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
