Test Two (GI,Fluids/electrolytes,Acid-base balance,Endocrine) Flashcards


Set Details Share
created 11 years ago by jnewman21
1,176 views
updated 10 years ago by jnewman21
show moreless
Page to share:
Embed this setcancel
COPY
code changes based on your size selection
Size:
X
Show:

1

Lipase

enzyme that aids in digestion of fats

2

trypsin and pepsin

aids in digestion of proteins

3

digestion

phase of the digestive process that occurs when enzymes mix with ingested food and when proteins, fats, and sugars are broken down into their component molecules.

4

absorption

phase of the digestive process that occurs when small molecules, vitamins, and minerals pass through the walls of the small and large intestine and into the bloodstream.

5

chyme

food moving from stomach to small intestine

6

mouth enzymes

saliva, salivary amylase

7

stomach enzymes

hydrochloric acid, pepsin, intrinsic factor

8

small intestine enzymes

amylase, lipase, trypsin, bile

9

dyspepsia

indigestion

10

information to obtain in assessing GI hx

Abdominal pain, dyspepsia, gas, nausea and vomiting, constipation, diarrhea, fecal continence, change in bowel patterns, characteristics of stool, jaundice, history of GI surgery or problems, appetite and eating patterns, teeth, and nutritional assessment including weight patterns
Psychosocial, spiritual, and cultural factors
Assess knowledge; need for patient education

11

aspirin can make:

black stool

12

berium enema can make

white stool

13

Blood tests for GI

CBC and Chemistry
AST (Aspartate Aminotranferase)
ALT (Alanine Aminotransferase)
Amylase and Lipase
Bilirubin
Carcinoembryonic antigen (CEA)

14

diagnostic stool tests

Fecal occult blood tests (False-positive NSAID’s, ASA, Red Meat, within 72 hours)

false-negative with vitamin C within 72 hrs

Stool examination for ova, parasites, and bacteria

15

see slides: 11 and 12

for referred pain and abdominal quadrants and regions

...

16

order to complete abdominal assessment

Inspection, auscultation, palpation, percussion

17

know times for diagnosing hypo,hyper active bowel sounds and what is normal

...

18

computed tomographic (CT scan)

Purpose- to detect tissue densities and abnormalities in the abd, liver, pancreas, spleen, and biliary tract
Client Prep- with or without contrast (IV or PO contrast may be used), NPO 4 hours prior if contrast used, IV access
Follow-up Care- none specific unless sedation was needed
If IV contrast used – hold Metformin 24 hours before and 48 hours after to prevent renal failure

19

false positive can occur for fecal occult blood tests with:

vit. C, NSAIDs, ASA, Red meat within 72 hours prior

20

high eisinophil count is indicative of:

parasitic infection

21

can be found through CBC count:

parasitic infection, ulcers, anemia

22

Upper GI radiographic series:

Purpose-detect abnormalities of the esophagus, stomach, or duodenum (hiatal hernias, ulcers)
Client Prep- NPO (6-8hrs), PO contrast, no opioids or anticholinergic meds for 24 hrs prior
Follow-up Care- drink plenty of fluids to eliminate barium. Laxative may be given. Stool may be chalky for 24-72 hrs after exam.

23

amylase is elevated within 12-24 hours of:

lipase remaining elevated is also extreme indicator of same issue

acute pancreatitis

24

Barium enema- Lower GI:

Purpose- detect changes in large intestines (polyps, tumors, and other lesions)
Client Prep- clear liquids only 12-24hrs prior, NPO 8hrs prior, bowel cleansing night before exam, might have cramping and discomfort during the procedure
Follow-Up Care- same as upper GI

25

Esophagogastroduodenoscopy (EGD)

Purpose- visualize the mucosal lining of esophagus, stomach, and duodenum
Client Prep- NPO at least 8 hrs prior
Follow-up Care- NPO until gag reflex returns, check temp freq for first 2 hrs post-procedure, begin with clears and advance as ordered.

26

breath test used for:

checking for h-pylori (ulcers)

27

Endoscopic Retrograde Cholangiopancreatogrophy (ERCP)

Purpose- visualize the liver, gallbladder, bile ducts and pancreas, and determine obstructions
Client Prep- same as EGD
Follow-up Care- same as EGD, also educate on s/s of possible pancreatitis (nausea, abdominal pain, and elevated temp)

28

Colonoscopy

Purpose- view large bowel for things such as: obtaining bx, removing polyps, evaluate cause of chronic bowel problems, locate source of GI bleeding
Client Prep- clear liquids 12-24 hrs prior, NPO 6-8hrs prior, bowel cleansing night before
Follow-up Care- VS monitoring freq, monitor for s/s of perforation and hemorrhage
Will have lots of gas afterwards (feeling of fullness & cramping)

29

monitor _____ after colonscopy

for hemorrhaging
and VS

patient will be gassy- bowel pumped with gas for procedure

30

hyatal hernia, cancer, GERD (Chapter 35) only for test

...

31

T or F:

When a colonoscopy is done, the flexible scope is passed through the rectum and sigmoid colon into the descending, transverse, and ascending colon.

True

32

Hiatal hernia

Protrusion of a portion of the stomach thru an opening (hiatus) in the diaphragm lying next to the esophagus.

33

sliding hiatal hernia:

part of stomach “slides” thru the hiatal opening into the thoracic cavity when pt is supine, and goes back into abd cavity when standing upright

34

Rolling (paraesophageal) hiatal hernia

fundus and greater curvature of the stomach “roll” up thru the diaphragm, forming a pocket alongside the esophagus.

35

see slide 26 for hernia pictures

...

36

causes of hiatal hernias

weakening of diaphragm muscles around esophagogastric opening, factors that increase intra-abdominal pressure (obesity, pregnancy, ascites, tumors, physical exertion, heavy lifting), trauma, poor nutrition, and a forced recumbent position (bedrest) are also predisposing factors.

37

clinical manifestations of hiatal hernia

similar to GERD, and may mimic GB disease, angina, and peptic ulcer disease. MAY BE ASYMPTOMATIC.

38

tests for hiatal hernias

Barium Swallow, x-rays, fluoroscopy

39

Gastroesophageal Reflux Disease (GERD)

Backward flow of GI contents in to the esophagus- at the lower esophageal sphincter

40

clinical manifestations of GERD

pyrosis (burning sensation in the esophagus), dyspepsia (indigestion), regurgitation, chronic cough especially at night, chest pain, dysphagia or odynophagia (painful swallowing)

41

things to ask about for assessing GERD

health history, evaluate complaints r/t heartburn, note relieving factors

42

diagnostics for GERD

Endoscopy or barium swallto

43

T or F

Barrett’s esophagus is a condition in which the lining of the esophageal mucosa is altered.

True

44

Barretts epithelium

epithelial lining that the body substitutes for the normal lining in the lower esophagus during the healing process that becomes more resistant to acid, but is considered pre-malignant and increases risk for CA in patients with prolonged GERD

45

Fibrosis and scarring accompanying healing process in GERD can

results in the narrowing of lumen (stricture) that causes dysphagia

46

GERD complications:

barretts epithelium, fibrosis and scarring, Esophageal ulceration, hemorrhage, aspiration pneumonia

47

Tx for GERD

Lifestyle changes- HOB up at least 6 in, stop alcohol and smoking b/c these cause decrease LES pressure, wt reduction for obese client, do not wear restrictive clothing
Diet therapy- avoid foods that dec LES pressure (choc, fat, mints) and foods that can delay esophageal healing (spicy, acidic i.e OJ and tomatoes) carb. bev increase intra-abdom pressure, eat 4-6 small meals/day, don’t eat for 3 hrs prior to sleep.
Drug Therapy- Antacids (Maalox, Mylanta, MOM, TUMS) for occ episodes, increase the pH of gastric contents, Histamine Antagonists (Pepcid, Zantac, Tagamet, ), PPIs (Prilosec, Prevacid, Protonix, Nexium

48

types of esophageal cancer

Squamous-cell most common, adenocarcinoma is increasing in incidence

49

predisposing factors for esophageal cancer

Smoking, Excessive alcohol intake, Chronic trauma, Barrett’s esophagus, Spicy foods, Poor oral hygiene, GERD

50

clinical manifestations of esophageal cancer

usually don’t appear until later stages but may include: dysphagia, pain (epigastric, substernal, back) that increases with swallowing

51

assessment for esophageal cancer

Assess risk factors for esophageal cancer, pain, dysphagia, and nutrition status

52

diagnostics for esophageal cancer

EGD, Biopsy

53

nursing DX with esophageal cancer

Altered nutrition (may necessitate need for feeding tube), Pain, Fluid Volume Deficit, Risk for aspiration, Anxiety

54

nasogastric tube is inserted:

through the nose to the stomach

55

gastrointestinal intubation done for:

Decompress the stomach
Lavage the stomach
Diagnose GI disorders
Administer medications and feeding
To treat an obstruction
To compress a bleeding site
To aspirate gastric contents for analysis

56

any kind of tube that provides nutrition

enteric tube...includes NG, gastric, duodenum, jejunum

57

gastric tubes

Levin – Single lumen
Sump - Refer to fig. 36-1 – One way valve that allows air to enter and prevents gastric contents to reflux

58

T or F:

The nasogastric tube is secured to the nose with tape to prevent injury to the nasopharyngeal passages.

True

59

nursing care of pt's with enteric tubes

Patient teaching and preparation
Tube insertion
Confirming placement
Securing the tube
Monitoring the patient
Maintaining tube function
Oral and nasal care
Monitoring, preventing, and managing complications
Tube removal

60

advantages of enteral feedings

Safe and cost-effective
Preserve GI integrity
Preserve the normal sequence of intestinal and hepatic metabolism
Maintain fat metabolism and lipoprotein synthesis
Maintain normal insulin and glucagon ratios

61

Gastrostomy or jejunostomy tubes are for:

long term feeding

62

Nasogastric or nasoenteral tubes are for:

shorter term feeding

63

advantages of tube feeding

Intermittent bolus feedings
Intermittent gravity drip
Continuous infusion
Cyclic feeding

64

air bolus is used for:

and how many mls?

checking for correct placement of enteral tubing

30 ml of air

can also check with ph strip for stomach acid being hit with tube

65

bolus gastrostomy feeding utilize ____ to administer bolus

gravity

66

once goal rate of ordered enteral feeding is reached and patient is tolerating it then:

continue checking every 8 hours

67

nasoenteric feeding rate is controlled by:

continuous controlled pump

68

What position should the patient’s head be in when receiving a tube feeding to prevent aspiration?

semi-fowlers...at least 30-45 degrees

69

assessment items for enteral tube feeding patients

Nutritional status and nutritional assessment
Factors or illnesses that increase metabolic needs
Hydration and fluid needs
Digestive tract function
Renal function and electrolyte status
Medications and other theories that effect nutrition intake and function of the GI tract
Compare the dietary prescription to the patient needs.

70

monitor _______ every 4 hours and admin ______ when needed for patients that are enteral

blood sugar, insulin

71

nursing Dx for enteral pt's

Imbalanced nutrition
Risk for diarrhea
Risk for ineffective airway clearance
Risk for deficient fluid
Risk for ineffective coping
Risk for ineffective therapeutic regimen management
Deficient knowledge

72

nursing Dx for gastrostomy pt's

Imbalanced nutrition
Risk of infection
Risk for impaired skin integrity
Ineffective coping
Disturbed body image
Risk for ineffective therapeutic regimen management

73

potential complications of enteral

Diarrhea
Nausea and vomiting
Gas/bloating/cramping
Dumping syndrome
Aspiration pneumonia
Tube displacement
Tube obstruction
Nasopharyngeal irritation
Hyperglycemia
Dehydration and

74

potential complications of gastrostomy feeding

Wound infection
GI bleeding
Premature removal of tube
Aspiration
Constipation
Diarrhea

75

dumping syndrome

can be caused by enteral feeding because food moves too quickly through the intestines....causes diarrhea, nausea, etc

76

goals when planning---enteral

nutritional balance, normal bowel elimination pattern, reduced risk of aspiration, adequate hydration, individual coping, knowledge and skill in self-care, and prevention of complications.

77

planning- goals---gastrostomy

attaining an optimal level of nutrition, absence of infection, adequate fluid volume, optimal level of activity, knowledge of self-care, and absence of complications.

78

enteral feeding

check for location, administer water, feeding, and admin water again

don't mix meds with feeding...admin water, give med, admin water again

79

enteral tube..what size syringe should you use

30 ml or larger

80

to avoid bacteria with enteral bags

don't hang more than 4 hours of feeding in open system

even though the feeding formula is good for 24 hours

can use same bag for 24 hours...just add more formula

81

rules for administering meds to enteral patient

Administer water before and after each medication and each feeding, before and after checking residual, every 4-6 hours, and whenever the tube feeding is discontinued or interrupted.

82

administer feeding slowly to avoid

dumping syndrome

83

when and how often should you measure residual of tube feedings?

Measure residual prior to intermittent feedings and every 4-8 hours during continuous feedings.

84

how do you maintain normal bowel elimination of enteral patient?

Selection of TF formula; consider fiber, osmolality, and fluid content
Prevent contamination of TF; maintain closed system, do not hang more than 4 hours TF in an open system
Maintain proper nutritional intake
Assess for reason for diarrhea and obtain treatment as needed
Administer TF slowly to prevent dumping syndrome
Avoid cold TF

85

proper dressing of G tube (gastrostomy tube)

usually 4x4 pad

and clean site every 8 hours around tube site

86

two ways to prevent aspiration of NG enteral patient

Elevate HOB at least 30-45 degrees during and for at least 1 hour after feedings

Monitor residual volumes

87

other interventions for enteral patients

Maintain hydration by supplying additional water and assessing for signs of dehydration
Promote coping by support and encouragement, encourage self-care and activities
Patient teaching

88

TPN

total parental nutrition

89

what is total parenteral admixture

An admixture of lipid emulsions, proteins, carbohydrates, electrolytes, vitamins, trace minerals, and water.

90

what is parenteral nutrition

A method to provide nutrients to the body by an IV route.
A complex mixture containing proteins, carbohydrates, fats, electrolytes, vitamins, trace minerals, and sterile water is administered in a single container.
The goals of parenteral nutrition are to improve nutritional status and to attain a positive nitrogen status.

91

what substance is best indicator of good nutrition and should be monitored for PN patients?

pre-albumin

92

when monitoring VS of PN patients always check

temperature- infection from tubing is common

93

reasons PN may be needed

Intake is insufficient to maintain anabolic state.
Ability to ingest food orally or by tube is impaired.
Patient is not interested or is unwilling to ingest adequate nutrients.
The underlying medical condition precludes oral or tube feeding.
Preoperative and postoperative nutritional needs are prolonged.

94

don't hang TPN over

24 hours

95

TPN is administered by

central line

96

potential problems and collaborative problems of TPN

Pneumothorax
Clotted or displaced catheter
Sepsis
Hyperglycemia
Rebound hypoglycemia
Fluid overload

97

goals for TPN patients

attaining an optimal level of nutrition, absence of infection, adequate fluid volume, optimal level of activity, knowledge of self-care, and absence of complications.

98

prevention measures for TPN infection

Appropriate catheter and IV site care
Strict sterile technique for dressing changes
Wear mask when changing the dressing
Assess insertion site
Assess for indicators of infection
Proper IV and tubing care

99

maintaining fluid balance of TPN patients

Use infusion pump. Flow rate should not be increased or decreased rapidly. If fluid runs out, hang 10% dextrose solution.
Monitor indicators of fluid balance and electrolyte levels.
I&O.
Weights.
Monitor blood glucose levels.

100

patient teaching for TPN

Goals and purpose
Components of PN
Emergency contact numbers
Demonstrate use of equipment and how to handle and hang the IV
Demonstrate dressing changes
Demonstrate how to flush or heparinize the catheter
Potential complications and actions

101

gastroenteritis (not in book)

Pathophysiology – inflammation of the stomach and intestinal tract that causes vomiting, diarrhea or both
Etiology – most common causes are viruses (rotavirus) and bacteria (Salmonella) in food or water.
Clinical Manifestations – episodes of vomiting and diarrhea and may develop symptoms of dehydration, malaise, abdominal cramps or fever
Prevention – handwashing, principle food handling (eggs and raw meat)
Assessment – abdomen assessment and hydration assessment.
Labs – CBC – for dehydration and elevated WBC’s
Nursing Dx – Fluid volume deficit

102

how are protozoa transmitted?

Infect humans through fecal-oral contamination or through ingestion of food or water contaminated with cysts or spores, through host-to-host contact, or by the bite of a mosquito or other insect that has previously bitten an infected person

103

signs and symptoms of protozoa infection

diarrhea, gastroenteritis, malaria

104

helminthic infection if transmitted by

skin pentration of larvae or ingestion of helminth eggs. Trichinelloisis (caused by roundworms) is a disease caused by eating raw or undercooked meat of pigs or wild animals that contain Trichinella larvae.

105

gastritis

Inflammation of the stomach (gastric mucosa)
A common GI problem

106

acute gastritis

rapid onset of symptoms usually caused by dietary indiscretion. Other causes include medications, alcohol, bile reflux, and radiation therapy. Ingestion of strong acid or alkali may cause serious complications.

107

chronic gastritis

prolonged inflammation due to benign or malignant ulcers of the stomach or by Helicobacter pylori. May also be associated with some autoimmune diseases, dietary factors, medications, alcohol, smoking, or chronic reflux of pancreatic secretions or bile.

108

Erosive gastritis

mucosal damage
cells secrete HCL or pepsinogen and intrinsic factor

109

acute gastritis S/S

abdominal discomfort, headache, lassitude, nausea, vomiting, hiccuping.

110

chronic gastritis S/S

epigastric discomfort, anorexia, heartburn after eating, belching, sour taste in the mouth, nausea and vomiting, intolerance of some foods. May have vitamin deficiency due to malabsorption of B12.

111

gastritis may be associated with

achlorhydria, hypochlorhydria, or hyperchloryhydria.

112

most common site of peptic ulcer

duodenum

113

gastritis is usually diagnosed by

UGI X-ray or endoscopy and biopsy.

114

gastritis nursing Dx's

Anxiety
Imbalanced nutrition
Risk for fluid volume imbalance
Deficient knowledge
Acute pain

115

peptic ulcer

Erosion of a mucous membrane forms an excavation in the stomach, pylorus, duodenum, or esophagus

Associated with infection of H. pylori

Risk factors include excessive secretion of stomach acid, dietary factors, chronic use of NSAIDs, alcohol, smoking, and familial tendency.

Manifestations include a dull gnawing pain or burning in the mid-epigastrium; heartburn and vomiting may occur

LABS- monitor H/H & coagulation studies

116

dietary assessment for peptic ulcer

Dietary intake and 72 hour diet diary

117

proton pump inhibitor for peptic ulcer should be taken when?

30 min prior to meal

118

two biggest factors for risk for gastric disorders and diseases

smoking and alcohol

119

clinical manifestations of gastric cancer

pain relieved by antacids early in the disease, dyspepsia, early satiety, weight loss, abdominal pain, loss or decrease in appetite, bloating after meals, nausea, and vomiting. Diagnosis of the disease is often late.

120

gastric cancer is diagnosed by

EGD with biopsy
Ultrasound –presence of tumors
CT

121

nursing Dx with gastric cancer

Anxiety
Imbalanced nutrition
Pain
Anticipatory grieving
Deficient knowledge

122

causes of constipation

medications, chronic laxative use, weakness, immobility, fatigue, inability to increase intra-abdominal pressure, diet, ignoring urge to defecate, and lack of regular exercise.

123

clinical manifestations of constipation

Fewer than 3 BMs per week
Abdominal distention, Indigestion
Decreased appetite
Headache, Fatigue
A sensation of incomplete evacuation
Straining at stool
Elimination of small-volume, hard, dry stools

124

complications with constipation

Hypertension
Fecal impaction
Hemorrhoids
Fissures
Megacolon

125

diarrhea

Increased frequency of bowel movements (more than 3 per day), increase amount of stool (more than 200 g per day), and altered consistency (i.e., looseness) of stool

126

metabolic and endocrine disorders can cause

diarrhea

127

Borborygmus

a rumbling or gurgling noise made by the movement of fluid and gas in the intestines

128

Tenesmus

a clinical sign, where there is a feeling of constantly needing to pass stools, despite an empty colon.

129

diagnosis criteria for IBS

criteria of recurrent abdominal pain or discomfort for at least 3 days a month in last 3 months

130

IBS is more common in

women than men

131

appendicitis is most common from

age of 10-30

132

S/S of appendicitis KNOW

increased WBCs, peri-umbilical pain (McBurney’s point) eventually shifting to RLQ, rebound tenderness (Rovsing’s sign), N/V, anorexia, possible low-grade fever

133

appendicitis is diagnosed by

abd assessment, CBC (shows elevated WBC’s), x-ray, ultrasound, CT

134

most common site of diverticulitis

sigmoid colon

135

never use warm compress for abdominal pain

could rupture appendix

136

diverticulum

sac-like herniation's of the lining of the bowel that extend through a defect in the muscle layer

137

diverticulosis

multiple diverticula without inflammation

138

diverticulitis

infection and inflammation of diverticula

usually caused by severe constipation

139

diverticular disease increases with

age
and low fiber diet

140

diverticulitis symptoms

mild or severe pain in lower left quadrant, nausea, vomiting, fever, chills, and leukocytosis.

141

ways to diagnose diverticular disease

Barium Enema, Colonoscopy, CT with contrast, CBC, ESR

142

complications of diverticular disease

Perforation, Peritonitis, Abscess formation, Bleeding, fistula (where bowel joins with another organ)

143

Abdominal pain and diarrhea are common clinical manifestations of

chrohn's disease

144

chrohns disease

chronic, nonspecific inflammatory bowel disorder that can affect any part of GI tract but mainly terminal ileum, jejunum, and colon

more commonly associated with smoking

145

S/S of chrohn's

DIARRHEA, abdominal pain, cramping, tenderness developing into weight loss, malnutrition, dehydration, electrolyte imbalances

146

tests for chrohn's

barium studies, colonoscopy, sigmoidoscopy, bx performed, CBC, ESR, Decreased albumin and protein

147

pre-albumin is decreased

with Chrohn's because they're not digesting protein well

148

ulcerative colitis

affects the superficial mucosa of the colon causing multiple ulcerations, diffuse inflammations and shedding of the colonic epithelium – usually in the rectum and lesions spread throughout the large intestine

149

in ulcerative colitis abscesses develop in the intestinal glands

breaking thru submucosa and leaving ulcerations that destroy mucosal epithelium causing bleeding and diarrhea, watery mucus

150

clinical manifestations of ulcerative colitis

exacerbations & remissions, diarrhea, passage of watery mucus & pus, LLQ abdominal pain, rectal bleeding, pallor, anemia, and fatigue

151

tests for ulcerative colitis

Barium series, Sigmoidoscopy, Colonoscopy, CBC (High WBC), Low H & H

152

mechanical intestinal obstruction

bowel is obstructed by disorders outside of the intestine or by blockages in the lumen of the intestine

153

Nonmechanical (paralytic ileus)- intestinal obstruction

result of neuromuscular disturbance resulting in decreased or absent peristalsis causing back up of intestinal contents

154

see slide 96 for three causes of intestinal obstructions

...

155

causes of hernias

increased inta-abd pressure by coughing, straining, and heavy lifting. Obesity, pregnancy, and poor wound healing are other risk factors

156

hernia

weakness in the abdominal muscle wall thru which a segment of bowel or other abd structure protrudes

157

inguinal hernia

located in the groin where the spermatic cord in males or the round ligament in females emerges from the abd wall.

158

umbilical hernia

are seen most often in obese women and in children. They are caused by a failure of the umbilical orifice to close

159

incisional hernia

(Ventral) usually result from a weakness in the abdominal wall following abd. surgery

160

see slide 98 for more hernia info

...

161

patho of colo-rectal cancer

cancer of colon and rectum predominantly adenocarcinoma.
The second cause of cancer deaths in the United States.

162

start again on slide 99

...

163

RBCs are broken down by liver...have life span of about 3 months...liver breaks it down into:

bile

164

liver stores glucose

for times of high energy requirements:
exercise, fight or flight, etc.

165

liver makes _______ factors

clotting

166

blood flows through liver by:

very fine capillary system...because blood has to come into contact with hepatocytes

167

symptoms of liver dysfunction

jaundice from bilirubin, cephalopothy (confusion), trembling, bilirubin binds to brain tissue, portal hypertension (filter clogged causes backup),blood goes into stomach because of portal hypertension (Ascites)

168

Ascites (Usitees)

blood in stomach from portal hypertenstion because vessels in esophagus swell and leak into stomach

cirrhosis of liver can cause bleed out and death via this route

tarry stool seen, faster bleed can cause vomitting of blood

169

clay color stool caused by:

lack of bile from liver dysfunction

170

diagnostic tests for liver function (enzymes)

these are ________ the more dead liver cells there are (A:higher)

Aspartate Aminotransfease - AST (also SGOT) 15 – 40 u/L
Alanine Aminotransferase – ALT 10 – 40 u/L
Leucine Aminopeptidase – 75 – 200 u/L
Gamma-Glutamyl Transpeptidase – GGTP 0 – 30 u/L
Alkaline Phosphatase – 0 – 93 u/L

171

other diagnostic tests for liver function

Erythrocyte Sedimentation rate
Serum Total Bilirubin
Unconjugated <1.1 mg/dL Conjugated <0.3 mg/dL
Urobilinogen * <1mg/dL
Prothrombin Time – PT <2.0 (times reference)
Serologic Tests – negative

172

ESR erythrocyte sedimentation rate

tells us there is inflammation in body

173

serum bilirubin unconjugated vs conjugated

unconjugated- not water soluble and hasn't been through liver yet

conjugated- has been changed by liver

may seem change in urine color if there is a lot of conjugated bilirubin

174

urobilirubin

bilirubin in urine

175

PT -- prothrombin time

test for clotting time
<2.0 (times reference)-- normal time for someone not on warfarin)

varies by age and gender

176

serologic tests

shows disease process

177

hepatitis (inflammation of cells of liver--usually caused by virus includes what cells?

HAV,HBV,HCV,HDV,HEV,HFV,HGV

or

H(A-G)V

178

transmission routes of hepatitis

concentrated in stool during incubation period (common transmission worldwide is contaminated H2O)

undercooked shellfish

179

prevention of hepatitis

cleanliness, vaccines (HAV,HBV), standard precautions

washing produce, hands, etc

180

hepatitis B transmitted

blood born: sexual contact, sharing drug needles, parenteral (in utero)

181

Stages of liver dysfunction:

prodromal stage- (1 week)- flu-like symptoms, RUQ pain

Icteric Stage- (2-6 weeks)- worsening symptoms, jaundice, rash/itching

Convalescent- (2-6 weeks)- return to normal function, lab values normal

182

autoimmune hepatitis

more common in women, rare

associated with graves, type I diabetes, myethenia gravis, etc

183

hepatitis A transmitted via:

hepatitis B transmitted via:

ingestion

body fluids

184

Fulminant Liver Failure

fatty liver disease
sudden massive loss of liver tissue replaced by massive amounts of fat (associated w/alcohol,drug toxicitiy, but can be idiopathic)
etiology- drug toxicity,hepatitis
people on TPN, wilson's disease, IDDM

185

S/S of fulminant liver failure

encephalopathy - confusion, coma

elevated liver enzymes, bilirubin, PT (same as hepatitis but no antibodies b/c of absence of virus)

ascites, GI discomfort, generalized edema,jaundice, eventually respiratory or renal problems

186

complications of Hepatitis and fulminant liver failure

Metabolic Alkalosis
Hypokalemia
Hypoglycemia
Clotting Disturbances
Sepsis
Renal Failure
Respiratory Failure

187

diagnostic tests for fulminant liver failure

ALT
AST
Serum Bilirubin
Urobilinogen
Biopsy
Blood Glucose
PT
Ultrasound

188

etiology of chronic liver failure -- Cirrhosis

Chronic Alcohol Ingestion
Hepatotoxins
Hepatitis
Gallbladder Obstruction
Heart Failure

189

pathophysiology of cirrhosis

Inflammation of Liver Cells
Infiltration with Fat and WBCs
Fibrotic Scar Tissue Replaces Liver Tissue

190

S/S of cirrhosis

portal hypertension, anemia, hepatic encephalopathy,hepatorenal syndrome (ammonia crystals cause itching), GI problems including clay color stool, ammenorhea (no period), testicular atrophy, low testosterone (ED and male breasts), hemorrhoids

191

complications of cirrhosis

renal failure, clotting defects, ascites, portal hypertension, encephalopathy

192

Dx testing for cirrhosis

liver enzymes, bilirubin, urobilinogen, serum ammonia, PT, abdominal x-ray, UGI series, liver scan, EGD (esophogus- endoscopic test), liver biopsy

193

Nursing DX for acute and chronic liver failure

Excess Fluid Volume
Imbalanced Nutrition
Pain
Risk for Disturbed Thought Processes
Risk for Ineffective Breathing Pattern
Risk for Deficient Fluid Volume
Risk for Infection

194

candidates for liver transplant

liver failure, no cancer, no complications, otherwise stable

195

pathophysiology of acute pancreatitis:

complications of acute pancreatitis

inflammation, autodigestion, elevated enzymes,fluid loss

shock,DIC (Disseminated intravascular coagulation)- microclotting through out body due to excessive bleeding, chronic pancreatitis

196

etiology of acute pancreatitis

Alcohol
Biliary Disease
Trauma
Some Drugs
scorpion and snake bites
Unknown (idiopathic)

not encapsulated so when there is disorder the surrounding tissue is affected (surrounding fat is digested)

197

S/S of acute pancreatitis

Abdominal Pain
Guarding
Rigid Abdomen
Hypotension or Shock
Respiratory Distress
Low Grade Fever
Nausea and Vomiting
Jaundice
grey turner (bluish color to flanks)

198

complications of acute pancreatitis

Cardiovascular Failure
Acute Respiratory Distrss Syndrome
Renal Failure
Hemorrhage
Infection

199

DX tests for acute pancreatitis

Serum Amylase – 30 – 110 u/L
Serum Lipase – 3 – 73 u/L
X-Ray
CT
Ultrasound

200

Nursing DX for acute and chronic pancreatitis

Pain
Imbalanced Nutrition
Risk for Ineffective Breathing Pattern
Risk for Injury

201

gall bladder disorders

Cholecystitis: Inflammation

Cholelithiasis: Stones

Choledocholithiasis: Stones in Common Bile Duct (can damage liver if left untreated)

202

etiology of gall bladder disorders

Stasis
High Cholesterol Intake
Fasting
Sedentary Lifestyle
Family History
More Common in Women
Pregnancy
Risk Increases with Age

203

S/S of gall bladder disorders

Increased Vital Signs
Vomiting
Jaundice
Epigastric Pain
RUQ Tenderness
Nausea
Indigestion
Positive Murphy’s Sign
Biliary Colic (pain)

204

complications of gall bladder disorders

Cholangitis
Necrosis/Perforation of GB
Empyema
Fistulas
Adenocarcinoma of GB
Pancreatitis

205

four F's of gall bladder disorder

female,fat,over 40,fertile

206

Dx tests for gall bladder

WBC
Serum Amylase
X-Ray
Nuclear Scan
Ultrasound

207

Nursing Dx for gall bladder disorders

Acute Pain
Risk for Deficient Fluid Volume
Risk for Impaired Skin Integrity
Risk for Ineffective Breathing Pattern

208

Third spacing

loss of ECF into space that does not contribute to equilibrium

209

ICF:

ECF:

fluid in cells-- 2/3rds of body fluid

fluid outside cells- intravascular,interstitial, and transcellular

210

transcellular ECF

cerebrospinal, percardial,synovial

211

interstitial ECF

lymph

212

intravascular ECF

fluid in lood vessels- aka plasma

213

Ascites that occurs with liver disease is categorized as

third spacing fluid

214

cations

positively charged ions

major types: sodium,potassium,calcium,magnesium,hydrogen ions

215

anions

negatively charged ions

chloride,bicarbonate,phosphate,sulfate, and proteinate ions

216

intracellular and extracellular fluids differ in terms of

electrolyte balance

217

hydrostatic pressure

exerted on walls of blood vessels (as in ascites)

218

osmotic pressure

exerted by protein in plasma

fluid is shunted to area higher in protein

219

Direction of fluid movement depends on differences of

hydrostatic and osmotic pressures

220

osmosis

area of low solute concentration to area of high solute concentration across membrane walls. No energy required. Water moves.

221

diffusion

solutes move from area of higher concentration to one of lower concentration . No membrane (like adding drop of food color to water). No energy required

222

filtration

movement of water, solutes occurs from area of high hydrostatic pressure to area of low hydrostatic pressure (like water leaking from hose) Takes energy

223

active transport

physiologic pump that moves fluid from area of lower concentration of one of higher concentration. (Example : Sodium-potassium pump) Takes energy.

required for movement against concentration gradient

224

soduim-potassium pump

maintains higher concentration of extracellular sodium, intracellular potassium

225

isotonic

has same osmolarity as blood plasma (0.9% salt)

226

hypertonic

has greater osmolarity than blood plasma -- higher concentration of salt

227

hypotonic

lower osmolarity than blood plasma (pt dehydrated but electrolytes are normal)

228

significant electrolyte blood levels

Potassium 3.5 – 5.0 mEq/L
Hypokalemia (jitters)
Hyperkalemia (heart failure)

Sodium 135 – 145 mEq/L
Hyponatremia (low EC salt- cells swell)
Hypernatremia (fluid moves out- cell shrinks)

Bicarbonate-regulated by kidneys

229

isotonic IV solutions

Normal Saline (0.9%NS)
Lactated Ringer’s (LR)- contains other electrolytes

230

hypotonic IV solution:

D5W:

½ Normal Saline (0.45%NS)

D5W has no salt

231

hypertonic IV solutions

Dextrose 5% in Normal Saline (D5NS)
Dextrose 5% in ½ Normal Saline (D51/2NS)
Dextrose 5% in Lactated Ringer’s (D5LR)

Dextrose makes it hypertonic

human albumin--rarely seen but used to pull off excess fluid off tissues b/c protein pulls water

232

route of fluid gain

Dietary intake of fluid, food or enteral feeding
Parenteral fluids

233

routes of fluid loss

Kidney: urine output – 1 to 2 L usual daily volume or 1ml/kg/h in all age groups (KNOW-math problem for test)

Skin loss: sensible (sweating), insensible losses (fever)
Lungs – loss is greater with increased respiratory rate or depth, or a dry climate.
GI tract – diarrhea and fistula cause larger losses.
Other – wounds
Must count all areas of fluid losses

234

study slide 15 for RAAS and effects of imbalance of fluids and electrolytes

...

235

if kidney blood flow is reduced it stimulates kidneys to produce ___________ which is converted to angiotensin I and that combined with ACE makes __________ which results in _______________

renin

Aldosterone

sodium and water retention thus increasing blood volume and pressure

236

Fluid volume deficit - FVD

hypovolemia- dehydration

237

Fluid volume excess - FVE

hypervolemia- fluid volume overload

238

dehydration

loss of water along with increased serum sodium level

239

GI suctioning can cause

dehydration

240

risk factors contributing to dehydration

diabetes insipidus, adrenal insufficiency, osmotic diuresis, hemorrhage, coma, third space shifts (ie, burn pt's, liver failure (ascites) and HF)

241

manifestations of dehydration

rapid weight loss, decreased skin turgor (tenting), oliguria, concentrated urine, postural hypotension, rapid weak pulse, increased temperature, cool clammy skin due to vasoconstriction, lassitude, thirst, nausea, muscle weakness, cramps

242

serum electrolyte changes associated with dehydration

Hypokalemia occurs with GI & renal losses
Hperkalemia occurs with adrenal insufficiency
Hyponatremia occurs with increased thirst & ADH release
Hypernatremia results form increased insensible losses and Diabetes Insipidus

243

factors contributing to FVE

heart failure, renal failure, cirrhosis of liver

excessive dietary sodium or sodium-containing IV solutions

244

manifestations of FVE

edema, distended neck veins, abnormal lung sounds (crackles), tachycardia, increased BP, pulse pressure and CVP, increased weight, increased UO (urinary output), shortness of breath and wheezing

245

pitting edema

stays down

regular edema returns

246

JVD is

jugular vein distention measured at 45 degree angle
should be 3 mm or less

247

hyponatremia

Serum sodium less than 135 mEq/L

248

causes of hyponatremia

adrenal insufficiency, water intoxication, Syndrome of Inappropriate Antidiuretic Hormone (SIADH) or losses by vomiting, diarrhea, sweating, diuretics

249

manifestations of hyponatremia

poor skin turgor, dry mucosa, headache, decreased salivation, decreased BP, tachycardia, nausea, abdominal cramping, neurologic changes (confusion)

250

nursing assessments for hyponatremia risk

dietary sodium and fluid intake, identify and monitor at-risk patients, effects of medications (diuretics, lithium), water intoxication (mental illness), monitor labs

251

nursing DX for hyponatremia

Risk for Hyponatremia r/t unreplaced loss or limited oral intake
Disturbed thought process r/t electrolyte imbalance
Risk for fluid volume excess r/t excessive intake of hypotonic fluids
Risk for injury r/t seizure, confusion (due to electrolyte imbalance

252

the nurse should monitor labs for ____________ and ________________________ when caring for the hyponatremic patient

Decreased serum and urine sodium
Decreased urine specific gravity & osmolarity

253

Education to provide to hyponatremic patient

Consult physician if vomiting or diarrhea >48 hr or weakness, dizziness, palpitations, cough or dyspnea, or CNS changes develop

Anyone with chronic disease should consult physician if manifestations last longer than 24 hours

254

hypernatremia

serum sodium greater than 145 mEq/L

255

causes of hypernatremia

excess water loss, excess sodium administration, diabetes insipidus, heat stroke, hypertonic IV solutions , hyperventilation

256

manifestations of hypernatremia

thirst; elevated temperature; dry, swollen tongue; sticky mucosa; neurologic symptoms; restlessness; weakness; increased pulse and BP

257

nursing assessments for hypernatremic patient

OTC sources of sodium, intake of fluids to meet patient needs, sufficient water with tube feedings; Neurologic symptoms – hallucinations, lethargy, restlessness, irritability, focal or grand mal seizures, monitor labs

258

Potassium facts

Primary intracellular cation
Vital role in cell metabolism

Balances Na in extracellular fluids (ECF) to maintain the electroneutrality of body fluids.

Promotes transmission & conduction of nerve impulses and contraction of skeletal, cardiac & smooth muscles

259

hypokalemia

Below-normal serum potassium (<3.5 mEq/L), may occur with normal potassium levels with alkalosis due to shift of serum potassium into cells

260

hypokalemia causes

GI losses (bulimia, starvation), medications, alterations of acid-base balance(alkalosis), hyperaldosterism, poor dietary intake

261

manifestations of hypokalemia

fatigue, anorexia, nausea, vomiting, dysrhythmias, muscle weakness and cramps, paresthesias, glucose intolerance, decreased muscle strength, DTRs (deep tendon reflexes)

262

nursing assessments for hypokalemic patients

severe hypokalemia is life-threatening, monitor ECG and ABGs, dietary potassium, IV potassium administration, monitor labs

263

DX and outcome for hypokalemia

Diagnosis
Risk for Injury r/t muscle weakness, hypotension, or seizures
Activity Intolerance r/t muscle weakness
Decreased cardiac output r/t dysrhythmia
Outcome
Client will not sustain injury

Diagnosis
Imbalanced Nutrition: Less Than Body Requirements related to insufficient intake of potassium-rich foods
Outcomes
Adequate intake of potassium-rich foods
Interventions
Educate regarding potassium-rich foods and supplements

264

hyperkalemia

Serum potassium greater than 5.0 mEq/L

265

tissue damage results in hyperkalemia D/T _____________ is released into blood stream resulting in ________________________________

potassium

heart failure

266

causes of hyperkalemia

usually treatment related, impaired renal function, hypoaldosteronism, tissue trauma, acidosis

267

manifestations of hyperkalemia

cardiac changes and dysrhythmias, muscle weakness with potential respiratory impairment, paresthesias, anxiety, GI manifestations, death

268

Hemolysis of blood specimen or drawing of blood above IV site may result in false laboratory result
when testing for

hyperkalemia

269

potassium sparing diuretics should not be used by

patients with renal dysfunction

270

nursing DX for hyperkalemia

Risk for Activity Intolerance
Risk for Decrease Cardiac Output

271

If patients is isotonic and isotonic solution is administered where will fluid be pulled? the circulatory system or tissues?

tissues

272

hypertonic solution- what direction will fluid be pulled?...circulatory or tissue

from cells into circulatory system

273

albumin in blood would pull fluid from where to where?

it's hypertonic and would pull fluid from cell to circulatory system...albumin is often used as a diurectic

274

two biggest electrolytes we are concerned with

potassium and sodium

275

role of calcium

Proper function of excitable tissues, especially cardiac muscle.
Adequate blood clotting
Structural support to bones and teeth

276

causes of hypocalcemia

hypoparathyroidism, malabsorption, pancreatitis, alkalosis, massive transfusion of citrated blood, renal failure, medications, open wounds

277

hypocalcemia

serum level less that 8.2 mg/dL

must be considered in conjunction with serum albumin level and pH

normal level is 8.2-10.2

278

S/S of hypocalcemia

tetany, circumoral numbness, paresthesias, hyperactive DTRs, Trousseau’s sign, Chovstek's sign, seizures, respiratory symptoms of dyspnea and laryngospasm, abnormal clotting, anxiety

279

nursing assessment for hypocalcemia

severe hypocalcemia is life-threatening, weight-bearing exercises to decrease bone calcium loss, patient understanding related to diet and medications, evaluate number of transfusions, monitor for dysrhythmia, monitor breathing, and monitor labs

280

nursing dx for hypocalcemia

Activity intolerance r/t neuromuscular irritability
Imbalanced nutrition
Ineffective breathing pattern r/t laryngospasm

281

tetany

tense muscles from hypocalcemia

282

hypercalcemia

serum level above 10.2 mg/dL

283

causes of hypercalcemia

malignancy of bone, hyperparathyroidism, bone loss related to immobility, prolonged use of thiazide diuretics

284

S/S of hypercalcemia

muscle weakness, incoordination, anorexia, constipation, nausea and vomiting, abdominal and bone pain, polyuria, thirst, ECG changes, dysrhythmias. Complication – renal/urinary calculi (stones)

285

nursing assessment for hypercalcemia

hypercalcemic crisis has high mortality, evaluate ambulation, fluids of 3 to 4 L/day containing sodium (rehydration/dilution) unless contraindicated, fiber for constipation, ensure safety (mental symptoms), monitor labs

286

often times with hypocalcemia

will see increase in CO2 levels because of insufficient breathing

287

nursing dx for hypercalcemia

Decreased Cardiac Output r/t bradycardia
Impaired mobility r/t decreased muscle tone
Risk for injury r/t decreased density of bones

288

trousseau's sign is seen with

hypocalcemia

289

role of magnesium

Most abundant intracellular cation after potassium
Involved in both carbohydrate and protein metabolism
Important in neuromuscular function
Acting peripherally to produce vasodilatation and decreased peripheral resistance
Calcium and magnesium work together – so an imbalance in magnesium will usually be accompanied by an imbalances in calcium

290

hypomagnesemia

Serum level less than 1.6 mg/dL (normal range 1.6 – 2.6 mg/dL), evaluate in conjunction with serum albumin

291

causes of hypomagnesemia

alcoholism, GI losses, enteral or parenteral feeding deficient in magnesium, medications, rapid administration of citrated blood; contributing causes include diabetic ketoacidosis, sepsis, burns, hypothermia

292

S/S of hypomagnesemia

neuromuscular irritability(Trousseau’s & Chvostek’s sign), muscle weakness, tremors, athetoid movements, ECG changes and dysrhythmias, alterations in mood (apathy & depression) and level of consciousness (delirium, confusion, hallucinations)

293

nursing assessment for hypomagnesemia

evaluate safety (seizure precautions and confusion), dysphasia screening, patient understanding related to diet, medications, alcohol use, monitor for dysrhythmia, and monitor labs

294

hypomagnesemia often accompanies

hypocalcemia

295

dysphagia is common in patients with

hypomagnesemia

296

nursing dx for hypomagnesemia

Risk for injury r/t disturb though processes, confusion
Risk for aspiration
Risk for decreased cardiac output r/t possible dysrhythmia

297

hypermagnesemia

Serum level more than 2.6 mg/dL

298

causes of hypermagnesemia

renal failure, diabetic ketoacidosis, excessive administration of magnesium, Addison’s disease

299

S/S of hypermagnesemia

flushing, lowered BP & shallow respirations, nausea, vomiting, hypoactive reflexes, drowsiness, muscle weakness, depressed respirations, ECG changes, dysrhythmias

300

nursing assessment for hypermagnesemia

evaluate for medications containing magnesium especially pt with renal failure, patient understanding regarding magnesium containing OTC medications, monitor labs, monitor LOC, monitor for dysrhythmia & respiratory rate

301

nursing dx for hypermagnesemia

Disturbed though processes r/t electrolyte imbalance
Activity intolerance r/t neuromuscular hypoactivity
Ineffective breathing pattern
Decreased cardiac output r/t dysrhythmia

302

role of phosphorous

Essential to the function of muscle and RBC’s and the formation of ATP
Facilitates the release of O2 from hemoglobin
Structural support to bones and teeth

303

hypophosphatemia

Serum level below 2.5 mg/dL (normal 2.5 – 4.5 mg/dL)

304

causes of hypophosphatemia

alcoholism, anorexia nervosa, refeeding of patients after starvation, pain, heat stroke, respiratory alkalosis, hyperventilation, diabetic ketoacidosis, hepatic encephalopathy, major burns, hyperparathyroidism, low magnesium, low potassium, diarrhea, vitamin D deficiency, use of diuretic and antacids

305

S/S of hypophosphatemia

neurologic symptoms (irritability, dysphagia, diplopia, seizures), confusion, muscle weakness, tissue hypoxia, muscle and bone pain (osteomalacia), increased susceptibility to infection

306

high glucose causes

hypophosphatemia

307

nursing assessment for hypophosphatemia

evaluate intake of foods high in phosphorus, monitor labs, monitor LOC

308

nursing dx for hypophosphatemia

similar to other electrolytes

309

hyperphosphatemia

Serum level above 4.5 mg/DL

310

causes of hyperphosphatemia

renal failure, excess phosphorus, excess vitamin D, acidosis, hypoparathyroidism, chemotherapy

311

S/S of hyperphosphatemia

few symptoms; soft-tissue calcifications, symptoms occur due to associated hypocalcemia

312

labs for hyperphosphatemia

Serum phos & Ca+, BUN & Creatitine (renal failure)

313

nursing assessment for hyperphosphatemia

evaluate avoiding high-phosphorus foods; patient understanding related to diet, phosphate-containing substances, signs of hypocalcemia

314

calcium and ____________________ have an antagonistic relationship (levels affect eachother)

phosphorous

if one goes up the other goes down

315

compare and highlight flashcards (see powerpoint slides)

...

316

normal pH of:

water
blood

7.0

7.35-7.45

317

normal cell function depends on regulating

hydrogen ions (H+)

318

as hydrogen production increases

pH decreases

319

acid

substance that releases Hydrogen ion

320

base (alkali)

binds hydrogen

321

serum pH interdependent systems

Chemical buffering in blood plasma and cells
Excretion of acids (CO2) by lungs
Excretion of acid or regeneration of base (HCO3) by kidney

322

______________ is the body's first attempt at maintaining pH levels

bicarbonate (carbonic acid buffering system)

323

the _______________ are the second line of defense in maintaining acid-base balance

lungs-- rapid compensation

324

the last line of defense in pH maintenance is

the kidneys- slow to compensate

325

other buffer systems (not as important to know)

ECF: inorganic phosphates, plasma proteins

ICF: proteins, organic, inorganic phosphates

Hemoglobin

326

excessive hydrogen ions means the patient will be

acidic

327

how do the lungs regulate volatile acid (convert it to gases)

CO2 produced by cells as by-product of energy production
CO2 diffuses into blood and mixes with H2O to produce H2CO3 (carbonic acid) which then separates into H+ and HCO3 (bicarbonate)
Carbonic acid releases CO2 thru aveoli recirculating H2O
Depending on need lungs either expel or retain CO2

328

fixed acids (not converted to gases) and bicarbonate are managed by

kidneys

329

how do kidneys regulate pH

by secreting H+ into urine or by regenerating HCO3 for reabsorption into the blood

330

CO2 lowers pH when you exhale you

alkalize the body -- get rid of hydrogen ions

CO2 is biggest portion of acid in blood stream

331

kidney regulation of acid-base works until

pH is <4.5

332

PaO2

partial pressure of oxygen in arterial blood

333

PaCO2

is the partial pressure of carbon dioxide and is a reflection of the pulmonary ventilation (35-45 mm Hg)

334

COPD causes build up of CO2 therefore the _______________ will try to step in but it may not be able to maintain acid-base balance

kidneys

335

bicarbonate (HCO3)

is a common base in the body and a major renal component of acid-base (22-26 mEq/L)

336

normal arterial blood gases (ABGs)

pH 7.35 - (7.4) - 7.45
PaCO2 35 - (40) - 45 mm Hg
HCO3ˉ 22 - (24) - 26 mEq/L
PaO2 80 to 100 mm Hg
Oxygen saturation >94%

337

What is the most common buffer system in the body?

Bicarbonate-carbonic acid

338

analysis of ABGs gives what info

Determines type of imbalance
Evaluates degree of compensation

339

the body's major extracellular buffer system is bicarbonate-carbonic acid buffer system which is assessed by

analysis of ABGs

340

blood draw for ABG should be from

an artery

341

acidemia

alkalosis

pH <7.35

pH >7.45

evaluate symptoms, med dx, tx's

342

order of analysis for ABGs

blood pH
assess PaCO2
assess HCO3 (healthy kidneys get rid of uric acid--if poor renal function will see uric acid combine with HCO3 and increase acidity)

343

see slide 73 for ABG value chart

...

344

metabolic alkalosis usually occurs

with ng suctioning or vomitting

345

metabolic acidosis is most commonly seen with

renal failure (uric acid problem) and diabetes (lactic acid problem)

will have low pH and low bicarbonate on ABG

346

causes of metabolic acidosis

Lactic acidosis, diabetic ketoacidosis, azotemic, diarrhea

347

S/S of metabolic acidosis

headache, confusion, drowsiness, increased respiratory rate and depth, decreased blood pressure, decreased cardiac output, dysrhythmias, shock; if decrease is slow, patient may be asymptomatic until bicarbonate is 15 mEq/L or less

348

with metabolic acidosis _________________ occurs as potassium shifts out of the cells (cell death) and into the circulatory system

hyperkalemia

349

_____________ should be monitored with metabolic acidosis

potassium levels

350

serum calcium levels should be corrected during tx of

acidosis

351

hypokalemia can cause

metabolic alkalosis

352

S/S of metabolic alkalosis

symptoms related to decreased calcium, respiratory depression, tachycardia, symptoms of hypokalemia

353

In metabolic alkalosis, Potassium in blood will decrease due to potassium being pulled into cells. This is due

to cell exchanging potassium for hydrogen ion (H+) to balance pH

354

respiratory acidosis is always due to

respiratory problem with inadequate excretion of CO2 (hypoventilatory states)

355

causes of respiratory acidosis

COPD, infections, cardiac diseases, Guillain-Barré syndrome, Drug overdose with a resp depressant, Paralysis of resp muscles, obesity, inadequate mechanical ventilation

356

seen with chronic respiratory acidosis

Symptoms may be suddenly increased pulse, respiratory rate and BP, mental changes, feeling of fullness in head
Potential increased intracranial pressure

357

respiratory alkalosis is always due to

hyperventilation (CO2 eliminated)

358

some causes of hyperventilation and thus respiratory alkalosis

Pulmonary disorders (pneumonia, embolism)
Acute anxiety
Stimulant drugs (epinephrine)
Neural disorders (stroke, intracranial lesions)

359

S/S of respiratory alkalosis

lightheadedness, inability to concentrate, numbness and tingling, hand feel like fingers are contracting, sometimes loss of consciousness

360

nursing dx for respiratory acidosis

Activity intolerance
Disturbed thought processes
Impaired gaseous exchange
Risk for decreased cardiac output (as acidosis increases)
Risk for injury

361

see slide 90 for tip to remember lab values

...

362

understand case study on slides 91 and 92

patient has metabolic acidosis
is kind of question that will be on test

sodium high due to dehydration
potassium high--mvmt from dead cells to circulation

363

steroids act

inside cell

364

peptides act

on cell surface

365

thyroid test

TSH
T3 and T4

366

parathyroid tests

PTH
Calcium
Phosphorus

367

endocrine system is closely linked to

nervous system and immune system

368

pituitary tests

GH
ADH
Urine Specific Gravity
ACTH(adrenocorticotropic hormone)

369

adrenal tests

Cortisol
24-Hour Urine for VMA( pheochromocytoma)

370

pancreatic function tests (diabetes)

Fasting Plasma Glucose
Oral Glucose Tolerance Test
Glycosylated Hemoglobin

371

diabetes insipidus and its patho

Is a disorder of the posterior lobe of pituitary gland

Insufficient ADH (vasopressin) or renal resistance to the hormone
Kidneys Do Not Reabsorb Water
Diurese 3-15 L per Day –large volumes of dilute urine.

372

causes of diabetes insipidus

Pituitary Tumor or Trauma
Infection of CNS –meningitis, encephalitis, tuberculosis
Drugs –lithium and declomycin
Psychogenic (extremely large fluid intake)
Nephrogenic (enough ADH but kidneys do not respond to it)

373

S/S of diabetes insipidus

Polyuria
Polydipsia (extreme thirst)
Nocturia
Dilute Urine (colorless)
Dehydration
Hypovolemic Shock
Decreased LOC
Death

374

urine specific gravity is biggest sign of diabetes insipidus and is what level

<1.005

375

diabetes insipidus often presents with

hypernatremia

376

nursing dx for diabetes insipidus

Risk for Deficient Fluid Volume
Risk for Electrolyte Imbalance
Risk for Ineffective Health Maintenance
Knowledge Deficit
Risk for Disturbed Thought Processes
Acute confusion
Disturbed Sleep Pattern
Impaired Comfort

377

The nurse is assessing a patient at admission with the diagnosis of Diabetes Insipidus. Assessment finding consistent with this diagnosis would be:

Warm/flushed skin, dizzy upon standing, B/P 108/54, T 99.4, “sticky” eyelids

378

primary disorder of endocrine system

organ/gland isn't functioning properly

379

secondary disorder of endocrine system

something else is causing malfunction of organ/gland

380

SIADH

syndrome of inappropriate ADH (antidiuretic hormone)

381

patho of SIADH

Too Much ADH
Water Retention
Hyponatremia
Decreased Serum Omolality

382

causes of SIADH

Cancers
Bronchogenic Lung Cancer
Drugs – oncovin, tricyclic antidepressants, thiazide diurestics, phenothiazines
Head Trauma
Brain Tumor

383

S/S of SIADH

Weight Gain Without Edema
Dilutional Hyponatremia
Serum Osmolality <275 mOsm/kg
Concentrated Urine
Muscle Cramps and Weakness
Brain Swelling, Seizures, Death

384

tests for SIADH

Serum/Urine Sodium
Serum/Urine Osmolality
Water Load Test

385

nursing dx for SIADH

Excess Fluid Volume
Risk for Ineffective Health Maintenance

386

A nursing assessment (nursing order) appropriate for nursing diagnosis of Excess fluid volume would be:

daily weight

387

S/S in adults with hypopituitary

Weakness
Hypoglycemia
Sexual Dysfunction
Risk for Cardiovascular Disease
Risk for Cerebrovascular Disease

388

tests for hypopituitary

GH Level
GH Response to Induced Hypoglycemia
CT/MRI for Tumor