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Endocrine Block 13
68WM6 Exam block 13- endocrine
| Question | Answer |
|---|---|
| Describe the location of the adrenal glands. | Small glands located on top of the kidneys |
| What hormones does the adrenal cortex release? | 1. Mineralcorticoids 2. Glucocorticoids 3. Sex hormones |
| What does the adrenal medulla release? | Epinephrine and norepinephrine during "Fight or Flight" response. |
| Causes of Cushing's Syndrome | 1. Hyperplasia of adrenal tissue 2. Tumor of adrenal cortex 3. Overuse of corticosteroid drugs |
| What is Cushing's syndrome? | Rare condition in which the plasma levels of adrenocortical hormones are increased, resulting in excess secretion of adrenal hormones. |
| Symptoms of Cushing's syndrome. | 1. Irritability 2. Emotional instability 3. Depression 4. Backache 5. Decreased libido 6. Increased appetite |
| Signs of Cushing's syndrome. | 1. Ecchymoses 2. Petechiae 3. Thin and fragile skin 4. Weight gain, edema 5. Hypertension 6. Muscle wasting 7. Moon face and buffalo hump 8. Prolonged wound healing 9. Hirsutism in women. |
| Medical management for Cushing's syndrome. | 1. Adrenalectomy for adrenal tumor. 2. Irradiated or removed surgically for pituitary tumors. 3. Mitotane (Lysodern) cytotoxic agent that is toxic to adrenal glands for inoperable adrenocoritcal cancer. |
| Another term for Cushing's Syndrome. | Adrenal HYPERfunction. |
| Another name for Addison's Disease | Adrenal HYPOfunction. |
| Causes of Addison's Disease. | 1. Adrenalectomy 2. Pituitary hypofunction 3. Longstanding steroid therapy 4. cancer of adrenal cortex 5. autoimmune disease 6. tuberculosis |
| What is Addison's disease? | inadequate secretion of glucocorticoids (cortisol) and mineralcorticoids (aldosterone) by adrenal glands |
| Signs/symptoms of Addison's | 1. Nausea, anorexia, salt craving 2. postural hypotension 3. vertigo, weakness, syncope 4. severe headache, abdominal pain 5. changes in color of mucous membranes 6. weight loss, vomiting, diarrhea 7. hypoglycemia, hyponatremia, hyperkalemia |
| Medical management of Addison's disease | 1. restore fluid and electrolyte balance 2. replace deficient adrenal hormones |
| Diet of patient with Addison's disease | High in sodium and low in potassium. |
| Definition of an Addisonian Crisis | an acute, emergency, life-threatening state of profound adrenal cortical insufficiency that occurs when the adrenal glands suddenly fail. |
| Signs of an Addisonian crisis | 1. Sudden, severe drop in BP 2. Anorexia, n/v 3. extremely high temp 4. diarrhea, abd. pain 5. profound weakness 6. headache, restlessness or fever |
| How is an Addisonian crisis treated? | 1. Corticosteroids via IV solution of NS and glucose 2. Antibiotics due to low resistance to infection. |
| What is pheochromocytoma? | Tumor, ususally found in adrenal medulla, causes excessive secretion of epinephrine and norepinephrine. |
| What is the principle manifestation of pheochromocytoma? | Hypertension (hypertensive crisis with BP as high as 300/175 may occur) |
| What hormones does the anterior pituitary release? | 1. Growth hormone (GH) 2. Thyroid stimulating hormone (TSH) 3. adrenocorticotrpoin hormone (ACTH) 4. Follicle stimulating hormone (FSH) 5. Luteinizing hormone (LH) 6. Melanocyte stimulating hormone (MSH) 7. prolactin |
| What hormones does the posterior pituitary release? | 1. Anti-diuretic hormone (ADH) 2. oxytocin |
| Which condition develops before puberty: acromegaly or gigantism? | Gigantism |
| What is acromegaly? | Overproduction of growth hormone after puberty. |
| Manifestations of acromegaly. | 1. Enlargement of cranium and lower jaw 2. Bulging forehead 3. Hands and feet become enlarged 4. Hepatomegaly, cardiomegaly, splenomegaly 5. Stiff joints 6. Impotence 7. Females- deepened voice, increased facial hair, amenorrhea |
| Drug of choice of acromegaly | Bromocriptine mesylate (Parlodel)- antiparkinson drug that inhibits release of GH |
| What is dwarfism? | deficiency in the growth hormone |
| Diagnosis of dwarfism is based on... | 1. Radigraphic evaluation 2. Decreased plasma levels of growth hormone |
| Medical management for dwarfism | 1. GH injections 2. Surgery for tumor removal |
| Most common complications associated with dwarfism | musculoskeletal and cardiovascular |
| What are dopamine agonists such as bromocrpitine, cabergoline, and octreotide used for? | to treat acromegaly |
| Side effects of dopamine agonists | 1. dizziness 2. drowsiness 3. visual disturbances 4. hypotension 5. nausea 6. abdominal pain 7. constipation 8. digital vasospasm (acromegaly only) |
| Patient teaching for dopamine agonists. | 1. Avoid use of alcohol 2. Do not double dose, take missed does w/in 4 hours. 3. May cause drowsiness and dizziness. |
| What is diabetes insipidus? | deficienty of ADH |
| Causes of diabetes insipidus | 1. Primary- malfunction of posterior pituitary 2. Secondary- head injury, intracranial tumor, intracranial aneurysm, infarct. 3. Infections |
| Common clinical manifestations of diabetes insipidus | polyuria, instense polydipsia, dilute urine. |
| Treatment of diabetes insipidus | 1. ADH administration (IM, SQ, nasal spray) 2. Eliminate caffeine 3. Monitor fluid and electrolyte balance |
| What is vasopressin (Pitressin) and what effect does it have? | ADH- decreases urine output and increases urine osmolality in diabetes insipidus |
| Side effects of vasopressin | 1. "pounding" sensation in head 2. belching, flatulence 3. paleness 4. perioral blanching 5. trembling |
| What are the s/s of toxicity and overdose of vasopressin? | s/s of water intoxication |
| What is desmopressin (DDAVP) and what is it used for? | ADH- to prevent nocturnal enuresis |
| What is Syndrome for Inappropriate Secretion of Anti-Diuretic Hormone (SIADH)? | Occurs when pituitary releases too much ADH, and kidneys absorb more water, results in: hyponatremia, hemodilution, and fluid overload |
| Risk factors for SIADH | 1. medications 2. duodenal, pancreatic cancer 3. tuberculosis or pneumonia 4. head trauma 5. meningitis 6. cerebral atrophy 7. hypothyroidism 8. lupus |
| S/S of SIADH | 1. hyponatremia 2. water retention 3. vague complaints (weakness, nausea, headache) 4. Changes in LOC 5. Intake exceeds output |
| T4 | thyroxine |
| T3 | triiodothyronine |
| Another name for hyperthyroidism | Graves disease, exophthalmic goiter, thyrotoxicosis |
| Major manifestations of hyperthyroidism | 1. anterior neck enlargement 2. exophthalmos |
| Laryngospasms, Trousseau's sign, and Chvostek's sign are signs of... | HYPOparathyroidism |
| What hormone do the parathyroid glands produce at what is it used for? | 1. Parathromone 2. Increases calcium concentration and regulates the amount of phosphorus in the blood. |
| What is the function of calcium in the body? | 1. makes muscles contract and gives bone rigidity 2. provides for normal conduction of electrical currents along nerves 3. essential element of the clotting process |
| What is the function of phosphorous in the body? | 1. energy storage and transfer 2. component of teeth and bones 3. decreased levels will lead to poor growth |
| What is the most common cause of hypoparathyroidism? | Accidental removal or destruction of the parathyroid glands during a thyroidectomy. |
| What are the s/s of hypoparathyroidism? | 1. hypocalcemia 2. hyperphosphatemia 3. hypocalcemic tetany 4. muscle spasms 5. kidney stones 6. dysrhythmias 7. muscle cramping 8. dysphagia |
| How will severe hypocalcemia manifest? | 1. laryngeal spasm 2. stridor 3. cyanosis with increased risk for asphyxia 4. calcification of basal ganglia in the brain |
| Management of hypoparathyroidism | 1. IV calcium gluconate/chloride 2. Vitamin D 3. Bronchodilators |
| Diet for hypoparathyroidism | High in calcium, low in phosphorous |
| What is hyperparathyroidism? | Overproduction of parathormone, resulting in increased urinary excretion of phosphorus, bones become demineralized because it enters the bloodstream from the bones. |
| Complications of hyperparathyroidism | 1. bones become weak 2. fractures 3. kidney stones 4. renal disease |
| Signs of tetany | 1. numbness or tingling 2. carpopedal spasm 3. tachycardia 4. tachypnea 5. hypertension 6. laryngeal spasm 7. Chvostek's and Trousseau's sign |
| What is a thyroid storm? | Over-release of thyroid hormone in bloodstream, resulting from manipulation of the thyroid |
| How do you treat a thyroid storm? | 1. IV fluids 2. Sodium iodide and corticosteroids 3. Antipyretics and oxygen as needed. |
| A severe form of hypothyroidism in adults is called... | Myxedema |
| CLinical manifestations of hypothyroidism | 1. hypothermia/cold intolerance 2. weight gain 3. impaired memory, slow thought 4. anorexia and constipation 5. menstrual irregularities 6. enlarged facial features 7. weakness, clumsiness |
| What is the medical management for hypothyroidism? | Thyroid hormone replacement therapy |
| Important dietary restrictions for hypothyroidism? | High-fiber, low-calorie |
| What is a goiter? | enlargement of the thyroid gland |
| Medical management for a goiter consists of what? | 1. oral potassium iodine 2. diet rich in iodine |
| Who is most commonly affected by thyroid cancer? | females and Caucasians |
| Types of thyroid cancer | papillary, follicular, anaplastic |
| What is the most dangerous and most rare type of thyroid cancer? | anaplastic |
| What is the most common, least severe type of thyroid cancer? | papillary |
| How is thyroid cancer diagnosed? | 1. Thyroid scan 2. Thyroid function tests 3. needle biopsy |
| What is the risk involved in needle biopsy? | Risk of "seeding" the cancer cells into surrounding tissue, causing metastasis |
| Who is the coolest guy ever? | RPB |
| Classic clinical manifestations of Diabetes Mellitus | Polyuria, Polydipsia, polyphagia |
| Classic laboratory findings used to diagnose diabetes mellitus? | 1. random blood glucose over 200 mg/dl 2. glycosuria 3. ketonuria |
| Causes of diabetes mellitus. | 1. unknown 2. genetic predisposition 3. viruses (coxsackievirus, rubella, mumps) 4. aging 5. diet and lifestyle |
| What causes glycosuria? | Body attempts to rid excess glucose that is in the body due to lack of insulin or misuse of insulin. |
| Why does diabetes mellitus cause polyphagia? | Glucose can not be used without insulin, so the cells starve, and the body tries to compensate by overeating. |
| Why are there excess ketones in the blood in a diabetic patient? | body's fat and protein sources are broken down for energy. |
| Accumulation of ketones in the blood causes... | ketoacidosis |
| Type 1 Diabetes Mellitus | Insulin Dependent Diabetes Mellitus (IDDM)- little or no insulin produced |
| Type II Diabetes Mellitus | Non-insulin dependent diabetes mellitus (NIDDM) |
| Differences in Type 1 and Type 2 DM | Type 1- 1. rapid onset 2. Thin clients due to muscle wasting 3. Manifestations- nocturia, blurred vision, halo around lights Type 2- 1. slow wound healing 2. legs and feet cold to touch 3. decrease sensation in extremities |
| Normal fasting blood glucose | 60-120 mg/dl, greater than 126 is abnormal |
| Difference in oral glucose tolerance test (OGTT) results for a non-diabetic and diabetic client | Non-diabetic: blood glucose returns to normal levels in 2-3 hours, urine negative for glucose Diabetic: blood glucose levels return slowly, urine is positive for glucose |
| What is done in a postprandial blood sugar? | Fasting client is given a measured amount of carbohydrate solution orally, blood drawn after 2 hours. BG > 160 indicates DM |
| What is HgbA1c? | glycosylated hemoglobin |
| Classic laboratory findings used to diagnose diabetes mellitus? | 1. random blood glucose over 200 mg/dl 2. glycosuria 3. ketonuria |
| Causes of diabetes mellitus. | 1. unknown 2. genetic predisposition 3. viruses (coxsackievirus, rubella, mumps) 4. aging 5. diet and lifestyle |
| What causes glycosuria? | Body attempts to rid excess glucose that is in the body due to lack of insulin or misuse of insulin. |
| Why does diabetes mellitus cause polyphagia? | Glucose can not be used without insulin, so the cells starve, and the body tries to compensate by overeating. |
| Why are there excess ketones in the blood in a diabetic patient? | body's fat and protein sources are broken down for energy. |
| Accumulation of ketones in the blood causes... | ketoacidosis |
| Type 1 Diabetes Mellitus | Insulin Dependent Diabetes Mellitus (IDDM)- little or no insulin produced |
| Type II Diabetes Mellitus | Non-insulin dependent diabetes mellitus (NIDDM) |
| Differences in Type 1 and Type 2 DM | Type 1- 1. rapid onset 2. Thin clients due to muscle wasting 3. Manifestations- nocturia, blurred vision, halo around lights Type 2- 1. slow wound healing 2. legs and feet cold to touch 3. decrease sensation in extremities |
| Normal fasting blood glucose | 60-120 mg/dl, greater than 126 is abnormal |
| Difference in oral glucose tolerance test (OGTT) results for a non-diabetic and diabetic client | Non-diabetic: blood glucose returns to normal levels in 2-3 hours, urine negative for glucose Diabetic: blood glucose levels return slowly, urine is positive for glucose |
| What is done in a postprandial blood sugar? | Fasting client is given a measured amount of carbohydrate solution orally, blood drawn after 2 hours. BG > 160 indicates DM |
| What is HgbA1c? | glycosylated hemoglobin-measures the amount of glucose bound to hemoglobin |
| Management of DM | Diet, exercise, educationA |
| Quantitative | Emphasis on total amount of complex carbohydrates consumed rather than type 45-50% kcals from COOH 10-20% kcals from protein no more than 30% kcals from fat |
| Qualitative | unmeasured and more unstructured, stresses moderation, reduce intake of simple carbs, saturated fats, and alcohol, food intake evenly throughout day |
| Humulin R | short/rapid acting insulin onset: 30-60 min peak: 3-6 hours duration: 6-8 hours |
| NPH, Novolin N, Humulin N | intermediate acting insulin onset: 60-90 minutes peak: 8-12 hours duration: 24 hours |
| Ultralente, Humulin U | long-acting insulin onset: 4-8 hours peak: 16-19 hours duration:36 hours |
| Humalog | insulin lispro, onset: 15 minutes, used in insulin pumps |
| Lantus | insulin glargine, long-acting synthetic insulin, administered once per day |
| How long is each cannula on an insulin pump good for? | 72 hours |
| Who is a good candidate for a pancreas transplant? | Type 1 diabetic with renal failure |
| What occurs in an islet cell transplantation? | islet cells are harvested from human donors and pigs, injected into the clients peritoneum to produce insulin. |
| What is neuropathy? | abnromal condition characterized by inflammation and degeneration of the peripheral nerves |
| What visual changes do diabetics need to watch out for? | diabetic retinopathy- microvascular changes affect retinal capillaries |
| Manifestations of diabetic ketoacidosis | 1. weakness, drowsiness 2. vomiting 3. thirst 4. abdominal pain 5. hot, dry skin, dry mouth, flushed cheeks LATE 1. Kussmaul's breathing 2. sweetish odor to breath (acetone) 3. hypotension 4. rapid, weak pulse |
| Blood glucose levels in diabetic ketoacidosis | 300-800 mg/dl |
| serum pH in diabetic ketoacidosis | 6.8-7.3. |
| Sulfonylureas (glipizide), meglitinides (repaglinide), biguanides (metformin) | types of oral hypoglycemics that lower blood glucose by stimulating insulin secretion by beta cells of the pancreas and increase insulin sensitivity at receptor sites *requires pancreatic function* |
| alphaglucosidase inhibitors (acarbase) | delays digestion of carbohydrates, lowering blood glucose. may combine with sulfonylureas |
| thiazolidinesdiones ((pioglitazone) | increase insulin sensitivity |
| Contraindications for oral hypoglycemics | 1. type 1 DM 2. hypoglycemia 3. any severe endocrine dysfunction 4. pregnancy and lactation |
| Ingestion of alcohol with oral hypoglycemics may cause | disulfiram-like reaction |
| levothyroxine | (Synthroid, Levothroid) T4 preparation for thyroid replacement therapy |
| liothyronine | (Cytomel, Triostat) T3 preparation for thyroid replacement therapy |
| liotrix | (Thyrolar) combination T3/T4 preparation |
| desiccated thyroid preparations | Armour Thyroid, Thyrar |
| Interactions of thyroid preparations | 1. may alter effectiveness of warfarin 2. may increase requirement for insulin or oral hypoglycemics in diabetic patients 3. increased cardiovascular effects 4. decrease response to beta blockers |
| For patients who have difficulty swallowing levothyroxine tablets: | 1. may be crushed and placed in 5-10 ml of water 2. must be administered immediately 3. do not store suspension |
| Only insulin that can be administered IV | short-acting (regular) insulin |
| methimazole and propylthiouracil are examples of.. | anti-thyroid agents |
| indications for use of anti-thyroid agents | 1. palliative treatment of hyperhtyroidism 2. adjuct to control hyperthyroidism in prep for thyroidectomy |
| Iodine-containing agents are used for | 1.adjunct therapy for preparation of thyroidectomy 2. treatment of thyrotoxic crisis |
| What is the effect of iodine-containing agents? | 1. rapidly inhibit release and synthesis of thyroid hormones 2. decrease vascularity of thyroid gland |
| hormones (like Ocreotide) are used for | 1. treatment of severe diarrhea and flushing episodes in patients with GI/ endocrine tumors 2. relief of symptoms in pituitary tumors |
| Oral and IV electrolyte replacement is used to | treat and prevent hypocalcemia |
| phentolamine (Regitine) | pheochromocytoma agent |
| Use of pheochromocytoma agents | IV: control of BP during surgical removal of a pheochromocytoma |
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hegaub
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