Chapters 33: Adrenal Drugs Chapters 20, 21: Cholinergic and Cholinergic Blocking Drugs Voice over power

point Chamberlain College of Nursing NR 292: Pharmacology II Adrenal Drugs- adrenal glands sit on top of the kidneys and consist of two parts, the cortex and the medulla. The cortex is the outer cap in the medulla is the inner layers. The cortex secretes the corticosteroids which are the glucocorticoids and mineralcorticiods. The medulla secretes epinephrine and norepinephrine. Chapter 33 Adrenal Cortex: Corticosteroids Also called glucocorticoids or steroids Hormones produced by adrenal cortex Affect almost all body organs in maintaining homeostasis Disease results from inadequate or excess secretion- p509 of the textbook Endogenous Corticosteroids Adrenal cortex produces 30 steroid hormones divided into Glucocorticoids Mineralcorticoids Gonadocorticoids- adrenal sex hormones

Feedback Control of Adrenal Cortex

If you have a hypo-secretion you have Addisons disease Hyper-secretion causes Cushings disease. Review in med surge for S&S so you can identify these symptoms Cushings Disease S&S: The signs and symptoms of Cushing's syndrome vary and most often develop gradually. You may have: Weight gain. Symptoms may include a round or puffy face (moon face), increased fat around the neck and upper part of the back (buffalo hump camera), or an enlarged waistline. Weight gain is the most common symptom of Cushing's syndrome.

Skin changes. These include thin, fragile skin that bruises easily; slow-healing wounds; wide, purplish stretch marks on the body (striae); acne; or a ruddy complexion. Changes in mental state. Irritability, anxiety, inability to sleep (insomnia), or feelings of sadness or depression may develop. Muscle and bone weakness. Symptoms may include backache; broken bones, especially the ribs and spine (caused by osteoporosis); or loss of muscle tone and strength. Weakness of the muscles in the arms and legs may make it difficult to rise from a chair or climb stairs. Sex hormone changes. Menstrual irregularity, facial hair growth in women, erection problems (erectile dysfunction), or loss of sex drive may occur. High blood pressure and diabetes. High blood pressure (hypertension) and diabetes may not be diagnosed until you have a checkup.

The eye conditions glaucoma and cataracts also may occur in Cushing's syndrome. In Cushing's disease (tumors on the pituitary gland), your field of vision can be affected. You may have loss of side, or peripheral, vision.

If a cancerous tumor on the lung is the cause, you may have rapid loss of appetite (anorexia) and weight loss. You also may have dark spots on the skin (hyperpigmentation).

Not everyone who has the classic signs and symptoms of Cushing's syndrome has the disorder. Also, not everyone who has Cushing's syndrome has the classic changes in physical appearance. This is often true in people who are very physically active. Addisons Disease S&S: Addison's disease symptoms usually develop slowly, often over several months, and may include: Muscle weakness and fatigue Weight loss and decreased appetite Darkening of your skin (hyperpigmentation) Low blood pressure, even fainting Salt craving Low blood sugar (hypoglycemia) Nausea, diarrhea or vomiting Muscle or joint pains Irritability Depression Body hair loss or sexual dysfunction in women Acute adrenal failure (addisonian crisis)

Sometimes, however, the signs and symptoms of Addison's disease may appear suddenly. In acute adrenal failure (addisonian crisis), the signs and symptoms may also include: Pain in your lower back, abdomen or legs Severe vomiting and diarrhea, leading to dehydration Low blood pressure Loss of consciousness High potassium (hyperkalemia) When to see a doctor See your doctor if you have signs and symptoms that commonly occur in people with Addison's disease, such as: Darkening areas of skin (hyperpigmentation) Severe fatigue Unintentional weight loss Gastrointestinal problems, such as nausea, vomiting and abdominal pain Dizziness or fainting Salt cravings Muscle or joint pains Glucocorticoids Overview Uses Anti-inflammatory Immunosuppressant Part of chemotherapy regimens for treatment of cancer

Prototype: prednisone (Deltasone) Others hydrocortisone (Cortef, Hydrocortone)-short acting cortisone (Cortone)- short acting methylprednisolone sodium succinate (Solu-Medrol) prednisolone (Delta-Cortef) triamcinolone (Aristocort, Kenacort) dexamethasone (Decadron)- long acting

Glucocorticoids (cont.)

Prototype: prednisone (Deltasone) Mechanism of action: immediate-acting synthetic analog of hydrocortisone Specific information for prednisone Given PO with meals- bc it can cause GI upset Give single doses early in the morning; multiple doses equally spaced around the clock Taper gradually; give every other day (if they are on it for more than two weeks at a time) cant stop quickly it will cause your body to go into a steroid crisis if you dont taper of slowly

Glucocorticoids (cont.) Specific information for hydrocortisone Oral, rectal, topical Phosphate: SC, IM, IV Succinate: IM, IV

S/A effects- lots of sa Abnormal fat deposits: moon face, buffalo hump, obese trunk with thin extremities (symptoms of Cushings disease) Hyperglycemia Labile emotions and behavioral changes- emotions are up and down Musculoskeletal effects: osteoporosis, muscle weakness F & E: FVE, edema, hypernatremia, hypokalemia, metabolic alkalosis AMINOGLYUTETHIMIDE (CYTADREN) Anti-adrenal used to treat the over production of adrenal hormones. Considered anti- adrenal steroid inhibitor. -MOA: stops the adrenal cortex from producing hormones. -Used to treat Cushings syndrome, metastatic breast cancer and adrenal cancers. -S/A: MC- Nausea vomiting, rash and diarrhea, dizziness A/E: Jaundice, hepatotoxicity, skin lesions, decr BP, and HA

Glucocorticoids (cont.)

S/A effects (cont.) CV (Cardiovascular effects): HTN, CHF GI: N, V; gastric ulcers; increased appetite; obesity Increased susceptibility to infection; poor wound healing Altered secondary sex characteristics: menstrual irregularities, acne, hirsutism (Excess hair) Eye changes: increased IOP; glaucoma, cataracts Skin: red, thin, striae (symptoms of Cushings also)

Mineralocorticoids- used to regulate mineral salts in our body, which are electrolytes in our body. In humans, the primary mineralocorticoid is aldosterone and that is the only one we have in our body. Overview Used to replace aldosterone (aldosterones main responsibility is to control sodium in our blood by exchanging sodium ions for potassium and hydrogen ions.) Prototype: fludrocortisone (Florinef)

Mineralocorticoids (cont.) Prototype: fludrocortisone (Florinef) Mechanism of action: long-acting synthetic mineralocorticoid Sodium retention, resulting in water reabsorption Potassium loss (monitor K+ and Na levels)

Specific information Given orally

Mineralocorticoid (cont.) S/A effects FVE Hypernatremia Hypokalemia and metabolic alkalosis Nausea Acne, slow wound healing it is a steroid

Watch diabetics for glucose levels bc it does cause hyperglycemia

Nursing Actions: Adrenocortical Hormones Medical alert bracelet Teach about life-long therapy ( unless they have an acute case like poison ivy, but most of them are life long) Teach about side effects and how to monitor for, prevent, and treat them Teach to avoid persons with infections- avoid fruit and flowers Treat any injury promptly- slow wound healing and prone to infections Do not miss doses; do not stop abruptly- bc the body is not producing themselves they are dependent on the medications Cholinergic Drugs are also called cholinergic agonists and they mimic Chapter 20 Parasympathomimetics (Muscurinic Agonists) Overview Direct-acting cholinergics Used to produce the effects of the PNS (parasympathetic nervous system) Prototype: bethanechol (Urecholine)

Indirect-acting cholinergics (cholinesterase inhibitors) Used to reverse the symptoms of myasthenia gravis (autoimmune disorder where the normal cells attack healthy tissue, the body produces antibodies that block the muscle cells from receiving messages from the nerve cells. What really happens then, bc the muscle cells are not getting messages form the nerve cells the muscles cant respond in the way that your brain is telling your hand or your foot to. So if your brain is saying pick up that ice tea, the nerves are getting the messages but the muscles cant receive them, therefore the muscles are weakened and you cant carry out the actions. MC in young females and older males. There is no known cause, but it may be associated with tumors of the thymus gland which is an organ in the immune system. S&S of myasthenia gravis: weakness of all voluntary muscles. This weakness increases with activity and decr with rest. So the more active they are the more weakness. Often the 1st symptom will be eye muscle weakness, blurred vision. TREATMENT- neostigmine Prototypes: Incr nerve cell communication with the muscles. Decr weakness.

neostigmine (Prostigmin) edrophonium (Tensilon)- tensilon test is used to diagnose myasthenia gravis. Test muscle strength and decide if tensilon makes a difference in muscle strength. If you have a pt with muscle weakness and they are ruling out myasthenia gravis. They have an IV in Pt sit and alternate their hands and dorsiflex and plantarflex their hands and count how many times they can do that rapidly. Or you can have the pt cross and uncross their legs very rapidly and count how many times they can do that. If the pt can only do it 20x. Then they give IV tensilon and retake the test about 15 20 min later. Perform the same exercise, if the tensilon makes a difference in muscle strength, they may have myasthenia gravis. If there is no improvement, then they probably dont have myasthenia gravis.

pyridostigmine (Mestinon) Prednisone is also used bc it suppresses the immune system response.

Used to prevent slow symptoms of Alzheimers disease Prototype: donepezil (Aricept)

Parasympathomimetics (cont.)- used to slow down symptoms of alzheimers disease. We know we cant stop the progression. Alzheimers is due to a short supply of acitocholin.

Cholinergic crisis: is when the body has too much of the cholinergic hormone and it causes respiratory muscles to get involved and become weak. Comes without warning. Can be caused by and overdose or underdose of medications. It is due to an incr amount of acitocholin. It now has spread from voluntary muscles to involuntary muscles. The pt may be on a ventilator for a while until the cholinergic crisis reverts. Mechanism of action Direct-acting: bind to cholinergic receptors to produce the rest-and-digest response; stimulates contraction of GI and GU muscle; used for urinary retention Indirect-acting: inhibit acetylcholinesterase; used for myasthenia gravis The anticholinergic effects are the same 5 effects: dry mouth, dry eyes, blurred vision, constipation, and urinary retention- teach pts that they will have these (normal) Cholinergic effects-S salivation, L Lacrimation, U urination, D diarrhea, G GI upset E emisis (SLUDGE) and tachycardia- things that pts on cholinergic pts should expect (normal)

Parasympathomimetics (cont.) Direct-acting cholinergic drugs Specific information Given orally, on an empty stomach to prevent n,v; peak effect in 60 90 minutes ( if they are having muscle weakness in their mouth give before food) Given subcutaneously, peak effect in 15 30 minutes

S/A effects Overdose: salivation, sweating, flushing, abdominal cramps, nausea, diarrhea (Cholinergic crisis); antidote is atropine sludge will be exaggerated Atropine can cause bradycardia and tachycardia so you have to be careful with it Dyspnea (acute asthma attack) Orthostatic hypotension and bradycardia (safety!) Diplopia (safety!)

Parasympathomimetics (cont.) Indirect-acting Specific information Given orally, subcutaneously, IM, IV Schedule around mealtimes to maximize benefit on chewing and swallowing Onset of action with oral dose = 2 4 hours; with IM/IV = 10 30 minutes With MG, note when weakness, diplopia, dysphagia occurs

Parasympathomimetics (cont.) Indirect-acting (cont.) S/A effects Increased salivation, sweating, flushing, abdominal cramps, nausea (again exaggerated to the max) treated with atropine again Hypotension and bradycardia Diplopia

Eye Medications- ophthalmic medications Cholinergic agonists: produce myosis (pupil constriction)- if pt has a head injury they may have dilated pupils

Cholinergic blockers: produce mydriasis (pupil dilation)- cholinergic blockers and adrenergic agonists Adrenergic agonists: produce mydriasis (pupil dilation) also used for eye surgery Anti-Cholinergics (Cholinergic Blocking Drugs)- blocking the cholinergic effects Chapter 21 Anticholinergic Drugs (Muscarinic Blockers) Overview Used to block PNS effects they allow the sympathetic nervous system to take over.

Belladonna alkaloids and derivatives Prototypes: atropine is our classic anticholinergic drug- 5 anticholinergic effects, dry mouth, eyes, blurred vision, constipation and urinary retention scopolamine (Hyoscine)- motion sickness, used continually during travel (patch)tachycardia oxybutynin (Ditropan) - used for nueurogenic bladder, incontinence or spasms due to head injury

Anticholinergic Drugs (Muscarinic Blockers) (cont.) Antisecretory/antispasmodic anticholinergics for GI disorders Prototype: propantheline bromide (Pro-Banthine) Others dicyclomine (Bentyl) tolterodine (Detrol)- overactive bladder they can dry up secretions and make muscle spasms stop, decr severe diarrhea

Anticholinergic Drugs (Muscarinic Blockers) Prototype: atropine Mechanism of action: Occupies muscarinic receptors so the action of acetylcholine is blocked; produces fight or flight responses Uses: reduce GI hypermotility; suppress respiratory secretions during surgery; reverse bradycardia; dilate pupils for eye examination, diahrrea, can also be given to incr HR if the pts hr rate is 50 and capillary refill is inadequate and their color isnt good

Anticholinergics (cont.) S/A effects Tachycardia CNS stimulation Urinary retention Constipation Dry mouth and dry eyes Blocked sweat glands, leading to hyperthermia Photophobia, dilated pupils (blurred vision)

Detrol has a low incidence of dry eyes and dry mouth compared to the others

An anecdote to much atropine would be Physofpigmine (antilirium). Symptoms of too much atropine would be severe delirium and agitation.