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GI > Pancreatitis: Acute and Chronic > Flashcards

Pancreatitis: Acute and Chronic Flashcards

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
Q

there is an increase in mortality associated with infected necrotic collections and ____ are necessary

A

antibiotics (fluoroquinolones)

26
Q

systemic complications of AP

A

organ failure (transient or persistent), cardiovascular: hypovolemia, hypotension from fluid loss

27
Q

most important laboratory tests for AP

A

elevation of serum amylase and lipase 3x ULN or greater

28
Q

longer half life: amylase or lipase?

A

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
Q

what findings are suggestive of gallstone disease

A

liver tests, direct bilirubin, and alkaline phosphatase

30
Q

why is fluid loss such an important problem

A

it means a loss of blood volume, leads to hypoperfusion or organs–> damages them.

31
Q

symptoms of fluid loss

A

decreased BP, increased HR, decreased urine output, increased hematocrit and BUN

32
Q

imaging for diagnosis

A

ultrasound if suspecting gallstones. CT and MRI to detect necrosis after 3 days if patient does not improve/gets worse.

33
Q

2/3 things for diagnosis of AP

A

characteristic pain, elevated amylase/lipase 3x ULN, positive imagine results

34
Q

3 treatment goals for AP

A

early fluid resuscitation, early initiation of nutrition (lowers mortality, prevents progression), relieve pain

35
Q

guidelines for fluid resuscitation

A

initiate within 12 hrs: lactated ringers or normal saline. monitor vitals, BUN elevated at 24 hours is a sign of increased mortality

36
Q

how does early nutrition help

A

counteracts the catabolic state, prevents damage to organs such as mucosal lining of intestines, reduces morbidity and mortality

37
Q

nutrition for mild AP

A

low fat soft/solid oral diet as early as 12h after diagnosis if it does not exacerbate pain.

38
Q

removal of the gallbladder is carried out as early as _____ if this is the cause

A

24-48h after diagnosis (before they leave the hospital)

39
Q

nutrition for moderately severe or severe AP

A

initiated about 24h after diagnosis and admission. oral if tolerated, enteral thru nasogastric or nasojejunal if not.

40
Q

what if there are contraindications for enteral feeding

A

parenteral can be initiated

41
Q

drugs for pain

A

opioids: IV LD, continuous IV, PCA. fentanyl is more potent and given in mcg (others are mg)

42
Q

why is meperidine not first line

A

because possible accumulation of its metabolite normeperidine has CNS effects/seizures

43
Q

prophylactic antibiotics?

A

not usually. can be initiated if infection is suspected. if infection is not confirmed then drug would be discontinued.

44
Q

what is chronic pancreatitis

A

progressive inflammation with structural and functional loss (permanent) of both endocrine and exocrine functions

45
Q

major cause of chronic pancreatitis

A

alcohol abuse

46
Q

other factors that increase the risk of CP

A

cigarette smoking, hereditary, obstruction of pancreatic ducts, previous AP episodes

47
Q

pathogenesis of chronic pancreatitis

A

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
Q

CP increases the risk of _____

A

pancreatic cancer

49
Q

diagnosis of CP: pain?

A

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
Q

diagnosis of CP: malnutrition?

A

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
Q

diagnosis of CP: endocrine function?

A

loss of endocrine function results in insulin-dependent diabetes mellitus

52
Q

diagnosis of CP: steatorrhea?

A

lack of lipase: dietary fat eliminated in the feces= steatorrhea

53
Q

how can you determine steatorrhea

A

evaluate 72 hour collection for fecal fat or measure elastase in feces (elastase not degraded in intestines)

54
Q

diagnosis of CP: serum amylase and lipase?

A

usually normal or below normal: loss of gland tissue is gradual, acinar cells no longer synthesizing and releasing the enzymes

55
Q

diagnosis of CP?

A

test of choice is MRCP. may be useful for observing calcified protein deposits that block pancreatic ducts and alcoholic CP

56
Q

guidelines for selection of a pancreatic enzyme supplement

A

administered to correct malabsorption (because of insufficient digestion). dosing/choice: focus on achieving nutritional goals.

57
Q

administration of the enzymes depends on

A

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
Q

the number associated with the name of the pancreatic enzyme preparation is the amount of _____ units in the preparation

A

lipase

59
Q

how to take pancreatic enzyme capsules

A

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.

GI (15 decks)

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