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68 Cards in this Set

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primarily a disorder of carbohydrate metabolism. Symptoms result from a deficiency of insulin or from resistance to insulin’s actions
Diabetes
it is the most common endocrine disorder, and the sixth leading cause of death by disease
Diabetes
Insulin pulls glucose out of the bloodstream and into the cells
Normal functioning, diabetes
Glucagon inhibits the effects of insulin thus preserving glucose levels in the blood
Normal functioning, diabetes
Symptoms from sustained hyperglycemia -- polyuria, polydipsia, ketonuria, and weight loss
Symptoms of Diabetes
Disorder of carbohydrate metabolism
– Deficiency of insulin
– Resistance to action of insulin
What is diabetes?
Over time develops into HTN, heart disease, blindness, renal failure neuropathy, amputations, impotence and stroke
Complications of diabetes
5% to 10% of all cases
Previously called insulin-dependent diabetes mellitus (IDDM)
Or juvenile-onset diabetes mellitus
Usually begins in childhood 11-13 y/o with abrupt symptoms
Primary defect is destruction of pancreatic beta cells thus a lack of insulin
Without insulin to get glucose for energy ketoacidosis (d/t Lipids being used for energy leaving Ketoacid as waste & lowers pH blood making it more acidic)
Type 1 diabetes
Most prevalent form of diabetes
Approximately 19 million Americans have it
Previously known as non–insulin-dependent diabetes mellitus (NIDDM) Or adult-onset diabetes mellitus
Obesity is almost always present
Little risk of ketoacidosis
S/S result from Insulin resistance and impaired insulin secretion
type 2 diabetes
Due to placenta producing hormones that antagonize insulin
Production of cortisol rises to a level 3X normal
Gestational diabetes
Heart disease
Hypertension
Atherosclerosis (develops early in DM)
Stroke
Hyperglycemia
Altered lipid metabolism
Macrovascular damage (cardiovascular leading cause of death)
DM
Short-term (usually seen with Type I)
Hyperglycemia, hypoglycemia, ketoacidosis (which is potentially fatal for untreated hyperglycemia)
Long-term -- most commonly d/t disrupted blood flow from macro or microvascular damage
Complications of diabetes
Retinopathy (eyes) – DM major cause of Blindness
Nephropathy (kidney) – proteinuria, decreased GFR, HTN
Neuropathy (nerve)
Gastroparesis affects 20-30% of DM
Amputations –50% of lower limb amputations
Erectile dysfunction 13% males, 8% females
Microvascular damage
Difficult to control since placenta-producing hormones that antagonize insulin’s action
Production of cortisol increases 3X
Hyperglycemia in Mother stimulates fetal secretion of insulin
Usually gone by post-partum period to 6 weeks after delivery
Gestationsal Diabetes
The diabetic woman who becomes pregnant will need her blood glucose checked 6-7 times a day due to the pregnancy.
Diabetes and Pregnancy
Excessive plasma glucose is diagnostic of diabetes.
Patient must be tested on two separate days, and both tests must be positive.
Diagnosis of diabetes
Three tests
Fasting plasma glucose (FPG)
Administered 8-10 hr after last meal (normal 100mg/dL (glucose >126 is POSITIVE)
Casual plasma glucose
Should be <200 mg/dL
Oral glucose tolerance (OGTT)
Give load of 75gm and measure glucose at 1-2 hr intervals (normal <200mg/dL at 1 hr, <140mg/dL at 2hr
Diagnosis of diabetes
Pancreas
Beta cell of the islets of Langerhans
Evidence of c-peptide in blood indicates pancreas is still producing some insulin
Insulin
Secretion controlled by sympathetic nervous system to release insulin (stimulus is glucose)
Beta 2 adrenergic receptor activation promote insulin secretion
Alpha adrenergic receptor stimulation inhibits insulin secretion
Insulin
Metabolic actions (See Table 56-4)
Anabolic actions:
Conserve energy and build energy stores
Promote synthesis of complex organic molecules
Metabolic consequences of lack of insulin
Catabolic mode where glycogen is converted to glucose leading to ketoacidosis
Proteins converted to amino acids
Fats into glycerol and fatty acids
Insulin deficiency promotes Hyperglycemia:
Increasing glycogenolysis
Process of changing glycogen to glucose
Increasing gluconeogenesis
Metabolic pathway that results in the generation of glucose from non-carbohydrate carbon substrates that occurs mostly in the liver (ketoacids are formed)
Ketoacidosis occurs secondary to disruption of glucose and fat metabolism
Reducing glucose utilization
Sulfonylureas (stimulate release of insulin)
Tolbutamide [Orinase]
Concomitant use of NSAIDs, Sulfonamide antibiotic, ranitidine and cimetidine can increase the risk of hypoglycemia
Avoid in pregnancy and breast feeding
Beta Blockers can mask hypoglycemic s/s and suppress insulin release

For type II
Meglitinides
Repaglinide [Prandin]
Interacts w/ gemfibrozil (lopid) to inhibit metabolism of Prandin (causing higher levels
Nateglinide [Starlix]

For type II
Biguanides
Metformin [Glucophage]
Monitor for elevated serum creatine levels (critical)
Causes freq. GI Disturbances (decreased appetite, N&V, diarrhea)
Lowers blood glucose by decreasing production of glucose by the liver (not by promoting the release of insulin)
Absorbed in intestine and excreted by kidneys
Used for polycystic ovary syndrome (PCOS)
Avoid ETOH (increases risk of lactic acidosis)
Toxicity includes lactic acidosis
Thiazolidinediones (Glitazones) increases target cell to respond to insulin (used in insulin-resistant patients)
Rosiglitazone [Avandia]
Well absorbed, half life 3-4 hr
May cause fluid retention
Lopid raises plasma levels of Avandia
Pioglitazone [Actos]

DO NOT GIVE GLITIZONES TO A CARDIAC PATIENT WITH HEART FAILURE
Alpha-glucosidase inhibitors
Acarbose [Precose] delays absorption of Carbs
Can decrease absorption of IRON in anemia
CAUTION: HEPATIC DYSFUNCTION
Miglitol [Glyset] effective in Hispanic and AA
NO ASSOC. W/ HEPATIC DYSFUNCTION
Muraglitazar [Pargluva] experimental
Educate you patient that Alpha-glucosidase inhibitors can cause GI problems (flatulence and diarrhea)
Does not cause hypoglycemia when used as monotherapy
Combination products
Glyburide/metformin
Glipizide/metformin
Rosiglitazone/metformin
Pramlintide [Symlin]
Supplement to mealtime insulin (type 1 or type 2) peaks in 20 min after SC injection
Adverse effects—hypoglycemia, nausea
Exenatide [Byetta]
Adjunctive therapy to improve glycemic control in patients with type 2 diabetes
Adverse effects
Hypoglycemia
Gastrointestinal effects (nausea)
Most severe manifestation
Pathogenesis – derangement of glucose and fat metabolism
Characteristics
Hyperglycemia
Ketoacids
Hemoconcentration
Acidosis
Coma

Ketoacidosis
Treatment
IV Insulin replacement
Bicarbonate for acidosis
Water and sodium replacement (large amts)
IV SALINE (EITHER 0.9% OR 0.45%)
Potassium replacement
MIX POTASSIUM IV SALINE AND MONITOR ECG
Normalization of glucose levels
WATCH FOR SWITCH TO HYPOGLYCEMIA

Ketoacidosis
Diet should consist of the majority of calories coming in the form of carbohydrates and monounsaturated fats
Regular glucose checking (at home) and follow up testing in office (glucose, Glycated Hemoglobin/ Hemoglobin A1c, urinalysis ever 3 months
If experiencing a severe Hypoglycemic episode always check the gag reflex before giving orange juice or cokes
If on a Beta Blocker, remember B-Blocker can mask the symptoms of hypoglycemia

Diabetic teaching
Wear Medic-Alert bracelet
Keep oral glucose source available
If in doubt of hypo or hyperglycemic episode, treat as hypoglycemic (progresses much slower)
Strict following of diet guidelines

Diabetic teaching
Rheumatoid arthritis (RA) is an autoimmune, inflammatory disorder that affects about 1% of the American population. RA follows a progressive course and can eventually cripple its victim.
Gout is a recurrent inflammatory disorder characterized by hyperuricemia and episodes of severe joint pain, typically in the large toe.
Rheumatoid arthritis (RA)
Autoimmune inflammatory disorder
Usually begins in 3rd to 4th decades
In younger 3X greater female, >60 equal gender
Treatment
Relieve symptoms
Maintain joint function and ROM
Minimize systemic involvement
Delay progression of disease

RA
Rheumatoid Arthritis:
Heralded by symmetric joint stiffness and pain (worse in AM)
Joints warm, tender and swollen
Weakness and fatigue
Anorexia and weight loss
Vasculitis
Therapy
3 objectives
Relief of symptoms
Maintenance of joint function
Prevention of deformity
Non-drug measures
PT, exercise and surgery
Need for a balance between rest and exercise
Classes differ in respect to time, course of action, toxicity, and ability to alter the progression of RA
NSAIDs
Nonsteroidal anti-inflammatory drugs
DMARDS
Disease-modifying antirheumatic drugs
Glucocorticoids
Adrenal corticosteroids

Classes of antiarthritic drugs
Protocol (based on severity of symptoms, patient’s response and ability to tolerate side effects)
NSAIDS add 1-2 DMARDs.
Fast acting and inexpensive (exception of COX-2)
Monitor liver and kidney functions
Usually maintenance dose 7.5-20 mg/week
Glucocorticoids may be added until DMARDs take effect.
Prednisone 10-20 mg/day until symptoms are controlled then taper off over 5-7 days

Drug selection for RA
First Choice of DMARDs
Most rapid-acting DMARD
Therapeutic effect—3 to 6 weeks
Monitor kidney and liver functions
Toxicity include hepatic fibrosis, bone marrow suppression GI ulceration and pneumonia
Usually maintenance dose 7.5-20 mg/week

Methotrexate [Rheumatrex]
Hydroxychloroquine (Placquenil)
Antimalarial drug used with Methotrexate to produce remission of RA symptoms (delayed onset of action 3-6 mo)
Toxicity – risk of irreversible retinal damage
Dosage –200 mg BID or 400mg QDay

Methotrexate [Rheumatrex]
Sulfasalazine (Azulfidine)
One used for IBS and now retards progression of joint deteriation
GI problems is #1 for discontinuing (give in divided dose to minimize GI effect)
Serous adverse effects (Hepatitis and Bone Marrow suppression BUT IS RARE)

Methotrexate [Rheumatrex]
Infliximab (Remicade) is often used in combination with Methotrexate in RA patients, (also Crohn's disease and ankylosing spondylitis)

Do Not use in patients with heart failure (it can also cause new-onset heart failure)
It increases the risk of lymphoma

Methotrexate [Rheumatrex]
New DMARD (usually combined with Methotrexate)
Inactivates tumor necrosis factor (TNF)
Use
Moderate to severe RA
Ankylosing Spondylitis, plaque psoriasis, psoriatic arthritis
Adverse effects
Infection
Injection site reactions in about 37% (given SC subcutaneous)
Interacts with live vaccines (avoid live vacc.)

Etanercept [Enbrel]
Powerful DMARD (equivalent to Methotrexate but more dangerous, more expensive and more side-effects)
Side Effects – GI (diarrhea) reversible alopecia, resp. infection, rash and nausea
Contraindication – PREGNANCY (STOP IMMEDIATELY)
Possible Effects – inhibit metabolism NSAIDs, add to liver damage with other hepatotoxic drugs

Leflunomide (Arava)
DMARD for serious active RA not responding to other treatments
Block receptors for Interleukins-1 (IL-1)
Approved for subcutaneous injections
Adverse effects
Injection site reactions
Especially during 1st month of treatment
Risk for serous infections

Anikanra (Kineret)
Recurrent inflammatory disorder
Hyperuricemia (excessive uric acid production and impaired renal excretion)
Episodes of severe joint pain
Deposits of uric acid crystals in joint that promotes inflammation

Gout
Gout progresses through four stages: (1)Asymptomatic hyperuricemia
(2) Attacks of acute gouty arthritis, (3)Asymptomatic intercritical period [so-called because symptoms subside]
(4)Tophaceous gout
Overview of therapy:
Relieve inflammation (Colchicine and indomethacin)
Reduce hyperuricemia (Allopurinol, Probenecid, and sulfinpyrazone)
Glucocorticoids and some NSAIDs

Gout
Colchicine (for Inflammation)
Indomethacin [Indocin]
(for Inflammation)
Allopurinol [Zyloprim]
(reduce hyperuricemia)
Probenecid [Benemid]
(reduce hyperuricemia)
Sulfinpyrazone [Anturane]
(reduce hyperuricemia)

Drug therapy for Gout
Anti-inflammatory agent that targets Gout
Uses
Treat acute gouty attack
Small doses decrease frequency and intensity
Reduce incidences of attack
Abort an impending attack
Take large amounts

Colchicine
Adverse effects
Gastrointestinal (n/v, diarrhea, abdominal pain)
Instruct to stop the drug regardless!
Use with caution w/ cardiac, renal, GI diseases and in elderly
Category C (oral) and Category D for IV pregnancy
If administering IV make sure the IV line is patent to avoid tissue necrosis
Mix with 20ml normal saline and inject IV push slowly over 5-10 min

Colchicine
Reduce blood levels of uric acid
Inhibits uric acid production
Uses
Chronic tophaceous gout (#1 choice)
Secondary Hyperuricemia due to cancer chemotherapy
Adverse effects
Well tolerated (discontinue if rash develops)
Hypersensitivity syndrome
Mild Gastrointestinal effects
Neurologic

Allopurinol [Zyloprim]
Drug interactions
Inhibits hepatic drug metabolizing enzymes
Problems with anticoagulants and cancer drugs
Decrease the warfarin dose
Rash with ampicillin
Administer
Consume plenty of liquids to avoid renal damage

Allopurinol [Zyloprim]
Actions
Inhibits reabsorption of uric acid in renal tubules
Drug interactions
ASA interferes with uricosuric action
Reduce Indocin and other sulfonamide dosages
Adverse effects
Well tolerated (some mild GI)
Administration
Take with 2-3 L water
Take with food

Probenecid
Calcium is an element that is critical to blood coagulation and to the functional integrity of bone, nerve, muscle, and the heart. Because these calcium-dependent processes can be seriously disrupted by alterations in calcium availability, calcium levels must stay within narrow limits. To regulate calcium, the body employs three factors: parathyroid hormone, vitamin D, and Calcitonin. Hypercalcemia or hypocalcemia results when these regulatory mechanisms fail.
For integrity of bone
Regulates excitability and transmitter release in nervous system
Excitation-contraction coupling and contraction of muscle
For cardiovascular system helps with myocardial and vascular contraction;

Calcium
Body stores
More than 98% stored in the bones
Absorption
Absorption in the small intestine
About 1/3 Ca ingested is absorbed
Ca requirements 9-18y/o = 1000mg/day
Ca requirements 51+y/o = 1200mg/day
Increased absorption by parathyroid hormone & vitamin D
Some foods interfere with absorption (brans and whole grain cereals and Spinach
Glucocorticoids decrease absorption

Calcium
Bone undergoes continuous remodeling Old bone deposits are osteoclasts New bone deposits are osteoblasts

Normal value for total serum calcium is 10 mg/dL (50% bound to proteins and 50% free)
Regulation of calcium levels
Absorption in small intestine
Absorb 1/3 of consumed increase by parathyroid hormone and Vit D
Excretion by the kidney
Reduced by parathyroid hormone and Vit D
Increased by loop diuretics and Calcitonin
Resorption by the bone
Regulated by
Parathyroid hormone
Vitamin D
Calcitonin
Physiologic regulation of calcium levels:
Body carefully adjusts Calcium in 3 ways:
(1) absorption from intestine (2) excretion by kidney (3) resorption or deposition of calcium in bone regulated by parathyroid hormone, vitamin D, and Calcitonin
Parathyroid hormone (PTH): Released from parathyroid glands in response to low levels of plasma calcium; elevates serum calcium by promoting resorption to form bone, promoting reabsorption filtered by glomerulus and activates vitamin D for absorption from intestine; also effects phosphate levels
Vitamin D: Similar to PTH; in addition, elevates phosphate levels
Calcitonin: Hormone produced by thyroid gland; decreases plasma levels; acts in opposition to PTH and vitamin D
Usually asymptomatic
S/S if seen are found in kidney, GI and CNS effects
Causes
Cancer
Hyperparathyroidism
Vit D intoxication
Sarcoidosis
Use of thiazide diuretics
Patients are pre-disposed who have Osteoporosis
Treatment
Drugs that promote urinary excretion
Decrease mobilization from bone
Decrease intestinal absorption

Hypercalcemia
Drugs
Furosemide [Lasix]
Glucocorticoids
Others: Calcitonin, bisphosphonates, inorganic phosphates, gallium nitrate


For treatment of hypercalcemia, IV isotonic saline and loop-diuretic

Hypercalcemia
S/S: Increases neuromuscular excitability (convulsions)
Clinical presentation
Tetany, convulsions, and spasm of the pharynx
Causes
Deficiency of parathyroid hormone (PTH), vitamin D, or dietary calcium intake
Treatment
IV calcium replacements (in severe cases) calcium chloride
Push IV slowly after warming to body temperature
Assess for Bradycardia if also administering Digoxin
Calcium supplementation (calcium gluconate)
Vitamin D

Hypercalcemia
Rickets (Usually a Childhood Disease)
d/t limited Vit D or exposure to sunlight causing defective bone growth (treat with Vit D)
Osteomalacia
Adult equivalent of Ricketts (back pain, bow-legs, Kyphosis)
Therapy is Vit D
Paget’s disease of bone
Seen over 40 y/o (increased bone reabsorption but replaced with abnormal bone (S/S fractures and deafness)
Osteoporosis (disorder of Calcium metabolism)
Low Bone Mass
Hyperparathyroidism (d/t parathyroid removal)
Hyperparathyroidism
Primary (caused by adenoma)
Secondary (common complication of chronic kidney disease and dialysis)

Others Disorders Involving Calcium
Most common disorder of calcium metabolism
Low bone mass and increased bone fragility
Primary prevention
Calcium, vitamin D, lifestyle
Diagnosis
Measuring bone mineral density (BMD)
Dual-energy x-ray absorptiometry (DEXA)

Osteoporosis
Prevention
Weight bearing exercises
Avoid alcohol
Avoid smoking

Osteoporosis
Antiresorptive therapy—drugs that reduce bone loss (does not reverse bone already lost)
Estrogen [Premarin]
Raloxifene [Evista]
Bisphosphonates
Alendronate [Fosamax]
Risedronate [Actonel]
Ibandronate [Boniva]
Calcitonin-salmon nasal spray [Miacalcin]
Drugs that promote bone formation
Teriparatide [Forteo] only drug that increases bone formation in osteoporosis

Osteoporosis
Alendronate (Fossomax)
Once daily in AM or Once Weekly in AM
Calcium and Antacids can decrease absorption of alendronate and should betaken 30 min after.
Also do not eat food for 30 min after taking
Take with a full glass of water, remain upright (sitting or standing) for 30 min afterwards, swallow whole do not chew or suck on pill.
Common side effect is GI

Osteoporosis
Raloxifene (Evista) increases the risk of DVT and pulmonary embolus.

Osteoporosis
For absorption of Vit D, bile is required along with sunlight
Absorption takes place in small intestines.
The elderly and school-age children are at the highest risk for failure to meet Vit D requirements
Children need 200 IU/day ( 50y/o to babies)
Elderly need 400 IU/day for 70y/o and under and 600 IU/Day over 70 y/o

Vitamin D
Thyroid hormones have profound effects on metabolism, cardiac function, growth, and development. These hormones stimulate the metabolic rate of most cells and increase the force and rate of cardiac contraction. Fortunately, most abnormalities of thyroid function can be treated effectively.

Throid
2 Active Thyroid Hormones
Triiodothyronine (T3)
More potent than T4
Thyroxine (T4)
Is converted to T3 in most tissues


Thyroid Hormone Actions
Stimulation of energy use
Stimulation of the heart
Promotion of growth and development

Thyroid
Serum TSH
Most sensitive method for diagnosing hypothyroidism
Serum T4 test
Measures total thyroxine for monitoring screening and replacement therapy
Confirms diagnosis
Serum T3 test
Measures total triiodothyronine
Used to test for hyperthyroidism and monitoring therapy

Thyroid Function Tests
Severe deficiency of thyroid hormone
Myxedema (adults)
Clinical presentation (adults)
Pale, puffy, and expressionless face
Cold and dry skin
Brittle hair or loss of hair
Heart rate and temperature lowered
Lethargy, intolerance to cold
May have mental impairment
May have enlarged thyroid gland
Associated with Hashimoto’s disease (chronic autoimmune Thyroiditis

Hypothyroidism
Lab values – low serum T4 and high TSH
Treatment with thyroid replacement is LIFE-LONG
Severe deficiency of thyroid hormone
Cretinism in children
Clinical Presentation in children
Mental retardation
Derangement of growth
Large protruding tongue, potbelly, dwarfish appearance
Impairment in nervous system, bones, teeth and muscles

CHECK FOR HYPOTHROIDISM DURING PREGNANCY TO PREVENT NEUROPSYCHOLOGIC DEFICITS AT BIRTH

Hypothyroidism
Two major forms of hyperthyroidism
Graves’ disease (most common)
Toxic nodular goiter (Plummer’s disease)
Graves’ disease --more common in Females
Thyrotoxicosis (Thyroid Crisis)
Exophthalmoses (Bugged Eyed)
Rapid HR with possible dysrhythmias
CNS effects -- Nervousness, rapid flow of speech, insomnia muscle weakness, intolerance to heat, sweaty skin and weight loss
Toxic Nodular Goiter (Plummer’s Disease)
Refer for surgery or radiation

Hyperthyroidism
Thyrotoxicosis (Thyroid Crisis)
Also called “Thyroid Storm”
Extremely high levels of Thyroid Hormones
Symptoms: Hyperthermia, Tachycardia, Profound weakness
Treat tachycardia with Propanolol

Hyperthyroidism
Lab values: low TSH Levels
Cause
Thyroid-stimulating Immunoglobulins (TSIs)
Treatment
Surgical removal of thyroid tissue
Destruction of thyroid tissue with radioactive iodine (potassium iodine or strong iodine solution) in cases of Thyroid Storm
Suppresses thyroid hormone release
May cause life-long Hypothyroidism
Suppression of thyroid hormone synthesis with anti-thyroid drugs

Hyperthyroidism
Levothyroxine (T4) [Synthroid]
Synthetic preparation of thyroxine (T4)
Conversion to T3
Half-life is 7 days
Highly protein bound
Used for all forms of hypothyroidism
Previously used as weight loss agent
Adverse effects (rare unless in excess/overdose) S/S Thyroid Toxicosis:
Tachycardia
Angina
Tremors

Thyroid Hormone Preparations
Levothyroxine (T4) [Synthroid] (cont’d)
Drug interactions
Drugs that reduce levothyroxine absorption
Cholestyramine (decreases absorption), colestipol, calcium supplements, aluminum antacids, iron supplements (give 2 hr apart)
Drugs that accelerate levothyroxine metabolism
Phenytoin, carbamazepine, rifampin, sertaline, phenobarbital
Warfarin
Synthroid accelerates the degradation of Vit K clotting factors enhancing the effects of Warfarin (TX --decrease warfarin dosage)
Catecholamines
Increases cardiac responsiveness to catecholamines

Thyroid hormone preparations
nhibits thyroid hormone synthesis by:
Preventing oxidation of iodine
Preventing iodinated tyrosine from coupling
Short half-life (about 75-120 minutes)
ONLY AVAILABLE ORALLY
Therapeutic uses
Graves’ disease
Adjunct to radiation therapy
Preparation for thyroid gland surgery
Thyrotoxic crisis
Adverse effects
Agranulocytosis (check serum WBC)
Hypothyroidism
Pregnancy and lactation
Stop drug immediately if jaundice, fever/chills, sore throat, bleeding gums

Propylthiouracil (PTU): Antithyroid Drug
Radioactive isotope of stable iodine
Emits gamma and beta rays
Half-life is 8 days
Used in Graves’ disease
Effect on the thyroid (destruction of thyroid tissue resulting in life-long hypothyroidism)
Advantages of 131I therapy
Low cost, less risk, less discomfort, no surgery or risk of death
Disadvantages of 131I therapy
Delay in effect and incidence of delayed Hypothyroidism

Radioactive Iodine-131 (131I)
Candidates
Patients over 30
Contraindicated in pregnancy and lactation
Action
The drug is taken up by the thyroid gland and destroys the cells to reduce hyperthyroidism
Produces clinical remission of hyperthyroidism with destruction of thyroid gland

Radioactive Iodine-131 (131I)
Strong iodine solution (Lugol’s solution)
Used to suppress thyroid function in preparation for thyroidectomy
Adverse effects
Brassy taste
Burning sensation in the mouth and throat
Soreness of the teeth and gums
Frontal headache
Coryza
Salivation
Various skin eruptions

Nonradioactive Iodine
The hypothalamus and pituitary work together to help regulate practically all bodily processes. To achieve their widespread effects, the hypothalamus and pituitary employ at least 15 hormones and regulatory factors. We will focus on just three agents: growth hormone (GH), antidiuretic hormone (ADH), and prolactin.

Hypothalamic and Pituitary Function
Hormones of the anterior pituitary
Growth hormone (GH)
Corticotropin hormone
Thyrotropin
Follicle-stimulating hormone (FSH)
Luteinizing hormone (LH)
Prolactin
Hormones of the posterior pituitary
Oxytocin
Antidiuretic hormone

Overview of Hypothalamic and Pituitary Endocrinology
Biologic effects
Promotes growth
Promotes protein synthesis
Carbohydrate metabolism
Pathophysiology
Deficiency
Pediatric—short stature
Adult—reduced muscle mass
Excess
Pediatric—gigantism
Adult—acromegaly

Somatropin Growth Hormone (GH)
Growth hormone excess
Acromegaly in Adults and Gigantism in children
Pituitary adenoma
Clinical manifestations
Treatment
Surgery
Radiation
Somatostatin
Octreotide and Pegvisomant

Acromegaly
Consequences of deficiency: Absence retards growth in all parts of the body; only treatment for deficiency is replacement with human GH
Some may respond to sermorelin, which promotes GH release
Growth hormone excess: Acromegaly in adults; gigantism in children; treated with surgery, radiation, or drugs
octreotide is synthetic analogue of somatostatin, which is most effective for suppressing GH release
pegvisomant (Somavert) may be our most effective drug for acromegaly

Somatropin Growth Hormone (GH)
Clinical Pharmacology
Therapeutic uses—Pediatric growth hormone deficiency (treat only those with proven GH deficiency; assess epiphyseal status annually); expected response is increase of 6 inches for adult; short stature only 2 inches and not recommended

Somatropin Growth Hormone (GH)
Adverse effects and interactions
Hyperglycemia
Antibodies to GH
Carpal tunnel syndrome
Fatality in Prader-Willi syndrome (PWS) patients
Interaction with glucocorticoids

CHECK TSH LEVELS PERIODICALLY

Somatropin Growth Hormone (GH)
Administration – comes in a powder, mix gently (do not shake)
Do not give if parentally if injection is cloudy
Administer 0.06mg/kg subcutaneous 3 days/week
Give until satisfactory adult height is reached or until epiphyseal closure occurs

Somatropin Growth Hormone (GH)
Produced by the anterior pituitary
Stimulation of milk production after giving birth
Hypersecretion (excessive secretion)
Female
Amenorrhea
Galactorrhea
Infertility
Male
Libido and potency are reduced
Galactorrhea
Cabergoline (Dostinex) for suppression of prolactin release
Dopamine agonist
Adverse effects: nausea, HA, dizziness

Prolactin
Thyrotropin (thyroid-stimulating hormone; TSH)—Role is stimulation of thyroid gland function; see increased thyroidal uptake of iodine, increased synthesis of thyroid hormones, increased release of thyroid hormone and thyroid growth; used to diagnose thyroid cancer

THYROTROPIN
Corticotropin (adrenocorticotropic hormone; ACTH)—Acts on adrenal cortex to stimulate production and release of adrenocortical hormones
Principal use is diagnosis of adrenocortical dysfunction

CORTICOTROPIN
Two hormones (FSH and LH)
FSH supports sperm production in males; in females, it promotes follicular growth and development
LH in females promotes ovulation and formation of corpus luteum; in males, LH promotes testosterone synthesis by Leydig cells
Employed clinically to treat infertility in men and women

GONADOTROPINS
Antidiuretic hormone (ADH) promotes renal conservation/reabsorption of water
Hypothalamic Diabetes insipidus
Deficiency of ADH
Polydipsia (excessive thirst)
Excretion of large volumes of dilute urine
Treatment—ADH replacement
Desmopressin (agent of choice)
Vasopressin
Adverse effects
Water intoxication
Side effects – drowsy, listless and complaints of recent HA
Excessive vasoconstriction

Antidiuretic Hormone
Desmopressin (Antidiuretic Hormone)
Therapeutic uses
Diabetes insipidus
Cardiac arrest
Postoperative abdominal distention
Preparation for abdominal radiography
Nocturnal enuresis (bedwetting)
Hemophilia A
Von Willebrand’s disease

Antidiuretic Hormone
May be administered:
PO
Intra-nasal
IV
Subcutaneous
BUT NOT IM

Antidiuretic Hormone
Produced by neurosecretory cells of hypothalamus and transported down axons of cells for storage in posterior pituitary
Two roles (promotion of uterine contraction during labor and stimulation of milk ejection during breastfeeding

OXYTOCIN
The hormones of the adrenal cortex affect multiple physiologic processes, including maintenance of glucose availability, regulation of water and electrolyte balance, development of sexual characteristics, and life-preserving responses to stress. The two most familiar forms of adrenocortical dysfunction are Cushing’s syndrome, caused by adrenal hormone excess, and Addison’s disease, caused by adrenal hormone deficiency.

Adrenal Cortex
Three classes of steroid hormones
Glucocorticoids
Mineralocorticoids
Androgens
Two most familiar forms of adrenocortical dysfunction
Adrenalcortical hormone excess
Cushing’s syndrome
Adrenalcortical hormone deficiency
Addison’s disease

Physiology of the Adrenocortical Hormones
Carbohydrate metabolism
Protein metabolism
Fat metabolism
Cardiovascular system
Skeletal muscle
Central nervous system and Mood
Stress and Respiratory system in neonates

Glucocorticoids—Physiologic Effects
Mineralocorticoids—Influence renal processing of sodium, potassium, and hydrogen; aldosterone most important
Physiologic effects — Aldosterone acts on collecting ducts of nephron to promote sodium reabsorption in exchange for secretion of potassium and hydrogen; water reabsorbed with sodium

Mineralocorticoids
Cushing’s syndrome
Causes
Hypersecretion of adrenocorticotropic hormone (ACTH)
Hypersecretion of glucocorticoids
Administering glucocorticoids in large doses
Clinical presentation
Obesity
Hyperglycemia
Glycosuria
Hypertension
Fluid and electrolyte disturbances

Adrenal Hormone Excess
Cushing’s syndrome (cont’d)
Treatment
Surgical removal of the adrenal gland
Replacement therapy
Irradiation of pituitary gland
Often ketoconazole is also given to inhibit glucocorticoid synthesis

Adrenal Hormone Excess
Addison’s disease (primary Adrenocortical insufficiency):
Clinical presentation and causes
Weakness
Emaciation
Hypoglycemia
Increased pigmentation of the skin and mucous membranes
Treatment
Replacement therapy with adrenocorticoids
Hydrocortisone is the drug of choice

Adrenal Hormone Insufficiency
Secondary and tertiary adrenocortical insufficiency
Secondary results from decreased secretion of ACTH
Tertiary results from decreased secretion of CRH
Adrenal secretion of glucocorticoids is diminished
Clinical presentation
Hypoglycemia
Malaise
Loss of appetite
Reduced capacity to respond to stress
Treatment
Replacement therapy with glucocorticoid

Adrenal Hormone Insufficiency
Acute adrenal insufficiency (adrenal crisis)
Clinical presentation
Hypotension
Dehydration
Weakness
Lethargy
GI symptoms
Causes
Adrenal failure
Pituitary failure
Inadequate doses of corticosteroids

Adrenal Hormone Insufficiency
Acute adrenal insufficiency (adrenal crisis) (cont’d)
Treatment
Rapid replacement of fluid, salt, and glucocorticoids
Glucose

Adrenal Hormone Insufficiency
Synthetic steroid
Therapeutic uses
Adrenal insufficiency
Allergic reactions, inflammation and treatment for cancer
Adverse effects
Low doses show no adverse effects, Large doses can be highly toxic with:
Adrenal suppression
Cushing’s syndrome

Hydrocortisone
Potent mineralocorticoid with significant glucocorticoid activity
The only mineralocorticoid available
Therapeutic uses
Addison’s disease
Primary hypoaldosteronism
Congenital adrenal hyperplasia
Adverse effects
Hypertension
Edema/retention of water and salt
Cardiac enlargement
Hypokalemia

Fludrocortisone [Florinef]