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NCLEX Content Review - Study Set 1

Terms in this set (1504)

- Accumulation of excess H+ ions/metabolic acids, not carbonic acids, not respiratory-related, or loss of HCO3

- Salicylate Intoxication = Ingesting an excessive amount of aspirin (salicylic acid)
- Hypoxia, shock, sepsis -> lactic acid build-up, basically, you are in a situation where you aren't getting enough perfusion to your tissues and causes the cells to work with anaerobic metabolism instead of aerobic metabolism producing a by-product called lactic acid
- DKA -> ketoacidosis or starvation, there's no insulin to deliver the glucose to the cells, cellular starvation cause fat to break down and produces the fatty acid called ketones
- Bicarbonate (base) loss:
> Renal failure - the kidney makes and reabsorbs bicarbonate, if this process malfunctions the bicarbonate is not around as much or you can't excrete bicarbonate causing a build-up
> Stool - contains bile, bilirubin, and bicarbonate so a diarrhea episode can cause a massive loss of bicarbonate

- tx the cause
- Oxygen + fluids especially for the shock pt to reestablish perfusion
- Fluids helps the pt get of anaerobic metabolism and back to aerobic metabolism
- Monitor e+lytes (K)
- If the K+ levels are too high -> dialysis
- Sodium Bicarb - for the renal failure pt bc they are having an issue w/ making & reabsorbing the bicarb & letting go of acid, giving sodium bicarb via IV is the last resort tx as in something like a code they probably were in cardiac/respiratory arrest (anaerobic metabolism), not a first-line drug for fixing metabolic acidosis bc there's a high risk making the patient alkalotic
- Dialysis - gives bicarbonate as part of the tx
- Antidiarrheal meds (stop bicarb loss) bc bicarb is in your stool, slow down peristalsis
- Diuretics (⬆ H+ loss) - i.e. Loop diuretic or a thiazide diuretic NOT a spiralolactone or K+ sparring, not for the shock patient

- Hyperkalemia (rare in respiratory acidosis)
- Dysrhythmias (vfib, PVCs)
- Confusion
- Respirations are initiated when the infant's lungs fill with air for the first time instead of fluid. Once the cord is clamped it becomes necessary for the infant to become self-sufficient because the mother is not supplying oxygen and nutrients anymore.
- Surfactant is a lipoprotein that starts to be produced at 24 weeks of gestation and completes production at 34 weeks. This is why HCP are especially concerned about premies who are less than 24 weeks because their lungs are not fully developed & they don't have enough surfactant to keep their alveoli (where gas exchange occurs) open outside of the uterus.
- It is thought that vaginal delivery is better than c-section because the extra "squeeze" infants get coming out of the birth canal allows for more of the amniotic fluid to come out of the lungs leading to a ⬇ risk for TTN in newborns.
- NV RR = 30 - 60, shallow & irregular w/ periods of apnea. These periods of apnea can be described as "pauses" because they last <10 secs & don't have HR changes or color changes
- Real apnea which is mostly seen with premies is accompanied by HR changes and color changes and last for 20+ secs with signs of decomp
- During premature labor mothers can receive betamethasone to help speed up the dvlpmt of the lungs if <34 wks
- Outside of the uterus premies can also receive surfactant directly into their lungs in a liquid form, you should make sure the med is dispersed, intially you will see sats go down and s/s of decomp
Respiratory distress = color changes (dusky/purple), grunting, retractions, ⬇ RR/effort or no RR at all
When premise have true apnea they sometimes "forget" to breathe and require stimulation to wake up, this is why they are likely on caffeine
Infants are obligate nose breathers
-(until about 4 weeks)
- They only breathe through their nose except when they are crying
- They have little mucus in their noses to help prevent infection, but when they do have excess mucus their small airways can be obstructed making it more difficult to breathe

Large tongues and tonsils
- Large tongues in relation to oral pharynx which can lead to airway obstruction
- As they get a little older, they have big tonsils and adenoids even when they are not sick. When they do get throat infection, tonsils can get so red and enlarged they touch each other which can occlude their airway

Small trachea
- 4mm in diameter compared to 20mm as an adult
- Anything that causes swelling, such as bronchospasm, or increase mucus causes resistance to airflow to the lungs

Underdeveloped larynx
- Cartilage surrounding it allows it to narrow, which can cause aspiration risk

Lower respiratory structures
- Bifurcation of the trachea, where it splits to go right/left so it can go to lungs
- Because of where its located in young children (3rd thoracic vertebrae compared to 6th in adults), there's an increased risk for aspiration
- Nurses should be aware of where they branch off so they know how far down they can safely suction in children

Lower airways
- Narrower bronchi and bronchioles - makes swelling a bigger issue (bronchiolitis/asthma)
- Fewer alveoli - where air exchange happens so if they have fewer to get oxygen, it puts them at higher risk for developing hypoxia and CO2 retention
-> Continue to develop alveoli until about 8 years old

Chest wall
- underdeveloped
- Muscles between ribs (which help move chest wall) are undeveloped and not supportive of lung expansion
-> Chest movement dependent on the diaphragm
- Children get much better delivery/release of med when using a spacer

- Using a Nebulizer to Delivery the Medication
-> Nebulizer uses a machine that makes a mist of medicine to breathe in through face mask or mouthpiece - your childs dr/nurse will tell you how much to put in
-> For best results when using one with a facemask follow these steps:
--->>> Wash hands thoroughly
--->>> Place face mask on nebulizer container
--->>> Attached one end of tubing to the bottom of nebulizer container
--->>> Attach other end to the nebulizer machine
--->>> Open plastic vile of medicine and pour into nebulizer container
--->>> Put on face mask covering nose and mouth - machine on flat, steady surface
--->>> Take slow deep breaths with mask on, treatment takes 6-10min
--->>> You'll know its complete when sounds changes to sputtering noise
--->>> Wipe face, and rinse mouth out and don't swallow the water

- Metered Dose Inhaler (MDI) Without the Use of a Spacer
-> Patient stands or sits as straight as possible
-> Take cap off, shake it 6-10 times
-> Hold head in neutral position or tilt back slightly
-> Exhale out all the way to empty the lungs
-> Place inhaler between teeth, over the tongue, with lips sealed tightly around mouthpiece
-> Aim inhaler at the back of the throat
-> Patient begins to inhale slowly while firing/pressing down on canister once
-> Firing should occur immediately after inhaling begins
-> Keep drawing air through month until breathing in stops
-> Keep inhaler in mouth throughout inhalation
-> Hold breath and count slowly to 10
-> Release breath slowly, relax and breath normal

- How to Use an MDI with a Spacer
-> Shake the inhaler for 10 seconds
-> Take cap off inhaler and attach to spacer
-> Sit up straight, place mask over nose and mouth, press down on inhaler
--->>> This puts medicine in spacer
-> Breathe in and out 5-10 times
-> If you need another puff of medicine, wait a minute and repeat process
- Immature

- Since the CNS is still immature their are skeletal fx that aren't present yet

- Can't coordinate certain movements yet as an infant

- Muscle mass is only 25 % of their body weight, they aren't using their muscles as much, so they aren't as large

- As the get used more the growth rate increases

- Bone healing - increased amount of cartilage, more flexible & porous they can absorb shock or trauma better bc it's less calcified & it can bend but not break, may buckle or bend in some injuries, bone healing happens quicker thatn in adults takes 1/2 the time

- curvature of the spine is more pronounced (buddha belly) a natural alteration to support the big head compared to their body, lordosis is normal, they might have kyphosis, girls are usually than the boys & may feel akward so they have a bent posture

- Positional alterations
▪ Metatarsus adductus (intoeing) r/t how the baby is inutero, not club foot bc there's no resistance
▪ Genu varum (bowlegs) - when they are first starting to walk, will resolve by 3 yrs
▪ Genu valgum (knock-knees) - "gum in b/t their knees", resolves by 8 yrs
▪ Flat feet until their arches start to dvlp'd

- Ossification is the process of cartilage turning into bone, not complete until the end of adolescence, one of the last system that is fully dvlp'd, tanner stage 5

- Long bones grow from the ends, damage that happens at the growth plate can lead to early or partial closure which means that later on the bone isn't going to grow how it needs to & lead to limb deformity

- Thick & strong periosteum
- Ax:
▪ Health history and risk factors - sudden onset of fever, photophobia, HA, irritability, neck pain, w/ infant poor sucking or high pitch cry
▪ Medical emergency!
▪ Neuro changes
▪ Nuchal rigidity - how to test it - stiff neck
▪ Petechial rash - pv by MCV4, can kill in 24 hrs, no blanching, can lose limbs, virulent type
▪ LP, CBC, blood & urine cultures
▪ CSF pressure increased w/ increased proteins and WBCs increased & glucose decreased due to BBB damage & bacteria feeding on glucose
▪ Bacterial vs Aseptic (viral) - similar appearances, bacterial looks worse
▪ Meningeal irritation - Brudzinski sign - lift head knees jerk up from pain, Kernig's sign - bend knee to 90 degrees + bend leg at hip - they try to stretch their leg out
▪ At risk for stroke, brain damage, tetanus, loss of limbs
▪ Vaccines decrease meningitis incidence (11 -12 y/o)- HiB, PCV13, MCV4

- Management (bacterial meningitis): Antibiotics ASAP for at least 3 days
▪ ***Maintain cerebral perfusion
-> Frequent neuro assessment
-> Reduce ICP - elevate HOB, burr holes,
-> Quiet environment
-> Reduce fever & pain

▪ Prevent injury from seizures
▪ Prevention
-> Droplet precautions
-> Post-exposure prophylaxis
-> Vaccination

▪ Corticosteroids to decrease inflammation of the meninges

- Ax (aseptic meningitis):
▪ Most common type of meningitis, better prognosis
▪ Caused by virus - self-limiting
▪ Once cultures come back and it's viral d/c antibiotics
Child usually less ill
▪ Majority < 5 years of age

- Nursing management
▪ Aggressive treatment to start
▪ Droplet precautions until identified
▪ Supportive care
- sick pancreas > no beta cells > no insulin > fat cell breakdown > ketone/acidosis in blood & urine
- rapid onset
- BG >300 (not set in stone)
- H+ ions ↑ > ↑ acid (blood pH >7.35 > ↑ RR to breathe off CO2 > ↓ acid)
- commonly caused by infection
- undx Type 1
- unmanaged Type 1 diabetes
- Thirsty
- N/V
- Flushed
- Fruity breath
- High fever
- kussmaul's RR
- high WBC + osmolarity
- 3 P's
- ICU admission
- BOLUS 0.1 units units/kg IV push + IV drip 0.1 units/kg/hr
- insulin drip, glucose checks q1h
- once glucose gets to 250 insulin dc = subq sliding scale/bicarbonate normalized or transition + dextrose to fluid, e.g. D5.+45NS
- 150 BG check q4h
Key Difference: Glucose doesn't get as high as in the case of HHS, ketones are produced, common with Type 1 diabetes

- gradual onset - over several days
- decreased thirst center
- NOT acidotic, blood pH or 7.35 -7.45 (normal)
- commonly caused by infection, drugs (diuretics/steriods), undx diabetic
- Polydipsia
- Polyphagia
- Polyuria
- Extreme dehydration due to high osmolarity (320+) > ↑ blood thickness > r/f clots
- High glucose levels
- electrolye disturbances
- 10 - 20 L of fluid loss > ↓ volume > ↓ BP + tachy❤> Perfusion to Kidneys > elevated BUN + creatinine
- treat slowly if not = cerebral edema (s/s = ALOC, coma, abn neuro checks), fluid = .9 or 045 NS 1L/hr
- once BP is over 100 systolic ↓ fluid to 100-200 ml/hr
- BOLUS IV push Reg insulin NOT humalog or lantus = 0.15 units/kg > IV drip 0.1 units/kg
- GOAL: lower BG by 50-70 to pv osmolarity shifts to fast
- 250 BG = check q2h > dc IV drip > sliding scale humalog subq
Key Difference: Glucose gets to extremely high levels (e.g. 600+), no ketones produced (no ketosis), insulin is still produced, common w/ Type 2 diabetes

- Multiple IV Access (20G)
- If pt can't eat/swallow/can't take oral fluids = NO dc insulin IV drip
- Don't tx hyperkalemia if insulin is admin bc insulin shift K+ into the cell > ↓ K+ levels
- If hypok+, UO (urine output) should be 30 ml+, min 60 ml/hr in/o to tx
- Crackles + wet cough = circulatory overload
- labs + I&Os frequently
- consider psychosocial issues w/ type 1 pts
- remember ABC + e+ ax