other GI disorders

Question 1

herniation

2 requirements

Answer 1

organ protruding through retaining str

requires
1=weakened abdm wall (muscle)
2=inc intra-abdm P most often provided by pregnancy orobesity

Question 2

how are diverticula and herniation formation diff

Answer 2

diverticula-out pouchings are in the wall of the gut but herniation is through the muscle wall

Question 3

patho of herniation

Answer 3

• weakened supporting str (eg muscles)
  
  • congenital or acquired
• inc intra abdm P eg pregnancy obesity leads to herniation

Question 4

2 types of hernia

Answer 4

hiatal hernia

inguinal hernia

Question 5

what is a hiatus?

Answer 5

a aperture or opening

Question 6

where is a hiatal hernia

Answer 6

the aperture in the diaphragm for esophagus

Question 7

what happens if hiatus enlarges

Answer 7

part of stomach will enter the thoracic cavity

Question 8

2 types of hiatal hernia

Answer 8

sliding and rolling or paraesophageal

Question 9

sliding hiatal hernia

Answer 9

• GEJ and upper stomach enter thoracic cavity
• some asymptomatic
• others: chest pain, heartburn, reflux? (gastroesophageal reflux)

Question 10

why is there pain and heartburn with sliding hiatal hernia

Answer 10

HCL has pH of 2 and when in esophagus it irritates it and leads to heartburn

Question 11

paraesophageal or rolling hernia

Answer 11

• 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)

Question 12

sliding or paraesophageal/rolling which has reflux

Answer 12

sliding

Question 13

tx for hernias

Answer 13

• 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)

Question 14

inguinal hernia

Answer 14

abdm organs protrude via inguinal ring

• peritoeum contains intestine and omentum
• sx correction

Question 15

diff bet direct and indirect hernia

Answer 15

direct=goes through a supporting str with no aperture

indirect goes through an existing aperture

Question 16

peptic ulcer disease
incidence
what is it

Answer 16

approx 10% incidence

• ulcerative disorder
  
  • stomach (20%) & duodenum (80%)
• primarily affects mucosa (can affect deeper layers)
• remissions and exacerbations

Question 17

et of peptic ulcer disease

Answer 17

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)

Question 18

risk factors of peptic ulcer disease

Answer 18

• 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

Question 19

defensive factors in PUD

Answer 19

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

Question 20

patho of pud

Answer 20

• h pylori infect
  
  • inflm and tisue damage
  • inc gastrin prod->inc acid sec->tissue damage
• defenses against gastric acid impeded by risk factors

Question 21

mnfts of PUD

Answer 21

• abdm pain, burning, cramping
• N&V (not d/t severe pain)
• constipation (according to Francesca)

(will have a minor fever)

Question 22

complic PUD

Answer 22

• 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)

Question 23

dx of PUD

Answer 23

• 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)

Question 24

tx of PUD

Answer 24

-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

Question 25

H2RA eg

Answer 25

Zantac and Tagamet

Question 26

PPI eg

Answer 26

Losec, Pariet, Nexium

Question 27

typical triple regimen for PUD

Answer 27

losec (PPI) amoxil flagyl

Question 28

hepatitis is

Answer 28

inflm of the liver

Question 29

et of hepatitis

Answer 29

- microbes (bact, viruses, fungi, parasites) - esp viruses - drugs (toxic hepatitis) (hepatotoxic drugs) - autoimmunity (10%)

Question 30

viral hepatitis

Answer 30

``` hep ABC (these 3 most common) DE (patho is same, virus is diff) -differences -virus and transmission -incubation period -severity -similar mnfts ```

Question 31

will liver show signs of damage quickly

Answer 31

no. it has v lg functional reserve and can be damaged extensively before showing signs

Question 32

liver functions

Answer 32

- 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

Question 33

Hep A

Answer 33

mild acute form (doesnt have to be treated actively.) (Transmitted via fecal oral route mostly, water borne, food borne) (Incubation-15-50 days)

Question 34

Hep B

Answer 34

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)

Question 35

Hep C

Answer 35

80% are chronic remissions and exacerbations (this isnt equal to carrier state) -often leads to cirrhosis (usually transmitted through blood and body fluids)

Question 36

patho of hepatitis

Answer 36

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

Question 37

mnfts of hepatitis

Answer 37

3 phases 1. prodromal 2. clinical 3. rcovery

Question 38

1st stage of mnfts of hepatitis

Answer 38

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

Question 39

2nd stage of hepatitis mnfts and how long is it

Answer 39

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

Question 40

3rd stage of hep mnfts

Answer 40

acute mnfts subside (~3wks) -full recovery within ~16wk

Question 41

how would you determine liver damage

Answer 41

look at liver enzymes in blood where they shouldnt be

Question 42

tx of hepatitis

Answer 42

- 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)

Question 43

hep c tx prophyaxis for post exposure

Answer 43

hygiene gammaglobulins antivirals

Question 44

autoimmune hepatitis

Answer 44

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...) ```

Question 45

et of autoimmune hep

Answer 45

idiopathic?? HLA and MHC on chr 6 enviro (viruses and chem agents)

Question 46

autoimune hepatitis mnfts

Answer 46

range from asymptomatic to mnfts of liver failure

Question 47

dx

Answer 47

exclude - viral hep - other liver disease - look for inc gammaglobulins (look at ANA and test abs in blood through serology)

Question 48

tx of autoimmune hepatiits

Answer 48

immunosuppressant drugs liver transplant? (may also give gamma globulins)