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COMPLEX > GI + sepsis > Flashcards

GI + sepsis Flashcards

1
Q

what are the GI alterations discussed in this lecture?

A
  • cirrhosis
  • pancreatitis
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2
Q

what is cirrhosis?

A

extensive fibrous buildup in the liver due to scarring from chronic inflammation (EtOH usual cause)

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3
Q

what are the various complications of cirrhosis?

A
  • hepatic encephalopathy
  • esophageal varices
  • ascites
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4
Q

what is the main function of the liver?

A

detoxifies the body of waste products

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5
Q

what is hepatic encephalopathy?

A

the liver’s failure to convert ammonia (toxic waste) affects the brain & induces changes in LOC and orientation

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6
Q

how is ammonia usually eliminated?

A

bowel movement

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7
Q

a client with cirrhosis starts showing neurological changes, what does the nurse expect to administer to manage these symptoms?

A

lactulose

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8
Q

how does the nurse confirm that a patient has ascites?

A

measure the patient’s ABD girth & monitor I&O daily and identify trends

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9
Q

what is the therapeutic procedure for ascites?

A

paracentesis

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10
Q

how does ascites occur?

A

portal hypertension

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11
Q

what are the nursing considerations in preparing the client for paracentesis?

A
  • assist to them void
  • weigh the client
  • supine positioning with HOB elevated
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12
Q

what are the nursing considerations AFTER paracentesis?

A
  • apply dressing over puncture site
  • maintain bed rest
  • measure fluid obtained
  • assess fluid color
  • send fluid specimen to lab
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13
Q

paracentesis can induce hypovolemic shock

A

true

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14
Q

what causes esophageal varices?

A

portal hypertension

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15
Q

what are esophageal varices?

A

fragile, collateral blood vessels that develop in the upper stomach & esophagus

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16
Q

the nurse finds out a patient has had bloody emesis, what is the cause?

A

esophageal varices have ruptured

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17
Q

what is pancreatitis?

A

an inflamed pancreas due to prematurely activated pancreatic enzymes

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18
Q

what are common s/s of cirrhosis?

(6)

A
  • asterixis
  • jaundice
  • ascites
  • lower extremity edema
  • itchy skin
  • ABD pain
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19
Q

what labs are elvevated for cirrhosis?

what is the liver responsible for?

A
  • bilirubin
  • ammonia
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20
Q

what labs are decreased for cirrhosis?

A
  • platelets
  • WBCs
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21
Q

what are common conditions included under nonalcoholic fatty liver disease?

A
  • Hepatitis B/C
  • fat collection in liver
  • inflammation of liver from excess hepatotoxic drugs
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22
Q

what can cause acute pancreatitis?

A

blocked bile ducts due to gallstones

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23
Q

what are some causes for chronic pancreatitis?

A
  • excess EtOH
  • cystic fibrosis
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24
Q

what are the manifestations for acute pancreatitis?

(7)

A
  • sudden LUQ pain
  • nausea
  • vomiting
  • ABD rigidity (boardlike)
  • Cullen’s sign
  • tachycardia
  • hypotension
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25
Q

what is Cullen’s sign in pancreatitis?

A
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26
Q

what labs are elevated in pancreatitis?

A
  • amylase
  • lipase
  • WBC
  • bilirubin
  • glucose
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27
Q

what labs are decreased in pancreatitis?

A
  • platelets
  • Calcium
  • Magnesium
28
Q

what are the s/s of chronic pancreatitis?

A
  • DM
  • jaundice
  • dark urine
  • steatorrhea
29
Q

what are the interventions for pancreatitis?

(5)

A
  • NPO
  • IV fluids
  • side lying on L side ONLY
  • NG tube
  • insulin drip
30
Q

why does a patient with pancreatitis need to be on NPO?

A

rest the pancreas and prevent autodigestion

31
Q

what does the patient with pancreatitis need an NG tube for?

A

gastric suctioning

32
Q

why does a patient with pancreatitis need an insulin drip?

A

acute hypoglycemia will occur due to decreased insulin from pancreatic damage

33
Q

what are the types of shock discussed in this lecture?

A
  • septic
  • neurogenic
  • hypovolemic
  • anaphylactic
34
Q

what is the earliest sign of septic shock?

A

tachypnea

35
Q

infection causes decreased perfusion (shock) due to uncontrolled immune response

A

true

36
Q

how does the body respond to an uncontrolled immune response?

A
  • vasodilation
  • edema from capillary leak
  • blood clotting that leads to blocked vessels
37
Q

with decreased perfusion during shock, organs become deprived of O2, what does the nurse expect to happen next?

A
  • multiple organ dysfunction
  • metabolic acidosis
38
Q

what is the optimal MAP to keep a patient with sepsis from detoriorating ?

A

> 65

39
Q

what is the calculation for MAP?

A
40
Q

what kind of relationship does cardiac output have with perfusion?

A

direct

41
Q

what are the s/s of sepsis?

(8)

A
  • tachycardia
  • tachypnea
  • hypotension
  • fever
  • diaphoresis
  • cool skin
  • AMS (hypoxemia)
  • decreased UOP
42
Q

the nurse discovers a patient has a MAP of less than 65, what pharmacological intervention do they need to take?

A

administer vasopressors

43
Q

what is the treatment for sepsis?

A
  • rapid fluid bolus
  • draw blood cultures
  • administer ABX
  • administer vasopressors
  • passive leg raise
44
Q

a patient who weighs 55 kg. has sepsis, and the nurse needs to give them a rapid fluid bolus of how much?

*30mL/ kg

A

1650 mL

LR (crystalloids)

45
Q

why is it most appropriate to draw blood culture from a patient who has sepsis BEFORE ABX treatment?

A

to identify the type of bacteria that caused infection and therefore administer the appropriate medication

46
Q

why does the nurse need to perform a passive leg raise on a patient who has sepsis?

A

increases circulation to the vital organs (which are located in the upper body)

47
Q

how is sepsis diagnosed?

A
  • elevated lactate (>4mmol)
  • positive blood cultures
48
Q

what is considered an elevated lactate in order to diagnose sepsis?

A

> 2 mmol/ L

49
Q

what are the stages of shock?

A
  1. initial
  2. compensatory
  3. progressive
  4. irreversible
50
Q

characteristics

initial stage

shock

A
  • asymptomatic
  • mild hypoxemia
51
Q

characteristics

compensatory stage

A
  • tachycardia
  • tachypnea
  • Renin & Angiotensin released
  • organs begin to fail
52
Q

characteristics

progressive stage

A
  • diaphoresis
  • cool skin

advancing hypovolemic shock/ progression to death

53
Q

characteristics

irreversible stage

A

imminent death

54
Q

what is the WBC level for septic shock?

A

> 10,000

55
Q

what is the pharmacological action in treating bradycardia from neurogenic shock?

A

atropine

56
Q

what is the medication for treating hypotension from neurogenic shock?

A

phenylephrine

57
Q

what are the characteristics of the skin in neurogenic shock?

A
  • warm
  • pink
  • dry

due to pooling of blood from systemic vasodilation

58
Q

how does hypovolemic shock occur?

A

there is a loss of intravascular blood volume due to severe bleeding or fluid loss

59
Q

what are the common causes of hypovolemic shock?

A
  • vomiting
  • diarrhea
  • bleeding
  • burns
60
Q

how should the patient with hypovolemic shock be positioned?

A

supine with legs elevated

trendelenburg

61
Q

how does neurogenic shock occur?

A
  • spinal cord injury at level T5 or above
  • intake of drugs that affect vasomotor center (opioids/ benzos)
62
Q

what is the primary treatment for anaphylactic shock?

A

epinephrine injection to the outer thigh (hold for 10 secs.)

63
Q

how often does epinephrine need to be administered for anaphylactic shock?

A

every 5-15 minutes (until rxn is resolved)

64
Q

what are the criteria for a patient to be given vasoactive meds or receive fluid resuscitation?

A
  • MAP < 65
  • SBP < 90
  • low UOP
65
Q

fluid resuscitation must be initiated before administering vasopressors

A

true

66
Q

what is the kidney’s response to impaired GFR?

A
  • increased sodium reabsorption
  • RAAS activation
67
Q

what does RAAS activation in response to impaired GFR lead to?

A

increased volume overload and compromised diuresis

COMPLEX (11 decks)

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