Med Surg 2 Chapter 54 Endocrine Exam 4

SIADH

Condition where inappropriate amount of ADH hormone released, causes body to retain water. These patients end up with low sodium, hyponatremia. We see big CNS changes here. Their pee will be very concentrated, body is not letting fluid go. Not a lot of pee, very concentrated.

In SIADH Body is hanging on to

a bunch of fluid so it is diluting our sodium levels which is below 135, if sodium is off we worry about seizures and swelling on the brain. We are worried they may get a headache and if they do then we may get more CNS changes that can lead to more problems. Not peeing very much, if they do it gross its thick and urine specific gravity is off.

SIADH signs and symptoms

•Muscle cramps/weakness

•Nausea and vomiting

•Headache

•Mental changes

•Seizures (severe cases)

SIADH Treatments

•Treat the causes

•Supplements

By the time seizures happen we probably

Missed the smaller signs

What should we do with fluid intake for these SIADH patients?

Limit fluid intake these patients are not getting fluids unless replacing sodium.

SIADH patients are given what med?

Demeclocycline will be given, blocks ADH. Going to go to renal tubules and tell it to start producing more pee. Then we will see increased urine output from this medication.

SIADH patients have low

sodium volume because so much fluid on board. Need to replace fluids and give high sodium diet.

These SIADH patients will be very thirsty so can give them

sugarless gum to chew to help with wanting to drink.

When treating SIADH we treat the

cause, both SIADH and DI have pituitary gland issues.

When brain swells so much it will move down and herniate, when brain herniates your done.

Hyperthyroidism

Sustained increase in thyroid hormones by thyroid gland. Thyroid usually occur in women between 20-40 years.

Thyrotoxicosis is in

Hyperthyroidism

Myxedema coma is in

Hypothyroidism

Hyperthyroidism most common form

Graves disease

Other causes:

•Thyrotoxicosis

-Physiologic effects/clinical syndrome of hypermetabolism

-Results from increased circulating levels of T₃, T₄, or both

•Hyperthyroidism and thyrotoxicosis usually occur together

What labs are checked for thyroid?

TSH, T3, and T4

Subclinical hyperthyroidism

•Serum TSH level below 0.4 mIU/L

•Normal T₄ and T₃ levels

Overt hyperthyroidism

•Low or undetectable TSH

•Increased T₄ and T₃ levels

•Symptoms may or may not be present

With hyperthyroid, everything will be high except

TSH, it will be low

Graves disease:

Autoimmune disease

-Diffuse thyroid enlargement

-Excess thyroid hormone secretion

•Risk factors may interact with genetic factors

•Women are five times more likely than men to develop Graves’ disease

Signs of graves disease:

•Related to effect of thyroid hormone excess

•Goiter

•Ophthalmopathy

•Exophthalmos: Increased fluid behind eyes

Big thyroid and eyeballs will look like popping out of head.

Graves disease usually treated with

antithyroid meds to treat, will take a couple months for these to really get on board and block thyroid to see improvement.

Can also use large doses of iodine which will inhibit thyroid synthesis as well.

Intervention for Graves disease:

Sometimes eye balls will poke so far they cant close eyes all the way, we can keep HOB elevated to promote postural drainage

Sometimes need eye drops because cant blink all the way to moisturize eye, they will end up with corneal abrasions

More manifestations of Hyperthyroidism:

High BP, high pulse, might have dysrhythmias, chest pain, increased RR, sob on activity, weight loss (metabolism is through roof), loose weight, diarrhea, skin and hair brittle, if respiratory issues may have clubbing, may feel nervous, hyperactive DTR

Men if get it will maybe end up with gynecomastia

Decreased libido and fertility in men and women

•Intolerance to heat

•Elevated basal temperature

•Lid lag, stare

•Eyelid retraction

•Rapid speech

Older adult may complain of palpitations, tremors, weight loss, and may not have some of the other issues.

Thyrotoxic crisis (thyroid storm)

•Excessive amounts hormones released

•Life-threatening emergency

•Death rare when treatment started early

•Results from stressors

•Thyroidectomy patients are at risk

Signs of thyroid storm:

•Severe tachycardia, heart failure

•Shock

•Hyperthermia (up to 106° F [41.1° C])

•Agitation

•Seizures

•Abdominal pain, vomiting, diarrhea

•Delirium, coma

Thyroid storm is storm of extra hormones. Patient you are worried may go into this will have tachycardia, signs of shock, elevated temp even up 1 degree says we might be headed there and need to intervene now

Diagnostic studies for hyperthyroidism:

•Decreased TSH (less than 0.4 mU/L

•Increased free thyroxine (free T₄)

•Total T₃ and T₄ (not definitive)

•Radioactive iodine uptake (RAIU): Distinguishes Graves’ disease from other forms of thyroiditis

Treatment of hyperthyroid

uAntithyroid medications (Tapazole)

uRadioactive iodine therapy (RAI)

uSurgery

When we use radiation or radioactive iodine, we run the risk of causing hypothyroidism. As nurse need to know the risk of swinging them the opposite way into hypothyroidism.

Radioactive Iodine Therapy (RAI)

•Treatment of choice for most  nonpregnant adults

•Damages or destroys thyroid tissue

•Delayed response of up to 3 months

•Treated with antithyroid drugs and β-blocker before and during first 3 months of RAI

•Given on outpatient basis

•Patient teaching

Teach them symptoms of hypothyroidism and need to give frequent oral care with this treatment.

Surgical therapy indications:

•Large goiter causing tracheal compression: Pushing on trach means cant breathe

•Unresponsive to antithyroid therapy

•Thyroid cancer

•Not a candidate for RAI

•Rapid reduction in T₃ and T₄ levels

Subtotal thyroidectomy

removes 90 percent of thyroid can be done scope or robotically

After any surgery to or near thyroid need to watch for

hypocalcemia causing tetany which will show as cramping or stridor. Doing BP on arm and hand twitches up that is tetany.

Stridor is medical emergency, caused by the low calcium. We need to give calcium.

If end up in thyroid storm because of this we can give beta blockers.

Nutritional therapy for hyperthyroidism

•High-calorie diet (4000 to 5000 cal/day)

•6 full meals/day with snacks in between

•Protein intake: 1 to 2 g/kg ideal body weight

•Increased carbohydrate intake

•Avoid highly seasoned and high-fiber foods, caffeine

•Dietitian referral

Lots of protein and carbs

Nursing assessment for hyperthyroidism:

History of thyroid problems, want to ask if having any symptoms for hyperthyroidism chest pain, rapid speech.

Will see big eyes, big goiter, forced speech, report dry skin, check mucus membranes and turgor

Acute thyrotoxicosis

•Necessitates aggressive treatment

•Give medications that block thyroid hormone production and SNS effects

•Monitor for dysrhythmias

•Ensure adequate oxygenation

•Fluid and electrolyte replacement

Potassium and calcium off so watch dysrhythmias

Acute thyrotoxicosis (hypo) we want room to be

•Cool, quiet room

•Light bed coverings

•Change linens often

These patients everything about this is high, we need to decrease external stimuli and that’s why we provide that type of room.

Also encourage and assist with exercise

In Acute thyrotoxicosis (hypo) if exophthalmos (eyes out from too much fluid behind) present:

•Apply artificial tears to relieve eye discomfort

•Restrict salt and elevate head of bed

•Dark glasses

•Tape eyelids shut if needed for sleep

•ROM of intraocular muscles

Surgical intervention for Acute thyrotoxicosis (hypo)

•Give medications to achieve euthyroid state

•Give iodine to decrease vascularization

Patient teaching:

•Comfort and safety measures

•Leg exercises, head support, neck ROM

•Routine postoperative care

Acute thyrotoxicosis (hypo) post op surgical care

•Monitor for complications

•Respirations may become difficult

•Maintain patent airway

•Assess frequently 24 hours for signs of bleeding or tracheal compression

•Semi-Fowler’s position

•Support head with pillows

•Avoid tension on suture line

If had thyroid surgery will be worried for hypocalcemia and electrolyte imbalances, infection, swelling in neck for airway risk, bleeding.

Would see tetany and stridor, we will give IV calcium

Avoid tension of suture line, want to keep head propped up and midline so no tension.

Would normally prepare to intubate for stridor, here we need calcium.

•The nurse is caring for a patient who just returned to the surgical unit following a thyroidectomy. The nurse is most concerned if which is observed?

•The patient makes harsh, vibratory sounds when breathing.

This is stridor, need to give calcium

Hypothyroidism:

Here is not enough thyroid hormone. More common in women, looking at TSH that's typically higher than 4 and a half or close to there.

Primary hypothyroidism etiology

•Caused by destruction of thyroid tissue or defective hormone synthesis

Hoshi motoes thyroid is sometimes primary cause which is autoimmune condition.

Iodine deficiency can cause this, just give iodine

Secondary hypothyroidism etiology

•Caused by pituitary disease (decreased TSH) or hypothalamic dysfunction or (decreased TRH)

Clinical manifestations of hypothyroidism

•Slow onset unless occurs after thyroidectomy

•Tired, lethargic, impaired memory, low initiative, weight gain

•Cardiovascular system

•Respiratory system

•Neurologic system

•GI system

•Integumentary system

•Musculoskeletal

•Reproductive

Metabolism is now slowed. Everything is slowed.

May be anemia, SOB easy on exertion, dry brittle nails, poor skin turgor, very puffy face

Treatment of hypothyroidism

uLevothyroxine (Synthroid)

uStart with low dose

uMonitor for chest pain, weight loss, nervousness, tremors, insomnia

uIncrease dose in 4- to 6-week intervals as needed based on TSH levels

uLifelong therapy

Can also use a med called armor, holistic med used.

Start with low dose because we don’t want to overthrow.

When we get into high levothyroxine levels we will see dysrhythmias (look up)

Older patient just started on it might have higher heart rate (also look up)

Teach patients this is lifelong therapy, the rest of life. After Synthroid have to wait 30-60 minutes before eating and at least 4-5 hours before taking antacid to not disrupt stomach pH.

After taking Synthroid have to wait

30-60 mins to eat

Nursing assessment for hypothyroidism

•Hyperthyroidism treatment

•Iodine-containing medications

•Changes in appetite, weight

•Activity level

•Speech, memory, or skin changes

•Cold intolerance

•Constipation

•Signs of depression

•Decreased heart rate

•Tenderness over thyroid gland

•Edema

•This usually goes undiagnosed because doctor assumes its just them getting older because its usually women in 30s.

•Tend to have cold intolerances (hyper has heat), these are all non specific symptoms which makes diagnosis less

•Female white, and getting older, down syndrome patients all at higher risk.

Hypothyroidism complications:

uMyxedema coma

Precipitated by infection, drugs, cold, trauma

Characterized by:

Impaired consciousness or coma

Subnormal temperature, hypotension, hypoventilation

Cardiovascular collapse

Treated with IV thyroid hormone

A lot of times will end up on vent with this

Need to give thyroid hormone

Common features of myxedema:

Dull, puffy skin; coarse, sparse hair; periorbital edema; and prominent tongue.

Cushing Syndrome

Cushing syndrome is a clinical condition that results from chronic exposure to excess corticosteroids, especially glucocorticoids.21 Several conditions can cause Cushing syndrome.

Cushing disease and primary adrenal tumors are more common in women in the 20- to 40-year-old age-group.

Hormonal disorder caused by prolonged exposure to high cortisol levels

Manifestations of Cushing syndrome

•Excess glucocorticoids

•Mineralocorticoid excess may cause: excess may cause hypokalemia from potassium excretion and hypertension from fluid retention

•Adrenal androgen excess may cause: may cause severe acne, the development of male characteristics in women, and feminization in men.

Thinning of hair, acne, moon face, red cheeks, buffalo hump, supraclavicular fat pad, increased body and facial hair, weight gain, purple striae, pendulous abdomen, ecchymosis from easy bruising, slow wound healing, thin skin and subcutaneous tissue, thing extremities with muscle atrophy

Diagnostic studies for Cushing syndrome

uConfirmation of increased plasma cortisol levels

uPlasma ACTH levels

uHypokalemia and alkalosis

Treatment of Cushing syndrome

•Normalize hormone secretion

•Treatment depends on cause

•If cause is prolonged use of corticosteroids

-Gradually decrease therapy

•Dose must be tapered gradually

Acute care of Cushing syndrome:

•Vital signs

•Daily weight

•Glucose

Assess for signs and symptoms of Inflammation/infection and VTE

Preop care for Cushing syndrome

•Optimize physical condition

•Control hypertension and hyperglycemia

•Correct hypokalemia

•High-protein diet to correct protein depletion

•Depends on planned surgical approach

Post op care for Cushing syndrome:

•Increased risk of bleeding

•Large release of hormones into circulation causes instabilities in BP, fluid balance, and electrolyte levels

•Monitor for acute adrenal insufficiency

Ambulatory care education for Cushing syndrome

•Home health nurse

•Always wear Medic Alert bracelet

•Avoid exposure to extremes temperatures, infection, and stress

•Teach how to adjust medication and when to call HCP

•Lifetime replacement therapy

Difference between Cushing syndrome and disease

Syndrome: caused by giving some steroids or something like that and its causing Cushing syndrome

Disease: Usually due to some pituitary adenoma

Defining presenting factors for Cushing:

Buffalo hump and moon face and huge purple striae on your belly (stretch marks), petichi little red spots on skin. And also muscle wasting so big belly but super thin wasting look arms

If cause is pituitary adenoma, patient goes to surgery, what is the biggest thing nurse needs to watch for postoperatively?

Sometimes have to surgically remove the adenoma or remove the whole adrenal, after this they are at high risk for fluid and electrolyte imbalances so you have to watch closely for those things. After we treat these patients with IV fluids and steroids. Also need to watch patients blood pressure, this will indicate if there is an issue with fluid volume status.

If starting to have signs of Cushing syndrome when on a steroid,

Doctor will say need to come off, or sometimes people can go every other day or just cut down somehow, but some people can not. We have to gradually discontinue these steroids.

Why do you have to gradually discontinue steroids?

We can throw the body into adrenal crisis.

Addison’s Disease:

Adrenocortical insufficiency (hypofunction of the adrenal cortex) may be from a primary cause (Addison disease) or a secondary cause (lack of pituitary ACTH secretion). In Addison disease, all 3 classes of adrenal corticosteroids (glucocorticoids, mineralocorticoids, and androgens) are reduced.

80% is autoimmune

Addison’s disease manifestations

•Insidious onset

-Anorexia

-Nausea

-Progressive weakness

-Fatigue

-Weight loss

•Disease often advanced before diagnosed

•Abdominal pain

•Diarrhea

•Headache

•Orthostatic hypotension

•Salt craving

•Joint pain

Complications of Addison’s disease:

•Addisonian crisis

•Manifestations of glucocorticoid and mineralocorticoid deficiencies

Addisonian crisis

Patients with adrenocortical insufficiency are at risk for acute adrenal insufficiency (addisonian crisis). It is a life-threatening emergency caused by insufficient adrenocortical hormones or a sudden sharp decrease in these hormones. Triggers of addisonian crisis is include (1) stress (e.g., infection, surgery), (2) sudden withdrawal of corticosteroid hormone therapy, (3) adrenal surgery, or (4) sudden pituitary gland destruction.

Manifestations of glucocorticoid and mineralocorticoid deficiencies

Glucocorticoid (cortisol) deficiency causes fatigue, weight loss, hypoglycemia, and hypotension, while mineralocorticoid (aldosterone) deficiency causes dehydration, severe hypotension, salt cravings, and hyponatremia/hyperkalemia. Together, these deficiencies (as seen in Addison's disease) can lead to hyperpigmentation, severe nausea, and life-threatening adrenal crisis,

Addison’s disease diagnostic studies:

uACTH stimulation test

uCRH stimulation test

uHigh potassium

uLow chloride, sodium, glucose

uAnemia

uIncreased BUN

uECG changes

uCT scan, MRI

Addison’s Disease Interprofessional care:

•Manage underlying cause

•Lifelong hormone therapy
-Hydrocortisone

-Increased during periods of stress

-Fludrocortisone (Florinef)

Women need androgen replacement

•Increase dietary salt intake

Addison’s Disease acute care:

•Frequent monitoring necessary

•Correct fluid and electrolyte imbalance

•Assess vital signs and neurologic status

•Daily weight

•Accurate I and O

•Obtain complete medication history

•Watch for signs of Cushing syndrome

Addison’s Disease patient teaching:

uReport signs and symptoms of corticosteroid deficiency and excess to HCP

uCarry identification and wear medical ID bracelet

uEmergency kit

uHow to administer IM hydrocortisone

uWritten instructions

uDosing

What do you do for Addisonian Crisis?

uShock management

uHigh-dose hydrocortisone replacement

u0.9% saline solution and 5% dextrose

Corticosteroid therapy:

•Effective in treating many diseases and disorders

•Complications and side effects with long-term use

•Potential benefits must be weighed against risks

•Expected effects of corticosteroid therapy

Corticosteroid therapy expected side effects:

uDecreased potassium and calcium

uIncreased glucose and BP

uDelayed healing

uSusceptibility to infection

uSuppressed immune response

uPeptic ulcer disease

uMuscle atrophy/weakness

uMood and behavior changes

uMoon facies, truncal obesity

uProtein depletion

uRisk for acute adrenal crisis if therapy is stopped abruptly

The nurse gives corticosteroids to a patient with acute adrenal insufficiency. The nurse determines that treatment is effective if what is observed?

The patient is alert and oriented.

Indication of improved perfusion and brain functioning, treatment is working.

An IV hydrocortisone infusion is started before a patient is taken to surgery for a bilateral adrenalectomy. Which explanation, if given by the nurse, is most appropriate?

“This medicine is given to help your body respond to stress after removal of the adrenal glands.”

After bilateral adrenalectomy patient is unable to produce cortisol, so we give IV hydrocortisone as stress dose steroids to prevent acute adrenal insufficiency (Addisonian crisis). Give it IV to ensure there is an adequate response during the stress of surgery, when in stress need more.

Biggest physical sign of Addison’s:

Hyperpigmentation, we call this bronzing.

Addison’s patients have to take steroids because

They don’t have enough

We need to teach our patients that if they are ill or under a lot of stress they may require more, if you don’t take it you will throw yourself into crisis. Being sick even can cause a need for more.

Addison’s disease patients need to be given

IV fluids and electrolytes, we often have to replace these.

For diagnostic studies we also see

BUN increase

EKG changes

Indications of going to Addison’s crisis

Hyponatremia, poor skin turgor, volume is low. Going to correct volume and hyponatremia with the D5 and NS

Which body system would be your priority in someone with Addison’s Crisis (life threatening)

The heart, can cause hyperkalemia when they are in crisis and high potassium causes hyperkalemia and need to put them on a monitor

Hyperaldosteronism

Hyperaldosteronism (Conn syndrome) is characterized by excess aldosterone secretion. The main effects of aldosterone are (1) sodium retention and (2) potassium and hydrogen ion excretion. Thus the hallmark of this disease is hypertension with hypokalemic alkalosis. Primary hyperaldosteronism (PA) is most often caused by a small solitary adrenocortical adenoma. Sometimes, multiple lesions are involved and are associated with bilateral adrenal hyperplasia.

Hyperaldosteronism clinical manifestations

•Increased aldosterone

•Sodium retention

•Hypokalemia and Hyperkalemia

Hypertension

Fluid and electrolyte imbalances

Hyperaldosteronism diagnostic studies

•Increased plasma aldosterone levels

•Increased sodium levels

•Decreased potassium levels

•Decreased plasma renin activity

•CT scan or MRI

•Plasma 18-hydroxycorticosterone level

Hyperaldosteronism Treatment:

•Adrenalectomy to remove adenoma

•Bilateral adrenal hyperplasia

Adrenalectomy to remove adenoma: preop

•Potassium-sparing diuretics

•Antihypertensives

•Oral potassium supplements

•Sodium restrictions

•Bilateral adrenal hyperplasia: preop

•Potassium-sparing diuretic

•Calcium channel blockers to control BP

•Dexamethasone to decrease adrenal hyperplasia

Hyperaldosteronism nursing management:

Careful assessment

•Fluid and electrolyte balance

•Cardiovascular status

Patient teaching

•Medications and side effects

•Signs and symptoms of hypokalemia and hyperkalemia

•Frequent monitoring

Often treated with potassium sparing diuretics and antihypertensives

Signs and symptoms of sodium retention:

Swelling

Will see hypertension but mainly also a headache

With hypokalemia puts at risk for

Dysrhythmias, put on monitor.

When we have hypokalemia over an extended time we will see

Glucose intolerance, fatigue, muscle weakness.

The hypertension is caused by

The sodium retention so if we can fix that then the hypertension will go away

What will be the electrolyte imbalances we see?

Problems with our sodium, potassium, problems with pH.