test 5 skin integrity and nutrition

dermatitis

inflammation of the skin
familial/hereditary
not contagious

is dermatitis an infection

no it is not an infection however it can become infected

atopic dermatitis

most common chronic, usually start at young age

tx. cortisone creams and light therapy

what do steroid creams do to the skin overtime

stain, thin, interrupt inflammatory process. can cause paperlike skin.
tx is usually 14 days

coricosteroid creams and where you use them

triamicinolone - face
clobetasol - body

h2 blockers

pepcid (famotidine)

can be used off-label in combination with H1 antihistamines (like Benadryl or Zyrtec) to treat allergic reactions.

It works by blocking H2 receptors on skin vessels, which can enhance relief from itching and hives

psoriasis

an autoimmune disorder

mostly plaque
usually effects trunk, elbows, knees and scalp
is a buildup of skin cells, the body attacking itself producing more rather than shedding

inflammatory response 3 parts

sequential
intensity of response
inflammatory response

sequential response to cell injury in inflammation process

neutralizes (destroying agent making it harmless) and dilutes (adds fluid to harmful agent to make it weaker) inflammatory agent

-removes necrotic material

-establishes environment for healing

"first we surround it, then we clean it."

intensity of inflammatory response (what it depends on)

-extent and severity of injury

-reactive capacity of injured person (the body's overall ability to initiate, manage, and resolve an inflammatory response following tissue damage)

what processes can the inflammatory response be divided into

-vascular response
-cellular response
-formation of exudate
-healing

vascular response to cell injury

1. injury occurs

2. brief vasoconstriction (to reduce blood loss)

3. chemical mediators are released (inflammatory chemicals- histamine, kinins, prostaglandins)

4. vasodilation (increase blood flow-hyperemia) causes redness and heat

5. capillary permeability increases (leaky) (allows fluid, proteins, immune cells to move out of bloodstream and into injured tissue)

6. local edema due to fluid leaking out of capillaries causing swelling

7. inflammatory exudate forms (fluid, WBCs, proteins- helps fight infection and start healing

Cellular response to cell injury

1. chemotaxis- WBCs chemically pulled to injury site

2. margination and diapedesis of leukocytes (WBCs move out of bloodstream) margination means move to edge of blood vessel wall, diapedesis means the WBCs squeeze through capillary wall into injured tissue. (essentially: blood -> vessel wall -> tissue)

3. migration of leuks to site of injury through chemotaxis signals

- neutrophils (first responders- arrive in mins to hrs, engulf bacteria (phagocytosis)

- monocytes- arrive next and transform into macrophages (macrophages live longer (long life span and can multiply) than neutrophils, continue phagocytosis, clean up dead cells and pathogens and help start healing)

- lymphocytes- immune response (recognize specific pathogens, coordinate adaptive immunity (identifies and destroys particular pathogens, creating long-lasting immunological memory), produce antibodies. arrive later; primary roles are cell mediated immunity, humoral immunity and chemical mediators like histamine, serotonin, and kinin

5. phagocytosis- neutrophils and macrophages engulfing and digesting pathogens and debris.

6. inflammatory exudate- produces pus in infected wounds, fights infection starts healing

pus components

dead neutrophils accumulated at site of injury, digested bacteria, other cell debris

what releases more neutrophils in response to infection, resulting in elevated WBC

bone marrow

complement system of cellular response

major mediator of inflammatory response, they destroy invading pathogens
- enhanced phagocytosis, increased vascular permeability (allowance of nutrients to move between bloodstream and tissues), chemotaxis (attracts and repels cells), cellular lysis (cell death)
final components of system create holes in cell membrane, causing targeted cell death by membrane rupture

pathway of generation

1st cell membrane injury, signals arachidonic acid (signals molecules that regulate inflammation, pain, and immunity). steroids inhibits this.

cyclooxygenase pathway = prostaglandins (pain fever inflammation) and thromboxane (clotting) - NSAIDS & Aspirin block these.

lipoxygenase pathway is leukotrienes (asthma, allergies)

steroids inhibits these pathways and weaken ability to fight things off

what meds inhibit the various steps in the pathway of generation

corticosteroids, nonsteroidal antiinflammatory drugs and acetylsalicylic acid (ASA)

left shift of inflammation

increased immature neutrophils, decreased grown neutrophils. because the body is trying to regenerate what's lost.
usually an indication of acute, active inflammation

acute inflammation

2-3 weeks, usually no residual damage.
neutrophils predominant cell type at site of inflammation

subacute inflammation

Same features as acute inflammation but persists longer (weeks or months)

chronic inflammation

-may last for years.
-injurious agent persists or repeats injury to site
-predominant cell types; lymphocytes and macrophages
-may result from immune system changes like an autoimmune disease

RICE

rest
ice
compression
elevate

primary intention of wound healing

wounds have little tissue loss like a surgical incision
edges can be approximated
low risk of infection and minimal scarring

secondary intention of wound healing

-occurs from trauma, burns, ulceration, infection
-large amounts of exudate, wide irregular wound margins with extensive tissue loss
-edges cannot be approximated
-high risk of infection, scarring and poss loss of tissue function

tertiary intention wound healing

when a wound is allowed to remain open for a time and then closed, allowing for debridement and other wound care - to reduce bacterial counts prior to closure

stages of wound healin

hemostasis (stop bleeding, initiating repair)
inflammation,
proliferation (repairing damaged tissue, preparing to close),
remodeling (tissue integrity restored)

what are two things wounds need to heal

oxygen and good blood flow

shearing

when skin sticks to a surface while muscles slide in the direction the body is moving
or bones in one direction, tissue in another
high fowlers is highest risk

blunt force wound

body hits a surface or is struck by a dull object, such as in assaults, falls, or car accidents

friction wound

caused when the skin is rubbed against another object

dehiscence

Bursting open of a wound, especially a surgical abdominal wound

evisceration

opening of wound, organs outside body cavity.
cover in moist gauze and call for help

hypertrophic scarring

too much collagen causes raised scarring, develop within the original boundary of a skin injury

keloid scar

firm, raised, and often itchy skin growths that extend beyond the boundary of an original injury, caused by excessive collagen production during healing

wound class;
superficial
partial thickness
full thickness

superficial- affects only the topmost layer of skin (epidermis) and sometimes the upper dermis, typically caused by scrapes, minor cuts, or light burns

partial thickness- involves damage to the epidermis and superficial dermis, appearing as a shallow, red/pink, and moist wound. Common causes include abrasions, skin tears, and second-degree burns

full thickness- extends through the epidermis and dermis into the subcutaneous tissue, often exposing adipose tissue, muscle, tendon, or bone

how do you measure a wound

treat like a clock.
head to toe, right to left.
measure in CM

fistula

an abnormal passage, usually between two internal organs or leading from an organ to the surface of the body
(ex. tunnel from buttocks to vagina)

What is undermining?

wound has more involvement under the skin than we can see on the surface

if you can't measure dead tissue, what do you do?

say where it is (ex, on clock measurement, at 3pm)

hyperbaric oxygen therapy for wounds

accelerates the healing of chronic, non-healing wounds—such as diabetic foot ulcers, radiation injuries, and, crush injuries—by having patients breathe 100% oxygen in a pressurized chamber. This increases blood oxygen levels, enhancing the body's natural healing, reducing swelling, and fighting infections

negative pressure wound therapy

activity that promotes wound healing and wound closure through the application of uniform negative pressure on the wound bed, reduction in bacteria in the wound, and the removal of excess wound fluid.

(black open pore polyurethane foam applied directly to wound, dressing applied and wound vac applied to wound, sucks in to srhink and pull wound together)

nursing implementation of wounds;
drug therapy

becaplermin (regranex) prescription topical medication used to treat diabetic foot and leg ulcers by stimulating healing

nursing implementation wounds;
nutritional therapy

high in proteins, carbs, vitamins, with moderate fat
vitamins needed include c, b complex and a

infection prevention nursing implementation of wound

don't touch recent injured area
keep free from contaminated items
antibiotics given prophylactically

infection control
nursing implementation of wound

culture
concurrent swab specimens obtained using levine's technique (by rotating a swab over a area of viable tissue for 5 seconds with sufficient pressure to express tissue fluid)

psychological implications of nursing implementation; wounds

fear of scar or disfigurement
drainage or odor concerns
be aware of facial expressions w dressing changes

PAD:

A- absence of pulse/hair

R - red round sores

T - toes and feet pale or black

S - sharp calf pain (intermittent claudication)

TX PAD

antiplatelets, walking exercise, bypass/stents
DO; inspect feet daily, encourage walking, hang legs
avoid cold exposure, no tight clothing

PVD

V - VOLUPTUOUS pulses

E -edema

I - irregular shaped sores (pools)

N - no sharp pain

Y -yellow and brown ankles

TX PVD

anticoagulants
compression stockings
elevate legs
hydrate
DO NOT massage if DVT is suspected
avoid long immobility

ulcer location of PAD and PVD

PAD; toes, heels, pressure points (dry, round, punched out)
PVD; ankles, lower legs (wet, irregular edges)

FRUITS OF WOUNDS
stages

stage 1; tomato (can push on it, doesn't turn white)

stage 2; potato (1st layer skin gone, skin broken)

stage 3; apple (1st layer and some tissue gone)

stage 4; peach (deep, down to bone)

unstageable; down through tissue, can't tell about skin. icky. deep but not how deep. under dead tissue.

deep tissue injury; eggplant; skin intact, deep purple

pyrosis

heartburn

indicators of hemorrhagic gastritis

hematemesis, tachycardia, hypotension

electrolyte imbalances and hypoglycemia

acute; several hours to few days, caused from NSAIDS, aspirin, corticosteroids, alcohol, radiation therapy

chronic; repeated exposure to irritating agents/recurring episodes of acute gastritis. caused by H pylori, autoimmune disorders, long term drug therapy, duodenal content reflux

what vitamins can chronic gastritis interfere with and what causes it

vitamin b12, diminished instrinsic factor production (reduced secretion of a protein by stomach parietal cells necessary for Vitamin absorption in the small intestine) leads to pernicious anemia

DX for gastritis

endoscopy, biopsy
CBC for anemia
H pylori tests

H pylori TX

proton pump inhibitor, abx, bismuth salts sometimes

what electrolyte should you monitor for gastric disorders

sodium

potassium

chloride

every 24 hours

peptic ulcers and what causes them

gastric, duodenal, esophageal erosion of mucosa due to HCL and pepsin, h pylori infection, NSAID use

zollinger-Ellison syndrome

hypersecretion of gastrin, leading to severe peptic ulcers
associated with MEN1 syndrome

symptoms of peptic ulcer

dul gnawing pain or burning sensation in mid epigastrium (upper middle abdomen) or back
pyrosis, vomiting, constipation or diarrhea, bleeding
hematemesis or melena if bleeding ulcer

difference between gastric and duodenal

gastric- immediate after food

duodenal 23 hr after means (most common)

meds of peptic ulcers

abx combination, proton pump inhibitors (-prazole), bismuth salts (pepto bismol), H2 blockers

how does smoking increase peptic ulcer risk

decreases bicarbonate secretion increasing duodenal activity

symptoms of hemorrhage, perforation, obstruction

hemorrhage; hematemesis, tachycardia, hypotension, melena

perforation; abdominal tension, tachycardia, signs of shock (fainting, dizziness, sweating)

obstruction; vomiting of undigested food, feeling full quickly

achalasia

absent or ineffective peristalsis of the
distal esophagus and failure of lower esophageal sphincter (LES) to relax

distal esophageal spasm

affects esophageal motility, making swallowing difficult

high resolution manometry is the standard for diagnosing esophageal motility disorders. what does it measure

peristalsis, contraction amplitude, esophageal pressure

hiatal hernia

opening in the diaphragm becomes
enlarged, part of the upper stomach moves up into
the thoraxopening in the diaphragm becomes
enlarged, part of the upper stomach moves up into
the thorax

sliding hernia
paraesophageal hernia

sliding hernia- upper stomach and gastroesophageal junction displaced upward

paraoesophageal hernia- stomach pushes through the diaphragm beside the esophagus

diagnostic of hiatal hernia

endoscopy, esophageal, manometry, pH monitoring, or esophagography (barium swallow)

clinical manifestation of perforation

• excruciating retrosternal pain (behind breastbone) followed by dysphagia

• infection, fever, leukocytosis, severe hypotension

• mediastinal sepsis with Boerhaave syndrome (rupture of distal esophagus), pneumothorax, subcutaneous emphysema

second line drugs GERD h2 receptor antagonists prokinetic drug

h2; famotidine, cimetidine; decrease gastric acid

prokinetic; metoclopramide; accelerate gastric emptying

proton pump inhibitors

prazole

decrease gastric acid production

baclofen

tx of GERD

reducing transient lower esophageal sphincter relaxations (muscle relaxant)

bethanechol chloride

reflux inhibitor

Barrett esophagus

altered esophageal mucosa lining predominantly white makes over 50. associated with family history, esophageal adenocarcinoma, GERD, smoking, obesity

symptoms of GERD

peptic ulcer disease

gastric acid injury causing inflammation and ulceration most common cause is H pylori

h pylori caused by

contaminated water or person to person

labs/dx peptic ulcer

urea breath test to test for h pylori upper GI h pylori and h pylori testing

nursing and medical care of peptic ulcer

nursing care; decrease gastric acid, determine cause of inflammation

medical care; h pylori tx antibiotics, ng tube decompression

two classifications of GERD

physiological (functional) and pathological (GERD)

GERD caused by

LES- lower esophageal sphincter tone

infants and GERD

peaks around 4 mos, and then declines
most common in premies and neurological deficit

functional GERD

painless effortless vomiting
normal nutrition criteria
factors increasing risk; small stomach size, short esophagus, liquid diet, horizontal positioning, frequent large feedings

pathological GERD

physical dysfunction
reflux greater than 18 mos
apnea
esophagitis
aspiration pneumonia

diagnosis GERD

history and physical
upper GI
barrium swallow
24 hour intraesophageally pH monitoring study (small catheter through nose to monitor pH of acid

normal pH of stomach acid

1-3, yellow or green in color for stomach contents