endocrine emergencies
A patient withy type 1 diabetes mellitus is admitted with Diabetic ketoacidois. Which type of insulin should a physician prescribe as an insulin infusion?
A) 50/50 B) 70/30 C) NPH D) Regular D.
Which dysfunction should you address first in a patient with DKA?
A) Acidosis B) Hyperkalemia C) Hyperglycemia D) Hypovolemia D. Fluids first and rehydrate Then hyperglycemia then hyperkalemia- acidosis will correct as correct other things
A client with type 1 diabetes mellitus has diabetic ketoacidosis. Which of the following findings has the greatest effect on fluid loss?
A) Hypotension B) Decreased serum potassium level C) Rapid, deep respirations D) Warm, dry, skin c. Vaporization can lose 1 L fluid
Antidiuretic Hormone Disorders (ADH)
Two most common: Diabetes Insipidus- DI Syndrome of inappropriate ADH (SIADH) Primary function of ADH is the regulation of water balance and serum osmolyte
Adrenal crisis presentation
Adrenal crisis is a life-threatening absence of cortisol and aldosterone Requires quick and astute response Signs and symptoms vary In the critically ill it should be considered with patient acutely ill with fever, vomiting ,shock, hypotension Cardiovascular system: in adrenal crisis the cardiovascular signs and symptoms are caused by hypovolemia, decrease vascular tone, and hyperkalemia In these patients most common presentation is hypotension refractory to fluids and requiring pressors ***hypotension that does not respond to fluids--- requires vasopressors ****!!!
Assessment
Abrupt onset is and may be unexpected Symptoms vary from person to person Symptoms vary related to the rapidity of decrease in blood glucose and usual blood glucose range Decreased adrenergic response may affect symptoms in persons who have had diabetes for many years probably related to autonomic neuropathy
Thyroid Storm:Collaborative Interventions
Administer medications Propylthiouracil (PTU) and methimazole (Tapazole) inhibit thyroid synthesis Iodine agents inhibits release of hormones Medication to block effects: beta-blockers, steroids Monitor cardiovascular status Monitor hyperthermia Promote oxygenation- O2 Fluid replacement Adequate nutrition Prevent injury Patient and family education
Hyperthyroidism: Nursing Diagnoses
Altered body temperature Ineffective breathing Decreased cardiac output Activity intolerance Imbalanced nutrition Ineffective coping Low self-esteem
Cushing's Syndrome: Clinical Manifestations
Altered fat metabolism ◦Protuding abdomen CLASSIC ◦"Buffalo Hump" APPEARANCE ◦"Moon Face" Protein Catabolism ◦Muscle wasting/Thin extremities ◦Thin, fragile skin ◦Striae - "Stretch marks" ◦Osteoporosis ◦Back Pain ** protruding abdoen and buffalo hump, moon face- classic appearance Retention of Na+ & water- increase in volume Hypertension Heart Failure Increased susceptibility to infection Gastric ulceration Virilization in women: characterized by Appearance of masculine traits Recession of feminine traits Mood swings Increase in fluid volume- increase BP Thin extremities, striae marks, increased bruising, excessive hair growth, more masculine features
Treatment of thyroid storm
Antagonize peripheral effects of thyroid hormone Inderal, beta blocker, or reserpine Inhibit hormone biosynthesis- tapazole Block release- potassium iodide, iodide tablets Secondary options- lopanoic acid, lithium Supportive care- hydrocortisone Decadron, High calorie high protein diet** High protein bc high metabolic state
Thyroid Storm: Treatment Goals
Antagonize peripheral effects of thyroid hormone Inhibit hormone biosynthesis Block thyroid hormone release Supportive Therapy Identify and treat precipitating cause Education
A nurse is caring for a patient with diabetic ketoacidosis. Urinalysis reveals proteinuria. Four days after admission, a repeat urinalysis is also positive proteinuria. Why should this result concern the nurse? A) Proteinuria increases susceptibility to UTIs B) Proteinuria is an early sign of nephropathy C) Proteinuria stores are catabolized in the early stages of DKA D) Proteinuria indicates the need for insulin reduction
B. Damage to glomerulus
DKA & HHS: Assessment
Based on severity of presentation Dehydration and hypovolemia Nausea and vomiting 3 P's - Polyuria Polyphagia Polydipsia Decreased level of consciousness (LOC)
Hypoglycemia
Blood glucose level (<70 mg/dL) Causes include too much insulin or oral hypoglycemic agents, too little food, and excessive physical activity 1st clinical sign - altered mental status* Manifestations Adrenergic symptoms: sweating, tremors, tachycardia, palpitations, nervousness, hunger Central nervous system symptoms: inability to concentrate, headache, confusion, memory lapses, slurred speech, numbness of lips and tongue, irrational or combative behavior, double vision, drowsiness Severe hypoglycemia: may cause disorientation, seizures, and loss of consciousnessv
cushing
C - Central obesity, Cervical fat pads, Collagen fiber weakness, Comedones (acne) U - Urinary free cortisol and glucose increase S - Striae, Suppressed immunity H - Hypercortisolism, Hypertension, Hyperglycemia, Hirsutism I - Iatrogenic (Increased administration of corticosteroids) N - Noniatrogenic (Neoplasms) G - Glucose intolerance, Growth retardation
Syndrome of Inappropriate ADH
Caused by central nervous system disorders such as head injury, infection, hemorrhage, surgery, and stroke that stimulate the hypothalamus or pituitary to produce EXCESS SECRETION OF ADH Inability to secrete dilute urine, have fluid retention, dilutional hyponatremia, Most important treatment is to withhold or restrict fluids*** May give 3% sodium iv, needs to be on a pump, monitor vitals & lung sounds, monitor serum sodium levels ,I&o. not to infuse greater than 50 cc hr. Very concentrated
DKA diagnosis
Clinical presentation is usually quick within 24 hours POLYURIA, POLYDIPSIA, polyphagia, AND WEIGHT LOSS MAY BE PRESENT FOR SEVERAL DAYS BEFORE THE DEVELOPMENT OF KETOACIDOSIS Vomiting and abdominal pain are frequently the presenting symptoms. Keep NPO
Myxedema Coma:Clinical Manifestations
Cognitive changes ◦"Myxedema Madness"- psychosis or hallucinations mixed with delirium Activity intolerance Cardiovascular ◦Bradycardia, hypotension ◦Cardiomegaly ◦Decreased CO ◦ECG changes- bradycardia and heart block, prolonged QT, T wave inversions without s-t changes ◦Edema ◦Shock Gradual progression Can be precipitated by infection, exposure to cold, sedatives, Cold, Tx- warm blankets, warming room, Pulmonary disturbances Hypoventilation CO2 retention Pleural effusion Upper airway and tongue edema Hypothermia Decreased reflexes and slow movements ***no shivering because cannot produce heat Low body- less 90--- increased risk mortality- poor prognosis If above 98.6- suspect infection
Feedback System
Hypothalamus : Pituitary - Increase/decrease secretion of hormone Controlled by feedback loops - Hormone low: stimulus to release more - Hormone high: stimulus to limit release
Myxedema Coma: Diagnostics
Decreased T3 and T4 Decreased T3 resin uptake Elevated TSH (primary) TSH normal or low if problem in hypothalamus or pituitary Hypoglycemia Hyponatremia Hyponatremia bc edema and fluid retention
Acute Adrenal Insufficiency: Interventions
Correct fluid and electrolyte imbalances (D5 normal saline) - prevents hypoglycemia Hormone replacement Hydrocortisone (glucocorticoid & mineralocorticoid properties) Fludrocortisone (mineralocorticoid) Patient and/or family education Hyperkalemia will improve with improvement of IV fluid status
Myxedema Coma: Nursing Diagnoses
Decreased cardiac output (CO) Ineffective breathing pattern Disturbed thought processes Hypothermia Excess fluid volume Risk for injury Activity intolerance Imbalanced nutrition Deficient knowledge
Acute Adrenal Insufficiency Addison's Disease
Two types Both types suppress the secretion of cortisol, aldosterone and androgens Primary: Destruction of adrenal glands (Addison's disease) Secondary: Interferes with secretion Deficiency of glucocorticoids (cortisol) seen in primary & secondary Deficiency of mineralcorticoids (aldosterone) primary only
A patient in the ER is admitted with HHS. What assessment findings should a critical care nurse expect when performing her admission assessment? A) Weakness, tachypnea, and hypertension B) Bradycardia, diaphoresis, and chest pain C) Shallow respirations, flushed skin and edema D) Change in LOC, decrease RR and hypotension
D.
What's an appropriate treatment measure for a patient with Addisonian crisis? A) IV fluid replacement B) IV corticosteroids C) Blood glucose management D) All of the above
D.
A patient is diagnosed with HHS. Which assessment finding is expected with HHS? A) Increase serum ketone level B) Decrease serum sodium level C) Decrease serum creatinine level D) Increase serum hemoglobin levels
D. Hemoconcentrated bc loss of fluid
DKA vs HHS
DKA: Plasma glucose > 250mg/dL (average: 675mg/dL) pH < 7.30 Bicarbonate < 15mEq/L Ketosis High anion gap Kussmaul's respirations Acetone breath Mortality Rate < 5% HHS: Plasma glucose >DKA (usually > 1000mg/dL) More "normal" ABG pH > 7.30 More electrolyte imbalances and renal dysfunction Higher serum osmolarity than DKA Tachycardia Mortality Rate 10-40% HHS longer period of time DKA: metabolic acidosis
DKA vs. HHS (AKA HHNC)
DKA: sustained/ absolute deficiet insulin- fatty acids/ breakdown, decreased pH, ketone formations, kussmaul respiration s HHS: decreased utilization or increased glucose production Both: start with deficiency in insulin, hyperglycemia, and diuresis
Lack of Cortisol
Decreased production of glucose Decreased metabolism of protein and fat Decreased vascular tone Decreased effect of catecholamines Decreased intestinal motility Inability to respond to stress Decreased serum calcium
Acute Adrenal Insufficiency: Nursing Diagnoses
Deficient fluid volume Ineffective tissue perfusion Disturbed thought processes Imbalanced nutrition (less than body requirements) Deficient knowledge Activity intolerance
Cushing's Syndrome: Diagnostics
Dexamethasone Suppression Test- administer 1mg oral in PM and get plasma cortisol level at 8Am Hyperglycemia/?DM Hypernatremia Hypokalemia Decreased eosinophils Loss of lymphoid tissue Plasma and urine cortisol levels ACTH levels 24 hr urine,
Pancreatic Disorders
Diabetic Ketoacidosis (DKA) Hyperglycemic Hyperosmolar State (HHS) Hyperglycemic Hyperosmolar, nonketonic coma (HHNC) More in elderly & Type II diabetes Hypoglycemia
Causes of SIADH
Ectopic causes Lung cancer Prostrate cancer Hodgkin disease CNS causes Head trauma Infections- meningitis, lupus, stroke, Gilliam barre Drugs: Amiodarone, Nicotine, Fentanyl, Morphine, Barbiturates, Cipro, Haldol, more listed in the text
Thyroid Storm: Diagnostics
Elevated T3 and T4 Elevated T3 resin uptake Decreased TSH Due to negative feedback Electrolyte imbalances Sodium & Calcium EKG: A-fib & / or SVT
Introduction
Endocrine system regulates physiologic processes Metabolic processes Energy production Fluid and electrolyte balance Stress reactions Linked closely to nervous and immune system Hypothalamus Conveys information to the pituitary Pituitary Response to hypothalamus Increased or decreased secretion of hormone Controlled by feedback loops Hormone low: stimulus to release more Hormone high: stimulus to limit production
Cushing's Syndrome
Excessive adrenocortical activity Prolonged exposure to elevated levels of either endogenous glucocorticoid or exogenous glucocorticoid Pituitary Tumors Adrenal Tumors Malignancies -> ectopic production of ACTH Long-term use of corticosteroid medications Manifestations of hypercortisolism Adrenal and pituitary hormones increase secretion **long term steroid use- asthma, COPD, immunosuppressants, transplant patients
Treatment Goal
Goal of treatment is to identify and correct underlying cause Restore normal fluid volume and osmolality, and electrolytes Most common drug used in treatment of neurogenic DI is DDAVP ( synthetic analog of vasopressin) When giving DDAVP monitor patient for headache, nausea, hypertension, hyponatremia Vasopressin- does not have vasopressor property
Thyroid Storm: Clinical Manifestations
High fever, heat intolerance, diaphoresis Increased cardiac workload ◦Tachycardia out of proportion to fever ◦Dysrhythmias, especially atrial Increased O2 demands & alterations in respirations Tremors, muscle weakness Fear, delirium, overt psychosis, convulsions, stupor, coma Fatigue Nausea, vomiting, diarrhea, cramps Irritability, restless, diplopia, Risk developing heart failure Bulding eyes- (exothalamus)* orbital edema, eyes can't close properly, need lubrication and tear formation to prevent eye dryness Goider
Causes of Diabetes Insipidus
Idiopathic- familial congenital Intracranial surgery Tumors hypothalamus pituitary Infections Tuberculosis sarcodosi Severe head injury Medications Renal diseases polycystic kidney
Emergency Measures
If the patient cannot swallow or is unconscious: Subcutaneous or intramuscular glucagon 1 mg 25-50 mL 50% dextrose solution IV Need good IV access when giving 50% dextrose bc hard to push
DKA
In both DKA and HHS- high extracellular glucose levels(hyperglycemia) produces an osmotic gradient between the intracellular and extracellular spaces= OSMOTIC DIURESIS As glycosuria and osmotic diuresis progress, urinary losses of water, sodium, potassium, magnesium, calcium ,and phosphorus occur. This osmotic diuresis with the fluid shifts causing worsening dehydration and low sodium levels on admission Large glucose pulls water in- that's why pee so much Hyponatremia- confusion, restless, agitation
Thyroid Storm
Inadequately controlled hyperthyroidism Onset is abrupt evoked by stress Caused by overproduction of t3 t4 Produces a hyperdynamic and hypermetabolic state Affects many major body functions Medical emergency, death within 24- 48 hours without treatment Mortality rate of 10% High BP, high heart rate, diaphoresis, fever, a-fib
DKA & HHS: Nursing Diagnoses
Ineffective breathing pattern Impaired gas exchange Deficient fluid volume Risk for ineffective therapeutic management
Etiology
Infections Severe stress - trauma, surgery, AMI Initial presentation of type 1 DM Missed or reduced insulin Non-adherence to insulin regimen Insulin pump failure Intentional omission Eating disorders Behavioral health issues Medications- Glucocorticoids Mismanagement of sick days Pregnancy in type 1 diabetes mellitus (DM)
HHS cont.
USUALLY SEEN IN UNDIAGNOSED DIABETES ABSENCE OF ABDOMINAL PAIN MORE FOCAL NEUROLOGICAL SIGNS AND SEIZURES ARE CLINICAL PRESENTATIONS MAY ALSO HAVE FEVER AND VOLUME DEPLETION Fever- dehydration, infection, Usually brought on by some type of infection
Acute Adrenal Insufficiency: Diagnostics
Lab Values ◦Hypoglycemia ◦Hyponatremia ◦Hyperkalemia ◦Eosinophilia ◦Increased BUN ◦Metabolic Acidosis ◦Hypercalcemia ◦Hyperuricemia Other symptoms decreased urine output, nausea vague abdominal pain Cosyntropin stimulation test. Give a dose and expect a response in the level of 7-9 mcg/dl from baseline. Those who don't respond are at high risk for increased mortality (diagnose and exclude primary and secondary_ ** solucortex drug of choice Give dose cosyntropin want to see response - don't respond- higher risk increased mortality - blood drawn prior to then draw blood after within an hour
Lack of Aldosterone
Loss of sodium and water Decreased circulating volume Potassium and hydrogen ion retention Seen in primary adrenal insufficiency
DKA & HHS: Interventions
Manage airway Fluid replacement 1st -> 0.9% NS, then 0.45% NS Electrolyte replacement Potassium, phosphorus (K-Phos replacement), magnesium Monitor blood glucose, UO, electrolyte, EKG, Once 200-250- change to fluids with dextrose Monitor potassium- once fluid shifts may create hypokalemia Insulin Therapy Loading dose- 10-15 units IVP Continuous Regular Insulin Infusion Hourly glucose monitoring Decrease rate when glucose approaches 200mg/dL AND Change IV to 5% dextrose with hypotonic saline (D5 0.45% NS) Treatment of Acidosis Assess respiratory compensation and LOC Usually corrected by fluids and insulin Bicarbonate only if pH < 6.9 Patient and family education
Hyperthyroidism:Thyroid Storm
Overproduction of thyroid hormones Affected by anterior pituitary and hypothalamus Positive and negative feedback
Which hormones are regulated by the following endocrine glands?
Pancreas- insulin & glucose Adrenal- medulla (catecholamines- epi, fight/flight), cortex (mineralcorticioids- aldosterone, glucocorticoids, sex hormones) Thyroid- T3, T4 (metabolism, calcitonin) Posterior pituitary- oxytocin and ADH, hemostasis, regulate water, glucose and salt Mineralcorticoids- Glucocorticoids- hydrocrotisone, solumedrol
Hyperglycemic Hyperosmolar State (HHS)
Pathophysiology Decreased use of glucose and/or increased production (gluconeogenesis) Hyperglycemia: increased extracellular osmolality Osmotic diuresis Profound dehydration / no thirst mechanism No ketoacidosis—hyperglycemia with hyperosmolarity blocks lipolysis Non-ketotic state **** NO THIRST increase, NO KETOSIS or ACIDOSIS because blocks breakdown of fats NO KETONES Undiagnosed diabetes, absence abd pain, more focal/ neuro changes-- decreased LOC, confusion, irritable, seizures
Myxedema Coma
Pathophysiology Hypofunction of the thyroid Hypometabolism and hypodynamic state Low and slow
DKA
Pathophysiology Relative or absolute insulin deficiency Increase in counter-regulatory hormones: glucagon, cortisol, catecholamines, and growth hormone Hyperglycemia: an increase in hepatic glucose production and a decrease in peripheral utilization Protein stores depleted by gluconeogenesis in liver Not producing enough insulin or if are produing enough- not being utilized 30-50% DKA caused by infection- UTI, pneumonia, etc. Alcohol or drug abuse, pancreatitis, thiazide, corticosteroids meds --- need to check blood sugar with cortisone and solumedrol ◦ Increase in lipolysis, release of free fatty acids ◦ Increase in ketone production: impaired ketone metabolism ◦ Impaired bicarbonate buffering of excess ketones -> Metabolic Acidosis ◦ Respiratory compensation (Kussmaul's respirations) ◦Osmotic fluid shifts; diuresis- polyuria ◦ Electrolytes vary often hyperkalemia Kussmaul- release ketones, fruity smell breath ◦Altered potassium balance ◦ Excess acids result in increased anion gap (8 - 16mEq/L = norm) (Na+ + K+) - (Cl- + HCO3-) ◦Altered consciousness relates to acidosis and dehydration Patients can lose up to 6 Liters of body water Don't need to know formula. ' Every tenth increase pH- potassium goes up by 6/10ths ***acidosis, dehydration, hyperglycemia
Myxedema Coma: Etiology
Primary Disease Hashimoto's Disease (autoimmune) Surgical or radioactive treatment for Graves' disease with inadequate follow-up Insufficient thyroid stimulation due to hypothalamus or pituitary disease Exacerbation of hypothyroid state
Causes of Adrenal Insufficiency
Primary: Autoimmune: idiopathic and polyglandular TB, Sarcoid Cancer Hemorrhagic destruction, trauma, sepsis Infectious: meningococcal staphylococcal TB AIDS Drugs: ketoconazole, phenytoin, barbiturates rifampin Irradiation Adrenalectomy Developmental or genetic abnormality Secondary Abrupt withdrawal of corticosteroids Pathology affecting the pituitary such as tumors, hemorrhage, radiation, cancers Systemic inflammatory states: sepsis, vasculitis sickle cell Postpartum pituitary hemorrhage Trauma especially head trauma or surgery Inadequate steroids in a highly stressed patient who has received chronic steroid therapy Hypothalamic disorders Taper solumedtol (methylprednisolone) Steroids- monitor blood sugars - Most common cause of acute adrenal insufficiency is the abrupt withdrawal of corticosteroid therapy Infection, sepsis, are both the most common causes of adrenal insufficiency in the critical care setting
Hyperglycemic Crises
Reduction in circulating insulin with elevation of counter-regulatory hormones Glucagon, catecholamines, cortisol & growth hormone elevated Occurrence DKA: Type 1 diabetes, Type II on Insulin HHS: Type 2 diabetes, elderly Relative insulin deficiency/ resistance, some drugs (thiazides in beta blockers) Gluconeogenesis and insulin resistance
Thyroid Hormone Effects
Regulates protein synthesis Regulates body heat production Increase gluconeogenesis and utilization of glucose Maintain appetite and GI motility Maintain calcium metabolism Maintain cardiac rate, contractility, and output Affect respiratory rate, oxygen utilization and carbon dioxide formation Affect RBC production Affect central nervous system Produce muscle tone and vigor
Other effects
Regulates protein synthesis Regulates body heat production Increase gluconeogenesis and utilization of glucose Maintain appetite and GI motility Maintain calcium metabolism Maintain cardiac rate, contractility, and output Affect respiratory rate, oxygen utilization and carbon dioxide formation Affect RBC production Affect central nervous system Produce muscle tone and vigor
Cushing's Syndrome: Nursing Diagnoses
Risk of injury* Risk of infection* Self-care deficit Impaired skin integrity Disturbed body image Disturbed thought processes Low salt, high protein, high calorie diet, no fresh fruit or veggies, high card, high potassium
Myxedema Coma:Collaborative Management
Treat with replacement drugs T4 - Synthroid T3 - Cytomel Combination of T3 + T4 Fluid and electrolyte replacement Thyroid replacement usually corrects Na+ Monitor respiratory status and gas exchange Warming devices, maintain thyroid replacement, If comatose and cant protect airway- may need mechanical ventilation Monitor cardiovascular status Manage hypothermia Protect from injury and infection Patient and family education Bradycardia and heart block Sedatives contraindicated bc slow metabolic rate Monitor blood glucose Need good skin care
Cushing's Syndrome Management
Surgery: Trans-sphenoidal Hypophysectomy, Adrenalectomy Irradiation Adrenal Enzyme Inhibitors Reduction or tapering of corticosteroid medications
Acute Adrenal Insufficiency: Assessment
Symptoms of hypovolemia Fluid and electrolyte imbalances ◦Postural hypotension ◦Change in LOC ◦Hyperkalemia Profound Fatigue/Weakness/headache GI complaints - abdominal pain, N/V/D Decreased renal perfusion & urine output Circulatory Shock -> Death in Addisonian Crisis Hypotension--- decreased renal perfusion & decrease UO ** most serious complication addisons disease - loss sodium and water, Potassium retention- increase risk heart probs
Thyroid Hormones
T3 (triiodothyronine) T4 (thyroxine) TSH ( thyroid stimulating hormone) Effects of the thyroid hormone: Major effects: increase metabolic activities of all tissues Increase rate of nutrient use/oxygen consumption in ATP production Increase rate of growth Increase activities of other endocrine glands
DKA Lab Values and Treatments
The triad of lab findings for DKA: Hyperglycemia Hyperketonemia Metabolic acidosis TREATMENTS: IV FLUIDS (for rehydration) 250-300ml/hr INSULIN (continuous infusion) -follow labs POTASSIUM AND ASSESS FOR BICARB *** don't use insulin drip protocol--- go by labs not titrating to blood sugar Once blood sugar down to 250- may change iv fluids to something that contains dextrose because need to provide some form sugar - may be able to start to feed patient Don't treat potassium until see glucose come down to normal
Hyperthyroidism: Etiology
Toxic diffuse goiter: Most common cause Graves' Disease (autoimmune) Toxic multi-nodular goiter Heart failure or severe muscle weakness Amniodorone - contains a lot of iodine Can cause a-fib
Management of Hypoglycemia
Treatment must be immediate Give 15 g of fast-acting, concentrated carbohydrate 3 or 4 glucose tablets 4-6 ounces of juice or regular soda (not diet soda) 6-10 hard candies 2-3 teaspoons of honey Retest blood glucose in 15 minutes, retreat if <70 mg/dL or if symptoms persist more than 10-15 minutes and testing is not possible. Provide a snack with protein and carbohydrate unless the patient plans to eat a meal within 30-60 minutes.
Diabetes Insipidus
Various disorders cause it but the primary cause is traumatic injury to posterior pituitary or hypothalamus* Clinical presentation is abrupt onset of POLYURIA WITH LITERS IN 24 HOURS- In conscious patients they become thirsty and dry to replace the fluids, in unconsous patients don't have the thirst mechanism Hypovolemia, dry skin poor turgor weight loss, tachycardia Monitor hypovolemia Polyuria and polydipsia I&Os Hypernatremia
A patient is diagnosed with adrenal crisis, a life- threatening deficiency of mineralocorticoid and glucocorticoid hormones. The nurse should monitor the patient for which electrolyte imbalance that is common with this condition? A) Hyponatremia B) Hyperglycemia C) Hypernatremia D) Hypokalemia
a
A patient is admitted to ICU in thyrotoxic crisis. Which findings indicated that the patient is improving? A) Respiratory rate increases B) Heart rate decreases C) Serum glucose levels increase D) Body temperature increases
b
A patient is experiencing thyroid storm. Which drug is contraindicated? A) IV beta-adrenergic blockers B) Aspirin C) Proplythiouracil (PTU) D) Corticosteroids
b
A patient with a history of hypothyroidism is admitted to the ER stuporous, hypotensive, and hypothermic. Admission labs show serum glucose level of 67 mg/dl and serum sodium levels of 12 mEq/l. Myxedema coma is diagnosed. Which finding indicates that treatment for myxedema coma is effective? A) Worsening cerebral hypoxia B) Increase in body temperature C) Decrease in heart rate D) Increase partial pressure of arterial carbon dioxide (PaCO2)
b
The nurse is completing a health history of a 42-year-old female with suspected Graves' disease. The nurse should assess this client for : A) Anorexia B) Tachycardia C) Weight gain D) Cold skin
b
The nurse should monitor the patient with Cushing's disease for which of the following? A) Postprandial hypoglycemia B) Hypokalemia. C) Hyponatremia D) Decreased urine calcium level
b
A patient with DKA is receiving normal saline solution for hydration and an infusion of regular insulin at 8units/hour. His serum potassium level is 6 mEq/l. A physician prescribes a sodium polystyrene sulfonate (Kayexalate) enema. The patient should: A) Receive calcium to protect his heart from negative effects of hyperkalemia B) Receive the enema to lower his potassium level because hyperkalemia can lead to cardiac dysfunction C) Not receive the enema because as acidosis and dehydration are corrected potassium will shift intra-cellulary D) Receive the enema because as acidosis and dehydration are corrected potassium will shift out of the cell and hyperkalemia will worsen.
c
After thyroid surgery for Graves' disease a patient develops rapid atrial fibrillation, tremors, palpitations, dyspnea, and anxiety. Which complications is the patient most likely experiencing? A) Hypocalcemic crisis B) Addisonian crisis C) Thyroid Storm D) Cushing syndrome
c
You are the nurse discharging an 82-y-old male after having a cardiac angioplasty for coronary artery disease. The patient is a non-insulin dependent taking glyburide, metformin, and jardience at home. As the nurse discharging the patient what are two important issues to discuss? A) Check your blood sugars three times a day B) Take all your medications as prescribed in the morning and only your statin at night C) Monitor your blood sugar closely while taking your new medication metoprolol and eat regular meals and a snack.
c. Patients taking beta blockers are at a risk of decreased awareness of hypoglycemia because of the sympathetic nervous system
A patient is admitted with hypotension, dehydration, disorientation, and hyperpigmentation. Which medication will most likely reverse this patients' symptoms? A) Parathormone B) Liothyronine (Cytomel) C) Prednisolone (Prelone) D) Vasopressin (Pitressin)
c. steroids- prevent fluid and electrolyte loss- maintains BP
A patient with type 1 Diabetes arrives in the ER with serum glucose level of 472 mg/dl. His ABG reveal pH 7.14, PaO2 90mm hg, PaCO2 35, HCO3- 18 mEq/l. These values suggest: A) Compensated Respiratory Alkalosis B) Respiratory Acidosis C) Compensated Metabolic Alkalosis D) Metabolic Acidosis
d
HHS etiology
◦Inadequate insulin secretion; usually with type 2 DM ◦Often in geriatric patients with decreased compensatory mechanisms ◦Stress response ◦Medications: Steroids (esp. glucocorticoids) Sympathomimetics Beta Blockers Analgesics Thiazide Diuretics Cimetidine (antacids) Calcium Channel Blockers Immunosuppressants Phenytoin Diazoxide Epinephrine Chemotherapeutic Agents Psychotropics (TCAs)Illicit Drugs (Cocaine, Ecstasy) Over longer period of time- higher blood sugars
