Nu 735 GI I /Pancreatic Flashcards

1
Q

Pancreatic Anatomy & Physiology

Role in Digestion
Pancreatic JUice - Enzymes
and
Release Hormones

A
  • Role of Pancreas: plays important role in Digestion
  • Located: Pancreas locating in upper abdomen, behind stomach size of the hand
  • During digestion Pancreas release juices called **enzymes **
  • Pancreatic enzymes released during digestion:

* lipase, protease and amylase

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2
Q

Lipase ?

A

***Lipase: (fat) - Fat w Bile ( in liver)
* **Enzyme that works together with bile that liver produces to breaks down fat in diet . **
i. When cells in pancreas are injured, increase amount of lipase enter blood steam and
ii. Resulting high level of Lipase concentration
iii. If you don’t have enough lipase, the body will have trouble observing fat and
And Important Fat Soluble Vitamins : A, B, E, & K
v. **How do we know that someone has poor fat absorption? **
Symptoms will include diarrhea and fatty bowel movements.

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3
Q

Amylase?

A
  • *Amylase > Break Down > Startches INTO Sugar > Lacke of Carbohydrates
  • Enzyme Breaks down starches into sugar which body can use for energy
    • When you don’t have enough Amylase:
      • Body may have diarrhea from undigested carbohydrates
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4
Q

Protease

A
  • Enzyme that break down proteins in diet
    - Undigested Protein can cause allergic reaction in some people
    - Also helps protect body from germs that may live in intestines like certain bacteria
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5
Q

Pancreatic Hormones

A

Pancreas helps digestion of producing hormones
A. Insulin:
B. Glucagon:
C. Amylin: supress glucagon

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6
Q

Ensymes:

Insulin

A
  • Produced by pancreatic beta cells, insulin helps regulate blood sugar (glucose) levels.
  • It promotes the uptake of glucose from the **bloodstream into cells, thereby lowering blood glucose levels.
  • Without insulin, cells cannot efficiently use glucose for energy, leading to high blood sugar levels (hyperglyce
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7
Q

Enzymes

Glucagon

A

.
* Produced by pancreatic alpha cells
* It raises blood sugar levels
* by promoting the breakdown of **glycogen (stored glucose) into glucose in the liver. **
* This process is called glycogenolysis.

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8
Q

Enzymes

Amylin

A

* co-secreted with insulin from pancreatic B/cells. **
* Blood sugar regulation: It helps to slow down the rate at which glucose enters the bloodstream after meals, reducing spikes in blood sugar levels.
* P
romotion of glucagon secretion:** Amylin can enhance the release of glucagon from pancreatic alpha cells, which helps to maintain blood sugar levels between meals.
* Delaying gastric emptying:
* Amylin slows down the emptying of the stomach after a meal, which helps to prevent sharp rises in blood glucose levels after eating

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9
Q

Pancreatic Injury

A

* Premature release of pancreatic enzymes
* Increased amounts of lipase & amylase enter bloodstream

o What happens when Pancreas becomes inflamed?
o Several mechanisms exist to limit Pancreatic enzyme activation after Procrit metabolism has occurred
o This is b/c premature pancreatic activation enzymes within pancreas leads to organ injury and pancreatitis
o Acute Pancreatitis occurs when factors involving maintaining cellular homeostasis become out of balance
o Digestion enzymes released in Pancreas
o Prematurely activated
o Than this enzymes start to digest Pancreas leading to inflammatory process

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10
Q

Pancreatitis Overview
Statistic

A
  • **Most common inpatient GI diagnosis **
    o Annual incidence ranges from 13-45 cases per 100,000 persons
    o Results in 250,000 hospitalizations/year
    o Most common nonsurgical abdominal condition for geriatric
    o **Mortality up to 40% above the age of 70 **
    o $2.6 billion per year cost to health care system

** Hospitalizations*
o Incidents of occurs : 200-fold after the age of 65
o 88% higher among Blacks
o Higher among males than females

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11
Q

Three Phases of
Acute Pancreatitis of Disease process

A
  • Initial Phase
  • Second Phase
  • Thirtd Phase
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12
Q

1st Phase:
Initial Phase

A

Enzyme activation & acinar cell injury

> ** Enzyme Activation: **characterized by intra pancreatic Enzyme activation
** Acinar Cell is : **
functional unit of exocrine pancreas

  • Responsible for producing and secreting digestive enzymes.
  • These enzymes, such as amylase, lipase, and proteases (like trypsinogen and chymotrypsinogen), are essenisl got breaking down carbohydrates, fats, and proteins in the small intestine ( duodenum )
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13
Q

Second Phase

A

**Cytokine Activation **
Resulting Inflammatory Injury

Cytokines ( IL interluekins, Interfersons) cell responsible to inhibits (prevent) T and B cells immune responses

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14
Q

Thirst Phase

A
  • **Leads to clinical findings: **
    like edema, interstitial hemorrhage, vascular damage, fat, cellular necrosis.
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15
Q

Pancreatitis Etiology

A

o Acute pancreatitis is an inflammatory condition of the pancreas, and while the exact cause of the initial event that triggers it is not fully understood,
o it is believed that an initial cellular injury can impair the secretion of digestive enzymes.
o This leads to the premature activation of zymogen granules (inactive enzyme precursors) within the pancreas, causing the pancreas to digest itself
o** Zymogen (inactive Enzyme Precursors)**: Special storage organs regulates secretion of digestion of enzymes

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16
Q

Most Common Causes

A

***Gallstones: **

Gallstones and Alcohol counts of 80% of all cases Pancreatitis in USA.
Amont those two, Gallstones, still leading cause of Pancreatitis. Than falling Alcohol.

Alcohol use:
During alcohol metabolism, toxic byproducts such as acetaldehyde and reactive oxygen species (ROS) are formed.
o These byproducts can cause cellular damage and oxidative stress within the pancreas.
o Enzymes **
usually released in digested track released in pancreas itself. Then damage pancreatic tissue promotes inflammation leads to further damage of pancreas
o Hypertriglyceridemia: mechanism not fully understood.
o But thought that high TG increase blood viscosity which may* induce ischemia in pancreatic tissue.
> inflammatory process
o Most of these pt showing derangement of lipid potassium.
o T
his pt prone to recurring episodes of pancreatis *
o ERCP procedure: **
**o Drugs: **due to hypersensitivity reaction or generation of metabolism
o
Trauma:
trauma and post up causes essentially direct insult to pancreas to some degree **
o P*ost operative

17
Q

The Revised Atlanta Criteria

A

*** Phases: **Defines phases of Acute Panreatitis
<Early></Early>

* Severity: Outlines Severity of Actute Pancratitis
* Based on Calssification: Mild, Moderate, Sever
*
* **Imaging: **Clarifiies imaging defenitions

18
Q

The Revised Atlanta Criteria

Phases of Acute Pancreatitis

EArly phase

A

<2 weeks

o Last 1 – 2 weeks
o Severity defined by clinical parameters (i.e. SIRS) rather than pathologic findings
o Organ failure occur if untreated **

o Occurs when inflammation mediators like neutrophils, macrophages are excreted into circulation

o Systemic complication can arrise like bacteremia , acute respiratory distress syndrome, pleural effusions, gastrointestinal hemorrhage, renal failure.

o Organ assessment system should me assessed at this point like RR, Cardiac, renal systems

19
Q

The Revised Atlanta Criteria
Late Phase

A

> 2 wks

Protracted Illness (progress over time )
Persistant organ demage

20
Q

**Acute Pancreatis
Clinical Findings **

A
  • Abdomimal pain, N/V, Fever, ST
  • Elevated S.Amylase& Lipase
  • Leukocytes: 15 - 20,000
  • Hematocrit >44% (severe disease process (i.e Pancreatic Necrosis )
  • Azotemia (significan riks factors for mortality)
  • Hyperglycemia
  • Hyperbilirubinemia (with transient jaundice)
  • Elevaed AST and ALT ( consider Gallbladder or Inflammation in Pancratic Head)

**Hematocrit : volume of red blood cells to the total volume of blood. *

21
Q

Revised Atrlanta Criteria
BAsed of what ?

A

**Dignosis Based on 2 out 3 Criteria
and

**Classification **

22
Q

Revised Atrlanta Criteria
Diagnosis

A

**Dignosis Based on 2 out 3 Criteria **

1)Epigastric Abdominal Pain

2)>3 -Fold Eleavation in Lipase and Amylase
Lipase 140 Normal ( elevated 360’s)
Amylase 30-110 Normal ( elevated 220’s -330)

3)AND /OR Confirmation Finding on Imaging

23
Q

THe Revised Atlanta Creteria
Severity: Classifation

A

*
* **Mild
* Without local Complications or organ Failure
* Subsides in 3 t 7 days after TX
*

  • ** Moderate Severtiy **
  • Transient organ Failure
  • Resoved <48 Hrs

*** Severe **
Persistan rgan Failure >48 hrs
Single or multiple organ failure

24
Q

CT Abdmen Acute Panreatitis

A

Interstitial or Necrotizing

25
Q

CT Abdomen
Intertitial Pancratis

A

o 90-95% of admission of pancreatitis
o Characterized By:
o diffuse gland enlargement

o contrast enhancement

o mild inflammation or peripancreatic stranding ( peripancreatic Stranding = Pancreatis )

26
Q

CT abdoment
Necrotizing pantreitis

A

 Occurs b/c of inflammation or injury
 Dead tissue getting infected
 Pancreatis become inflamed and injured. Pancreatic enzymes leakes > Harm tissue of Pancreas > > If damage cannot be reversed > Necrotitis effect can be sterile but in some cases can be infected
o 5-10% of admissions
o May not involved like several days hospitalization
o lack of pancreatic parenchymal enhancement by IV contrast
o peripancreatic necrosis
o greater risk of mortality

27
Q

o Organ failure & Mortality associated with necrosis

A

o Organ failure & Mortality associated with necrosis
 Slightly higher infected then non- infected
o median prevalence is 54%
o mortality 3-10% with single organ
o Mortality 47% in multi system organ Failure

28
Q

BISAP

A

**Determine Severity of Pancreatis
>3 or More > ICU
**
* B= BUN: >25mg/dl
*I= Impaired Mental Status
* S= SIRS
* A Age >60
* P Pleurial Effusion
*

29
Q

TX Actute Pancreatis

A
  • Fluid Resusitation
  • Intially: 200 to 250ml/Hr (15 to 20ml/kg)
  • Follow: 2 to 3 ml/kg
  • LR perfer ; NSS can be
  • LR superior to NSS
30
Q

Target Resucintation

A

HCT and BUN Q 8 to 12 HRS
Indicatio of Sufficent Fluid: Decrease HCT and BUN with in 8 hrs
Risinng BUN indicates up proper hydration also assiciates with highter Mortality

31
Q

Diet

A

NPO IV pain meds
**Mild case: **
Start CLD advance slowly to low fat diet
Tolerance indication that there is not abdominal pain
No rise in Lipase
Severe casess
2 to 3 days after admission
Enternal Nutrition rather than TPN b/c lesser complication

32
Q

Necrotizing Acute Panreatitis
**Treamtne via multiple approach **

A

** * Sterile Necrosis: **
* Conservative Managent
**
Sigh of Infection **
* Leukocytosis, Fever, Organ Failure
* Percutenious Aspiration
* To obtain Granm stain and cultute
*** Antibiotics **
No role for prophylactic ABT
Broad Spectrum ABT
D/c A BT if gram stain native

**If fever persist **: Repeat FNA with gram stain and cultute in 5 to 7 days
**Follow up with CT /MRI **

If infection only then Percutanious Aspiration

Conservative TX 1st

33
Q

Step Up Approach

A

Percutaneous Endoscopic Drainage 1st
Necrosectomy if needed
Pancreatic Debridement : Definitive Management of Infected Necrosis