disorders of the pancreas - tosto

first branch of superior mesenteric artery

pancreatoduodenal artery

gastric ulcer in posterior wall could damage

inflammation or infection of pancreas

pancreatitis

what is consumed in saponifcation

calicum → hypocalcemia, calcifications in chronic

inflammatory disease with little or no fibrosis

initiated by several factors:

• acute cholelithiasis or ETOH abuse

acute pancreatitis

single or recurrent episode of pain

abdomen with elevated pancreatic enzymes

acute focal/diffuse swelling/inflammation

symptoms resolve after acute attack, blood biochem becomes normal

acute pancreatitis

GET SMASHED: GET part

gallstone: female, fat, fifty, fertile

ethanol

trauma: mva

GET SMASHED: SMASHED part

steroid

mumps/virus

autoimmune

scorpion bites

hyperlipidemia

ERCP

Drugs: so many, NSAIDS, thiazide diuretic

clinical presentations of acute panc

abdominal pain

N/V, bloating

low grade fever

guarding

tachy, tachypnea, hypotn, hyperthermia

elevated hematocrit, pre renal azotemia

abdominal pain in acute pancreatitis

epigastric pain

radiates to back, flank, chest, lower abdomen

worse in supine, better leaning forward

clinical sequelae of acute panc

respiratory sx: atelectasias, pleural effusions, ARDS

abdom: CULLEN sign (umbilicus bluish), Grey Turner (bluish flanks)

hypovolemic shock: 3rd spacing, hemorrhage, increased vascular perm, vasodilation, cardiac depresh, vomiting

grey turner and cullens sign

serum amylase: normal doesn’t exclude. nonspec. doesn’t predict severity

amylase

what best predicts disease severity in acute panc

BUN

found in pacna nd salivary glands, low levels in many tissues

may be normal , poor specificity

amylase

found predominantly in panc but also in gastric, intestinal mucosa, and liver

better specificity

2-3x normal level is good cutoff

lipase

renal failure and lipase

lipase is cleared by the kidneys so levels would be elevated

diagnosis acute panc: xray

rules out other diagnoses too

may see calcifications if chronic

may see sentinel loop, elevated hemidiaphragm, pleural effusion

US and acute panc

may detect gallstones

ct scan abdomen and acute panc

estimates severity and prognosis

complications → phlegmons, abscesses, pseudocysts. 2-3 wks after acute pancreatitis

pathophy of acute panc

central cause → acitvation of digestive zymogens in acinar cells and subsequent autodigestion of pancreas

and then they digest cellular membranes within pancreas → edema, interstitial hemorrhage, vascular damage, coag, and cellular necrosis

scoring criteria for panc

ranson’s criteria

also apache-2

biochemical markers and CT scan

RANSON CRITERIA Admission

age, wbc, glucose, LDH, AST

from first aid: Drugs generate a violent abdominal distress

Diuretics

glucocorticoids, valproate, alcohol, azithoprine

ranson crit wbc count

>18000

ranson criteria during first 48 hours

hematocrit

serum calcium

base deficity

increase in bun

fluid sequestration

ransons WBC admission

>18000

ranson glucose admission

>220

ranson ldh admission

>400

ranson admission AST

>250

ranson hematocrit drop

>10%

ranson serum calcium 48hrs

<8

ranson base deficit

>5.0r

ranson Increase in BUN

>2

ranson fluid sequestration

>4L

<2 pos signs ranson criteria

mortality rate is 0

3-5 positive signs ranson criteria

mortality rate is 10-20%

>=7 pos signs ranson criteria

>50% mortality rate

pancreatic necrosis

tx mild pancreatitis

rest

supp care

• fluid resus → watch BP and urine output

• pain control

• NG tubes

refeeding (3-7 days)

tx severe pancreatitis

rest and supp care

• fluid resus: may req 5-10 liters a day (norm is 2-3)

• careful pulm and renal monitoring

• maintain HCT of 26-30

• pain ctl (pump)

• correct electrolytes

• prophy AB

• nutritional support (may be NPO for weeks, TPN)

local complications of pancreatitis

abscess, pseudocyst, ascites, phlegmon

adjacent organ involvement

systemic complications

pulm effusions, hypoxemia, ards

myocardial depress, hemorrhage, hypovolemia

hypocalcemia, hyperglycemia, hyperlipidemia, coagulopathy

renal failure

gi hem

fat necrosis

irreversible damage to panc, incurable

chronic pancreatitis

70% of chronic panc caused by

ETOH

steady and boring pain, epigastric

not colicky

N/V

anorexia

malabsorption, weight loss

apancreatic diabetes

chronic pancreatitis

chronic pancreatitis calcifications

abnormally dilated ducts

chronic panc

minimally invasive test that allows simultaneous assessment of ductal and parenchymal structure

endoscopic ultrasound

noninvasive alternative to ERCP for imaging pancreatic duct

MRCP

highly sens test for CP (radiographic)

ERCP

splenic and portal vein thrombosis

complication of chronic panc

tc for chronic panc

stop alcohol

enzyme tx

analgesia

ppis

surg,