Endocrine System 1

Hypothalamus/Pituitary & Thyroid

What do they do? Work together to regulate certain hormones

Hypothalamus = body’s thermostat

1. coordinates changes in SNS & PNS

2. communicates with pituitary via “releasing” and ”inhibiting” hormones and neuronal input

3. Hormones: GHRH, TRH, CRH, GnRH, PIF, dopamine

Pituitary = controls growth and metabolism

• master gland

• communicates with the hypothalamus by blood and nerves

• hormones: GH, ACTH, TSH, LH, FSH

Measuring hormone output determines what is wrong

* know what is wrong when labs are strange

Thyroid

Thyroid → Located on top of the trachea

• Regulates metabolism

• Hormones: Thyroxine (T4), Triiodothyronine (T3),

• Calcitonin

• Disorders: Hypo/hyperthyroidism, Cancer

Parathyroid Glands → Located on the posterior

• Surface of the thyroid

• Superior/Inferior – responsible for eucalcemia

Hypothyroidism

Hypo is slow! Slows things down!

Etiology

• Autoimmune Disease (Hashimoto’s Thyroiditis)

• Surgical removal of the thyroid

• Radiation treatment

• certain medications

In autoimmune disease: body mistakes thyroid gland cells & their enzymes for invaders destroys cells, leaves no thyroid cells or enzymes to produce thyroid hormone

• Causes: primary (loss of the gland itself), secondary (pituitary gland issue, if issue with TSH) or tertiary (hypothalamus issue), Goiter (not enough Iodine),

Hair loss, fatigue, sensitivity to cold, bradycardia, menstrual change, weight gain, dry skin

Diagnostic Studies

 History and physical examination

 Laboratory tests

• Serum TSH (Determines location of hypothyroidism – pituitary & secondary)

• Free T4 - biologically active

• Serum T3 – usually free T3 and bound T3

• Serum T4 (Total T4) - biologically active & protein bound inactive T4

• Increased Cholesterol & trig, increased CK, anemia

• TRH Stimulation test – increased TSH after TRH injection = hypothalamic dysfunction

T4 can convert to T3

Treatment

 Goal: Restoration of euthyroid state as safely and rapidly as possible

 Low calorie diet

 Synthetic T4 (levothyroxine): levitating thyroid levels

 Monitor thyroid levels

Thyroid Disorders: Thyroid Replacements: levothyroxine

Thyroid Replacements:

levothyroxine (Synthroid)

MOA

• Synthetically prepared T4; T4 is converted to T3

Therapeutic Use

• hypothyroidism

Adverse Drug Reactions (rare) (hyperthyroidism)

• Thyrotoxicosis (toxic amt of thyroid hormones, doesnt tell u whats going on tho), hyperthyroidism

• Tachycardia

• Headache, Insomnia, irritability

• Diarrhea

• Tremors

Interventions

• Monitor thyroid function (thyroid labs every 6-8 weeks)

• Monitor for s/sx hyperthyroid

Client Instructions

• Take in the morning on empty stomach

• Must taper when discontinuing

• May require lifelong therapy

• Taper medication

• Formulations are not interchangeable

Contraindications

• Thyrotoxicosis

• Recent Myocardial Infarction

• Severe renal impairment

Drug Interactions

• Ca supplements (reduces absorption)

• Antacids (reduces absorption)

• Increases anticoagulant effects of warfarin

Precautions

• CV disease

• Renal Impairment

• Diabetes Mellitus

• Older adults

Hyperthyroidism

 What does it mean? Speeds things up

Thyroid is over functioning, increasing metabolic rate

 Definition: sustained increase in synthesis & release of thyroid hormones (from thyroid)

 Causes: Autoimmune overproduction (Graves’ Disease), exogenous iodine excess, pituitary tumor, too much Synthroid, thyroid cancer

 More common in women & 20–40-year-olds

Graves' Disease

 Precipitating factors

• Infection

• Stressful life events (interacting with genetic factors)

• accounts for 75% of hyperthyroidism cases

Antibodies are developed to TSH receptor

• Thyrotropin receptor antibody (TRAb)

• Leads to clinical manifestations of thyrotoxicosis (may progress to Thyroid storm)

• Antibodies attached to receptors on thyroid causing an increase in T3. T4

• May progress to destruction of thyroid tissue, leading to hypothyroidism

Treatment

 Reduce symptoms of hyperthyroidism (Betablockers)

 Thyroidectomy (requires lifelong replacement)

 Pharmacotherapy

• PTU

• Radioactive Iodine

Thyroid Disorders: Antithyroid Drugs (Thioamides): propylthiaouracil/ PTU

Antithyroid Drugs (Thioamides)

propylthiaouracil/ PTU

MOA

• Limits the synthesis of thyroid hormones by blocking iodine from being integrated in tyrosine. Also inhibits peripheral conversion of T4 to T3.

Therapeutic Use

• Hyperthyroidism (Grave’s Disease)

• Thyrotoxic Crisis

• Suppression of thyroid in prep for thyroidectomy: if thyroid is so large

*can be used alone or in combination with radiation

Adverse Drug Reactions

• Hepatotoxicity

• Hypothyroidism

• Agranulocytosis (uncommon) (fever, sore throat but pain in throat!)

• Aplastic anemia (rare)

• Rash

• N/V and headache

Interventions

• Monitor thyroid function (thyroid labs every 6-8 weeks)

• Monitor for s/sx hypothyroid

• Baseline CBC then as needed (for agranulocytosis)

Client Instructions

• Take every 8h (short half-life)

• Report fever and sore throat (s/sx of agranulocytosis)

• Monitor for rash/bone pain

• Medication must be tapered

• Can takes 3-12 weeks to normalize

*pt saying something not making sense “i should feel affects in a week” FALSE!

Contraindications

• Hypersensitivity

Drug Interactions

• Additive effect when used with antineoplastics or radiation on bone marrow suppression. : monitor for hyperthyroidism

Precautions

• Immunosuppression

• Bone marrow depression

• Infection

• Liver dysfunction: jaundice, pain, ascites (abdominal distention)

• Pregnancy

Thyroid Disorders: Antithyroid Drugs (Thioamides): methiamazole/ Tapazole

Antithyroid Drugs (Thioamides):

methiamazole/ Tapazole

MOA

• Limits the synthesis of thyroid hormones by blocking iodine from being integrated in tyrosine. no impact on synthesis of t4 or t3.

Therapeutic Use

• Hyperthyroidism (Graves’ Disease)

• Thyrotoxic Crisis Thyroid storm—as part of combination treatment.

• Methimazole can be used; it is not sufficient by itself.

• May be used as primary drug therapy or to control hyperthyroidism before definitive treatment with radioactive iodine or surgery.

*can be used alone or in combination with radiation

Adverse Drug Reactions

• Hypothyroidism

• Agranulocytosis (uncommon)

• Aplastic anemia (rare)

• Rash

• N/V and headache

• Liver injury

Interventions

• Monitor thyroid function (thyroid

• labs every 6-8 weeks)

• Monitor for s/sx hypothyroid

• Baseline CBC then as needed (for agranulocytosis)

Client Instructions

• Report fever and sore throat (s/sx of agranulocytosis)!

• Monitor for rash/bone pain

• Medication must be tapered

• Can take 3-12 weeks to normalize

Contraindications

• Hypersensitivity

Drug Interactions

• Additive effect when used with antineoplastics or radiation on bone marrow suppression.

• May increase the effect of warfarin—monitor PT/INR

Precautions

• Immunosuppression

• Bone marrow depression

• Infection

• Liver dysfunction

• Risk for fetal harm

Thyroid Disorders: Antithyroid Drugs: iodine-131

Antithyroid Drugs:

iodine-131 (Radioactive Iodine)

MOA

• Over time the thyroid will take in radioactive iodine, which will eventually destroy thyroid tissue and glandular function

Therapeutic Use

• Hyperthyroidism (Grave’s Disease)

• Thyroid Cancer (much higher dose given for cancer)

Adverse Drug Reactions

• Hypothyroidism

• Bone marrow depression (rare)

• Radiation sickness (rare)

Interventions

• Monitor thyroid function

• Monitor for s/sx hypothyroid

• Baseline CBC then as needed

• Monitor for radiation sickness

Client Instructions

• Limit exposure to others (radiation) especially children & pregnant women

• Report fever and sore throat (s/sx of agranulocytosis)

• Report bloody nose:

Contraindications

• Pregnancy

• Breastfeeding (does enter breastmilk)

Drug Interactions

• Do not give other antithyroid medications while giving, because they will reduce the uptake

Precautions

• Use caution in pre-pubescent children

*body still having radiation when on this even tho only targeting in thyroid gland.

Adrenal Glands

What does it do? Stress response, blood pressure, fight-or-flight

Adrenal Glands → Located on top of the kidneys (think add to renal)

• Cortex: cortisol (stress/metabolism) & Aldosterone (BP)

• Medulla: Adrenaline & noradrenaline (fight-or-flight) & sex hormones

Disorders of the Adrenal Glands → causes

• Primary – the gland itself (JFK)

• Secondary – stimulating gland is the problem (pituitary)

• Tertiary – releasing organ is the problem (hypothalamus)

Addison’s Disease

*ADD more hormones

Disordered Adrenal Function - INSUFFICIENCY

• Mental Status → mood changes, irritability

• Glycemic Response → Hypo*

• Hydration/Electrolytes → lose Na+ & H20, ↑K+

• Low cortisol, aldosterone, sex hormones

• (symptoms of hyperkalemia?) Fast & Irregular heartbeat, muscle twitching, spasms, weakness

• Addison’s Disease

Clinical Manifestations → Anorexia/nausea, hyperpigmentation, GI upset

• Fluid Balance → Hypotension (d/t increase capillary permeability & vascular collapse - losing Na+ & water (but retaining K+)

• What happens to glucose? DECREASE

Adrenal insufficiency”= addison’s disease

• LOW cortisol and LOW aldosterone

Adrenals regulate BP, Na & H20 balance, Stress, Body hair during puberty

Autoimmune (mostly) or idiopathic atrophy (Tumor or poor pituitary function)

• Abruptly stopped steroids

Give steroids because the Adrenals stop producing and releasing steroids

Treatment

• Increase Na+ (broth, salty foods): retain salt

• Daily I&O (weight gain/loss)

• Meds (corticosteroids) – DON’T ABRUPTLY STOP!

• Address fluid volume deficit

Addison’s Crisis may occur (who is most at risk?)

• Immediate parenteral hydrocortisone!

• Profound dehydration: NS + D10 (ultimately hypotensive)

• Cyanotic: Give O2

• Tachycardia

• Hypoglycemic/Hyperkalemia

Adrenal Disorders: Glucocorticoids: hydrocortisone (Cortef)

Glucocorticoids:

hydrocortisone (Cortef)

MOA

• A synthetic preparation of Cortisol

• Mimics cortisol- increases availability of glucose

Therapeutic use

• acute or chronic adrenal insufficiency (Addison’s disease) without these patients will die

Adverse Drug Reactions

• Adrenal insufficiency

• Cushing’s syndrome (overshoot!)

• (both rare if therapeutic doses)

Interventions

• Monitor for weight changes

• Monitor for adrenal insufficiency: not enough

• Monitor for Cushing

Client Instructions

• Report stress

• Avoid live vaccines: steroid that dampens immune response

• Monitor weight changes

• Minimize carbohydrates

Contraindications

• Small doses – none.

• Large doses – severe infection

• Live vaccines

Drug Interactions

• Birth control (if large dosing)

• Phenobarb (if large dosing)

Precautions

• None

Adrenal Disorders: mineralocorticoids: fludrocortisone

mineralocorticoids

fludrocortisone

MOA

• Mimics the action of aldosterone (ADH)

• Regulates sodium potassium and water levels

• Usually give with hydrocortisone

Therapeutic Use

• Acute or chronic adrenocortical insufficiencies (Addison’s disease, primary

• Hypoaldosteronism and congenital adrenal hyperplasia)

Adverse Drug Reactions

• Few at low doses

• Fluid & electrolyte imbalances

• Hypo K

• Heart failure

Interventions

• Monitor for s/sx of ADR

• Monitor for fluid/elec imbalance

Client Instructions

• Report weight gain

• Follow a diet high in potassium

• Report weakness or heart changes: potassium

• Have BP checked regularly

• Take with milk

• Must taper dose!

Contraindications

• Hypersensitivity

Drug Interactions

• Potassium depleting diuretics

• Salt and foods high in sodium (increases sodium retention and potassium loss)

Precautions

• Heart failure

• Addison’s Disease (may have exaggerated response)

• OB

Cushing’s Syndrome

Disordered Adrenal Function - EXCESS

• Mental Status → mood changes, cranky

• Glycemic Response → Hyper* due to which 3 pathways?

• Immune Response → Suppression - @ risk for?

• Physical Hallmark → Moon face

• High Cortisol

Cushing’s syndrome

• Causes → tumors of adrenal gland, lung cancer, iatrogenic

• Mental Status → mood changes, euphoria

• Glycemic Response → Hyper* due to which 3 pathways?

• Immune Response → Suppression - @ risk for?