Pancreatitis: Acute and Chronic Flashcards

(59 cards)

1
Q

AP is _____

A

inflammation of the pancrea

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2
Q

the leading cause of ER visits and hospitalizations for GI diseases in the US

A

pancreatitis

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3
Q

3 strategies to increase positive outcomes for AP patients

A

diagnose rapidly, fluid initiate within 12 hours and nutrition within 24 hours, follow up

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4
Q

__% of AP cases are severe

A

20

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5
Q

most common cause of pancreatitis

A

gallstones

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6
Q

second most leading cause of AP

A

alcohol consumption

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7
Q

third most leading cause of AP

A

hypertriglyceridemia

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8
Q

pathogenesis of AP

A

obstruction of common duct, ampulla of vater–> bile refluxed back into pancreas and damages acini. pancreatic secretions accumulate in the pancreas, proteolytic enzymes are activated= initiate AP.

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9
Q

what indicates that gallstones/sludge were the cause of AP

A

cholecystetomy or removal of gallbadder with subsequent recovery

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10
Q

how high are triglycerides to cause AP

A

> 1000 mg/dL

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11
Q

what are some more rare causes of AP

A

ERCP, some drugs

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12
Q

classification: mild AP

A

inflammation, edema of pancreas. peripancreatic fluid collections, pancreatic fluid collections. no organ failure, no systemic complications. recover in 3-7 days

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13
Q

classification: moderately severe AP

A

necrosis, inflammation, edema, fluid collections, transient organ failure <48 hours

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14
Q

classification: severe AP

A

necrosis, persistent organ failure, 20% mortality

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15
Q

_____ increases the severity of AP

A

infection of the pancreas and peripancreatic collections (fluid and necrotic tissue)

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16
Q

______ is death of cells & tissues associated with moderate and severe AP

A

necrosis

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17
Q

what 2 things contribute to organ failure with AP?

A

the pancreatic enzymes are activated in the pancreas and damage the surrounding tissue, they can leak into the circulation and damage other organs thus leading to organ failure. also: the immune response, systemic inflammatory response syndrome (SIRS)

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18
Q

diagnostic marker for severe AP

A

C reactive protein, CRP > 150 at 48 hours: indicates systemic disease.

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19
Q

symptoms of AP

A

severe pain, acute onset, epigastric, may radiate to the back. nausea, vomiting, fever

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20
Q

AP physical exam indications

A

abdominal distention

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21
Q

history to gather for AP

A

past hx of AP (pt and fam), identify possible cause, gallstone disease, alcohol use, medications, etc

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22
Q

if the fluid collection is still there at 4 weeks it is called

A

pseudocyst

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23
Q

when the fluid collections include necrotic tissue at 4 weeks they are called

A

walled off necrosis

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24
Q

if the necrotic collection becomes infected, they are called

A

infected walled off necrosis

25
there is an increase in mortality associated with infected necrotic collections and ____ are necessary
antibiotics (fluoroquinolones)
26
systemic complications of AP
organ failure (transient or persistent), cardiovascular: hypovolemia, hypotension from fluid loss
27
most important laboratory tests for AP
elevation of serum amylase and lipase 3x ULN or greater
28
longer half life: amylase or lipase?
lipase: so it remains elevated for a longer time 8-14 days. whereas amylase has shorter half life and returns to normal in 3-5 days
29
what findings are suggestive of gallstone disease
liver tests, direct bilirubin, and alkaline phosphatase
30
why is fluid loss such an important problem
it means a loss of blood volume, leads to hypoperfusion or organs--> damages them.
31
symptoms of fluid loss
decreased BP, increased HR, decreased urine output, increased hematocrit and BUN
32
imaging for diagnosis
ultrasound if suspecting gallstones. CT and MRI to detect necrosis after 3 days if patient does not improve/gets worse.
33
2/3 things for diagnosis of AP
characteristic pain, elevated amylase/lipase 3x ULN, positive imagine results
34
3 treatment goals for AP
early fluid resuscitation, early initiation of nutrition (lowers mortality, prevents progression), relieve pain
35
guidelines for fluid resuscitation
initiate within 12 hrs: lactated ringers or normal saline. monitor vitals, BUN elevated at 24 hours is a sign of increased mortality
36
how does early nutrition help
counteracts the catabolic state, prevents damage to organs such as mucosal lining of intestines, reduces morbidity and mortality
37
nutrition for mild AP
low fat soft/solid oral diet as early as 12h after diagnosis if it does not exacerbate pain.
38
removal of the gallbladder is carried out as early as _____ if this is the cause
24-48h after diagnosis (before they leave the hospital)
39
nutrition for moderately severe or severe AP
initiated about 24h after diagnosis and admission. oral if tolerated, enteral thru nasogastric or nasojejunal if not.
40
what if there are contraindications for enteral feeding
parenteral can be initiated
41
drugs for pain
opioids: IV LD, continuous IV, PCA. fentanyl is more potent and given in mcg (others are mg)
42
why is meperidine not first line
because possible accumulation of its metabolite normeperidine has CNS effects/seizures
43
prophylactic antibiotics?
not usually. can be initiated if infection is suspected. if infection is not confirmed then drug would be discontinued.
44
what is chronic pancreatitis
progressive inflammation with structural and functional loss (permanent) of both endocrine and exocrine functions
45
major cause of chronic pancreatitis
alcohol abuse
46
other factors that increase the risk of CP
cigarette smoking, hereditary, obstruction of pancreatic ducts, previous AP episodes
47
pathogenesis of chronic pancreatitis
chronic inflammation and damage to acinar cells, islets, duct cells--> permanent structural/functional losses. lost cells replaced by fibrous material. calcified pancreatic proteins block or damage ducts, inflammation, activation of enzymes
48
CP increases the risk of _____
pancreatic cancer
49
diagnosis of CP: pain?
usually not as severe as AP. in epigastric area, can be intermittent or chronic episodic flare-ups. can radiate to the back. nausea and vomiting common
50
diagnosis of CP: malnutrition?
loss of exocrine function= malabsorption of nutrients leading to malnutrition and weight loss (because loss of enzymes for digestion of the 3 major foods, digestion must occur before absorption of nutrients). loss of lipase: malabsorption of fats, fat soluble vitamins
51
diagnosis of CP: endocrine function?
loss of endocrine function results in insulin-dependent diabetes mellitus
52
diagnosis of CP: steatorrhea?
lack of lipase: dietary fat eliminated in the feces= steatorrhea
53
how can you determine steatorrhea
evaluate 72 hour collection for fecal fat or measure elastase in feces (elastase not degraded in intestines)
54
diagnosis of CP: serum amylase and lipase?
usually normal or below normal: loss of gland tissue is gradual, acinar cells no longer synthesizing and releasing the enzymes
55
diagnosis of CP?
test of choice is MRCP. may be useful for observing calcified protein deposits that block pancreatic ducts and alcoholic CP
56
guidelines for selection of a pancreatic enzyme supplement
administered to correct malabsorption (because of insufficient digestion). dosing/choice: focus on achieving nutritional goals.
57
administration of the enzymes depends on
amount of food, rate of consumption. entire dose may be taken with first bite, or half at the beginning and other half in the middle of the meal
58
the number associated with the name of the pancreatic enzyme preparation is the amount of _____ units in the preparation
lipase
59
how to take pancreatic enzyme capsules
can be swallowed whole or opened/sprinkle contents on acidic food such as applesauce. follow consumption with a beverage. do not chew or crush capsules or their contents.