Gallbladder Flashcards
Inflm of gallbladder aka
Cholecystitis
Gallstones aka
Cholelithiasis
Cholelithiasis et
Abnormal bile composition (eg inc cholesterol, dec bile salts)
Bile stasis leads to precipitation
(Either of the above can lead to gallstone formation)
(In order to form precipitate you need a particle that isn’t part of composition of bile, the precipitates will then attach to the particle called nuclei)
(Those who dev infection from E. coli or strep faecalis are more susceptible to gallstones most likely d/t composition of bile)
Inflm debris leads to nuclei for stone formation
-genetics? (If person dev stones very quickly)
Types of gallstones
Which is more common
Cholesterol stones 80% -composed of bile and lots of cholesterol
Pigment stones 20% made of bilirubin and calcium salts (bilirubin is usually only present in small amounts)
Mixed stones
Gall bladder fx
What do disorders involve
Disorders involve inflm, infection, stones and tumors
composition of bile
97% fluid and electrolytes bile salts bilirubin fats (cholesterol, fatty acids and lecithin) inorganic salts
mnfts of gallstones
colic intermittent, radiating pain. (can be confused as MI)
nausea, vomiting d/t pain and GI symptom
dx gallstone
hx, px
ultrasounds
scans
tx gallstones
Complications
- pain
- dissolving agents eg actigall
- sx eg retrograde endoscopy (from duodenum wire will go into bile ducts
tx complications eg cholecystitis, pancreatitis, perforation that could lead to peritonitis
how does actigall work
for cholelithiasis
it contains bile acid which dissolves the stones
acute pancreatitis
what enzymes does pancreas release
inflm of pancreas
auto digestion (not autoimmunity)
can be life threatening
et pancreatitis
alcohol abuse (~70%) gallstones idiopathic (~10%) others pancreatic trauma, drugs
patho of pancreatitis
Pancreatic enzymes are produced in inactive form and are activated once in duodenum in presence of bile
-bile flow obstr->premature activation of Ex-> enzymatic damage of pancreas. autodigestion, hemmorhage, necrosis (if gallstone forms and blocks below the pancreatic duct, bile may flow up pancreatic duct and activate enzymes)
- alcohol?
- inc pancreatic sec (when the duct fills with pancreatic sec which will also have bile it leads to enzyme activation…the sphincter of Oddi opens…)
- constricts sphincter in pancreatic duct
enymes prod by pancreas
(pancreatic enzymes: 99% of pancreas is exocrine eg produces pancreatic amylase, lipase, trypsinogen, chymotrypsinogen.)
mnfts of pancreatitis
acute onset usually following large meal (inc bile release) or alcohol (inc pancreatic sec)
- severe abdm pain
- epigastric (could be mistaken for appendicitis)
- radiates to back
- 3rd spacing +++
- vascular collapse and shock is possible
dx of pancreatitis
blood amylase and lipase
be aware that amylase is also prod in mouth so dont run only this
tx pancreatitis
based on severity
Mild=1wk recovery NPO (because when you ingest food this inc bile and inc Es) pain lytes/fluid correct metb abn
Severe=ICU
renal, circulatory, hepatobiliary support
IV opiates
Sx? for stones
liver cancer how is it divided, which is more common and why
primary or secondary
secondary tumors are more common
d/t size, portal drainage, inc perfusion
primary liver CA 2 types
which is more common
hepatocellular carcinoma-90%
cholangiocarcinoma
hepatocellular carcinoma
90% of liver CA
- origin in hepatocytes
- et linked to (like risk factors)
- chronic liver disease eg hepatitis (viruses cause mutation)
- environ toxins eg arsenic
mnfts of hepatocellular carcinoma
insidious onset
then masked by underlying liver disease
youll often have preceding hep C infection with similar mnfts
tx of hepat. carc.
poor prognosis
partial hepatectomy
chemo and radiation (palliative)
ademona who is at risk cell of origin risk of what tx
20-30yr old women on the pill at risk
affects hepatocytes
vascular (risk of hemmorhage)
sx and withdraw the hormones->prognosis is good
cholangiocarcinomas
cell of origin
assoc with what
origin in bile duct epithelium
assoc with chronic inflm of duct epithelium
metastatic secondary tumours usually come from where
from colon, lung, breast
mnfts of metastatic secondary tumors
those of liver disease
- hepatomegaly, ascites, abdm pain
- anorexia, fever, wt loss
whenever a pt has ____ youll check for cancer
unexplained wt loss
tx of metastatic secondary tumours
very poor prognosis
supportive and palliative
pancreatic cancer is more prevalent in who
black men who smoke
pancreatic cancer
leading cause of death from CA
-90% mortality in the first year
-
what is et of pancreatic CA linked to
unclear but linked to
- smoking (major risk. Organ specific carcinogens)
- alcohol
- DM, chronic pancreatitis
- age (>50yr)
- poor diet
why does pancreatic CA risk inc with age
-age (>50yr) when prevalence inc with age it suggest cumulative exposure/damage to cause mutation)
what type of tumours form in pancreatic CA
90% adenocarcinomas (duct epith)
not in fx cells of organ
mnfts of pancreatic CA
d/t mass rather than dec fx
jaundice (dont know why)
wt loss
abdm pain
all general s/s that dont point to pancreas
dx of pancreatic CA
u/s and CT
it will have already metastaized at dx
tx of pancreatic CA
pain control is key
sx is primary approach. (Must be caught earlyt o be successful)
what are the infant disorders
cleft lip cleft palate pyloric stenosis GER.. Hirschsprung disease intussusception
cleft lip
- ranges from indentation to fissure
- unilateral or bilateral
- ~1/700 births
- teratogens
- smoking, viral infect, folic acid deficiency (nec for DNA synthesis and cell division)
- maxillary and nasal str do not fuse (wk 5-8) sensitive period
(congenital and teratogen)
cleft palate
incomplete fusion of palatine strs (wk 9-12)
- strong link to smoking in pregnancy
- 1/2000 births
- malformed nasal strs
- sx
(smokin is teratogen again)
pyloric stenosis
muscle hypertrophy and constriction at pylorus
-2-8 wks of age (after birth not sensitive period)
1/100 births
-4:1 male to female ratio
et of pyloric stenosis
idiopathic
-linked to hypergastrinemia, PGE & erythromycin exposure
(infants have immature organs. Duodenum only has weak buffers so sphincter may hypertrophy to compensate and try to stay closed)
patho and mnfts of pyloric stenosis
hypertrophy->constriction->inflm->obstr
projectile vomitiing, dehydration, malnourishment
dx pyloric stenosis
hx and px (when palpating in RUQ there may be mass. Hx of projectile vomit)
US (shows enlargement)
tx of pyloric stenosis
sx
