Med Surg Final Flashcards
Hormonal Regulation Glucose Regulation (Diabetes and Hypoglycemia) Gas Exchange (Upper airway obstruction, allergic rhinitis/sinusitis, Influenza, sleep apnea) Lower Respiratory/Impaired Transportation (Anemia PE, Pneumonia, Tuberculosis, Asthma & COPD,) Blood Administration
Pituitary Gland
Located at the base of the skull. Divided in two two lobes 1.anterior and 2. posterior.
Secretes regulatory hormones that in turn regulates many bodily functions.
Anterior pituitary secretes (6 hormones)
Posterior pituitary secretes (2 hormones) - these hormones are produced in the hypothalamus and stored in the posterior pituitary gland where they’re secreted as needed.
Anterior Pituitary
- Thyroid Stimulating Hormone (TSH)
- Luteinizing Hormone (LH)
- Follicle stimulating hormone (FSH)
- Prolactin
- Growth Hormone (GH) ( TOO MUCH= acromegaly in adults)
- adrenocorticotropic hormone ( ACTH)- stimulates the secretion of glucocorticoids from the adrenal glands ( TOO MUCH= Cushings)
FLATPG
For this exam- just need to focus on TSH and GH
Posterior Pituitary
- Antidiuretic Hormone ( ADH; Vasopressin): Increases reabsorption of water in the kidneys ( deficiency = diabetes insipidous) Excessive = SIADH)
- Oxytocin
Disorders of the Posterior pituitary result in fluid/electrolyte imbalances
Acromegaly
Too much growth hormone that causes widespread overgrowth ( but not height), untreated can cause hypertension, Diabetes, and heart problems)
-onset is gradual
Risk Factors: Age, benign tumors ( Pituitary Adenoma
S/S:
- severe head aches
- visual disturbances (diplopia (double vision), decreased visual acuity)
- joint pain
- decreased labido
- enlarged hands and feets
- HYPERglycemia
- Barrel-shaped Chest
- lower jaw protrusion
- big head
- change in voice characteristics
- menstrual pattern changes
- sleep apnea
- Increased ICP ( decreased level of consciousness, pupillary changes, sever hypertension, widened pulse pressure, bradycardia and Seizures)
Diagnostics:
- X-ray
- CT/MRI
- Cerebral Angiography
Labs:
Growth Hormone suppression test- where GH is measured at baseline as well as after receiving glucose ( increase Glucose is expected to decrease GH) pts. With acromegaly with show either no decrease or only minor decrease in GH following administration of Glucose
Nursing Actions:
- obtain baseline GH and glucose levels
- administer glucose
- obtain Gh and blood glucose at 10, 60 and 120 min post glucose administration
( patients should be NPO, except water for 6-8 hrs prior to test)
Medications:
dopamine agonists- inhibit release of GH
( mesylate, cabergoline)
Somatostatin analogs - inhibit GH release
GH receprot blocker-
Surgical Interventions:
Hypophysectomy (Removal of pituitary gland/ tumors via endoscopic transnasal or oronasal approach)
Radiation- radiate the tumor
Patient Teaching:
If pituitary gland removed- pt will need life long hormonal replacement
- avoid activities that increase ICP
- oral care- to minimize effects of mouth breathing post surgery
- High fiber diet to minimize straining post op
Diabetes Insipidus
Primarily DI = decreased ADH
Decreased ADH reduces the ability of the distal renal tubules in the kidney to collect and concentrate urine, resulting in excessive diluted urination, excessive thirst, electrolyte imbalance and excessive fluid intake
Think *WATER WASTING
Types (4):
1. Primary - low ADH production caused by defects in hypothalamus or pituitary gland
- Secondary- lack of ADH caused by infection, tumor, head trauma or brain surgery
- Nephrogenic- inherited , renal tubules do not react to ADH
- Drug-induced- Lithium or demeclocycline can alter how the kidneys respond to ADH
Risk Factors:
- head injury, tumors or lesions, surgery, radiation near or around the pituitary gland.
- infections like meningitis or encephalitis
- clients on lithium/ demeclocycline
- older adults are at higher risk of dehydration due to generally lower water content in the body, decreased thirst response, decreased kidney function, increase use of diuretics, swallowing difficulties and inadequate food intake
S/S:
- polyuria ( abrupt onset of excessive urination) output of 4-30 L/day
- polydipsia ( excessive thirst)
- nocturia
- fatigue
- dehydration ( excessive thirst, weight loss, muscle weakness, headache, constipation, dizziness)
Physical Assessment findings:
- sunken syes
- tachycardia
- hypotension
- loss or absence skin turgor
- dry mucous membranes
- weak, poor peripheral pulses
- decreased cognition
Lab Tests:
Serum Chemistry ( THINK HIGHLY CONCENTRATED)
-increased osmolarity
-increased sodium
-increased potassium
-serum volume is lower, but serum concentration is higher
Urine Chemistry:
- Decreased Specific gravity ( less that 1.005)
- decreased osmolality
- decreased PH
- decreased sodium
- decreased potassium
- urine volume is increased and concentration decreases
Nursing Assessment/Considerations:
- Monitor vitals , urinary out put, I/O,
- Monitor Lab Values: specific gravity, BUN, potassium, sodium, creatinine)
- daily weights
- regular diet, but avoid foods/beverages with diuretic effects
- IV therapy: hydrate to match output, electrolytes replacement
- promote safety ( access to bathroom, bed pan, assist with ambulation as dizziness may be present)
- assess skin turgor and mucous membranes
- drink in response to thirst
Medications:
ADH replacement agents
( desmopressin, vasopressin ( IV, orally or intranasally)
- monitor vitals
- give cautiously to patients with coronary artery disease because it can cause vasoconstriction
- monitor I/O, labs
- monitor for headache, confusion or other signs of water intoxication
- for nasal preparations, teach clients to blow nose prior to clear nasal passage and have them sit up prior to inhalation
SIADH ( syndrome of inappropriate Antidiuretic Hormone)
SIADH is excessive release of ADH (OPPOSITE OF DI)
- common in lung cancers
THINK WATER HOLDING / NA WASTING
-leads to renal reabsorption of water and suppression of renin-angiotensin mechanism, causing renal excretion of sodium leading to water intoxication
Risk factors: conditions that stimulate the hypothalamus to hyper secrete ADH include malignant tumors, increased intrathoracic pressure ( like positive pressure ventilation), head injury, meningitis, stroke, tuberculosis, and medications such as ( TCAs, Chemo agents, SSRIs, Opioids, fluoroquinolone antibiotics)
S/S: early manifestations: - headache -weakness -muscle cramps -anorexia -weight gain (without edema because water, not sodium is retained)
As serum sodium levels decrease:
- personality changes
- hostility
- sluggish deep tendon reflexes
- nausea
- vomiting
- diarrhea
- oliguria with dark yellow concentrated appearance
Physical Assessment Findings
- confusion, lethargy, cheyne-stokes respirations,
- seziures, stroke, coma or death
manifestations of fluid volume excess ( hypervolemia) include: tachycardia, bounding pulses, possible hypertension, crackles in lungs, distended neck veins, taut skin, weight gain w/o edema, intake greater than output
Lab values:
Urine chemistry- Think Concentrated
- increase sodium
- increase urine osmolarity
- as urine volume decreases, urine osmolarity increases
Blood Chemistry - Think Diluted
- decreased sodium - dilution hyponatremia
- decreased osmolarity
- as serum volume increases, serum osmolarity decreases)
Nursing Care:
-restrict oral intake of fluid to 500-1,000ml/day to prevent further hemodilution- provide comfort measures for thirst, such as oral care, ice chips, lozenges and stagger water intake
- Flush all enteral and fastric tubes with normal saline- NOT WATER to replace sodium and prevent further hemodilution
- monitor I/O - report decrease output of urine
- monitor vitals for signs of increased BP, tachycardia and hypothermia
- auscultate lungs sounds- monitoring for Pulmonary edema
- daily weights
- report altered mental status
- reduce environmental stimuli
- provide safe environment, initiate seizure protocol
- monitor for indications of heart failure, which can occur from fluid overload, use of loop diuretics can be indicated
Medications : Vasopressin- promote water secretion without causing sodium loss -administer in acute care setting -monitor blood glucose -monitor serum sodium -I/O -bowel movement patterns -frequent oral care -monitor for sins of dehydration
Loop diuretics:
- increase water secretion in the kidneys
- caution for hyponatremia
- tell client to change positions - orthostatic hypotension
- monitor signs of hyponatremia (nausea/vomiting and decreased appetite)
- Hypertonic sodium chloride IV therapy
(3%-5%)
-monitor for fluid over load ( distended neck veins, crackles in the lungs, trouble breathing, onset of cough)
-changes in LOC
Thyroid
Thyroid gland produces 3 hormones
- thyroxine ( T4)
- Triiodothyronine ( T3)
- thyrocalcitonin ( calcitonin)
Secretion of T3 and T4 is regulated by the Anterior pituitary gland through a negative feedback mechanism
When T3 and T4 level decrease, TSH is released from the anterior pituitary , this stimulates more hormones to be released until normal levels are reached.
T3 and T4 affect all body systems by regulating overall metabolism, energy production, and controlling tissue use of fats, proteins and carbohydrates
Calcitonin- inhibits mobilization of calcium from bone and reduces blood calcium levels. Dietary intake of protein and iodine are necessary for the production of thyroid hormones
Hyperthyroidism
Excessive thyroid hormones- exaggerating normal body functions and produces a hyper-metabolic state
Risk Factors:
-Graves disease is the most common cause-autoimmune antibodies result in hypersecretion of thyroid hormones- AUTOSOMAL RECESSIVE TRAIT passed to females
- Toxic nodular goiter, is caused by over production due to thyroid nodules
- exogenous hyperthyroidism is caused by excessive dosages of thyroid hormone
S/S:
- nervousness, irritability, hyperactivity, emotional lability, low attention span, crying/laughing without cause, change in mental status/emotional status
- weakness, easily fatigability, exercise intolerance
- muscle weakness
- heat intolerance
- weight change( usually loss), increased appetite
- insomnia, change in sleep patterns
- frequent stools and dirrhea
- menstrual irregularities ( usually amenorrhea, decreased flow or infertility)
- initial increase in libido, then gradually decrease as the disease progresses
- warm, sweaty, flushed skin with velvety smooth texture
- hair thinning, fine, soft, silky texture
- tremors, hyperkinesia, hyperreflexia
- Bulging eyes
- enlarged thyroid ( goiter)
- vision changes
- elevtaed systolic blood pressure
- widened pulse pressure
- tachycardia, palpatations, dysrhythmia
- dyspnea
- older adults may present with heart failure, angina or afib
Lab Tests:
Serum TSH: decrease in graves disease, but possibly elevated in secondary or tertiary hyperthyroidism
T4, T3- elevated in presence of disease
Diagnostic procedures:
- Ultrasound images of thyroid gland and surrounding tissues
-electrocardiogram - used to evaluate the effects of excessive TH on the heart(tachycardia, dysrhythmias) ECG changes include a-fib and changes in P and T waves)
- Radioactive Iodine uptake - nuclear medicine test
- clarifies size and function of gland
- contraindicated in pregnancy
- assess for allergy to iodine/shellfish
- the uptake of radiactive iodine orally, 24 hours prior to test is measured
- elevated uptake is indicative of hyperthyroidism
nursing considerations pre scan
- med list- to determine use of iodides
- allergies
- confirm not pregnant
- recent use of contrast media/ birth control- can cause false positives
- severe illnesses, malnutrition, use of aspirin, steroids, phenytoin sodium can cause false decreases in TH levels
- inform provider if pt received iodine contrast recently
-advise client to avoid foods high in iodine for 1 week suggest the use of non-iodized salt, avoid fish shellfish and medications containing iodine
Nursing Considerations:
- minimize clients energy expenditure, encourage alternation of activity and rest and assist with activities as necessary
- promote calm environment
-assess mental status changes and decision-making ability
-Monitor nutritional status, providence increase calories and protein- other nutritional support as necessary
-I/O
-Daily weights
- provide eye protection/lubricants, tape eyes closed for pts. with exophthalmos
- monitor vitals and hymodynamic parameters
-reduce room temperature
- provide cool showers/sponge bath to promote comfort
-provide frequent linen changes
- MONITOR TEMPERATURE- an increase of 1* could indicate impending thyroid crisis
-monitor for ECG changes
-avoid excessive palpation of thyroid
-administer antithyroid medications or if goiter is obstructing airway
if unresponsive to med prepare for total/subtotal thyroidectomy
Medications:
Thiaonamides -inhibit productino of thyroid hormones ( methimazole, propylthiouracil)
beta-blockers ( -OLOL)
help with sympathetic nervous system effects of hyperthyroidism
Radioactive iodine therapy- higher doses destroys some of the hormone-producing cells- one dose could be sufficient, or two to three may be needed. - destruction of cells caries and lifelong thyroid replacement therapies may be needed ( effects can take 6-8 weeks to be evident, stay away from pregnant women, children or infants for the first week following treatment, avoid contact closer than 3 feet - and limit for no more than 1 hr daily )
-monitor for sign of hypothyroidism (edema, intolerance to cold, bradycardia, weight gain and depression)
Thyroidectomy -
pre-procedure:
-thianomides for 4-6 weeks prior to surgery
-iodine 10-14 days prior to surgery to help shrink glands
-high protein high carb diet prior to surgery
Post-precedure:
- support the neck when doing deep breathing and coughing exercises ( q30-60mins)
- keep pt in semi fowlers- support head and neck with pillows
- avoid neck extensions
- vitals q15 until stable then q30
- provide oral/trach suctioning as needed
- check surgical site and BACK OF NECK for signs of bleeding ( hemorrhage most likely in first 24 hrs)
- respiratory distress due to swelling and surgical site/compression of trachea
- humidify air
- ask pt to speak upon waking from anesthesia and q2 hrs to check for laryngeal nerve damage
-Hypocalcemia and Tetany can occur if parathyroid glands are damage or removed
( indications are tingling of toes or around mouth, muscle twitching)
-check for chvosteks (face) and trousseaus (wrist) signs
- ENSURE IV CALCIUM GLUCONATE AND CALCIUM CHLORIDE ARE IMMEDIATELY AVAILABLE)
voice may be hoarse
notify nurse of any tingling sensations
-scant bleeding after 24 hrs
Thyroid Storm/Crisis
sudden surge of large amounts of thyroid hormones into the bloodstream
MEDICAL EMERGENCY- high mortality rate
-most commonly in graves disease, infection, trauma, emotional stress, diabetic ketoacidosis and digitalis toxicity , post surgical procedure or thyroidectomy
S/S:
- hyperthermia
- hypertension
- delirium
- vomiting
- abdominal pain
- tachydyrhythmias
- chest pain
- dyspnea
- palpitations
Nursing Considerations:
- maintain paten airway
- provide cardiac monitoring
- administer acetaminophen to decrease temp
- provide cool sponge baths
- administer thionamides
- 1 hr later administer iodide
- administer beta-blockers for heart sxs
- administer glucocorticoids if adrenal insufficiency is suspected or to treat shock
- IV fluids to provide adequate hydration and vascular collapse
- give O2
Hypothyroidism
Low levels of circulating T3 and T4 causing a decrease in metabolic rate
*hypothyroidism can have manifestations that mimic the aging process, so it goes often undiagnosed in elder clients, leading to serious adverse effects from medications ( sedatives, opiates and anesthetics)
Primary- dysfunction of the gland, typically caused by autoimune thyroiditis, medications that decrease synthesis of TH, and loss of thyroid gland due to surgery, radiation, iodine deficiency
secondary- caused by failure of anterior pituitary to stimulate thyroid gland or failure of surrounding tissues to respond to tyroid hormones, ( pituitary tumors)
Tertiary - failure of hypothalamus to produce thyroid-releasing hormone
Risk Factors:
women 30-60 effected 7-10Xs more than men
-mild hypothyroid often goes undiagnosed, but can contribute to increase acceleration of atherosclerosis and complications of medical treatment
-can be cause by lithium or amiodarone
-inadequate intake of iodine
-radiation to head/neck
S/S: ( often vague and varied sxs that develop slowly over time)
- fatigue
- irritabilty
- intolerance to cold
- constipation
- weight gain without increased caloric intake
- pale skin
- thick, brittle fingernails
- depression/apathy
- periorbital edema
- joint/muscle pain
- bradycardia, hypotension, dysrhythmias
- slow thought/speech
- hypoventilation, pleural effusion
- thickening of the skin
- swelling in face, hands and feet ( myexedema: non-pitting mucinous edema)
- decrease acuity of taste and smell
- hoarse, raspy speech
- abnormal menstrual periods
- decreased libido
Lab results
- decreased T3 and T4
- increased serum cholesterol
- increase in TSH in primary hypothyroidism
- decrease in TSH in secondary hypothyroidism
Diagnostic procedures:
-radioisotope scan- clients will have a low uptake of iodine
-ECG: sinus bradycardia, dysrhythmias
Nursing Considerations:
- monitor for cardiovascular changes (low BP, bradycardia, dysrhythmias)
- monitor weight
- assess for peripheral edema
- increase clients activity level gradually, provide frequent rest periods to avoid fatigue and decrease myocardial oxygen demand
- compression stalkings and elevation of legs to assist in venous return
- monitor respiratory status including rate, depth, o2 sat, arterial blood gas
- encourage cough and deep breathing to prevent pulmonary complications
- provide good skin care, avoid alcohol based products, provide emollient lotion after bathing
- provide clothing/blankets for client with cold intolerance- adjust room temp
- caution client in using heating blankets
- CAUTION with mediations due to alteration in metabolism
Medication MGMT:
levothyroxine- thyroid hormone replacement therapy
-increase the effects of warfarin and can increase the need for insulin and digoxin
-medications that accelerate the metabolism of levothyroxine ( phenytoin, carbamazepine, rifampin, sertraline, phenobarbital ) - thus increased dose may be needed to reach therapeutic effects
-begin slowly in elder adults who may have CAD to avoid coronary ischemia because of increased oxygen demands of the heart.
-take medication on empty stomach
-avoid supplements unless discussed with provider- excessive calcium, iron or antacids can interfere with absorption
- lifelong replacement will be necessary
Myxedema Coma
life-threatening condition that occurs when hypothyroidism is untreated or when a stressor (acute illness, surgery, chemo, discontinuation of thyroid replacement meds or use of sedative/opiates) affects a client who had hypthyroidism
S/S:
- respiratory failure
- hypotension
- hypothermia
- bradycardia
- hyponatremia
- hypoglycemia
- coma
Nursing Considerations:
- maintain airway- with ventilator if necessary
- provide continuous ECG monitoring
- Monitor ABGs to detect hypoxia, hypercapnia ( aka hypercarbia, aka co2 retention) and respiratory acidosis
- monitor mental status
- cover client with warm blankets
- monitor temperature hourly until stable
- replace fluids with normal saline
- replace thyroid hormones by IV bolus
- monitor vitals cause rapid correction can cause cardiac issues
- monitor I/Os and daily weights
- treat hypoglycemia with glucose
- administer corticosteroids
- initiate aspiration precautions
- check for sources of infection that may have precipitated the coma, treat underlying illness
Control of Hormonal Secretions:
Negative feedback
Positive feedback
Biological rhythms
Central nervous system control
Hormonal Circadian Rhythms
Growth hormone- increases during sleep, decreases during wakeful state
cortisol- highest in morning, slowest during sleep
prolactin- resembles growth hormone cycle
aldosterone-peaks in afternoon, declines in evening
testosterone- low in afternoon, high in night
Cushings syndrome
hypercortisolism- cause by over excretion cortisol from the adrenal cortex
Risk Factors: women ages 20-40
Causes:
Tumor of pituitary gland that results in the release of ACTH ( Adrenocorticotropic hormone) that then stimulates cortisol excretion in adrenal cortex.
-can also be cause by hyperplasia( increase or enlargement of an organ or tissue due to increased reproduction of its cells) of the adrenal cortex
-carcinomas of the lung, GI tract or pancreas ( these tumors can secrete ACTH)
-exogenous causes of increased cortisol:
therapeutic use of glucocorticoids for the following:
-organ transplant
-chemo
-autoimmune diseases
-asthma
-allergies
-chronic inflammation
Health promotion/disease prevention:
- take meds!
- eat foods high in calcium and vitamin D
- monitor for gastric bleeds ( coffee ground emesis)
- monitor daily weights
- avoid infections
S/S:
- weakness
- fatigue
- sleep disturbances
- back and joint pain
- altered emotional state (irritability, depression)
- decreased libido
Physical Assessment findings:
- evidence of decreased immune function and decreased inflammatory responses( infections without fever, swelling, drainage, redness)
- thin, fragile skin
- bruising and petichia
- hypertension ( caused by sodium and water retention)
- tachycardia
- gastric ulcers due to over secretion of hydrochloric acid
- weight gain and increased appetite
- irregular periods
- dependent edema
- fat accumulation in the face, truncal obesity, BUFFALO HUMP
- fractures
- bone pain
- muscle wasting
- impaired glucose control
- hirsutism
- acne
- striae ( stretch marks, very red)
- hyperglycemia
- emotional lability
LAB Values:
-elevated cortisol ( check urine for elevated free cortisol as well) in the absence of acute illness or stress
if caused by increase in ATCH by anterior pituitary- ACTH level will be elevated
if caused by disorders of adrenal cortex or medication therapy - ACTH levels will be decreased
-salivary cortisol confirms the diagnosis of cushings
- decreased Potassium and Calcium levels
- increased glucose
- increased sodium
- decreased lymphocytes
Diagnostics:
X-ray, CT, Radiological imaging
Nursing Care:
- Monitor I/O
- assess for hypervolemia (edema extended neck veins, shortness of breath, adventitious lung sounds, hypertension, tachycardia)
- maintain safe environment
- meticulous skin care
- decrease infection risk
- change clients position q2hrs
- monitor WBCs daily
Medication treatments ( depend on the cause of the disease) -
- Ketoconazole ( antifungal agent that inhibits adrenal corticosteroid synthesis at high doses) ( used supplementally with radiation or surgery)- monitor for hepatotoxicity
- Mitotane- produces selective destruction of adrenocortical cells ( purpose to reduce tumor size)
hydrocortisone- for replacement therapy for clients who have adrenocortical insufficiency
Risk Factors for altered Hormone Regulation
Hormonal supplement therapy Advanced age Obesity Sedentary lifestyle Genetics Chromosomal deficiencies/abnormalities Family history, especially autoimmune responses/conditions Stress Trauma Chronic medical conditions Cancer treatment
transsphenoidal hypophysectomy
Avoid activities that increase pressure at site
Monitor patient for
- Meningitis
- CSF leakage ( halo sign, yellow around the edges, clear in the middle fluid) or glucose containing clear fluid from nose
- Diabetes Insipidus
- Increased intracranial pressure
Post operative Assessment:
- Neuro exam( q1 hr for the first 24 hrs)
- I/O – monitor drainage
- Urine specific gravity
- Desmopressin or vasopressin
- IV access
- Increase HOB
- Mouth care ( due to mouth breathing, given the drip padding under nose)
- Give glucocorticoids to prevent and abrupt drop in cortisol levels
- Give stool softener or laxative to reduce strain
- teach pt they may experience numbness at incision site and diminished sense of smell for 3-4 months post op
- avoid bending at the wait
- avoid teeth brushing for 2 weeks ( floss and rinse mouth instead)
- advise on head ache, confusion and bleeding
- these patients are also at risk or GI bleeds ( monitor for coffee group emesis, due to increased cortisol levels, levels of protective gastric mucosa are diminished*
Adrenal Cortex- Hormones
Sugar, salt, sex
Sugar- glucocorticoids (cortisol) - cortisol affects glucose, protein and fat metabolism; the bodys response to stress; and the bodys immune function
Salt- mineralcorticords (aldonsterone)- aldosterone increases sodium absorption and causes potassium excretion by the kidneys
Sex- mineralcorticords (androgens/estrogens; testosterone)
Addison’s disease
adrenocortical insufficiency - caused by damage or dysfunction of adrenal cortex
( DECREASE IN ALDOSTERONE AND CORTISOL)
Risk factors for primary Addisons:
- Ideopathic autoimmune
- tuburculosis
- histoplasmosis
- adrenalectomy
- cancer
- radiation therapy of the abdomen
Causes of secondary Addisons:
- steroid withdrawal
- hypophysectomy
- pituitary neoplasim
- high dose radiation of pituitary gland or entire brain
S/S:
- weight loss
- craving for salt
- hyper-pigmentation
- weakness and fatigue
- nausea and vomiting
- abdominal pain
- constipation or diarrhea
- orthostatic hypotension
- dizziness
- severe hypotension
- dehydration
- hyponatremia
- hyperkalemia
- hypoglycemia
- hypercalcemia
- manifestations of chronic Addison develop SLOWLY*
- manifestations of acute adrenal insufficiency develop rapidly-
Lab Values:
- Increased Potassium
- decreased sodium
- increased calcium
- Increased BUN and Creatinine
- decreased serum cortisol
Nursing Care:
- monitor for fluid/electrolyte imbalances
- give saline infusions to restore fluid volume
- observe for dehydration
- give hydrocortisone infusion or bolus
- monitor for and treat hyperkalemia
- obtain serum K+ values and ECG
- assess vitals frequently
- give insulin, calcium, glucose and bicarb as needed
- monitor and treat hypoglycemia (monitor for neurological changes)
- safety precautions- fall risk
Hyperaldosteronism (CONN’s Disease)
Primary and Secondary etiology
Cause: -most common cause is ideopathic -second most common is adenoma Manifestations – hypertension and hypokalemia -increase urine potassium -increase in plasma levels of aldosterone and sodium -decrease in renin plasma levels -Increased BP
Collaborative Care:
( when you see hypokalemia and HTN- suspect CONNS)
Diagnostics:
- CT Scan
- EKG changes
- Labs
Parathyroid Disorders
Hyperparathyroidism
Hypoparathyroidism
PTH increased the excretion of calcium by the kidneys into the urine
PTH enhances the release of calcium from bones into the bloodstream
Hyper- Increased serum calcium
Hypo - decreased serum calcium
BONES,STONES, GROANS
Hypo/hypercalcemia
Goiter
Hypertrophy and enlargement of the thyroid
Caused by excessive TSH stimulation from inadequate thyroid hormones
Can be caused by Goitrogens (foods or drugs that suppress gland function)
Enlargement of gland
Interferes with iodine uptake
Surgery may be necessary
What is a priority nursing diagnosis for this patient?
( airway)
Nodules
Palpable deformity
May be benign or malignant
Major sign of thyroid cancer is a hard, painless, nodule on an enlarged gland
Diagnostics:
Ultrasound, CT scan, thyroid scan, MRI and/or Fine Needle Aspiration (FNA)
Thyroiditis
Inflammation of thyroid
Can be viral, bacterial, fungal, or autoimmune
Can lead to hypothyroidism (Hashimoto’s)
Usually thyroid hormones are elevated but then may become depressed
TSH low, then elevated
Treatment depends on cause and manifestations
Thyroidectomy Post-op Care
Airway – tracheostomy tray at bedside WHY?
ANS: bleeding, swelling of the airway
Assess for bleeding. How? Where?
ANS: behind the neck
Position – Semi Fowlers
Avoid flexion of neck, neutral position of neck
Monitor vital signs and which electrolyte imbalance?
hypocalcemia ( if the parathyroid was damaged or removed)
Diet – permitted to take fluid as soon as tolerated and soft diet the next day
adrenal Crisis ( acute adrenal insufficiency)
RAPID onset due to Sudden drop in corticosteroids is due t sudden tumor removal, stress of illness, trauma, surgery or dehydration, or abrupt withdrawal of steroid medications
if not quickly diagnosed and treated- prognosis is poor.
S/S:
- hypotension
- hypoglycemia
- hyperkalemia
- abdominal pain
- weakness
- weight loss
Nursing Actions:
- start IV line and administer rapid infusion of Normal saline
- administer glucocorticoids to treat acute insufficiency
- administer insulin with dextrose or loop diuretic to treat the hyperkalemia ( move potassium into cells)
- give calcium to counteract the effects of hyperkalemia and protect the heart
- if acidosis occurs, give bicarb
- administer glucagone or iv glucose for the hypoglycemia
- monitor vitals and gluose levels
- monitor for ECG changes
adrenal Crisis ( acute adrenal insufficiency)
RAPID onset due to Sudden drop in corticosteroids is due t sudden tumor removal, stress of illness, trauma, surgery or dehydration, or abrupt withdrawal of steroid medications
if not quickly diagnosed and treated- prognosis is poor.
S/S:
- hypotension
- hypoglycemia
- hyperkalemia
- abdominal pain
- weakness
- weight loss
Nursing Actions:
- start IV line and administer rapid infusion of Normal saline
- administer glucocorticoids to treat acute insufficiency
- administer insulin with dextrose or loop diuretic to treat the hyperkalemia ( move potassium into cells)
- give calcium to counteract the effects of hyperkalemia and protect the heart
- if acidosis occurs, give bicarb
- administer glucagon or iv glucose for the hypoglycemia
- monitor vitals and glucose levels
- monitor for ECG changes
Homeostasis of blood glucose regulation requires (3)
Balanced Nutrient intake
Balanced Hormonal signaling
Balanced Glucose uptake by the cell
Hypoglycemia
State of insufficient or low blood levels, defined as less than 70 mg/dL
Possible Causes:
- Insufficient Nutritional Intake
- Adverse Reaction to Medication
- Excessive Exercise
S/S:
- irritability
- fatigue
- mental confusion
- seizures
- unconsciousness
- potentially leads to cellular death
TREATMENT:
Rule of 15s
- eat/drink 15g carbs
- wait 15 min
- check blood glucose
- less than 70mb- repeat steps 1-5
Once BG >70 mg/dL – give complex CHO with protein or fat
If pt is crashing or unconscious- give glucagon 1 mg, sub Q or IM
OR
50% Dextrose (D50) 25-50ml IV push
Hyperglycemia
State of elevated blood glucose levels, defined as more than 100 mg/dL in a fasting state or 140 mg/dL when not fasting
- Insufficient Insulin -Production/Secretion
- Deficient Hormone Signaling
- Excessive Counter-regulatory Hormone Secretion
Short-term consequences :
Inadequate glucose reaching the cells
Dehydration
Long-term consequences: End-organ disease due to microvascular damage Retinopathy Nephropathy Peripheral neuropathy
Macrovascular angiopathy:
Hypertension
Cardiovascular and peripheral vascular disease
Collaborative Care:
- Education about glucose regulation
- Nutrition therapy
- Pattern management: monitoring meal-related blood glucose values
- Pharmacological agents
- Oral hypoglycemic agents
- Insulin
ketones in urine associated with hyperglycemia- greater than 300mg=medical emergency
Diagnostic test for diabetes
- Fasting Plasma glucose
- No caloric intake for at least 8 hrs.
-Impaired Fasting Glucose = 100-126
Critical Values :
<60 mg/dl or >500 mg/dl
2.Random Glucose test
-Can be drawn any time
-Meals, drugs, stress can cause increase
-Critical values
>180 mg/dl on two occasions
>200 mg/dl with s/s hyperglycemia
- Two-Hour Glucose Tolerance Test ( OGTT)
-Multiple blood draws over 2 hrs. after a glucose load of 75 g
-200 mg/dl or more = diabetes
>140 and <199 = pre-diabetes
Glycosylated Hemoglobin A1c (HbA1c)
A blood test that measures the amount of glycosylated hemoglobin in the blood (Hemoglobin is a protein found in the blood)
Glycosylated hemoglobin means that glucose (sugar) has attached to the hemoglobin protein
The higher the blood sugar, the more that glucose gets attached to the hemoglobin
Glucose attaches to Hgb and remains attached to the RBC for it’s lifespan (90 days)
- Indicates overall long term average glucose control for previous 60-90 days
- Near-normal levels over time markedly reduce risk of complications
Conditions that affect RBC turnover may alter HbA1c (sickle cell, anemia, hemolysis, etc.)
Normal range: 4 to 5.6 %
Prediabetes: 5.7-6.4%
Goal: 6.5% or less
Other diagnostic testing for glucose regulation disorders
Urine- checking for protein and/or ketones
Kidney function tests
people with a BMI of >25 at risk for glucose regulation issues
Diabetes Mellitus
- Multi-system disease related to abnormal insulin production, impaired insulin utilization or both
- Disturbance in carbohydrate, protein and fat metabolism
- heart disease, cerebral vascular accidents, renal failure, blindness, and non traumatic limb amputation
Glycemic control reduces complications of diabetes
Treatment of hypertension and hyperlipidemia is essential
Types of DM
- Pre-diabetes (Impaired Glucose Tolerance)
- Type 1
- Type 1.5 - Latent autoimmune diabetes in adults (LADA)
- Type 2
- Type 3
- MODY (maturity onset diabetes of the young)
- Gestational
-Secondary diabetes: Chemical induced
Disease induced
Hormonal
Type 1.5
- Slow progressing form of autoimmune diabetes
- Occurs because your pancreas stops producing adequate insulin, most likely from some “insult” that slowly damages the insulin-producing cells in the pancreas.
- Often won’t need insulin for several months up to years after being diagnosed.
- Usually diagnosed over 30 years
- At first, LADA can be managed by controlling blood glucose with diet, weight reduction if appropriate, exercise and, possibly, oral medications.
- As the body gradually loses its ability to produce insulin, insulin injections will eventually be needed.
Type 3 Dm
alzheimers related DM
- Evidence suggests that AD represents a form of diabetes that selectively involves the brain and has molecular and biochemical features
- Rapid growth in the literature pointing toward insulin deficiency and insulin resistance as mediators of AD
- People with type 2 diabetes have an increased risk of suffering fromAD disease estimated to be between 50% and 65% higher.
MODY ( maturity onset diabetes of the young)
- 1-5% of DM cases
- Autosomal dominant
- Leads to Beta cell dysfunction
- Usually before age of 25
- Not associated with obesity or hypertension
- Treatment depends on the genetic mutation
Pre-diabetes
Prediabetes/Impaired Glucose Tolerance (IGT)/Impaired Fasting Glucose (IFG)
- Beta cells become fatigued from overproduction
- Beta cell dysfunction is mild (with slight increase in glucose)
- Patients with IGT are increased risk for DM II (usually within 10 years)
Fasting glucose levels above 100
- pre-diabetes can prevent or delay the development of Type 2 diabetes through changes to their lifestyle that include modest weight loss and regular exercise
- long-term damage, especially the cardiovascular system, already may be occurring during pre-diabetes
Type 1
-Failure of the pancreas
-May be genetic – recessive
-Can be caused by toxins or virus
5-10 % of all diabetics
-Usually under age of 40
-Peaks before 20 years of age
- same incidence in males and females
- Patients are usually thin/lean but may be obese
- Progressive destruction of Pancreatic B cells
- Requires exogenous Insulin
- Diabetic Ketoacidosis (DKA)
Acute onset- 3Ps
- polydipsia
- polyphagia
- polyuria
- weight loss
Type 2 DM
- Most prevalent (90% of patients)
- Genetics – dominant and multifactorial (
- Insulin resistance
- Highest among Native Americans and Hispanics followed by African Americans
correlated with obesity
- over the age of 35
- also identified in young people- especially with the increase of childhood obesity
- pancreas still manufactures SOME insulin
- but its usually insufficient to meet the needs of the body and/or poorly utilized by tissues
- body tissues do not respond to insulin
- insufficient number of receptors or the receptors are unresponsive
- hyperglycemia
- hyperinsulinemia
can result in HHNK
( hyperosmolar hyperglycemic nonKetotic state)
s/s: non specific manifestations Can be 3 P's -fatigue -recurrent infections -visual changes -prolonged healing
Metabolic Syndrome
-primarily occurs in Type 2 Diabetes
Metabolic Syndrome - cluster of abnormalities working synergistically to greatly ↑ risk for CV disease and diabetes
- Elevated insulin levels (insulin resistance)
- High triglycerides
- Decreased HDL
- Increase LDL
- Hypertension
- Obesity (esp. central obesity)
- Sedentary Lifestyle
- Estimated 34% of Americans fit the criteria
- Can be treated with weight loss and exercise
Insulin Therapy
Drug Therapy- Exogenous Insulin
Why can’t exogenous insulin be taken orally?- destroyed by gastric enzymes before it can reach the cells
Onset-Peak-Duration
Sliding Scale
insulin pumps, ports, pens, Omnipods, insulin jets
Nutritional Therapy for glucose regulation
Nutritional Therapy – Individualized to patient (Table 44.6)
CHO:
include fruits, vegetables whole grains and low-fat milk
Fiber intake 25-30 g/day
Protein:
High protein diets for weight loss not recommended
15-20% of daily intake
Fats:
Minimize trans fats
Dietary cholesterol <200mg/day
At least 2 servings/week of fish
Alcohol:
Limit to moderate amounts
Effect of Alcohol on sugar?
alcohol decreases serum blood glucose and can cause hypoglycemia
Collaborative care for DM
*Lowers blood glucose by increasing CHO metabolism
Fosters weight reduction & maintenance
Increases insulin sensitivity
Increases high-density lipoprotein (HDL) levels
Decreases triglyceride levels
Lowers blood pressure
Reduces stress & tension
Monitor blood sugars before and after exercise
Best done after meals
Moderate activity level such as brisk walking or active housework
If BS <100 mg/dL – delay exercise
If BS >250mg/dL and with ketones in urine– postpone exercising
Monitor by healthcare providers – adjustment of medications
Illness and DM
Illness causes increased BS… Eat regular diabetic diet Increase non-caloric fluids Continue with oral agents and/or insulin Monitor BS every 4 hrs. If > 240 check urine for ketones and report \+ ketones to physician
If Illness leads to decreased PO intake…
Supplement CHO food intake with CHO-containing fluids while continuing with oral agents and/or insulin
Notify physician immediately if unable to keep any food or fluids down
Foot Care and DM
Risk of amputation 15X higher in diabetics
Foot care/assessment
Proper footwear
Podiatrist
Somogyi Effect
Somogyi Effect: A rebound effect in which an overdose of insulin induces morning hyperglycemia
Results in ↓ B.S. in middle of night as a response to ↑ insulin
Compensatory mechanisms occur to raise glucose (release of counter-regulatory hormones → gluconeogenesis etc.)
Results in overcompensation, leading to rebound hyperglycemia and ketosis noted in the AM.
Problem: Possible undetected hypoglycemia during the night
Treatment
Check B.S. between 2 AM and 4 AM
If this AM B.S. is low …then reduce PM dose of insulin OR eat a more substantial bedtime snack
Dawn Phenomenon
Hyperglycemia noted on awakening in AM due to release of hormones in predawn hours
- Growth hormone is possible factor
- Affects majority of those with diabetes but most severe in adolescence and young adulthood
Problem: high B.S. usually after 3 AM
Treatment
Check B.S. between 2 AM and 4 AM
If high, then increase insulin and eat bedtime snack
Change timing of evening intermediate acting from dinnertime to bedtime
Diabetic Ketoacidosis ( DKA)
Onset Over 4-10 hours - Medical EMERGENCY- Type 1 only
SERUM GLUCOSE GREATER THAN 300
serum sodium - normal, low or high
sodium potassium depends on how long DKA existed prior to treatment- decreases with treatment
Increase in BUN (>30) and Creatinine (>1.5)
ketones present in serum and urine
metabolic acidosis with respiratory compensation
PH less than 7.3
Causes:
- lack of sufficient insulin related to undiagnosed type 1 or nonadhearance to medication regimen
- reduced or missed dose of insulin
- any condition that increases carbohydrate metabolism (physical or emotional stress, illness, infection (#1 cause of DKA), surgery or trauma)
- increased hormone production( cortisol, glucagon, epinephrine), stimulates the liver to produce glucose and decreases the effects of insulin
Expected findings:
- polyuria
- polydipsia
- polyphagia
- weight loss
- GI effects ( N/V/Abdominal pain)
- blurred vision
- orthostatic hypotension
- fruity odor of breath
- kussmaul respirations ( deep labored breathing)
- metabolic acidosis
- mental status changes
Hyperglycemic Hyperosmolar State (HHS)/Hyperosmolar Hyperglycemic Nonketotic State (HHNK)
MEDICAL EMERGENCY -Occurs in patients who produce enough insulin to prevent DKA- Type 2 only
SERUM GLUCOSE GREATER THAN 600
serum sodium- normal or low
serum potassium- normal to high as a result of dehydration
Increase in BUN (>30) and Creatinine (>1.5)
ketones NOT present in urine or serum
- Not enough insulin to prevent osmotic diuresis, hyperglycemia or ECF depletion
- Increase in serum osmolarity
- BS >400mg/dl
- Ketones are absent
absence of acidosis
PH :greater than 7.4
Causes:
lack of insulin related to undiagnosed DM, enough to prevent ketosis, but not enough to prevent hypoglycemia.
-inadequate fluid intake or poor kidney function
-most common in elder adults 50-70
-mortality rates in elders are between 40-70%, due to late treatment and overall poorer health
-medical conditions such as MI, Stroke or sepsis can cause HHNK
- can be caused by some medication such as : glucocorticoids, thiazide diuretics, phenytoin, beta blockers, calcium channel blockers
-infection and stress
Expected findings:
- polyuria
- polydipsia
- polyphagia
- weight loss
- blurred vision
- orthostatic hypotension
- mental status changes
- seizures, myoclonic jerking
- reversible paralysis
Treatment for DKA and HHNK
Medical emergency
-IV administration of NSS the hypotonic- ½ NSS
-Regular insulin IV
-When glucose falls < 250 add IV glucose
(D5 ½)
-monitor serum potassium - initially they will be increased but with iv insulin potassium will shift back into the cell and pt is at risk for hypokalemia
-Electrolyte replacement
-Bicarbonate for pH<7.10
-Treat underlying cause and complications
-cardiac monitoring- why?
pts with known DM should monitor blood glucose every 1-4 hours when ill
-wear medical alert bracelet
Medication treatments for type 2 DM
biguanides- metformin
-reduces the production of glucose in the liver ( glycogenesis)
-take with food
STOP taking it 48 hours before/after any tyoe of radigraphic test with iodinated contrast dye- can cause lactic acidosis and kidney failure
second gen. sulfonylureas - glipizides, glyburide
-stimulates insulin release from pancreas causing decrease blood glucose
-take 30 min before meals
Gas exchange
Conceptually: process by which oxygen is transported to cells and carbon dioxide is transported from cells.
Process: interaction among the following systems…
Neurologic
Respiratory
Cardiovascular
Impairment of gas exchange occurs when the diffusion of gases (oxygen and carbon dioxide) becomes impaired because of
- Ineffective ventilation
- Reduced capacity for gas transportation (reduced hemoglobin and/or red blood cells)
- Inadequate perfusion
Consequences of impaired gas exchange include:
- reduced oxygen in blood( hypoxia)
- absence of oxygen in blood ( anoxia)
- oxygen-deprived tissues
- CELL DEATH
Risk Factors for Impaired Gas Exchange
- Age
- Smoking
- Chronic medical conditions,
- Immunosuppression
- Reduced state of cognition
- Brain injury
- Prolonged immobility
Primary Prevention of impaired Gas exchange
-Infection control
-Smoking cessation
-Immunizations
-Influenza – Given Yearly - Check for egg allergies prior to flu shot
-Pneumococcal
-PCV13 (Pneumococcal Conjugate) -recommended @65 yrs.
or younger who are high risk
-PPSV23 (Pneumococcal Polysaccharide) – recommend @65 yrs. or younger if smoker or have asthma
-Preventing postoperative complications
Diagnostic Tests for impaired gas exchanged
Screening Tests:
Mantoux skin test
Interferon-gamma release assays (IGRAs).
Laboratory tests: Throat culture Arterial blood gases Complete blood count D-Dimer test Sputum Biopsy
-Pulse Oximetry
-Radiologic studies
(Chest x-ray,
CT scan and Spiral CT scan
MRI scans,
ventilation/perfusion (V/Q) scan,
positron emission tomography (PET) scan)
-Pulmonary function studies/Peak Flow
Bronchoscopy
-transbronchial needle biopsy
Thoracentesis
Collaborative interventions for Impaired gas exchange
Pharmacotherapy: β-adrenergic Agents (short and long acting) Corticosteroids Anticholinergic Agents Methylxanthines Mucolytics Antibiotics Decongestants/Expectorants/Antitussives
Cor Pulmonale
Alveolar hypoxia–>pulmonary capillary vasoconstriction–>increased pulmonary artery pressure (pulmonary hypertension)–> hypertrophy of right ventricle–> right-sided heart failure
Polycythemia
- Physiologic compensation for hypoxemia.
- Increased RBC’s but not able to carry increased O2 as oxygen not available –>cyanosis.
Anemia
- Deficiency in # of RBC or a deficiency in the quantity of hemoglobin concentration OR both
- Not a specific disease but rather a manifestation of a pathologic process
- Manifestations stem from hypoxia
S/S variable: Mild, Moderate, Severe -possibly asymptomatic in mild cases -pallor -irritability -numbness or tingling of extremities -dyspnea on exertion -yellowing of eyes -pale, cold yellow skin -shortness of breath -muscle weakness - changes in stool color -fatigue -dizziness -fainting ( severe) -low BP -heart palpitations -Tachycardia -chest pain (severe) -angina (severe) -heart attack ( severe) -enlarge spleen -orthostatic hypotension -nail bed deformities( spoon-shaped nails) -smooth, sore, bright-red tongue ( b12 deficiency)
*Collaborative Care: Administer oxygen as needed Alternate rest/activity Monitor blood H/H Medication teaching Diet teaching- b12, folate, iron
A causes of Anemia:
- bood loss
- inadequate RBC production (hypoproliferative anemia)
- Increased RBC destruction ( Hemolytic)
- deficiency of necessary components such as folic acid, iron, erythpoietin, and/or vitamin b-12
Risk Factors for Anemia:
- Acute or chronic blood loss
- trauma
- menorrhagia
- GI bleeds ( ulcers, tumor)
- Intra or post-surgical blood loss or hemorrhage
- Chemical or radiation exposures
- Increased Hemolysis
- defective Hgb ( sickle-cell disease) RBCs become malformed during periods of hypoxia and obstruct capillaries in joins and organs
- immune disorders or destruction (transfusion reactions, auto immune diseases)
- mechanical destruction of RBCs (mechanical heart valve, cardiopulmonary bypass)
- inadequate dietary intake or malabsorption
- iron deficiency
- vitamin b-12 deficiency
- folic acid deficiency
- pica
- bone-marrow suppression
- exposure to radiation or chemo
- aplastic anemia
- age
- older clients are at risk for nutrition-deficient anemia
- anemia can be misdiagnosed as depression or debilitation in older adult clients
- gastrointestinal bleeding is a common cause of anemia in older adult clients. check stools for occult blood
pernicious anemia
anemia due to deficiency of intrinsic factor produced by gastric mucosa, which is necessary for absorption of b-12
-dietary intake of b12 would do nothing
Collaborative Care:
Supplemental B-12 ( cobalamin) injections for pernicious anemia
Cobalamin= B-12
Gas Exchange and Upper Airway
Epistaxis ( nose bleed)
Rhinitis
Sinusitis
NOTE: These conditions typically do not interfere with a person’s ability to maintain oxygenation or adequate tissue perfusion unless complications (such as Bronchitis, Pneumonia etc.) develops
Epistaxis
Etiology: Trauma Foreign bodies Nasal sprays Street drug use Anatomic malformation Allergic rhinitis Tumors Medications Hypertension (doesn’t increase risk but makes bleeding more difficult to control)
Anterior ( most common):
Keep patient quiet
Place in sitting position, lean forward
Pinch entire soft portion of nose 10 minutes
Apply ice to nose
Partially insert gauze into bleeding nostril
Obtain medical assistance if bleeding continues
Posterior ( More serious): If tubes are used to control bleeding… Observe for respiratory distress Humidified oxygen Bedrest Pain management Hydration and oral care
Rhinitis
Viral (“Common Cold”):
Viruses invade the upper respiratory system
Spread by droplet
Increased in winter months
Risk factors:
Overcrowding/staying indoors
Compromised immune system
Stress
Allergic:
Triggered by a sensitivity reaction to airborne allergens
“Seasonal” or “chronic”
Nursing considerations:
- Rest, fluids, diet, analgesics
- Antihistamine and decongestant therapy
- Recognize symptoms of secondary bacterial infection
- Prevention – avoid crowded areas, good hand washing, etc.
Sinusitis
Exit (ostia) from sinus is narrowed or blocked by inflammation or hypertrophy (swelling) of the mucosa
- Secretions build up behind the obstruction
- Excellent medium for organism growth leading to infection
Clinical Manifestations: Pain over affected sinus Purulent nasal drainage Nasal obstruction Congestion Fever Malaise Dental pain Headaches
Collaborative Care: Control underlying cause (i.e. allergies etc.) Antibiotics Decongestants Nasal Corticosteroids Increase fluids Nasal Clearing/Cleaning Techniques (hot showers nasal rinse, etc.) Avoid smoking or exposure to smoke Increase HOB
Obstructive Sleep Apnea
Partial or complete airway obstruction during sleep
Apnea is cessation of airflow >10 seconds (adults)
Narrowing of passages – reduction of muscle tone during sleep
Tongue falling back to obstruct airway
Decreased O2 and increased CO2
Long term effect: Hypertension, Cardiac dysrhythmias, heart failure, CAD etc.
Chronic OSA: impaired memory, inability to concentrate, failure to accomplish task, interpersonal difficulties
Risk factors: Obesity, smoking, cranial abnormalities, acromegaly, men>women (until menopause than women = men)
Manifestations:
- insomnia
- daytime sleeping
- partner may notice snoring
- restless behaviors
Treatments: Mild (5-10 apnea episodes per hour) – positioning, Avoid sedatives and ETOH Weight loss CPAP (>15 apnea episodes per hour)
Gas Exchange
Infectious Respiratory Disorders
Ventilation and Perfusion Concerns
Influenza
TB
Pneumonia
Acute Bronchitis
**Seriousness of above conditions and/or complications that may occur can result in altered ventilation and perfusion concerns
Influenza
Highly contagious that may cause serious morbidity and mortality (estimated 20,000 death each year)
Flu season starts in September and extends to April
Need annual flu vaccinations due to different Influenza virus strains mutating over time
s/s: headache fever (usually high) extreme muscle tiredness join aches runny or congested nose sore throat aches coughing Vomiting
Diagnosis:
History & Physical
Viral Cultures (usually take 3-10 days)
Rapid Flu Tests (nasal secretions) – best done within 48 hours of onset of symptoms
Collaborative Care:Prevent:
-Good hand-washing and Vaccine (nasal vaccine not available)
-Check for egg allergies prior to flu shot
Antiviral – inhaler, oral or IV- best if given within 48 hours of s/s onset
-Supportive therapy (rest, analgesics/antipyretics, hydration)
Acute Brochitis
- Inflammation of the bronchi
- Viral or Bacterial (Most are viral)
Manifestations: Cough Sputum production Headache Shortness of breath on exertion Rhonchi, wheezing
Collaborative Care: Supportive (rest, fluids etc.) Antitussives Anti-inflammatory agents Bronchodilators
Tuberculosis (TB)
- Infectious disease caused by Mycobacterium tuberculosis
- Lungs most commonly infected
- 1/3 of world’s population is infected with TB
- Leading cause of death in patients with HIV/AIDs
- Prevalence is decreasing in the United States
Multidrug-Resistant Tuberculosis (MDR-TB)
Resistance to 2 of the most potent first-line anti-TB drugs
Extensively Drug Resistant TB (XDR-TB)
Resistant to any fluoroquinolone plus any injectable antibiotic
Risk Factors: Homeless Residents of inner-city neighborhoods Foreign-born persons Living or working in institutions (includes health care workers) IV drug users Poverty, poor access to health care Immunosuppression
Etiology and Pathophysiology
- Spread via airborne particles
- Can be suspended in air for minutes to hours
- Transmission requires close, frequent, or prolonged exposure
- NOT spread by touching, sharing food utensils, kissing, or other physical contact
- Once particles lodge in bronchioles and alveoli -> local inflammatory reaction occurs -> calcified lesions and further spread stopped
- Has affinity for lungs but can spread and grow in other organs
Classifications
-Primary infection
When bacteria initiate inflammatory response – encapsulate organisms preventing disease
-Latent TB infection (LTBI)
Infected but no active disease
-Active TB disease
Primary TB
Reactivation TB (post-primary)
Clinical Manifestations:
LTBI – asymptomatic
Pulmonary TB:
Takes 2-3 weeks to develop symptoms
Initial dry cough that becomes productive
Symptoms (fatigue, malaise, anorexia, weight loss, low-grade fever, night sweats)
Dyspnea and hemoptysis late symptoms
Hospitalization not necessary for most patients
Infectious for first 2 weeks after starting treatment
Drug therapy used to prevent or treat active disease
Need to monitor compliance
Vaccine
Bacille-Calmette-Guérin (BCG) vaccine to prevent TB is currently in use in many parts of world
In United States, not recommended
Can result in positive PPD reaction
Active Disease:
Four-drug regimen (Isoniazid, Rifampin (Rifadin) Pyrazinamide Ethambutol)
Teach side effects and when to seek medical care
Monitor liver function
Avoid Alcohol
May need Direct Observed Therapy (DOT)
Latent TB infection: Positive TB test Drug therapy to prevent TB infection from becoming active disease Usually treated with Isoniazid for 6 to 9 months HIV patients should take Isoniazid for 9 months
Acute care for TB
Airborne isolation
Single-occupancy room with 6-12 airflow exchanges/hour
Health care workers wear high-efficiency particulate air (HEPA) masks
Immediate medical workup
Appropriate drug therapy
Patient wears mask if outside of negative-pressure room
Identify and screen close contacts
Ambulatory Care
Can go home even if cultures positive
Monthly sputum cultures
Teach patient how to minimize exposure to others
Ensure that patient can adhere to treatment
Negative cultures are needed to declare the patient not infectious
Notify Health Department
Smoking Cessation
Pneumonia
Acute infection of lung parenchyma
Associated with significant morbidity and mortality rates
Pneumonia and influenza are 8th leading cause of death in the U.S.
Etiology :
- When defense mechanisms become incompetent or overwhelmed
- ↓ Cough and epiglottal reflexes may allow aspiration
- Chronic diseases suppress immune system
Three ways organisms reach lungs:
- Aspiration from nasopharynx or oropharynx
- Inhalation of microbes present in air
- Hematogenous spread from primary infection elsewhere in body
Mucociliary mechanism impaired : Pollution Cigarette smoking Upper respiratory infections Tracheal intubation Aging
Types pf Pneumonia
- Can be classified according to causative organism
- Community Acquired Pneumonia (CAP)
- Hospital-Acquired Pneumonia (HAP)
- Ventilator Associated Pneumonia (VAP)
- Multidrug-resistant (MDR) organisms (risks factors, advanced age, immunosuppression, history of antibiotic use, prolonged mechanical ventilation)
- Aspiration Pneumonia
- Necrotizing Pneumonia
- Opportunistic Pneumonia
- Pneumocystis jiroveci pneumonia (PJP)
pathophysiology of pneumonia
- Inflammatory response- attraction of neutrophils, release of inflammatory mediators, Accumulation of fibrinous exudates, red blood cells and bacteria
- alveoli fill with fluid and debris (consolidation)
and increased production of mucus (airway obstruction) - Decreased gas exchange
- Resolution of infection
- macrophages in alveoli ingest and remove debris
- normal lung tissue restored
- gas exchange returns to normal
Pneumonia continued…
S/S:
- cough ( productive cough: blood streaked, yellow, rusty sputum=infection)
- fever
- chills
- tachycardia
- tachypnea
- dyspnea
- pleural pain
- malaise
- respiratory distress
- decreased breath sounds
Diagnostic orders:
- sputum culture
- chest X-ray
- ABGs
Collaborative Care:
- oxygen
- hydration
- rest and activty
- patient teaching
Medications: antibiotics analgesics/antipyretics cough sepressants corticosteroids bronchodilators
Lower Airway Exemplars of Gas exchange impairment
-pulmonary embolism
-asthma
-COPD
(chronic bronchitis vs. emphysema)
Pulmonary Embolism
PE occurs when a blood clot becomes lodged in a lung artery, blocking blood flow to lung tissue. Blood clots often originate in the legs
Risk Factors: > 90% arise from thrombi in the deep veins of the legs -Immobilization -Surgery within last 3 months (especially orthopedic surgery i.e. hip/knee replacements) -Stroke -Malignancy -Obesity -Smoking -Hypertension/Chronic -Heart Disease
PE Classifications:
Massive
Sub-massive
Low risk
s/s:
- Dyspnea (most common - 85% of patients)
- Anxiety
- Tachycardia
- Cough/Hemoptysis
- Chest pain
- Syncope
- Sudden change in MS
- Massive emboli produce abrupt hypotension and shock; sudden collapse of the patient
Collaborative Care:
- O2 therapy
- Bed rest – Semi-Fowler’s
- Call for assistance
-Drug Therapy
Anticoagulant Therapy
Thrombolytic agent
-Surgery
Embolectomy
Vena Cava Filter
Asthma
-Reversible expiratory airflow limitation
-Disease of Inflammation along with bronchial hyper-responsiveness
-Parasympathetic Dominance :
Mucosal Inflammation
Bronchial smooth muscle construction
Excess mucus production
Risk Factors:
- inflammatory factors
allergens, respiratory infections, environmental factors
-irritants
change in temp, exercise, cold air, stress and emotions, strong odors
-other
medications, tobacco, gastric reflux, pollutants, food additives
S/S: Wheezing Coughing Dyspnea Chest tightness Use of accessory muscles to breath Anxiety Tachycardia, Diminished breath sounds
Classification-severity: Intermittent Mild persistent Moderate persistent Severe persistent Treatment is based upon stages
Collaborative Care:
-Medications
β-agonists, anti-inflammatory, mucolytics, methylxanthines, anticholigenerics, Leukotriene modifiers)
- Oxygen
- Nebulizer Treatments
- Elimination of causative factors
- Daily monitoring of PEFR
- Self-management plan (Green, Yellow, Red Zone) Asthma Action Plan -
Meter dose inhalers (MDI) Use instructions
- Hold inhaler 2-3 cm from mouth, shake canister, spray one puff and inhale; hold for 10 seconds
- 1-2 minutes in-between each puff of the same type of inhaler
- Rinse mouth after use of steroid inhalers
COPD
COPD (Chronic Obstructive Pulmonary Disease)
Disease state characterized by the presence of airflow obstruction
-Chronic bronchitis
Presence of chronic productive cough for 3 months X 2 years
-Emphysema
Abnormal enlargement of airspaces accompanied by destruction of walls
Chronic Bronchitis ( Blue Bloater)
Hypertrophy & hyperplasia of bronchial glands
Increased # goblet cells increased mucus
Decreased cilia
Chronic Inflammation- airway narrowing
Altered function of alveoli macrophages
S/S: Cough-frequent, productive Frequent respiratory infections Dyspnea on exertion (DOE) Hypoxemia & Hypercapnia Edematous Coarse rhonchi & wheezing
Emphysema ( Pink Puffer)
Destruction of alveolar walls 2o proteolytic enzymes–>destroys elastin & collagen
Alveolar air trapping–> hyperinflation–>alveoli meld together–> bleb/bullae
Lose normal elastic recoil
S/S: Dyspnea Cough-minimal Thin and underweight Finger Clubbing Pursed-lip breathing Diminished breath sounds Hypercapnia
Collaborative Interventions for COPD
-Oxygen Therapy
( “O2 drive” -CO2 narcosis)
- My carbon dioxide can be raised- do not give me high flow O2- low flow only 24%
Hypoxic Drive theory:
is a form of respiratory drive in which the body uses oxygen chemo-receptors instead of carbon dioxide receptors to regulate the respiratory cycle
it is believe when a patients has chronically elevated CO2, that CO2 levels stop being the drive to breath, and that low oxygen level becomes the main drive to breath.
Treatment: -STOP SMOKING -Poisitioning- high fowlers -breathing exercises- pursed lip breathing -coughing Nebulizer treatments Chest physiotherapy Postural drainage Airway suctioning Tracheostomy tubes Mechanical intubation Chest tube management
Gas Exchange and NUTRITION THERAPY
Nutrition therapy Modifications depending on condition: -Encourage 3L/Day -Small, frequent meals -Fluids between meals -Rest 30 minutes before eating -Bronchodilator may be needed before eating -Frozen & microwave foods – conserve energy in food preparation (be careful of sodium content-read labels) -Sodium restriction may be necessary -Avoid foods that cause bloating and gas -5-6 small meals/day -Liquid commercials diets -Avoid food that requires significant chewing -Avoid exercises for 1 hour after eating -Low carbohydrate diets
COPD and sexual activity
Explore patient concerns
Bronchodilator before sex
Less stressful positions
O2 if needed
Blood Administration
Transfusion Therapy:
Injection/administration of blood or blood products into the blood stream
Universal donor: is 0-
Universal Recipient is: AB+
RH Factor
Rh factor is an antigen that is a component of the Rh blood groups and is made up of numerous complex antigens
Rh(+) indicates a person has Rh factor on surface of RBCs
Rh(-) indicates person does not have Rh factor on surface of RBCs
Rh factor is a powerful antigen
Rh(-) person may only be transfused with Rh(-) blood to prevent formation of antibodies to
Rh(+) blood
Rh(+) person may be transfused with either Rh(-) or Rh(+) blood
Fresh Frozen Plasma
With FFP… Liquid portion of blood (no cells) Contains clotting factors AB is considered the universal donor O is the universal recipient
Type and Cross
Blood Typing: Blood test that determines blood type
Cross-matching: Blood test that indicates compatibility between blood of donor and recipient
Clumping in test tube=BAD not compatible
Types of blood products
Whole Blood Packed RBCs Platelets Granulocytes Fresh Frozen Plasma (FFP) Anti-hemophilic Factor VIII Cryoprecipitate Albumin Immune Serum Globulins
Nursing Protocols
- 19 gauge IV line or greater
- Establish patency before requesting blood!
- Sterile technique
- NSS/”Y-type” IV tubing set-up at bedside (or as per institution protocol)
- Baseline VS
- Check orders
- Double-check patient ID and blood product ID data with another licensed RN (or RN and MD)
- Administer blood as soon it arrives to floor (within 2-4 hours)
- Minimal handling of bag
- Vital signs at start of infusion, 15 minutes into infusion (and as per institution protocol)
- Stay with patient for first 15 minutes
- Administer very slowly for the first 15 minutes
DO NOT:
-do not use dextrose solution or LR for blood administration - will cause RBC hemolysis
-DO NOT give any additives (including meals) via same tubing unless cleared with NSS
Post Transfusion:
-Vital signs/necessary assessments at end of transfusion
- Document findings after transfusion
- Complete any adverse reaction forms if needed
- Monitor lab values
H/H (generally one unit of packed RBC raises the HCT by 3% and
hemoglobin by 1g/dL)
Transfusion Reactoins
Nursing Responsibilities: -STOP THE INFUSION -Maintain patency of cannula via NSS -Monitor vital signs and urine output -Notify the physician -Emergency equipment at bedside -Implement appropriate interventions -Written documentation -Follow appropriate protocol for reporting incident and collecting blood bag for lab
Acute hemolytic Reaction
- Most dangerous
- Infusion of ABO-incompatible whole blood, RBCs, or components containing 10 mL or more of RBCs
- Antibodies in recipient’s plasma attach to antigens on transfused RBC = RBC destruction
s/s:
- chills
- fever
- hypotension
- uncontrollable bleeding
- heat sensation in the transfused vein
- BACK PAIN
- increased heart rate
- constricting chest pain
- heboglobinuria
- hyperbilirubinemia
- acute kidney injury
- vascular collapse
- cardiac arrest
- Death
Nursing Actions:
STOP THE BLOOOD
Discontinue blood
Emergency fluids/drugs/dialysis to maintain renal perfusion/blood pressure
Treat shock
Red urine appears on next void – need to collect urine
Collect blood specimen
Allergic Reaction to blood
-Can be mild or severe
-Results from recipient’s sensitivity to donor plasma proteins
-Flushing, itching, Antihistamines/
corticosteroids
-Monitor closely
-Can lead to anaphylaxis
s/s:
- anxiety
- chills
- flushing
- itching
- shortness of breath
- chest pain
Anaphylactic reaction
- Emergency situation
- Sensitivity to donor plasma proteins
- Usually follows quickly - after only a few milliliters of blood
S/S:
Anxiety, urticaria, dyspnea, wheezing, bronchospasm, shock, possible cardiac arrest
- swelling of the conjunctiva
- runny nose
- swelling of lips, tongue, throat
- increase or decrease in HR
- low BP
- Hives, flushing itching
- pelvic pain
- dizziness, LOC, confusion, headache
- OSB, wheezes or stridor
- hoarseness
- pain with swallowing
- coughing
- crampy abdominal pain
- diarrhea/comiting
- loss of bladder contorl
Circulatory Overload
-Occurs when blood is administered more rapidly that the circulatory system can accommodate
S/S:
Cough, dyspnea, chest tightness, tachycardia, pulmonary edema, HTN, restlessness, JVD
-dyspnea
-cyanosis
-orthopnea
-headache
-systolic hypertension . increase >50 mm hg
Nursing actions:
- Stop transfusion
- Increase HOB
- IV NSS to KVO
- Notify MD
Sepsis reacton
-Due to transfusion of bacterially infected blood components, or when blood sits around too long
S/S: Rapid onset chills, high fever, vomiting, diarrhea, marked hypotension, shock
Nursing actions: Stop blood NSS to KVO Notify MD Blood bag and tubing sent back to lab
Transfusion-Related Acute Lung Injury (TRALI)
- Possible reaction between recipient’s leukocytes and donor’s antibodies = pulmonary inflammation and capillary leak = sudden development of non-cardiogenic pulmonary edema
- Usually 2-6 hours after transfusion
S/S:
Fever, hypotension, tachypnea, dyspnea, ↓O2 sat, frothy sputum
Nursing actions: Stop blood O2 Steroids IV KVO
Delayed Hemolytic Reaction
Occurs days to weeks after infusion
Usually less severe
S/S:
Fever, malaise, gradual decrease in H/H
No red urine
Important to monitor because may be a precursor to a more severe reaction in further transfusions
Infections- delayed usually
Hepatitis B & C HIV Malaria EBV Lyme disease West Nile virus
Transfusion Hyperkalemia- prolonged storage of blood, cell destruction, improper handling of blood products
Transfusion Hypocalcemia- preservative used to store blood binds to calcium to cause a deficiency
