Pancreatitis and Adrenal Insufficiency Flashcards

1
Q

How are pancreas functions classified?

A

1) Exocrine

2) Endocrine

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2
Q

What are exocrine pancreatic functions?

A

Release of digestive enzymes and sodium bicarb into GI tract (85% of pancreas responsible for this)

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3
Q

Where are digestive enzymes and bicarbonate produced?

A

Pancreas in the acini cells

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4
Q

What does amylase, lipase, and trypsin break down?

A

Carbs, fats, and proteins respectively

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5
Q

What does the sphincter of Oddi do?

A

When food enters duodenum, sphincter of Oddi relaxes and releases digestive enzymes and sodium bicarb into the duodenum

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6
Q

What are endocrine pancreatic functions?

A

Release of substance into the blood, pancreatic cells clustered around blood capillaries (Islets of Langerhans) responsible for serum glucose regulation

Only 2% of gland responsible for this

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7
Q

What do beta cells do?

A

Release insulin into the blood, shifts sugar from blood into cells

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8
Q

What do alpha cells do?

A

Release glucagon into the blood, shifts glycogen (stored sugars) into the blood

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9
Q

Why is glycemic control important in ICU?

A

Reduces mortality by 42%, reduce renal failure and septicemia

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10
Q

What is the basic pathophys of pancreatitis?

A

In pancreatic, normally inactive digestive enzymes become activated and begin to digest pancreatic tissue (autodigestion)

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11
Q

What are the two main classifications of pancreatitis?

A

1) Chronic
2) Acute
(Mild acute, moderate acute, severe acute)

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12
Q

What is chronic pancreatitis?

A

Slow, gradual destruction of pancreas. Most common etiology is alcohol consumption.

Destruction persists despite removal of causative agent.

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13
Q

What is acute pancreatitis?

A

Sudden autodigestion of the pancreas due to a specific causative agent. Associated with inflammation, hemorrhage, necrosis.

Once causative agent addressed, complete resolution of disease usually occurs.

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14
Q

What are the most common etiologies of acute pancreatitis?

A

Alcohol consumption, gallstones

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15
Q

What is the difference between the 3 types of acute pancreatitis?

A

1) Mild acute pancreatitis (No organ failure)
2) Moderate acute pancreatitis (Organ failure resolves within 48hrs, some local / systemic complications but not persistent)

3) Severe acute pancreatitis (Persistent organ failure with systemic complications, requires ICU admission)

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16
Q

What is trypsinogen and why is it significant for pancreatitis?

A

Is a digestive enzyme produced in the pancreas, remains inactive while in pancreas normally. When it enters duodenum, it activates into trypsin and breaks down proteins in the GI tract. In pancreatitis, trypsinogen activates early into trypsin while still in the pancreas and starts auto-digestion

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17
Q

What are the phases of severe acute pancreatitis?

A

Phase 1)
Trypsinogen early activates into trypsin while in the pancreas and starts auto-digesting pancreatic proteins. Trypsin starts a cascade activating other pancreatic digestive enzymes

Phase 2)
Early activated enzymes cause localized damage to pancreas. Breakdown of blood vessels cause bleeding, breakdown of fatty acids necrotize the pancreas. Damaged cells release pro-inflammatory cytokines and cause inflammation.

Phase 3)
Enzymes and pro-inflammatory mediators spread to other organs in the body leading to systemic damage. Digestive enzymes leak to liver, stomach, spleen, diaphragm. Organs suffer from systemic inflammation

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18
Q

What are neuro manifestations of pancreatitis?

A

Restlessness, decreased LOC, coma

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19
Q

What are respiratory manifestations of pancreatitis?

A

Atelectasis, decreased air entry, hypoxia, pleural effusions, resp distress

20
Q

What are cardiovascular manifestations of pancreatitis?

A

Tachycardia, hypotension, edema, shock, low grade fever

21
Q

What are the GI manifestations of pancreatitis?

A

Dull epigastric pain radiating to back, nausea and vomiting, hypoactive bowel sounds, intra-abdominal hypertension, TURNER’s and CULLEN’s SIGN

22
Q

What are GU manifestations of pancreatitis?

A

Oliguria, anuria

23
Q

How is acute pancreatitis diagnosed?

A

2 of the 3 findings:

1) Presentation of pain consistent with disease (epigastric, radiating to left side, back, flank, constant severe)
2) Elevated lipase or amylase (3 times the upper limit)
3) Abnormal CT or MRI imaging

24
Q

What are common lab changes for acute pancreatitis?

A

Elevated amylase, lipase, bilirubin, liver enzymes (AST/ALT/ALP), triglycerides, WBCs, serum glucose

Hypocalcemia, decreased albumin, metabolic acidosis

25
Q

What happens to the patient in ICU for acute pancreatitis?

A

First two weeks characterized by multi-system organ failure and inflammation (systemic inflammatory response syndrome SIRS)

Afterwards pt is at high risk of infection due to necrotic pancreatic tissues. Pt is immunocompromised so nosocomial infections are common.

26
Q

Is routine use of antibiotics for acute pancreatitis recommended in ICU?

A

NO, prophylactic antibiotics NOT recommended

27
Q

What are some recommendations for acute pancreatitis management?

A

Goal to identify and reverse cause, provide supportive care, and treat complications.

Aggressive hydration within first 24hrs (250-500mls/hr), enteral nutrition, U/S and CT, prophylactic antibiotics NOT recommended

28
Q

Where are the adrenal glands?

A

Found on top of each kidney

29
Q

What are the 2 components of the adrenal gland?

A

1) Outer cortex

2) Inner medulla

30
Q

What hormones are formed by the outer cortex?

A

1) Glucocorticoids (Cortisol)
2) Mineralcorticoids (Aldosterone)
3) Sex hormones (Testosterone)

31
Q

What hormones are formed by the medulla?

A

Epinephrine, norepinephrine

32
Q

What is the hypothalamic-pituitary-adrenal axis responsible for?

A

Regulation of adrenal secretions

33
Q

Where is the hypothalamus and what does it do?

A

Lies just below the thalamus at the base of the brain.

Integrate functions between nervous system and the endocrine system, secretes Corticotropin Releasing Hormone (CRH)

34
Q

What is Corticotropin Releasing Hormone and what does it do?

A

Secreted by the hypothalamus, stimulates anterior pituitary to release Adrenocorticotropic Hormone (ACTH)

35
Q

Where is the pituitary gland and what does it do?

A

Suspended from the hypothalamus, regulates bodily function along with the hypothalamus. Divided into an anterior and posterior lobe, secrete many hormones including Adrenocorticotropic Hormone (ACTH)

36
Q

What is Adrenocorticotropic Hormone (ACTH)?

A

Secreted by the pituitary gland, stimulates adrenal cortex to release hormones such as cortisol

37
Q

What is the function of cortisol and where does it come from?

A

Released by the adrenal cortex during a stress response, regulated by negative feedback. High levels suppress hypothalamus and pituitary from secreting CRH and ACTH.

It raises blood sugar and is anti-inflammatory

38
Q

What is adrenal insufficiency?

A

Deficiency in either production or use of glucocorticoids (cortisol). Low cortisol can be suspected when pts have hypotension from unidentifiable cause or are vasopressor dependent.

39
Q

What pts are at risk for adrenal insufficiency?

A

Septic, multi-trauma, long term critical illness, previous glucocorticoid use, brain injury

40
Q

What are the 4 types of adrenal insufficiency?

A

1) Primary
2) Secondary
3) Relative adrenal insufficiency
4) Peripheral adrenal resistance

41
Q

What is primary adrenal insufficiency?

A

Intrinsic failure of adrenal gland to produce cortisol, may be due to adrenal tumors, rare in ICU

42
Q

What is secondary adrenal insufficiency?

A

Adrenal glands stop production of hormones due to exogenous glucocorticoid administration. May occur with pts on long term steroids, which is why they have to be tapered off so adrenal glands can slowly resume functioning

43
Q

What is relative adrenal insufficiency?

A

Most common in ICU. Critical illness related corticosteroid insufficiency.

Inadequate glucocorticoid activity for the severity of pt’s illness, pt is exposed to high amount of stress for long period of time.

44
Q

What is peripheral adrenal insufficiency?

A

Occurs in septic shock, inflammatory mediators cause cellular resistance to adrenal hormones. Body loses ability to recognize and respond to cortisol

45
Q

How is adrenal insufficiency diagnosed?

A

Adrenal stimulation test:

1) Draw baseline serum cortisol
2) Administer Cosyntropin (synthetic ACTH) which should stimulate the adrenal gland to produce cortisol
3) 30 mins / 60 mins post, draw another cortisol level

Adrenal sufficiency suspected if baseline is low or if only a small rise in cortisol level after Cosyntropin

46
Q

How is adrenal insufficiency treated?

A

Low dose hydrocortisone, 50mg IV q6h until pt condition improves. Then it should be tapered off slowly.

Risk of immunosuppression and infection

47
Q

Why does acute pancreatitis cause metabolic acidosis?

A

Decrease in acid due to loss of bicarb secretions due to pancreatic duct disruption. Lactic acidosis occurs from shock and renal failure