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Flashcards in 05a: Da Pancreas Deck (37)
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1
Q

Diagnosis of acute pancreatitis requires 2 out of which criteria?

A
  1. Characteristic abd pain
  2. Elevated serum lipase/amylase (3x ULN)
  3. Characteristic imaging findings
2
Q

Characteristic pain in acute pancreatitis is quite similar to (X) pain, but is (exacerbated/alleviated) by (Y).

A

X = biliary cholic (acute onset, persistent and severe epigastric pain that radiates to back and exacerbated by eating)
Alleviated
Y = leaning forward

3
Q

(Lipase/amylase) elevation is more specific for acute pancreatitis. It stays elevated for (shorter/longer) period of time.

A

Lipase (can increase 10x normal!); longer (72-96h)

4
Q

Which imaging modalities used to diagnose acute pancreatitis? Star the preferred method.

A

CT*, MRI, US

5
Q

Most (50%) cases of acute pancreatitis are attributed to:

A

Gallstones

6
Q

Second most common cause of acute pancreatitis is:

A

EtOH (30%)

7
Q

Patient presenting with acute pancreatitis. Which finding is considered incredibly high predictor of gallstone etiology (95% PPV!)?

A

ALT elevated 3x ULN

8
Q

You diagnose patient with acute pancreatitis. What are your initial steps for therapy?

A
  1. NPO
  2. Analgesics
  3. Early, aggressive IV fluid resuscitation
9
Q

Acute pancreatitis: IV fluids are preferentially (normal saline/lactate ringers) to prevent which complications?

A

Lactate ringers;

Metabolic acidosis and increased trypsinogen activation

10
Q

“BISAP” scoring system used to predict (X). What does it stand for?

A

X = severity of acute pancreatitis

BUN over 25 mg/dL
Impaired mental status
SIRS
Age over 60
Pleural effusion on imaging
11
Q

T/F: Like other zymogens, pancreatic amylase and lipase are secreted in inactive forms.

A

False

12
Q

Based on experimental models, the initiating event in acute pancreatitis is:

A

Intra-acinar conversion of trypsinogen to trypsin (resulting in acute intracell injury)

13
Q

T/F: The magnitude

of serum amylase/lipase elevation correlates with the severity of pancreatitis.

A

False

14
Q

Which two main complications of acute pancreatitis occur due to toxic materials (liberated by pancreas) reaching systemic circulation?

A

SIRS and MODS (multiple organ dysfunction syndrome)

15
Q

T/F: All pancreatic pseudocysts are removed to avoid infection/compression.

A

False - asymptomatic ones are just followed

16
Q

Fat necrosis is an example of (autodigestion/local spread/systemic spread) in acute pancreatitis.

A

Local spread

17
Q

(X) tool is useful for distinguishing between interstitial and necrotizing pancreatitis. What is the difference between these?

A

X = CT (with contrast)

Interstitial: intact microcirculation (uniform enhancement)
Necrotizing: disrupted microcirculation (large areas won’t enhance with contrast)

18
Q

(X) is the leading cause of mortality (80%) in acute pancreatitis.

A

X = infected necrosis

19
Q

Treatment of infected necrosis (in acute pancreatitis) includes which drugs?

A

Antibiotics that penetrate pancreatic necrosis:

Carbapenems, quinolones, metronidazole

20
Q

T/F: All patients with infected necrosis (secondary to acute pancreatitis) require debridement.

A

False - stable patients may only require antibiotics

21
Q

Mild pancreatitis: when should oral diet be restarted?

A

Immediately after resolution of pain, N/V (early re-feeding associated with short hospital stays, decreased complications)

22
Q

T/F: In severe pancreatitis, parenteral nutrition is preferred to avoid additional stress on the gut.

A

False! Enteral preferred;

TPN only if enteral route unavailable/not tolerated (higher risk of infection, organ failure, mortality)

23
Q

T/F: The changes in chronic pancreatitis are fibro-inflammatory and irreversible.

A

True

24
Q

Almost 75% of chronic pancreatitis is due to which etiology?

A

EtOH

25
Q

Three main clinical manifestations of chronic pancreatitis:

A
  1. Abdominal pain (similar to that in acute pancreatitis)
  2. Fat and fat-soluble vitamin malabsorption (exocrine insufficiency)
  3. Diabetes (endocrine insufficiency)
26
Q

Which 3 main imaging methods used to diagnose chronic pancreatitis?

A

CT, MRCP, EUS

27
Q

(X) CT finding is pathognomonic (indicative of) chronic pancreatitis. Which other findings might be present?

A

X = calcifications in pancreas

Atrophy, fatty replacement, ductal dilation

28
Q

(X) imaging modality is excellent for evaluation of biliary/pancreatic duct changes in chronic pancreatitis.

A

X = MRCP

29
Q

(X) imaging modality is useful for detecting mild chronic pancreatitis (before radiographic abnormalities are evident).

A

X = EUS (Endoscopic ultrasound)

30
Q

Diabetes is a(n) (early/late) complication of chronic pancreatitis. About (X)% of gland is damaged when clinical diabetes becomes apparent.

A

Late;

X = 80-90

31
Q

(X) is the gold standard functional test for diagnosis of chronic pancreatitis.

A

X = secretin stimulation

With diagnostic decrease in HCO3 production, even in early pancreatitis

32
Q

(Fecal/serum) measurement of (X) is seen as superior to serum trympsinogen and fecal chymotrypsin in testing function of (Y).

A

Fecal
X = elastase
Y = pancreas (i.e. for chronic pancreatitis)

33
Q

Chronic pancreatitis Rx is focused on managing:

A
  1. Pain

2. Exocrine/endocrine insufficiency

34
Q

Diet/supplementation in chronic pancreatitis involves:

A
  1. Low fat diet
  2. Vitamin and pancreatic enzyme supplementation
  3. Diabetes control
35
Q

Patient with CKD and HCV infection can be treated with (X) combo for which genotypes?

A

X = Grazoprevir (NS3/4A inhibitor) and Elbasvir (NS5A inhibitor)

Genotypes 1 and 4

36
Q

Patient with decompensated cirrhosis and HCV (Genotype 2) should be treated with (X) drug combo, which covers which genotypes?

A

X = Velpatasvir (NS5Ai) and Sofosbuvir (NS5Bi)

All (1-6) genotype

37
Q

Patient with decompensated cirrhosis and HCV (Genotype 5) can be treated with (X) drug combo, which covers which SELECT genotypes?

A

X = Ledipasvir (NS5Ai) and Sofosbuvir (NS5Bi)

Genotypes 1,4-6