NUS 111 Test #3 Flashcards
this releases thyroid stimulating hormone
pituitary gland
iodine is needed to synthesize these
T3 and T4
what does the thyroid gland affect
metabolic rate, growth and developement, brain function and metabolism
decreased basal metabolic rate creating weight gain, supresses glucose
hypothyroidism
weight loss, caloric requirement goes up; graves disease causes 75% of this
hyperthyroidism
this is caused by the destruction of the thyroid gland and/or defect in the production of hormones
hypothyroidism
decreased production of ____ leads to the stimulation of the secretion of _____ which stimulates the secretion of T3
T4
TSH
T3 increases the secretion of _____ which leads to the hypertrophy of the thyroid gland
T4
what is transient hypothyroidsm
temporary/reversible
waht is primary hypothyroidism
disfunction of thyroid gland itself; or not enough iodine
this is thyroid deficiency is present at b irth
cretinism
drugs for hypothyroidism
lithium
what is the most common cause of hypothyroidism in the world
iodine deficiency
modifiable risk of hypothyroidism - 2
use of lithium
diet iodine deficiency
Non modifiable risk factors of hypothyroidism - 6
age, 30-60 yrs old
genetics
autoimmune disease
females
hyperthyroidism, part of thyroid removed, meds for hyperthyroid at any point, head or neck radiation
old ppl considerations for hypothyroidism - 6
depression
decreased mobility
presents atypically*
constipation
thyroid replacement therapy
CV & neurologic side effects with thyroid replacement therapy
early symptoms of hypothyroidism - 8
- fatigue
- amenorrhea
- loss of libido
- non pitting edema
- mental sluggishness
- parasthesia and nerve entrapment syndrome
- hair loss, dry skin, brittle nails
- constipation
late symptoms of hypothyroidism - 10
- slow speech
- cold intolerance
- subdued emotional response,
- apathy
- absence of sweating
- constipation
- thickening of skin
- dyspnea
- weight gain (without increase in food consumption)
- thinning of hair, alopecia (Severe)
severe hypothyroidism resulting in decompensated metabolic state and mental status change
myxedema coma
what part of myxedema coma is pt a medical emergency
enlarged tongue
depressed resp drive
advanced stage of hypothyroidism
personality and congnitive changes - looks like dementia
respiratory issues:
-muscle weakness
-pleural effusion
-sleep apnea
severe stage of hypothyroidism
elevated level of serum cholesterol
CAD/ Poor left ventricular function
myxedema coma
-hypothermic
-Lethargy/unconscious /coma
-Non pitting and periorbital edema
-Enlarged tongue (hoarseness)
-Depressed respiratory drive
how do you manage myxedema coma
- supportive (airway, rewarming)
- hydrocortisone
- levothyroxine, T4
- +/- T3 supllementation
what are the laboratory findings for myxedema coma
hypoglycemia
hyponatremia
hypoxemia
prolonged QT, low voltage
pericardial effusion
hypercapnia
precipitating factors of myxedema comma
infection, cold exposure, stroke, meds (amiodarone, lithium)
nursing assessments - hypothyroidism
vitals - low pulse, bp, RR is tachy
palpate thyroid - is it enlarged, soft, rubbery
skin changes
constipation
weight gain
hair loss, brittle nails
how tolerate cold
cardiac function
assess mouth for enlarged tongue
slurred speech
dyspnea
numbness/tingling
nursing interventions for hypothyroidism
nutritional support - iodine, risk for weight gain healthy diet
assess for signs of myxedema, LOC, CV changes, sedatives/opioids - avoid
teach pt -
1. dont switch brands without talking to provider
2. take meds 1-2 hours before breakfast
3. how to manage symptoms
4. mild soap, use lotion, avoid skin breakdown
5. constipation, stool softener, increase fiber
medication for hypothyroidism
levothyroxine
what are the considerations for levothyroxine
benzos & sedatives - can cause myxedema coma
anticoagulants - watch for bleeding, increased risk
insulin - may need more
digoxin - can cause angina & arrhythmias
dilantin - decreases effect
tricyclic antidepressant - effects decreased
should levels of TSH be low or high for hypothyroidism
high if thyroid issue
low if pituitary or hypothalamus
hypothyroidism
low or high T3
low
hypothyroidism
low or high T4
low
hypothyroidism
low or high LDL
high
hypothyroidism
low or high anemia
low
hypothyroidism
low or high hemoglobin
low
BMR - hypothyroidism low or high
low
safety measures for hypothyroidism
- chest pain
- HR over 100
- medications
- supportive management; education, oral and written instructions if needed
- monitoring physical status; CV collapse; respiratory issues
collaborative goals for hypothyroidism
-adhere lifelong therapy
-weight reduction
-monitor thyroid hormones, keep within normal range
-report herbal and OTC meds to provider
modifiable risks of hyperthyroid
smoking
overmedication
too much iodine
diet meds
non modifiable risks of hyperthyroid
graves disease
female
cancer, thyroid, pituitary
20-40 year old
raidation
thyroiditis
non modifiable risks of hyperthyroid
graves disease
female
cancer- thyroid, pituitary
20-40 years
radiation
thyroiditis
when the thyroid gland makes too much T3 and T4 so pituitary gland will not produce TSH
hyperthyroidism
this is the clinical effects of hyper metabolism from too much circulation T3 & T4
thyrotoxicosis
this is associated with goiter
thyrotoxicosis
hyperthyroidism for old ppl - considerations
- unexplained weight loss
- isolated episodes of atrial fibrillation
- less common in elderly
- new or worsening heart failure
- difficulty climbing stairs when it wasnt before
- mental deterioration
- may need beta blockers
symptoms of thyroid storm (Thyrotoxic crisis)
high fever
agitation
delirium
congestive heart failure
loss of consciousness
nursing assessments for hyperthyroidism
vital signs
thyroid gland - enlarged, soft, thrill-palpable pulse
respiratory - watch for airway, possible stridor, resp distress, difficulty swallowing
peripheral edema
tachycardia
dyspnea; crackles; jugular vein distention
nursing intervention for hyperthyroidism
high calorie diet - 4000-5000
avoid stimulants
low fiber food
peristalsis increases risk for diarrhea
cool environment
monitor for thyrotoxic crisis
already stimulated so avoid; nicotine, caffeine, soda, alcohol
clinical manifestations of hyperthyroidism
exophthalmos - bulging/buggy eyes
nervousness/ emotionally excitable
Tremors
weight loss
Thinning of hair
high HR
palpitations
elevated systolic BP
hyperhidrosis
heat intolerance/Hyperthermia
itchy skin
Systolic murmur
increased peristalsis
increased appetite
muscle fatigue
these block synthesis of hormones
antithyroid meds
what are the antithyroid meds
PTU
methimazole
meds for hyperthyroid
antithyroid meds
adjunctive therapy
radioisotopes iodine
what is the priority during post op of a thyroidectomy
airway - assess airway every 2 hours for first 24 hours. high risk for airway issue
how much of thyroid is removed during thyroidectomy
5/6th
hyperthyroidism lab
TSH - high or low
low
hyperthyroidism lab
T3 - high or low
high
hyperthyroidism lab
T4 - high or low
high
hyperthyroidism lab
BMR - high or low
high
pt education for post treatment of thyroidectomy
see physician
2-3 mos before improvement of symptoms
continue meds as directed
monitor for a year closely for hypothyroid
education on diet
which system is activated causing hunger which activates the sympathetic nervous system
parasympathetic
this mimics alcohol intoxication early on
hypoglycemia
what are the risk factors of hypoglycemia
too little or delayed food intake
too much exercise
medication or food taken at right time
manifestations of hypoglycemia
hunger
shaking, nervous, anxious
diplopia
lethargic, weakness
slurring
faint, lightheadedness, syncope
nursing assessment hypoglycemia
blood glucose level
cold clammy skin
slurred speech
diaphoretic
tachycardia, palpitations
seizure, coma, loss of consciousness
unsteady walking, impaired coordination
nursing intervention of hypoglycemia
PB - carb + protein
eating snack at peak insulin time
medications for hypoglycemia
glucagon IM
50% dextrose IN
medical alert bracelet
collaborative safety goals - hypoglycemia
watch for signs and symptoms
watch for N & V
if pt is unconscious, treat blood sugar then once conscious give snack
this is a group of metabolic disease characterized by elevated blood glucose levels in the blood
diabetes
what do you have, if you have sweet urine
diabetes
what are the four types of diabetes
prediabetes
DM type 1
DM type 2
gestational diabetes
this is produced by the pancreas that controls blood glucose levels by regulating production, use and storage of glucose
insulin
in this type of diabetes - insufficient release, damage to pancreatic cells. not enough made. betas cells damaged or destroyed
type 1
deficient hormone signals - insulin resistance - which diabetes is this
type 2
what is the function of insulin
transports and metabolizes glucose for energy
signals to stop release of glucose
enhances storage of dietary fat
inhibits breakdown of glucose
facilitiates transport of K+ to cells
stimulates storage of glucose as glycogen in liver and muscle cells
characteristics of prediabetes
- impaired glucose intolerance
- not high enough numbers to be diabetes
- increased glucose levels
manifestations of metabolic syndrome
- hypertension
- high blood sugar
- abnormal cholesterol levels
- abdominal obesity
non modifiable risk factors of prediabetes
ethnicity - native americans, latinos
gestational diabetes - can develop to type 2 later in life
age 45 +
modifiable risk factors of prediabetes
weight
hypertension
sedentary lifestyle
HDL cholesterol level
primarily autoimmune - immune destruction of beta cells
type 1a diabetes
failure without an immune mediated etiology
type 1b
children and young adults mostly get this type of diabetes
type 1
nonmodifiable risk factors for type 1 diabetes
onset can occur at any age but usually under 30
genetics
exposure to virus
clinical manifestations for type 1 diabetes
polyuria
polydipsia
polyphagia
weight loss
vision changes
numbness/tingling in hands/feet
dehydration
priority assessment for type 1 diabetes
thin, below ideal body weight
slow wound healing
lethargic
eye exam
numbness/tingling in hands/feet
GI assessment, urinary assessment, skin assessment
CV assessment, tachycardia, hypotension
kussmaul breathing
sweet breath/urine
3 Ps
manifestations of diabetic ketoacidosis
feeling tired and sleepy
confusion, passing out
stomach pain, feeling sick
high ketones, polyuria
blurred vision
sweet smelling breath
polydipsia
high blood sugar levels
priority interventions for type 1 diabetes
assess and monitor blood glucose levels
educate on meal planning
urine glucose testing
educaton on exercise
educate on alcohol usage and its effects
educate on insulin choices and how to admin
reading food labels, carrying snacks with them at all times
pay attention to blood sugar when high
educate to know signs/symptoms of hyper and hypoglycemia
medications for type 1 diabetes - types of insulin
exogenous insulin admin
insulin pumps
insulin
-rapid - lispro
-short - regular insulin
-intermediate - NPH
-long acting - glargine/detemir
priority diagnostics of type 1 diabetes
fasting blood glucose levels
random glucose level
urine
hemoglobin A1C >6.5%
urinalysis
C peptide test
what age of population tends to get type 2 diabetes
older population
pathophysio of DM type 2
insulin resistance
impaired insulin secretion
b-cells become fatigued from compensatory overproduction of insulin
-don’t get ketosis
HHNS
impaired insulin secretion - type 2 diabetes
body tissues do not respond to action of insulin
DKA
gets ketosis
insulin resistance - type 2 diabetes
nonmodifiable risk factors - DM type 2
age 45
family history
ethnicity - minorities
gestational diabetes
modifiable risk factors -DM type 2
weight
smoking
sedentary lifestyle
HTN
high cholesterol
high blood sugar
clinical manifestations pf type 2 diabetes
fatigue
visual changes
slower onset
reoccuring infections
polyuria
polydipsia
polyphagia
prolonged wound healing
nursing assessment for type 2 diabetes
body mass index
measuring abdominal girth
skin assessment
CV assessment
numbness/tingling
cognition status
priority nursing interventions for DM type 2
nutrition
exercise
monitor blood sugar
signs/symptoms of hyper/hypoglycemia
medications for type 2
biguanides - metformin
sulfonylureas - glipizide
nonsulfonylureas
a glucosidase inhibitors
dipeptidyl peptidase - 4
exogenous insulins
amylin analog - pramlintide
diagnostics for DM type 2
HgA1C
fasting blood glucose >126
lipid profile
CPB
urine - high glucose, mincroalbuminuria (protein)
collaborative and safety goals type 1 & 2 diabetes
nutrition
blood sugar within normal limits
miaintain good quality of life
control caloric intake to maintain healthy body weight
exervcise, cholesterol levels and have good lipid levels and BP
15g carbs = 1 carb = 1 unit of insulin
affects of alcohol
drinking a lot at risk of DKA
type 1 higher change to get hypoglycemia
important to know effects of exercise
risk factors for old ppl and pre diabetes
liver or pancreatic disease, heart disease
diet, inactivity
altered insulin secretion and resistence
age related changes for old ppl and pre diabetes
cognitive impairment
kidney functions decrease
decrease GI motility
dental and oral care
chronic disease
socioeconomic factors
potential drug interactions
activity/exercise
sensory changes
clinical manifestations of pre diabetes
slow wound healing
fatigue
3 Ps - polyuria, polydipsia, polyphagia
assessment of pre diabetes
screening of blood glucose levels
check ATI or honan
interventions of pre diabetes
education on diet
education on glucose screening
pre diabetes medication
metformin
this produces antidiabetic effects by decreasing hepatic production of glucose and facilitating the action of insulin on peripheral receptor sites
metformin
diagnostics pre diabetes
impaired fasting 100-125
impaired glucose tolerance 140-199
hemoglobin A1C 5.56-6.5
lipids - low hdl, high ldl
See ATI
collaborative goals pre diabetes
monitor risks factors
maintain healthy weight
meds - statin for cholesterol
healthy diet
at risk for CV
education on prediabetes for risk factors
3 main types of macrovascular complications
CAD, CVA, PVD
what are the macrovascular complications of diabetes
-changes in medium to large vessels
-blood vessel walls thicken, sclerosis occurs and become occluded by plaque
-changes tend to occur at earlier stage in patients whose diabetes is poorly managed
microvasulcar complications of diabetes
thickening of membrane of capillaries due to formation of abnormal glucose molecules in basement membrane of small blood vessels
three types of microvascular complications of diabetes
diabetic retinopathy
nephropathy
neuropathy
what is this
microvascular damage to retina is the leading cause of blindness
glacuoma and cataracts occur more frequently
diabetic retinopathy
this results from damage to small blood vessels that supply glomeruli of kidney
shows 10-15 yrs with type 1
10 year with type 2
nephropathy
nerve damage that occurs bc of the metabolic derangements associated wtih diabetes
neuropathy
this happens to 60-70% of pts with diabetes
neuropathy
increased incidence of MI due to . Typical ischemic symptoms may not be present in diabetics
CAD
cerebral blood vessels affected by accelerated arthrosclerosis
CVA
usually affects vascular of lower extremities, smoking couple with diabetes greatly increases risk
PVD
life threatening syndrome that can occur in pts with diabetes who are able to produce enough insulin to prevent hyperglycemia, osmotic diuresis and extracellular fluid depletion
hyperglycemic hyperosmolar nonketotic syndrome (HHNS)
type 2 blood sugar is high, normal blood sugar is 600-1200
hyperglycemic hyperosmolar nonketotic syndrome (HHNS)
infection, medication or acute/chronic condition can cause this. the medication is glucocorticoid steroids
hyperglycemic hyperosmolar nonketotic syndrome (HHNS)
risk factors of hyperglycemic hyperosmolar nonketotic syndrome (HHNS)
pts over 60 with undiagnosed type 2 diabetes
impaired thirst sensation
functional inability to replace fluids (aspiration)
inadequate fluid intake
prevention of illness/infection
clinical manifestations of HHNS
dehydration
hypotension
skin turgor, dry mucus membranes
confusion
tachycardia
stroke symptoms
hemiparesis
aphasia
polyuria
polydipsia
nursing assessment of HHNS
hypotension
CV and skin assessment - dry mucous membranes, skin turgor
neuro assessment - confusion, alteration of sensorium, seizures, hemiparesis
nursing interventions HHNS
-replacement of fluid is initiated that is dependent on pts cardiac status and degree of fluid volume deficit
-insulin - IV and pen
-monitor electrolytes
-monitor i & o
-monitor blood sugars, vital signs and skin turgor
-have on cardiac monitor, EKG
-watch symptoms of overload
-pt education - how to prevent, how to respond, include family in teaching
-determine the cause
medications for HHNS
insulin
half normal saline or normal saline, potassium as needed
diagnostics HHNS
-blood glucose >600 as blood sugar
-serum osmolarity >340 mOsm/L produces severe neurological symptoms
-glucose in urine
-ketones absent or minimal
-elevated BUN and creatinine
the higher the serum ____, the more profound the dehydration, and the greater risk for ____ _____ and ____ status changes
glucose
renal impairment
mental
this is not a disease but a syndrome
gastroesophageal reflux disease
Chronic symptom of mucosal damage caused by reflux of stomach acid into the lower esophagus
GERD
risk factors for GERD
Advanced age (delayed gastric emptying and weakening tone of sphincter)
Obesity
Sleep apnea
NG Tube
Hiatal hernia
H.Pylori
Diet (spicy foods citrus foods caffetine, chocolate)
calcium channel blockers,
metra nitrates
manifestations of GERD
dyspepsia - indigestion
pyrosis- heartburn
dysphagia- difficulty swallowing
odynophagia- painful swallowing
regurgitation- acid in mouth
esophagitis
Excessive salivation
how often do GERD symptoms need to happen to be diagnosed
4-5x/week
what is odynophagia
pain on swallowing
what is pyrosis
heartburn
what is dyspepsia
pain/uncomfortable feeling in upper middle part of your stomach area
assess for GI symptoms for GERD
-wakes up at night, pain when it occurs
-pain in upset stomach, upper gastric
-regurgitation - bitter, hot in mouth
what other symptoms of GERD that aren’t GI
respiratory - wheezing, coughing, hard time sleeping
sore throat, hoarse voice
globus sensation
hypersalivation
pain worse after eating - lasts 20 to 2 hours
increase in faltus
what serious condition does GERD mimic
heart attack
how do you tell if pt is having heart attack or GERD
give antacid and if pt gets better then its gerd
diagnostics of GERD
upper GI endoscopy with biopsy and cytolic analysis
esophagogram - barium swallow
motility (manometry) tests
pH monitoring
radionuclide test
what does the radionuclide tests detect
reflux and rate of esophageal clearance
medications for GERD
antacids - magnesium calcium carbonide
H2 receptor antagonists - Famotidine etc
proton prump inhibitors - omeprazole etc
prokinetic agents - metoclopramide (reglan)
what do prokinetic agents do
increases motility of esophagus. blocks effects of dopamine - has extrapyramidal effects especially pts with parkinsons
give slowly eg iv over 10 mins
do you take antacids with other meds
no. take seperate.
take at bedtime or 1-3 hours after eating or taking other meds
how do you take H2 receptors?
With food
Caution with kidney disease
PPI medication considerations
risk for CDiff, Fractures, Hypoglycemia, Electrolyte imbalance
Surgical nursing intervetions for GERD
after endoscopy - make sure gag reflux is back, have pt swallow and drink something afterwards
make sure pt signs consent
tell pt to avoid smoking, alcoho,, and carbonated beverages
Priority nursing interventions for GERD
Avoid tight fitting clothes
Avoid eating 2-3hrs before bed
raise head of bed 30 degrees
Take meds as prescribed
Weight
dietary changes. avoid peppermint/spearmint, carbonated drinks, caffeine alcohol
what is the surgerical intervention for GERD
fundoplication
what is a fundoplication
reconstructing sphincter to make it work better to reduce reflux
–only ppl not getting relief from meds will get this
lifestyle modifications for GERD
eat smaller meals
break time between meals and lying down
dont smoke
control weight
avoid wearing tight clothes
relaxation techniques
medications
food to avoid - acidic foods, alcohol, caffeine, spicy foods, fried foods, carbonated beverages
a condition characterized by erosion of gastroduodenal mucosa resulting from digestive action of hcl and pepsin
peptic ulcer disease
this is due to increased concentration or activity of acid pepsin
peptic ulcer disease
decreased resistance of mucosa —- less mucus production
peptic ulcer disease
Occurs in small intestine
result of increase in acid
Most common
Often have multiple
duodenal ulcer
less common than duodenal ulcer.
Higher mortality rate because of age @ onset and complications
Occur near pyloric sphincter
Mucosal breakdown is cause
Acid levels normal
H.Pyloric bacteria
choronic gastric ulcers
this is caused by H. pylori bacteria
chronic gastric ulcers
Located in esophagus
Result of acid reflux/GERD
esophageal ulcer
risk factors for peptic ulcers
stress
age (40-60 years average)
men more likely - once women hit menopause it’s equal
smoking
type O blood
alcohol
caffeine
milk
spicy foods
H.Pylori
NSAIDs/corticosteroid use
COPD & Chronic Kidney disease
Pernicious anemia
manifestations of peptic ulcer
chest pains
reflux, heartburn in epigastric (can look like cardiac pain)
eating helps pain
pain - type/onset/comes back 2-5 hours after eating /straight after meal/ or at night?
bowel movements - constipation or diarrhea
vomiting if obstruction
bleeding
hematemesis
melena - dark tarry stools
sharp, localized tenderness when doing abdominal assessment
assessments of peptic ulcer
-black tarry stools
-history of diet
-medications - NSAIDs, corticosteroids, aspirin
-what makes it worse/better
-how does pain relate to when you eat, not eat, does it happen overnight
-onset, duration pain assessment
-family history
-lifestyle
-stress
-alochol use
-smoking
-dyspepsia
-any bleeding
-do a full focused abdominal assessment
-check labs and studies
nursing interventions of peptic ulcer
- teach pt about medications - understand side effects, any interactions, etc
- make lifestyle changes
- decrease stress
- have them pay attention to what is aggravating or alleviating pain
what are the 3 major complications of peptic ulcer
- hemorrhage
- perforation
- pyloric obstruction
nursing intervention for hemorrhage of peptic ulcer
-test vomit and stool
-blood pressure, shock, vital signs (check for bleeding severity)
-intake and output - check hourly
-check HR, mental status, faintness/dizziness
-stop bleeding - gastric lavage
-give blood products (?????)
-keep checking for signs of bleeding
potentially need NG tube for gastric decompression
nursing intervention for perforation of peptic ulcer
monitor fluid and electrolyte balance
look for signs of shock, infection
listen for bowel sounds
any abdominal pain
-stomach will be distented
-sudden, severe upper abdominal pain, vomiting, callapse, extremely tender and rigid, hypotension and tachycARDIA
nursing intervention for pyloric obstruction of peptic ulcer
first consider NGtube to decompress stomach
upper GI study or endoscopy is performed to confirm this
this is the erosion of ulcer through the gastric serosa into the peritoneal cavity without warning. it’s an abdominal catastrophe.
needs emergency surgery.
perforation
what labs for peptic ulcer
CBC, AST (liver enzymes), ABG
amylase and lipase - stool, rapid urea test, biospy
diagnostics for peptic ulcer
diagnostic studies for H. pylori
upper endoscopy (EGD)
biopsy and histologic exam
barium contrast study
stool tested for H. pylori
medications for peptic ulcer healing
H2 receptor antagonists
proton pump inhibitors
what medications are H2 receptors antagonists
ranitidine
nizatidine
famotidine
cimetindine
what meds are PPIs - proton pump inhibitors
omeprazole
lansoprazole
rabeprazole
esomeprazole
what meds do you use for h. pylori bacteria for first line therapy
PPI + clarithromycin + amoxicillin or metronidazole
what meds do you use for h. pylori bacteria for second line therapy
bismuth salt compound + tetracycline + metronidazole + PPI
what meds do you use for NSAID ulcers
PPIs
surgical therapy for peptic ulcers
vagotomy
dumping syndrome
pyloroplasty
antrectomy
severing of the vagus nerve. this decreases gastric acid by diminishing cholinergic stimulation to the parietal cells, making them less responsive to gastrin.
vagotomy
nursing interventions for surgical therapy of peptic ulcer
-stop drinking fluids with meals, and not to drink for one hour afterwards.
-education
-help relieve stress
when the circular area of muscle surrounding the pylorus hypertrophies and obstructs gastric emptying.
hypertrophic pyloric stenosis
risk factors of hypertrophic pyloric stenosis
genetic disposition
hyential hernia
history of reflux
newborns at greatest risk
what race is at greatest risk of hypertrophic pyloric stenosis
caucasian
what gender is at greater risk of getting hypertrophic pyloric stenosis
male
are preterm, term or postterm babies at greatest risk of getting hypertrophic pyloric stenosis
term babies
clinical manifestations of hypertrophic pyloric stenosis
projectile vomiting (becomes worse as obstruction worsens)
pt is hungry, thin, pale, failure to thrive
vomiting happens after eating typically, but can be several hours after
dehydration signs on newborns
Olive shaped mass in RUQ
Peristaltic waves move left to right when baby supine
Metabolic alkalosis
Assessments of hypertrophic pyloric stenosis
Abdominal assessment:
see peristalsis after eating
firm round mass
right upper quad - olive shaped mass
Distention
Hypoactive bowel sounds
History of feeding and timing of vomiting
baby will be irritable after eating
pH status is alkaline
metabolic alkaosis - acid is coming out so less in system
signs of dehydration
Poor skin turgor
No tears
Dry mucus membranes
Sunken eyes and fontanelle
Weak cry
Electrolytes blood work CMP BMP
Airway
Weight
I & O
Priority nursing interventions for hyertrophic pyloric stenosis
Educate parents on care for baby
maintain fluids
watch for dehydration, electrolytes and I&O
assess vomit - color consistency
Raise bedhead to prevent aspiration
Monitor for signs of aspiration
Monitor O2
Monitor for signs of Metabolic alkolosis
Pre-op Nursing interventions for Hypertrophich Pyloric stenosis
Pass NG tube for decompression
Monitor how much and quality of what is removed
NPO
IV Fluids
Educate parents on procedure and expected outcomes
how to diagnosis hypertrophic pyloric stenosis
abdominal ultrasound
whatis the treatment for hypertropic pyloric stenosis
laparoscopic pyloromyotomy - ramstedts operation
pre op nursing interventions for hypertrophic pyloric stenosis
weight
monitor I &O
electrolytes - CMP, CBC
airway
check for olive shape mass
peristalsis
bowel sounds will be hypoactive
weigh baby daily
vital signs
NG tube for decompression
baby needs to be NPO, fluid via IV
monitor lab values
raise head of bed to prevent aspiration
assess for signs/symptoms for respiratory distress
teach parents what to expect and why doing what doing
post op nursing interventions for hypertrophic pyloric stenosis
Post op Vital signs
check gag reflex
Respiratory monitoring
assess bowel sounds as at risk of delayed peristalsis
start clear liquids 4-6 hrs post op (pedialyte)
Advance to breast milk/formula 24-48hrs post op
Document tolerance to feeding
Continue IV until feeding established
I&O and daily weights
teach parents what to do if newborn starts vomiting again, not eating, signs of infection
how to diagnose hypertrophic pyloric stenosis
ultrasound - see mass
Flat plate X-ray eliminates constipation
Barium swallow study, however not a good option if unable to flush barium through system because of blockage
what labs do you do for hypertrophic pyloric stenosis
check electrolytes - low Cl, K, Na
high pH (metabolic alkolosis)
Bicarb and Bilirubin high
Priority collaberative management hypertrophic pyloric stenosis
Drugs: none
Safety considerations: Resolve symptons and problem so baby can thrive
Collaberative management: Proper education for parents so they are able to manage recovery at home
this occurs when small, bulging pouches develop in your digestive tract.
Diverticulosis
when one or more Diverticula pouches become inflamed or infected, the condition is called
Diverticulitis
what are the small pouches that develop in the digestive tract called…
diverticula
Potential complications of Diverticulosis
Perforation
Obstruction
Abscesses
Hemorrhage
Fistula
Sepsis
Peritonitis
Modifiable risk factors for diverticulosis
not enough fiber in diet
low volume poop, high pressure in colon
constipation
Non-Modifiable risk factors for Diverticulosis
Advanced age (80 or over)
Congenital disposition (under 40)
the decrease muscle strength in the colon wall, from harden fecal masses create
constipation
can include bowel irregularity, with intervals of diarrhea, nausea, anorexia and abdominal distention
diverticulosis
this is acute onset of mild-severe pain in lower left quadrant
pt will have nausea, vomiting, fever, chills,
Leukocytosis (elevated WBC)
rebound tenderness indicative of perforation
can lead to sepsis
diverticulitis
rebound tenderness for diverticulitis can suggest what
perforation
what assessments do you do for diverticulosis/itis
get history, perform physical exam
look for signs of fever, vital signs (afebrile in older )
assess labs - look at WBC, occult blood in stool
get diet history - low fiber?
obtain weight and height
find out how active pt is - exercise?
do focused abdominal assessment
Signs and symptoms of peritonitis (rebound tenderness)
Possible palpable mass if abscess
Priority Labs for diverticulosis
CBC
Blood culture (has it progressed to diverticulitis)
Urinalysis
Stool for occult blood
ESR (erythrocyte sedimentation rate) inflammatory marker
Priority diagnostics for Diverticulosis
CT of the abdomen with contrast
Abdominal Xray for free air and fecal matter
Colonoscopy risky because of pre op sedation and possibility of perf
Barium enema visualizing colon and large intestines
Define cretinism
Thyroid deficiency present at birth
What is Euthyroid?
Thyroid hormone production that is within normal limits
What is exophthalmos
an abnormal protrusion of one or both eyeballs that produces a startled expression. Often seen in Grave’s disease
What is Chvostek’s sign ?
Facial twitching in response to tapping over the massetal muscle
what do you look for during focused abdominal assessment for diverticulosis/itis
abdominal tenderness
distention
palpable mass
watch for signs/symptoms of peritonitis,
rebound pain
loss of bowel sounds
what do you expect to see on abdominal xray for diverticulosis/itis
free air/fecal matter
What is Trousseau’s sign?
Is a specific type of muscle spasm in the hand and wrist that is a sign of latent tetany
what do you expect to see on CT of abdomen with contrast diverticulosis/itis
thickening of bowel and presence of abscesses
what labs do you look at for diverticulosis/itis
CBC, blood cultures, urinalysis, stool for occult blood and ESR
How do we assess for Trousseau’s sign?
Inflate a BP cuff to a number above the systolic rate of the patient and leave it for 3 minutes. A positive Trousseau’s will induce spasm in wrist and hand
what do you expect to see on colonoscopy for diverticulosis/itis
pockets
What does Trousseau’s sign assess for?
Hypocalcemia
waht medications do you use for diverticulosis/itis
antibiotics to treat infection
antispasmodics for pain and to relax area
bulk forming laxative - increase volume in colon
what is the surgery used for diverticulitis
bowel resection and anastemosis
Possible temporary colostomy to rest bowel before reanastemosis
*this is last resort
What does Chvostek’s sign assess for?
Hyperexcitability of the facial nerve due to Hypocalcemia
when is surgery used for diverticulitis
hemorrhaging, abscess, obstruction, peritonitis
what are the outpatient nursing interventions for diverticulosis/itis
Medications: Oral antibiotics antispasmotics, bulk forming laxatives,
dietary changes: clear liquids 2-3L per day to stay hydrated, high fiber and low fat, fresh veg
Lifestyle changes: No straining, wear loose fitting clothing
Goal- increase stool volume and decrease poop inside body time
What is Goiter?
An enlarged thyroid gland that presents as swelling of the neck
what are the inpatient nursing interventions for diverticulosis/itis
-NPO, NGtube
-if vomiting or distention - clear out (abdominal decompression)
-give IV fluids/antibiotics
-avoid NSAIDs give opioids
- advance diet as tolerated
- monitor for infection/complications
what can happen if give NSAIDs to pt with diverticulosis/itis
can cause perforation
What is Grave’s Disease?
An autoimmune disease of the thyroid gland that results in the binding of antibodies to TSH which causes over production of T3 and T4. A common cause of Hyperthyroidism
what do you teach a pt to get them ready for discharge if they have diverticulosis/itis
-how to avoid constipation
-high fluid intake
-reduce weight
-what factors would increase abdominal pressure (straining to poop, bending, lifting, vomiting, tight clothing, etc)
-eat lots of fresh vegetables
-avoid exacerbation of disease
- know what to look for
What is cushing’s syndrome?
A Pituitary tumor that causes overproduction of ACTH. Hypothyroidism occurs
What are striae ?
Purple stretch marks
What is truncal obesity?
Obesity of the trunk and thinness of the extremeties.
What is tetany?
Abnormal muscle spasms and overly stimulated peripheral nerves related to hypocalcemia
What is metabolic rate?
the rate at which a person metabolizes
What is Myxedema?
swelling of the skin and underlying tissues giving a waxy consistency, typical of patients with underactive thyroid glands. (Hypothyroidism)
What is Thyrotoxicosis?
Symptoms of hyperthyroxinimea
Why is the use of heating pads and electric blankets discouraged in Hypothyroid patients?
Because of the risk of peripheral vasodilation, further heat loss and vascular collapse
