
explain where things occur
2
1. pepsinogen
## Footnote
released y chief cells in the stomache in response to food, which ins then activated by the low pH to **_PEPSIN_**, then becomes inactivated in the duodenum from alkaline pH
2. pancreatic enzymes trypsin
chymotrypsin
carboxypeptidase
elastase
61
malabsorption syndrome
get **_osmotic diarreah**_ with _**fatty stool "steatorrhea"_**
sxs
muscle wasting
weight loss
failure to thirve
62
what are 6 things that can influence annorexia?
influences on appetite
hunger
hypothalamus
smell
emotional factors
drugs and disease
63
vomiting
## Footnote
5 ways this system can be triggered?
3 things these triggers stimulate?
limits the possibility of damage from ingested noixious agents by emptying contents of the stomach and portion of SI
triggers:
**_1. GI tract/organs_**
**_2. CNS system_** respinding to sights, sounds, or emotions
**_3. vestibular apparatus_**-mostion sickness
**_4. chemoreceptors_**-drugs or toxins
**_5. hypoxia_**
stimulates:
**1. salivary centers**
**2. respiratory center**
-stops breathing
**3. abdominal muscles**
- contraction/increased pressure
- LES relazation
64
gastroesophageal reflux disease
## Footnote
what is this?
population common in?
percent in US?
5 complications it can lead to
most common dxs of esophagous 15-20% US, common in pregnancy
## Footnote
**_transient relaxation of lower esophageal spincter LES_** leading to gastric acid reflux that causees damange to esophagus and spincter and can lead to:
**1. esphagitits- 50% will get this!!!**
**2. esophageal stricutre**
**3. _barrettes esophagous_**
**4. _esophageal adenocarcinoma_**
5. **hiatial hernia**
-
65
GERD
what are 6 sxs?
1 thing to keep in mind about sxs?
1. heartburn, restrosternal and postprandial
## Footnote
**_substernal pain/discomfort most commong 30-60 minutes after a meal_**
**_worsens when laying down or recumbant_**
2. regurgitation (vomit burp)
**_spontaneous reflux of sour bitter gastric contents in mouth_**
3. dysphagia (discomfort)
cough at night from acid asipiraiton
4. reccurent pneumonia
5. sxs temp relieved with antacids
6. can radiate to arm/jaw
\*\*\*keep in mind sxs don't correlate with dxs progression so can't tell how much damage has been done\*\*
66
GERD
3 dx options
6 reasons of when it is not appopropriate to use the first line dx
1. empirically first line unless (below)
2. esphagogastroduodenoscopy(EGD) if high risk or tx has failed
a. over 50
b. weight loss
c. melena
d. odynophagia _pain with eating_
e. heavy alcohol or tabacco
f. non repsonsive to tx
3. modified/full barium swallow
67
what is the pathway for txing GERD?
6
1. lifestyle adjustments
2. OTC antacids-2 weeks
3. H2 receptor antagonists
4. Proton pump inhibitors
\*\*if these fail EDG\*\*
5. prokinetics
6. surgical
68
what are the lifestyle changes a patient should make to relieve sxs of GERD?
5
1. _avoid eating 2-3 hours before bed_
## Footnote
_2. elevate head of bed_
_3. loose weight_
4. avoid acidic food, chocolate, peppermint, ETOH, coffee
5. stop smoking
69
why is it important to treat GERD?
prevent cancer aka barrette esophagus because the damange from acid makes this more likely to occur
70
what is the emergency cocktail you give someone in the ED for heart burn?
1. benadryl
2. lidocaine
3. maalox
71
in child with asthma, what is one thing you want to look for? why?
look for GERD! asthma and GERD coexist in 50% of children with asthma dx
72
what is the most common cause of esophagitits?
GERD, 50% of patients with GERD have esophagitits
73
esophagitits
## Footnote
what is this?
5 general causes?
4 sxs
inflammation of the esophagus, esp in immunocomprimised
## Footnote
1. viral
2. bacterial
3. paraistic
4. abx induced
5. radiation or chest cancers
sxs;
1. odyniaphagia
2. dysphagia
3. substernal chest pain
4. oral thursh
74
esophagitis
herpes liabilis (HSV)
3 SXS?
2 DX?
1 TX
N/V/ chills
**herpetic vesicles on nose/lips**
dx:
**_1. endoscopy_** showing small vesicles or superficial lesions
**_2. culture esophageal lesions_**
TX:
ACYCLOVIR 7-21 DAYS!!!
75
ESOPHAGITIS
VARICELLA-ZOSTER
1 dx?
tx?
N/V fever chils
**DX:**
**endoscopy: vesicles or confluent ulcers**
Tx:
1. usually resolve spontaneously but can cause _necrotizing esophagitits_
2. ACYCLOVIR!!!!
76
esophagitis
CMV
who does this occur in?
characteristics of ulcer? 2
3 sxs?
1 tx?
**only occurs in immunocomprimised patients**
**_CREEPING ULCER_** or can be GIANT ULCER
sxs:
odyniaphagia
persistent CP
hematememis
Tx:
**_IV GANCICLOVIR_**
77
esophagitis
candidia
who does it occur in?
3 complications?
1 dx?
1 tx?
**occurs in immunocomprimised host**
can cause complications:
1. bleeding
2. perforation
3. stricture
dx:
**_endoscopy: small yellowwhite raised plaques_**
tx:
**_oral or IV fluconazole!!_**
78
barrett's esophagus
## Footnote
how does this occur? what hcanges?
what are they at increased risk for? how much?
metaplastic changes in which the **_stratified squamous**_ is replaced by the _**columnar epithelium that is typically found in the duodenum_**....extens poximally from LES from repeated exposure to acid esp with GERD (thats why the cells change to this type because its the same exposure the duodenum gets)
increases risk for **_adenocarcinoma_** 5-10%
this change increases risk for neoplastic changes/cancer 40-100 times greater than general public
79
barettes esophagus
## Footnote
2 dx rules?
3 tx?
DX:
**_EDG every 2 years with bx to check for neoplastic changes_**
if there is high risk dysplasia, consider **_surgrical resection_**
TX:
\*\*more txing symtpoms unless surgical intervention\*\*
1. antacids
2. H2 blockers OTCs
3. PPIs
80
achalasia
## Footnote
what is this?
what is it caused by?
3 things you are at greater risk for?
4 sxs?
**loss of peristalsis in distal esophagus and _failure of the LES to relax**_ (LES tone increased) caused by _**dennervation to LES_**
obstruction of esophagus from LES relaxtion failure from failed stretch receptors or nerves
increased risk for:
1. aspiration
2. irritation
3. _cancers_
sxs:
**_dysphagia is most common_**
**_substernal cp_**
**_regurgitation_**
difficulty belching
81
achalasia
## Footnote
4 dx? 1 key word
4 tx options?
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_**
82
mallory-weiss tear
## Footnote
what is this?
what does it occur from?
who commonly seen in?
MC location?
3 RF?
2 sxs?
linear mucosal tear in the distal esophagus or gastric cardia from forceful _vomiting_ or retching, causing _hematemesis_ commonly seen in _alcoholics_
## Footnote
**most common location: gastroesophageal junction**
**RF:**
**alcholic**
**hiatial hernia**
**eating disorder BULEMIA**
**SXS:**
1. multiple bouts of vomiting and retching followed by **_PAINLESS HEMATEMESIS_**
2. abdominal pain
\*\*\*keep in mind the bleeding usually stops spointaneously as teh condition is usually benign\*\*
83
mallory weiss tear
## Footnote
1 dx?
2 tx?
DX:
ENDOSCOPY
TX:
1. **stabliazation**
- transfusion/gastric lavage if needed
2. **control bleeding via endoscopy**
\*\*keep in mind most bleeding stops spontaneously and condition is usually benign\*\*
84
in mallory weise syndrome what is somethign you want to do before releasing someone from hospital?
obtain occult negative stool to insure not bleeding still or hemmoraging
85
esophageal cancer
## Footnote
what are the two types?
frequency?
prognisis?
who is more common?
types:
1. adenocarcinoma
2. squamous cell carcinoma
prognosis typicaly poor, 5 year survival **_10-13%_**
both appeare with **_equal_** frequency
males more common than females
86
esophageal cancer:
**_adenocarcinoma_**
where do you find this?
4 most important RF?
2 protective
_distal esophagus_
## Footnote
RF:
1. reflux over 20 years
2. Barrettes esophagus-almost all cases
3. obesisty
4. caucasion males
5. smoking increases risk (not main)
Protective effects:
1. fiber
2. NSAIDS (seems counterintuitive)
87
esophageal cancer:
_squamous cell carcinoma_
prevalence?
location?
4 RF?
key point to remember?
prevalence is decreasing
_middle esophagus_
RF:
1. smoking
2. alchohol
3. diet low in fruits and veggies
4. achalasia increases risk 16 x
\*\*\* accounts for 90% of all squamous carcinoma in US\*\*\*
88
esophageal cancers
## Footnote
sxs
1 early
3 late
SXS:
early:
**_1. transient "sticking" of food that turns to PROGRESSIVE DYSPHAGIA_**
_later:_
1. retrosternal pain/burning
**_2.iron deficient anemia_** -loss from chronic cancer, but not enough to notice hememensis or occult
**_3. tracheobronchial fistula_**
late complication where the **esophageal wall infilates the stem bronchus causeing** _i**ntractable coughing with frequent pneumonia**_
_**\*\*\*if this occurs person has less than four weeks to live\*\*\***_
89
in esophageal cancer, when would you expect to see the weight loss and dysphagia?
when the lumen is less than 13 mm
90
esophageal cancer
## Footnote
2 DX
2 STAGE
dx:
1. barium studies
2. endoscopy
Staging:
1. **CT OF CHEST AND UPPER ABDOMENT**
**2. PET SCAN**
91
of the esophageal cancers, which is dxed more?
adenocarcinoma and squamous cell carcinoma are both dxed with equal amouth these days
92
what is the 5 year survival rate if dxed with esophageal cancer?
10-13% :-/
93
is smoking a RF for developing esophageal cancer?
yep! just like everything else!!!
94
where are adenocarcinomas and squamous cell esophageal cancers found?
adenocarcinoma: lower 1/3
## Footnote
squamous: middle esophagus
95
esophageal varices
## Footnote
what is this?
what causes this?
mortaltiy rate?
MOST COMMON CAUSE?
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_
96
where is the most common stie for esophageal varices? why?
distal esophagus at gastroesophageal junction because veins are most superficial here!!
97
what is a random syndrome that can cause portal HTN?
budd chiari syndrome
98
esophageal varices
## Footnote
6 sxs
3 dx
sxs:
**_1. hematemesis!!! over 50% stop bleeding spontaneously_**
2. melena
3. tachycardia
4. hypotension
5. syncope
6. jaundice
DX:
**1. emergent endoscopy**
CBC
BUN/creatine
type and cross
99
esophageal varices
## Footnote
4 immediate tx options
1. immediate tx-stop bleeding because mortaltiy approaches 75%
2. visceral ligation- rubber band
3. sclerotherapy
4. balllon tamponade
100
esophageal varices
## Footnote
long term tx considerations
5
1. abx
2. decrease portal HTN BB/nirates
3. shunts
4. liver transplant
5. _STOP ETOH_
101
what is boerrhave syndrome
esophageal rupture
102
oropharyngeal dysphagia
## Footnote
what is this?
what does it ususally come from?
diffiiculty inititating the swalling reflex
usually comes from neuromuscla disorders that cause weakness or lack of coorindatio of the muscles involved in swallowing
Ex: CVA, parkinsons
103
esophageal dysphagia
## Footnote
what is this?
where?
arises within the body of the esophagus, LED, or cardia most commonly from _mechanical or motility disturnances_
ex: stricuture, radiation
104
odynophagia
## Footnote
what dioes this present as?
reflect what?
substernal sharp pain on swalloing
_usually reflects SEVERE erosive disease_
105
esophageal spasm
## Footnote
what is this?
what is a specific subset of this? qualification?
2 tx options
motiltiy disorder usually associated with CP or dysphagia
**_NUTCRACKER ESOPHAGUS: increased pressure over 180 during peristalsis which creates the dysphagia_**
DX:
mamometry
TX:
1. nitrates (relaxes)
2. CCB diltiazem (relaxes)
106
esophageal manometry
## Footnote
what is this test and what are 2 things it is helpful in dxing?
measures the pressure in the esophagus, signifying the effectiveness of peristalsis
## Footnote
**_used frequently for achalsaia (NO PERISTALSIS) and NUTCRACKER ESOPHAGUS (hyper peristalsis/contractions)_**
107
esophageal ring
## Footnote
what is this?
sxs?
dx?
1 tx?
ring of tissue located at the _gastroesophageal_ junction called
**_schatzkis ring_**
sxs:
1. dysphagia with **_foods, but not typically liquds_**
DX:
barium esophagram
TX:
mechanical dilation with balloon
108
esophageal web
## Footnote
what is this?
where?
1 simple example of this?
1 dx?
1 tx?
**mid to upper esophagus**
**membranes of squmous mucosa that causes intermittent dysphagia with solid food**
_plummer vinson syndrome-WEB WITH IRON DEFICIENT ANEMIA AND GLOTTITIS_
DX:
barium esophagram
Tx:
mechanical dilation with balloon
109
pearl: in eldery patient esp after a stroke who is getting reccurent pnuemonia, what should you always check?
modified barium swallow
110
nissen fundoplication
## Footnote
what is this procedure used to tx?
how does it work?
laproscopic procedure used to treat GERD or hiatial hernia
1. gastric fundus is wrapped around the lower end of the esophagus
2. stablaizes this area and spincter and prevents hernia and GERD
111
hiatial hernia
## Footnote
what is this?
what are the sxs?
tx?
occurs at the LES where the **_upper part of the stomach moves into the upper chest and through the small opening in the diaphram_**
the diaphragmatic hiatus acts as an additional spincter around the lower end of the esophagus
SXS:
produces symptoms of GERD or dysphagia
TX:
surgical
112
systemic scleroderma
## Footnote
what is this? what are the **5 common presentations**? what is the **#1 think you worry about in this?** what test do you do in the lab? what are the treatments?
thickening and harderning of the skin **via collagen deposition**
1. raynauds (75%)
2. vascular changes in nail bed
3. GI dysmotility "watermelon stomache"
4. puffy hands
5. fixed face
\*\*\*\*\*WORRY ABOUT PULMONARY FIBROSIS AND ACUTE RENAL FAILURE\*\*\*\*\*\*\*
DX: ANA-SPECKLED
Tx: treat system effected
renal-ACE inhibitors
raynauds-calcium channel blockers
Gi: promotility
lungs: cyclophosphamide
113
CREST Syndrome
what is the pneumonic to remember the symptoms and what do you need to monitor annually in these patients?
LIMITED SCLERODERMA
**C- calcinosis** of joints leading to puffy hands
**R- raynauds**
**E-Esophageal dysmotility**
**S-sclerodactyly** of _MCPs_
**T: telangiectasis**
\*\*complication=pulmonary hypertension so need to get _annual PFT/DLCO to make sure no lung fibrosis_\*\*
Tx: symptoms
114
what do you need to avoid in schleroderma pts because it can cause a RENAL CRISIS?
high dose corticosteroids.
don't do it!
115
gastritis
## Footnote
what is this?
5 causes?
2 sxs
dx
**inflammation or irritation of the gastric lining**
causes:
ETOH
H. pylori
NSAIDS
STRESS
autoimmune
SXS:
**_often asymptomatic_**
**_initial presentation may be GI blleeding_**
"coffee ground, melena, emesis
DX:
_endoscopy_
differentiates from PUD
116
gastritis-ETOH
## Footnote
how do you tx this?
nausea, dyspepsia, hematemesis
TX:
H2, PPI, or sucralfate
**_4 week tx_**
117
gastritis-H. pylori
## Footnote
how presents?
2 things associated with?
**_usually symptomatic_**
cofactor for PUD
**two things associated with:**
**1. gastric adenocarcinoma**
**2. B-cell gastritis-mucosal associated lymphoid tissue (MALT)**
118
NSAID gastritis
## Footnote
common?
recognized early?
2 tx? (how)
VERY COMMON 25-50%
**MOST GO UNREGOGNIZED BECAUSE OF NO SXS**
**TX:**
**1. D/C NSAIDS**
**2. TX EMPIRICALLY IF ON NSAIDS**
**3. PPI 2-4 WEEKS**
119
stress gastritis
## Footnote
who do you find this in?
because?
3 causes?
1 tx?
prophylaxsis
common in **_ICU patients_**
develop quickly in this population
caused by **decreased mucosal flow**
Seen in:
1. trauma
2. _respiration failure/mechanical ventilation_
3. _coagulation problems_
**prophylaxisis in high risk:** PPI oral or NG tube to decrease bleeding
**tx:** PPI
120
stomach neoplasms
## Footnote
where do these occur?
appearance? 4
sxs?
3 dx?
1 tx
occur in antrum, MC in lesser curvature
**_bulky, irregularly shaped_**
**_firm, jagged edges_**
usually asymptomatic till late disease
early detection is therefore difficult
DX:
1. barium swallow xray
2. endoscopic studies with bx
3. cytologic (screening in atrophic gastritis/polyps)
TX:
**_surgery-radical subtotal gastrectomy TOC_**
121
what are 6 RF for stomach neoplasms?
1. genetic predisposition
2. carcinogenic diet
_smoked food/perserved food_
3. autoimmune gastritis
_increased inflammation_
4. gastric adenomas
5. polyps
6. h. pylori, cofactor for some
122
Peptic ulcer disease
## Footnote
what this this?
2 causes?
1
3
size?
**break in the gastric or duodenal mucosa that _extends through the muscularis mucosa_ that comes from**
**1. _impaired normal mucosal defense factors_**
NSAIDS
**_2. defense factors overwhelmed by aggressive luminal factors_**
acid
pepsin
infection
greater than 5 mm in diameter
123
what are the 5 common causes of PUD?
1. NSAIDS
2. H. pylori
3. idiopathic
4. hypersecretory states
5. smoking
124
3 locations of PUD?
which one is most common?
how long do they take to heel?
what do you need to keep in mind that is very important depending on location?
1. duodenal
## Footnote
a. **_MOST COMMON LOCATION!!_**
b. 90% heal in 4 weeks
2. pylorus
3. gastric
\*\*CAN BE MALIGNANT\*\*
\*\*must get bx at endoscopy time\*\*
a. take longer to heal 8 weeks!
b. increased length of tx
125
peptic ulcer disease
NSAIDS
cause?
why?
4 RF?
2 tx? length of time?
caused by long term NSAID use esp nonselective COX1 and COX2 blockers
_COX1 decreases prostaglandins_ which have a _protective effect on gastric mucosa_, it the lack of this **_impairs gastric mucous and HCO3 secretion_**
\*\*this is why COX2 selective are better option since decrease risk of bleeding\*\*
RF:
1. ASA
2. corticosteroids
3. over 60
TX:
**_1. PPI_** or H2
\*\*\*4 weeks duodenal\*\*\*
\*\*\*8 weeks gastric\*\*\*
**_2. D/C NSAID_**
126
peptic ulcer disease:
h. pylori
KEY?
characteristic?
acute/chronic characteristics?
what is key about this?!
**_nesscary cofactor for 75-90% of duodenal/gastric ulcers_**
characteristics:
PRODUCE UREASE
ACUTE:
a. infectious "gastroenteritis"
CHRONIC:
a. **_ASYMPTOMATIC_**
b. DIFFUSE SUPERFICIAL MUCOSAL INFLMMATION WITH POLYPS
\*\*ERRADIACATION IS ESSENTIAL OTHERWISE _85% WILL RECURR!!!!!\*\*_
127
what is a RF for all ulcers?
smoking!
128
explain the patho for duodenal ulcer with h. pylori?
6 steps
1. H. pylori infection **increases acid production**
2. causes **gastric metaplasia in duodenal bulb**
3. H. pylori infection
4. causes **duogenitis**
5. causes **mucosal breakdown**
6. causes **duodenal ulcer from breakdown**
129
explain te patho of stomach ulcers caused by h. pylori?
1. infection in body
2. causes **gastritis and chronic inflamation that overwhelms immune system**
3. causes **mucosal breakdown**
4. creates gastric ulcer
130
PEPTIC ULCER DISEASE
## Footnote
2 sxs
3 dx
when do you use each?
1 think must do?
SXS
1. _epigastric like pain "hunger like" in 80-90%_
2. _50% have relief by eating antacids within 2-4 hours_
\*\*physical exam is often unremarkable so need to watch for changes in pattern, indicating perforation or penetration\*\*
DX:
1. endoscopy EDG TOC!
allow so for visulaization and also bx!!
2. fecal antigen test (noninvasive)
3. c-urear breath test (noninvasive)
\*\*\*\*OPTIONS 2 AND THREE AT THE TOC FOR ACTIVE PUD AND PROOF OF ERADICATION\*\*\* _MUST D/C PPI 7-14 DAYS PRIOR OR MAY GET FALSE POSITIVIVE!_
131
peptic ulcer disease
tx without h. pylori
2
3 for first
1 second
1. _antisecretory agents_
A.**_PPIs_** 1st DOC-inhibit 90% acid secretion
**_ompreazole_**
**_lansoprazole_**
B. H2-inhibit histamine mediated secertion
C. OTC anti-secretory
2. _mucosal defense agents_
2nd line can be used as adjunct for _symptom relief_
**sacralfate, busmuth**
132
peptic ulcer disease:
## Footnote
Treatment for H. pylori
what is the tx regimen?
what must you do after tx and when?
2/3 abx, PPI, +/- bismuth
## Footnote
**_1. amoxicillin_** 1 g BID
**_2. clarithromycin_** 500 mg BID
**_3. HIGH DOSE 40 mg PPI_** BID
\*\*\*no reason shouldn't use quadrople therapy see in this pic\*\* KNOW BOTH
\*\*must confirm eradication with C-urea breath test or fecal antigen test
4 weeks post abx
2 weeks post PPI\*\*\*
133
peptic ulcer disease:
post H. pylori tx tx
2 considerations
**DUODENAL f still large or bleeding post tx:**
_continue PPI for 2-4 weeks_
**GASTRIC if large ot blleding post tx:**
_continue PPI for 4-6 weeks_
134
in reccurent ulcers what must you do!?
rule out H. pylori and NSAID use
135
peptic ulcer disease:
complication!
bleeding ulcers
what percent of people?
times increase in mortality?
2 sxs?
2 dx?
4 tx? but keep in mind?
**occur in 10-20% of pts with PUD**
## Footnote
\*\*may be the first sign of an ulcer\*\*
**REBLEEDING INCREASES MORTALITY 10X**
SXS:
_hematemensis_
_melena_
DX:
**_endoscopy!_**
predicts liklihood of rebleeding
**_HgB, Hct_**
TX:
**80% OF THESE STOP BLEEDING SPONTANEOUSLY**
1. _isotonic fluids to replace volume_
2. _endoscopy can help stop bleeding_
3. _HIGH DOSE PPI_ to decrease bleeding
4. surgery in extere
136
peptic ulcer disease:
## Footnote
COMPLICATIONS
PENETRATION/PERFORATION
results in?
2 sxs?
tx?
results in chemical peritonitis
a. severe generalized abdominal pain
b. _rigid abdominal rebound_
_TX:_
_1. laproscopic perforation closure_
_2. increased RX TX_
137
peptic ulcer disease:
refractory ulcers
what is this caused by?
3 contributing factors
uncommon, contributed to non compliance with medication
Contirbutory factors:
1. cigs
2. NSAIDS
3. failutre to eradicate H. pylori! MUST DO THIS
138
gastroparesis
## Footnote
what is this?
issue with what?
5 causes?
2 sxs?
3 dx?
3 tx?
**delayed stomach emptying caused by partial paralysis of the stomach**, so food remains in the stomache for abnormally long time
vagus nerve issue
causes:
1. DM
2. bulemia
3. parkinsons
4. abdominal surgery
5. cigarettes
SXS:
_1. **chronic nausea**_
**_2. fullness after just a few bites_**
3. vomiting
DX:
1. xray
2. mamometry
3. gastric emptying scans
TX:
**_1. dietary changes, lowe fiber, low residue diets_**
**_2. SMALLER MEALS_**
3. antidepressant mirtazapine
139
pyloric stenosis
## Footnote
who do you find it in?
m/f?
caused by?
2 main sxs?
2 dx?
1 tx?
\*2 key buzz words\*\*
children 4-6 weeks old
## Footnote
more comme males
gastric outlet is blocked by **_pyloric hypertrophy_**
SXS:
**_1. progressive projectile vomiting in child who remains hungry_**
2. oval shaped mass right of the umbilicus, esp right after eating!!
DX:
US
barium swallow with **_"STRING SIGN"_**
TX:
SURGERY!!!!!
140
zollinger-ellison syndrome
## Footnote
what is this?
by the time of dx...?
rate?
what can it cause?
3 locations?
met site?
_gastrinoma_ that secretes large amounts of _gastrin_ so causes recurrent and refractory gastric ulcers, 1/3 have mets by dx
## Footnote
SLOW GROWTH
the increase in gastrin **increases the osmoliarty of the lumen so it draws water out and can cause _diarreah_**
locations:
1. pancreas
2. duodenum
3. lymph nodes
**metastasizes to _liver_**
141
zollinger-ellison syndrome
## Footnote
what are the 3 sxs?
3 dx options?
2 tx depending if isolated or mets?
SXS:
GERD
diarrhea
malabsorption weight loss
DX:
1. serum gastrin over 500
2. pH less than 3
3. somatostatin receptor scintigraphy endoscop US
_finds primary tumor and mets_
tx:
**isolated primary tumor:** _PPI and resection_
**mets:** _PPI high dose_
142
what percent of gastinomas are malignant?
2/3
143
gallbladder
## Footnote
2 functions
when is it filled?
when is it released?
1. STORES BLADDER
2. CONCENTRATES BILE
filled when the spincter of oddi is closed
contracts in response to **_cholecystokinin to release bile into the duodenum_**
144
bile
## Footnote
what does it do?
3 things it is made of?
digests _fats_ in SI, terminal ileum, and recycled to liver for reexcretion
## Footnote
CONTENTS
1. bile salts (from cholesterol)
2. bilirubin (waste product RBC)
3. alkaline fluids
145
cholecystic
referring to gallbladder
146
cholecystitis
inflammation (chronic or acute)
147
cholithiasis
stones in GB
148
choledocholithiasis
stone in the bile duct
149
cholecystectomy
surgical removal of GB
150
pancreas
exocrine portion
2 cell types?
which more common?
things it secretes?
3
1
ducts enter the duodenum
ENCOMPASSES:
1. acinar cells-95% of pancreas
**1**. secrete proteolytic enzymes including **_trysinogen, chymotrypsinogen, procarboxypeptidases for protein digestion_**
2. **_amylase for carb digestion_**
3. **_lipase-fat digestion_**
2. ductal epithelial cells
a. **_alkaline secretion_** to decrease the acidic pH of the duodenal contents
151
cholecystalgia
pain (aka billiary colic)
152
pancreas
## Footnote
3 location descriptors
during development
2 things contains
in **retroperitoneum**
**head near _duodenum_**
tail posterior to stomach
during development two pancreat buds come together to fuse
CONTAINS:
exocrine portion
endocrine portion
153
what are the most common cells in the pancreas?
acrinar cells
154
pancreas:
endocrine portion
where do secretions go?
what are the cells made into?
what are the 3 cell types??
secretion into the blood stream
1. islets of langerhans
"islands of endocrine cells" 1-2% of pancreas
**_beta-cells:_** insulin synthesis/secretion
**_alpha cells:_** glucagon
**_deta cells_**: somatostatin, inhibits GH and TSH
155
tumor markers:
ca 19-9
pancreas
156
tumor markers
## Footnote
ca-125
ovarian cancer
157
tumor markers
AFP
liver cancer
158
tumor markers
CEA
colon cancer
159
acute pancreatitis
## Footnote
6 sxs
where is pain?
severity?
what makes worse/better?
pain with...?
two key signs you dont want to miss?
1. **_epigastric radiates to back_**
2. **_billiary colic PERSISTS DOESN"T GO AWAY_**
3. **_worse SUPINE, BETTER LEANING FORWARD_**
4. **_PAINFUL INSPIRATION, SHALLOW BREATHS_**
5. _TACHYCARDIA_
**_6. hemmoragic pancreatitis_**
_cullens sign_: periumbical ecchymosis
_grey tuner's sign:_ flank eccymosis
160
tumor markers
PSA
prostate
161
explain the pathophys of pacreatitis?
what are 2 theories that cause this?
1. inflammation of the pancreas causes damage to the **_acrinar cells_**
2. the inactive proenzymes like _trysinogen_ are activated early while still in the pancreas
3. early activated _lipases_ disolve the fat
4. so the _pancreatic enzymes_ start to DIGEST THE PANCREASE "EATS ITSELF"
theories:
1. obstruction of the pancreatic duct due to stones
2. failure of the two parts of the pacreas to fully join during development _pancreatic divism_
162
acute pancreatitis
## Footnote
what are 2 MC causes? account for what? 6 others?
causes:
1. gallstones 45%-**MC**
2. alcohol 35%
\*\*these two are most common and make up 80% of cases\*\*
other causes:
trauma
drugs (iatrogenic)
obstruction (tumors)
infections (mumps)
metabolic (hyperlipidemia)
toxins (methyl alcohol, scorpion stings)
\*\*MOST RECOVER AND HAVE NORMAL FUNCTING PANCREASE\*\*
163
when dxing pancreatitis and looking at labwork, what test is most effective?
lipase
(this is better than amylase)
164
acute pancreatitis
## Footnote
5 labs tests?
TOC for dx?
LAB TESTS:
**_elevated cbc_** (infection)
**_elevated lipase_** (pancreas)
**_elevated LFT_**
**_elevated glucose_**
**_decreased calcium_**
TEST OF CHOICE FOR DX: **_CT SCAN!!!_**
scored A-E, A is good, E is bad
165
acute pancreatitis
## Footnote
5 labs tests?
TOC for dx?
LAB TESTS:
**_elevated cbc_** (infection)
**_elevated lipase_** (pancreas)
**_elevated LFT_**
**_elevated glucose_**
**_decreased calcium_**
TEST OF CHOICE FOR DX: **_CT SCAN!!!_**
scored A-E, A is good, E is bad
166
acute pancreatitis
## Footnote
6 tx options?
what is the process dependent on?
mostly supportive
## Footnote
a. NPO 48-72 hours **_NO ALCOHOL_**
**_b. ERCP if presense of stone**_ _**on CT scan_**
b. maintain hydration
c. pain control
d. NG tube in extreme
e. abx if infectious
f. incision and drainage if infected/necrosis
167
chronic pancreatitis pathophysiology
## Footnote
what is this?
what should you think about when thinking of this?
what happens?
inflammatory disease of the pancreas
**_irreversible**_ _**changes occur_**
**_can lead to permanent loss of function_**
HINT: think necrosis fibrosis theory of alcoholic pancreatitis
alcohol to tissue damage to fibrosis to partial obstruction
168
chronic pancreatitis
## Footnote
what is the MC cause of this?
3 others?
NOT CAUSED BY WHAT?
what can this lead to?
1. alcohol cause #1!!
\*\*\*THIS IS **_NOT_** CAUSED BY GALLSTONES LIKE ACUTE\*\*
2. **_obstructive causes of spincter of oddi by neoplasms_**
3. **_malnuitirion_**
4. metabolic
chronic pain leads to opoid addiction! keep this in mind
169
chronic pancreatitis
## Footnote
4 dx options
fat stranding
1. amylase/lipase **_NORMAL_**
## Footnote
body gets used to working under these circumstances
2. _secretin stimulation test "gold standard" for **early** chronic pancreatitis dx_
3. plain xray films QUICK AND CHEAP-see calcifications
4. CT SCAN-better at seeing calcifications but $$/rad
_"arrowhead and fat stranding"_
170
chronic pancreatitis
4 sxs?
sxs:
1. **_epigastric abdominal pain_** that radiates to the **_LEFT_**
2. insufficiency of pancreatic function leads to
**_a. steatorhhea_** damages decreases lipase
**_b. diabetes_** once islets damaged
**3. asymptomatic and found incidently**
171
chronic pancreatitis
## Footnote
5 tx options
most important!!
2 drugs?
1. _stop the alcoho_l!!
2. controls sxs
a. **pain control**
**b. prancreatic enzyme supplements _viokase and pancrease_**
3. endoscopic duct decompression
4. surgical draingage of duct
5. celiac plexsus nerve block
172
what are 4 things that that increase persons chance of bad outcome/mortality with pancreatitis?
1. organ failure
2. pancreatic necrosis
3. obesity
4. old age
173
what are the two criteria used to identify the mortality with pancreatitis?
1. Ranson's criteria
## Footnote
_Take home: higher numbers means more severe disease and increased risk of death_
-measured at time of admission and during first 48 hours
**6+=50% mortality**
2. APACHE II score
\*\*typically impatient ICU use\*\*
over **_8_** is severe!!!
174
pancreatic cancer
## Footnote
what are thet wo tumor markers?
survival?
1 RF?
tumor markers:
1. CA19-9 85%
2. CEA 40-45%
5 year survival is only 4% _really bad_
only RF: _chronic pancreatitis_
175
pancreatic cancer
## Footnote
4 sxs?
toc? 1
sxs:
1. _painless **jaundice** is PC until prove otherwise_
2. **_virchows node_-**supraclavicular node
3. **_trouseaus signs- recurring superficial thrombophlebitis_**can be anywhere
4. weight loss
TOC: _CT scan dual phase helical_
176
pancreatic cancer
## Footnote
what two lab findings supposrt this?
3 tx options?
LABS:
**_1. elevated direct bilirubin_**
**_2. elevated alkaline phosphatase_**
(significantly elevated in cancer)
**_TX:_**
**_1. chemo_**-poor respinse only reduces size to buy little time
2. _whipple surgery_-only at cancer specialties
3. **_pallaitive care_**
177
acute cholecystitis
## Footnote
what happens in this?
what is most likely to cause this?
leads to 3 things? possible worst case?
2 _key_ sxs?
the **_cystic duct**_ becomes blocked _**most commonly from gallstone!_**
less common:
cancer, sludge, infection
blockage causes distention and edema that cauess _ischemia, necrosis, perforation_ and possible _generalized sepsis_
SXS
1. RUQ/epigastric pain _radiate to shoulder/scapula_
2. _murphys sign_ (tenderness and pt stops inspiration on palpation)
178
acute cholecystitis
## Footnote
2 dx tests? when to use?
2 labs?
TOC #1: **_US_**
## Footnote
find gallstones and _wall thickening over **3 mm**_
TOC #2: **_HIDA nuclear med scan_** (cholescintigraphy) GOLD STANDARD and _BEST TEST_
\*\*\*\*not usually used since it is $$$$$$$, so US becomes TOC\*\*\*\*\*\*
Two elevated labs:
**_elevated gamma-glutamyl transpeptidase_**
**_elevated bilirubin_**
179
acute cholycystitis
## Footnote
TXOC?
3 others?
TreatOT: TAKE IT OUT!! MOST COMMON!! via _laproscopic cholecystectomy_
2. leave in if very mild
3. drain it if patient too sick
4. abx if elevated WBC
180
cholelithiasis
two types of stones?
percentage?
what do they look like?
**1. cholesterol stones**
MC-75% of stones!!
don't show up on xray
2. **calcium bilirubinate/ca salts**
25% of stones
pigmented black/brown sludge stones
181
explain 3 pathphys concepts of cholelithiasis?
## Footnote
one population more at risk
1. cholesterol supersaturation of bile
2. nucleation
cholesterol comes together and crystalizes, propogates
3. GB hypermotility
slower emptying=more time for stones for form
**THINK PREGNANT WOMAN!!!**
182
acute cholithiasis
## Footnote
what do you need to keep in mind about sxs?
how do they present? 3
dx TOC?
what do you need to keep in mind?
_asymptomatic in 50-60%_
## Footnote
symptomatic patients:
**biliary collic with _RUQ pain/epigastric areas_**
**_refers to back, scapula or R shoulder_**
DX:
TOC: transabdominal US
**_shows stone without wall thickening_**
\*\*_keep in mind not great for stones in common bile duct\*\*_
183
what are the four RF for cholithiasis?
1. over 40
2. obesity (or rapid weight loss)
3. female/pregnant
4. native american
**"FEMALE, FAT, FORTY, FERTIL" 4, F's**
184
acute cholelithiasis
## Footnote
what are you 3 tx options and who are they appropriate for?
1. cholecystectomy-MOST COMMON "it hurts
## Footnote
2. leave in if doesn't hurt _UNLESS_ high risk to keep in
a. diabetics
b. sickle cell
c. Native americans with _calfieiced "porcelain" stone_
3. dissolve cholesterol stones with _actigal, urodeoxycholic acid_ but $$$
185
acute ascending cholangitis
## Footnote
what is this?
why is it important?
sxs? KEY
infection and inflammation of the billiary tract **_COMMON BILE DUCT_**
obstruction then infection
**_potentially life threatening_**
**_CAN LEAD TO SEPSIS OR SHOCK!!!!_**
**_sxs:_**
**_charcots triad_**
1. abdominal pain
2. jaundice
3. fever
\*KNOW IT\*
186
acute ascending cholangitis
## Footnote
what are the 3 things seen on labs?
what must you make sure to do?
2 tx options?
LABS:
1. leukocytosis
2. hyperbilirubinemia
3. alkaline phosphatase increasing
**_\*\*\*\*\*\*MAKE SURE TO ORDER BLOOD CULTURES X2\*\*_**
TX:
**1. ABX TO COVER _GRAM NEGATIVE ANAEROBES, ENTEROCOCCI_**
penicillin
aminoglycoside
**_2. REMOVAL OF OBSTRUCTED STONES ERCP_**
187
choledocholithiasis
## Footnote
where is the stone?
where does it come from?
where is pt?
sxs? 4
stone in the **_COMMON BILE DUCT_**
usually migrate from the gallbladder
patient very sick and likely in ICU!! compared to cholelithiasis
sxs:
asymptomatic in 30-40%
**_BILLARY COLIC_**
**_jaundice, pancreatitis_**
188
choledolithiasis
## Footnote
what are the two dx/tx options?
what must you keep in mind?
1. MRCP magnetic resonance cholangiopacreatogprahy ONLY DX
## Footnote
2. ERCP-endoscopic retrograde cholangioancreatography DX **_AND TX so GOLD STANDARD!!_**
\*\*\*\*keep in mind contraindicated in pancreatitis/cholecystomy\*\*\*
189
niacin
2 functions
4 sources
1 presentation
FUNCTION:
1. energy
2. fat metabolism
Soucres:
1. tuna/ salmon
2. chicken/beef
Presentation:
**FLUSHING**
190
thiamine
## Footnote
4 sources
2 functions
4 presentations
SOURCES
1. pork
2. grains
3. dried beans
4. peas
FUNCTION:
carbohydrate metabolism
_nerve function_
PRESENTATION
berberi
**nervous tingling**
**poor coordination**
**edema**
**cardia dysfrunction**
191
vitamin A
## Footnote
4 sources
2 presentations
3 toxicities
SOUCRES
1. liver
2. fish oils
3. fortified milk
4. eggs
CLINICAL PRESENATION
**night blindness**
**dry skin**
TOXICITY
1. skin disorders
2. hair loss
3. teratogenicity
192
riboflavin
4 sources
1 function
2 presentations
sources:
1. milk
2. spinach
3. liver
4. grains
functions
ENERGY
presentation
**oral inflammation**
**eye disorders**
193
vitamin C
## Footnote
4 sources
3 functions
3 presentations?
SOURCES
**1. citrus berries**
**2. starberies**
**4. broccoli**
**4. greens**
functions:
1. collagen synthesis
2. hormone function
3. neurotrasmitter synthesis
PRESENTATION!
**_scurvy_**
**poor would healing**
**petechiae**
**bleeding gums**
194
what does the toxicity of vitamin C cause?
diaareah
195
vitamin D
## Footnote
1 source
2 functions
2 at risk
source
FORTIFIED MILK
functions
**CALCIUM REGULATION**
**CELL DIFFERENTIATION**
at risk:
elderly
and those without sun exposure
196
vitamin D
## Footnote
2 preseentations
3 toxicitiy
rickets
osteomalacia
toxicity;
1. hypercalemia
2. kidney stones
3. soft tissue deposits
197
vitamin K
## Footnote
4 sources
1 function
1 presentation
2 toxicity
sources:
1. liver
2. green leafy veggies
3. broccoli
4. peas
5. green beans
functions
**_clotting_**
presentation:
**_bleeding_**
toxitiy presents as:
**_1. anemia_**
**_2. juandice_**
198
folate
## Footnote
4 sources
1 function
4 presentations of deficiency
sources
1. green leafy veggies
2. organe juice
3. grains
4 organ meats
RF:
**_PREGNANCY!!!!!_**
presentation:
1. megaloblastic anemia
2. sore tongue
3. diarreah
4. mental disorder
199
appendicitis
## Footnote
what is this?
MC cause?
2 risks?
3 presentations?
**inflammation of the appendix causing leakage of cecum contents and blockage** _MC common due to fecalith_
RISK OF SEPSIS AND DEATH IF RUPTURES
SXS:
**1. sudden onset of abdominal pain**
2. **_umbilicus progresses to RLQ pain_**
3. pain to palpation
200
appendicitis
## Footnote
5 physical tests to do to confirm?
2 tests to do to confirm suspicion?
TESTS:
1. rovsings sign
2. obturatory sign
3. psoas sign
4. mcburneys
5. _rebound tenderness_
6. CT-inflammation
7. surgical consult
201
appendicitis
## Footnote
what is the tx for this?
what is the controversy concerning this?
surgical tx is standard of care
## Footnote
\*\*\*\*\***abx in recent studies conclude that 80% could be txed IV but 25% required emergency removal of appendix within first year post op....SO NOT IDEAL\*\*\***
202
constapation
## Footnote
what is the qualification for this classification?
what are the 7 causes?
difficult passing stool
qualification:
difficulty in over 25% of attempts for over 3 months with NO obstructive or peristalsis disorder
causes:
nervous system disorders
neural transmitter malfunction
hormone malfunction
heighten immune response
poor diet
poor activity
mediation Se
203
constapation
## Footnote
what must you rule out?
2 DX options?
3 tx options?
must r/o obstruction, impaction
## Footnote
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
constapation
## Footnote
what are the 3 classes of drugs you can use to tx this?
what is the function of each?
\*\*add the drugs from table\*\*
1. bulk forming laxatives
## Footnote
- absorbs water and increases fecal mass
- Fiber
2. ostmotic laxatives
causes H2O retnetion in the stool (pull water into the stool)
- PEG
3. stimulant laxatives
increase acteylcholine regulated GI motility peristalsis
-senna
205
celiac disease
## Footnote
what type of condition is this?
what is the patho of this and the specific component?
nickname?
autoimmune dx of _SI_
## Footnote
introlerance to **_gluten and the alpha-gliadin_**
gluten triggers immune response in turn causing damage to the small intestine
causes _nuitritional deficits secondary to absorption issues_
"celiac sprue"
206
celiac disease
## Footnote
what are 6 sxs that come with this?
explaination of the last?
1. unintended weight loss
## Footnote
2. persistently underweight
3. sxs of poor nuitrition
4. "failure to thrive in child"
5. diarreah
6. _dermatitis herpetiformis_
a. ***intense itching***
***b. blisterning rashes***
***c. 10-15% of patients***
207
celiac disease in children
## Footnote
when does this start?
4 causes in children
2 things at increased risk for
GI issues start when there is gluten introduced to the diet
irritablitly
anxious
distention
abdominal pain
high risk for:
1. dehydration
2. hypokalemia due to increased fluid loss
208
celiac disease
## Footnote
what are the 3 dx options of this?
key thing to remeber?
1. anti-tissue transglutaminase antibodies OR anti-endomysium IgA antibodies
## Footnote
2. _bx if small intestine_ and blood + for antibody
\*\*\*\*if they have dermatitis herpetiform with + antibody skin bx, THEN NO NEED FOR INTESTINAL BX\*\*\*
209
celiac disease
## Footnote
what are the 2 tx for this?
what about screening?
1. gluten free diet
## Footnote
- wheat
- rye
- barley
2. abx for dermatitis herpetiformis
\*\*\*make sure to screen if family hx using blood test for autoantibodies\*\*
210
diverticula
## Footnote
what are these?
how are they formed?
sac-like protrusions in the colonic wall
**blood vessels penetrate the mucosal wall**
**internal layers penetrate through weak areas creating diverticula**
211
diverticulosis
## Footnote
what is this?
where does it most commonly occur?
what is important to know about this?
presentation?
2 things to avoid?
condition of having divericula
typically asymptomatic
MC in SIGMOID COLON, _account for 50% of all lower GI bleeds, bright red blood in rectum earliest finding MOST COMMON_
diet restricted in
seeds, strawberries
212
diverticulitis
## Footnote
what is this?
3 sxs?
2 tests?
inflammation of the pocuhes
1. severe **_LLQ_** pain
2. change in bowel habit
3. constapation
Tests:
1. **_CT TOC with IV and oral contrast_**
2. WBCs
3. barium enema
4. colonoscopy
213
who is diverticulosa most common in?
## Footnote
2 percents?
western/industerialized societies
## Footnote
30% by 60
65% have by age 85
214
what are 3 RF for diverticulosa?
1. connective tissue disorders
2. low fiber diet
3. too little exercise
215
what are the two conditions that make up inflammatory bowel disease?
1. crohns disease
2. ulcerative colitis
216
crohns disease
## Footnote
3 populations common in
1. common in 15-35
2. jewish population
3. increased risk with family hx
217
Inflammatory bowel disease
crohns disease
where are the lesions?
how deep are lesions?
where is the pain?
3 things that can occur as complications?
4 things that are common?
3 other things it can effect?
bowel appearance?
1. legions mouth to anus; spread out with healthy tissue between
_2. transmural_
**_3. RLQ pain MC_**
4. fistulas, abscesses, fibrotic stricutres
5. bleeding common
6. weight loss common
7. obstruction common
8. perianal disease common
8. can effect skin eyes joints liver
9. _large volume_ diarreah and mucous (trash bag)
218
what 2 are tests you want to do to look for crohns?
1. anti-saccharomyces cervisial (ASCA)- 44% of crohns are pos
## Footnote
2. _colonoscopy TOC_
219
what are the 4 tx options for crohns?
1. 5-aminosalcyclics (5-ASA)
## Footnote
**-mesalamine**
**-sulfasalazine**
2. corticosteroids
3. cimzia-certolizumab
4. humira-adalmumab
\*\*surgery doesn't work since it involves the entire GI tract\*\*
220
which is more common crohns or ulcercerative colitis?
ulcerative colits 3x more likely
221
what groups of people does ulcerative colitis effecT?
1. ages 20-30
2. caucasions and jewish descent
3. family hx is strongest RF
222
ulcerative colitis
## Footnote
where is this?
pain presents?
what is most common and worse?
what does person have increased?
what might they develop?
describe lesions and how deep?
what does the colon look like on colonscopy?
what are 3 things aren't present?
1. primarily localized in _colon_
**_2. LLQ_**
3**_. bleeding from rectum_** **_is most common_**
3. _urgency need of BM_
_4. potenital anemia due to blood loss_
4. lesions are continuous starting at the rectum and in mucosa only
5. _colon wall thin with continuous inflammation_
6. no granulomas
(weight loss/obstruction very rare with this)
223
what do you use to dx ulcerative collitis?
colonoscopy
224
what are the 3 tx options for ulcerative collitis?
1. 5-ASA
- sulfasalzine
- mesalamine
2. corticosteroids
3. **_colonectomy CURE best choice_**
removal of colon
225
irritable bowel syndrome
## Footnote
what is this?
who most common in?
age?
pathogenIsis? 3 **causes**
**_dx of exclusion, no other cause_**
FUNCTIONAL BOWEL WITH MUCOSAL INFLAMMATION
women more than men
presents before age **_45_**
**_1. abnormal motiltiy_**
_2. **visceral hypersensitivity**_ lower visceral pain threshold
**_3. psychosocial interaction_**-emotional stress
226
irritable bowel syndrome
## Footnote
3 tx options?
4 medications tx options
1. pt education and behavior/ emotional support
## Footnote
2. dietary therapy
3. pharm
a. antispasmotics
b. antidiarreals
c. psychotropic
d. serotonin receptor agonists
227
mesenteric ischemia
## Footnote
what are the two categories? sxs associated with
2
1
what are 5 causes?
Acute (embolus)
## Footnote
**_SUDDEN SEVERE ABDOMINAL PAIN_**
**_FEVER_**
or chronic (athlerosclerosis)
**_ABDOMINAL PAIN POST EATING_**
**causes:**
**1. CVD impacting flow**
**2. trauma**
**3. neoplasm**
**4. physical obstruction**
**5. systemic illness**-_DM, sickle cell, PVD, even dehydration_
228
mesenteric ischmia
## Footnote
2 dx methods?
1 tx
DX:
1. **_mesenteric angiogram TOC_**
2. CT or abdomen with contrast-bowel wall edema
Tx:
SURGERY with stent or emboli removal
229
ischemic colitis
## Footnote
what is this?
who get its?
inflammation and injury to the large intestine resulting in decreased BF
most common in elderly patients
230
small intesine neoplasms
when are these found?
common?
4 types?
dx? 2
**_NOT TYPICALLY DETECTED TILL LATE STAGES!!!_**
\*rare.\*
98% of adenocarcinomas, carcinoids, sarcomas, and lymphomas
**_often not dxed until metastisized to other parts of the body!!_**
sxs vague and non specific
DX:
1. colonoscopy with bx TOC!!
2. CT
231
what is the most common GI cancer? in US?
**_COLORECTAL MOST COMMON GI CANCER!!! 3rd most common in US for males and females!!_**
232
colorectal cancer
## Footnote
what are 3 risk factors?
1. genetic predisposition
2. presence of _adenomatous polyps)_
_3. diets high in fats and refined carbs that are low in plant fiber \*industerialized world\*_
233
colonrectal cancer
## Footnote
4 sxs
2 key dx
3 others
sxs:
1. **_colic type pain_**
**_2. anorexia_**
**_3. thin appeareance_**
**_4. pallior/anemia_**
dx:
1. xray: _classic apple core/npaking ring appearance_
2. endoscopy with bx
3. iron deficient anemia
4. hypoalbuminemia
5. occult blood in stool
234
what does colonrectal cancer come from?
the progression of adenomatous polyp into malgnancy
235
obstruction
## Footnote
5 causes
explain last 3
4 sxs
1. tumor
2. foreign body
3. **paralytic ileus-trauma, surgery, infection, metbaolic disease with DM**
**4. volvulus-twisting of intesinte**
**5. intusssception-telescoping of intestine**
sxs;
1. severe abdominal cramping
2. inability to pass stool
3. **_increased bowel sounds first, then decreased_**
4. **_abdominal swelling, distention_**
236
obstruction
## Footnote
3 dx
3 tx
1. abdominal xray
2. CT
3. barium enema
tx:
1. NG tube (relieve pressure)
2. relieve obstruction
3. surgery often needed
237
what are four complications from obstruction?
tissue death
perforation
sepsis
death
238
intussusception
## Footnote
what is this?
who most common in?
2 causes?
3 sxs?
2 dx children and adult
1 tx?
telescoping of the intestines
**_MC in children_**, but also in adults with **obstruction or neoplasms**
1. currant jelly stools
2. sausage like mass felt on abdominal palpation
3. coliky pain
DX:
children: barium enema
adult: CT is best
TX: SURGERY
239
toxic megacolon
## Footnote
what is this?
typically caused by? and 3 others?
what are 2 risks worry about?
**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
what are the requirements to dx toxic megacolon?
4
4
must contain 3 of 4 of these
## Footnote
temp over 101.5
HR over 120
leukocytosis over 10.5
anemia
and 1 of these
dehydration
altered mental status
electrolyte abnormality
hypotension
241
toxic megacolon
## Footnote
5 sxs
dx, and finding?
SXS:
1. abdominal pain
2. bloating
3. fever
4. tachycardia
5. **_LOSS OF BOWEL SOUNDS_**
DX:
xray, dilation of colon over 6 cm in transverse colon
242
toxic megacolon
## Footnote
4 tx options?
1. _decompress bowel immediately_
2. if not successful, colectomy
3. abx and steroids
4. tx fluid and electrolyte imbalances
243
lactose intolerance
## Footnote
what is this?
4 populations common in?
5 sxs? key 1?
**_difficulty digesting lactose from lack of lactulase_**
MOST COMMON IN:
1. AFRICAN AMERICANS
2. HISPANIC/LATINO
3. ASIAN AMERICANS
4. NATIVE AMERICANS
SXS:
1. bloating
2. pain
3. increase passage of gas
4. diarrhea and nausea
**_5. 2 hours post consumption of milk or dairy_**
244
lactose intolerance
## Footnote
1 dx?
1 tx?
dx:
## Footnote
hydrogen breath test
tx:
dietary avoidance
245
angiodysplasia
## Footnote
what is this?
why does it happen
3 sxs?
**swollen fragile blood vessels in the colon so considered _vascular lesions_**
patho:
**_aging and degen_** of the structure of **blood vessels** causes formation of **arteriovenous malformation**
*often the cause of GI bleed in elderly not attributed to other causes*
_*1.* maroon/melena colored stool_
2. pallor
3. SOB from anemia
246
angiodysplasia
## Footnote
3 dx?
3 tx options?
DX
1. colonscopy
2. CT scan
3. angiography
TX:
1. majority stop bleeding without intervention
IF NOT
**_2. cautery via colonscope_**
**_3. clotting through angiography_**
247
what is the dentate line?
## Footnote
senstion?
divides the rectal mucosa from the squamous epithelium in the canal
## Footnote
above in anorectal canal: INSENSATE (no pain)
below in _andoderm_: _SENSATE AND PAINFUL!!_
248
what does the dentate line divide?
3
1. nervous system
2. vascular supply
3. _nervous system_
\*\*most important, divides where a patient can feel and where they can't so important when determine sxs!!\*\*
249
anal fissure
## Footnote
what is this?
where do these occur?
signicant stat?
2 causes?
**Tear in the andoderm of rectal canal**
90% are posterior along midline
**_most common cause of painful rectal bleeding_**
causes:
1. passage or hard stool
2. prolonged diarreah
250
a kid with tearing pain with bowel movements and bright red blood when he or she whipes with toitlet paper
shuld mak eyou think of...
ANAL FISSURE!!
251
anal fissure
## Footnote
3 sxs?
what not to do?
sxs:
1. "tearing" pain with BM since below dentate line
2. hematochezia during BM
3. SPREAD BUTTOCKS to examine
\*\*NEVER DO RECTAL EXAM, TOO PAINFUL!..and cruel\*\*
252
anal fissure
## Footnote
2 tx categories
4
1 (also, who not to do in)
1. 90% heal without tx
## Footnote
a. bulk agents
b. stool softeners
c. sitz baths
d. hydrocortizone ointment Anusol
2. _surgical-lateral internal anal spincterotomy GOLD STANDARD if failure conservative_
\*\*can't do if patient incontinent\*\*
253
rectal abcess
## Footnote
where do these most commonly occur?
where does it come from?
4 causes?
most in posterior rectal wall, originate in the crpyts with gland obstruction
## Footnote
s. aureus
bacteroides
proteus
strep
254
rectal abcess
## Footnote
2 causes
3 steps
1. crypt gland obstruction
2. increased muscle tone causing obstruction
STEPS
1. stasis
2. dilation
3. infection
255
once a anal abcess in a crypt has formed...where can go if infection spreads? 4
most common?
1. _superficially to external spincter_ to make perianal abcess **_most common_**
## Footnote
2. deep through the external spincter into fat of ischioretal fossa
3. deep into supralevator space
4. interspincteric
256
who are rectal abcess most common in?
how do they present?
5 (3 key)
MEN!!!!!!!!!!!
1. _sever pain while sitting_
2. _drainage on PE_
3. _palpable fluctuant mass_
4. worse with coughing, sitting, defectatin
5. really really painful DRE
257
rectal abscess
## Footnote
how to dx? 1
how to tx? 2
outcomes?
DX
1. CT-size and location, fistula presence
TX:
1. surgical drainage if not fistula
2. post op sitz bath
50% will be cured
50% will have fistula formation
258
fistula in ano
"rectal fistula"
6 associations?
1. crohns
2. GC procitis
3. carcinomas
4. hodgkins lymphoma
5. radiation fibrosis
6. immunocomprimised states
259
what do you need to remember if someone has an abcess or resctal fistula?
DO NOT DO DRE!
260
anorectal fistulas
Goodalls rule
what does it tell you?
2 rules?
\*\*used to determine the location of the internal opening of the fistula\*\*
anterior external opening
goes to _interally via straight line_
posterior exernal opening, _tracts internally via curved line_
261
anorectal fistulas
## Footnote
2 sxs patient presents with
1 tx?healing?
\*be careful of\*\*
1. embaressing persistent discharge
2. not painful but itchy
TX:
1. fistulotomy (opening tract)
healed by _secondary intention with granulation tissue_
left open to heal on its own
\*\*\*watch out for spincter!! must preserve its function\*\*
262
fecal impaction
## Footnote
what is this and when typcailly does it occur?
2 key sxs?
PE? 1
TX 3
large mass of dried hard stool _typically after chronic constapation_
SXS:
_1. sudden watery diarreah in patient that has had cronic constapation_
_2. straining with passage of liquid or small stool_
PE:
DRE shows hard mass or dry stool in vault
TX:
**_1. removal manually_**
**_2. prevention with stool softeners, colase, bulk (fiber) and H20_**
**_3. high fiber diet_**
263
what is the most common anorectal complain in adults over 50?
hemmoroids
264
what percent of people over 50 have hemmoroids?
50%`
265
explain the pathophysiology of hemmoroids?
5
1. anal canal is lined with "cushions" that are **_vascualr and connective tissue and make the hemmorrhoidal plexsus_**
2. exist in 3 columns
3. **_cushions encorge during defecation_** to profect the anal canal from abrasion
4. when venous engorgement is increased with conditions like pregnancy, straining, and increased abdominal pressure it **prompts production of abnormal hemorrhoidal tissue** which can be symptomatic
266
what are 6 RF for hemmoroids?
constapation
straining at stool
pregnancy
obesity
chronic liver disease
portal HTN
267
internal hemmoroids
## Footnote
4 key sxs with these!
above the denate line!!
veins surrounded by mucosa
1. **_PAINLESS, above denate_**
**_2. bright red bleeding with defecation_**
**_3. may prolapse and be palpable on DRE_**
**_4. bleed_**
268
what are the stages used to define internal hemmoroids?
**_first_**-bleed
**_second-_**bleed and prolapsed, spontanously reduce
**_third_**-bleed, prolapse, and require manual reduction
**_fourth degree_**-bleed/incarcerate
269
Internal hemmoroid tx categories
## Footnote
5
2
1-2 degree:
## Footnote
a. fiber
b. water
c. stool softner
d. anusol hydrocortisone
e. numbing agent nupercainal ointment
3-4 degree:
a. SURGICAL
b. EXCESIONALHEMMOIROIDECTOMY
270
external hemmoroids
## Footnote
whe do they occur/what are they covered in?
3 sxs
dx method?
1 tx?
below the dentate line and covered with andoderm
1. usually don't **_bleed_**
2. may **_thrombose_** which is VERY painful
3. cause **_pain, discomfort and most severe at time of defecation_**
dx
"either present or not"
tx:
1. excision of outside of the mucotaneous junction leaving wound open **_hemroidectomy_**
271
rectal polyps
what are these?
why is it improtant to know type?
1 type concerned about?
why?
2 shapes?
small outcropping that grows in the rectum or colon
\*\*need to deterine the type since some are associated with carcinoma\*\*
_adenomas_
**_PREMALIGNANT POLYP_**
**_PRECURSOR TO COLORECTAL CANCER_**
**_sessile_**: flat and intimately attacted to mucosa
**_peduclated_**: round and attached be stalk
272
what are the 3 types of adenoma polys? which is most common? which has higest risk of cancer? risk of cancer and prevalance for each?
1. tubular adenoma
## Footnote
**_MOST COMMON TYPE 65-80%_**
pedunculated, little cancer risk
2. tubulovillous adenoma
10-25% of adenomas
22% risk of cancer
3. **_vilous adenomas_**
**_40% RISK OF CANCER_**
only 5-10% so least common but most deadly
273
what is the least common but the most prognostic for cancer of the adenoma polyps?
vilous adenoma
\*think vilian=evil\*
274
what are the two tests that are reccomended annually to screen for colorectal cancer?
1. guiac fecal occult blood test (gFOBT)
## Footnote
2. immunochemical-based fecal occult blood test (iFBT)
275
what are the 3 screening tests that are reccomended for colorectal cancer? which is most reccomended? what age do you start?
age 50 to less than 10 years life expectancy
## Footnote
1. **_optical colonscopy_**-10 years
2. flexible sigmoidoscopy-5 years
3. CT colonography-10 years
276
when should you screening african americans for colorectal cancer?
45 rather than 50 according to the college of gastroenterology
277
what are the sxs associated with polyps/colorectal cancer?
they might bleed
**more important to think about family hx**
278
pilonidal cyst/disease
## Footnote
what is this?
what does it look like?
location?
who is it in? age? KEY!!!!!!
common, _congenital abnormality_
_"opening of a sinus tract that may conttain a **tuft of hair**"_
location:
midline, post sacral intergluttal fold superoir to anus
**ALMOST ALWAYS MEN 20-30, _always under 40_**
279
pilonidal cyst/disease
## Footnote
4 key sxs?
1 tx otpion? why?
1. **_fluctuant mass with erytmatous "halo"_**
2. purluent d/c
_3. NO ANAL PAIN OR DEFECATION ISSUES_
4. painful but in gluteal area
Tx:
**_1. MOST LIKELY SURGERY with secondary closure (leaving open) vs ID with abx_**
HIGH RATE OF RECURRANCE SO SURGERY IS BETTER OPTION TO GET DEEPER TRACTS!!!
280
incisional hernia
associated with vertical incisions esp in pts with wound infection or obesity
## Footnote
tx: surgery!
281
inguinal hernia
## Footnote
3 types?
where are they?
which is most common?
1. direct
## Footnote
**_passage of intesine through external inguinal ring at hesselbachs triangle_**
2. indirect
**_MOST COMMON_**
**_passage through inguinal canal INTO SCROTOM, often_**
3 femoral
less common through femoral ring
282
umbical hernia
## Footnote
when do they get it?
how is it txed?
congenital and appears at birth
most resolve on their own
283
vental hernias
when does this occur?
occur when weakening in the anterior abdominal walla and can be either incisional or unilical
284
portal vein
## Footnote
lacks what?
internal pressure?
supplies what percent of blood
formed from?
valvless
pressure 3-5 mmHg
75% of the livers total blood supply by volume
formed by the superior mesenteric artery
285
hepatic vein
## Footnote
where does it go?
structure?
2
3
2
venous drainage of liver through 3 **_valveless_** hepatic veins into inferior vena cava
## Footnote
right: **5, 8**
middle: **4, 5, 8**
left: **2, 3**
286
neural innervation of the liver
2
1. parasympathetic of **_vagus nerve_**
2. parasympathetic from the **_celiac plexsus_**
287
explain the 2 cels in the liver and when you see them?
parenchyma is made up of actively diviiding **_hepatocytes_**
in damaged tissue this becomes **_fibrotic**_ and you will see _**oval cels indicating damage_**
288
what are the 3 main functions of the liver? subgroups?
## Footnote
3
4
1
1. metabolic and catabolic
## Footnote
**_a. glucogenesis_**
**_b. synthesis of phospholipids and cholesterol_**
**_c. detoxification of meds and alchohol_**
2. storage
glycogen
protein
iron
vitamins
3. excretory functions
synthesis and secretion of bile
289
what are 6 synthetic functions of the liver that occur in the hepatocytes?
1. **_coagulation factors_****_: PT/INR, PTT_**
2. plasma proteins: albumin
3. acute phase proteins
4. carbohydrate metabolism
5. lipid metabolism
6. bilirubin metabolism: bile excretion
290
what are the two tests that suggest hepatocellular damage/inflammation?
1. AST
2. ALT
291
what 3 LFTs suggest obstructive disease?
1. bilirubin
## Footnote
direct=conjucated
indirect=unconjugated
2. ALP/alkaline phosphatase
3. GGTP/gamma-glutamyl transferase \*ordered sepereately
292
conjugated bilirubin=
direct bilirubin
293
unconjugated bilirubin=
indirect bilirubin
294
asartate aminotransferase
(AST)
elevated in?
specific?
elevated in **_acute_** conditions
## Footnote
found in the muscle, kidney, and heart so low specificity for liver damage since mreasures more than just the liver
295
alanine aminotransferase
(ALT)
elevated in?
specific?
elevated in **_chronic_** conditions
## Footnote
primarily found in the liver so more specific than AST
296
if the ration of AST:ALT is greater than 2:1 ration, what should you think of?
alcoholism or drug toxicity
297
unconjugated (indirect) bilirubin
## Footnote
what is this?
if increased indicates? 3
broken down RBC in speel bind to albumin and go to hepatocytes
## Footnote
if increased indicates:
PREHEPATIC PROBLEM
**_1. hemolysis of RBC_**
**_2. imparied hepatocyte function_**
298
direct bilirubin (conguated)
## Footnote
what happens to this?
where does it usually go?
if increased indicates 2 things?
enzymatically conjugation occurs with glucuronic acid...goes into bile...into small intestine where aprox 95% is reabsorbed
## Footnote
if increased:
INDICATEDS POSTHEPATIC PROBLEM
_1. **obstruction of biilary system=CHOLESTASIS**_
299
is bilirubin in the urine common?
no, it should not be present in the urine!!
300
alkaline phosphatase
## Footnote
where is this found?
found in the **liver, intestine, kidney, and placenta**
therefore, not specific to the liver
301
gamma-glutamyltransferase
## Footnote
what does this indicate?
what does this help rule in/out?
liver specific
\*\*helps differentiate if the liver is the problem if the alkalne phosphatase is increased\*\*
302
if you have increased alk phos and increased GGTP....what should this make you think?
OBSTRUCTION
303
what are the first and second most common causes of chronic liver disease?
1. hep C
2. alcohol
304
gilberts disease
## Footnote
what is this?
why does it happen?
2 key sxs?
most common hereditiary cause of increased bilirubin
## Footnote
_impaired enzymatic conjugation of Indirect bilirubin_
sxs:
1. **_jaudice at birth_**
2. icteric sclera
305
gilberts disease
## Footnote
what are the 3 tests done to dx?
1 tx option?
DX:
1. **_elevated INDIRECT bilirubin_**
**_2. normal direct bilirubin_**
**_normal US_**
tx
only in infancy with "bili lights" to prevent liver failure
306
nonalcoholic fatty liver disease
(NASH)
6 causes
1. certrain drugs
2. obesity
3. starnation
4. diabetes melltius
5. high blood tryglicerides
6. alcohol
307
nonalchoholic liver disease
(NASH)
what are the sxs?
3 dx findings? 1 key
what should you consider if more than more one abnormal finding?
sxs
NON UNLESS CIRROSIS
DX
**_1. increased echotecture at times HSM on US_**
**_2. AST/SLT increased sometimes alk phos_**
2. ALT more than AST
(opposit of ETOH)
\*\*CONSIDER BX IF MORE THAN ONE POTENTIAL CAUSE OF ABNORMAL LFTS\*\*
308
non alcoholic fatty liver dxs
## Footnote
5 tx options?
TX
1. lifestyle: weightloss, lowfat diet
2. management of high triglycerides, BS
3. decrease ETOH
4. meds/supplements
- vitamine E,
- ursodiol
309
hemochromatosis
## Footnote
what is this?
who does it present in?
sxs? 4
3 important labs for dx
autosomal recessive causing iron deposition in orgams
## Footnote
OVER 50 years
often asymptomatic
**can include:**
**arthalagias**
**hepatomegaly**
**_gray skin_**
**DM**
Labs
**_1. high ferritin and iron % saturation_**
**_2. HFE gene analysis_**
**_3. liver bx with iron stain_**
310
what is the tx for hemochromatosis?
phlebotamy, remove the iron
311
wilson's disease
what is this?
what happens in this?
3 things it causes?
2 labs must check
rare autosomal recessive disorders
liver unable to exrete copper, so get _copper overload_ in brain, bone, kidney, cornea
1. _basal ganglia sxs (parkinson like)_
_2. liver disease_
_3. kayser-fleicher rings_
brown on green pigment in cornea
Labs.
1. **_LOW CERULOPLASMIN_**
**_2. 24 hour urine copper_**
312
wilsons disease
## Footnote
what are 2 key sxs?
1 tx option?
sxs:
**_1. visual disturbances_**
from the kayser fleischer rings get brown ring causing visual disturbances
**_2. neurologic/psychiatric changes_**
TX:
1. copper chelators like zinc
313
alpha 1 antitrypsin deficiency
## Footnote
what is this?
what 2 organs does it effect?
2 effects?
tx?
genetic condition effecting **_lung and liver_**
alpha-1 antitrypsin (A1A) synthesized in liver resulting in reduced circulating levels
increase in A1A in liver=obstruction
decrease A1A circulation=obstructive lung disease
tx:
replace A1A
314
alchoholic hepatitis
## Footnote
what is this?
what is the ratio you see?
2 labs might see?
**_most common cause of cirrohosis_**
## Footnote
**_AST\>ALT 2:1 rarely over 300_**
labs:
1. vitamin and calorie deficiency
2. **megaloblastic anemia (folate, B1, B6)**
315
what is the ration associated with alcoholic hepatitis?
AST greater than ALT 2:1 rarely over 300
316
acute phase alcholic hepatitis
## Footnote
associated with what?
how serious?
3 sxs of this?
what must you calculate?
typically with heavy use or binge
can be **_fatal, pts often encephalopathic_**
sxs:
1. **HEPATOSPLENOMEGALY**
**2. ASCITIES**
**3. JAUNDICE**
\*\*calculate discriminant function\*\*\*
over 31=poor 1 month prognosis
317
what is consider tylenol OD?
## Footnote
what precent of acute hepatitis?
serious?
tx?
single or total dose exceeding 10 grams
accounts for 45% of cases of acute hepatitis
_fatal if untreated_
tx:
1. **_N-acetylcysteine_**
use this if hepatoxicity or ingestion time unknown
318
autoimmune hepatitis
## Footnote
who is this common in?
2 labs to check?
2 biomarkers to check?
_1 test needed to dx?_
2 tx options!
most common in females 14-50 **_WHO MOST LIKELY HAVE ANOTHER AUTOIMMUNE CONDITION_**
LABS:
1. elevated enzymes
2. elevated alk phos
BIOmarkers:
1. ANA
2. anti-smooth muscle
Dx:
**_need bx to make dx_**
tx:
**_prednisone and imuran_**
319
primary biliary cirrhosis
## Footnote
what is this strongly associated with?
what is key finding on testing?
test?
2 tx options?
75% cases are patients with ulcerative colitis, males
## Footnote
"**_beading"_** of bile ducts on MRCP (MRI)
Tx:
**_1. ursodiol_**
**_2. transplant cure!_**
320
if person has family hx of colorectal cancer, when do you start screening?
start 10 years prior to the dx of your 1st degree relative and do every 5 years from there with _colonoscopy_
321
acute hepatitis
## Footnote
what is the mortalty?
3 most common causes?
what are 4 sxs associated with this? **_KEY!!_**
**mortality 40-80%**
sudden onset deterioration of hepatocyte function causing coagulopathy
1. tylenol 45% of cases
2. alcohol and drugs
3. heptitis A and B
sxs:
**_1. jaundice_**
**_2. elevated transmidates AST/ALT_**
**_3. coagulopathy INR over 1.5_**
**_4. encepalopathy-alteration in mental status due to evelated ammonia_**
322
viral infections account for what percent of hepatitis?
50% of all cases
hep a b c d e account for 95% of thse
323
hepatitis A
## Footnote
precentage?
virus type?
incubation?
transmission route? (3)
**65% of all cases**
**RNA**occurs exclusively in liver cells
**incubates 2-6 wks**
transmission **_FECAL ORAL_**
1. travel
2. contanimated food and water
3. close contact with infected individuals
324
hepatitis A
## Footnote
sxs?
1 (time)
7 after sxs
SXS
1. prodrome, flu like
_most infectious here 12-21 days_
_2. icteric phase_
**1. dark urine appeares first (bilrubinuria)**
**2. pale stool follows**
**3. jaundice 70-85%**
**4. abdominal RUQ pain 40%**
**5. _prurits, indicates bilirubin_**
6. arthralgias
7. hepatomegally
325
hepatitis A
## Footnote
3 dx findings
tx
DX:
1. anti-hep A IGM and IGG
2. LFTS
- increase AST/ALT over 1000
- increased bilirubin 5-10 x
TX: selflimiting supportive
326
what are 5 prevention methods for hepatitis A?
improvement in hygiene and sanitation
cooking food
avoidance of water foods and endemic areas
avoidance of raw shellfish
immunization
327
who gets vaccinated for hep A? 4
Harvix
**travelers**
**miliary personnel**
**lab workers**
**immunocomprimised**
328
when you think of raw shellfish think..
hep A!
329
hepatitis B
## Footnote
what type of virus?
what percent of people have it and who?
3 transmission pathways?
**_KEEY THING TO KNOW ABOUT THIS_**
DNA virus
1/3 of population infected, majority immigrants or 1st gen
transmission:
1. perianatal
2. sexual
3. blood containing med equiment
**_\*\*\*\*\*\*\*causes 80% of hepatocellular carcinoma=fatal!!!!\*\*\*\*\*_**
330
what type of hepatitis can lead to hepatocellular carcinoma?
HEPATITIS B!! vaccines for this mandated
331
what are the categories of hepatitis B?
3
**immunity**
- vaccination
- natural infection
**actue infection**
**chronic infection**
- active
- chronic
332
\*\*\*what are the **_2_** test results you want to keep in mind when looking at hepatits infection\*\*\*
**_hepatitis B surface antibody (HBsAB)=_**IMMUNITY--ONLY PRESENT IN VACCINATED PEOPLE
## Footnote
**_hepatitis B envelope antigen (HBeAg)_**: NEEDS TREATMENT, current infection
333
surface=
core=
envelope=
surface=**immunity (vaccine or exposure)**
core=**exposed to virus**
envelope=**present infection with active replication**
334
acute hepatitis B
## Footnote
what is the breadown for how they present? (%)
1 key dx? 2 supportive?
tx2? why?
70% are subclinical (no jaundice or aniteric)
30% get icteric hepatitis
dx
**_1. HBcIGM for dx_**
2. elevated AST/ALT
3. elevated bilirubin
TX:
1. supportive
\*\*many will seroconvert to HBsAB and HBeAB meaning they develop immunity on their own!!\*\*
2. high calorie diet
335
chronic hepatitis B
## Footnote
three phases of this?
3 tx options and length of time?
initial phase:
**positive HBeAG**
immune clearance phase
**HBsAg, HBeAG**
**elevated ALT**
**inflammation on liver bx**
inactive carrier
tx:
1. tenofovir DOC
2. entecavir DOC
\*\*\*both of these are lifelong drugs!!!\*\*\*
3. interferone alpha 6 months
336
hepatitis prevention and vaccination
## Footnote
2
1. recombinant hepatitis vaccine
2. hep B immune globulin (exposued)
337
what is key to know about _hepatitis D_?
transmission?
RNA coinfection with **_HEP BE IS REQUIRED!!!_**
**_HBsAg_**
transmission: sexual contact
338
hepatitis C
## Footnote
what is this?
3 RF/transmission?
virus type?
age?
**_most common chronic blood borne infection in the US_**
## Footnote
1. injection drug use/cocaine
2. sexual contact
3. transfusion
RNA virus, 30-49 y/o
339
\*\*what important people do you need to test for hepatitis C?\*\*
**_test everyone born between 1945 to 1965_**
340
what percent of people proceed to the chronic state? what are two things you are at increased risk for?
80% proceed to the chronic state
HIGH RISK OF CIRRHOSIS AND HEPATOCELLULAR CARCINOMA
341
hepatitis C
## Footnote
3 tx options?
when do you start tx?
2 main options?
how long is the tx?
1. supportive first since can clear on their own
2. avoid hepatotoxic drugs
3. \*\*most wait **_6 months_** for posisble clearance before starting antiviral therapy\*\*
- harvoni (sofosbuvir/ledipasvir)
- daklinza (daclatasvir)
\*\*12-24 weeks tx depending tx naive and if cirrhosis\*\*
\*\*some regimens still include ribaviran, but not all of them\*\* NO INTERFERON
342
what do you want to check when txing someone for hep C?
viral load after **_12 weeks_** to confirm cure
343
what is cool about treating hep C?
IT IS CURABLE!!! nearly 100!!!!!
there is no vaccine and no post exposure immunoglobulin **_THEREFORE YOU WANT TO SCREEEN!!!_**
344
what is interesting about hep G?
if coinfected with HIV, helps reduce the HIV replication
345
HEP E
## Footnote
2 places you find this?
transmition
_AT RISK POP?_
North Africa
South Asian
fecal oral
self-limiting
***issues in pregnacy!!! EXTREMELY SEVERE!!!! esp in third trimester 20% mortality!!!!!! KEY***
346
cirrhosis
## Footnote
what is this?
2 classifications?
**chronic end stage dxs of the liver marked by _degeneration of cells_ from inflammation resulting in _fibrous thickening of tissue_**
4 stages of fibrosis and cirrhosis is the last
**_compensated_**: although fibrotic can still preform functions
**_decompensated_**: fibrotic with loss of essential function
347
cirrohosis
## Footnote
4 sxs of compensated?
7 sxs of decompensated?
_compensated sxs:_
ammenorreah
impotence
gynecomastica
**_hematemesis as present features in 15-25% (esophageal varices)_**
_decompenstated_:
**1. spider angiomas**
**2. muscle wasting**
**3. palmar erythema**
**4. dilated superficial veins of abdomen**
**5. ascities**
**6. portal HTN**
**7. encepalopathy**
348
cirrohsis
5 labs
3 tests
LABS:
low platelets
**_prolonged PT_**
moderate elevations enzymes
**_elevated bilirubin_**
**_low serum albumin_**
**_1. abdominal US WITH DOPPLER_**
- nodular appearing liver +/- hepatosplenomegaly
2. LIVER BX! TOC to confirm, determine staging
349
cirrhosis
## Footnote
5 tx
1. alcohol abstinence
2. vitamin supp
3. nuitrional supp
4. BB for portal HTN
5. _CURE IS TRANSPLANT_!!!
350
what MUST you do for someone with cirrhosis?
_**\*\*\*\*\*must screen for alpha fetal protein and imaging ever 6 months\*\*\***_
351
what is used to stage liver disease?
what does it determine?
MELD SCORE
\*\*determines prognosis of patient in order to determeine priorty of patient for transplant\*\*
352
hepatocellular carcinoma (HCC)
## Footnote
what is this strongly associated with?
5 year survival?
3 sxs? 1 key
3 dx methods
**one key think you want to order**
associated with **_cirrhosis_**
## Footnote
4-6 months from time of dx
5 year survival is 25%
SXS:
1. _painless jaundice_
2. weight loss
3. hepatomegaly
dx
1. triple phase CT or MRI
2. **_percutaneous bx of lesions!!! TOC_**
**_3. Alpha fetoprotein tumor marker is PATHOPNEUMONIC_**
353
hepatocellular carcinoma
## Footnote
4 tx
1. surgical ressection
2. chemo
3. portal vein embolizations
4. _transplant_ if small and localized
354
metastatic liver lesions
## Footnote
what is this?
3 ways it gets there?
3 dx methods?
3 tx options
**_MOST COMMON NEOPLASM OF THE LIVER!!!_**
## Footnote
1. portal venous circulation
2. direct extension
3. lymphatic spread
DX
1. triple phase CT or MRI
2. Percutaneous bx of lesions
3. **_PETS scan and tumor markers for primary tumor_**
TX:
1. ressection
2. chemo
3. not option for transplant
355
hepatic ressection
## Footnote
how much can you take?
can remove up to 80% because it regenerates!! woah!
## Footnote
regains albumin ability by 3rd week
356
portal HTN
## Footnote
what are the 3 classifications of this?
5 things it can cause?
1. **presinusoidal**: slpenic or protal vein
2. **sinusoidal**: cirrhosis
3. **postsinusoidal**: hepatic veins, ouflow problem
CAN CAUSE:
1. _esophageal varices_
2. ascites
3. encephalopathy
4. splenomegaly
5. hepatorenal syndrome
357
what are the most common PORTAL HTN locations?
presinusoidal and sinusoidal
358
what is basically the only cause of postsinusoidal portal HTN?
budd-chiari syndrome
359
portal HTN
## Footnote
5 tx options depending on cause
1. nonselective BB
## Footnote
2. banding for varices
3. diuretics for ascites
4. lactulose and xifaxan for encephalopathy
5. surgical if meds fail
_TIPS-transjugular intrahepatic portosystemic shunt_
