other GI disorders Flashcards
herniation
2 requirements
organ protruding through retaining str
requires
1=weakened abdm wall (muscle)
2=inc intra-abdm P most often provided by pregnancy orobesity
how are diverticula and herniation formation diff
diverticula-out pouchings are in the wall of the gut but herniation is through the muscle wall
patho of herniation
- weakened supporting str (eg muscles)
- congenital or acquired
- inc intra abdm P eg pregnancy obesity leads to herniation
2 types of hernia
hiatal hernia
inguinal hernia
what is a hiatus?
a aperture or opening
where is a hiatal hernia
the aperture in the diaphragm for esophagus
what happens if hiatus enlarges
part of stomach will enter the thoracic cavity
2 types of hiatal hernia
sliding and rolling or paraesophageal
sliding hiatal hernia
- GEJ and upper stomach enter thoracic cavity
- some asymptomatic
- others: chest pain, heartburn, reflux? (gastroesophageal reflux)
why is there pain and heartburn with sliding hiatal hernia
HCL has pH of 2 and when in esophagus it irritates it and leads to heartburn
paraesophageal or rolling hernia
- non upper part of stomach enters thoracic cavity
- GEJ below diaphragm
- chest pain, dyspnea, fullness after meals
- no reflux why? (no reflux d/t pressure going back into stomach we feel full from stretch receptors in stomach, here there is a smaller volume & the small pocket may get stretched and the stretch receptors there are triggered)
sliding or paraesophageal/rolling which has reflux
sliding
tx for hernias
- lifestyle modifications (eg change diet, dont eat before be, dont bend over, raise HOB. thi is often sufficient
- drugs for reflux
- antacids (can lead to kidney stones)
- H2RA
- PPI
- sx (approx 15%) (fundoplication, like a boot being laced)
inguinal hernia
abdm organs protrude via inguinal ring
- peritoeum contains intestine and omentum
- sx correction
diff bet direct and indirect hernia
direct=goes through a supporting str with no aperture
indirect goes through an existing aperture
peptic ulcer disease
incidence
what is it
approx 10% incidence
- ulcerative disorder
- stomach (20%) & duodenum (80%)
- primarily affects mucosa (can affect deeper layers)
- remissions and exacerbations
et of peptic ulcer disease
helicobacter pylori infection (which is transient and often harmeless)
- site (H pylori colonize in stomach or duodenum in stomach epithelia tissue. they secrete urease (enzyme) that breaks down urea into NH3& C02. Nh3 is a buffer. You will end up with bicarbonate which buffers in a local area - adhesion - urease - mechanism is unclear - inflm (induced when colony established - hypergastrinemia (the infection stim gastrin prod which stimulates secretion of chief cells and HCL)
risk factors of peptic ulcer disease
- Hcl and biliary acid
- steroids and NSAIDs (d/t damage to mucosal lining and inc acid prod)
- chronic gastritis
- smoking, alcohol, caffeine (inc acid sec)
- stress
defensive factors in PUD
1-reg of acid sec (so that there isnt excess/too little
2-intact perfusion (to take away wastes/bring resources etc)
3-mucus
4-regen of mucosal cells
patho of pud
- h pylori infect
- inflm and tisue damage
- inc gastrin prod->inc acid sec->tissue damage
- defenses against gastric acid impeded by risk factors
mnfts of PUD
- abdm pain, burning, cramping
- N&V (not d/t severe pain)
- constipation (according to Francesca)
(will have a minor fever)
complic PUD
- perforation (could lead to peritonitis)
- hemmorrhage (occult blood but not frank as its in stomach and duodenum)
- gastric obstr (or duodenal)
- d//t edema, spasm or scar tissue contraction
(muscle spasm (not vasospasm. the walls of the muscles spasm) when ulcers begin to dev theyll be some regen, with scar tissue. the scars make the stomach smaller d/t contraction. There will be exudate and mucus that inc P in lumen)
dx of PUD
- hx
- urea breath test (theres chemical rxn where urea is transformed into NH3 and C02 by urease which is prod by bacteria. Pt will be given urea soln labeled with C14. If bact is in there it will be turned into NH3 & C(14)02. The C(14)02 will be taken into lungs and exhaled. 2.5hrs later theyll exhale into bag and if theres C1402 it will be present inthe gases int the bag)
- serology (looking for Abs in blood)
- fecal Ag (look for proteins in stool)
- barium swallow
- endoscopy (beneficial as you can see the ulcers)
tx of PUD
-antacids (symptomatic mgmt)
-triple regimen: H2RA (histamine facilitates acid synthesis by binding to receptor) + 2Abx or PPI (blocks hydrogen ion se and 2 Abx
-sx for complic
H2RA eg
Zantac and Tagamet
PPI eg
Losec, Pariet, Nexium
typical triple regimen for PUD
losec (PPI)
amoxil
flagyl
hepatitis is
inflm of the liver
et of hepatitis
- microbes (bact, viruses, fungi, parasites)
- esp viruses
- drugs (toxic hepatitis) (hepatotoxic drugs)
- autoimmunity (10%)
viral hepatitis
hep ABC (these 3 most common) DE
(patho is same, virus is diff)
-differences
-virus and transmission
-incubation period
-severity
-similar mnftswill liver show signs of damage quickly
no. it has v lg functional reserve and can be damaged extensively before showing signs
liver functions
- produces bile
- metb hormones and drugs
- synthesizes proteins, glucose and clotting factos
- stores vitamins and minerals
- changes ammonia to urea
- metb of fats, carbs, proteins
- filters blood and removes bacteria and particulate matter by Kupffer
Hep A
mild
acute form (doesnt have to be treated actively.)
(Transmitted via fecal oral route mostly, water borne, food borne)
(Incubation-15-50 days)
Hep B
most severe
-10-15% are chronic
(“serum hep”)
(blood and saliva)
(1-10% fatality rate)
(incubation 28-160 days)
(you can be a carrier without having it yourself)
Hep C
80% are chronic
remissions and exacerbations (this isnt equal to carrier state)
-often leads to cirrhosis
(usually transmitted through blood and body fluids)
patho of hepatitis
2 mechanisms in all types
- IR->inflm and necrosis
- viral injury-> necrosis (the virus damages the liver by causing lysis d/t infction of the hepatocytes - hepatocyte necrosis
- dec fx
- vasulature & ducts are damaged by inflm
- healing in ~4months
mnfts of hepatitis
3 phases
- prodromal
- clinical
- rcovery
1st stage of mnfts of hepatitis
prodromal
- lethargy (liver processes metabolites to prod energy if not working leads to lack of energy)
- myalgia
- fever
- anorexia
- abdm pain (inflm-> stretching of capsule around liver)
- N
- V
2nd stage of hepatitis mnfts and how long is it
5-10 days after prodromal stage is clinical stage (aka icterus)
(RBC breakdown prod heme which has the intermediate of bilirubing which should be processed by liver but d/t liver fx being impaired it accum in blood as its insoluble. it therefore deposits in the tissues)
-jaundice
-pruritus (d/t deposits of bile salts in integument
-hepatomegaly and tender liver
3rd stage of hep mnfts
acute mnfts subside (~3wks)
-full recovery within ~16wk
how would you determine liver damage
look at liver enzymes in blood where they shouldnt be
tx of hepatitis
- rest to dec energy requirements
- diet (small, high calorie meals that are high in carbs and low in fat because bile emulsifies fat)
- no alcohol or other hepatotoxic drugs
- relief from pruritus
- post exposure prophylaxis (eg Hep a is largely d/t poor hygiene so good hygiene, gammaglobulins, vaccines good. all this for A and B)
hep c tx prophyaxis for post exposure
hygiene
gammaglobulins
antivirals
autoimmune hepatitis
severe chronic form
type 1:
- more common
- 30% in women less than 40 who tend to have immune problems
- anti nuclear antibodies and smooth muscle antibodies
type 2 -2-14yrs -abs against cytosol and microsomes (cytosol is just the fluid without organelles) (vesicles from ER...)
et of autoimmune hep
idiopathic??
HLA and MHC on chr 6
enviro (viruses and chem agents)
autoimune hepatitis mnfts
range from asymptomatic to mnfts of liver failure
dx
exclude
- viral hep
- other liver disease
- look for inc gammaglobulins (look at ANA and test abs in blood through serology)
tx of autoimmune hepatiits
immunosuppressant drugs
liver transplant?
(may also give gamma globulins)
