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What is the most significant risk factor for COPD
Smoking cessation
biggest impact in reducing risk of developing COPD
accelerated decline in pulmonary function slows to almost nonsmoking levels
Carbon monoxide
decrease O2 carrying capacity
increase heart rate
impaired psuchomotor performance and judgment
What is a cardiac complication of COPD
respiratory insufficiency and failure
pneumonia
chronic atellectasis
pneumothorax
cor pulmonale (right sided heart failure)
Why do patients with COPD lose weight
thre primary symptoms
chronic cough
sputum production
dyspnea
Weight loss due to dyspnea- encourage easy to eat foods
“barrel chest” and club fingers
what classification of drugs are used first for fast relief of airway obstruction in COPD and asthma
Bronchodilators: Short-Acting and Long-Term Inhaled Beta2- Adrenergic Agonists
administering bronchodilators by inhalation is most effective and the treatment of first choice to relieve acute asthma
two general types of inhaled beta 2-adrenergic agonists are used for asthma management:
rescue inhalant medications (quick relief, short-acting drugs) used during periods of acute symptoms and exacerbations
Albuterol (Proventil HFA, Ventolin HFA, Pro AirResp Click)
maintenance inhalant medications (long term control drug used to achieve and maintain prophylactic control of persistent asthma
MOA: stimulates the beta 2 adrenergic receptors in the smooth muscle of the bronchi and bronchioles. The enzyme adenyl cyclase causes increased production of cyclic AMP, resulting in bronchodilation
What deficiency is seen in younger people diagnosed with COPD
Alpha-1 Antitrypsin
Protein that protects the lung
produced in the liver
deficiency increased risk of lung and liver disease
the destruction is all over
panlobular (panacinar) emphysema
the destruction is all over- its a genetic problem
What clinical manifestation occurs with chronic hyperinflation of the lungs and “dead space”
barrel chest
AP diameter: 1:1
PAIN
what is pain
complex experience
dynamic interactions between physical, cognitive, spiritual, emotion and environmental factors
not just a response to injury
Acute pain is protective → promotes withdrawal from painful stimuli, allows injured parts to heal, and teach avoidance
Pain can be defined as whatever the patient says it is, and it exist whenever the patient say it does
what happens during the transduction phase of the pain process
physiology of pain (nociception)
transduction → transmission → perception → modulation
during transduction, painful stimuli is converted to action potentials at the sensory receptor
occurs at the end of A-delta fibers and C-fibers
what is the difference between A-delta fibers and C-fibers in pain transmission
A-delta
small diameter
myelinated- rapid tranmsission of pain
pain is sharp, stinging, cutting, and pinching, it localized (know where to pull hand away from)
C-fibers
small diameter
unmyelinated, slow transmission of pain
pain is dull, burning, aching, poorly localized (can’t pin point where it hurts)
what are some examples of therapies related to the Gate Control Theory of pain
during modulation
synaptic transmission of pain signals is altered
can be amplified or dampened
neurotransmitters
opioids such as ENDORPHINS mediate pre synaptic (inhibit)
morphine MIMICS the effect of endorphins
Gate Control Theory
theory that if we block the pain before it gets to the brain we can stop or lower pain perception
touch, rubbing skin, massage, distraction acupuncture, getting active, TENS units
What is the difference between referred and phantom pain
refee
what are the indications for the drug gabapentin
atypical pain medications
gabapentin (Neurontin) and pregablin (Lyrica)
Anti convulsants
MOA: though to spontaneously suppress neuronal firing
Indications: to complement effects of opioids
used specifically for neuropathic pain
AE: drowsy, dizzy, visual problems
con only be partially reverses with Naloxone
What are the indications of naloxone or when would it be used
naloxone (Narcan)
opioid antagonist
MOA: binds to opioid receptors but DOES NOT ACTIVATE (just clogs them up)
onset is < 2 mins
route: IV, IM or intranasal
Indications: antidote to reverse effects of morphine and morphine-like drugs (opioids) - respiratory depression
AE:
abrupt reversal of opioid effects with Recurrent pain
increased blood pressure
What are the bodys “natural” painkillers
endorphines
Urological and Male Reproductive
What are the signs of testicular cancer
early clinical manifestations
enlargement of testicle
painless mass noted
if discomfort present (30-40%)
dull ache in groin
sensation of heaviness
Late clinical manifestations
possible acute pain
mainfestations based on metastatic spread
cough
hemoptysis
swelling of lower extremities
back pain
dizziness
What are risk factors for prostate cancer
non-modifiable
age
family history
race/ethnicity
modifiable
obesity and metabolic syndrom
caffeine
physical activity
what are the clincal manifestations of BPH
frequencey and urgency
delay in initation
reduction in force
increased urination time
dribbling
Who is at risk for urosepsis
definition: severe systemic response to UTI that can be life threatening
who at risk
elderly patients
diabetics
immunosuppressed patients
prognosis
high mortality
treatment : source control is key, administration of ABX, follow cultures and supportive care
who would not be able to take bactrim for a complicated UTI
bactrim: AKA Septra, Sulfatrim (sulfa drug)
works on synthesis of folate inside bacteria, halting DNA and protein synthesis
metabolized by liver, and CYP450. excreted in urine, metabolized in liver
used for treatment of uncomplicated UTI and MRSA coverage
SE: nausea/vomitting, can cause sunburn
safe in pregnancy after trimester 1
What is the MOA of phenazopyridine (Pyridium)
urinary tract analgesic
prototype: phenazopyridine (Pyridium)
Therapeutic use; reliefe
MOA: dye used in paints- local analgesic action
Side/Adverse effects
well tolerated
reddish-orange urine
what are some atypical UTI symptoms in the elderly
anxiety
confusion
lethargy
anorexia
history of falling may be exacerbated due to UTI symptoms
URI and atelectasis
the nurse is administering diphenhydramine to a client. the nurse would monitor the client for which of the below side effects of this medication?
ataxia, drowsiness, vertigo, slurred speech
drowsiness
diphenhydramine is a first gen antihistamine
suppresses activity in key regions of the subcortical area of the central nervous system
Ataxia, vertigo and slurred speech are not associated with 1st gen antihistamines.
the nurse instructs a client to breathe deeply to open collapsed alveoli. which explanation could the nurse offer to explain the relationship between alveoli and improved oxygenation?
the alveoli need oxygen to live
the alveoli have no direct effect on oxygenation
collapsed alveoli increase oxygen demand
oxygen is exchanged for CO2 in the alveolar membrane
oxygen is exchanges for CO2 in the alveolar membrane
the exchange of oxygen and carbon dioxide occurs in the alveolar membrane
if the alveoli collapse this exchange cannot occur because pulmonary ventilation is reduced
which of the conditions below causes a steeple sign on X-ray
epiglottis
What are the classic signs and symptoms of allergic rhinitis
inflammatory disorder
upper airway, lower airway, and eyes
clinical manifestations: sneezing, rhinorrhea, prutitus, nasal congestion, watery, ithcy eyes
triggered by allergens- binds to IgE antibodies on mast cells- release inflammatory mediators
environmental triggers: dust mites, mold, etc- avoid contact as part of treatment
Upper GI
peptic ulcer (PUD) etiology
H. pylori
Injury causing substances
NSAIDS, ASA, alcohol
excess secretion of acid
stress- physiologic stress
smoking
family history
what is the connection between proton pump inhibitor omeprazole, instrinstic factor, and vitamin B12 level?
acid degrades meat, releasing vitamin B-12 (colabalamin)
parietal cells secrete intrinsic factor
in the duodenum, B12 binds to intrinsic factor
instrinsic factor shuttles B12 into the cells of the illeum
(B12 binds to transcobalamin once in the plasma)
What is the MOA of pantoprazole (Protonix)
Proton Pump Inhibitors (PPI)
Prototype
omeprazole (Prilosec)
Pantoprazole (Protonix)
MOA
binds to proton pump
irreversibly inhibits the secretion of HCL
Indication
short term treatment of PUD and GERD
explain difference between COX-1 and COX-2
How do NSAIDS cause PUD
NSAIDS work by inhibiting (blocking) 2 enzymes
COX-1:
found in all tissues
one of its jobs is to protect gastric mucosa by secreting prostaglandin E (PGE)
COX-2:
found at site of injury
mediates inflammation and pain
So what happens if you inhibit COX-1
when NSAIDS block or inhibit the COX-1 pathway, they reduce levels of protective prostaglandins which protect the gastric mucosa which can lead to peptic ulcer disease
NSAID EX: ibuporfen, naproxen, aspirin, and celecoxib
What is GERD and what are the risk factors
Gastroesophageal reflux disease
backflow from the stomach into esophagus
highly acidic material
what can it result in
Inflammation
pain
complications: ulceration, scarring, strictures, Barrett esophagus
Anything that alters closure strength of LES or increases abdominal pressure
EX
fatty foods
caffeine
large amounts of alcohol
ciagaretter smoking
sleep position
obesity
pregnancy
pharmacologic agents
Lower GI
A post op patient is receiving morphine for pain. which of the below medications might you expect to see on the MAR
docusate sodium
senna
psyllium
magnesium hydroxide
docusate sodium
docusate sodium lubricate fecal material and walls, promotes fat absorption into fecal mass
used often in conjunction with opioids in the hospital to prevent opioid-induced constipation
a client with a clostridium difficile is a risk for which of the complications listed below? what is the treatment for c. diff?
bowel perforation
abdominal cramping
low grade fever
dumping syndrome
bowel perforation
bowel perforation is a complication of having c diff. infection
abdominal cramping and fever are expected manifesations of c diff infection
dumping syndrome is associated with impaired stomach function (after bariatric surgery, for example)
the best treatment for C diff is the antibiotic vancomycin
What are the classic signs and symptoms of IBS
Manifestations
diarrhea, constipation, combination of both
cramping abdominal pain
nausea
mucus in stool
pharmacotherapy
antidiarrheals
anticholinergic/antispasmotics
laxatives
What is dumping syndrome and what are the S/S
dumping of stomach contents into small intestine
Manifestations
nausea
weakness
sweating
diarrhea
pharmacotherapy
Octrotide (Sandostatin)
antidiarrheal
Route: SQ
SE: nausea, vomitting, and upset stomach
what dietary changes can a patient make to decrease risk of constipation
defined: small, infrequent, or difficult BM
fewer than 3 BMs/week
causes
diet (low in fiber) - increase fiber
lack of exercise
slowed peristalsis
pathologic conditions
obstruction or diverticulitis
which of the mechanisms listed below would a nurse recall when caring for a client prescribed bisacodyl (Ducolax) for constipation?
producing bulk
softening feces
lubricating feces
stimulating peristalsis
stimulating peristalsis
bisacodyl stimulates the intestinal mucosa, precipitating a bowel movement
stimulant laxative
which of the actions below is responsible for the therapeutic effect of docusate sodium
lubricates the feces
creates an osmotic effect
stimulates intestinal wall muscle activity
absorbs water and increases bulk
lubricates the feces
docusate sodium promotes the drawing of fluid into the stool, which softens and lubricates the feces
creating an osmotic effect in the GI tract is the action of saline laxatives, such as magnesium hydroxide or other hyperosmotic, such as lactulose
stimulating motor activity of the GI tract is the action of peristaltic stimulants such as bisacodyl
Diabetes
Type 1 diabetes
most common pediatric chronic disease
diagnosis about 12 years old
aout 5-10% of DM
Two types
idiopathic