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Critical Care > Abdominal Disorders > Flashcards

Abdominal Disorders Flashcards

1
Q

Liver functions (10)

A
  1. Synthesize plasma (albumin/globulins)
  2. Nutrient metabolism (Glycogen to glucose)
  3. Sunthesize bile
  4. Provides for fat/vitamin storage (B12/iron/copper)
  5. Eliminate bilirubin
  6. Steroid hormons/polypeptides inactivate
  7. Kupffer’s cells (break down drugs/toxins)
  8. Coagulation factors
  9. Fat metabolism
  10. Detoxify ammonia
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2
Q

Hepatitis

Define

A

Inflammation of the liver
(virus,bacteria, drugs )
* obstructs ducts/circulation
* impedes liver function
* necrosis of tissue

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3
Q

Hepatitis

Treatment

A

supportive care
* rest
* nutrition
* avoid stress
* avoid hepatotoxic substance

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4
Q

Cirrhosis

Define

A

chronic liver inflammation
caused by chronic alcohol abusehepatitis/biliary obstruction

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5
Q

Cirrhosis

Pathophysiology

A
  • Initially fatty infilitration/obstruction
  • oxidation of alcohol yield acetaldehyde
    (damages hydrochondria / necrosis)
  • necrotic tissue becomes scar tissue –> distorting blood flow

results in dysfunction and liver failure
CAUSING
portal hypertension

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6
Q

Portal vein hypertension

A

venous congestion and dilation
nutrient rich blood shunted away from liver
* results in poor metabolism of nutrients, drugs, toxins
* vascular changes –> varicose veins

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7
Q

Impaired liver function

Edema

A

decreased osmotic pressure by lack of plasma proteins

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8
Q

Impaired liver function

ALL

A
  • edema
  • jaundice
  • malnutrition
  • hyperlipidemia
  • hormones
  • unstable glucose
  • bruising/hemorrhage
  • cognitive change
  • hepatic encephalopathy
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9
Q

Impaired liver function

Jaundice

A

increased bilirubin

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10
Q

Impaired liver function

Fatigue, malnutrition

A

liver cannot process nutrient rich blood

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11
Q

Impaired liver function

hormones

A

Inappropriate ADH/aldosterone levels

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12
Q

Impaired liver function

ALT/AST

A

high levels – feedback function no longer valid

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13
Q

Impaired liver function

glucose

A

poor carbohydrate metabolism

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14
Q

Impaired liver function

cognitive change

A

somnolence/agitation
irritability/hostility

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15
Q

Liver disease labs

A
  • ↑ALT/AST
  • ↑ammonia
  • ↑ bilirubin
  • ↑ PT/PTT
  • decreased protein
  • decreased h/h
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16
Q

Hepatic encephalopathy

Define

A

accumulation of neurotoxins ammonia
progress with change in personality, irritability
* aserixis –> hand flapping –> cannot keep hand still

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17
Q

Hepatic encephalopathy

Management

A

maintain safe environment
* remove/decrease nitrogenous waste
* Lactulose (clear toxin)
* Xifaxan (prevents bacterial action)

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18
Q

Ascites

Define

A

accumulation of fluid in peritoneum
decreased colloid pressure
↓
increased hydrostatic pressure
↓
ald/ASH remain in blood –> retain fluid
↓
increase abd girl, fluid wave
↓
respiratory distress

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19
Q

Acites

Treatment

A
  • Bed-rest
  • Low sodium-diet
  • Diuretics
  • Paracentesis (hypotension/infection)
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20
Q

Ascites

LeVeen shunt

A

relieves resistant ascities
complications sepsis, peritonitis, occlusion

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21
Q

Ascites

Trans jugular Intrahepatic Porto system shunt

A
  • decompress portal venous system
  • decrease portal hypertension
  • stop/reduce ascites

Contraindications –> CHF

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22
Q

Circulatory Effects of Cirrhosis `

A

enlarged liver
↓
increased resistance to blood flow
↓
increased PHT
↓
varices develop in esophageal/gastic/ hemorrhoidal veins

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23
Q

Esophagogastic varices

A

Engorged and distended blood vessels of the esophagus and proximal stomach that develop as a result of portal hypertension.

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24
Q

Varices

Complications

A
  • Acute GI hemorrhage
  • Life-threatening (severe can rupture)
  • treatment/management similar to acute GI bleed
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25
Q

Acute Gastrointestinal Bleeding

three disease

A
  • peptic ulcer disease
  • stress-related erosive
  • esophageal varices
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26
Q

Peptic ulcer disease

Define

A

results from breakdown of gastromucosal lining

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27
Q

Normal protection of gastic mucosa

A
  • glyocoprotein
  • gastic mucosal blood supply
  • cells connected by tight junctions
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28
Q

Peptic ulcer disease

2 main causes

A
  • NSAIDs
  • H. pylori

breakdown barriers

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29
Q

Stress-related erosive syndrome

Define

A

increased gastric acid production resulting in decreased blood flow (ischemia)

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30
Q

Stress-related erosive syndrome

at risk

A

ventilation patients
shock
burns
trauma
major surgery
stress

31
Q

GI bleed

Assessment - coffee ground

A

more gastic content in contact with blood

32
Q

GI bleed

Assessment - maroon

A

less gastric contact with blood

33
Q

GI bleed

Assessment - hematemesis

A

vomiting bright red blood

34
Q

GI bleed

Assessment - hematochezia

A

bright red blood from profuse bleeding from lower gi per rectum

35
Q

GI bleed

Assessment - melena

A

tarry stool d/t old blood moving through GI tract

36
Q

GI bleeding

early sign

A

postural hypotension

37
Q

GI bleeding

later signs

A
  • decreased h/h
  • tachycardia
  • pale, SOB
  • axiety
  • elevated BUN with normal creatinine
38
Q

GI bleeding

Management

A
  1. Fluid resuscitation
  2. Packed RBC
  3. Endoscopy
  4. Billroth I + II
39
Q

GI bleeding

Sclerotherapy

A

Creates inflammatory reaction that induces vasoconstriction and results in the formation of venous thrombus.

40
Q

GI bleeding

Band ligation

A

hematemesis could be loss of clip

41
Q

Bleeding Esophageal Varices

Baloon tamponade

A

esophagogastric tubes
internal pressure within varices

  • Aspiration
  • Asphyxiation
  • esophageal erosion

deflate q12h to allow perfusion (bleeding status)

42
Q

Vasopressin

GI bleeding

A

given IV to constrict splanchnic
* decrease portal HTN
* systemic ischemia
* short term use with lowest dose

43
Q

Somatostatin/octreotide

GI bleed

A

decrease portal venous pressure

44
Q

H2 antagonist
pepcid/zantac

GI bleed

A

prophylaxis
block acid secretion

45
Q

Proton pump inhibitor
omeprazole, protonix

GI bleed

A

treat the bleed –> help healing
block final stage in acid production

46
Q

Antacid

GI bleed

A

neutralize acid/ bind phosphates in GI

47
Q

Blocking agent
carafate

GI bleed

A

cover ulcer sit with protective bonding

48
Q

Pancreas

Exocrine functions

A

digestive enzymes
acinar cells secrete: amylase/lipase

49
Q

Pancreas

Endocrine functions

A

hormones
islets of langerhans: glucagon, insulin, somatosatin

50
Q

Pancreatitis Exocrine

A

digest protein, fat, starch
↓
enzymes activated in duodenum
↓
bile obstruction
↓
premature activation
↓
autodigestion
↓
break down tissue

51
Q

Acute Pancreatits

Pathophysiology

A
  • autodigestion
  • increasing capillary permeability (edema)
  • fibers of blood vessels (hemorrhage)
  • cell membranes
  • lipase moves into systemic circulation
    ↓
    fat necrosis
52
Q

Acute Pancreatitis

Assessment

A
  • epigastric to midabd pain
  • nausea/vomiting
  • grey turner (L)
  • cullen sign(L)
  • edema
53
Q

Acute Pancreatitis

Lab results

A
  • ↑amylase/lipase
  • hypocalcemia
  • ↑glycemia/bilirubinemia
54
Q

Acute Pancreatitis

Diagnostic procedures

A

CT scan
ABD IS

55
Q

Acute Pancreatitis

Treatment

A

pain relief
fetal position
rest –> NPO FULL WEEK
*TPN
* I/O

56
Q

CT imagining revealed a pus-like pseudocyst. What order would the nurse anticipate to be ordered?

A

Antibiotic for peritonitis prophylaxis

57
Q

Acute Pancreatitis

Patient is at risk for:

A
  • third spacing
  • hemorrhage
  • SIRS
  • Shock
  • coagulation issues
58
Q

Hyperglycemic Hypersmolar State

Define

A

extremely high levels of plasma glucose leading to osmotic diuresis

59
Q

Hyperglycemic Hypersmolar State

Etiology

A

Still has some insulin
pancreas produces insufficent amount of insulin for high glucose
dehydration d/y hyperglycemia

60
Q

Hyperglycemic Hypersmolar State

Causes

A
  • infection
  • CVA, MI, trauma
  • Steroids, beta-blocker, dobutamine, phenytoin
61
Q

Hyperglycemic Hypersmolar State

Pathophysiology

A
  • reduced insulin allows more glucose to accumulate
  • triggers glucagon release
  • glucose increase = osmolality increase
  • body pulls intracellular into vascular
  • excessive fluid loss = hypovolemia
    reduced kidney perfusion/oliguria
62
Q

Hyperglycemic Hypersmolar State

Assessment

A

s/s ignored
* polyuria
* polydipsia
* weight loss
* weakness
* dehydration

63
Q

Hyperglycemic Hypersmolar State

Labs

A
  • Glucose over 600
  • Serum osmolality over 320
  • pH >7.3
  • bicarb over 15
  • ketonuria
  • elevated hematocrit
  • low potassium
64
Q

Hyperglycemic Hypersmolar State

Treatment

A
  • rapid rehydration
  • hypotonic then isotonic (9-12L)
  • insulin replacement - low dose
  • correct electrolytes (K+)
    Monitor K+
  • treat cause
65
Q

What should you do before giving insulin for a patient in Hyperglycemic Hypersmolar State?

A

CHECK POTASSIUM
(if low insulin will make it lower)

66
Q

Solid organs

A

BLEED
* spleen
* liver
* kidney
* pancreas

67
Q

Hollow organs

A

generally do not bleed
* stomach
* gallbladder
* duodenum
* small intestines

68
Q

Abdominal trauma

Assessment

A
  • location
  • cullen/grey
  • hematoma
  • distension
  • auscultation
  • rebound tenderness
  • subcutaneous emphysema
69
Q

Abdominal trauma

Diagnostics

A
  • NG/urinary cath COLOR
  • H/H, amylase
  • CT
  • Ultrasound
  • Perioneal lavage –> DPL
  • Laparoscopy
70
Q

Abdominal trauma

Medical management

A

Non-op –> management
OP –> nonstable hemodynamics
Intestinal injuries require surgical intervention

71
Q

Spleen

Define

A

Most likely to be injured
lymphoid tissues serves as reservor
* control leukocyte production
* recycles iron/rbc
* antibody production

72
Q

Spleen Injury

Assessment

A
  • LUQ pain, radiating to left shoulder (Kehr’s)
  • Peritoneal irritation, hypotension, tachcardia
  • increase WBC
  • less effective RBC
73
Q

Spleen Injury

Treatment

A

Pain control
Antibiotics
Surgery (splenectomy)

Critical Care (9 decks)

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