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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
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Diabetes
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it is the most common endocrine disorder, and the sixth leading cause of death by disease
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Diabetes
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Insulin pulls glucose out of the bloodstream and into the cells
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Normal functioning, diabetes
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Glucagon inhibits the effects of insulin thus preserving glucose levels in the blood
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Normal functioning, diabetes
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Symptoms from sustained hyperglycemia -- polyuria, polydipsia, ketonuria, and weight loss
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Symptoms of Diabetes
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Disorder of carbohydrate metabolism
– Deficiency of insulin – Resistance to action of insulin |
What is diabetes?
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Over time develops into HTN, heart disease, blindness, renal failure neuropathy, amputations, impotence and stroke
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Complications of diabetes
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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
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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
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Due to placenta producing hormones that antagonize insulin
Production of cortisol rises to a level 3X normal |
Gestational diabetes
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Heart disease
Hypertension Atherosclerosis (develops early in DM) Stroke Hyperglycemia Altered lipid metabolism |
Macrovascular damage (cardiovascular leading cause of death)
DM |
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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
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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
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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
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The diabetic woman who becomes pregnant will need her blood glucose checked 6-7 times a day due to the pregnancy.
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Diabetes and Pregnancy
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Excessive plasma glucose is diagnostic of diabetes.
Patient must be tested on two separate days, and both tests must be positive. |
Diagnosis of diabetes
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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
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Pancreas
Beta cell of the islets of Langerhans Evidence of c-peptide in blood indicates pancreas is still producing some insulin |
Insulin
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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
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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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.
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Gout is a recurrent inflammatory disorder characterized by hyperuricemia and episodes of severe joint pain, typically in the large toe.
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Rheumatoid arthritis (RA)
Autoimmune inflammatory disorder Usually begins in 3rd to 4th decades In younger 3X greater female, >60 equal gender |
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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 |
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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 |
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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] |
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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] |
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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] |
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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) |
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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 |
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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 |
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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 |
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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] |
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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.
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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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) |
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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 |
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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 |
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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 |
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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) |
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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) |
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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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] |
