Endo

Question 1

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)

Answer 1

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)

Question 2

Organs of the Endocrine System (9)

Answer 2

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

Question 3

Neuroendocrine Response to Critical Illness

Answer 3

Severe illness and stress activate hypothalamic-pituitary-adrenal (HPA) axis, resulting in release of Cortisol (stress hormones) from adrenal cortex (fight/flight)

Question 4

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?

Answer 4

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

Question 5

Acute neuroendocrine response to critical illness: Liver and pancreas in acute stress

Answer 5

Glucagon -> glycogen -> gluconeogenesis and increased blood glucose (fight/flight response)

Question 6

Acute neuroendocrine response to critical illness: Thyroid gland in acute stress

Answer 6

Increased levels of T3 and T4

Question 7

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?

Answer 7

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

Question 8

Adrenal dysfunction in critical illness: Causes (5)

Answer 8

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

Question 9

Assessment of adrenal function

Answer 9

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)

Question 10

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)

Answer 10

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

Question 11

Insulin management in the critically ill (5)

Answer 11

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

Question 12

Hypoglycemia management

protocols?

rule of ?

Answer 12

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

Question 13

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

Answer 13

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)

Question 14

Diabetes Mellitus

what?

what is associated with DM

diagnosis of DM (4)

Answer 14

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)

Question 15

Types of diabetes (2) - explain pathophysiology

Answer 15

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

Question 16

Glycated hemoglobin (HgB A1C numbers for diabetic, pregnant, ad older)

Answer 16

Diabetic target: less than 7%
Pregnant: <6.5%
Older: <8%

Question 17

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

Answer 17

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)

Question 18

Type 2 diabetes (90% to 95%)

patient population mostly?

assocaited with?

what is it?

Answer 18

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

Question 19

Diabetic Ketoacidosis: epidemiology and etiology

what?

typically effects who?

what kind of deficiency?

manifests with 3?

elevation of? (4)

Answer 19

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

Question 20

Diabetic Ketoacidosis: Pathophysiology (5)

Answer 20

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

Question 21

Diabetic Ketoacidosis: Diagnostic criteria for diabetic ketoacidosis (DKA) (6)

Answer 21

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

Question 22

Diabetic Ketoacidosis: causes (9)

Answer 22

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

Question 23

Diabetic Ketoacidosis: Assessment and diagnosis - clinical manifestations

tip: 3 P’s, respiratory/cardiac issues (3)

other signs of hyperglycemia

Answer 23

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

Question 24

Diabetic Ketoacidosis: Laboratory studies (4)

Answer 24

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

Question 25

DKA lab values (6)

Answer 25

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

Question 26

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?

Answer 26

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

Question 27

Insulin Therapy (4)

Answer 27

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

Question 28

DKA treatment: too low pH (1)

Answer 28

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

Question 29

DKA treatment: Transfer to from IV to SQ (2)

Answer 29

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

Question 30

Diabetic Ketoacidosis: Medical management goals (4)

Answer 30

Reverse dehydration Replace insulin Reverse keto-acidosis Replenish electrolytes (specifically potassium)

Question 31

Diabetic Ketoacidosis: Nursing management (4)

Answer 31

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

Question 32

Hyperglycemic Hyperosmolar State (HHS): Epidemiology and etiology complication of which DM hallmarks? (2)

Answer 32

1) Potentially lethal complication of type 2 DM 2) Hallmarks: - *Extremely* high levels of plasma glucose - Elevation in hyperosmolarity causing osmotic diuresis

Question 33

Hyperglycemic Hyperosmolar State: Differences between hyperglycemic hyperosmolar state (HHS) and DKA (5) what occurs in HHS that doesn't occur in DKA

Answer 33

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

Question 34

Hyperglycemic Hyperosmolar State: Pathophysiology (3)

Answer 34

1) Deficit of insulin (not absolute) 2) Excess of glucagon release 3) Results in - Hemo-concentration - Hypovolemia - Dehydration - Risk for Thromboemboli

Question 35

Hyperglycemic Hyperosmolar State: Incidence/predisposing factors (2)

Answer 35

Recent onset of T2 diabetes Receiving TPN or high-caloric feedings

Question 36

Hyperglycemic Hyperosmolar State: causes (5)

Answer 36

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

Question 37

Hyperglycemic Hyperosmolar State: Assessment and diagnosis, Clinical manifestations a) ____,_____ onset b) intiial symptoms are nonspecific: (3) c) ____ _____ findings d) very elevated ____ ____

Answer 37

a) Slow, subtle onset b) Initial symptoms are nonspecific: - Marked fatigue/malaise - confusion - s/sx dehydration Physical examination findings Very elevated glucose levels (>1000)

Question 38

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 ______

Answer 38

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

Question 39

Hyperglycemic Hyperosmolar State: Medical management (2)

Answer 39

Rehydration Insulin administration to facilitate the cellular use of glucose

Question 40

Hyperglycemic Hyperosmolar State: Insulin treatment usually less then DKA (3)

Answer 40

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

Question 41

HHNK Treatment (2)

Answer 41

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.

Question 42

Hyperglycemic Hyperosmolar State: Nursing management (6)

Answer 42

Administration of fluids, insulin, and electrolytes Monitor response to therapy Surveillance for complications Monitor for signs of infection Patient education Collaborative management

Question 43

Anticoagulation for DKA/HHS (3)

Answer 43

1) Increase risk for thrombosis (HUGE RISK) - Prophylactic heparin administration should be considered unless contraindicated. - At risk for DIC

Question 44

Diabetes Insipidus (3)

Answer 44

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)

Question 45

Diabetes Insipidus: 3 types (3)

Answer 45

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)

Question 46

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

Answer 46

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

Question 47

Diabetes Insipidus: clinical manifestations (2)

Answer 47

Dramatic increase in dilute urine output Absence of diuretics, fluid challenge, or hyperglycemia

Question 48

Diabetes Insipidus: Laboratory studies (4)

Answer 48

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)

Question 49

Diabetes Insipidus: medical mgmt (2) 1) ______ restoration 2) medications: - central DI: ? - nephrogenic DI: ?

Answer 49

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)

Question 50

Diabetes Insipidus: nursing mgmt (5)

Answer 50

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)

Question 51

Syndrome of Inappropriate Secretion of Antidiuretic Hormone (SIADH) (4)

Answer 51

Opposite of DI Excess Anti-Diuretic Hormone (ADH) (too much ADH) Kidneys reabsorb too much water Dilutional hyponatremia (drop Na)

Question 52

SIADH: etiology (4)

Answer 52

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)

Question 53

SIADH: Pathophysiology (3)

Answer 53

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)

Question 54

SIADH: Clinical manifestations (5) tip: CLAMS

Answer 54

- Clinical presentation in SIADH relates to water and sodium imbalance - Lethargy - Anorexia - Mental confusion - Seizures, coma, death

Question 55

SIADH: Laboratory values (2 (2/3))

Answer 55

1) Serum laboratory values - Serum osmolality low - Serum sodium low 2) Urine laboratory values (high – super concentrated) - Urine osmolality - Urine sodium - Urine specific gravity

Question 56

SIADH: Medical management (3)

Answer 56

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)

Question 57

Goal of treatment (2)

Answer 57

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

Question 58

SIADH: nursing mgmt (4)

Answer 58

Restriction of fluids Surveillance for complications Patient education Collaborative management

Question 59

Conditions Associate With Hyperthyroidism (3)

Answer 59

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

Question 60

Thyroid Storm: etiology (3)

Answer 60

Excessive uptake of thyroid hormone Increased metabolic activity Sympathetic nervous system response tip: sympathetic stressor causes increased uptake thyroid hormone

Question 61

Risk Factors for Development of Thyroid Crisis in the presence of pre-existing conditions (3) precipitating factors (6)

Answer 61

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

Question 62

Thyroid Storm: pathophysiology (sympathetic overload) (3)

Answer 62

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

Question 63

Thyroid Storm: Assessment and diagnosis 1) combination of ___ and _____ critical manifestations 2) laboratory findings: (4) 3) diagnostic tests (3)

Answer 63

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

Question 64

Thyroid Storm: Medical management goal (4)

Answer 64

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

Question 65

Thyroid Storm: medication (4)

Answer 65

1. 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 2. 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 3. B-Blockers – Blocks sympathetic effects of thyroid storm - Propanolol/Esmolol - Lopressor to block tachycardia/HTN 4. Steroids – Blocks peripheral conversion of T4/T3 - Hydrocortisone

Question 66

Thyroid Storm: Nursing management (6)

Answer 66

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

Question 67

Pheochromocytoma: rare adrenal medulla tumor (6)

Answer 67

Pressure (HTN) Pain (HA) Perspiration Plapitation Pallor Paroxysm’s

Question 68

Hypothyroid -> Myxedema Coma (what) (2)

Answer 68

hypothyroid: severe deficiency or absence of thyroid hormone myxedema coma: severe hypothyroidism

Question 69

Myxedema Coma: Etiology (4)

Answer 69

1) Deficiency of circulating thyroid hormone - Decreased metabolic rate and mental status change - Often associated with other conditions - Afflicts elderly more commonly

Question 70

Myxedema Coma: Symptoms (slow onset) (8)

Answer 70

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

Question 71

Myxedema Coma: Laboratory studies (2)

Answer 71

Low T4 Elevated TSH levels (pituitary gland recognizes absence of thyroid hormone)

Question 72

Myxedema Coma: Pharmacologic management (5)

Answer 72

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

Question 73

Myxedema Coma: Nursing management (8)

Answer 73

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