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125 Cards in this Set
- Front
- Back
______ gland regulates Ca levels
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Parathyroid gland (PTH)
- Disorders result in alt. of serum Ca levels (less common than throid disorders) |
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- Increase in the secretion of PTH
- Affects kidneys and bones - Occurs rarely |
Hyperparathyroidism
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Patho of ______
- increased resorption of Ca and excretion of phosphorus by kidneys - increased HCO3 excretion and decreased H+ ion excretion - increased release of Ca and Phophorus by bones - Deposits of Ca in soft tissues / renal calculi |
Hyperparathyroidism
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S&S of ______
- Asymptomatic - Bone pain/ pathological fractures - Renal calculi - Abdominal pain - Muscle weakness - Acid-base disorder - Electrolyte disorder |
Hyperparathyroidism
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DX for Hyperparathyroidism
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- Serum Ca levels
- Serum PTH levels - Phosphorus - Electrolytes - Bone Scans |
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Low levels of PTH hormone, decreased serum Ca levels, occurs rarely
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Hypoparathyroidism
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S&S of ______
- Parathesia - Tetany - Numbness - Muscle spasms - Hyperactive reflexes - Malabsorption - Seizures |
Hypoparathyroidism
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DX for Hypoparathyroidism
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- Serum Ca level
- Serum Phosphorus level - Positive Chvostek & Trousseaus's signs |
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Constructive phase; Requires energy, synthesis of protoplasm for growth and repair.
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Anabolism
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The destructive phase; Complex substances converted to ATP.
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Catabolism
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T/F - Brain & Nervous depend exclusively on glucose metabolism for energy.
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True
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T/F - Brain & NS can store and synthesize glucose.
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False, must extract it from the blood.
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How much glucose does the body need daily?
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100-115 grams / day
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Liver's role in glucose metabolism?
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Liver regulates entry of glucose into the blood.
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1. breakdown of glycogen to produce glucose for energy
2. Occurs while in the liver or after stored |
Glycogenolysis
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Hormone control of _______ ?
- Glucagon - in liver - Epinephrine - in skeletal muscle |
Glycogenolysis
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1. Synthesis of glucose from sources other than glycogen
2. Amino acids, lactate, & glycerol converted 3. Occurs mostly in liver 4. Glucose stored as glycogen or released into blood |
Gluconeogenesis
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Hormonal control of ______ ?
- Glucagon (in blood) - Glucocorticoid (adrenal hormone) - Thyroid hormone |
Gluconeogenesis
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Enzymes & lipases breakdown triglycerides.
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Fat metabolism
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Most amino acids contained in body proteins excess are converted to fatty acids, ketones, & glucose
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Protein metabolism
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Hormonal control of Metabolism
Pancreas secretes insulin (b cells) which: |
1. Provides for glucose storage
2. Prevents fat breakdown into ketones (acids) 3. Increases protein synthesis |
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Hormonal control of Metabolism
Pancreas secretes Glucagon (a cells) which: |
- Breakdown of glycogen via glycogenolysis
- Synthesis of glucose via gluconeogenesis - increase Fat & protein breakdown |
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The ratio of glucagon to insulin actually determines _____ ?
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blood glucose levels
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_______ _________ levels are the amount of sugar which is released into blood by liver and removed by body tissues
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Blood glucose
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Hormones helping maintain or increase Blood Glucose Levels (besides insulin or glucagon)
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1. Epinephrine
2. Growth Hormone 3. Glucocorticoid |
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Identify the following:
1. ACTH 2. FSH 3. TSH 4. GH 5. ADH |
1. adrenocorticotropic hormone
2. follicle-stimulating hormone 3. thyroid stimulating hormone 4. somatotropin 5. antidiuretic hormone |
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Alpha cells produce ________ which _______ blood glucose.
Beta cells produce _______ which ______ blood glucose. |
glucagon, elevates
insulin, lowers |
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Which hormones promote glycogenesis and gluconeogenesis?
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- glucagon
- epinephrine - GH - glucocorticoid |
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Feedback Mechanisms
increase hormone levels = _______ decrease hormone levels |
decreased hormone synthesis and release
increased hormone synthesis and release |
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- Secreted by pituitary
- Children = req. for growth - Adults = maintain organ size/ protein synthesis |
GH (somatotropin)
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Causes Deficiency of ______ ?
- Idiopathic (lack of _____ releasing factor) - Pituitary tumors (cause decrease in _____) - Dwarfism (levels are present but body unable to utilize them) |
GH
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Causes Excess _______ ?
- Usually pituitary tumor - Gigantism - excess _____ before puberty - Acromegaly - over-stimulation of Beta cells in pancreas; excess _____ after puberty |
GH
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Clinical Manifestations of ______ ?
- Usually adults, thickened bones and soft tissue - enlargement of hands and feet |
Excess GH
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_________ which primarily secrete thyroglobulin regulate pressence of Iodine. Takes up & concentrates large amts. of Iodine (in the form of Iodine) for T4 (thyroxine) and T3 (triodothyronine)
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Follicular cells
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What hormones are these?
- Thyroglobulin - T4 (Thyroxine) - T3 (Triodothyronine) |
Thyroid Hormones
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Function of _______ ?
- increase metabolism of all cells - Helps regulate metabolism of carbohydrates, lipids, protein - increase protein synthesis - Catabolizes protein - promotes G & D in children - Synergistic effect with catecholamines |
Thyroid
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Congenital hypothyroidism
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cretinism
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Aquired (Etiological factors) of _______ ?
- Hashimoto's Thyroiditis - Aging - Thyroidectomy - Radiation to neck/head - Scleroderma - Iodine Deficiency - Antithyroid medications - Defective hormone synthesis |
Hypothyroidism
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Clinical manifestions of _______ ?
- from decreased BMR, mild initially - fatigue - weight gain - cool dry skin - hoarseness - goiter - cold intolerance - decreased sweating |
Hypothyroidism
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Complications from _______ ?
- Arteriosclerosis and coronary heart disease - Anemia - Increased risk of infections - Respiratory distress - Myxedema (acute hypothyroidism) |
Hypothyroidism
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Develops in undiagnosed or undertreated hypothyroidism
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Myxedema
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Precipitating factors of _______ ?
- physical stress - trauma - exposure to extreme cold - drugs (anesthesia, sedatives, narcotics) - excess antithyroid medication |
Myxedema
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S&S of _______ ?
- slowed movement - cool dry skin - fatigue - hoarseness - cold intolerance - facial & body puffiness - weight gain - goiter - decreased sweating |
Myxedema
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Grave's Disease; autoimmune disorder
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Hyperthyroidism
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Causes of ________ ?
- Thyroid carcinoma - Toxic nodular goiter - too much thyroid replacement medication - most common cause is Grave's Disease |
Hyperthyroidism
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- Primarily affects women 30-40 years old
- thought to be autoimmune diseases -> antibody production -> TSH receptors -> excessive TH secretions - primary characteristics: Hyperthyroidism, goiter |
Grave's Disease
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Clinical Manifestations of ________ ?
- nervousness - irritability - fatigue - weight loss with large appetite - increased HR - SOB - excess sweating - heat intolerance - fine motor tremor - exophthalmos - goiter |
Hyperthyroidism
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Lab finding with _______ ?
- decreased TSH - increased T3 and T4 |
Hyperthyroidism
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Complications of ________ ?
- Exophthalmus - can lead to corneal ulceration (bulging eyes) - Heart disease - Atrial fibrillation, tachycardia CHF - Thyroid Storm |
Hyperthyroidism
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Also called vasopressin. Synthesized in hypothalamus; stored in pituitary gland. Secretion stimulated by increase in osmalality of the blood and decrease in blood pressure.
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Anti-diuretic hormone
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Function of ADH
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controls the excretion of water by the kidneys. has "antidiuretic" effect
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Decreased ADH
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Diabetes Insipidus
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Causes of _______ ?
- Head trauma - Brain tumor - Removal of pituitary - CNS infection - Unresponsive renal tubules |
Diabetes Insipidus
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Lab findings of _______ ?
- Low urine osmolality - Serum osmolality - Hypernatremia - Hypokalemia |
Diabetes Insipidus
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Complication of _______ ?
- Hypovolemic shock |
Diabetes Insipidus
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Increased ADH
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Syndrome of Inappropriate Anti-diuretic Hormone (SIADH)
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Causes of _______ ?
- Small cell carcinoma - Brain trauma - Infections - Some chemotherapy agents - Excessive treatment with DDAVP |
SIADH
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Lab finding of _______ ?
- Hyponatremia - Increased urine sodium - BUN increased - Decreased serum osmolality - Increased urine osmolality |
SIADH
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Complications of _______ ?
- seizures - brain damage |
SIADH
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Adrenal gland hormone of the Inner Medulla
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Epinephrine/Norepinephrine
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Adrenal gland hormone of the Outer cortex
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Corticosteroids
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Adrenal gland hormone of the Mineralcorticoids
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Aldosterone
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Control mechanisms of _______ ?
- high serum potassium - low serum sodium - ACTH - adrenocorticotropin |
Mineralcorticoids
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Functions of _______ ?
- Increases sodium absorption - Increases potassium excretion |
Mineralcorticoids
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Adrenal gland hormone of the Glucocorticoids
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Cortisol
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Functions of _______ ?
- regulated through a neg. feedback system - increases blood glucose levels - Stimulates appetite - Increases blood concentrations of amino acids - Increases use of fatty acids as energy - Decreases capillary permeability - Inhibits prostaglandin synthesis |
Glucocorticoids
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Steroid hormone, such as testosterone or androsterone that controls the development and maintanance of masculine characteristics
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Androgens
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Excess production of glucocorticoids, mineralcorticoids, and androgens
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Hyperfunctioning Adrenal Gland
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Cushing's Syndrome
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Hypercortisolism
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Causes of ________ ?
- High-dose glucocorticoid use (Most common iatrogenic cause) - Adrenal tumors - Pituitary tumors |
Hypercortisolism
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Manifestations of _______ ?
- Fat deposition - protruding abdomen "buffalo hump" "moon face" - muscle wasting and weakness - thin extremities |
Hypercortisolism
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Excess production of mineralcorticoid hormone (aldosterone) by adrenal cortex.
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Primary aldosteronism
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Causes of _______ ?
(primary) - defect or tumor of adrenal (secondary) - CHF - Cirrhosis of liver - Nephrotic syndrome |
Primary aldosteronism
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Clinical manifestations of _______ ?
- Hypertension - decrease K+ - hypernatremia |
Primary aldosteronism
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Autoimmune disorder; 90% of gland destroyed before symptomatic.
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Addison's Disease
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Addison's Disease
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Hypofunctioning of Adrenal Gland
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Risk factors for ________ ?
- history of other endocrine disorders - sudden cessation of glucocorticoids if taken > 3 weeks - Tuberculosis - Adrenalectomy - Primary vs. Secondary -> life long tx |
Addison's Disease
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Clinical Manifestations of ________ ?
- Anorexia - weight loss - N/V - Myalgia - arthralgia - orthostatic hypotension - hyponatremia - hyperkalemia |
Addison's Disease
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A severe phase or attack of a chronic adrenocortical disorder, characterized by insufficient amounts of the adrenocortical hormones and resulting in nausea, vomiting, low blood pressure, and life-threatening imbalances in electrolytes.
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Adrenal Crisis (Addisonian Crisis)
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Inadequate or lack of insulin resulting in hyperglycemia
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Diabetes
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Types of Diabetes (8)
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1. Type I
2. Type II 3. Maturity Onset Diabetes of the Young (MODY) 4. Idiopathic Type I Diabetes (Type 1b) 5. Latent Autoimmune Diabetes in Adults (LADA) 6. Youth Onset Atypical Diabetes (YOAD) 7. Impaired Glucose Tolerance 8. Gestational Diabetes |
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Insulin Dependent Diabetes
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Type I Diabetes (IDDM)
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- characterized by destruction of pancreatic beta cells
- absolute insulin deficiency - was named "Juvenile Diabetes" - more common occurence in younger people but can occur at any age - immune mediated more common - Idiopathic |
IDDM
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Non-insulin Dependent Diabetes
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Type II Diabetes (NIDDM)
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- presence of hyperglycemia in association w/ relative insulin deficiency
- can have high, low or normal insulin levels - Dysfunction of both insulin levels and insulin function |
NIDDM
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Clinical manifestations of _______ ?
- polyuria - polydipsia - polyphagia - dry flushed skin - confusion - Kussmaul resp. - N/V - fruity breath - lethargy - coma |
NIDDM
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Routine Monitoring Lab Test
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- fasting blood glucose
- Hgb A1C - measures glucose control over time - urine glucose & ketones - urine protein |
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S&S of _______ ?
- pallor - diaphoresis - hunger - nausea - anxiety - irritability - difficulty concentrating - decreased LOC - coma |
Hypoglycemia
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Acute complications of Diabetes (3)
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- Hypoglycemia
- Diabetic Ketoacidosis - Hyperosmolar Coma (HHNK) |
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- accumulation in blood & tissues large quantities of ketone bodies --> metabolic acidosis; ketone production by the liver exceeds cellular utilization & renal excretion; lack of insulin --> breakdown of fats
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Diabetic Ketoacidosis
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Diabetic Ketoacidosis occurs with which diabetes?
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Type I
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Clinical manifestations of _______ ?
- slow onset - polyuria - polydypsia - N/V - fatigue progressing to coma |
Diabetic Ketoacidosis
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Extreme hyperglycemia and serum osmolality.
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Hyperosmolar Coma (HHNK)
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Hyperosmolar Coma (HHNK) occurs with which diabetes?
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Type II
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Occurs with
- acute pancreatitis - severe infections / MI - hyperthyroidism - hyperalimentation - Type II diabetes |
Hyperosmolar Coma (HHNK)
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Clinical manifestations of ________ ?
- dehydration - neurological symptoms (seizures) - excessive thirst |
Hyperosmolar Coma (HHNK)
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Complications of Diabetes
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- Metabolic syndrome
- Microvascular - Macrovascular |
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- increased triglycerids
- decreased HDL - HTN - CHD (coronary artery disease) - increased waist ratio |
Metabolic syndrome
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- Capillary basement membrane thickening
- Diffuse glomerular sclerosis - Nodular glomerulosclerosis - Leading cause of ESRD - First manifestation of microalbuminemia |
Nephropathy
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- Leading cause of blindness
- Abnormal retinal permeability - Microaneurysms - Neovascularization - Hemorrhage - scarring - retinal detachment - on exam hemorrhages & exudates |
Retinopathy
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What are the two Microvascular Diabetes complications?
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1. Nephropathy
2. Retinopathy |
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What are the two Macrovascular Diabetes complications?
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1. Cardiovascular
2. Neuropathy |
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Diabetes appears to act as an amplifier of CV risk, multiplying the impact of underlying risk factors.
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Cardiovascular diabetes complications
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- Hyperlipidemia
- HTN (very important risk factor) - Particularly true for microvascular complications - CVA, CAD, PVD - Hyperlipidemia |
Cardiovascular diabetes complications
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- decreased sensation
- peripheral pulses - "stocking ang glove" - can affect cranial nerves - diabetic foot leading cause of non traumatic amputation - More at risk for infection |
Peripheral Neuropathic diabetes complications
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- Impotence
- gastroparesis |
Autonomic Neuropathic diabetes complications
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Age related changes (diabetes)
- Other chronic illnesses cause problems. |
Elderly
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Age related changes (diabetes)
- usually type I - diet challenges - puberty |
Child
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What hormone corresponding to adrenergic receptors (SNS) causes vasodilation in kidneys, heart, and viscera
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Dopamine
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What adrenergic receptor (SNS) causes
- vasoconstriction of blood vessels - decreased renin - glycogenolysis/gluconeogenesis - GU contraction - Uterine contraction - Myadriasis |
Alpha 1 Receptors
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What controls involuntary responses in smooth muscle and secretory glands & visceral organs
- Functions to maintain homeostasis - Responds to stress and repair tissues. |
Autonomic Nervous System (ANS)
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What causes:
- "fight or flight" / stress state (adrenergic response) - sympathetic neurotransmitters - catecholamines (epinephrine, norepinephrine, dopamine) |
Sympathetic Nervous System (SNS)
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What does mnemonic SLUDGE stand for?
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S alivation
L acrimation U rinary incontinence D iarrhea G I cramps E mesis |
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What action is the mnemonic SLUDGE describing?
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PNS Acetylcholine action
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What is responsible for:
- Rest and Digestion / Calming (cholinergic response) |
Parasympathetic Nervous System (PNS)
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What is the primary cholinergic neurotransmitter and where is it active?
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Acetylcholine (ACh), active with the PNS. (75% nerve fibers in vagus nerve.)
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What adrenergic receptor (SNS) causes:
- increased HR - increased myocardial contraction - increased automaticity - increased rate of conduction - increased renin |
Beta 1 Receptors
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What adrenergic receptor (SNS) causes:
- bronchodilation - vasodilation - decreased GI motility - gluconeogenesis/glucogenolysis - GU relaxation - uterine relaxation |
Beta 2 Receptors
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What adrenergic receptor (SNS):
- inhibits release of norepinephrine - inhibits receptory |
Alpha 2 Receptors
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What system regulates the body levels of thyroid hormone?
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hypothalamic-pituitary-thyroid feedback system
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What hormone causes these actions?
- constricts bronchioles - decreases HR - vasodilation - increased GI motility - constricts pupils - contracts bladder |
Actions of Acetylcholine (ACh)
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What are the two main pancreas secretions?
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- insulin (b cells)
- glucagon (a cells) |
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which adrenergic receptors (SNS) inhibit release of norepinephrine; (inhibitory receptor)
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Alpha 2 receptors
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The actions below are from what hormone?
- provides for glucose storage - prevents fat breakdown into ketones (acids) - increases protein synthesis |
Insulin (b cells)
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The actions below are from what hormone?
- breakdown of glycogen via glycogenolysis - synthesis of glucose via gluconeogenesis - increased fat & protein breakdown |
Glucagon (a cells)
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