Lipase
enzyme that aids in digestion of fats
trypsin and pepsin
aids in digestion of proteins
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.
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.
chyme
food moving from stomach to small intestine
mouth enzymes
saliva, salivary amylase
stomach enzymes
hydrochloric acid, pepsin, intrinsic factor
small intestine enzymes
amylase, lipase, trypsin, bile
dyspepsia
indigestion
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
aspirin can make:
black stool
berium enema can make
white stool
Blood tests for GI
CBC and Chemistry
AST (Aspartate Aminotranferase)
ALT (Alanine Aminotransferase)
Amylase and Lipase
Bilirubin
Carcinoembryonic antigen (CEA)
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
see slides: 11 and 12
for referred pain and abdominal quadrants and regions
...
order to complete abdominal assessment
Inspection, auscultation, palpation, percussion
know times for diagnosing hypo,hyper active bowel sounds and what is normal
...
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
false positive can occur for fecal occult blood tests with:
vit. C, NSAIDs, ASA, Red meat within 72 hours prior
high eisinophil count is indicative of:
parasitic infection
can be found through CBC count:
parasitic infection, ulcers, anemia
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.
amylase is elevated within 12-24 hours of:
lipase remaining elevated is also extreme indicator of same issue
acute pancreatitis
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
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.
breath test used for:
checking for h-pylori (ulcers)
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)
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)
monitor _____ after colonscopy
for hemorrhaging
and VS
patient will be gassy- bowel pumped with gas for procedure
hyatal hernia, cancer, GERD (Chapter 35) only for test
...
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
Hiatal hernia
Protrusion of a portion of the stomach thru an opening (hiatus) in the diaphragm lying next to the esophagus.
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
Rolling (paraesophageal) hiatal hernia
fundus and greater curvature of the stomach “roll” up thru the diaphragm, forming a pocket alongside the esophagus.
see slide 26 for hernia pictures
...
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.
clinical manifestations of hiatal hernia
similar to GERD, and may mimic GB disease, angina, and peptic ulcer disease. MAY BE ASYMPTOMATIC.
tests for hiatal hernias
Barium Swallow, x-rays, fluoroscopy
Gastroesophageal Reflux Disease (GERD)
Backward flow of GI contents in to the esophagus- at the lower esophageal sphincter
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)
things to ask about for assessing GERD
health history, evaluate complaints r/t heartburn, note relieving factors
diagnostics for GERD
Endoscopy or barium swallto
T or F
Barrett’s esophagus is a condition in which the lining of the esophageal mucosa is altered.
True
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
Fibrosis and scarring accompanying healing process in GERD can
results in the narrowing of lumen (stricture) that causes dysphagia
GERD complications:
barretts epithelium, fibrosis and scarring, Esophageal ulceration, hemorrhage, aspiration pneumonia
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
types of esophageal cancer
Squamous-cell most common, adenocarcinoma is increasing in incidence
predisposing factors for esophageal cancer
Smoking, Excessive alcohol intake, Chronic trauma, Barrett’s esophagus, Spicy foods, Poor oral hygiene, GERD
clinical manifestations of esophageal cancer
usually don’t appear until later stages but may include: dysphagia, pain (epigastric, substernal, back) that increases with swallowing
assessment for esophageal cancer
Assess risk factors for esophageal cancer, pain, dysphagia, and nutrition status
diagnostics for esophageal cancer
EGD, Biopsy
nursing DX with esophageal cancer
Altered nutrition (may necessitate need for feeding tube), Pain, Fluid Volume Deficit, Risk for aspiration, Anxiety
nasogastric tube is inserted:
through the nose to the stomach
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
any kind of tube that provides nutrition
enteric tube...includes NG, gastric, duodenum, jejunum
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
T or F:
The nasogastric tube is secured to the nose with tape to prevent injury to the nasopharyngeal passages.
True
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
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
Gastrostomy or jejunostomy tubes are for:
long term feeding
Nasogastric or nasoenteral tubes are for:
shorter term feeding
advantages of tube feeding
Intermittent bolus feedings
Intermittent gravity drip
Continuous infusion
Cyclic feeding
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
bolus gastrostomy feeding utilize ____ to administer bolus
gravity
once goal rate of ordered enteral feeding is reached and patient is tolerating it then:
continue checking every 8 hours
nasoenteric feeding rate is controlled by:
continuous controlled pump
What position should the patient’s head be in when receiving a tube feeding to prevent aspiration?
semi-fowlers...at least 30-45 degrees
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.
monitor _______ every 4 hours and admin ______ when needed for patients that are enteral
blood sugar, insulin
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
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
potential complications of enteral
Diarrhea
Nausea and vomiting
Gas/bloating/cramping
Dumping syndrome
Aspiration pneumonia
Tube displacement
Tube obstruction
Nasopharyngeal irritation
Hyperglycemia
Dehydration and
potential complications of gastrostomy feeding
Wound infection
GI bleeding
Premature removal of tube
Aspiration
Constipation
Diarrhea
dumping syndrome
can be caused by enteral feeding because food moves too quickly through the intestines....causes diarrhea, nausea, etc
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.
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.
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
enteral tube..what size syringe should you use
30 ml or larger
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
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.
administer feeding slowly to avoid
dumping syndrome
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.
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
proper dressing of G tube (gastrostomy tube)
usually 4x4 pad
and clean site every 8 hours around tube site
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
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
TPN
total parental nutrition
what is total parenteral admixture
An admixture of lipid emulsions, proteins, carbohydrates, electrolytes, vitamins, trace minerals, and water.
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.
what substance is best indicator of good nutrition and should be monitored for PN patients?
pre-albumin
when monitoring VS of PN patients always check
temperature- infection from tubing is common
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.
don't hang TPN over
24 hours
TPN is administered by
central line
potential problems and collaborative problems of TPN
Pneumothorax
Clotted or displaced catheter
Sepsis
Hyperglycemia
Rebound hypoglycemia
Fluid overload
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.
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
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.
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
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
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
signs and symptoms of protozoa infection
diarrhea, gastroenteritis, malaria
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.
gastritis
Inflammation of the stomach (gastric mucosa)
A common GI problem
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.
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.
Erosive gastritis
mucosal damage
cells secrete HCL or pepsinogen and intrinsic factor
acute gastritis S/S
abdominal discomfort, headache, lassitude, nausea, vomiting, hiccuping.
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.
gastritis may be associated with
achlorhydria, hypochlorhydria, or hyperchloryhydria.
most common site of peptic ulcer
duodenum
gastritis is usually diagnosed by
UGI X-ray or endoscopy and biopsy.
gastritis nursing Dx's
Anxiety
Imbalanced nutrition
Risk for fluid volume imbalance
Deficient knowledge
Acute pain
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
dietary assessment for peptic ulcer
Dietary intake and 72 hour diet diary
proton pump inhibitor for peptic ulcer should be taken when?
30 min prior to meal
two biggest factors for risk for gastric disorders and diseases
smoking and alcohol
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.
gastric cancer is diagnosed by
EGD with biopsy
Ultrasound –presence of tumors
CT
nursing Dx with gastric cancer
Anxiety
Imbalanced nutrition
Pain
Anticipatory grieving
Deficient knowledge
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.
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
complications with constipation
Hypertension
Fecal impaction
Hemorrhoids
Fissures
Megacolon
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
metabolic and endocrine disorders can cause
diarrhea
Borborygmus
a rumbling or gurgling noise made by the movement of fluid and gas in the intestines
Tenesmus
a clinical sign, where there is a feeling of constantly needing to pass stools, despite an empty colon.
diagnosis criteria for IBS
criteria of recurrent abdominal pain or discomfort for at least 3 days a month in last 3 months
IBS is more common in
women than men
appendicitis is most common from
age of 10-30
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
appendicitis is diagnosed by
abd assessment, CBC (shows elevated WBC’s), x-ray, ultrasound, CT
most common site of diverticulitis
sigmoid colon
never use warm compress for abdominal pain
could rupture appendix
diverticulum
sac-like herniation's of the lining of the bowel that extend through a defect in the muscle layer
diverticulosis
multiple diverticula without inflammation
diverticulitis
infection and inflammation of diverticula
usually caused by severe constipation
diverticular disease increases with
age
and low fiber diet
diverticulitis symptoms
mild or severe pain in lower left quadrant, nausea, vomiting, fever, chills, and leukocytosis.
ways to diagnose diverticular disease
Barium Enema, Colonoscopy, CT with contrast, CBC, ESR
complications of diverticular disease
Perforation, Peritonitis, Abscess formation, Bleeding, fistula (where bowel joins with another organ)
Abdominal pain and diarrhea are common clinical manifestations of
chrohn's disease
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
S/S of chrohn's
DIARRHEA, abdominal pain, cramping, tenderness developing into weight loss, malnutrition, dehydration, electrolyte imbalances
tests for chrohn's
barium studies, colonoscopy, sigmoidoscopy, bx performed, CBC, ESR, Decreased albumin and protein
pre-albumin is decreased
with Chrohn's because they're not digesting protein well
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
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
clinical manifestations of ulcerative colitis
exacerbations & remissions, diarrhea, passage of watery mucus & pus, LLQ abdominal pain, rectal bleeding, pallor, anemia, and fatigue
tests for ulcerative colitis
Barium series, Sigmoidoscopy, Colonoscopy, CBC (High WBC), Low H & H
mechanical intestinal obstruction
bowel is obstructed by disorders outside of the intestine or by blockages in the lumen of the intestine
Nonmechanical (paralytic ileus)- intestinal obstruction
result of neuromuscular disturbance resulting in decreased or absent peristalsis causing back up of intestinal contents
see slide 96 for three causes of intestinal obstructions
...
causes of hernias
increased inta-abd pressure by coughing, straining, and heavy lifting. Obesity, pregnancy, and poor wound healing are other risk factors
hernia
weakness in the abdominal muscle wall thru which a segment of bowel or other abd structure protrudes
inguinal hernia
located in the groin where the spermatic cord in males or the round ligament in females emerges from the abd wall.
umbilical hernia
are seen most often in obese women and in children. They are caused by a failure of the umbilical orifice to close
incisional hernia
(Ventral) usually result from a weakness in the abdominal wall following abd. surgery
see slide 98 for more hernia info
...
patho of colo-rectal cancer
cancer of colon and rectum predominantly adenocarcinoma.
The second cause of cancer deaths in the United States.
start again on slide 99
...
RBCs are broken down by liver...have life span of about 3 months...liver breaks it down into:
bile
liver stores glucose
for times of high energy requirements:
exercise, fight or flight, etc.
liver makes _______ factors
clotting
blood flows through liver by:
very fine capillary system...because blood has to come into contact with hepatocytes
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)
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
clay color stool caused by:
lack of bile from liver dysfunction
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
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
ESR erythrocyte sedimentation rate
tells us there is inflammation in body
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
urobilirubin
bilirubin in urine
PT -- prothrombin time
test for clotting time
<2.0 (times reference)-- normal time for someone not on warfarin)
varies by age and gender
serologic tests
shows disease process
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
transmission routes of hepatitis
concentrated in stool during incubation period (common transmission worldwide is contaminated H2O)
undercooked shellfish
prevention of hepatitis
cleanliness, vaccines (HAV,HBV), standard precautions
washing produce, hands, etc
hepatitis B transmitted
blood born: sexual contact, sharing drug needles, parenteral (in utero)
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
autoimmune hepatitis
more common in women, rare
associated with graves, type I diabetes, myethenia gravis, etc
hepatitis A transmitted via:
hepatitis B transmitted via:
ingestion
body fluids
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
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
complications of Hepatitis and fulminant liver failure
Metabolic Alkalosis
Hypokalemia
Hypoglycemia
Clotting Disturbances
Sepsis
Renal Failure
Respiratory Failure
diagnostic tests for fulminant liver failure
ALT
AST
Serum Bilirubin
Urobilinogen
Biopsy
Blood Glucose
PT
Ultrasound
etiology of chronic liver failure -- Cirrhosis
Chronic Alcohol Ingestion
Hepatotoxins
Hepatitis
Gallbladder Obstruction
Heart Failure
pathophysiology of cirrhosis
Inflammation of Liver Cells
Infiltration with Fat and WBCs
Fibrotic Scar Tissue Replaces Liver Tissue
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
complications of cirrhosis
renal failure, clotting defects, ascites, portal hypertension, encephalopathy
Dx testing for cirrhosis
liver enzymes, bilirubin, urobilinogen, serum ammonia, PT, abdominal x-ray, UGI series, liver scan, EGD (esophogus- endoscopic test), liver biopsy
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
candidates for liver transplant
liver failure, no cancer, no complications, otherwise stable
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
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)
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)
complications of acute pancreatitis
Cardiovascular Failure
Acute Respiratory Distrss Syndrome
Renal Failure
Hemorrhage
Infection
DX tests for acute pancreatitis
Serum Amylase – 30 – 110 u/L
Serum Lipase – 3 – 73 u/L
X-Ray
CT
Ultrasound
Nursing DX for acute and chronic pancreatitis
Pain
Imbalanced Nutrition
Risk for Ineffective Breathing Pattern
Risk for Injury
gall bladder disorders
Cholecystitis: Inflammation
Cholelithiasis: Stones
Choledocholithiasis: Stones in Common Bile Duct (can damage liver if left untreated)
etiology of gall bladder disorders
Stasis
High Cholesterol Intake
Fasting
Sedentary Lifestyle
Family History
More Common in Women
Pregnancy
Risk Increases with Age
S/S of gall bladder disorders
Increased Vital Signs
Vomiting
Jaundice
Epigastric Pain
RUQ Tenderness
Nausea
Indigestion
Positive Murphy’s Sign
Biliary Colic (pain)
complications of gall bladder disorders
Cholangitis
Necrosis/Perforation of GB
Empyema
Fistulas
Adenocarcinoma of GB
Pancreatitis
four F's of gall bladder disorder
female,fat,over 40,fertile
Dx tests for gall bladder
WBC
Serum Amylase
X-Ray
Nuclear Scan
Ultrasound
Nursing Dx for gall bladder disorders
Acute Pain
Risk for Deficient Fluid Volume
Risk for Impaired Skin Integrity
Risk for Ineffective Breathing Pattern
Third spacing
loss of ECF into space that does not contribute to equilibrium
ICF:
ECF:
fluid in cells-- 2/3rds of body fluid
fluid outside cells- intravascular,interstitial, and transcellular
transcellular ECF
cerebrospinal, percardial,synovial
interstitial ECF
lymph
intravascular ECF
fluid in lood vessels- aka plasma
Ascites that occurs with liver disease is categorized as
third spacing fluid
cations
positively charged ions
major types: sodium,potassium,calcium,magnesium,hydrogen ions
anions
negatively charged ions
chloride,bicarbonate,phosphate,sulfate, and proteinate ions
intracellular and extracellular fluids differ in terms of
electrolyte balance
hydrostatic pressure
exerted on walls of blood vessels (as in ascites)
osmotic pressure
exerted by protein in plasma
fluid is shunted to area higher in protein
Direction of fluid movement depends on differences of
hydrostatic and osmotic pressures
osmosis
area of low solute concentration to area of high solute concentration across membrane walls. No energy required. Water moves.
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
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
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
soduim-potassium pump
maintains higher concentration of extracellular sodium, intracellular potassium
isotonic
has same osmolarity as blood plasma (0.9% salt)
hypertonic
has greater osmolarity than blood plasma -- higher concentration of salt
hypotonic
lower osmolarity than blood plasma (pt dehydrated but electrolytes are normal)
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
isotonic IV solutions
Normal Saline (0.9%NS)
Lactated Ringer’s (LR)- contains other electrolytes
hypotonic IV solution:
D5W:
½ Normal Saline (0.45%NS)
D5W has no salt
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
route of fluid gain
Dietary intake of fluid, food or enteral feeding
Parenteral fluids
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
study slide 15 for RAAS and effects of imbalance of fluids and electrolytes
...
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
Fluid volume deficit - FVD
hypovolemia- dehydration
Fluid volume excess - FVE
hypervolemia- fluid volume overload
dehydration
loss of water along with increased serum sodium level
GI suctioning can cause
dehydration
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)
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
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
factors contributing to FVE
heart failure, renal failure, cirrhosis of liver
excessive dietary sodium or sodium-containing IV solutions
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
pitting edema
stays down
regular edema returns
JVD is
jugular vein distention measured at 45 degree angle
should be 3 mm or less
hyponatremia
Serum sodium less than 135 mEq/L
causes of hyponatremia
adrenal insufficiency, water intoxication, Syndrome of Inappropriate Antidiuretic Hormone (SIADH) or losses by vomiting, diarrhea, sweating, diuretics
manifestations of hyponatremia
poor skin turgor, dry mucosa, headache, decreased salivation, decreased BP, tachycardia, nausea, abdominal cramping, neurologic changes (confusion)
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
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
the nurse should monitor labs for ____________ and ________________________ when caring for the hyponatremic patient
Decreased serum and urine sodium
Decreased urine specific gravity & osmolarity
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
hypernatremia
serum sodium greater than 145 mEq/L
causes of hypernatremia
excess water loss, excess sodium administration, diabetes insipidus, heat stroke, hypertonic IV solutions , hyperventilation
manifestations of hypernatremia
thirst; elevated temperature; dry, swollen tongue; sticky mucosa; neurologic symptoms; restlessness; weakness; increased pulse and BP
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
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
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
hypokalemia causes
GI losses (bulimia, starvation), medications, alterations of acid-base balance(alkalosis), hyperaldosterism, poor dietary intake
manifestations of hypokalemia
fatigue, anorexia, nausea, vomiting, dysrhythmias, muscle weakness and cramps, paresthesias, glucose intolerance, decreased muscle strength, DTRs (deep tendon reflexes)
nursing assessments for hypokalemic patients
severe hypokalemia is life-threatening, monitor ECG and ABGs, dietary potassium, IV potassium administration, monitor labs
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
hyperkalemia
Serum potassium greater than 5.0 mEq/L
tissue damage results in hyperkalemia D/T _____________ is released into blood stream resulting in ________________________________
potassium
heart failure
causes of hyperkalemia
usually treatment related, impaired renal function, hypoaldosteronism, tissue trauma, acidosis
manifestations of hyperkalemia
cardiac changes and dysrhythmias, muscle weakness with potential respiratory impairment, paresthesias, anxiety, GI manifestations, death
Hemolysis of blood specimen or drawing of blood above IV site may result in false laboratory result
when testing for
hyperkalemia
potassium sparing diuretics should not be used by
patients with renal dysfunction
nursing DX for hyperkalemia
Risk for Activity Intolerance
Risk for Decrease Cardiac Output
If patients is isotonic and isotonic solution is administered where will fluid be pulled? the circulatory system or tissues?
tissues
hypertonic solution- what direction will fluid be pulled?...circulatory or tissue
from cells into circulatory system
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
two biggest electrolytes we are concerned with
potassium and sodium
role of calcium
Proper function of excitable tissues, especially cardiac muscle.
Adequate blood clotting
Structural support to bones and teeth
causes of hypocalcemia
hypoparathyroidism, malabsorption, pancreatitis, alkalosis, massive transfusion of citrated blood, renal failure, medications, open wounds
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
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
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
nursing dx for hypocalcemia
Activity intolerance r/t neuromuscular irritability
Imbalanced nutrition
Ineffective breathing pattern r/t laryngospasm
tetany
tense muscles from hypocalcemia
hypercalcemia
serum level above 10.2 mg/dL
causes of hypercalcemia
malignancy of bone, hyperparathyroidism, bone loss related to immobility, prolonged use of thiazide diuretics
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)
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
often times with hypocalcemia
will see increase in CO2 levels because of insufficient breathing
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
trousseau's sign is seen with
hypocalcemia
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
hypomagnesemia
Serum level less than 1.6 mg/dL (normal range 1.6 – 2.6 mg/dL), evaluate in conjunction with serum albumin
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
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)
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
hypomagnesemia often accompanies
hypocalcemia
dysphagia is common in patients with
hypomagnesemia
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
hypermagnesemia
Serum level more than 2.6 mg/dL
causes of hypermagnesemia
renal failure, diabetic ketoacidosis, excessive administration of magnesium, Addison’s disease
S/S of hypermagnesemia
flushing, lowered BP & shallow respirations, nausea, vomiting, hypoactive reflexes, drowsiness, muscle weakness, depressed respirations, ECG changes, dysrhythmias
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
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
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
hypophosphatemia
Serum level below 2.5 mg/dL (normal 2.5 – 4.5 mg/dL)
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
S/S of hypophosphatemia
neurologic symptoms (irritability, dysphagia, diplopia, seizures), confusion, muscle weakness, tissue hypoxia, muscle and bone pain (osteomalacia), increased susceptibility to infection
high glucose causes
hypophosphatemia
nursing assessment for hypophosphatemia
evaluate intake of foods high in phosphorus, monitor labs, monitor LOC
nursing dx for hypophosphatemia
similar to other electrolytes
hyperphosphatemia
Serum level above 4.5 mg/DL
causes of hyperphosphatemia
renal failure, excess phosphorus, excess vitamin D, acidosis, hypoparathyroidism, chemotherapy
S/S of hyperphosphatemia
few symptoms; soft-tissue calcifications, symptoms occur due to associated hypocalcemia
labs for hyperphosphatemia
Serum phos & Ca+, BUN & Creatitine (renal failure)
nursing assessment for hyperphosphatemia
evaluate avoiding high-phosphorus foods; patient understanding related to diet, phosphate-containing substances, signs of hypocalcemia
calcium and ____________________ have an antagonistic relationship (levels affect eachother)
phosphorous
if one goes up the other goes down
compare and highlight flashcards (see powerpoint slides)
...
normal pH of:
water
blood
7.0
7.35-7.45
normal cell function depends on regulating
hydrogen ions (H+)
as hydrogen production increases
pH decreases
acid
substance that releases Hydrogen ion
base (alkali)
binds hydrogen
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
______________ is the body's first attempt at maintaining pH levels
bicarbonate (carbonic acid buffering system)
the _______________ are the second line of defense in maintaining acid-base balance
lungs-- rapid compensation
the last line of defense in pH maintenance is
the kidneys- slow to compensate
other buffer systems (not as important to know)
ECF: inorganic phosphates, plasma proteins
ICF: proteins, organic, inorganic phosphates
Hemoglobin
excessive hydrogen ions means the patient will be
acidic
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
fixed acids (not converted to gases) and bicarbonate are managed by
kidneys
how do kidneys regulate pH
by secreting H+ into urine or by regenerating HCO3 for reabsorption into the blood
CO2 lowers pH when you exhale you
alkalize the body -- get rid of hydrogen ions
CO2 is biggest portion of acid in blood stream
kidney regulation of acid-base works until
pH is <4.5
PaO2
partial pressure of oxygen in arterial blood
PaCO2
is the partial pressure of carbon dioxide and is a reflection of the pulmonary ventilation (35-45 mm Hg)
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
bicarbonate (HCO3)
is a common base in the body and a major renal component of acid-base (22-26 mEq/L)
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%
What is the most common buffer system in the body?
Bicarbonate-carbonic acid
analysis of ABGs gives what info
Determines type of imbalance
Evaluates degree of compensation
the body's major extracellular buffer system is bicarbonate-carbonic acid buffer system which is assessed by
analysis of ABGs
blood draw for ABG should be from
an artery
acidemia
alkalosis
pH <7.35
pH >7.45
evaluate symptoms, med dx, tx's
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)
see slide 73 for ABG value chart
...
metabolic alkalosis usually occurs
with ng suctioning or vomitting
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
causes of metabolic acidosis
Lactic acidosis, diabetic ketoacidosis, azotemic, diarrhea
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
with metabolic acidosis _________________ occurs as potassium shifts out of the cells (cell death) and into the circulatory system
hyperkalemia
_____________ should be monitored with metabolic acidosis
potassium levels
serum calcium levels should be corrected during tx of
acidosis
hypokalemia can cause
metabolic alkalosis
S/S of metabolic alkalosis
symptoms related to decreased calcium, respiratory depression, tachycardia, symptoms of hypokalemia
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
respiratory acidosis is always due to
respiratory problem with inadequate excretion of CO2 (hypoventilatory states)
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
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
respiratory alkalosis is always due to
hyperventilation (CO2 eliminated)
some causes of hyperventilation and thus respiratory alkalosis
Pulmonary disorders (pneumonia, embolism)
Acute anxiety
Stimulant drugs (epinephrine)
Neural disorders (stroke, intracranial lesions)
S/S of respiratory alkalosis
lightheadedness, inability to concentrate, numbness and tingling, hand feel like fingers are contracting, sometimes loss of consciousness
nursing dx for respiratory acidosis
Activity intolerance
Disturbed thought processes
Impaired gaseous exchange
Risk for decreased cardiac output (as acidosis increases)
Risk for injury
see slide 90 for tip to remember lab values
...
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
steroids act
inside cell
peptides act
on cell surface
thyroid test
TSH
T3 and T4
parathyroid tests
PTH
Calcium
Phosphorus
endocrine system is closely linked to
nervous system and immune system
pituitary tests
GH
ADH
Urine Specific Gravity
ACTH(adrenocorticotropic hormone)
adrenal tests
Cortisol
24-Hour Urine for VMA( pheochromocytoma)
pancreatic function tests (diabetes)
Fasting Plasma Glucose
Oral Glucose Tolerance Test
Glycosylated Hemoglobin
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.
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)
S/S of diabetes insipidus
Polyuria
Polydipsia (extreme thirst)
Nocturia
Dilute Urine (colorless)
Dehydration
Hypovolemic Shock
Decreased LOC
Death
urine specific gravity is biggest sign of diabetes insipidus and is what level
<1.005
diabetes insipidus often presents with
hypernatremia
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
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
primary disorder of endocrine system
organ/gland isn't functioning properly
secondary disorder of endocrine system
something else is causing malfunction of organ/gland
SIADH
syndrome of inappropriate ADH (antidiuretic hormone)
patho of SIADH
Too Much ADH
Water Retention
Hyponatremia
Decreased Serum Omolality
causes of SIADH
Cancers
Bronchogenic Lung Cancer
Drugs – oncovin, tricyclic antidepressants, thiazide diurestics, phenothiazines
Head Trauma
Brain Tumor
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
tests for SIADH
Serum/Urine Sodium
Serum/Urine Osmolality
Water Load Test
nursing dx for SIADH
Excess Fluid Volume
Risk for Ineffective Health Maintenance
A nursing assessment (nursing order) appropriate for nursing diagnosis of Excess fluid volume would be:
daily weight
S/S in adults with hypopituitary
Weakness
Hypoglycemia
Sexual Dysfunction
Risk for Cardiovascular Disease
Risk for Cerebrovascular Disease
tests for hypopituitary
GH Level
GH Response to Induced Hypoglycemia
CT/MRI for Tumor