Endo Flashcards
Communication between body systems occurs by what system?
_____ ______ of chemicals that are released into the ______ _______
- IE Inflammatory response with ________, _______ and _________
Cellular secretion of chemicals that are circulated through the blood stream
- _________ secretion (stimulate)
- _______ and _______ by specialized cells and released into blood vessels to exert _________ effects on target cells distant from the site of origin (needs to bind on target)
Nervous system
Cellular secretion of chemicals that are released into the interstitial fluid
- IE Inflammatory response with histamine, complement and prostaglandins
Cellular secretion of chemicals that are circulated through the blood stream
- Hormonal secretion (stimulate)
- Synthesized and secreted by specialized cells and released into blood vessels to exert biochemical effects on target cells distant from the site of origin (needs to bind on target)
Organs of the Endocrine System (9)
Pituitary Gland: where we store most of our hormones, hypothalamus – production of said hormones, sends to PTG
Pineal Gland
Thyroid Gland
Parathyroid Glands: can see problems in adrenal glands (can see problems with adjacent glands if one isn’t working), regulates calcium
Adrenal Glands: mostly regulates stress
Islet Cells of Pancreas
Testes
Ovaries
Gastrointesinal Tract: new weightloss medications target these hormones (GLP-1 inhibitors)
- Gastrin, motilin, incretin
Neuroendocrine Response to Critical Illness
Severe illness and stress activate hypothalamic-pituitary-adrenal (HPA) axis, resulting in release of Cortisol (stress hormones) from adrenal cortex (fight/flight)
Acute neuroendocrine response to critical illness: Hypothalamic-pituitary-adrenal axis in acute stress (T6 – direct innervation of adrenal glands)
what is released from medulla of adrenal glands?
what occurs in the posterior and anterior pituitary gland?
what occurs with the release of cortisol (4)
what is the role of aldosterone?
Epinephrine released from medulla of adrenal glands (direct innervation of T6 spinal column)
Pituitary gland:
— Posterior:
* Release of Antidiuretic hormone (ADH) vasopressin -> Increase in blood pressure
— Anterior
* Growth hormone/androgens (reticularis)
* Corticotropin -> stimulates release of cortisol + aldosterone
Cortisol (glucocorticoid)
- increases glucose levels
- increase BP by sensitizing norepinephrine binding sites
- suppresses immune system (prolonged cortisol release causes reduction in immune cells)
- increases osteoclastic activity (bone break down to increase calcium in the blood, leading to osteopenia/osteoporosis)
Aldosterone (mineralocorticoids) ->
- causes kidneys to resorb Na and H2O to raise BP
Acute neuroendocrine response to critical illness: Liver and pancreas in acute stress
Glucagon -> glycogen -> gluconeogenesis and increased blood glucose (fight/flight response)
Acute neuroendocrine response to critical illness: Thyroid gland in acute stress
Increased levels of T3 and T4
Prolonged neuroendocrine response to critical illness
Hypothalamic-pituitary-adrenal axis in prolonged stress?
Liver and pancreas in prolonged stress?
Thyroid gland in prolonged stress?
Gonads in prolonged stress?
Hypothalamic-pituitary-adrenal axis in prolonged stress
- Production of hormones lessened
Liver and pancreas in prolonged stress
- Gluconeogenesis (high levels of glucose)
- Results in elevated serum glucose levels in patients without diabetes
Thyroid gland in prolonged stress
- Normal TSH responses flattened
Gonads in prolonged stress
- Hypogonadism develops
TIP: hormones are NOT as robust
Adrenal dysfunction in critical illness: Causes (5)
1) Primary hypoadrenalism (Addison’s disease) – aldosterone insufficiency (quite rare, BRONZE TONE TO SKIN, harder to identify with darker skin)
2) Secondary hypoadrenalism (from the pituitary gland) – stops releasing hormones from glands
3) Critical illness - related corticosteroid insufficiency** (most common)
- Failed adrenal glands -> Result in drop of BP (looks similar to septic shock, benefit from steroids)
4) Peripheral cortisol resistance
5) Corticosteroid replacement (ex. Asthmatic taking prednisone) for other conditions followed by abrupt D/C -> want to taper doses done, abrupt disruption can lead to vascular collapse
Assessment of adrenal function
Cosyntropin stimulation test (draw baseline adrenal hormone level, give cosyntropin, draw 2 more panels to assess for increase in adrenal function -> if not, desired effect NOT reached)
Hyperglycemia in critical illness
1) Guidelines related to blood glucose management in critically ill patients: (2)
2) Hyperglycemia and the cardiovascular system: (1)
3) 3) Hyperglycemia and brain injury: (2)
1) Guidelines related to blood glucose management in critically ill patients:
- a) Intensive Insulin therapy (aka tight glycemic control) has been found to be beneficial in patients undergoing Coronary Artery Bypass surgery, but goal glucose levels <100 have lead to hypoglycemia (cardiac patients want lower BG)
- b) Patients with other conditions increased mortality due hypoglycemia
2) Hyperglycemia and the cardiovascular system:
a) Elevated serum glucose levels that remain persistent can worsen HF symptoms
3) Hyperglycemia and brain injury:
a) Hyperglycemia can cause cerebral dehydration due to osmotic diuresis
b) Avoid hypoglycemia -> can have negative effects on brain
TIP: any shock patient -> worsening outcomes d/t hypoglycemia
Insulin management in the critically ill (5)
1) Tight glucose control
- Controversial due to risk of hypoglycemia
2) Frequent blood glucose checks
- Need every 1-2 hours for IV infusion
- Should be done 4-5 times daily (Q6 at least)
3) Continuous insulin infusion
4) Transition from continuous to intermittent insulin coverage (via IV)
- Combination of Long Acting and short acting is necessary.
- Regular insulin –> half life is 15 minutes, metabolized out quickly, can become acidotic if not transitioned correctly
5) Intermittent insulin coverage
- Insulin sliding scales for rapid acting insulin
Hypoglycemia management
protocols?
rule of ?
Follow protocols:
- D50 (25g sugar into veins)
- Glucose tablets (can take PO or alert)
- Orange Juice
Rule of 15’s
- 15 grams of rapid acting carbohydrate, wait - 15 minutes and check blood glucose. If still low, repeat
Neuroendocrine Response to Critical Illness: Nursing management
monitor _____ side effects of ____ therapy
administer?
monitor ______ ______ and insulin effectiveness
provide?
maintain surveillance for?
patient and family education about effects of disease and glycemia control
Monitor glycemic side effects of vasopressor therapy (if on max dose of 1 vasopressor – make sure to get venous sample because finger stick will NOT be accurate)
Administer prescribed corticosteroids (will cause hyperglycemia)
Monitor blood glucose and insulin effectiveness (need to address hyperglycemia)
Provide nutrition
Maintain surveillance for complications
Patient and family education (about effects of disease and glycemia control)
Diabetes Mellitus
what?
what is associated with DM
diagnosis of DM (4)
1) carbohydrate intolerance and insulin dysregulation
2) Morbidity and mortality associated with DM
3) Diagnosis of diabetes
- A1C > 6.5% or <7% for diabetics
- Fasting plasma glucose = 126 mg/dL or
- Two-hour plasma glucose level 200 mg/dL or more during an oral GTT. or
- Patients with classic symptoms of hyperglycemia or hyperglycemic crisis, random plasma glucose level of 200 ml/dL or more (suggestive of diabetes)
Types of diabetes (2) - explain pathophysiology
Type 1: beta-cell destruction, usually leading to absolute insulin deficiency (need insulin to live)
Type 2: progressive insulin secretory defect in addition to insulin resistance (don’t produce enough insulin or insulin resistance)
Other types have been identified
Glycated hemoglobin (HgB A1C numbers for diabetic, pregnant, ad older)
Diabetic target: less than 7%
Pregnant: <6.5%
Older: <8%
Type 1 diabetes (5% to 10%)
what?
_______ disease
first manifestation of disease for children and adolescents
mgmt?
what is required to keep t1dm alive?
2 types of insulin required? what is the indication
1) B cells no longer secrete insulin
2) Autoimmune disease (body is attacking beta cells, causing no secretion of insulin)
3) Diabetic ketoacidosis (DKA) may be first manifestation of disease for children and adolescents
4) Management of type 1 diabetes
- IV (initial) or subcutaneous insulin (transitioned)
5) Insulin is required to keep T1DM patients alive. They require:
a) Basal (continuously acting insulin) to control glucose levels that would otherwise increase secondary to glycogenolysis (release of glycogen) by the liver (liver is always secreting blood glucose, basal insulin acts in the opposite)
—-Insulin pump basal rates (inject continuously, 24/7 once programed) (rapid acting insulin), long acting insulin (Lantus, Levemir)
b) Bolus (single doses) to control carbohydrate intake and subsequent glucose release into the bloodstream
—-Insulin pump bolus (Programmed by user before meals), novolog/humalog injections in non pump users (take a dose before meals)
Type 2 diabetes (90% to 95%)
patient population mostly?
assocaited with?
what is it?
1) Majority of patients are adults, but with increasing child obesity we are seeing increase incident in children
2) Associated with metabolic syndrome
3) Imbalance between insulin production and use
- Inadequate insulin response versus insulin resistance syndrome or combination of both
tip:
Insulin pump: can augment basal rate (best type of therapy for T1DM)
Lantus: “lasts” 24H – takes a while to build therapeutic level
NPH: peak 30 minutes – 2 hours, cheapest insulin on the market
Diabetic Ketoacidosis: epidemiology and etiology
what?
typically effects who?
what kind of deficiency?
manifests with 3?
elevation of? (4)
1) Life-threatening complication of DM
2) Typically affects patients with type 1 diabetes, but can affect patients with type 2 diabetes (rare).
3) Absolute Insulin deficiency
4) Manifests with severe hyperglycemia (not as high as HHS), metabolic acidosis & fluid and electrolyte imbalances (peeing all of the volume out to get rid of solute, leading to a waste in fluid and electrolytes)
5) Elevation of counter-regulatory hormones (stimulate SNS)
- GH, cortisol, epinephrine and glucagon
tip:
High BG -> Insulin is no longer in our body, cells can’t get glucose and undergo anaerobic metabolism -> metabolic acidosis and ketones in the urine
Diabetic Ketoacidosis: Pathophysiology (5)
1) Insulin deficiency
- Leads to disordered metabolism of proteins, carbohydrates and fats
- Concomitant elevation of counter-regulatory hormones such as growth hormone, Cortisol, epinephrine and glucagon exacerbates the condition of elevated glucose levels
2) Hyperglycemia
3) Fluid volume deficit
- hypovolemia
4) Ketoacidosis
5) Acid-base balance
Diabetic Ketoacidosis: Diagnostic criteria for diabetic ketoacidosis (DKA) (6)
Blood glucose < 500 mg/dL
Metabolic Acidosis from accumulation of ketoacids- pH below 7.3
Serum bicarbonate below 15 mEq/L (buffered by low pH)
Moderate or severe ketonemia or ketonuria (blood and urine)
Hyperosmolality from hyperglycemia and dehydration
Volume depletion from osmotic diuresis
Diabetic Ketoacidosis: causes (9)
Infection
Inadequate Insulin therapy (most common cause)
Severe illness (CVA, MI, pancreatitis)
Alcohol abuse
Trauma
Drugs
Sudden discontinuation of insulin
- Underserved patients
- Pump failure
- Rapid acting only has a duration of 4 hours, can go into DKA if pump isn’t fixed
Present in DKA with initial diagnosis DM Type 1 (due to lack of knowledge about need to take insulin)
Some Type 2 Diabetics can develop in catabolic stress associated with severe critical illness
Diabetic Ketoacidosis: Assessment and diagnosis - clinical manifestations
tip: 3 P’s, respiratory/cardiac issues (3)
other signs of hyperglycemia
Malaise
Headache
*Polyuria (peeing a lot)
*Polydipsia (drinking a lot)
*Polyphagia (eating a lot r/t treatment of hyperglycemia)
Nausea and vomiting
Extreme fatigue
Dehydration
Weight loss (overtime)
Central nervous system depression and decreased level of consciousness, stupor
Coma
Dehydration
Flushed, dry skin
Tachycardia
* Hypotension (esp. in older population)
* Kussmaul respirations (rapid breathing patterns to get rid of CO2)
* Fruity odor of acetone
Diabetic Ketoacidosis: Laboratory studies (4)
Bedside finger stick – only good until 500-600 mg/dL (if high, repeat, and if high again, send to PCP)
Arterial blood gases
Chemistry panel (electrolytes – K+)
- Anion gap (surrogate for acidosis)
Urine analysis for ketones
DKA lab values (6)
Anion Gap: 20+ (normal: <14)
Elevated Glucose
Ketones in blood and urine
Hypercholesterolemia may be present
Hypertriglyceridemia may be present
Hyperamylasemia (amylase) may be present
DKA treatment (3)
what is the most acute and critical problem? how do you fix it?
administer what medication and what are the parameters?
monitor what else?
1) Hypovolemia most acute and critical problem
- Replace fluids with 0.9NS (4-8L deficit depending on hydration state)
- As soon as serum BS drops to 200 change fluid to D5/.45NS to prevent cerebral edema and hypoglycemia at 150-250 ml/hr (Expect 4-8L in first 24 hours)
2) Administer IV KCL 20-30meq/liter of fluid in first 2-3 hours of therapy unless potassium levels exceed 5.0mEq/L (Maintain K+ between 4-5 mEq/L (will cause an intracellular shift, causing decrease, If K+ is < 3.3, hold insulin and give KCL until K>3.3)
3) Monitor other electrolytes
tip:
problems - hyperglycemia, acidosis, dehydration
Insulin Therapy (4)
1) Start initial IVP of 0.1unit/kg of REGULAR INSULIN (Ie. 100kg patient would get 10U IVP (weight based))
2) Then IV infusion 0.1-0.2 units/kg/hr (Ie. 10U/hr. (regular insulin))
3) Expected BS drop of 50-75dL/hr, expect drop of 10%
- When plasma glucose <200-250 mg/dL, decrease infusion to decrease insulin until DKA Resolves
- *Alternatively, a long acting insulin will allow the drip to come off
4) Q1 hr BS monitoring
tip:
- While BG is coming down, it’s also getting rid of the anaerobic metabolism
- Give insulin to get rid of hyperglycemia and acidosis, and continue to even if BG is okay
DKA treatment: too low pH (1)
1) NaHCO3: replacement rarely needed and may be used if pH <6.9, but stop once pH reaches > 7.0
- Most often ordered as a bicarbonate drip as opposed to IVP
- Treat myocardial death
DKA treatment: Transfer to from IV to SQ (2)
1) Continue IV insulin infusion for 1-2 hr after SC insulin begun to ensure adequate plasma insulin levels.
- If Long acting insulin is given during the acute phase (shot), no need to maintain insulin drip if blood sugar and acidosis is corrected
- Eliminates risk of anaerobic metabolism
2) Look for precipitating causes for elevated
- infection, trauma, inflammatory process
Diabetic Ketoacidosis: Medical management
goals (4)
Reverse dehydration
Replace insulin
Reverse keto-acidosis
Replenish electrolytes (specifically potassium)
Diabetic Ketoacidosis: Nursing management (4)
1) Administer fluids, insulin, and electrolytes
2) Monitor response to therapy
3) Surveillance for complications
- Fluid overload
- Hypoglycemia
- Hypokalemia/hyperkalemia
- Hyponatremia
- Risk for cerebral edema** (be slow with fluids)
- Risk for infection
4) Patient and family education
Hyperglycemic Hyperosmolar State (HHS): Epidemiology and etiology
complication of which DM
hallmarks? (2)
1) Potentially lethal complication of type 2 DM
2) Hallmarks:
- Extremely high levels of plasma glucose
- Elevation in hyperosmolarity causing osmotic diuresis
Hyperglycemic Hyperosmolar State: Differences between hyperglycemic hyperosmolar state (HHS) and DKA (5)
what occurs in HHS that doesn’t occur in DKA
1) Extremely elevated serum glucose levels 600+
- Higher mortality than DKA (acute process), HHS is a more chronic process
2) More profound dehydration (high solutes)
3) Minimal or absent ketosis
4) Proteins and fats are not used for glucose
5) HHS does not develop in patients with type 1 diabetes
Hyperglycemic Hyperosmolar State: Pathophysiology (3)
1) Deficit of insulin (not absolute)
2) Excess of glucagon release
3) Results in
- Hemo-concentration
- Hypovolemia
- Dehydration
- Risk for Thromboemboli
Hyperglycemic Hyperosmolar State: Incidence/predisposing factors (2)
Recent onset of T2 diabetes
Receiving TPN or high-caloric feedings
Hyperglycemic Hyperosmolar State: causes (5)
1) Thiazide diuretics, steroids, hypertonic solution
2) Illness (ex. Septic), trauma, or stress
3) Diet-controlled diabetes (progressive)
4) Pancreatitis
5) Increased incidence in diabetic patients of advanced age
Hyperglycemic Hyperosmolar State: Assessment and diagnosis, Clinical manifestations
a) ____,_____ onset
b) intiial symptoms are nonspecific: (3)
c) ____ _____ findings
d) very elevated ____ ____
a) Slow, subtle onset
b) Initial symptoms are nonspecific:
- Marked fatigue/malaise
- confusion
- s/sx dehydration
Physical examination findings
Very elevated glucose levels (>1000)
Hyperglycemic Hyperosmolar State: Laboratory studies (7)
Blood glucose level greater than _____ mg/dL
Serum osmolality greater than ________ mOsm/kg
________ usually absent
Elevated ________ level
Decreased ____ and ____ levels
Increase _____/____ ratio (suggestive of pre-renal failure)
Absent ______
Blood glucose level greater than 600 mg/dL
Serum osmolality greater than 320 mOsm/kg
Acidosis usually absent
Elevated hematocrit level
Decreased potassium and phosphorus levels
Increase blood urea nitrogen/creatinine ratio (suggestive of pre-renal failure)
Absent ketones
Hyperglycemic Hyperosmolar State: Medical management (2)
Rehydration
Insulin administration to facilitate the cellular use of glucose
Hyperglycemic Hyperosmolar State: Insulin treatment usually less then DKA (3)
Initial bolus of 0.1-0.15 units/kg IV followed by 1-2 units/hours titrated until BG levels are acceptable OR
0.1 units/kg per hour to achieve a decrease of serum glucose of 50-75 mg/dl per hour
Electrolyte replacement
tip: anaerobic metabolism (DKA) requires more insulin treatment
HHNK Treatment (2)
Critical care monitoring is indicated. Consider CVP or PA catheter depending on patients pulmonary and cardiac status
Replacement of fluids depends on degree of dehydration, age and CVS.
Hyperglycemic Hyperosmolar State: Nursing management (6)
Administration of fluids, insulin, and electrolytes
Monitor response to therapy
Surveillance for complications
Monitor for signs of infection
Patient education
Collaborative management
Anticoagulation for DKA/HHS (3)
1) Increase risk for thrombosis (HUGE RISK)
- Prophylactic heparin administration should be considered unless contraindicated.
- At risk for DIC
Diabetes Insipidus (3)
1) Insufficiency or hypofunction of antidiuretic hormone (ADH)- made in the hypothalamus, stored and released from pituitary
2) ADH stimulates kidney tubules to be permeable to water so that water is reabsorbed back into the bloodstream
3) Inadequate ADH means that large quantities of dilute urine are passed
tip: may be easier to call ADH -> vasopressin (maintain good normal BP, not wasting fluid)
Diabetes Insipidus: 3 types (3)
Three types
1) Central DI – pituitary issue
2) Nephrogenic DI. - loss via kidneys (not responding to adh/vasopressin)
3) Psychogenic DI. -excessive drinking causing excessive urination (bipolar, schizophrenia)
Diabetes Insipidus: pathophysiology (3)
1) _____ _____ excreted in urine
2) Extracellular dehydration (3)
3) ________ – with NO ____ in urine (dilute)
- Serum ________ (unless it is psychogenic- then you’ll see ____natremia) when drawing blood
1) Free water excreted in urine
2) Extracellular dehydration
- Hypotension
- Hypovolemic shock
- Decreased cerebral perfusion (mental status changes)
3) Polyuria – with NO sodium in urine (dilute)
- Serum Hypernatremia (unless it is psychogenic- then you’ll see hyponatremia) when drawing blood
Diabetes Insipidus: clinical manifestations (2)
Dramatic increase in dilute urine output
Absence of diuretics, fluid challenge, or hyperglycemia
Diabetes Insipidus: Laboratory studies (4)
Serum sodium level greater than 145 mEq/L. (Unless psychogenic -> hyponatremia)
Serum osmolality greater than 295 mOsm/kg water
Urine osmolality less than 300 mOsm/kg water (very dilute urine)
Measurement of ADH (central or nephrogenic issue)
Diabetes Insipidus: medical mgmt (2)
1) ______ restoration
2) medications:
- central DI: ?
- nephrogenic DI: ?
1) Volume restoration
2) Medications
a) Medications used for central DI
- Vasopressin (Pitressin) (replace what we’re not getting)
b) Medications used for nephrogenic DI (have ADH, but kidneys aren’t responding to it)
- Hydrochlorothiazide (diuretic)
Diabetes Insipidus: nursing mgmt (5)
Administration of fluids and medications
Evaluation of response to therapy
Surveillance for complications
Patient education
Collaborative management (hard to track down so work with nephron and endo)
Syndrome of Inappropriate Secretion of Antidiuretic Hormone (SIADH) (4)
Opposite of DI
Excess Anti-Diuretic Hormone (ADH) (too much ADH)
Kidneys reabsorb too much water
Dilutional hyponatremia (drop Na)
SIADH: etiology (4)
1) Head or central nervous system injury
- Trauma, anoxia (post arrest)
2) Malignancy
3) Other conditions
4) Positive end-expiratory pressure (PEEP) with mechanical ventilation
- Will give body a false sense of low volume.
-> body will create ADH (vasopressin)
tip:
High peep causes hypotension (increased intrathoracic pressure in lungs will compress IVC and decrease blood return to heart, decreasing CO and BP)
SIADH: Pathophysiology (3)
1) ADH released by posterior pituitary gland
2) ADH regulates water and electrolyte balance
3) Excessive ADH
- Over-hydration
- Low sodium (dilutional)
- Concentrated urine (super concentrated)
SIADH: Clinical manifestations (5)
tip: CLAMS
- Clinical presentation in SIADH relates to water and sodium imbalance
- Lethargy
- Anorexia
- Mental confusion
- Seizures, coma, death
SIADH: Laboratory values (2 (2/3))
1) Serum laboratory values
- Serum osmolality low
- Serum sodium low
2) Urine laboratory values (high – super concentrated)
- Urine osmolality
- Urine sodium
- Urine specific gravity
SIADH: Medical management (3)
Fluid restriction
Sodium replacement – only when it gets critically low
Medications
- Stop drugs that may cause SIADH
- Medications that increase renal water excretion
- Demeclocycline
- Vasopressin receptor antagonists: Conivaptin (chronically low sodium)
Goal of treatment (2)
1) Reasonable correction parameters consist of a maximal rate of correction of serum sodium in the range of 1–2mEq/L per h as long as the total magnitude of correction does not exceed 25 mEq/L over the first 48 h.
- (a) the patient‘s symptoms are abolished,
- (b) a safe serum sodium (generally 120 mEq/L) is achieved, or
- (c) a total magnitude of correction of 20 mEq/L is achieved
2) Replacement rates beyond the recommendations result in “osmotic demyelination” (Central Pontine Myelinolysis- CPM) resulting in spastic quadriplegia (permanent, locked in syndrome) and delirium
tip:
Too fast of replacement – can demyelinate (strips myelin sheath, leading to locked in syndrome) and cause CPM
SIADH: nursing mgmt (4)
Restriction of fluids
Surveillance for complications
Patient education
Collaborative management
Conditions Associate With Hyperthyroidism (3)
1) Endocrine Disorders
- Graves disease
- Nodular goiter
- Toxic multinodular adenoma
- Radiation-induced thyroiditis
- Sub-acute thyroiditis
2) Drugs
- Iatrogenic thyroid replacement
- Accidental or purposeful ingestion of thyroid medication
- Contrast media dye
- Amiodarone
- B-Blockers
3) Tumors
- Metastatic thyroid cancer
- Hypophyseal tumors
- Hypothalamus tumor
- Hydatidiform mole
Thyroid Storm: etiology (3)
Excessive uptake of thyroid hormone
Increased metabolic activity
Sympathetic nervous system response
tip:
sympathetic stressor causes increased uptake thyroid hormone
Risk Factors for Development of Thyroid Crisis
in the presence of pre-existing conditions (3)
precipitating factors (6)
1) In the Presence of a Known Preexisting Condition
- Hx of graves disease
- Hx of nodular Goiter
- Thyroid adenoma
Precipitating factors
- Infection
- Trauma
- Stress
- Coexistent medical illness (MI, Pulmonary disease)
- Pregnancy
- Exposure to cold
hyperthyroidism -> thyroid storm
Thyroid Storm: pathophysiology (sympathetic overload) (3)
1) Increased metabolic rate
- Febrile, Diaphoretic, agitated, nervous, tremulous, abdominal cramping/pain/weight loss
- Tachycardia, high blood pressure (Wide pulse pressure), fever, agitation –> delirium
2) Increased cellular oxygen consumption
- Metabolic acidosis
3) Hypersensitivity to increased adrenergic-binding sites
Thyroid Storm: Assessment and diagnosis
1) combination of ___ and _____ critical manifestations
2) laboratory findings: (4)
3) diagnostic tests (3)
1) Combination of PMH and current clinical manifestations
2) Laboratory findings
- The TSH level will be LOW due to feedback system being altered by the high amount of hormone in the system. (too much thyroid hormone in our body)
- Total T4, free T3 & free T 4 elevated
- Serum calcium levels are decreased if calcitonin release is suppressing osteoclastic activity
- Hyperglycemia from insulin resistant.
3) Diagnostic tests: Radioactive iodine uptake test, ECG, TMS
Thyroid Storm: Medical management goal (4)
1-Treat precipitating factor or factors (treat septicemia)
2-Block excessive thyroid hormone release
3-Block the conversion of T4 into T3 (peripheral conversion)
4-Block the peripheral (Sympathetic) effects of thyroid hormone
Thyroid Storm: medication (4)
- Thionamide’s – Block production/Release of T4, prevent peripheral conversion T4-T3
- PTU (Propylthiouracil)
- MMI (Methimazole)
- T3 more potent in the body than t4, so want to prevent conversion - Iodine – must be given 1 hr. AFTER administration of thionamides to prevent peripheral conversion
- Potassium Iodide
- Lugol’s solution
- Lithium Carbonate
- Given too soon: Can exacerbate production of t4 - B-Blockers – Blocks sympathetic effects of thyroid storm
- Propanolol/Esmolol
- Lopressor to block tachycardia/HTN - Steroids – Blocks peripheral conversion of T4/T3
- Hydrocortisone
Thyroid Storm: Nursing management (6)
1) Hyperkinesis/Agitation
- Benzodiazepine (Ativan)
2) Hyperthermia
- Cooling blanket and antipyretic (Tylenol, not ASA – can exacerbate production of thyroid hormone)
3) Rehydration
- Fluid replacement therapy
- Electrolytes
4) Nutritional needs are elevated
5) Patient education
6) Collaborative management
Pheochromocytoma: rare adrenal medulla tumor (6)
Pressure (HTN)
Pain (HA)
Perspiration
Plapitation
Pallor
Paroxysm’s
Hypothyroid -> Myxedema Coma (what) (2)
hypothyroid: severe deficiency or absence of thyroid hormone
myxedema coma: severe hypothyroidism
Myxedema Coma: Etiology (4)
1) Deficiency of circulating thyroid hormone
- Decreased metabolic rate and mental status change
- Often associated with other conditions
- Afflicts elderly more commonly
Myxedema Coma: Symptoms (slow onset) (8)
Depression
Weight gain
hypothermia
hypoglycemia
hyponatremia
hypoventilation (most dangerous, comatose, not breathing well)
Hx of Thyroid surgery (hypothyroid state), radioablative surgery, previously on thyroid hormone
Myxedema Coma: Laboratory studies (2)
Low T4
Elevated TSH levels (pituitary gland recognizes absence of thyroid hormone)
Myxedema Coma: Pharmacologic management (5)
1) Levothyroxine or thyroid hormone
- Levels should increase slowly
2) Glucocorticoids (Hydrocortisone)
- Impaired adrenal function seen with profound hypothyroidism
- Can worsen hypothyroid state d/t blocks of t3-t4 conversion
3) Fluid replacement/Electrolyte replacement (Correct Hyponatremia)
4) Re-warm with blankets
5) Monitor LOC
Myxedema Coma: Nursing management (8)
Pulmonary care
Cardiac concerns
Thermoregulation
Thyroid replacement therapy
Skin care
Elimination
Patient education
Collaborative management
tip:
synthroid instructions -> take in morning as it has a lot of interactions with other medsications, take on empty stomach, 1 hour before anything else
