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CCRN Study Deck > Gastrointestinal System 5% > Flashcards

Gastrointestinal System 5% Flashcards

1
Q

Abdominal Girth Increase : Intra-abdominal blood accumulation

A

1-inch increase = 500 to 1000ml intra-abdominal blood accumulation

Normal total blood volume is approx 5 L

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2
Q

Differentiate Cause of Jaundice Based on Lab

A

Increased Direct Bilirubin = Biliary Obstruction

direct bilirubin is conjugated Increased Indirect Bilirubin = Hepatic Disease or Excessive Hemolysis

indirect bilirubin is unconjugated

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3
Q

Focused Abdominal Sonography for Trauma (FAST)

A

Preferred screening study for patients with abdominal trauma

Bedside ultrasound

Accurately predict the need for laparotomy

Quickly detect free intra-abdominal fluid (hemoperitoneum) or blood around the heart (pericardial effusion)

Good sensitivity and Excellent specificity

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4
Q

Signs of Hypovolemia

A

Crack lips

Poor skin turgor

Hypotension

Tachycardia

Restlessness

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5
Q

What is required for the absorption of the following?

Vitamin B12

Fat-soluble vitamins (A, D, E, K)

Calcium

A

Vitamin B12 = Intrinsic factor (produced by parietal cells in the atrum of the stomach)

Fat-soluble Vitamins (A, D, E, K) = Bile

Calcium = Vitamin D

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6
Q

Gastrin

A

Hormone Stimulates the secretion of hydrochloric acid

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7
Q

What type of abdominal pain is most specific to peritoneal irritation?

A

Pain lessened by lying still with knees flexed

Limits movement and relieves abdominal tension

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8
Q

Enteral Feeding Tube Placement in Acute Pancreatitis

A

Jejunum

Below duodenum to avoid stimulating release of pancreatic enzymes

Feed the gut, dont “tell” the pancreas.

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9
Q

H&H Redraw Timing Following Transfusion

A
  • 1 HOUR post transfusion
    • Evaluate current status, determine if patient still bleeding or if more blood is required
  • 4 to 6 HOURS post transfusion
    • Evaluate effect of transfusion on hemoglobin/hematocrit levels.
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10
Q

Lab profiles Seen in Alcoholism and Cirrhosis of the Liver

A

Prolonged prothrombin time

Prolonged aPTT

Low albumin

Low transferrin

Elevated liver enzymes (ALT, AST, LDH)

Elevated bilirubin Low potassium

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11
Q

Mechanical Bowel Obstruction Bowel Sounds

A

Early mechanical bowel obstruction = hyperactive (rushes)

Late intestinal bowel obstruction = hypoactive and then absent

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12
Q

Kehr Sign

A
  • Pain in the left shoulder referred pain from the spleen Indicates splenic rupture
  • Diaphragmatic irritation causes referred pain
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13
Q

Chvostek Sign

A

Spasm of the facial muscles elicited by tapping on the facial nerve Indicates hypocalcemia

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14
Q

Cullen Sign

A

Bluish tint around the umbilicus

Ecchymosis of periumbilical area

Indicates intra-abdominal (intraperitoneal) bleeding

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15
Q

Coopernail Sign

A

Ecchymosis of scrotum or labia Indicates pelvic fracture

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16
Q

Clay colored stool is a sign of what?

A

Biliary obstruction

Bilirubin cannot get into the gastrointestinal tract and into the stool

Conjugated bilirubin normally excreted in the urine and the stool

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17
Q

Early Dumping Syndrome

A

Hypovolemia

Hyperosmolar

food being “dumped” into the duodenum

Symptoms occur within 30 min of eating

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18
Q

Late Dumping Syndrome

A

Result of Increase in insulin secretion stimulated by hyperglycemia after eating

When part or all of the stomach is removed, food is “dumped” into the duodenum and jejunum instead of the food gradually being released

Hyperglycemia & resultant surge of insulin secreted by the pancreas

Symptoms occur 1 to 2 hours after eating

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19
Q

Patient with upper gastrointestinal bleeding and chronic renal failiure, what kind of antacid should be avoided?

A

Magnesium-containing antacid

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20
Q

Grey Turner Sign

A
  • Bluish discoloration in the flank area
  • Indicates retroperitoneal hemorrhage
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21
Q

Acute Pancreatitis Labs

A

Elevated serum amylase

Elevated serum lipase

Elevated bilirubin

Decreased calcium

Decreased albumin

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22
Q

Most Common Causes of Acute Pancreatitis

A

Alcoholism

Biliary Disease

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23
Q

Hepatic Encephalopathy Stages and Symptoms

A

Stage I: Mild Confusion (confusion progressively worsens until the patient is unconscious in stage IV)

Stage II: Asterixis (motor disorder is characterized by an inability to maintain a position, which is demonstrated by jerking movements of the outstretched hands when bent upward at the wrist.)

Stage III: Constructional apraxia (the inability to reproduce simple figures [e.g., a star or triangle])

Stage IV: Neurologic changes indicative of severe cerebral failure (e.g., Positive Babinski), areflexia, fetor hepaticus, electroencephalogram abnormalities

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24
Q

Nutritional deficiencies anticipated in a patient with biliary obstruction and acute pancreatitis include:

A
  • Protein and fat-soluble vitamins
  • Exudates from the pancreas are high in protein, which reduces serum albumin and total proteins
  • Biliary obstruction causes an inability to absorb fat-soluble vitamins
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25
Q

Signs of Esophageal Tear

A

Severe retrosternal pain

Hematemesis

Patient history often includes binging and purging

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26
Q

Peritonitis

A
  • Most likely cause is anastomosis leak following gastric or bowel resection
  • Indications are that GI contents are leaking into the peritoneal cavity.
  • Symptoms include:
    • abdominal pain
    • abdominal distention
    • diminished bowel sounds
    • fever
    • leukocytosis
27
Q

Pancreatitis Pain

A

Epigastric pain that is described as “boring”/radiating through to the back.

28
Q

Large Intestinal Obstruction Pain

A

Dull, diffuse abdominal pain

Generalized pain with abdominal distention

29
Q

Inflammatory (itis) Conditions Cause What Kind of Pain?

A

Sharp

30
Q

Intra-Abdominal Pressure Monitoring

A

Decompression laparotomy should be considered when the pressure exceeds 20 mm Hg

Bladder pressure closely reflects intraperitoneal pressure

Physiologic compromise begins at a pressure of 12 to 15 mm Hg.

Transducer is leveled to the symphysis pubis.

31
Q

Exploratory Laparotomy Indicated for Acute Appendicitis with Intestinal Perforation why?

A
  • Prevent further bacterial contamination and chemical irritation of the peritoneum.
  • Patient may show signs of:
    • peritoneal irritation
    • generalized abdominal pain
    • increasingly severe pain
    • link board-like abdomen to an acute abdomen
    • diffuse tenderness
    • board-like rigidity
    • fever
    • tachycardia
    • tachypnea
32
Q

Stress Ulcer Care

A

Goal gastric pH between 3.5 and 5

Hydrochloric acid has a pH of 1.0 to 3.0

Give medications to decrease acidity of gastric secretions

33
Q

Medications to reduce gastric secretion acidity

A
  • Histamine2 receptor antagonists (e.g., ranitidine)
  • Proton-pump inhibitors (e.g., pantoprazole)
  • Antacids

Decreasing the caustic nature of the secretions decreases the risk of stress ulcers.

34
Q

True Alkalinization of Gastric Secretions

A

pH greater than 7

Not desirable

Would allow proliferation of bacteria

35
Q

S/S of Small-Bowel Obstruction

A

Vomiting of Fecal Material

Causes reverse peristalsis and movement of bowel contents into the stomach and vomiting of fecal material

Abdominal pain and change in bowel habits could occur in small- or large-bowel obstruction

36
Q

S/S of Inflammatory Bowel Disease

A

Mucus and blood in the stool

37
Q

Vasopressin in Patients with Gastrointestinal Bleeding

A

Slows blood loss by constricting the splanchnic arteriolar bed and decreasing portal venous pressure.

Vasopressin is another name for antidiuretic hormone It causes water (but not sodium) retention and may cause SIADH.

Vasopressin does not inhibit hydrochloric acid secretion Decreases mesenteric blood flow and may cause ischemia

38
Q

Sengstaken-Blakemore Tube

A

Used for patients with esophageal varices

Requires scissors to be kept at the bedside

39
Q

Pulmonary Artery Occlusive Pressure (PAOP)

A

Normal PAOP is 12 to 15 mm Hg

Dehydration would indicate decreased PAOP.

40
Q

Why is a morbidly obese patient at increased risk to develop a hospital-associated pneumonia?

A

Body habitus causes hypoventilation leading to atelectasis, particularly when in the supine position.

Body habitus does not lead to elevated intra-abdominal pressure or alter immune responses.

41
Q

Lactulose

A

Chelating agent of ammonia

Decreases ammonia levels

Decreases neurologic toxic effects

Osmotic laxative, which will move nitrogenous wastes through the gastrointestinal tract rapidly to reduce additional increases in ammonia

42
Q

Normal Right Atrial Pressure

A

2 to 6 mm Hg

43
Q

Normal Serum Osmolality

A

280 to 295 mOsm/L

44
Q

Normal Urine Output

A

0.5 ml/kg/hr

45
Q

Early Indications Alcohol Withdrawal Syndrome

A
  • Diaphoresis
  • Pruritus
  • Mild Tachycardia
  • Mild Hypertension
  • Nausea
  • Vomiting
  • Visual Distrubances
  • Tremors
  • Anxiety
  • Agitation
  • Sleep Disturbances
46
Q

Late Indications Alcohol Withdrawal Syndrome

A
  • Marked Tachycardia
  • Marked Hypertension
  • Hyperthermia
  • Dehydration
  • Delirium
  • Hallucinations
47
Q

Trousseau Sign

A
  • Indication of hypocalcemia or hypomagnesemia
  • Calcium levels become low in acute pancreatitis because of fat necrosis and precipitation of calcium
  • Carpopedal spasm caused by inflating the blood-pressure cuff to a level above systolic pressure for 3 minutes
48
Q

Upper GI Bleed

A
  • Approximately 80% of acute GI bleeding
    • peptic ulcer disease
    • esophageal
    • stress ulcers
    • mallory-weiss tear
    • cancer
  • Higher mortality
49
Q

Lower GI Bleed

A
  • 20% of acute GI bleeding
    • diverticulosis
    • angiodysplasia (AVMs)
    • tumor
    • radiation
    • colitis
    • inflammatory (chrons)
    • infectious (clostridium difficile or e. coli)
50
Q

Management of Upper GI Bleeding

A
  • Address Cause
  • Isotonic fluid resuscitation as for hypovolemic shock
  • PRBCs
  • Replace clotting factors (FFP, Platelets)
  • Medications
    • Vasopressin
      • Constricts splanchnic arteriolar bed
      • Decreases portal venous pressure
      • Watch for chest pain and ST elevation
    • Octreotide (Sandostatin)
      • reduces splanchnic blood flow, gastric acid secretion, and GI mobility
    • Osmotic laxatives (sorbitol)
      • removes nitrogenous materials (blood) out of gut to prevent ammonia conversion
      • important in the presence of liver disease
    • Beta blockers
      • constrict mesenteric arterioles reducing portal venous flow
51
Q

Acute Pancreatitis

A
  • Diffuse inflammation, destruction, and auto-digestion of the pancrease from premature activation of exocrine enzymes.
  • Is NOT always caused by an infection
  • Up to 6 L fluid may be secreted into interstitial spaces
  • Activation of inflammatory mediators (cytokines, kinins, histamine, clotting factors)
  • Results in systemic inflammatory response syndrome (SIRS)
52
Q

Systemic Inflammatory Response Syndrome (SIRS)

A
  • ↑ vascular permeability
  • vasodilation
  • vascular stasis
  • microthrombosis
53
Q

Etiology of Acute Pancreatitis

A
  • Alcoholism
  • Obstruction (gall stones)
  • Abdominal surgery
  • Drugs
  • Hyperlipidemia
  • Trauma
  • Infection (although it is seldom an infection)
54
Q

Pulmonary Complications of Acute Pancreatitis

A
  • Atelectasis, left lower lobe
  • Left pleural effusion
  • Bilateral crackles
  • ARDS
55
Q

S/S of Acute Pancreatitis

A
  • Abdominal pain – boring
  • Pain radiates to all quadrants and lumbar area
  • N/V, rigid abdomen, no rebound tenderness
  • ↓ or absent bowel sounds
  • Low-grade fever
  • ↓Calcium
  • ↑WBC
  • ↑Amylase – peaks in 4-24 hours, returns to normal in 4 days
  • ↑ Lipase, stays elevated longer than amylase
  • ↑ Blood sugar
56
Q

Signs of Hemorrhagic Pancreatitis

A
  • Cullen’s sign
    • methemalbumin forms from digested blood and tracks around the abdomen from the inflamed pancreas
  • Grey Turner’s sign
    • Hemorrhagic pancreatitis
57
Q

Acute Pancreatitis Treatment

A
  • Fluid replacement
  • Calcium, K+, and Mg++ replacement
  • H2 blockers or proton pump inhibitors (PPIs) to decrease gastric pH
  • NG suction to decrease gastric secretion
  • Pain management, morephine
  • Glucose control
  • Enteral feeding below duodenu
  • Monitor for pulmonary complications
    • ARDS
    • Elevation of diaphragm and bilateral basilar crackles
    • Atelectasis especially left base
58
Q

Liver Failure Lab Abnormalities

A
  • ↑ AST, ALT, alkaline phosphatase, GGT
  • ↑Serum bilirubin
  • ↑NH3 (ammonia)
  • ↑Serum creatinine, BUN - late
  • ↓Serum protein
  • ↓Serum albumin and ascites
  • ↓Blood sugar
  • Pancytopenia (↓WBC, RBC, platelets)
  • Coagulopathies (↑PT, PTT)
  • Hyperventilation, respiratory alkalosis > ↑ lactate - metabolic acidosis
59
Q

Clinical Findings of Liver Failure

A
  • Mental status change
  • Asterixis (flappy hand tremor due to elevated ammonia)
  • Ascites due to low albumin and protein, risk of spontaneous bacterial peritonitis
  • Jaundice due to elevated bilirubin
  • Renal failure (hepatorenal syndrome), not fully understood, high mortality (-80%) usually due to bleeding or infection
  • Sepsis, bacterial or fungal due to decreased immune function
  • Liver becomes enlarged, tender during acute inflammatory state
  • Liver becomes non-palpable as hepatocellular necrosis progresses
60
Q

Factors that Increase Serum NH3

A
  • Hypokalemia: triggers ammonia genesis in the kidneys (mechanism entirely unclear)
  • ↑ BUN: breakdown of nitrogen
  • ↑ Protein: breakdown of nitrogen
  • ↑ Lactic acidosis: may be precipitated by administration of Ringer’s lactate – normally it is converted into bicarb by healthy liver
61
Q

Differentiation of Abdominal Pain

A
62
Q

Appendicitis - Nursing Study Card

A
63
Q

Peritonitis “Hot Belly”

A
64
Q
A

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