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355 test 3
| Question | Answer |
|---|---|
| Endocrine Glands | Endocrine glands make & release special chemical messengers called hormones ● Secrete hormones directly into the blood |
| Exocrine Glands | Exocrine glands are not part of the endocrine system ● Secrete their substances into ducts that then empty into a body cavity |
| ducts | Salivary glands produce saliva, secreted through salivary ducts ○ Kidneys secrete: erythropoietin & stimulate RBC production ○ Heart secretes: [ANP, BNP] ○ GI Tract secretes: Peptide Hormones [Gastrin |
| Endocrine System Roles | Role in reproductive and CNS development in fetus 2. Stimulating growth and development during childhood and adolescence 3. Sexual reproduction 4. Maintaining homeostasis 5. Responding to emergency demands |
| Endocrine Hormones | Exert effects by: ○ Recognizing target tissues ○ Attaching to receptor sites in a “lock-and-key” type of mechanism |
| lock and key | A hormone will act only on cells that have a receptor specific for that hormone |
| Regulation of Hormonal Secretion | Simple Feedback ■ Negative feedback ● Think: “Stop! That’s enough!” ● Most common form ■ Positive feedback ● More rare form 2. Nervous system control 3. Physiologic rhythms |
| Negative Feedback – Insulin Release from Pancreas | High blood glucose After eating, glucose levels in the blood rise Increases insulin release Pancreas detects high sugar, releases insulin Lowers blood glucose As insulin works, sugar returns to normal levels, then decreases insulin release |
| Nervous System Control | Nervous system activity directly affects some endocrine glands Pain, fear, stressors can stimulate the nervous system to control hormone secretion |
| Catecholamines: | Epinephrine Norepinephrine |
| CNS and SNS | Central Nervous System (CNS): Senses stress Sympathetic Nervous System (SNS): Secretes catecholamines to stimulate heart and lung function |
| Circadian rhythm | Sleep-wake cycles Cortisol peaks early in day and at the end of sleep GH, TSH, Prolactin peak during sleep |
| Glycogenolysis | Breakdown of glycogen into glucose Glycogen: Stored form of glucose in the body |
| Gluconeogenesis | Formation of glucose from non-carbohydrate molecules When glycogen stores are used, glucagon makes the liver create new sugar |
| Ketogenesis | Make ketones for energy When glucose is very low, body breaks down fat + makes ketones |
| Amylin | Glucose-Regulating hormone Slows gastric emptying, promotes satiety, prevents spikes in blood glucose levels Amylin helps insulin work better after meals |
| Insulin | Regulates metabolism and stores ingested carbohydrates, fats, and proteins Facilitates glucose transport into cells Out of the blood stream Builds protein Helps amino acids enter cells |
| insulin function | “Storage” Hormone: Helps move sugar (glucose) from the blood into the cells to use for energy Extra glucose: Stored as glycogen in liver and muscles |
| High Insulin (After Eating): | Stops the body from making new glucose Helps store fat Helps build proteins |
| Low Insulin (Overnight Fasting): | Releases stored glucose from liver Releases fat from fat stores Breaks down protein from muscles |
| high/low insulin tip | High Insulin: Use and store nutrients Low Insulin: Mobilize stored fuel to keep blood sugar steady |
| Somatostatin | Inhibitory to insulin, glucagon, gastrin, growth hormone Slows GI motility allowing more time for food to absorb Decreases the spike in blood glucose levels after eating |
| Somatostatin tip | Somatostatin: Body’s balancer. Makes sure that insulin & glucagon don’t go overboard. Slows both down when needed. |
| Pancreatic Polypeptide | Released in response to eating a meal, especially a high protein or high fat meal Suppres the release of digestive enzymes from pancreas, preventing excessive digestion Signals brain to feel full, reducing food intake, Slows insulin & glucagon |
| Pancreatic Polypeptide controls | digestion & appetite |
| Diabetes Mellitus (DM) | Chronic disease that affects how the body uses sugar, fat, and protein Body either doesn’t make enough insulin or can’t use it well Causes high blood sugar (hyperglycemia) due to: Lack of insulin Insulin resistance |
| A1C | average blood sugar over the last 2-3 months Glucose attaches to hemoglobin molecule RBCs live 120 days, A1C levels reflect long-term glucose control Used to diagnose, monitor response to therapy, and screen patients with prediabetes |
| A1C goal | Less than 6.5% - 7% [reduces complications] |
| Fasting plasma glucose (FPG) level: | No food for 8 hours before > 126 mg/dL x 2 tests |
| 2-hour plasma glucose level: | Oral Glucose Tolerance Test (OGTT) > 200 mg/dL |
| Random plasma glucose level: | > 200 mg/dL |
| Impaired glucose tolerance prediabetes | Oral Glucose Tolerance Test (OGTT): 140 to 199 mg/dL |
| Impaired fasting glucose prediabetes | Fasting glucose: 100 to 125 mg/dL |
| A1C prediabetes | 5.7 – 6.4 |
| prediabetes tip | OGTT for DM: > 200 Fasting Glucose for DM: > 126 A1C for DM: > 6.5 |
| Type 1 Diabetes Mellitus (DM1): | Autoimmune disease Body attacks and destroys insulin-producing cells in pancreas Body makes little to no insulin No insulin → Glucose can’t get into cell → stays in blood → high blood sugar |
| 3 P’s if blood sugar is high enough | Polyuria: Excess glucose pulls water into urine – urination Polydipsia: Losing fluid – thirst Polyphagia: glucose can’t get into cells – cells are “starving” – hunger |
| Type 2 Diabetes Mellitus (DM2): | Most common type Body makes insulin, but doesn’t use it well Insulin is there → cells ignore it → glucose stay in blood → high blood sugar |
| Metabolic Syndrome | Cluster of conditions that occur together and increases risk of DM2 Abdominal obesity High Blood Pressure High Blood Sugar High Triglycerides Low HDL “Good” cholesterol 3 or more= MBLC SYNDROME |
| Metabolic Syndrome tip | Body isn’t using insulin well so it affects Blood Sugar, Blood Pressure, and Cholesterol |
| diabetes nursing care | Nutrition Exercise Drug therapy: Insulin Oral agents (OAs) and noninsulin injectable agents Self-monitoring of glucose |
| Oral Antidiabetic Agents | Stimulate the pancreas to produce & use more insulin Slow down glucose absorption from food Help the kidneys excrete extra glucose |
| Who takes PO DM Meds? | DM1: NO! Not effective. No endogenous insulin. DM2: YES! First line therapy + lifestyle changes. |
| Exogenous Insulin | Genetically engineered in laboratories Multiple daily injections or insulin pump Required for type 1 diabetes Prescribed for patients with type 2 diabetes During times of stress As disease progresses and unable to manage glucose levels |
| Endogenous Insulin Vs. Exogenous Insulin | Endo: Produced in pancreas Exo: Produced outside of body |
| Bolus | : Rapid or short-acting insulin before meals based on glucose Quick burst or bolus of insulin before meal to handle rise in sugar after eating |
| Basal | Intermediate or long-acting (background) insulin once or twice a day Keeps blood sugar steady between meals & overnight Most common insulin regimen for DM management |
| Basal-Bolus Regimen goal | Glucose level as close to normal as possible as often as possible |
| Mealtime Insulin (Bolus) | Rapid-Acting synthetic (bolus): Mimic natural insulin in response to meals Short-Acting regular (bolus): More likely to cause hypoglycemia Fast onset & Short duration: Drops sugar fast Strong peak: When hypoglycemia is most likely |
| Long-acting (Basal) insulin | detemir (Levemir), glargine (Lantus) Released steadily & continuously with no peak action for many; onset varies Administered once or twice a day, Never given IV Do not mix or dilute with any other insulin or solution |
| Intermediate-Acting Insulin (NPH) | Can mix with short- and rapid-acting insulins Never given IV Cloudy never push |
| Combination Insulin Therapy | Short or rapid-acting insulin + intermediate-acting insulin in same syringe Short/Rapid first NPH second Provides mealtime and basal coverage in one injection COMBO Not” (NPH) “Retired” (Regular) “RN” (Regular, NPH) |
| Insulin Storage | Extreme temperatures can make insulin less effective Hot climates Use thermos or cooler Refrigerate extra unopened insulin Avoid exposing to direct sunlight Store prefilled syringes upright |
| Insulin Administration | Given by SQ injection Avoid IM Risk of hypoglycemia Regular insulin may be given IV What should we never push? Abdomen is preferred site Don’t inject in site that will be exercised |
| Insulin Pen | Portable, convenient, compact, discreet Various lengths and gauges Good option for patients with vision |
| Insulin Pump | Continuous subcutaneous infusion of rapid-acting insulin Device connected to a catheter inserted into SQ tissue in abdominal wall |
| Dawn Phenomenon | Cause- Normal morning effect Growth Hormone & Cortisol rise in early morning hours Hormones tell liver to release glucose – HIGH morning sugar 3AM Glucose-Normal or HIGH Treatment-Increase insulin dose or administration time Normal?-Yes |
| Somogyi Effect | Man made – poor diabetes management “SO MOCH (much) insulin” Too much insulin causes hypoglycemia overnight Body detects LOW sugar – releases hormones – HIGH morning sugar 3am glucose-low, give bedtime snack normal?-no |
| Inhaled Insulin - Afrezza | Rapid-acting inhaled insulin Administered at beginning of each meal or within 20 minutes after starting meal adverse reactions: hypoglycemia, cough, throat pain or irritation Not recommended for treatment of DKA, smokers, asthmatics, or COPD |
| Biguanides: Metformin (Glucophage) | Most effective 1st line treatment for DM2 Available in immediate-release, extended-release, and liquid forms, works without insulin release Action Reduces glucose production by liver May cause weight loss Used in prevention of DM2 |
| Metformin: Drug Alert | Hold if undergoing surgery or radiologic procedure with contrast medium bc it is cleared by kidneys → IV Contrast harm kidneys →metformin can accumulate in body & cause lactic acidosis Hold 24-48 hours before procedure and 48 hours post-procedure |
| Sulfonylureas | Action Increases insulin production from pancreas over several hours Check for sulfa allergy Examples Glipizide (Glucotrol), Glyburide (Glynase), Glimepiride (Amaryl) hypoglycemia bc force insulin release, weight gain bc insulin is fat storage |
| Meglitinides (-glinides) | Quicker onset of insulin production from pancreas during and after meals… this mimics the normal response Take with first bite of food Major side effects Hypoglycemia, weight loss Examples Repaglinide (Prandin), Nateglinide (Starlix) |
| α-Glucosidase Inhibitors | “Starch blockers” Slows down carbohydrate digestion, decreasing the postprandial sugar rise Take with first bite of each meal Side effects GI symptoms: Flatulence, cramps, abdominal distension Examples Acarbose (Precose) |
| Dipeptidyl Peptidase–4 (DDP-4) Inhibitors (-gliptins) | DDP-4 normally inactivates incretin hormones So when DPP-4 is inhibited: More active incretins (hormones released after eating to help regulate glucose) Decrease in blood glucose levels, increase in insulin release |
| Dipeptidyl Peptidase–4 (DDP-4) Inhibitors (-gliptins) effects and examples | Side effects Pancreatitis, hypersensitivity reactions Examples Alogliptin (Nesina), linagliptin (Tradjenta), saxagliptin (Onglyza), sitagliptin (Januvia) |
| Sodium-Glucose Co-Transporter 2 (SGLT2) Inhibitors (-flozins) | Increase glucose excretion via urine By inhibiting SGLT-2 in the kidney tubules, decreasing glucose levels and inducing weight loss via caloric loss through the urine Examples Dapagliflozin (Farxiga), Empagliflozin (Jardiance) |
| Glucagon-Like Peptide-1 (GLP-1) Receptor Agonists | Non-insulin injectable given subcutaneously Simulate glucagon-like peptide–1 (GLP-1) Increase insulin synthesis and release Slow gastric emptying, increased satiety + reduced food intake |
| Amylin Analogs | Non-insulin injectable Pramlintide (Symlin) Slows gastric emptying, reduces postprandial glucagon secretion, increases satiety Administer subcutaneously before meals with at least 250 calories |
| Glucagon-Like Peptide-1 (GLP-1) Receptor Agonists caution care and examples | Give PO meds an hour before due to delayed gastric emptying Examples Albiglutide (Tanzeum), Semaglutide (Ozempic), Liraglutide (Victoza) |
| Glucagon | Can be administered subcutaneously, intramuscularly, or intravenously Used to treat insulin-induced hypoglycemia when the client is semiconscious or unconscious and is unable to ingest liquids Blood glucose level begins to increase within 5 to 20 min |
| Dextrose | Hypoglycemia Stupor, coma, or seizures, unsuspected hypoglycemia Adverse effects Hyperglycemia Phlebitis and cellulitis after extravasation (with concentrations ≥10%) from the intravenous injection site |
| Nutrition Therapy: Type 1 Diabetes | Based on usual food intake and preference Balanced with insulin and exercise consistency makes it easier to manage glucose Rapid-acting insulin, multiple daily injections, and insulin pump offer flexibility based on current glucose and carbs |
| Nutrition Therapy: Type 2 Diabetes | achieve glucose, lipid, and BP goals Moderate weight loss (5% to 7%) improves insulin sensitivity Nutritionally adequate meal plan appropriate serving sizes and reduced saturated and trans fats and low CHO can decrease calories |
| Nutrition Therapy: Carbohydrates | Complex carbohydrates are preferred Carbohydrate Counting Track amount of carbohydrates with each meal Nutritive and nonnutritive sweeteners may be used Serving size is 15 g of CHO Typically, 45 to 60 g per meal |
| complex carbs | Whole grains, beans, veggies - Digest slower - Glucose enters gradually - Slower rise in sugar & insulin |
| Insulin dose based on number of | grams of CHOs consumed For example, 1 unit per 15 grams CHO Meal with 60 grams of carbs = 4 units of insulin |
| Alcohol Intake | Inhibits gluconeogenesis by liver Prevents glucose release into the blood Can cause severe hypoglycemia Eat carbohydrates when drinking unless drinks have sweetened mixers Limit to moderate amount if no risk for other alcohol-related problems |
| Exercise | Minimum of 150 minutes/week aerobic activity Resistance training 3 times/week Decreases insulin resistance and glucose Weight loss Reduce need for DM2 medications Reduce triglycerides and LDL , ↑ HDL Decrease BP and improve circulation |
| Glucose-lowering effect of exercise may last up to | 48 hours Never exercise without a pre-workout meal Check glucose before exercise |
| 15-15 Rule for Hypoglycemia | 15 gram SIMPLE CARBOHYDRATE snack Wait 15 minutes & recheck blood sugar Repeat if needed Exercise at same time every day if its low after 2-3 times contact hcp |
| Do not inject insulin into an | area of the body that will be exercised! Exercise speeds up absorption |
| simple carbs | Raise sugar FAST Glucose tabs, hard candies, glucose ge |
| When to test blood glucose | Before meals Two hours after first bite When hypoglycemia is suspected Every 4 hours during illness Before and after exercise Consider impaired vision, cognition, or dexterity; use adaptive devices, identify caregiver |
| Nursing Implementation: Acute Illness glucose | Physical and emotional stress can increase glucose Stress hormones tell the liver to release more glucose, reducing insulin effectiveness Encourage to check glucose at least every 4 hours when ill DM2 patients may need insulin during illness |
| Hypoglycemia | Too much insulin in proportion to glucose in the blood Glucose level < 70 mg/dL Autonomic nervous system activated & epinephrine released Shakiness, palpitations, nervousness, diaphoresis, anxiety, hunger, & pallor |
| Hypoglycemia s/s | T-tachycardia I-irritability R-restless E-excessive hunger D-diaphoresis/depression Cold & Clammy? Need some candy! |
| Causes of Hypoglycemia | Too much insulin or oral hypoglycemic agents Too little food Delaying time of eating Too much exercise Usually occurs at peak time for meds or with disruption in daily routine |
| Moderate Hypoglycemia | (<40 mg/dL, Confusion Double vision Drowsiness Emotional changes Headache Impaired coordination Confusion |
| Severe Hypoglycemia | (<20 mg/dL) - Neuroglycopenia, Difficulty arousing Disoriented behavior Loss of consciousness Seizures Mimics alcohol intoxication |
| Untreated hypoglycemia | → Loss of consciousness → Seizures → Coma → Death |
| Hypoglycemia: Acute Care Setting | Patient alert? Start with oral CHO Patient not alert & IV access? 50% dextrose 20 to 50 mL (D50) Patient not alert & no IV access? Glucagon 1 mg Watch for nausea: Prevent aspiration |
| Diabetic Ketoacidosis (DKA) | Caused by profound deficiency of insulin Glucose typically > 250! Characterized by Hyperglycemia Ketosis Acidosis Dehydration Most likely to occur in DM1 May occur in people with type 2 DM with severe illness or stress |
| DKA: Precipitating Factors | Illness Infection Inadequate insulin dosage: Not enough! Undiagnosed type 1 DM Lack of education, understanding, or resources Neglect |
| So… What REALLY Happens in DKA? | Insulin Deficiency Body needs to find another source of energy! Body burns fat as fuel Since cells can’t use glucose properly, body burns fat instead for energy Fat breakdown → acidic ketones → alters pH → metabolic acidosis Ketones in urine |
| So… What REALLY Happens in DKA? pt 2 | Impairs protein synthesis Protein (muscle) breakdown due to insufficient insulin → nitrogen loss from tissues Leads to malnutrition (over time) Still no insulin → Body starts to panic Liver makes even more sugar Blood sugar gets extremely high |
| So… What REALLY Happens in DKA? pt 3 | Too much sugar in blood → you urinate it out Sugar pulls water with it! Urinate a LOT (Polyuria) Polyuria → dehydration Lose water Lose electrolytes Blood volume drops, Organs don’t get enough blood Kidneys slow down, ketones build up |
| DKA untreated | Shock, coma, death |
| acidosis DKA | Vomiting increases Fluid loss increases Electrolytes drop further |
| Simplified DKA Explanation | No insulin makes the body create more sugar and burn fat. Extra sugar makes you pee out all your water and electrolytes. Dehydration makes kidneys get less blood flow so acid / ketones |
| DKA: Clinical Manifestations | Glucose > 250 mg/dL Blood pH < 7.30 Too acidic High ketone levels in urine or serum Body burning fat instead of sugar Sunken eyes, dry skin Dehydration Nausea/vomiting From acidosis, fruity breath, kussmal resp. |
| DKA: Emergency Management | Monitor and replace potassium before starting insulin therapy Insulin drives water, K+, & glucose into cells → hypovolemia & hypokalemia; potentially life-threatening Continuous infusion: IV regular insulin drip to correct hyperglycemia and ketosis |
| DKA: Emergency Management pt 2 | Cardiac monitoring because of electrolyte imbalances Protect from cerebral edema due to rapid drops in glucose Hourly urine output for fluid overload, renal and cardiac compromise |
| Hyperosmolar Hyperglycemia Syndrome (HHS) | Life-threatening syndrome Less common than DKA Occurs with type 2 diabetes Common Causes: Acute illness (causes stress), Impaired thirst sensation and/or inability to replace fluids, polyuria |
| Hyperosmolar Hyperglycemia Syndrome (HHS) tip | DM1: No Insulin: Ketones: DKA DM2: Some Insulin: No Ketones: HHS |
| HHS Manifestations | Enough circulating insulin to prevent ketoacidosis Some insulin but not enough to control the sugar Fewer early symptoms lead to higher glucose levels Greater than 800 mg/dL! More severe neurologic manifestations |
| HHS Manifestations pt 2 | More severe neurologic manifestations because of increased serum osmolality High osmolality draws water out of brain cells Somnolence, coma, seizures, hemiparesis, aphasia; similar to stroke Ketones absent or minimal in blood and urine |
| HHS Management | More fluid replacement needed than DKA Need hemodynamic monitoring to avoid overload during fluid replacement IV insulin and NaCl infusions Fluid and electrolytes (*K+), serum osmolality, VS, I&O, cardiac |
| HHS Management tip | Super-high glucose Glucose spills into urine Lots of urine Lots of water lost SEVERE dehydration |
| Retinopathy | Chronic & progressive impairment of the retinal circulation Most common cause of new cases of adult blindness Assessment: Visual changes due to microaneurysms in retinal blood vessels Blurred vision Retinal detachment Cataracts Glaucoma |
| Nephropathy | Damage to small blood vessels that supply the glomeruli of the kidney Risk factors Hypertension, genetics, smoking, chronic hyperglycemia Treatment Early prevention-glucose & BP Restrict dietary protein, Na, and K Avoid nephrotoxic meds |
| Neuropathy | Deterioration of the nervous system throughout the body Persistent hyperglycemia causes: Accumulation of sorbitol and fructose that damages nerves |
| Neuropathy s/s | Affects distal portion of nerves Most frequently in lower extremities – loss of protective sensation Paresthesia – tingling, burning, itching Poor peripheral pulses Skin breakdown and signs of infection |
| Gerontologic Considerations | Increased prevalence and mortality Higher rate of death, functional disability, and coexisting illness Polypharmacy Many undiagnosed and untreated Signs resemble changes associated with aging such low energy levels, dizziness, confusion, uti |
| Hypothalamus | Located next to pituitary gland & controls how it works Release substances that tell the pituitary to start or stop releasing hormones Contains neurons that receive signals from the brain & nervous system Acts as a control center |
| Hypothalamus tip | connects the endocrine system, autonomic nervous system, body functions, & emotions Anger, fear, pleasure Hypothalamus is brain’s control center: Links nervous system + hormone system Tells pituitary gland what to do |
| hypothalamus releasing hormones | Corticotropin-releasing hormone (CRH) Thyrotropin-releasing hormone (TRH) Growth hormone–releasing hormone (GHRH) Gonadotropin-releasing hormone (GnRH) Prolactin-releasing factor (PRF) Signals a “GO” to pituitary to make / release hormones |
| hypothalamus inhibiting hormones | Somatostatin (inhibits growth hormone release) Prolactin-inhibiting factor (PIF) Signals a “STOP” to pituitary to not make / release hormones |
| Pituitary GLAND | Located under hypothalamus at base of brain Known as the master gland |
| Pituitary GLAND anterior lobe | (Makes Hormones) Regulated by hypothalamus Tropic hormones (TSH, ACTH, FSH, LH) Growth hormone (GH) Prolactin Think: FLAT PiG |
| Pituitary GLAND posterior lobe | (Stores Hormones) Connected to hypothalamus via nerve tracts Antidiuretic hormone (ADH) Regulates fluid volume Potent vasoconstrictor |
| Hyperpituitarism (Excess hormone secretion) | TOO MUCH Acromegaly Cushing’s disease Hyperprolactinemia |
| Hypopituitarism (Deficiency of hormones) | NOT ENOUGH Dwarfism Adrenal insufficiency Hypothyroidism |
| Anterior Pituitary Disorders | Most commonly caused by Pituitary Tumors |
| BOTH Hyperpituitarism & Hypopituitarism are | RARE Disorders Because the Pituitary gland is usually well-protected in the brain |
| acromegaly | Overproduction of growth hormone (GH) Excess GH leads to abnormal enlargement: Excess GH makes liver release IGF-1 (Insulin-like growth factor-1) IGF-1 causes bone & tissue growth Too much IGF-1 leads to abnormal enlargement of bones & soft tissues |
| acromegaly diagnose and risks | typically at 40 to 45 years old After growth plates have closed Risk factors: age & benign tumors |
| acromegaly tips | GH: The signal IGF-1: Hormone that does the growing Growth plates close… So… Bones can’t grow taller… So… They grow thicker & wider |
| Acromegaly manifestations | Severe headaches Tumor: pushes on surrounding tissues Thick lips with coarse facial structures Lower jaw protrusion Bulging of forehead Joint pain, muscle weakness Enlarged hands and feet Hyperglycemia GH makes the body insulin resistant htn |
| Acromegaly Labs & diagnostics | Insulin-like Growth Factor (IGF-1) Serum test Shows amount of IGF-1 in blood X-rays of skull: Identify abnormalities CT or MRI of head: Detects soft tissue lesions Cerebral angiography: Detect presence of vascular malformation or aneurysms |
| Acromegaly Labs & diagnostics pt 2 | Growth Hormone Suppression Test: Client is NPO before test Baseline GH level is drawn Client drinks glucose solution Blood is drawn again after Expected Results: Normal: GH levels drop after glucose Acromegaly: GH levels stay high |
| When you drink glucose…your body should stop | releasing growth hormone |
| hypopituitarism | Rare disorder Involves a decrease in 1 or more of the pituitary hormones Most common hormone deficiencies GH Gonadotropins (e.g., LH, FSH) Manifestations & diagnosis are specific to the hormone deficiency |
| Hypophysectomy | Surgical removal of pituitary gland via craniotomy or transsphenoidal approach Prevent increased intracranial pressure (ICP): Elevate head of the bed at least 30° Avoid sneezing, coughing, blowing the nose Monitor patient status |
| Hypophysectomy complications | Infection CSF Leak: Clear nasal drainage Check drainage for glucose Monitor “mustache” dressing, strict I and O |
| Hypophysectomy further Post-op care | Oral care Immediate post-op: Avoid toothbrushes 10-14 days post-op: Ultra-soft toothbrush Lifelong replacement of ADH, cortisol, and thyroid hormone if entire pituitary gland is removed No longer produce tropic hormones that stimulate other glands |
| Hypophysectomy educate | Follow-up importance Regular IGF-1 & MRI scans Medication adherence Lifelong! Healthy Lifestyle |
| SIADH | Overproduction of ADH despite low plasma osmolarity ADH is stuck “ON” button: Kidneys hold water Kidneys reabsorb: Less urine Blood gets watery: Diluted blood (plasma osmolality drops) Kidneys try to filter more: Sodium gets out. Fluid OVERLOAD |
| Siadh manifestations | Early: Headache, weakness, muscle cramps, weight gain without edema since water, not sodium, is retained So if you’re SOAKED INSIDE… Fluid retention Low urine output Decreased serum osmolality Dilutional hyponatremia High water but low sodium |
| SIADH labs | Blood / Serum: Dilutional Hyponatremia: Serum Sodium less than 135 mEq/L Too much water for the sodium – ADH traps water so sodium is washed out Dilute Blood: Decreased serum osmolality Urine: Concentrated Urine: High urine osmolality High SG |
| SIADH tip | Diluted blood (LOTS OF WATER INSIDE) Concentrated urine (WATER ISN’T GOING OUT) |
| SIADH Client-centered care | Address underlying cause & fluid restriction Assess & monitor for worsening hyponatremia Confusion, lethargy, Cheyne-Stokes respirations Restrict oral fluids to 500-1000 mL/day Oral care, ice chips per MD order Strict I & O + Daily Weights |
| Tetracycline derivative (Demeclocycline) | for SIADH, Unlabeled use to correct fluid & electrolyte imbalances Stimulates urine flow Makes kidneys ignore ADH Contraindicated with impaired kidney function Monitor effectiveness: Urinary output increases, says NO to ADH & makes you GO |
| Vasopressin antagonists (‘Vaptans’) | for SIADH, Block vasopressin from working on kidneys Kidneys let go of extra water Urine output increases Serum sodium increases Urine becomes more dilute Tells the kidneys to STOP holding onto water |
| Loop Diuretics (Furosemide): | for SIADH, Increase water excretion from the kidneys Causes sodium excretion & can worsen hyponatremia Change position slowly-orthostatic hypotension |
| Diabetes insipidus (DI) | Deficient production or secretion of ADH Decreased ADH reduces ability of the renal tubules to concentrate urine Less water More sodium Excessive diluted urine, thirst, electrolyte imbalance, excessive fluid, incr thirst |
| Central (Neurogenic) DI | Interference with ADH Most common type Risk Factors: Brain tumor, head injury, brain surgery, CNS infections Demeclocycline Remember: Used to treat SIADH (DemecLOcycline says NO to ADH and makes you GO) |
| DI Manifestations | Polyuria Polydipsia Dry mucous membranes Weak, poor peripheral pulses Constipation Weight loss Fatigue Muscle weakness Dilute urine |
| DI Labs & diagnostics | Blood / Serum: Increased serum sodium & potassium Concentrated Blood: Increased blood osmolality More concentrated because losing water Urine: Diluted Urine: Decreased urine osmolality diluted bc kidneys cant hold water Decr SG, inc output |
| DI - Water Deprivation Test | Also known as ADH stimulation test Purpose: See if the body can concentrate urine when water is withheld Stop giving patient water for 8-12 hours… dehydration Normally: ADH Increases, kidneys save water, urine becomes concentrated |
| If urine is still diluted after Water Deprivation Test | Suggestive of Diabetes Insipidus Give Desmopressin (DDAVP) (“Fake” ADH) intranasally or IV Check labs q 2hrs and rehydrate |
| DI Client-centered care | central venous pressure I & O, Weight potassium, sodium, BUN, creatinine, specific gravity, osmolarity IV therapy to match output & replace electrolytes Fall precautions Regular diet Add bulk food & fruit juices for constipation: May add laxative |
| T4 (Thyroxine) | needs iodine to be made Made only in the thyroid gland Thyroid combines Iodine + Tyrosine to form T4 90% of thyroid hormone produced STORAGE hormone controls metabolism, HR, energy, temp |
| T3 (Triiodothyronine) | Mostly made by conversion of T4 to T3 More potent hormone Causes stronger metabolic effects ACTIVE hormone – does most of the work |
| thyroid hormone tip | Thyroid Hormones: Control metabolism Affect energy use, oxygen use, brain function |
| goiter | Thyroid gland gets bigger Can happen with overactive or underactive thyroid Most common cause: Not enough iodine in the diet TSH & T4 Levels: Can be normal, high, or low |
| what worsens goiter | Certain foods, drugs high in iodine, Thyroid inhibitors: Methimazole, Propylthiouracil |
| thyroiditis | Inflammation of the thyroid gland Hashimoto Thyroiditis [Chronic Autoimmune Thyroiditis]: Caused by the destruction of thyroid tissue by antibodies Most common cause of hypothyroid goiters |
| hallmark of thyroiditis | Goiter is hallmark of Hashimoto Thyroiditis: Can enlarge rapidly, may compress structures in neck, changing the voice/affecting breathing |
| hyperthyroidism | high and hot, Excessive circulating thyroid hormones Exaggerates normal body functions & produces hypermetabolic state Most common in females aged 30-50 Etiology: Graves Disease: Autoimmune, toxic diffuse goiter, causes hyperthyroidism |
| hyperthyroidism manifestations | Nervousness, irritability, hyperactivity, Weakness, fatigue, exercise intolerance Weight loss, ↑ appetite Insomnia Frequent stools & diarrhea Warm, sweaty, flushed skin Exophthalmos, excessive tearing, bloodshot appearance, vision changes Goiter |
| Exophthalmos | Ophthalmopathy: Abnormal eye appearance or function Exophthalmos Inflammation causes fluid buildup in eye muscles Increased fat deposits behind eyeball Outward eyeballs, retracted + elevated eyelids, occurn wt graves disease |
| Exophthalmos Management | Tape the eyelids closed or use eye patches AVOID 5 S’s - Can Trigger THYROID STORM: NO Sodium (eye swelling) + HOB Up (drain the eyes) NO Stimulants (Cluster care) NO Smoking, Stress, Sepsis Don’t touch neck... release MORE T3 & T4, sunglasses |
| Hyperthyroidism Labs & diagnostics | Low or undetectable TSH Pituitary senses too much thyroid hormone Pituitary stops sending TSH; shuts off TSH Increased T4 and T3 levels Thyroid is overactive Ultrasound to view thyroid gland & surrounding tissues |
| Radioactive iodine uptake (RAIU) | Nuclear scan to measure how much radioactive iodine the thyroid gland absorbs Shows how active your thyroid is Distinguishes thyroiditis & other causes of hyperthyroidism Discontinue iodine-containing medications week priot hold 6 weeks after |
| Methimazole, Propylthiouracil (PTU) | for hyperthyroidism, Inhibit production of thyroid hormone Monitor T3 & T4 levels for effectiveness Block thyroid from making new T3/T4 hormones Monitor for hypothyroidism manifestations |
| Beta-adrenergic Blockers | for hyperthyroidism, Treat symptomatic nervous system effects Don’t fix the thyroid, but calm body’s response |
| Lugol’s Solution & Saturated solution of potassium iodine (SSKI) | for hyperthyroidism, Stops thyroid from releasing hormones Use: Short-term use only in preparation for surgery Tips: Mix with juice to mask taste; use a straw to avoid teeth stain Watch for fever, sore throat, metallic taste, mouth ulcers |
| radioactive iodine (ablation) therapy | How it works: Thyroid takes up radioactive iodine & destroys some of the hormone-producing cells After: May require life-long thyroid hormone therapy BEFORE: Pregnancy test Hold antithyroid meds 5-7 days prior Client should be awake, Fast after/bef |
| radioactive iodine (ablation) therapy avoid what? | everyone, Take a laxative 2-3 days after to help rid body of stool contaminated with radiation. can swing pt into hypothyroidism |
| Hyperthyroidism: Surgical Therapy | Subtotal is preferred: Minimally invasive procedure 90% is removed (balance) Less risk of damaging nearby structures Preserves some thyroid function |
| Thyroidectomy Care pre op | Administer propylthiouracil or methimazole, & iodine before surgery to reduce size & prevent bleeding Goal is to calm the thyroid down before removal |
| Thyroidectomy post op care | Monitor for respiratory distress AIRWAY! Trach Tray + Suction + O2 at bedside Humidify air Avoid neck flexion & stress on the suture line Support neck when coughing & deep breathing Monitor for laryngeal nerve damage Pain Management |
| Thyroidectomy Care: Discharge Teaching | Monitor hormone balance periodically Decrease caloric intake Metabolism slows down post-operatively Adequate but not excessive iodine intake If complete thyroidectomy: Symptoms of hypothyroidism Need for lifelong thyroid hormone replacement |
| Thyroidectomy complications | Hemorrhage at site,Hypocalcemia, tetany, Thyroid Storm (Crisis): surge of large amounts of thyroid hormones in blood.emergency risk factors: Uncontrolled hyperthyroidism, surgery, stress s/s- Hyperthermia, HTN, delirium, vomiting, abdominal pain |
| Thyroid storm (crisis) client-centered care | Administer IV fluids to provide adequate hydration & prevent vascular collapse Supplemental oxygen to meet metabolic demands Teach client to notify provider of fever, ↑ restlessness, palpitations, chest pain Cool, hydrate, oxygenate! |
| hypothyroidism | Inadequate amount of circulating thyroid hormones: Decreased metabolic rate Often undiagnosed in older clients since manifestations mimic the aging process, opiates, anesthetics.Primary: Dysfunction of thyroid gland |
| Hypothyroidism risk factors | Females 30-60 years of age Inadequate intake of iodine Radiation therapy to head & neck Often slow progression & undiagnosed due to vague & varied findings |
| Hypothyroidism: Clinical manifestations | Cold & Slow! Fatigue, lethargy Irritability Cold intolerance Bradycardia, hypotension, dysrhythmias Slow thought processes and speech Hypoventilation weight gain, swelling, pallor, thick nails, constipated |
| Hypothyroidism Labs & diagnostics | Remember… thyroid gland is underactive It can’t make enough T3 & T4 So the Pituitary senses the low thyroid and tries to fix it… releases more TSH ↓ T3 & T4 TSH ↑ in primary |
| thyroid hormone replacement therapy | Levothyroxine: Synthetic thyroid hormone replacement; most common medication Use cautiously with CAD to avoid ischemia due to ↑ O2 demand of heart Too much hormone makes heart work harder; can trigger angina or MI |
| thyroid hormone replacement therapy pt 2 | Dosing is weight-based & ↑ every 2-3 weeks until desired response: Use TSH to monitor effectiveness Monitor for cardiovascular compromise Lifelong therapy Empty stomach 30-60 minutes before breakfast |
| Complication: Myxedema coma | Life-threatening condition Result of: Untreated / poorly managed hypothyroidism Acute stress Discontinuation of thyroid replacement therapy |
| Myxedema coma s/s | Respiratory failure, hypotension, hypothermia, bradycardia, dysrhythmia, hyponatremia, hypoglycemia, coma |
| Myxedema coma Client-centered care | ICU admission with hourly VS or more frequently if needed Maintain airway & ventilatory support as needed Aspiration precautions Continuous ECG monitoring Monitor mental status, Replace fluids with 0.9% NS Administer levothyroxine as IV bolus |
| Parathyroid hormone (PTH) | Regulates serum calcium levels Bones: Signals bones to release calcium into blood Kidneys: Tells kidneys to keep calcium & excrete phosphate Intestines: Activates Vitamin D – increases calcium absorption from food, Ca keeper |
| hyperparathyroidism | Over-secretion of PTH causes increased serum calcium levels Primary: Problem is parathyroid gland itself Parathyroid adenoma (most common) Makes too much PTH Secondary Tertiary |
| hyperparathyroidism manifestations | Hypercalcemia PTH makes the bone weak by taking calcium from its storages Stones Moans Groans Bone pain, fractures, deformities Kidney stones, renal failure Fatigue & muscle weakness Anorexia, nausea, vomiting, weight loss, constipation HTN |
| Hyperparathyroidism Labs & diagnostics | ↑ PTH levels ↑ serum calcium level ↓ serum phosphorus level ↓ bone density Weakened bones PTH steals calcium from bones, bones get thin MRI, CT, and/or ultrasound can detect an adenoma, Asymptomatic hypercalcemia found thru routine chem panel |
| Hyperparathyroidism Client-centered care | IV furosemide to flush out calcium in urine Isotonic Normal Saline IV: to maintain hydration IV phosphate: to reduce ca reabsorption in kidneys (help decrease) Calcitonin: to decr skeletal calcium release & increase renal excretion Ca, bisphospnates |
| Hyperparathyroidism Client-centered care (cont…) | Monitor vital signs Monitor I & O & signs of renal stones Monitor for skeletal pain; move the client slowly & carefully Monitor calcium & phosphorus levels Emphasize the importance of exercise |
| Parathyroidectomy Care pre op | Monitor electrolytes, calcium, phosphate, magnesium Ensure that calcium levels are decreased to near-normal values Inform the client that talking may be painful for 1-2 days after surgery |
| Parathyroidectomy Care post op | Assess airway! Trach Tray + Suction + O2 at bedside Monitor for hypocalcemia + Trousseau’s or + Chvostek’s Monitor for voice pattern changes & hoarseness Monitor for laryngeal nerve damage and hypocalcemia, can cause heart issues/kidney/bone |
| hypoparathyroidism | Uncommon condition of inadequate circulating PTH Characterized by hypocalcemia due to a lack of PTH to maintain serum calcium levels Most common cause: Accidental removal of the PTH glands or damage to glands during thyroidectomy |
| Hypoparathyroidism manifestations | Positive Chvostek’s & Trousseau’s sign Numbness or tingling in fingers, toes, lips Muscle twitching or spasms Signs of overt tetany: Bronchospasm, laryngospasm, dysrhythmias, seizures |
| Hypoparathyroidism labs | Hypocalcemia Low PTH levels High phosphate levels |
| Hypoparathyroidism Client-centered care | IV Calcium Gluconate Given slowly; Can cause dysrhythmias, cardiac arrest Oral calcium & vitamin D supplements ↑ calcium diet: Dark green vegetables, soybeans, tofu Seizure precautions Check calcium levels 3-4 times per year |
| Adrenal Glands | Keep body balanced, fuel metabolism, manage stress, influence sexual development One adrenal gland on top of each kidney Adrenal Medulla: Inner core Adrenal Cortex: Outer shell Regulates sodium & electrolyte balance Sustains fight-or-flight response |
| Adrenal Medulla – Inner: | Catecholamines: Epinephrine, norepinephrine, dopamine Fight-or-Flight response |
| Adrenal Cortex – Outer: (Sugar, Salt, Sexual Characteristics) | Glucocorticoids (Cortisol): Anti-inflammatory & affects glucose metabolism Mineralocorticoids (Aldosterone): Influence fluid and electrolyte balance Adrenal androgens: Sexual characteristics |
| Cortisol | Most abundant and potent glucocorticoid Necessary to maintain life and protect the body from stress Regulates blood glucose concentration by stimulating glucose formation in liver Decreases inflammatory response Body stresses |
| Aldosterone | Maintains extracellular fluid volume Promote renal reabsorption of sodium & water & excretion of potassium Synthesis & secretion are stimulated by hyponatremia, hyperkalemia, and angiotensin II |
| Cushing’s syndrome - hypercortisolism | Chronic exposure to excess corticosteroids, especially glucocorticoids “Especially glucocorticoids” = too much cortisol Can occur from: Long-term use of corticosteroids (Prednisone) Most common |
| ACTH | Adrenocorticotropic Hormone Main job is to stimulate adrenal cortex to make & release cortisol |
| Cushing’s syndrome manifestations | Glucocorticoids (Cortisol [sugar]) excess may cause: Hyperglycemia related to glucose intolerance and increased gluconeogenesis Cortisol makes more glucose- hyperglycemia Muscle wasting causes weakness Breaks down protein, low collagen=thin skin |
| Mineralocorticoid (Aldosterone [salt]) excess may cause: | Hypokalemia Excretion of potassium Hypertension Due to sodium & water retention |
| Adrenal androgen (sexual characteristics) excess may cause: | Severe acne Male characteristics in women Feminization in men |
| Cushing’s syndrome Labs & diagnostics | 24-hour urine cortisol Measures total cortisol over entire day High cortisol: Cushing’s X-ray MRI CT Scans Identify lesions |
| Cushing’s syndrome treat | Surgical removal or irradiation of pituitary adenoma Hypophysectomy Adrenal tumors or hyperplasia Adrenalectomy Removal of ACTH-secreting tumors |
| Cushing’s syndrome monitor | Monitor I&O, daily weights Assess for hypervolemia Minimize risk of pathologic fractures & skin trauma Infection prevention Monitor WBC ↑ calcium & vitamin D diet |
| Hyperaldosteronism: Conn’s Syndrome | Excess mineralocorticoid (aldosterone) secretion from the adrenal cortex Causes: Adrenal adenoma, renal artery stenosis Remember… aldosterone has 2 main effects: Sodium and water retention Potassium excretion |
| Conn’s Syndrome hallmark sign | Hypertension with hypokalemic alkalosis |
| Hyperaldosteronism: Conn’s Syndrome diagnose and treat | Diagnosis: ↑ plasma aldosterone & Na levels ↓ plasma potassium Treatment: Adrenalectomy (if tumor present) Spironolactone (aldosterone antagonist) Be sure to monitor I & O, weight, VS, electrolytes! |
| Addison’s disease & Addisonian Crisis | Chronic adrenocortical insufficiency: Addison’s Disease Acute adrenal insufficiency: Addisonian Crisis (life-threatening) Caused by damage or dysfunction of adrenal cortex ↓ mineralocorticoid & glucocorticoid, low aldosterone and cortisol |
| Addison’s Disease Manifestations | Persistent fatigue, muscle weakness Hyperpigmentation (bronze skin) Low cortisol = high ACTH = increased melanin = bronze skin Hypotension, dehydration ↑ K, Ca, BUN ↓ Na, glucose Anemia Salt cravings due to aldosterone deficiency GI disturbance |
| Addison’s disease Labs & Diagnostics | ↓ blood & salivary cortisol Adrenocorticotropic hormone (ACTH) Stimulation Test: Give IV synthetic ACTH Normally, adrenals respond by releasing more cortisol within 30-60 minutes If cortisol stays low, Addison’s Disease |
| Addison’s disease Client-centered care | Stabilize BP Correct electrolytes Give IV steroids (IV Hydrocortisone) Continuous monitoring Provide safe environment Recumbent position + elevate legs Increases blood flow back to the heart Treats hypotension |
| Client-centered care: glucocorticoids | Hydrocortisone, prednisone, cortisone Replacement for adrenal insufficiency & anti-inflammatory Monitor weight, BP, & electrolytes Increase dosage in times of stress Administer with food Taper dose when discontinuing |
| Adrenal Medulla Disorders | Catecholamine release (epinephrine & norepinephrine) in response to stress: Stimulate the heart Constrict blood vessels Dilate bronchioles Increase respiration and metabolism Promotes hyperglycemia |
| Pheochromocytoma | Tumor causes release of excessive amounts of catecholamines Rare, typically benign If left untreated: Encephalopathy Cardiomyopathy Multiple organ failure Death |
| Pheochromocytoma Manifestations: 5 Ps | Pressure: Severe hypertension Pain: Severe, pounding headaches, chest pain, abdomen Palpitations: Tachycardia Perspiration: Excessive sweating Pallor |
| Pheochromocytoma Lab & diagnostic tests | 24-hour urine catecholamines CT/MRI of adrenal glands Do not palpate client’s abdomen if suspected pheochromocytoma May cause the sudden release of catecholamines Severe hypertension as result |
| Pheochromocytoma Client-centered care | Monitor vital signs, especially BP & HR Monitor for hypertensive crisis & complications from hypertensive crisis Avoid stimuli that can precipitate hypertensive crisis, such as increased abdominal pressure and abdominal palpation No smoking/caffeine |
| Pheochromocytoma Management | Monitor serum glucose level Epinephrine increases glucose in the blood Secondary diabetes mellitus Promote rest and a non-stressful environment Prepare client for an adrenalectomy Laparoscopic surgical removal of an adrenal gland |
| Adrenalectomy | Catecholamine levels drop as a result of surgery Can result in cardiovascular collapse, hypotension, and shock Need to monitor closely Vital signs are key in assessment |
| Adrenalectomy Pre-Op Therapy | α-adrenergic receptor blockers β-adrenergic receptor blockers Used to decrease tachycardia and dysrhythmias Therapy can cause orthostatic hypotension Pre-Op care is about controlling BP! |
| Adrenalectomy Pre-Op Therapy monitor | correct electrolyte imbalances Assess for dysrhythmias Monitor for hyperglycemia Administer glucocorticoids to prevent adrenal hypofunction & prepare for stress of surgery |
| Adrenalectomy: Postoperative Care | Monitor vital signs Monitor I&O Monitor daily weight Monitor serum electrolyte & glucose levels Administer IV fluids to maintain blood volume Watch for hypotension, fever, and shock due to low catecholamine |
| A1C is your | glycosylated hemoglobin levels, reflects 2-3 months of glucose, want less than 6.5% |
| fasting plasma glucose | blood sugar test after no food for 8 hrs. baseline glucose not influenced by recent meals, sugar >126mg/dl x 2 |
| 2 hour plasma glucose | done with oral glucose tolerance test, glucose drink, sugar checked 2 hrs later to see how body handled glucose load, sugar >200mg/dl |
| random plasma glucose level | any random time of day without fasting, sugar >200 mg/dl plus symptoms |
| rapid acting insulin chart | lispro, aspart, glulisine-take around meal time onset: 10-30 min peak: 30min-3hr duration: 3-5hr |
| short acting insulin chart | humulin r. novolin r. onset: 30min- 1 hr peak: 2-5 hr duration: 5-8 hr higher hypoglycemia risk-if no extra snack- hypoglycemia |
| intermediate acting insulin chart | NPH, never IV - cloudy onset: 1.5-4 hr peak: 4-12h4 duration: 12-18hr |
| long acting insulin chart | admin one or twice daily, never IV glargine, detemir, degludec onset: 0.8-4hr peak: none duration: 16-24hr |
| inhaled insulin chart | afrezza. onset: 12-15min peak: 60min duration: 2.5-3hr |
| highest risk for hypoglycemia | peak |
| liver produces | glycogen |
| if your sugar is low | pancreas releases glucagon, liver breaks down glycogen, blood glucose rises |
| glucagon | glucose is GONE, make more |
| dawn vs somogyi | how to tell difference- check glucose 2-3am-will be low treat- may need to decrease evening insulin or add bedtime snack |
| meds for acromegaly | dopamine agonists, somatostatin analogs, gh receptor blockers |
| posterior pituitary disorder | regulates water balance and uterine contractions through release of ADH and oxytocin, helps your body save water |
| hashimoto thyroiditis | your immune system attacks your thyroid, slowly destroying it so it cant make enough thyroid hormone,leads to hypothyroidism |
| thyroid storm can lead to | uncontrolled hyperthermia, fever, tachydysrhythmias, chest pain |
| iodine solutions | hyperthyroidism. when you give high doses of iodine, it temporarily shuts down the thyroid from making and releasing hormones "woah too much iodine stop production of T3 and T4" |
| levothyroxine is | WEIGHT BASED. take on empty stomach 30-60 min before breakfast |
| parathyroid main job is to | keep Ca levels in blood normal, pulls Ca from bones into blood, tells kidneys to hold on to ca, activates vitamin D to help intestines absorb Ca |
| adrenal glands make | cortisol, aldosterone, adrenaline, norepinephrine |
| adrenalectomy control | blood pressure |
| The nurse teaches a client newly diagnosed with type 1 diabetes about storing Humulin N insulin. Which statement indicates to the nurse that the client understood the discharge teaching? | "I can store the open insulin bottle in the kitchen cabinet for 1 month." |
| Metformin is prescribed for a client with type 2 diabetes mellitus. What is the most common side effect that the nurse would include in the client's teaching plan? | GI disturbances |
| In the client with type 2 diabetes mellitus, an elevated temperature may indicate | infection. Infection is a leading cause of hyperosmolar hyperglycemic syndrome in the client with type 2 diabetes mellitus. The other findings are within normal limits or are expected. |
| The nurse is caring for a client with a diagnosis of Addison's disease and is monitoring the client for signs of Addisonian crisis. The nurse would assess the client for which manifestation that would be associated with this crisis? | severe abd pain |
| The nurse is reviewing the record of a client admitted to the hospital with a diagnosis of pheochromocytoma. The nurse reads the assessment findings and expects to note documentation of which major symptom associated with this condition? | HTN |
| The nurse is performing an assessment on a client with a diagnosis of myxedema (hypothyroidism). Which assessment finding would the nurse expect to note in this client? | dry skin |
| findings consistent with a diagnosis of adrenal insufficiency include | nausea, vomiting, and diarrhea; hyponatremia; salt craving; hyperkalemia; and orthostatic hypotension. Irritability and depression may also occur in primary adrenal hypofunction. |
Created by:
cwehner125