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Critical Care > Abdominal Disorders > Flashcards

Abdominal Disorders Flashcards

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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
Acute Gastrointestinal Bleeding | three disease
* peptic ulcer disease * stress-related erosive * esophageal varices
26
Peptic ulcer disease | Define
results from breakdown of gastromucosal lining
27
Normal protection of gastic mucosa
* glyocoprotein * gastic mucosal blood supply * cells connected by tight junctions
28
Peptic ulcer disease | 2 main causes
* NSAIDs * H. pylori breakdown barriers
29
Stress-related erosive syndrome | Define
increased gastric acid production resulting in decreased blood flow (ischemia)
30
Stress-related erosive syndrome | at risk
ventilation patients shock burns trauma major surgery stress
31
GI bleed | Assessment - coffee ground
more gastic content in contact with blood
32
GI bleed | Assessment - maroon
less gastric contact with blood
33
GI bleed | Assessment - hematemesis
vomiting bright red blood
34
GI bleed | Assessment - hematochezia
bright red blood from profuse bleeding from lower gi per rectum
35
GI bleed | Assessment - melena
tarry stool d/t old blood moving through GI tract
36
GI bleeding | early sign
postural hypotension
37
GI bleeding | later signs
* decreased h/h * tachycardia * pale, SOB * axiety * elevated BUN with normal creatinine
38
GI bleeding | Management
1. Fluid resuscitation 2. Packed RBC 3. Endoscopy 4. Billroth I + II
39
GI bleeding | Sclerotherapy
Creates inflammatory reaction that induces vasoconstriction and results in the formation of venous thrombus.
40
GI bleeding | Band ligation
hematemesis could be loss of clip
41
Bleeding Esophageal Varices | Baloon tamponade
esophagogastric tubes internal pressure within varices * Aspiration * Asphyxiation * esophageal erosion deflate q12h to allow perfusion (bleeding status)
42
Vasopressin | GI bleeding
given IV to constrict splanchnic * decrease portal HTN * systemic ischemia * short term use with lowest dose
43
Somatostatin/octreotide | GI bleed
decrease portal venous pressure
44
H2 antagonist pepcid/zantac | GI bleed
prophylaxis block acid secretion
45
Proton pump inhibitor omeprazole, protonix | GI bleed
treat the bleed --> help healing block final stage in acid production
46
Antacid | GI bleed
neutralize acid/ bind phosphates in GI
47
Blocking agent carafate | GI bleed
cover ulcer sit with protective bonding
48
Pancreas | Exocrine functions
digestive enzymes acinar cells secrete: amylase/lipase
49
Pancreas | Endocrine functions
hormones islets of langerhans: glucagon, insulin, somatosatin
50
Pancreatitis Exocrine
digest protein, fat, starch ↓ enzymes activated in duodenum ↓ bile obstruction ↓ premature activation ↓ autodigestion ↓ break down tissue
51
Acute Pancreatits | Pathophysiology
* autodigestion * increasing capillary permeability (edema) * fibers of blood vessels (hemorrhage) * cell membranes * lipase moves into systemic circulation ↓ fat necrosis
52
Acute Pancreatitis | Assessment
* epigastric to midabd pain * nausea/vomiting * grey turner (L) * cullen sign(L) * edema
53
Acute Pancreatitis | Lab results
* ↑amylase/lipase * hypocalcemia * ↑glycemia/bilirubinemia
54
Acute Pancreatitis | Diagnostic procedures
CT scan ABD IS
55
Acute Pancreatitis | Treatment
**pain relief** fetal position rest --> NPO FULL WEEK *TPN * I/O
56
CT imagining revealed a pus-like pseudocyst. What order would the nurse anticipate to be ordered?
Antibiotic for peritonitis prophylaxis
57
Acute Pancreatitis | Patient is at risk for:
* third spacing * hemorrhage * SIRS * Shock * coagulation issues
58
Hyperglycemic Hypersmolar State | Define
extremely high levels of plasma glucose leading to osmotic diuresis
59
Hyperglycemic Hypersmolar State | Etiology
Still has some insulin pancreas produces insufficent amount of insulin for high glucose dehydration d/y hyperglycemia
60
Hyperglycemic Hypersmolar State | Causes
* **infection** * CVA, MI, trauma * Steroids, beta-blocker, dobutamine, phenytoin
61
Hyperglycemic Hypersmolar State | Pathophysiology
* 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
Hyperglycemic Hypersmolar State | Assessment
s/s ignored * polyuria * polydipsia * weight loss * weakness * dehydration
63
Hyperglycemic Hypersmolar State | Labs
* Glucose over 600 * Serum osmolality over 320 * pH >7.3 * bicarb over 15 * ketonuria * elevated hematocrit * low potassium
64
Hyperglycemic Hypersmolar State | Treatment
* rapid rehydration * hypotonic then isotonic (9-12L) * insulin replacement - low dose * correct electrolytes (K+) Monitor K+ * treat cause
65
What should you do before giving insulin for a patient in Hyperglycemic Hypersmolar State?
CHECK POTASSIUM (if low insulin will make it lower)
66
Solid organs
BLEED * spleen * liver * kidney * pancreas
67
Hollow organs
generally do not bleed * stomach * gallbladder * duodenum * small intestines
68
Abdominal trauma | Assessment
* location * cullen/grey * hematoma * distension * auscultation * rebound tenderness * subcutaneous emphysema
69
Abdominal trauma | Diagnostics
* NG/urinary cath COLOR * H/H, amylase * CT * Ultrasound * Perioneal lavage --> DPL * Laparoscopy
70
Abdominal trauma | Medical management
Non-op --> management OP --> nonstable hemodynamics Intestinal injuries require surgical intervention
71
Spleen | Define
Most likely to be injured lymphoid tissues serves as reservor * control leukocyte production * recycles iron/rbc * antibody production
72
Spleen Injury | Assessment
* LUQ pain, radiating to left shoulder (Kehr's) * Peritoneal irritation, hypotension, tachcardia * increase WBC * less effective RBC
73
Spleen Injury | Treatment
Pain control Antibiotics Surgery (splenectomy)

Critical Care (9 decks)

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