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pathways > Gallbladder > Flashcards

Gallbladder Flashcards

1
Q

Inflm of gallbladder aka

A

Cholecystitis

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2
Q

Gallstones aka

A

Cholelithiasis

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3
Q

Cholelithiasis et

A

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)

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4
Q

Types of gallstones

Which is more common

A

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

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5
Q

Gall bladder fx

What do disorders involve

A

Disorders involve inflm, infection, stones and tumors

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6
Q

composition of bile

A 
97% fluid and electrolytes
 bile salts
bilirubin
 fats (cholesterol, fatty acids and lecithin)
inorganic salts
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7
Q

mnfts of gallstones

A

colic intermittent, radiating pain. (can be confused as MI)

nausea, vomiting d/t pain and GI symptom

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8
Q

dx gallstone

A

hx, px
ultrasounds
scans

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9
Q

tx gallstones

Complications

A
  • 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

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10
Q

how does actigall work

A

for cholelithiasis

it contains bile acid which dissolves the stones

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11
Q

acute pancreatitis

what enzymes does pancreas release

A

inflm of pancreas
auto digestion (not autoimmunity)
can be life threatening

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12
Q

et pancreatitis

A 
alcohol abuse (~70%)
gallstones
idiopathic (~10%)
others
   pancreatic trauma, drugs
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13
Q

patho of pancreatitis

A

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
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14
Q

enymes prod by pancreas

A

(pancreatic enzymes: 99% of pancreas is exocrine eg produces pancreatic amylase, lipase, trypsinogen, chymotrypsinogen.)

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15
Q

mnfts of pancreatitis

A

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
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16
Q

dx of pancreatitis

A

blood amylase and lipase

be aware that amylase is also prod in mouth so dont run only this

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17
Q

tx pancreatitis

A

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

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18
Q

liver cancer how is it divided, which is more common and why

A

primary or secondary

secondary tumors are more common
d/t size, portal drainage, inc perfusion

19
Q

primary liver CA 2 types

which is more common

A

hepatocellular carcinoma-90%

cholangiocarcinoma

20
Q

hepatocellular carcinoma

A

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
21
Q

mnfts of hepatocellular carcinoma

A

insidious onset

then masked by underlying liver disease
youll often have preceding hep C infection with similar mnfts

22
Q

tx of hepat. carc.

A

poor prognosis
partial hepatectomy
chemo and radiation (palliative)

23
Q 
ademona
who is at risk
cell of origin
risk of what
tx
A

20-30yr old women on the pill at risk
affects hepatocytes
vascular (risk of hemmorhage)
sx and withdraw the hormones->prognosis is good

24
Q

cholangiocarcinomas

cell of origin

assoc with what

A

origin in bile duct epithelium

assoc with chronic inflm of duct epithelium

25
Q

metastatic secondary tumours usually come from where

A

from colon, lung, breast

26
Q

mnfts of metastatic secondary tumors

A

those of liver disease

  • hepatomegaly, ascites, abdm pain
  • anorexia, fever, wt loss
27
Q

whenever a pt has ____ youll check for cancer

A

unexplained wt loss

28
Q

tx of metastatic secondary tumours

A

very poor prognosis

supportive and palliative

29
Q

pancreatic cancer is more prevalent in who

A

black men who smoke

30
Q

pancreatic cancer

A

leading cause of death from CA
-90% mortality in the first year
-

31
Q

what is et of pancreatic CA linked to

A

unclear but linked to

  • smoking (major risk. Organ specific carcinogens)
  • alcohol
  • DM, chronic pancreatitis
  • age (>50yr)
  • poor diet
32
Q

why does pancreatic CA risk inc with age

A

-age (>50yr) when prevalence inc with age it suggest cumulative exposure/damage to cause mutation)

33
Q

what type of tumours form in pancreatic CA

A

90% adenocarcinomas (duct epith)

not in fx cells of organ

34
Q

mnfts of pancreatic CA

A

d/t mass rather than dec fx
jaundice (dont know why)
wt loss
abdm pain

all general s/s that dont point to pancreas

35
Q

dx of pancreatic CA

A

u/s and CT

it will have already metastaized at dx

36
Q

tx of pancreatic CA

A

pain control is key

sx is primary approach. (Must be caught earlyt o be successful)

37
Q

what are the infant disorders

A 
cleft lip
cleft palate
pyloric stenosis
GER..
Hirschsprung disease
intussusception
38
Q

cleft lip

A
  • 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)

39
Q

cleft palate

A

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)

40
Q

pyloric stenosis

A

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

41
Q

et of pyloric stenosis

A

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)

42
Q

patho and mnfts of pyloric stenosis

A

hypertrophy->constriction->inflm->obstr

projectile vomitiing, dehydration, malnourishment

43
Q

dx pyloric stenosis

A

hx and px (when palpating in RUQ there may be mass. Hx of projectile vomit)
US (shows enlargement)

44
Q

tx of pyloric stenosis

A

sx

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