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NURS 487 > GI > Flashcards

GI Flashcards

1
Q

subjective data for abdominal assessment

A 
Appetite
Dysphagia
Food intolerance
Abdominal pain
Nausea/vomiting
Bowel habits
Past abdominal history
Medications
Nutritional assessment
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2
Q

objective data for abdominal assessment

A 
Inspect
(contour, symmetry, umbilicus, skin, hair, movement and demeanor)
Ausculate
(hyperactive, hypoactive and absent)
Percuss
Palpate
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3
Q

gastritis

A

inflammation of the stomach

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4
Q

acute gastritis

A

Acute is usually due to local irritants

May or may not be symptomatic

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5
Q

chronic gastritis

A

Chronic leads to atrophy of the glandular epithelium of the stomach
H. pylori gastritis is most common
Autoimmune and multifocal least common but increases risk of carcinoma
Chemical from reflux of duodenal contents, pancreatic secretions, bile

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6
Q

patho of gastritis

A

Occurs as a result of the breakdown of the normal gastric mucosal barrier
Hydrochloric acid moves back into the mucosa
Results in tissue edema, disruption of capillary walls with loss of plasma into the gastric lumen and possible hemorrhage

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7
Q

clinical manifestations of gastritis

A

Anorexia, nausea and vomiting, epigastric tenderness and a feeling of fullness
Hemorrhage is commonly associated with alcohol abuse
Acute gastritis is self limiting, lasting from a few hours to days with complete healing
Chronic gastritis, patients lose intrinsic factor (a substance secreted by gastric mucosa that is essential for absorption of cobalamin (vitamin B12) leading to cobalamin deficiency  changes in RBC production anemia and neurological complications

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8
Q

assessment for gastritis

A

GI: Nausea/vomiting, pain, blood noted in stool or emesis, nutritional intake, ETOH, stress

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9
Q

drug causes of gastritis

A

aspirin
corticosteroids
nonsteroiddal anti-inflammatorys

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10
Q

diet causes of gastritis

A

alcohol
spicy food
irritating food

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11
Q

microorganism causes of gastritis

A

heliobactorer pylori
salmonella
staphylococcus

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12
Q

environmental factor causes of gastritis

A

radiation

smoking

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13
Q

patho condition causes of gastritis

A 
burns 
large hiatal hernia 
physiological stress 
reflux of bile and pancreatic secretions 
renal failure (uremia)
sepsis 
shock
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14
Q

other factors causes of gastritis

A

endoscopic procedures
nasogastric suction
psychological stress

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15
Q

gastroesophageal reflux disease (GERD)

A

Backwards movement of stomach contents into esophagus

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16
Q

patho of GERD

A

Backflow regulated by a sphincter at stomach entrance; transient relaxation common after meals, especially fatty foods

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17
Q

clinical manifestations of GERD

A

Most common symptom epigastric pain or heartburn, sometimes belching, chest pain
Respiratory symptoms include: wheezing, coughing, and dyspnea
Otolaryngologic symptoms include: hoarseness, sore throat, lump in the throat (globus sensation), and choking

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18
Q

nursing assessment for GERD

A

NEURO: dysphagia, pain (PQRST); CV: identify if chest pain is cardiac in nature or a result of GERD, tachypnea, changes in BP; RESP: sore throat, lump in throat, hoarseness of cords, wheezing, coughing, dyspnea, crackles if aspiration pneumonia has occurred; GI: nutritional status, odynophagia (painful swallowing), heartburn, nausea/vomiting, weight loss

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19
Q

complication of GERD

A

Barrett esophagus -scarring, edema, spasm (strictures)

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20
Q

peptic ulcer disease

A

Group of disorders resulting from exposure of upper GI tract to acid-pepsin secretions. Mostly duodenal and gastric; duodenal much more common. Men 55-70 most commonly affected
Caused often by H. pylori, Non-Steriodal Anti-Inflammatory Drugs (NSAIDs)

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21
Q

patho of peptic ulcer disease

A

Only develop in the presence of an acid environment
Mucosa barrier becomes impaired, and back-diffusion of acid lead to PUD
Can affect all layers of mucosa and eventually penetrate through

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22
Q

clinical manifestations of peptic ulcer disease

A

Primary symptom is pain usually on empty stomach; relieved by food or antacids*
Exacerbations occur

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23
Q

complications of peptic ulcer disease

A

Complications include hemorrhage, gastric outlet obstruction (from edema, spasm, contraction of scar tissue), perforation (which can lead to peritonitis)

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24
Q

GI bleed

A

Can happen anywhere in GI tract- (UGIB or LGIB)
Site of bleeding indicated by colour and texture: bright red to tarry black (melena)
Think EMERGENCY Situation!!!
Patients may also develop lower GI bleeding where primary symptom is frank red blood

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25
Q

site of GI bleed

A

Upper GI often coffee-ground material (partially digested) or bright red
Brighter red means bleeding closer to the source; darker means further from source (e.g. source is duodenum, which is high up, blood in stools will be dark; hemorrhoids often produce bright red blood)
May be hard to pinpoint source; e.g. with hypermotility blood may be bright red even if source is high in GI tract

26
Q

GI bleed assessment

A

NEURO: LOC, alert, orientated, lethargic, dizziness, light headedness, anxiety, confusion, stupor, coma (due to low cerebral blood flow); CV: color, hemodynamic status- is the patient pale, pink, grey, cyanotic, low CO, low BP, tachycardia, changes in perfusion, capillary refill, cool to touch, changes in pulses especially in lower extremities, chest pain or angina present, dysrhythmias (AF); RESP: tachypnea, dyspnea, cyanosis, crackles due to pulmonary edema or heart failure; GI: absent of hypoactive bowel sounds, epigastric tenderness, anorexia; RENAL: urine output, < or > 30 cc/hr (due to decreased blood flow to kidneys), monitoring for tubular necrosis, colour, consistency, frequency, 24 hour fluid balance
LAB Values: CBC (Hgb, platelets, hematocrit), All electrolytes with careful attention to potassium, creatinine, BUN, GFR

27
Q

ileus obstruction

A

What is an obstruction?
Any condition that prevents normal flow of chime through intestine
Loss of intestinal motility in the absence of an ileus
Classified as simple or functional

28
Q

primary cause of small bowel obstruction

A

Primary Cause of Small Bowel Obstruction:
Adhesions *
Hernia
Tumors

29
Q

primary cause of large bowel obstruction

A

Primary Cause of Large Bowel Obstruction:
Malignancy
Volvulus
Strictures related to diverticulitis

30
Q

clinical manifestations of of intestinal obstruction

A

Symptoms based on degree and duration of obstruction
May be sudden and dramatic symptoms of pain (intermittent), vomiting, distention, borborygmus**, peristaltic rushes, restlessness and awareness of peristaltic movements

31
Q

treatment for intestinal obstruction

A

based on cause. May respond to decompression, but may require surgery

32
Q

stomach and intestinal dysfunction key assessment points

A 
Changes or Absent Bowel Sounds
Complaints of Nausea, Vomiting, Anorexia and Distention
Abnormalities noted in Lab Values
GI Pain
Usually sharp or burning
May be steady or intermittent
May be referred
As with all pain, assessment of timing, quality, and intensity of pain is key
33
Q

liver structure

A

Largest; divided into R & L lobes
Located RUQ
Main blood supply from hepatic artery and portal vein. Portal vein drains from alimentary canal, spleen and pancreas.
Blood drains into sinusoids, and from there into central veins and then to Inferior Vena Cava
Hepatic circulation important b/c obstruction leads to portal hypertension

34
Q

liver function

A

Multi-skilled organ
Secretes bile
Metabolism of Bilirubin
Hematologic(hematopoeisis, clotting, storage)
Metabolism of Nutrients (CHO, CHON, Fat)
Detoxifies (at risk for further injury)
Stores Minerals (Vitamins B12, D, A, E, and K)

35
Q

hepatitis a patho

A

Widespread inflammation of the liver tissue
Liver damage is mediated by cytotoxic cytokines and natural killer cells that cause lysis of infected hepatocytes
Damage results from liver necrosis
Inflammation of periportal areas may interrupt flow of bile
Hepatitis A is transmitted through feces (fecal-oral route; contaminated water and food; blood)
Hepatitis A has an incubation period of 2-7 weeks.

36
Q

clinical manifestations of hepatitis a

A

Fatigue, nausea vomiting, fever, hepatomegaly, jaundice, dark urine, anorexia, rash, but is usually a mild disease

37
Q

fulminant viral hepatitis

A

Clinical syndrome that results in severe impairment or necrosis of the liver cells
May occur with Hepatitis B or C virus
Tylenol overdoses are common to cause this severe syndrome
Edematous hepatocytes and patchy areas of necrosis and inflammatory cell infiltrates disrupt the parenchyma
Acute liver failure develops within 6-8 weeks after initial symptoms of hepatitis

38
Q

clinical manifestations of fulminant viral hepatitis

A

Anorexia, vomiting, abdominal pain, progressive jaundice, followed by ascites and gastrointestinal bleed

39
Q

jaundice

A

May occur as a result of liver dysfunction
Results from 1. extrahepatic (post-hepatic) obstruction to bile flow, 2. intrahepatic obstruction, 3. prehepatic excessive production of unconjugated bilirubin
Conjugated bilirubin cannot flow out of the liver because of obstruction or inflammation of the bile ducts stools become light or clay coloured
Pruritis can occur due to bile salts accumulating under the skin
Urine may become dark brown or brownish red

40
Q

portal hypertension

A

Abnormally high blood pressure in the portal venous system caused by resistance to portal blood flow

41
Q

patho of portal hypertension

A

Intrahepatic result from vascular remodelling with intrahepatic shunts, thrombosis, inflammation or fibrosis such as in cirrhosis of the liver, viral hepatitis, or schistosomiasis (parasitic infection)
Posthepatic causes occur from hepatic vein thrombosis or cardiac disorders that impair the pumping ability of the right side of the heart (RV HF); blood backs up and there is increased pressure in the portal system
Prehepatic causes occur with narrowing of the hepatic portal vein
Long term complications include: varices, splenomegaly, hepatopulmonary syndrome and portopulmonary hypertension

42
Q

clinical manifestations of portal hypertension

A

Most common clinical manifestation is vomiting of blood from bleeding esophageal varices, then slow, chronic bleeding from varices causes anemia or melena

43
Q

portal hypertension complications

A

Backup leads to varices, ascites and right sided heart failure

Varices can result in profound bleed: melena, frank red blood, vomiting

Rapid treatment needed - volume replacement, drugs, endoscopy, balloon tamponade, surgery
(portacaval shunt)

44
Q

non-alcoholic fatty liver disease (NAFLD)

A

Hepatocytes are infiltrated with fat (triglycerides)
Occurs in absence of alcohol
Associated with obesity, high levels of cholesterol and triglycerides, metabolic syndrome and type 2 diabetes
May develop NASH

45
Q

non-alcoholic steatohepatitis (NASH)

A

Hepatocellular injury, inflammation and fibrosis

May progress to cirrhosis and end-stage liver disease

46
Q

cirrhosis of the liver

A

Irreversible inflammatory, fibrotic liver disease
Fibrosis occurs when the liver tries to regenerate after an injury but the regenerative process is disorganized
Overgrowth of new and fibrous tissue distorts the structure, resulting in lobules of irregular size and shape impeding blood flow
Leads to poor cellular nutrition, and hypoxia causing inadequate flow and scar tissue decreasing the function of the liver

47
Q

clinical manifestations of cirrhosis of the liver

A

Abnormal liver function tests; AST, ALT, GGT, Alk Phos,
Normal blood values; Albumin, Bilirubin (initially but then increases as the disease progresses), PTT
Initially, patient’s complain of abdominal pain, fatigue, slight weight loss, and enlargement of the liver and the spleen
As the illness progresses, patients develop: jaundice, skin lesions, peripheral neuropathy, portal hypertension, esophageal and gastric varices, peripheral edema and ascites, hepatic encephalopathy, hepatorenal syndrome

48
Q

ascites

A

Sodium, water and protein accumulate
in peritoneal cavity due to pressure changes in
lymph system, capillaries. Oncotic and osmotic
pressures rise
May require paracentesis as pressures in
abdomen increase
Sodium restriction, diuretics
Colloids to increase oncotic pressure
Accumulation of fluid in the peritoneal cavity reducing amount of fluid available for normal physiological functions
Most common complication of cirrhosis but can also occur with right sided heart failure, abdominal malignancies, nephrotic syndrome, and malnutrition

49
Q

patho of ascites

A

Contributing factors include: portal hypertension, decreased synthesis of albumin by the liver, splanchnic arterial vasodilation, and renal sodium and water retention

50
Q

clinical manifestations of ascites

A

Increased abdominal distention, increased abdominal girth, and weight gain
Dyspnea caused by decreased lung capacity leading to increase in respiratory rate
Peripheral edema
May develop bacterial peritonitis (fever, chills, abdominal pain, decreased bowel sounds, and cloudy ascitic fluid)

51
Q

patho of hepatic encephalopathy

A

AKA portosystemic encephalopathy
Complex neurologic syndrome characterized by impaired cognitive function, asterixis, and EEG changes
May develop rapidly and become an EMERGENCY situation quickly
Increased amounts of Ammonia and GABA (inhibitory transmitter) may contribute to reduced LOC

52
Q

clinical manifestations of hepatic encephalopathy

A

subtle changes in personality, memory loss, irritability, lethargy and sleep disturbances are common. Symptoms can progress to confusion, flapping tremor of the hands, stupor, convulsions and coma

53
Q

treatment for hepatic encephalopathy

A

lactulose, lactulose, lactulose

54
Q

gallbladder structure and function

A

Saclike organ
Primary function is to store and concentrate bile between meals
Bile is an alkaline, bitter tasting, yellowish green fluid that contains bile salts, cholesterol, bilirubin, electrolytes, and water
Aids in digestion of fats
Bile is released in response to food
Conditions slowing or obstructing flow of bile out of the gallbladder lead to gallbladder disease

55
Q

cholelithiasis (gallstones) patho

A

Gallstones are formed from impaired metabolism of cholesterol, bilirubin, and bile salts
3 types of gallstones: cholesterol (most common), pigmented (black-hard, brown-soft), and mixed
Form when there is decreased motility and biliary stasis
Stones may lay dormant and silent until they become lodged in the cystic or common duct, causing pain when the gallbladder contracts

56
Q

clinical manifestations of gallstones

A 
Often asymptomatic
Epigastric and RUQ pain and intolerance to fatty foods are cardinal manifestations
Vague symptoms include heartburn, flatulence, epigastric discomfort, pruritus, jaundice, and foot intolerances particularly to fats and cabbage
Biliary colic (pain) occurs 30 to several hours after eating a fatty meal
57
Q

cholecystitis patho

A

Can be acute or chronic
Caused by the lodging of a gallstone in the cystic duct
Gallbladder becomes distended and inflamed
Colic pain but decreased blood flow can result in ischemia, necrosis, and perforation of the gallbladder

58
Q

clinical manifestations of cholecystitis

A

Fever, leukocytosis, rebound tenderness, and abdominal muscle guarding
Serum bilirubin and alkaline phosphatase (ALP) may be elevated

59
Q

nursing assessment for gallbladder disorder

A

RUQ or epigastric pain may be referred
May be severe- peak in 30 minutes and can last for several hours
Pain may be dull, constant and radiate to back, waist, shoulder, and scapula
Lab tests with cholelithiasis and biliary colic often normal
Monitor for high WBC in cholecystitis
AST, ALT may be elevated with CBD stone
Serum amylase may be elevated
Increased bilirubin
Urine culture and sensitivity to rule out pyelonephritis or renal stones

60
Q

diagnostic tests associated with gallbladder disorder

A

ERCP (Endoscopic Retrograde Cholangiopancreatography)
Radiographic and endoscopic; diagnosis & treatment
Computed Tomography Scan (CT misses 20%)
Plain x-rays (show calcium ring on some stones, air in biliary tree, other sources of obstruction)
Ultrasound most common and probably most reliable with least risk (90-95% sensitive for cholecystitis)
Scintigraphy (HIDA) (nuclear scanning)

NURS 487 (8 decks)

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