GI: Stomach Flashcards
define gastroparesis
delayed gastric emptying in absence of mechanical gastric outlet obstruction
*common in DM
Gastritis
-acute vs chronic
*inflamm disorder of the gastric mucosa
ACUTE: caused by injury of protective mucosal barrier–superficial inflammation—- “rug burn” of the stomach aka SUPERFICIAL
CHRONIC:
- chronic fundal gastritis (type A–IMMUNE)–pernicious anemia for ex
- chronic antral gastritis (type B–NONimmune)–aka infectious–>HP infection for ex or chronic NSAID use
*symps are vague for both* anorexa fullness n/v epigastric pain
patho behind
Autoimmune Metaplastic Atrophic Gastritis
- T cell mediate auto destruction of the gastric mucosa
- Autoimmune gastritis leads to chronic gastritis–anti-parietal and anti-intrinsic factor antibodies–leads to development of pernicious anemia (B12 malabsoprtion)
*lack of parietal cells can lead to: hypochlorhydria + hypergastrinemia
list/explain the stress-related mucosal dz
*general cause
Acute form of PUD–related to severe illness or major trauma
- ischemic ulcers–>w/in hours of trauma, burns, hemorrhage, HF or sepsis
- curling ulcers–>dev as a result of burn injury
- cushing ulcers–>result of brain injury or brain surgery
stress gastritis
- MC causes/major RFs
- what can reduce the risk?
- focus should be on?
RFs:
- mechanical ventilation
- coagulopathy
- truama
- burns
- shock
- sepsis
- CNS injury
- liver failure
- kidney dz
- multiorgan failure
***use of enteral nutrition reduces the risk of stress related bleeding
Focus should be on PREVENTION
Atrophic (Chronic) gastritis
- due to ?
- explain the types
- inr risk of what
due to gland atrophy + intestinal metaplasia **
- ->small intestine bacterial overgrowth
- ->decr IF secretion–>B12 deficiency–>pernicious anemia
- ->risk of adenocarcinoma increase THREE fold**
- ->achlorhydia too
types:
1. Immune AKA pernicious Anemia aka Type 1
- –>auto immune disorder involving the fundic glands
- Non-immune AKA type 2 aka HP infection
- ->malabsorption secondary to chronic HP infection
Autoimmune gastritis affects what part of stomach and spares whihc?
affects– fundus (top part)
spares–antrum (lower part)
parietal cells produce
*what will happen if this cell is damaged
Antral G cells produce?
IF–B12 absoprtion
acid–help with iron asboprtion
damage leads to:
- iron def anemia
- pernicious anemia
Antral G cells produce gastrin
deifine PUD
- a break or ulceration in the protective mucosal lining
- disruption of mucosal integrity of stomach lining or duodenal lining—- leads to local defect due to active inflammation
define dyspepsia
epigastric pain exacerbated by fasting— improves with meals
basically upset stomach
do majority of PTs with dyspepsia have PUD?
NO—- over 90% do not have ulcers
how do majority of PTs with PUD present
asympto..
occurance of acid peptic disorders in US
- lifetime prevalnce in US?
- death rate?
very common–4 million individuals/yr
Lifetime prevalence–about 12% men and 10% women
15,000 deaths/yr due to complications
how to differentiate b/w gastric and duodenal ulcer?
change in PT’s symptoms with food is key
- Duodenal ulcer–s/s get better with food
- gastric ulcer–s/s get worse when eating
which is MC– duodenal or gastric ulcers?
duodenal–4 times more common
which is usually benign– duodenal or gastric ulcers
proximal duodenal MC benign
Gastric–4% associated with gastric adenocarcinoma
duodenal ulcer
*developmental factors (2)
Dev Factors
- HP infection**
- NSAIDs
gastritis tends to develop where in stomach vs gastric ulcers?
gastritis– fundus
ulcer–antrum (lower) next to the acid-secreting mucosa of the body—why it can be associatd with adenocarcionoma (intestinal cells met to stomach)
primary defect in gastric ulcers?
increased mucosal permeability to hydrogen ions
—gastric secretion tends to be normal or less than normal
Helicobacter Pylori
- what kind of bacteria
- affect on body?
- what happens during acute infection
- what happens after acute infection
- when is eradication achieved?
Spiral, gram (-) rod
*causes gastric mucosal inflammation
acute infection:
-causes transient illness of nausea and abdominal pain for several days–>acute gastritis with polymorphonuclear neutrophils (PMNs)
After infection or once s/s resole:
-majority progress to a chronic infection–>chronic diffuse mucosal inflammation characterized by PMNs and lymphocytes
eradication is achieved when:
ABX leads to >85% resolution of the chronic gastritis
Majority of chronic infection are asympto***** and no sequelae
why does eating make gastric ulcer more painful?
because food stimulates production of MORE acid
HP infection’s affects on:
- Gastrin
- acid production
since the HP infections usually attack the antrum– this can lead to:
1. increased gastrin–>turns on parietal cells–>secrs more acid
- Increased acid production
***all this leads to incr risk of devl PUD–esp duodenal
gastric ulcers are mostly caused by imbalance with?
decreased protective mechanisms (decr mucus, bicarb, prostaglandins)
duodenal ulcers are mostly caused by imbalance with?
aggressive factors (HP infection, incr HCL production)
chronic HP infection gastritic leads to:
duodenal or gastric ulcers–10%
gastric CA–.1-3%
Low grade B cell gastric lymphoma–SUPER rare
how to test for HP infection
-two genral ways
Noninvasive
- Fecal antigen immunoassay
- C-urea breath test
Invasive:
endoscopic + biopsy
patho behind urea breath test
urea pill–>pill has carbon-urea (tagged carbon/radioactive)
NPO and off PPI****
normally NO urea in the stomach…. but HP makes urease–which breaks down urea into CO2 and ammonia– so if + HP infection… the CO2 will be breathed out WITH the carbon isotope.
+ test is breathing out the radioactive isotope
- test is just peeing out the substance and not breathing out any tagged C in CO2
other conditions that cause PUD:
Zollinger-Ellison syndrome CMV CD Lymphoma Medications Chronic medical illneses like cirrhosis or CKD
prevalence of HP infection with duodenal ulers?
70-90%
chance of developing ulcer dz with an active HP infection?
10%
HP infection increases risk of?
NSAID induced ulcers and complications
Zollinger-Ellison Syndrome -also called? -what is it MC found where -asoc with what dz?
(Gastrinoma)
gastrin-secreting neuroendocrine tumor that often leads to severe PUD and diarrhea DUE TO HYPERSECRETION OF GASTRIC ACID
>90% of PTs develop PUD
the s/s are identical to PUD– so this dz might go undiagnosed for years
MC in duodenal wall (45%), pancreas (25%), lymph nodes (5-15%) or other sites
Associated with MEN 1
NSAIDs can cause PUDs by?
their prostaglandin production— leads to impaired defenses
what is the MCC of UGIB
PUD
Avg age for:
- duodenal ulcers
- Gastric ulcers
Duodenal: 30-55
Gastric: 55-70
why does diarrhea occur in 1/3 of PTs with Zolliner-Ellison syndrome
Gastric acid hypersecretion–>direct intestinal mucosal injury –> pancreatic enzyme inactivation–> resulting in diarrhea, steatorrhea, and weight loss
Gastric CA
- MC assoc with?
- other Rfs
- MC ??
- four types? (most favorable and worst prognosis?)
assoc with HP and atrophic gastritis—>gastric adenocarcinoma
other RF
- consumption of heavily salted and preseved foods
- low intake of veg/fruits
- smoking
- etoh
MC: adenocarcinoma–90%
TYPES:
- Polypoid carcinoma–solid mass projects into the stomach luemn
- ulcerative–looks like PUD
- superficial spreading–most favorable diagnosis
- Linitis plastica or “leather bottle”–infiltrates early– all layers–stomach wall becomes thick and rigid–poor prognosis
