NURS 366 exam 3 study guide

normal changes in the integumentary system due to aging

-skin injuries and infection become more common
-the sensitivity of the immune system is reduced
-muscles become weaker and bone strength decreased
-sensitivity to sun exposure increases
-the skin becomes dry and often scaly
-hair thins and changes color
-sagging and wrinkling occur
-the ability to lose heat decreases
-skin repairs process slowly

skin injuries and infection become more common with age due to

epidermis thins as stem cell activity declines

the sensitivity of the immune system is reduced with aging due to

the amount of macrophages residing in the skin decreasing

muscles become weaker and bone strength decreases with age due to

reduced calcium and phosphate absorption from declined vitamin D3 production

sensitivity to sun exposure increases with age due to

less melanin production from decreased melanocyte activity (pale skin)

skin becomes dry and scaly with age because

glandular activity declining reducing oil and sweat production

hair thins and changes color with age because

follicles stop functioning or produce thinner finer hairs

decreased melanocyte activity creates gray or white hair

sagging and wrinkling of the skin occurs with age due to

dermis becomes thinner and the elastic fiber network decreases in size

the skin becomes weaker and less resilient

the ability to lose heat decreases with age because

blood supply to the dermis is reduced

sweat glands become less active

combination makes older clients less able to lose heat

overexertion and overexposure to high temperatures can be dangerous

skin repair in older adults

takes 6-8 weeks when compared to 3-4 weeks for younger adults

pruritus s/s

itching

eczema s/s

-red to brownish gray colored patches
-itching, which may be severe especially at night
-small, raised, bumps which may leak fluid and crust over when scratched
-thickened, cracked, or scaly skin
-raw sensitive skin from scratching

dermatitis s/s

-swelling
-red
-itchy
-lesions

psoriasis vulgaris s/s

-bright red areas of raised patches (plaques) on the skin, often covered with loose silvery scales
-localized or general
-itchy

acne vulgaris s/s

-blackheads
-whiteheads
-pustules
-on the face, neck, upper back

skin tear s/s

-acute traumatic wounds
-not pressure ulcers
-separation of epidermis and dermis

stage I pressure ulcer

reddened area
nonblanchable

pressure ulcer is starting to develop

stage II pressure ulcer

-skin blisters
-forms open sore
-may be red and irritated

stage III pressure ulcer

breakdown looks like a crater

damage to the tissue below the skin

stage IV pressure ulcer

deep damage to the muscle and bone and sometimes tendons and joints

sunburn s/s

UV rays exceed what can be blocked by melanin resulting in a burn on the skin

cellulitis s/s

-heat
-tenderness
-edematous
-erythema
-chills
-fever
-malaise

shingles s/s

-grouped vesicles
-unilateral on trunk, face, and lumbosacral areas
-burning
-mild to severe during outbreak
-neuralgia preceding outbreak

causative agent for pallor (skin color)

anemia

causative agent for cyanosis (skin color)

respiratory issues

causative agent for jaundice (skin color)

liver issues

compartment syndrome (orthopedic treatment complication)

increased pressure in a limited anatomical space (splint, cast, crush injury, edema)

fat emboli (orthopedic treatment complication)

catecholamines mobilize fatty acids from adipose tissue

Discuss the care of patient's in traction regarding mobility and skin care

-assess skin throughout
-weights keep hanging free
-maintain ropers over midline
-maintain patient alignment

normal anatomy and physiology of the musculoskeletal system

206 bones, tendons, ligaments, cartilage

musculoskeletal system functions

-support
-movement
-protection
-blood cell production
-calcium and phosphorous storage

bone remodeling

resorption
reversal
formation
resting

resorption (bone remodeling)

osteoclasts remake bone mineral and metric, creating an erosion cavity (3-4 weeks)

reversal (bone remodeling)

mononuclear cells prepare bone surface for new osteoblasts to begin building bone

formation (bone remodeling)

osteoblasts synthesize a matrix to replace resorbed bone with new bone (3-4 months)

resting (bone remodeling)

a prolonged resting period until a new remodeling cycle begins

normal changes of the musculoskeletal system with aging

-decreased muscle mass, size and muscles look smaller
-decreased muscle tone
-decreased amount of elastic tissue
-slower muscle response
-decrease in elasticity of tendons and ligaments
-decreased range of motion (stiffness)
-decreased joint mobility
-osteoporosis: thinning and softening of the bone

knee replacement pre-op education

-weight bearing within 24 hours of surgery
-elevate leg when sitting
-s/s of infection, PE, atelectasis, urinary retention, skin breakdown, constipation, pain, DVT
-weight bearing restrictions, isometric exercises, need for early ambulation, pneumatic compression (SCD)
-drains
-heparin, lovenox, aspirin
-labs: CBC, coagulation, CXR, EKG, UA

knee replacement post-op education

-VS, LOC, TCDB, pain management, nutrition, prevention of infection
-watch for: constipation, urinary retention, venous stasis, CMS, respiratory complications, changes in skin integrity
-PT, PTT, INR, check for bleeding
-correct position of the operative extremity, neuromuscular checks, progressive ambulation

home care for knee replacement

-1-3 days hospitalization then rehab
-rehab phase post-op is a year
-maximum strength and flexibility takes about 3 years to return
-anticoagulant use continues
-need for low impact exercises
-venous foot pumps and or pneumatic compression
-blood transfusions (autologous or homologous)
-weight bearing restrictions
-assistive devices: cane, crutches, walker

patient education & home care for hip replacement

-do not bend hip more than 90 degrees
-do not cross legs when sitting
-do not bend body forward to pick up objects
-do not rotate leg when standing, keep leg straight, no pigeon feet
-possible high blood loss during surgery
-drains: hemovac, JP
-cell saver
-keep legs abducted: use of pillows
-HOB 45 degrees or less
-do not flex operative, bend, or scissor legs
-ambulate POD 1-2
-check CMS

lumbar laminectomy and discharge needs

-gradually return to normal ADLs
-no heavy lifting for 4-6 weeks
-no bending, twisting or lifting
-no sitting for extended periods of time for 6 weeks including car rides
-instruct patient to take short walks to avoid fatigue
-change position frequently
-may resume sex in two weeks
-return to work dependent on occupation
-assure patient has assistance for ADLs, cleaning, and child care

portal hypertension

the elevation of blood pressure within the portal venous system

portal hypertension complications

-Right sided HF
-Anorexia
-Esophageal and gastric varices
-Periumbilical varices
-Ascites
-Uncontrolled bleeding
-Associated with cirrhosis
-When alcoholic liver disease is left untreated it can lead to cirrhosis, portal hypertension and liver failure

causative factors of pancreatitis

alcohol, biliary sludge, trauma, post-ERCP, hypertrogliceridemia, biliary tract obstruction, hyperparathyroidism, steroids, cancer, mumps, smoking, nicotine

pancreatitis pathophysiology

stimulant / irritant → enzymes activated in pancreas → autodigestion → severe inflammation and necrosis
-Enzymes and necrosis leaks into circulation→ shock, DIC, ARDS
-Enzymes leak into peritoneum; destruction and inflammation → severe pain, hemorrhage shock, peritonitis, sepsis

liver lab tests

-Total protein
-Albumin
-AST/ALT (liver tissue): show inflammation and injury
-Alk Phos: seen in bile duct disorders
-Bilirubin
-Ammonia: changed into urea
-GGT (obstruction): needed for protein synthesis, most sensitive to hepatobiliary diseases
-Coagulation labs
-Ammonia
-ALP (obstruction)

Cirrhosis AST/ALT ratio

>1

Hepatitis AST/ALT ratio

<1

hepatitis A labs

elevated ALT & AST

hepatitis B labs

elevated ALT & AST

hepatitis C labs

elevated ALT & AST

cirrhosis labs

LFT elevated then normal

primary biliary cirrhosis labs

elevated GGT and alk phos

+ ANA

alcoholic cirrhosis labs

-elevated ALT & AST
-thrombocytopenia
-hypoglycemia
-elevated neutrophils

alcoholic steatohepatitis labs (alcoholic liver disease)

Decreased neutrophils and phagocytes

Reduced NKs

Impaired cytotoxic T cells

fibrosis labs
(alcoholic liver disease)

Decreased NKs

alcoholic cirrhosis labs
(alcoholic liver disease)

Decreased NK
Decreased dendritic cells (DC)
Decreased B cells

alcoholic liver disease labs

elevated ALT & AST

fatty liver disease labs

-Increased LDLs
-Increased interleukin 6
-Increased CRP
-Hyperglycemia
-Hyperlipidemia
-Hyperinsulinemia

In general levels of ALT and AST are ___ in liver impairment

elevated

purpose of common medications utilized with liver impairment

???

cirrhosis nursing care

-Health promotion and prevention of risk factors: malnutrition, alcohol use, hepatitis, biliary obstruction, obesity, right sided HF
-Urge patients to abstain from alcohol
-Conserve muscle strength
Prevention of pneumonia and thromboembolic problems
-Modification of the activity rest schedule

causes of hepatitis

-Viruses: A,B,C,D,E
-Autoimmune
-Other viruses: mono, CMV, Epstein-Barr, herpes, coxsackie, rubella
-Bacteria: salmonella
-Parasites: amoebiasis

hepatitis A cause

fecal oral transmission

hepatitis B cause

STD

hepatitis C risk factors

IV drug abusers, high risk behavior, healthcare workers

hepatitis treatments

-Prevention = #1
-Vaccination for A, B
-Serum antibody screening
-Symptom management: rest, nutrition, fluids, medications

hepatitis medications

-direct acting antivirals
-supplementation
-antihistamines
-antiemetics

cirrhosis medications

-diuretics
-beta blockers (carvedilol)
-silymarin

alcoholic liver disease medications

corticosteroids for inflammation

nonalcoholic fatty liver disease medications

-vitamin E
-antidiabetics
-statins
-antihypertensives

GERD (adult)

-most common upper GI problem, C/O heartburn, epigastric pain, dyspepsia
-stomach acid refluxes into esophagus, stomach HCL and pepsin irritate and inflame

GERD etiology

no single cause, foods, medications, hiatal hernia

ETOH chocolatemedications fatty foodpeppermint nicotine tea/coffee

GERD treatments

-identify and eliminate cause
-stop eating 2 hours before bedtime
-lifestyle management
-medicationsL PPIs, H2 receptor blockers, antacids, pro kinetic therapy -endoscopic therapy -surgery

GERD diagnosis

H&P exam
EDG barium swallow mobility studies

hiatal hernia

-herniation of part of the stomach above the diaphragm
-most common upper GI problem
-found on x-ray
-acute paraesophageal hernia is a medical emergency

sliding hiatal hernia

top of stomach slides through when patient is supine and slides back down when patient is upright

paraesophageal or rolling hiatal hernia

the funds and greater curvature of the stomach roll up through and form a pocket

hiatal hernia etiology

structural changes, weak diaphragm at esophageal opening, increased intraabdominal pressures, obesity, pregnancy, ascites, tumors, heavy lifting, physical exertions

hiatal hernia s/s

similar to those of GERD

hiatal hernia complications

GERD
esophagitis hemorrhage esophageal erosion esophageal stenosis
ulcerations aspiration into trachea

hiatal hernia diagnosis

barium swallow EGD

hiatal hernia treatment

-conservative treatment similar to GERD treatment
-avoid straining or lifting
-surgery: fundoplacations, mesh placements, herniorrhaphy, gastroplexy

gastritis

-inflammation of gastric mucosa
-very common-acute or chronic
-the result of breakdown in gastric mucosa = inflammation

gastritis etiology

drugs, diet, alcohol, microorganisms, environmental factors, diseases, disorders, procedures, stress

gastritis s/s

anorexia n/v epigastric tenderness
fullness

some asymptomatic

gastritis diagnosis

H&P
drug and ETOH use
occ CBC
EGD

gastritis treatment

-eliminate cause
-supportive care
-NPO if n/v
-PRN: NG to monitor bleeding, lavage, and empty
-clear liquids
-medications: PPIs, H2RB, antibiotics if bacterial
-lifestyle changes

gastric peptic ulcers

-burning or gas pressure in epigastrium, pain 1
-2 hours after eating
-common in women, H pylori is the cause of 80% of cases
-NSAID most common cause of non H pylori cases -less common than duodenal ulcers
-increased cancer risk -high recurrence
-management: stop NSAIDs, antibiotics for H pylori, WTOH and smoking cessation, eliminate coffee, medications (H2 or PPI)

duodenal peptic ulcers

-burning, cramping, pressure like pain across midepigastrium and abdomen, back pain, pain 2-5 hours after meal midmorning or middle of night, pain relief with food and antacids
-most common peptic ulcer
-in men more than women -high recurrence
-management: similar to gastric, ETOH and smoking cessation, stop NSAIDs, H2 or PPI medications

chronic PUD complications

hemorrhage
upper GI bleed

perforation (most lethal)

gastric outlet obstruction

IBD

-common onset 15-30 years but can occur at any age
-difficult to diagnose, symptoms similar to other diseases/condition -no cure but remissions are possible
-thought to be autoimmune
-urban > rural and highest in white, and Jewish, genetic link

ulcerative colitis involves only the

colon

Crohn's disease can involve

the small intestine or colon

Crohn's disease

a chronic relapsing disease that can occur segmentally in the smallbowel and colon

crohn's s/s

-involves the entire thickness of wall, especially submucosa
-common in terminal ileum and colon but can occur anywhere
-not common in the rectum
-diarrhea usually without blood
-onset mid 30s or >60
-abdominal pain, cramping, diarrhea, rectal bleeding, fever, weight loss, malabsorption

relief during remission

crohn's complications

-cancer (esp small bowel)
-perianal abscesses and fistulas
-perforation
-strictures

ulcerative colitis s/s

-onset teens
-30s or over 60
-severe abdominal pain
-diarrhea
-fever
-rectal bleeding
-tenesmus
-pseudopolyps

ulcerative colitis complications

-colorectal cancer
-c diff
-perforation
-toxoic megacolon