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Endocrine Diseases
Pathophysiology 9 - Endocrine disease
| Question | Answer |
|---|---|
| define endocrine | hormones are released to circulation to act on a target organ (TSH, ADH) |
| define paracrine | hormone acts locally on cells close to where they are released (estrogen, testosterone) |
| define autocrine | hormones produce a biologic action on the cell that released them (insulin) |
| what are the different structural types of hormones (3) | 1 - amines and amino acids 2 - peptides and protein 3 - steroids (from cholesterol) |
| what are the functions of hypothalamus | - links nervous system with endocrine system - regulates homeostasis (body temp, hunger, behavior, emotion, pain) - produces releasing hormones that stimulates the pituitary |
| what is the role of pituitary gland | "master gland" - stimulates target organs to secretes their hormones |
| explain the concept of negative feedback | - how the body maintains homeostasis or equilibrium - prevents over-secretion of any hormone - helps to keep hormone levels within certain range or set-point |
| give an example of negative homeostasis | (There are MANY) - the action of ADH which dilutes the blood - once blood is dilute - hypothalamus detects diluted blood - brain stops releasing ADH |
| explain the concept of positive feedback | - enhances or increases the amount of the hormone that is released |
| give an example of positive feedback | oxytocin during labor |
| at least 4 ways hormones can be over-secreted | 1) pathology with target gland 2) target gland over stimulated by pituitary/hypothalamus 3) hormones are being produced from a different site (tumor) 4) hyperactive genetic mutation of the target hormone receptors |
| at least 5 ways decreased hormone secretion can occur | - disorder of target gland (congenital/acquired) - pituitary is not secreting enough stimulating hormone - hypothalamus not secreting enough releasing hormone - defective hormone - receptors of the target organ not responding |
| 3 ways adrenal insufficiency can be caused | - primary adrenal insufficiency (Addison's d/t dysfunction of the adrenal glands) - decreased ACTH stimulation - decreased CRH from hypothalamus |
| what is second adrenal insufficiency | decreased adrenal stimulation by ACTH |
| what is tertiary adrenal insufficiency | decreased hypothalamic release of CRH |
| with Addison's disease, what hormones will be altered | both cortisol and aldosterone are decreased and ACTH are elevated |
| with Addison's disease, what lab values will be altered | (low aldosterone) - low sodium and increased potassium - hypotension can result |
| name 4 things that can cause Cushing Syndrome | 1) latrogenic (long term use of steroids) 2) over-secretion of adrenal gland(s) (d.t adrenal adenoma or carcinoma) 3) over-stimulation of the adrenal glands by an ACTH-secreting tumor in pituitary (Cushing's Disease) 4) ectopic ACTH-producing tumor |
| what are signs and symptoms of Cushing syndrome (name at least 7) | - buffalo hump (on back) - abdominal obesity - moon face - muscle weakness - easy bruising - thin skin -osteoporosis/necrosis - acne - hirsutism - virilization - immunosuppression - diabetes - mental changes (mood and psychosis) |
| what lab values will be altered in primary hyperthyroidism | - TSH will be LOW |
| what lab values will be altered in secondary hyperthyroidism | - TSH will be HIGH |
| why is TSH low in primary hyperthyroidism | thyroid secreting a lot of hormone without being told by the pituitary |
| why is TSH high in secondary hyperthydroidism | pituitary is over secreting TSH |
| what is hyperthyroidism | elevated T3 and T4 |
| what are signs and symptoms of hypothyroidism | - weight gain - fatigue - weakness - bradycardia - hypoventilation - cold intolerance - constipation - joint pains - muscle aches - anemia - goiter may be present |
| what is the role of insulin | moves glucose in to the cells to reduce blood sugar |
| what is the role of glucagon | causes a release of glucose into the blood when levels are low |
| the role of insulin and glucagon work together to _____________________________ | maintain normal blood sugar |
| what is glycogenesis | when cells uptake sugar and store it as glycogen, fat, or protein |
| what hormone encourages glycogenesis | insulin - released from beta cells in pancreas |
| what is glycolysis | when energy is broken down for energy |
| what hormone encourages glycolysis | insulin |
| what is gluconeogenesis | glucose formation (usually from a source that is not glycogen like fat or protein) |
| what hormone regulates gluconeogenesis | glucagon - from alpha cells in pancreas, ---- also helps decrease glycolysis |
| what is glycogenolysis | the breakdown of glycogen to release glucose |
| what hormone regulated glycogenolysis | glucagon |
| what is insulin resistance | when insulin does not work effectively |
| _____________ leads to a decreased number of insulin receptors | obesity |
| what is typically seen in Type 2 diabetes | insulin resistance, specifically with obese patients |
| what is metabolic syndrome | a myriad of conditions that increase one's risk for - heart disease - stroke - type 2 diabetes |
| what is metabolic syndrome, is a myriad of conditions that increase one's risk for - heart disease - stroke - type 2 diabetes what conditions are included in metabolic syndrome? | - elevated blood sugar - high cholesterol - hypertension - obesity (particularly increased fat around the waist) |
| what is polydipsia | increased thrist |
| what is polyphagia | increased hunger |
| what is polyuria | increased urination |
| what are primary microvascular complications of diabetes | - retinopathy - nephropathy - neuropathy |
| what is retinopathy | - primary microvascular complication of diabetes - in the retina of the eye - can lead to blindness |
| what is nephropathy | - primary microvascular complication of diabetes in the kidney - leads to renal failure |
| what is neuropathy | - primary microvascular complication of diabetes in the nerves - leads to nerve damage - causes weakness, numbness, or pain - usually in hands and feet |
| what are the primary macrovascular complications of diabetes | - peripheral vascular disease - coronary artery disease - heart attack - stroke |
| what types of hormones does the hypothalamus release? What is there function | hypothalamus releases RELASING hormones these hormones stimulate the pituitary to release STIMULATING hormones |
| list the hormones released by the hypothalamus | - corticotropin-releasing hormone (CRH) - growth hormone-releasing hormone (GHRH) - thyrotropin-releasing hormone( TRH) - somatostatin - dopamine - Gonadotropin Releasing hormone (GnRH) |
| function of corticotropin-releasing hormone | release of ACTH |
| function of Gonadotropin-releasing hormone | release of LH and FSH |
| function of thyrotropin releasing hormone | release of TSH |
| function of growth hormon-releaseing hormone | release of growth hormone |
| list the hormones of the anterior pituitary | - GH - ACTH - TSH - FSH - LH - prolactin |
| list the hormones of the posterior pituitary | - ADH - oxytocin |
| what hormones control the release of pituitary hormones (general name)? where do they come from | - releasing and inhibiting hormones ----- CRH, TRH, GHRH, GnHR - from hypothalamus |
| what is the function of somatostatin (hypothalamus origin) | - inhibits GH and TSH release |
| what is the function of dopamine (hormone)? where does it come from? | - inhibits prolactin, FSH, and LH - from the hypothalamus |
| what is the function of growth hormone | - stimulates growth (bone and muscle) - promotes protein and fat metabolism |
| where is growth hormone secreted from | anterior pituitary |
| what is the function of ACTH | - stimulates synthesis/secretion of adrenal cortex hormones |
| where is ACTH released from | anterior pituitary |
| what is the function of TSH | - stimulated production and release of thyroid hormone |
| where is TSH secreted from | anterior pituitary |
| what is the function of FSH | (male) sperm production (female) ovarian follicle stimulation, ovulation |
| where is FSH released from | anterior pituitary |
| what is the function of LH | (male) testosterone release (female) corpus luteum, oocyte release (ovulation), estrogen/progesterone release |
| what is the function of prolactin | prepares breast for breast-feeding |
| where is LH released from | anterior pituitary |
| where is prolactin released from | anterior pituitary |
| what is the function of ADH | increased water reabsorption by kidneys |
| where is ADH released from | posterior pituitary |
| what is the function of oxytocin | - uterine contractions - milk production |
| what is the function of aldosterone (and other mineralcorticosteroids) | increased sodium absorption and decrease potassium loss |
| where is aldosterone (and other mineralcorticosteroids) released from | adrenal cortex |
| what is the function of cortisol (and other glucocorticoids) | - regulate metabolism of nutrients - regulate blood glucose levels - affected growth *** anti-inflammatory action *** decrease effects of stress |
| where is cortisol (and other glucocorticoids) released from | adrenal cortex |
| what is the function of adrenal androgens (i.e. DHEA and androstenedione) | - converted to testosterone and DHT - minimal androgenic activity |
| what is the function of epinepherine and norepinepherine | neurotransmitters for the Sympathetic Nervous System |
| where are the catecholmines released | adrenal medulla |
| what is the function of T3 and T4 | - increase metabolic rate - protein and bone turnover - fetal/infant growth/development |
| where is T3 and T4 released from | thyroid gland |
| what is the function of calcitonin | - decreased calcium/phosphate levels |
| where is calcitonin released from | thyroid gland |
| what is the function of parathyroid hormone | regulate blood serum calcium levels |
| where is PTH released from | parathyroid gland |
| what is the function of somatostatin (from pancreas) | - delays intestinal absorption of glucose |
| where is somatostatin released from (there are two) | - pancreas - hypothalamus |
| what is the function of 1,25-Dihydroxyvitamin D | stimulates Calcium absorption from intestine |
| where is 1,25-Dihydroxyvitamin D released from | kidneys |
| what is the function of estrogen | - female sex organ maturation/development - secondary female sex characteristic |
| what is the function of progestrone | - influences menstrual cycle - growth of uterine wall - maintain pregnancy |
| what is the function of testosterone (androgens) | - male sex organ (maturation/development) - secondary sex characteristics - sperm production |
| what is primary hypothyroidism | thyroid not producing enough thyroid hormone |
| at least 4 causes of primary hypothyroidism | - congenital thyroid disease - Hashimoto's thyroiditis - thyrotoxic drugs (i.e. amiodarone) - iodine deficiency - post-surgical damage/removal - radiation therapy |
| what is hashimoto's thyroiditis | autoimmune disease antibodies attack the thyroid gland |
| discuss iodine deficiency and primary hypothyroidism | - iodine is needed for hormone synthesis of T3 and T4 - decreases negative feedback loop for TSH - increased TSH leads to increased thyroid size leads to goiter - |
| discuss goiters in the US | - uncommon in US - salt includes Iodine in western culture |
| what is the primary cause of secondary hypothyroidism | - not enough TSH is secreted |
| lack of TSH secretion can result from | - infection - inflammation - infiltration - hemorrhage - tumor |
| signs and symptoms of hypothyroidism (name at least 5) | - weight gain - fatigue - weakness - bradycardia - hypoventilation - cold intolerance - constipation - joint pains - muscle pains - hair becomes coarse/brittle - dry skin - myxedema |
| what is myxedema | nonpitting swelling in the connective tissues of the body |
| how is hypothyroidism diagnosed | - low levels of T3 and T4 - elevated TSH (primary); decreased TSH (secondary) - presence of anti-TPO and anti-TG (Hashimoto's) |
| how is hypothyroidism treated | - synthetic thyroid hormone (T4...thyroxine) |
| what is primary hyperthyroidism | - thyroid over-secretes thyroid hormone |
| some conditions that lead to primary hyperthyroidism | - grave's disease - toxic nodule |
| what is grave's disease | an autoimmune disease |
| what is a toxic nodule on the thyroid | thyroid nodule that secretes excess thyroid hormone (not triggered by the pituitary) |
| what causes secondary hyperthyroidism | when the pituitary over-stimulates the thyroid to secrete thyroid hormone |
| possible causes of secondary hyperthyroidism | - pituitary tumor - ectopic source of thyroid hormone |
| name an ectopic source of thyroid hormone release as seen in hyperthyroidism | ovarian tumor |
| signs and symptoms of hyperthyroidism | - weight loss - increased appetite - tachycardia (a-fib on occasion) - dyspnea - heat intolerance - tremor - nervousness |
| signs and symptoms of Grave's disease | - s/s of hyperthyroidism (plus) - ophthalmopathy - exopthalmos - pretibial myxedema - diffuse goiter - thyroid bruit |
| another term of hyperthyroidism | thyrotoxicosis |
| why is weight loss and increased appetite seen in hyperthyroidism | high metabolism |
| what is thyroid bruit | a rushing sound over the thyroid on auscultation |
| how is hyperthyroidism diagnosis | - differs by type (different hormones with be elevated or decreased) - (primary) TSH is low - (secondary) TSH is high - T3 and T4 is high - (Grave's disease) presence of anti-TSH receptor antibodies |
| imaging tests for hyperthyroidism diagnosis that help detect thyroid function and nodules | - radioiodine uptake test - thyroid scans |
| imaging tests for hyperthyroidism that will help differentiate between cystic and solid lesions | ultrasound |
| imaging tests for hyperthyroidism that will help differentiate between benign v. malignant thyroid disease | fine-needle aspiration biopsy |
| in hyperthyroidism, what is used for treatment for tachycardia and anxiety | beta-blockers |
| in hyperthyroidism, what is done to reduce the amount of circulating thyroid hormone | - (medication) methimazole and propylthiouricil - surgical thyroid removal - thyroid destruction by radioactive iodine |
| what is a problem with surgical removal of thyroid or radioactive iodine treatment | hypothyroidism |
| name the three layers of the adrenal cortex and the hormones they secrete | - zona glomerulosa (aldosterone) - zona fasciculata (glucocorticoids (cortisol)) - zona reticularis (sex hormones) |
| what is addison's disease | - insufficient cortisol and aldosterone secretion, accompanied by elevated ACTH - low sodium - increased potassium - hypotension |
| clinical presentation of addison's disease | - hyponatremia - water loss (subsequent dehydration) - hyperkalemia - decreased CO - fatigue - weakness - salt craving |
| a decrease in glucotoricoids will lead to | - lethargy - hypoglycemia - nausea - vomiting - lack of appetite - weight loss |
| increased levels of ACTH can lead to | - high levels of melanocyte-stimulating hormone - hyperpigmentation of the skin |
| diagnosis of Addison's disease | - decreased cortisol levels in blood - (aldosterone is not measured in labs) low sodium and high potassium - elevated ACTH |
| what is the ACTH stimulation test | - ACTH injected - see if this increases blood cortisol levels of not |
| what is the purpose of the ACTH stimulation test | to differentiate whether or not the cause of Addison's disease is primary, secondary or tertiary |
| in the ACTH stimulation test, if cortisol levels increase this means | the problem lies with the adrenals and it is primary adrenal insufficiency |
| what is the treatment for Addison's disease | - hormones replaced daily for life |
| what medication is used for cortisol replacement in Addison's disease | - glucocorticoids - hydrocortisone |
| what medication is used for aldosterone replacement in Addison's disease | - mineralcorticoid - fludrocortisone |
| why do people with Addison's disease need regular meal times | people with this disease had a high likelihood for hypoglycemia and hyponatremia |
| discuss the ways to check for cortisol with patients suspected of having Cushing disease | - 24-hr urinary collection for free cortisol - check the level of cortisol in saliva in late evening - check for suppressed cortisol with administration of exogenous glucocorticoids |
| what is the dexamethasone suppression test | - administration of exogenous glucocorticoids - check to see if cortisol levels are increased |
| if ACTH is low during Cushing disease, signifies | adrenal glands hyper-secreting on their own |
| if ACTH is high during Cushing disease, signifies | something else is over-secreting cortisol on its own (something like a tumor) |
| what other labs should be checked with Cushing disease | - hypokalemia (increased potassium excretion) - hypertension (increased sodium retention) - decreased immune and inflammatory response |
| how is Iatrogenic disease treated | - tapering off the glucocorticoid therapy |
| how are other types of Cushing diseases treated | - surgical removal for radiation of the offending tumor |
| what races have the highest rates of diabetes mellitus | - American Indians/Alaska Natives - African Americans - Hispanic Americans |
| islet of Langerhans in the pancreas | - endocrine portions - secrete insulin and glucagon |
| with diabetes mellitus, there is either an _____________________ or a ____________________ . | insensitivity to insulin; decreased insulin secretion |
| what is the ultimate cause of type 1 diabetes | no insulin production (therefore no insulin secretion) |
| what is the ultimate cause of type 2 diabetes | insulin resistance |
| compare and contrast type 1 and type 2 diabetes regarding age of onset | Type 1 - usually before 20 Type 2 - usually after 30 |
| compare and contrast type 1 and type 2 diabetes regarding type of onset | Type 1 - Abrupt, symptomatic often with DKA Type 2 - Gradual, subtle, often asymptomatic |
| compare and contrast type 1 and type 2 diabetes regarding usual body weight | type 1 - normal, recent weight loss is common type 2 - overweight |
| compare and contrast type 1 and type 2 diabetes regarding family history | type 1 - <20% type 2 - > 60% |
| compare and contrast type 1 and type 2 diabetes regarding monozygotic twins | type 1 - 50% concordant type 2 - 90% concordant |
| compare and contrast type 1 and type 2 diabetes regarding beta cell mass | type 1 - markedly reduced type 2 - normal or slightly reduced |
| compare and contrast type 1 and type 2 diabetes regarding circulating insulin levels | type 1 - markedly reduced type 2 - elevated or normal |
| compare and contrast type 1 and type 2 diabetes regarding clinical management | type 1 - insulin is REQUIRED type 2: - weight loss improves condition - insulin not needed initially, but will be needed later |
| what is ketosis | when the body breaks down fat as if the body was starving and forms ketones |
| what is diabetic ketoacidosis | - ketosis (breakdown of fat and formation of ketones) can lead to this - type of metabolic acidosis |
| clinical presentation of diabetic ketoacidosis | - polydipsia - polyuria - polyphagia - weakness - weight loss - tachy cardia - dry mucous membranes - poor skin turgor - hypotension - n/v - mental status changes - shock (sometimes) - fruity breath smell |
| when does DKA usually occur | - after extreme stress (i.e. pregnancy, infection, anxiety) |
| how is diabetic ketoacidosis diagnosised | - hyperglycemia (blood glucose > 250 mg/dL) - low serum bicarbonate (< 15 mmol/L) - low pH (<7.35) - ketonemia - moderate ketonuria |
| treatment for DKA | - IV insulin - electrolyte replacement |
| what is hyperosmolar hyperglycemic state (HHS) | - type 2 diabetic version of DKA - (AKA) non-ketotic hyperglycemic hyperosmolar syndrome - occurs with either dehydration/infection |
| how does hyperosmolar hyperglycemic state (HHS) present clinically | - confusion |
| how is hyperosmolar hyperglycemic state (HHS) diagnosed | - hyperglycemia (blood sugar > 500 mg/dL) - hyperosmolality - dehydration without ketoacidosis |
| how is HHS treatment | - correcting hyperglycemia - electrolyte imbalances - dehydration |
| what is the mortality rate for DKA and HHS | high mortality rate |
| what is the leading cause of blindness and vision loss in the US | diabetic retinopathy |
| pathology of diabetic retinopathy | - microaneurysm formation - abnormal retinal vascular permeability - hemorrhage - neovascularization - scarring - retinal detachment |
| how to control progression of diabetic retinopathy | - control blood glucose - control blood pressure - control cholesterol |
| why should diabetics have an annual dilated eye examp | to check for diabetic retinopathy |
| what is the leading cause of chronic kidney disease | diabetic neuphropathy |
| an early detection of diabetic nephropathy is done through | urine microalbumin test (when 30-300 mg is lost per day) |
| ways to prevent/control kidney disease in diabetics | - tight glycemic control - blood pressure control (<130/80) - hyperlipidemia treatment - smoking cessation - limiting proteinuria with ACE inhibitors or ARBs or protein restriction |
| what are the two pathologic changes in the presence of hyperglycemia that lead to neuropathy | - thickening of the walls of nutrient vessels that supply nerve leading to vessel ischemia - demyelination of the Schwann cell and slowed nerve conduction |
| describe the clinical presentation of diabetic neuropathy | - loss of feeling, sensation, touch, sense of position, occasional pain |
| why is diabetic neuropathy a problem | - greater risk for falls - greater risk for burns - increased injuries on the feet - limited ability to empty the bladder - erectile dysfunction |
| what is a common cause of amputations in diabetics | neuropathy and foot ulcers |
| how do foot ulcers become a problem with diabetics | - trauma/infection that is undetected (d/t neuropathy) - the trauma/infection is worsened by vascular insufficiency and unable to heal |
| what is a monofilament test | - in diabetic patients with foot ulcers - assesses sensation - assesses vascular status - assesses skin integrity - administered annually |
| ways to prevent diabetic foot ulcers | - proper fitting shoes - daily feet inspection for blisters/sores/signs of infections |
| what are macrovascular complications | - diabetic damage to large blood vessels |
| macrovascular complications is a major risk factor for | - development of peripheral vascular disease - heart attack - stroke |
| 50-75% of diabetics die from (micro/macro)vascular disease | macrovascular disease |
| leading cause of nontraumatic amputations in diabetics | peripheral vascular disease |
| what are risk factors for macrovascular disease in diabetics | - hyperglycemia - hypertension - hyperlipidemia - obesity - altered platelet function - endothelial dysfunction - elevated fibrogen levels - systemic inflammation |
| chronic complications of diabetic mellitus (autonomic neuropathy) | - dizziness - syncope |
| chronic complications of diabetic mellitus (eye) | - retinopathy - cataracts - glucoma |
| chronic complications of diabetic mellitus (microangiopathy in brain) | - cerebral infarcts - hemorrhage |
| chronic complications of diabetic mellitus (cardiovascular) | - ischemic heart disease - MI - hypertension - peripheral vascular disease (gangrene and infections) |
| chronic complications of diabetic mellitus (disorders of the gastrointestinal motility) | - delayed gastric emptying - diarrhea - constipation |
| chronic complications of diabetic mellitus (genitourinary tract) | - bladder stasis - bladder infection - erectile dysfunction (male) |
| chronic complications of diabetic mellitus (nephropathy) | - glomerulosclerosis - chronic kidney disease |
| chronic complications of diabetic mellitus (somatic neuropathy) | -abnormal sensory and motor function - foot ulcers |
| who should be tested for diabetes | - everyone 45 and older - younger than 45 IF: ------ obese ------ has a family history with HTN or hyperlipidemia |
| for patients who have normal glycemia what is the Hemoglobin A1c | 4 - 5.6% |
| for patients who have normal glycemia what is the fasting plasma glucose (FPG) | < 100 mg/dL |
| for patients who have normal glycemia what is the 2-hour oral glucose tolerance test (OGTT) | <140 mg/dL |
| for prediabetic patients what is the hemoglobin A1c | 5.7 - 6.4 % |
| for prediabetic patients what is the fasting plasma glucose (FPG) | 100 - 125 mg/dL |
| for prediabetic patients what is the 2-hour oral glucose tolerance test (OGTT) | 140 - 199 mg/dL |
| for diabetic patients what is the hemoglobin A1c | >= 6.5% |
| for diabetic patients what is the fasting plasma glucose (FPG) | >= 126 mg/dL |
| for diabetic patients what is the 2-hour oral glucose tolerance test (OGTT) | >= 200 mg/dL |
| to diagnose diabetes what criteria needs to be met | - A1c >= 6.5% - FPG >= 126 mg/dL - OGTT >= 200 mg/dL - symptoms of DM - casual plasma glucose >= 200 mg/dL |
| diabetes treatment | - keep glucose as normal as possible - (type 1) REQUIRES insulin replacement - (type 2) weight loss, heart healthy diet and exercise - (type 2) aggressive management of hyperglycemia, hyperlipidemia, and antiplatelet therapy |
| 5 main categories of antidiabetic agents | - insulin secretagogues - biguanides - alpha-glucosidase inhibitors - thiazolidinediones (TZDs) - dipeptidyl peptidase-4 (DPP-4 enzyme inhibitors) |
| the injectable diabetes medication class | glucagon-like peptide-1 (GLP-1) agonists |
| name a couple insulin secretagogues | - glipizide (sulfonylureas) - glyburide (sulfonylureas) - repaglinide (nonsulfonylureas) - nateglinide (nonsulfonylureas) |
| the mechanism of insulin secretagogues | stimulate release of insulin from beta cells in pancreas |
| side effects of insulin secretagogues | - hypoglycemia - should be avoided in elderly and patients with impaired hepatic/renal function |
| difference between sulfonylureas and nonsulfonylureas insulin secretagogues | nonsulfonylureas must be taken shortly before meals |
| name a biguanides | metformin |
| the mechanism of biguanides | - decreases hepatic glucose production - intestinal glucose absorption - increases insulin sensitivity |
| other beneficial side effects of biguanides | - weight loss - lower blood lipids |
| biguanides should be avoided when | - dehydration - liver disease - elevated creatinine levels |
| name some alpha-glucosidase inhibitors | - acarbose - miglitol |
| mechanisms for alpha-glucosidase inhibitors | inhibits pancreatic alpha-amylase and intestinal alpha-glucose hydrolase (delays carbohydrate absorption) |
| name thiazolidinediones (or glitazones) | - pioglitazone - rosiglitazone |
| what is the mechanism of thiazolidinediones | - increasing insulin sensitivity of fat, muscle and liver |
| problems with thiazolidinediones | - increased risk of cardiac events (especially with rosiglitazone) - (therefore) they are contraindicated in heart failure patients d/t exacerbation of fluid accumulation in CHF |
| name some dipeptidyl peptidase-4 enzyme inhibitors (DPP-4 inhibitors) | - sitagliptin - saxagliptin - alogliptin - linagliptin |
| DPP-4 inhibitors is a type of ________________ therapy | incretins |
| mechanism of DPP-4 inhibitors | inhibit the enzyme DPP-4 (which increases GLP-1 and GIP) increases insulin release and decreases glucagon release |
| name Glucagon-like peptide-1 (GLP-1) agonists | - exenatide - liraglutide |
| mechanism of GLP-1 agonists | - activate GLP-1 receptors - increase insulin secretion - decreasing glucagon secretion - delays gastric emptying (incretin imitator) |
| main side effects of GLP-1 agonists | - nausea - weight loss |
| types of insulin used for diabetes treatment | - rapid-acting - short-acting - long-acting |
| insulin must always be administered by | subcutaneous injection |
| what is multiple delayed injections (MDI) for insulin | mimics the normal patten of insulin secreted in the body |
| what is continuous subcutaneous insulin infusion (CSII) | uses an insulin pump; giving a continuous basal injection in addition to bolus doses around meal time |
| what is hypoglycemia | serious side effect of insulin therapy and some oral hypoglycemic drugs and some cognitive impairments - blood glucose < 60 mg/dL |
| hypoglycemia is caused by | - change in medication - lack of drug adherence - not eating - increased exercise |
| symptoms of hypoglycemia | - headache - confusion - anxiety - tachycardia - cool/clammy skin - seizures (severe) - coma (severe) |
| how is hypoglycemia treated | - (immediately) 15-20 g of glucose (it works quickly) - complex carbs given once levels are controlled - (in life-threatening) IV, IM, or subcutaneous glucose given |
| ways diabetes can be monitored | - checking weight - checking BP - fasting glucose - hemoglobin A1c - monitor glycemic control - regular dental exams |
| how to prevent/delay diabetes | - good nutrition - exercise - preventative care |
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