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Adult Health > AHII Endocrine > Flashcards

AHII Endocrine Flashcards

1
Q

hypocalcemia

A 
watch for laryngospasm--> stridor
lack of PTH
CATS (convulsions, arrhythmias, tingling and tetany, stridor and spasms)
Ca gluconate
Ca chloride
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2
Q

patient reports tightness in throat following thyroidectomy

A

suspect hematoma-need suture removal tray and sterile 4X4’s, PRBC’s and be ready to send back to OR

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3
Q

changes in volume, quality and tone following a thyroidectomy

A

indicate possible laryngeal nerve damage

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4
Q

thyroid storm (due to thyroid getting squeezed like a sponge)

A

TH release
hypermetabolism
increased O2 needs
SNS overdrive

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5
Q 
tachycardia/palpitations
afib
elevated temp, flushing
O2 hunger, chest pain
tremors, hyperhidrosis (excessive sweating)
agitation
watch for hypoglycemia!!
A

thyroid storm

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6
Q

pheochromocytoma

A

EPI, NE secreting tumor
happens spontaneously lasts minutes to hours
PHE (Palpitations, HA, hyperglycemia, hypertension, Excessive sweating)
ONLY REGULAR INSULIN IV
Remove adrenal gland is primary tx.

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7
Q

treating thyroid storm

A

maintain airway and support o2 status

circulation and metabolic needs: treat dehydration, DEXTROSE fluids (D5W NOT Glucagon!!) Propanolol, Digoxin (body may have used up all of glycogen stores, making Glucagon ineffective)

cooling blanket, ice packs, NO ASA, protect the skin, NSAIDS

block conversion of T4 to T3: PTU monitor CBC, fever, chills, sore throat, agranulocytosis, rigors

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8
Q

hyponatremia, hypotonic blood, concentrated urine, no edema

A

suspect SIADH-implement seizure precautions!-cells will swell bc they are hypertonic to the blood-this includes the brain

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9
Q

What might cause SIADH?

A

Cancer, CNS disorder, meds, pulmonary issues, CYCLOPHOSPHAMIDE

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10
Q

Hyponatremia

A

think neuro changes: disorientation, restlessness, lethargy, unresponsive, coma, seizures

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11
Q

large urine output, hypernatremia, increased serum osmolality, decreased urine osmolality and specific gravity, dehydration (dry MM, tenting skin, sunken eyes, insatiable thirst)

A

diabetes insipidus; treat with 1/2 NS, push PO fluids, vasopressin in neurogenic, if nephrogenic, ADH (Vasopressin) wont work bc kidney tubules cannot response, so remove the source with LITHIUM, give NSAIDS to reduce polyuria, encourage a low salt, low protein diet to reduce urine output, and give Thiazide diuretics (thiazide diuretics slow the GFR to decrease urine output)
neugenic: result of hyposecretion of ADH
Nephrogenic: kidney tubules fail to reabsorb water in response to ADH

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12
Q

buffalo hump, moon face, purple striae on abd

A

cushings

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13
Q

solu-cortef

A

IV hydrocortisone: doesnt fit if patient has Cushings which is too much glucocorticoids-why would you give IV Steriords?

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14
Q

confusion, weakness, pale, palpitations

A

acute adrenal insufficiency from stopping steriods abruptly

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15
Q

hyponatremia, hyperkalemia, hypotension

A

cushings

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16
Q

what do endocrine glands do?

A

maintenance and regulation of vital functions
response to stress and injury
growth and development
energy metabolism
reproduction
fluid, electrolyte, and acid-base balance

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17
Q

hypothalamus

A

body temp, sleep, appetite (activates, controls and integrates ANS)

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18
Q

pituitary gland

A

growth of body tissues, influences water absorption by the kidney, and controls sexual development and function

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19
Q

adrenal gland

A

sodium and electrolyte balance, affects carb, fat, and protein metabolism, influences developemnt of sexual characteristics, sustains fight or flight response

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20
Q

adrenal cortex

A

outer shell; synthesizes glucocorticoids and mineralocorticoids and secretes small amounts of sex hormones

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21
Q

adrenal medulla

A

inner core; SNS-produces NE, EPI

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22
Q

thyroid gland

A

metabolism and growth

makes T4, T3 and thyrocalcitonin

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23
Q

parathyroid glands

A

controls calcium and phosphorus metabolism, produces PTH

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24
Q

pancreas

A

influences carb metabolism, indirectly influences fat and protein metabolism, produces insulin and glucagon

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25
Q

a life threatening disorder caused by adrenal hormone insufficiency. Crisis is precipitated by infection, trauma, stress, or surgery. Death can occur from shock, vascular collapse, or hyperkalemia

A

addisonian crisis

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26
Q

hyposecretion of adrenal cortex hormones (glucocorticoids and mineralocorticoids) from the adrenal gland, resulting in deficiency of the corticosteriod hormones. The condition is fatal if left untreated.

A

Addison’s disease

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27
Q

temporary replacement of glucocorticoids and mineralocorticoids may be necessary for up to 2 years

A

unilateral adrenalectomy

if bilateral adrenalectomy, lifetime replacement with hydrocortisone and development of addison’s disease

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28
Q

a sign of hypocalcemia. A spasm of the facial muscles elicited by tapping the facial nerve just anterior to the ear.

A

Chvostek’s sign

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29
Q

a metabolic disorder characterized by abnormally increased secretion (endogenous) of cortisol, caused by increased amounts of adrenocorticotropic hormone (ACTH) by the pituitary gland

A

Cushing’s diease

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30
Q

a metabolic disorder resulting from the chronic and excessive production of cortisol by the adrenal cortex or by the administration of glucocorticoids in large doses for several weeks or longer (exogenous or iatrogenic)

A

Cushing’s syndrome

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31
Q

a nocturnal release of growth hormone, which may cause blood glucose level elevations before breakfast in the client with DM. Treatment includes administering an evening dose of intermediate acting insulin at 10 pm.

A

dawn phenomenon

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32
Q

the hyposecretion of antidiurectic hormone from the posterior pituitary gland, resulting in failure of tubular reabsorption of water in the kidneys and diuresis

A

diabetes insipidus

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33
Q

a chronic disorder of glucose intolerance and impaired carb, protein, and lipid metabolism caused by a deficiency of insulin or resistance to the action of insulin. A deficiency of effective insulin results in hyperglycemia.

A

Diabetes Mellitus

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34
Q

a life-threatening complication of diabetes mellitus that develops when a severe insulin deficiency occurs. Hyperglycemia progresses to ketoacidosis over a period of several hours to several days. Acidosis occurs in clients with type 1 diabetes, persons with undiagnosed diabetes, and persons who stop prescribed treatment for diabetes

A

diabetic ketoacidosis

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35
Q

elevated blood glucose as a result of too little insulin or the inability of the body to use insulin properly

A

hyperglycemia

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36
Q

extreme hyperglycemia without acidosis. A complication of type 2 diabetes mellitus, which may result in dehydration or vascular collapse but does not include the acidosis component of diabetic ketoacidosis. Onset is usually slow, taking from hours to days

A

hyperglycemia hyperosmolar nonketotic syndrome (HHNS)

initiate immediate cardiac monitoring because of the changes in potassium level related to fluid and insulin therapy and the osmotic diuresis from the elevated serum glucose level. There will be a large amount of IV fluid administtered.

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37
Q

low blood glucose level that results from too much insulin, not enough food, or excess activity

A

hypoglycemia

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38
Q

A rare but serious disorder that results from persistently low thyroid production. Coma can be precipitated by acute illness, rapid withdrawal of thyroid medication, anesthesia and surgery, hypothermia, and use of sedatives and opioid analgesics

A

myxedema coma

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39
Q

a rebound phenomenon that occurs in clients with type 1 diabetes. Normal or elevated blood glucose levels are present at bedtime. hypoglycemia occurs at about 2-3am. counterregulatory hormones, produced to prevent further hypoglycemia, result in hyperglycemia (evident in the prebreakfast blood sugar level). Treatment includes decreasing the evening (predinner or bedtime) dose of intermediate-acting insulin or increasing the bedtime snack.

A

Somogyi Phenomenon

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40
Q

an acute, potentially fatal exacerbation of hyperthyroidism that may result from manipulation of the thyroid gland during surgery, severe infection, or stress

A

thyroid storm

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41
Q

a sign of hypocalcemia. Carpal spasm can be elicited by compressing the brachial artery with a blood pressure cuff for 3 minutes.

A

Trousseau’s sign

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42
Q

thyroid function test

A

measures the absorption of an iodine isotope to determine how the thyroid gland is functioning. A small dose of radioactive iodine is given by mouth or IV, and the amount of radioactivity is measured in 2-4 hours and again at 24 hours.
Normal values are 3-10% at 2-4 hours; and 5-30% in 24 hours.
elevated values indicate hyperthyroidism, decreased iodine intake, or increased iodine production while decreased values indicate a low T4 level, the use of antithyroid meds, thyroiditis, myxedema, or hypothyroidism.

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43
Q

T3 T4 resin uptake test

A

T3 and T4 regulate TSH
T3 normal: 80-230 ng/dL
T4 normal 5-12 mcg/dL
Thyroxine, free (FT4) 0.8-2.4 ng/dL
T3 is elevated in hyperthyroidism, decreases with the aging process, and may be decreased in hypothyroidism
T4 is elevated in hyperthyroidism and decreased in hypothyroidism

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44
Q

Thyroid stimulating hormone

A

blood test is used to differentiate the diagnosis of primary hypothyroidism. Normal value is 0.2-5.4 microunits/mL; elevated values indicate primary hypothyroidism while decreased values indicate hyperthyroidism or secondary hypothyroidism.

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45
Q

what is an important consideration prior to a thyroid scan?

A

determine whether the client has received radiographic contrast agents within the past 3 months, bc these may invalidate the scan
Check with HCP regarding DC meds containing iodine for 14 days before the test and need to DC thyroid meds before the test

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46
Q

glucose tolerance test

A

a 2-hour post load glucose level higher than 200 mg/dL confirms the diagnosis of DM

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47
Q

cortisol, cortisone, corticosterone

A

responsible for glucose metabolism, protein metabolism, fluid and electrolyte balance, suppression of the inflammatory response to injury, protective immune response to invasion by infectious agents, and resistance to stress=glucocorticoids

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48
Q

aldosterone

A

mineralocorticoid: regulation of electrolyte balance by promoting sodium retention and potassium excretion

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49
Q

increased HbA1C level (normal 4-6%)

A

is usually the result of hyperglycemia in a diabetic client

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50
Q

mild-moderate obesity

A

suspect GH or TSH deficiency

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51
Q

reduced cardiac output

A

suspect GH or ADH deficiency

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52
Q

infertility, sexual dysfunction

A

suspect gonadotropins or ACTH deficiency

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53
Q

fatigue and low BP

A

suspect TSH, ADH, ACTH, or GH deficiencies

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54
Q

tumors here may cause HA and visual defects

A

pituitary gland (located near optic nerve)

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55
Q

cushings disease or acromegaly

A

result from hypersecretion of GH due to pituitary gland tumor

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56
Q

water intoxication and hyponatremia

A

SIADH-implement seizure precautions d/t hyponatremia-cells will swell bc they are hypertonic to the blood-this includes the brain

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57
Q

vanillymandelic acid: VMA

A

a product of catecholamine (NE, EPI) metabolism that is tested for in urine to determine pheochromocytoma; catecholamine levels above 14 mcg/100mL indicate pheochromocytoma

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58
Q

What actions may precipitate a hypertensive crisis, and should thus be avoided in a patient with pheochromocytoma?

A

abdominal pressure or vigorous palpation

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59
Q

hypotension, bradycardia, hypothermia, hyponatremia, hypoglycemia, generalized edema, respiratory failure, coma

A

symptoms of myxedema coma

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60
Q

airway, aspiration precautions, NS or a hypertonic IV fluid, IV levothyroxine, IV Glucose, IV corticosteriods, assess body temp hourly, keep client warm,

A

treatment of myxedema coma

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61
Q

Graves Disease

A

hyperthyroidism; keep client cool and give sedatives, high calorie diet, antithyroid meds such as propylthiouracil, PTU, iodine preps that inhibit the release of thyroid hormone, Administer Inderal (Propranolol) for tachycardia, prepare client for radioactive dye therapy to destroy thyroid cells or thyroidectomy

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62
Q

fever, tachycardia, Systolic HTN, N/V/D, agistation, tremors, anxiety, irritability, restlessness, confusion, and seizures may lead to delirium and coma

A

Thyroid Storm

airway, antithyroid meds, iodides, propranolol, and glucocorticoids, monitor VS, monitor for cardiac dysrhythmias.

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63
Q

What is important to know about salicylates and thyroid storm?

A

salicylates increase free thyroid hormone levels so give NSAIDs instead to lower fever assoc with thyroid storm
Aspirin will displace TH from carrier proteins and increase TH blood levels

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64
Q

What do you need at bedside following a thyroidectomy?

A

trach set, oxygen, and suction

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65
Q

hypocalcemia and hyperphosphatemia, numbness and tingling in face, muscle cramps, TETANY: bronchospasm, laryngospasm, carpopedal spasm, dysphagia, photophobia, cardiac dysrhythmias, seizures. Hypotension, anxiety, irritability, depression

A

hypoparathyroidism
seizure precautions, trach set, oxygen and suction at bedside, administer Ca Gluconate, calcium and Vit D supplements, phosphate binders, medic alert bracelet

66
Q

decreased muscle tone, muscle weakness and shortened QT interval

hypercalcemia, hypophosphatemia, fatigue and muscle weakness, skeletal pain and tenderness, bone deformities that result in pathological fractures, renal stones, cardiac dysrhythmias

A

hyperparathyroidism:
monitor for cardiac dysrhythmias, move client slowly and carefully, encourage fluids, administer Lasix to lower calcium levels, NS for hydration, phosphates to decrease calcium absorption, calcitonin to decrease skeletal calcium release and increase renal excretion of calcium

prepare for parathyroidectomy

67
Q

type 2 diabetes

A

a relative lack of insulin or resistance to the action of insulin. Usually insulin is sufficient to stabilize fat and protein metabolism, but not carb metabolism.

68
Q

Type 1 Diabetes

A

a nearly absolute defiency of insulin (primary beta cell destruction); if insulin is not given, fats are metabolized for energy, resulting in ketonemia (acidosis).

69
Q

Metabolic Syndrome

A

Syndrome X: individual has coexisting risk factors for developing DM2. abdominal obesity, hyperglycemia, hypertension, high triglyceride levels, and lowered HDL

70
Q

polyuria, polydipsia, polyphagia

weight loss

A

more common in type 1 diabetes

71
Q

What about blood glucose level of 250 mg/dL and urinary ketones?

A

tell the DM1 patient not to exercise until blood glucose is closer to normal and urinary ketones are absent

72
Q

What is important to caution diabetic patients about if they take a sulfonylurea?

A

avoid alcohol

73
Q

Why is it important to rotate insulin injection sites?

A

avoid lipoatrophy: the development of fibrous fatty masses at the injection site

74
Q

kussmauls respirations, fruity breath, nausea, abdominal pain

A

signs of Ketosis

75
Q

What is important to remember when giving insulin IV?

A

use only short-duration insulin for IV administration. Flush the insulin solution through the entire IV tubing and discard the first 50-100mL of solution before connecting and administering to the client (insulin molecules adhere to the plastic of IV infusion sets). Mix the prescribed does on insulin for continuous infucion in NS or 1/2NS.

Monitor potassium and glucose levels and for signs of IICP

76
Q

What blood glucose levels warrant a call to the HCP?

A

250-300mg/dL

77
Q

Why do you monitor for IICP during insulin administration via IV or when treating a patient for DKA?

A

If blood glucose level falls too far or too fast before the brain has time to equilibrate, water is pulled from the blood to the cerebrospinal fluid and the brain, causing cerebral edema and IICP

78
Q

How do you treat HHNS?

A

insulin is less critical in the treatment of HHNS than it is for the treatment of DKA. Rehydration alone may decrease glucose levels in HHNS.

79
Q

microalbuminuria, thirst, fatigue, anemia, weight loss, signs of malnutrition frequent UTI’s neurogenic bladder

A

diabetic nephropathy

dialysis, pancreas/kidney transplant

80
Q

Kussmauls respirations

A

deep, rapid breathing: think DKA

81
Q

shakiness, palpitations, and lightheadedness

A

signs of hypoglycemia

82
Q

polyuria, blurred vision, and fruity breath

A

signs of hyperglycemia

83
Q

A client is admitted to a hospital with a diagnosis of DKA. The initial blood glucose level was 950 mg/dL. A continuous IV infusion of short-acting insulin is initiated, along with IV rehydration with NS. The serum glucose is now 240mg/dL. What are the nurse’s next steps?

A

Change IV rehydration fluids from NS to dextrose.
During management of DKA, when the blood glucose levels falls to 250-300mg/dL, the infusion rate is reduced and a dextrose solution is added to maintain a blood glucose level of about 250 mg/dL

84
Q

To correct DKA, what is the primary action?

A

IV insulin along with potassium to avoid hypokalemia

85
Q

when is the peak of NPH insulin?

A

4-12 hours

86
Q 
The nurse is caring for a client with pheochromocytoma who is scheduled for adrenalectomy.  In the preoperative period, what should the nurse monitor as priority?
A. VS
B. I&O
C. BUN
4. Urine for glucose and ketones
A

A. VS especially BP for pheochromocytoma due to the risk of hypertensive crisis.

87
Q 
A client has just been admitted to the nursing unit following thyroidectomy.  Which assessment is the priority for this client?
A. hypoglycemia
B. Level of hoarseness
C. Respiratory distress
D. Edema at the surgical site
A

C. Respiratory distress

88
Q

PTU

A

antithyroid med that causes agranulocytosis: monitor for fever or sore throat and notify HCP if these develop

  • often used with iodine to produce euthyroid before surgery
  • blocks peripheral conversion of T4 to T3
89
Q

Exenatide (Byetta)

A

is an incretin mimetic used for type 2 diabetes only. It is not recommended for clients taking insulin. This medicaiton is administered within 60 minutes before the morning and evening meals. Monitor the client for GI side effects

90
Q

growth hormone

A

elevated AST/ALT
recommend annual bone age determinations for children receiving GH
monitor for hyperglycemia

91
Q

Antidiuretic Hormone: Desmopressin (DDAVP, Stimate, Minirin) Vasopressin (Pitressin)

A

enhance reabsorption of water in the kidneys
used to treat Diabetes Insipidus
watch for water intoxication**
DDAVP is used to treat diabetes insipidus by replacing ADH that the patient is lacking. Inhaled DDAVP can cause nasal irritation, headache, nausea, and other signs of hypernatremia.

92
Q

thyroid hormones: levothyroxine sodium (Synthyroid, Levothroid, Levoxyl)

A

treat hypothyroid or myxedema coma
drug interactions
take in the am without food
**Any chest pain or heart palpitations or HR >100bpm should be reported immediately and an ECG and cardiac enzymes should be ordered.

93
Q

anti thyroid meds: Methimazone (Tapazole), Propylthiouracil (PTU), Strong iodine solution (Lugor’s Solution)

A

treat hyperthyroidism, Graves disease
agranulocytosis with leukopenia and thrombocytopenia
alopecia and hyperpigmentation
Iodism (vomiting, abd pain, metallic or brassy taste, rash, sore gums)
THYROID STORM is abrupt discontinuation

94
Q

mineralocorticoids

A

treat addisons disease
mineralocorticoids enhance reaborption of sodium and chloride and excrete potassium and hydrogen (think Aldosterone). SE hypernatremia, edema, hypokalemia, osteoporsis, compression fractures

95
Q

glucocorticoids

A

watch for Cushings syndrome: moon face, puffy eyelids, edema, increased bruising, dizziness, bleeding, and menstraul irregularities

96
Q

Androgens: Fluoxymesterone, Methyltestosterone

A

can cause bleeding if client is taking oral anticoags
can decrease serum glucose concentration, thereby reducing insulin requirements in clients with DM
Avoid hepatotoxic meds with androgens
androgens stimulate growth of existing prostate or breast cancers
cause hypercalcemia
take with meals or snack
notify HCP if priapism or fluid retention develops

97
Q

iodine preparations

A

Iodine preparations decrease blood flow through the thyroid gland and reduce the production and release of thyroid hormone; they are not used to treat hypothyroidism.

98
Q

cushings syndrome abnormal labs

A

The client with Cushing’s syndrome experiences hyperkalemia, hyperglycemia, an elevated WBC count, and elevated plasma cortisol and adrenocorticotropic hormone levels.

99
Q

addisonian crisis symptoms

A

Addisonian crisis is a serious life-threatening response to acute adrenal insufficiency that most commonly is precipitated by a major stressor. The client in Addisonian crisis may demonstrate any of the signs and symptoms of Addison’s disease, but the primary problems are sudden profound weakness; severe abdominal, back, and leg pain; hyperpyrexia followed by hypothermia; peripheral vascular collapse; coma; and renal failure.

100
Q

signs of adrenal insufficiency

A

The nurse should be alert to signs and symptoms of adrenal insufficiency after adrenalectomy. These signs and symptoms include weakness, hypotension, fever, and mental status changes.

101
Q

A hospitalized client is experiencing an episode of hypoglycemia. The nurse plans care, knowing that which is the physiological mechanism that should take place to combat the decline in the blood glucose level?

A

Glucagon is secreted from the alpha cells in the pancreas in response to declining blood glucose levels. At the same time, hypoglycemia triggers increased cortisol release, decreased secretion of insulin, and increased epinephrine release.

102
Q

A client with diabetes mellitus who refuses to take insulin as prescribed exhibits markedly increased blood glucose levels after a meal. The nurse caring for the client anticipates that which initial body response to elevated glucose levels will worsen the situation for the client?

A

As blood glucose levels rise when glucose is not being carried into the cells, the body interprets this to mean that more glucose is needed. The initial response by the body is to use up the stores of glycogen in the liver. The conversion of glycogen to glucose for use by the body is called glycogenolysis. If this mechanism fails, the body breaks down fats and proteins and converts them into glucose; this process is called gluconeogenesis. Glucose binds onto cell membranes and is transported across them into the cells when there is sufficient circulating insulin.

103
Q

PTU indications

A

PTU is prescribed for the treatment of hyperthyroidism. Excessive dosing with this agent may convert a hyperthyroid state to a hypothyroid state. If this occurs, the dosage should be reduced.

104
Q

During routine nursing assessment after hypophysectomy, a client complains of thirst and frequent urination. Knowing the expected complications of this surgery, what should the nurse assess next?

A

After hypophysectomy, temporary diabetes insipidus can result from antidiuretic hormone deficiency. This deficiency is related to surgical manipulation. The nurse should assess urine specific gravity, and notify the health care provider if the result is less than 1.005.

105
Q

What special considerations need to be made with regard to a 24 hour urine collection for VMA?

A

Clients are reminded not to take medications for 2 to 3 days before a 24-hour urine collection for vanillylmandelic acid (VMA).

106
Q

oral glucose tolerance test guidelines

A

The normal reference values for oral glucose tolerance tests are lower than 140 mg/dL at 120 minutes; lower than 200 mg/dL at 30, 60, and 90 minutes; and lower than 115 mg/dL in the fasting state. 160 mg/dL is higher than the normal reference range so therefore is the correct answer.

107
Q

Why does hyperkalemia develop during shock?

A

The body can exchange like charges for like. If the body is acidotic (anaerobic respiration due to lack of perfusion to cells results in lactic acidosis), the body will want to rid of H+ by swapping with K+.

108
Q

What happens during a MI when the left ventricle isn’t ejecting blood like it should?

A

RAAS is activated to try to give the heart more blood to pump

109
Q

What does CVP indicate?

A

right preload normal is 2-6 mm Hg (usually obtained through a central line)

110
Q

What measure gives you the Left Preload?

A

pulmonary artery occlusive pressure (PAOP) or PAWP or WEDGE. Normal is 8-12 mm Hg

111
Q

SvO2 = mixed venous oxygenation saturatoin

A

normal is 70%. after the blood circulates the body, how much of the oxygen did the cells take? If SvO2 is low (below 60%), then the oxygen supply is insufficient or oxygen demand has increased. If SvO2 is high, (above 80%) then the oxygen demand has declined (are cells dying?) or the oxygen supply has increased.

112
Q

what does shunting of blood away from GI tract in order to maintain perfusion of heart and brain do?

A

ischemia breaks down protective mocosal barrier of GI tract resulting in ulcers, GI bleeding, and even aids in bacterial migration to the blood stream. Decreased perfusion of the liver means that the Kupffer cells that aid in immune function cannot attack these bacteria, and bacteremia develops

113
Q

why should most vasopressors be given via central line?

A

vasoconstrictive properties may be harmful if administered peripherally and the drug extravasates

114
Q

When do you administer vasopressors

A

when the patient has not responded to fluid resusitation. Goals of vasopressor therapy are to maintain a MAP>65 mmHg. Monitor end-organ perfusion (urine output, LOC) and serum lactate levels (every two hours for the first 6 hours) to ensure that tissue perfusion is adequate

115
Q

What drugs do you give to cardiogenic shock patients? vasopressors or vasodilators?

A

vasodilators: patients in cardiogenic shock have decreased myocardial contractility, and vasodilators may be needed to reduce the afterload. This reduces myocardial workload and oxygen requirements. Use of vasopressors increases SVR, which adds to the workload of the heart and makes cardiogenic shock worse.

the rationale for using vasodilator therapy for a patient in cardiogenic shock is to break the harmful cycle in which widespread vasoconstriction causes a decrease in CO and BP, resulting in further sympathetic-induced vasoconstriction (which leads to less tissue perfusion)

116
Q

what labs do you see in DIC?

A

positive D-dimer, coag times increased, FDP levels increase

117
Q

What labs tell you how the liver is synthsizing proteins?

A

monitor plasma transferrin and prealbumin

118
Q

clinical manifestations of MODS

A 
respiratory distress
decreased renal perfusion
decreased serum albumin and prealbumin
decreased GI motility
acute neuro changes
myocardial dysfunction
DIC
change in glucose metabolism
119
Q

How is septic shock characterized?

A

decreased circulating blood volume. Septic shock requires large amounts of fluid (6-10 L isotonic crystalloids and 2-4L colloids in first 6 hours) to achieve a target CVP or 8-12 mmHg. Once CVP is 8, consider adding vasopressors such as NE or dopamine. Also give Dobutamine to increase stroke volume. Start antibiotics in the first hour, and Xigris (protein C) has been proven to improve patient outcomes-monitor for bleeding because Xigris has antithrobotic and anti-inflammatory properties. FInally, maintain glucose levels 80-110. (or less than 150)

120
Q

Which nursing diagnosis is more emergent? Decreased Cardiac Output or Ineffective Tissue Perfusion?

A

The many deleterious effects of shock are all related to inadequate perfusion and oxygenation of every body system. Ineffective Tissue Perfusion supercedes the other nursing diagnoses.

121
Q

hyperglycemia with no history of diabetes, oliguria, tachypnea and tachycardia

A

sepsis clinical manifestations

122
Q

cardiogenic shock manifestations

A

Clinical manifestations of cardiogenic shock include tachycardia, hypotension, a narrowed pulse pressure, tachypnea, pulmonary congestion, cyanosis, pallor, cool and clammy skin, diaphoresis, decreased capillary refill time, anxiety, confusion, and agitation

123
Q

what is relative hypovolemia?

A

Relative hypovolemia results when fluid volume moves out of the vascular space into extravascular space, such as with sepsis and burns.

124
Q

clinical manifestations of hypovolemic shock

A

Clinical manifestations depend on the extent of injury or insult, age, and general state of health and may include anxiety; an increase in heart rate, CO, and respiratory rate and depth; and a decrease in stroke volume, pulmonary artery wedge pressure (PAWP), and urine output.

125
Q

what is neurogenic shock?

A

Neurogenic shock is a hemodynamic phenomenon that can occur within 30 minutes of a spinal cord injury at the fifth thoracic (T5) vertebra or above and last up to 6 weeks, or in response to spinal anesthesia.

126
Q

what are manifestations of neurogenic shock?

A

Clinical manifestations include hypotension, bradycardia, temperature dysregulation (resulting in heat loss), dry skin, and poikilothermia

127
Q

Septic shock has three major pathophysiologic effects:

A

vasodilation, maldistribution of blood flow, and myocardial depression

128
Q

Octreotide (Sandostatin)

A

a somatostatin analog that reduces growth hormone levels to within the normal range in many patients. Octreotide is given SC three times a week. Two long-acting analogs, octreotide (Sandostatin LAR) and lanreotide SR (Somatuline Depot) are available as IM injections given every 2-4 weeks.

129
Q

hypercalcemia manifestations

A

muscle weakness, polyuria, constipation, n/v, lethargy, and memory impairment

130
Q

Care of a patient with SIADH

A
  • limit fluids to 1000mL/day to decrease weight, increase osmolality, and improve symptoms.
  • HOB at 10 degrees or less to enhance venous return to the heart and increase left atrial filling pressure, thereby reducing the release of ADH.
  • Monitor for s/sx of hyponatremia
  • frequent turning, positioning and ROM are important to maintain skin integrity and joint mobility.
  • implement seizure precautions! cells will swell bc they are hypertonic to the blood-this includes the brain
  • if hyponatremia is severe, consider giving 3%NaCl (remember this should go into a central line) but correct SLOWLY-if you make blood very hypertonic quickly, the fluid will come out of the brain cells so quickly that it wrecks the myelin sheath around the nerve (demyelination syndrome or central pontine myelinolysis)-watch for decreased LOC
131
Q

hypothyroidism presentation

A

puffy face, decreased sweating, dry,coarse hair, muscle aches and pains, slow mvmts, and decreased appeatite and pallor

132
Q

hyperthyroidism presentation

A

aka Graves disease; systolic HTN and increased HR and increased thirst, exophthalmos

133
Q

What do you suspect when HTN does not respond to traditional treatment?

A

Pheochromocytoma: a 24-hour urine collection for fractionated metanephrines is simple and reliable with elevated values in 95% of people with Pheochromocytoma. In a patient with pheochromocytoma preoperatively an alpha adrenergic receptor blocker is used to reduce BP.

134
Q

The patient with an adrenal hyperplasia is returning from surgery for an adrenalectomy. For what immediate post op risk should the nurse plan to monitor the patient?

a. vomiting
b. infection
c. thromboembolism
d. rapid bp changes

A

d. rapid bp changes
The risk of hemorrhage is increased with surgery on the adrenal glands as well as large amounts of hormones being released in the circulation, which may produce hypertension and cause fluid and electrolyte imbalances to occur for the first 24-48 hours after surgery. Vomiting, infection, and thromboembolism may occur post operatively with ANY surgery.

135
Q

when do you suppress pituitary ACTH synthesis?

A

cushings syndrome

136
Q

What may need to be increased in the diet of a person with Addison’s disease?

A

sodium

137
Q

kussmaul respirations

A

deep and non labored often displayed in DKA to blow off the acidosis.

138
Q

Metformin (Glucophage) mechanism of action

A

metformin is a biguanide that reduces glucose production by the liver and enhances the tissue’s insulin sensitivity.

139
Q

which anitdiabetic meds increase insulin production from the pancreas?

A

sulfonylureas and meglitinides

140
Q

which antidiabetic meds slow the absorption of carbs in the intestine?

A

alpha glucosidase inhibitors

141
Q

A patient with diabetes mellitus who has multiple infections every year needs a mitral valve replacement. What is the MOST important preoperative teaching the nurse whould provide to prevent a cardiac infection post-op?

a. avoid sick people and wash hands
b. obtain comprehensive dental care
c. maintain hemoglobin A1C below 7%
d. coughing and deep breathing with splinting

A

B. Obtain comprehensive dental care
a person with DM is at high risk for post-op infection. The most importnat pre-op teaching to prevent a post-op infection in the heart is to have the patient obtain comprehensive dental care bc the risk of septicemia and infective endocarditis increases with poor dental health. Avoiding sick people, hand washing, maintaining hemoglobin A1C below 7%, and cough/deep breathing would be important for ANY type of surgery, but not the priority with mitral valve replacement for this patient.

142
Q

why do you give propranolol for Graves, thyroid storm?

A

propranolol blocks SNS stimulation and decreases conversion of T4 to T3 in periphery

143
Q

what is the reversal agent for anxiolytics such as benzos or lorazepam

A

flumazenil

144
Q

whats the reversal agent for narcotics?

A

naloxone

145
Q

methimazole (Tapazole)

A

antithyroid med that blocks synthesis of TH

146
Q

SSKI, Lugol’s solution

A

give SSKI with straw to avoid staining teeth. SSKI blocks TH release

147
Q

adenoma

A

benign tumor (but it can GROW)

148
Q

pheochromocytoma meds

A

alpha adrenergic blocker: phentolamine
smooth muscle relaxant: nitroprusside (Nipride) drip
CCB: nifedipine
beta blocker: propranolol if cardiac arrhythmias or no response to phentolamine
catecholamine synthesis inhibitor: methyl-p-tyrosine
insulin to reduce BG levels

149
Q

overscretion of cortisol by adrenal cotex caused by either a faulty adrenal gland or too much ACTH from the anterior pituitary

A

Cushings

150
Q

cortisol

A

glucocorticoid, stress hormone. makes body more sensitive to catecholamines, raises blood sugar by stimulating liver to breakdown glycogen and by having anti-insulin effects. decreases inflammation and protein synthesis, increases fat metabolism

151
Q

Dexamethason suppression test for diagnostics of cushings

A

give 1 mg dexamethasone PO at 2300 and obtain plasma cortisol at 0800. Cortisol < 5 (suppressed) means HPA axis negative feedback is intact.

152
Q

addisonian crisis manifestations

A

circulatory collapse and shock: pallow, hypotension, rapid, weak pulse, rapid RR
HA, nausea, ab pain, diarrhea
confusion, restlessness (d/t hyponatremia)
extreme weakness
hyperkalemia-cardiac dysrhythmias, T wave fluttering, PVC’s
hyperpigmentation of skin folds

153
Q

Treatment priorities Addisonian crisis

A

id cause and treat (infection, dehydration, stress)
IV fluids and dextrose+electrolyte replacement (esp Na)
Vasopressors (d/t circulatory collapse)
IV cortocosteriods (fix the problem of adrenal insufficiency)
monitor labs and daily weights

Avoid overexerting your patient-turn them do all the bathing, etc!

154
Q

orthostatic hypotension

A

SBP<20 mmHg when moving from lying to sitting

155
Q

normal serum osmolality

A

285-295 mOsm

156
Q

normal urine specific gravity

A

1.003-1.030

expect 1.030 in SIADH (too concentrated)

157
Q

potassium iodide

A

decreases release of thyroid hormones

used to decrasse size and vascularity of thyroid gland preoperatively

158
Q

radioactive iodine (131 I)

A

treatment of choice against hyperthyroidism in non pregnant adults
decreases thyroid secretion by damaging the thyroid gland
often causes hypothyroidism over time

159
Q

When a patient with parathyroid disease experiences symptoms of hypocalcemia, a measure that can be used to raise serum calcium levels temporarily is to

a. abminister IV NS
b. have the patient rebreathe in a paper bag
c. administer Lasix as ordered
d. administer oral phosphorus supplements

A

b. have the patient rebreathe in a paper bag.
rebreathing in a paper bag promotes carbon dioxide retention in the blood, which lowers pH and causes acidosis. An acidemia enhances the solubility and ionization of calcium, increasing the proportion of total body calcium available in physiologically active form and relieving the symptoms of hypocalcemia. NS and Lasix promote calcium excretion. Phosphate levels in the blood are reciprocal to calcium, and an increase in phosphate promotes calcium excretion.

160
Q

A patient with Addison’s diases comes to the ED with complaints of n/v/d and fever. The nurse would expect collaborative care to include

a. parenteral injections of ACTH
b. IV administration of vasopressors
c. IV administration of hydrocortisone
d. IV administration of D5W with 20 mEq KCl

A

c. IV administration of hydrocortisone.
vomiting and diarrhea are early indicators of addisonian crisis, and fever indicates an infection, which is causing additional stress to the patient. Treatment of a crisis requires immediate glucocorticoid replacement, and IV hydrocortisone, fluids, sodium, and glucose are necessary for 24 hours. Addison’s disease is a primary adrenal insufficiency and ACTH is not effective. Potassium levels are increased in Addison’s disease, and KCl would be contraindicated.

161
Q

During discharge teaching for a patient with Addison’s disease, the nurse identifies a need for additional instruction when the patient says

a. I should always call the doctor if I develop vomiting or diarrhea.
b. If my weight goes down, my dosage of steriod is probably too high.
c. I should double or triple my steriod use if I undergo rigorous physical exercise.
d. I need to carry an emergency kit with injectible hydrocortisone in case I can’t take my medication by mouth.

A

b. If my weight goes down, my dosage of steriod is probably TOO LOW (corrected statement)
A weight reduction in the patient with Addison’s disease may indicate a fluid loss and a dose replacement therapy that is too low rather than too high. Patients with Addison’s disease are taught to take two to three times their usual dose of steriods if they become ill, have teeth extracted, or engage in rigorous physical activity and should always have injectable hydrocortisone available if oral doses cannot be taken. Because vomiting and diarrhea are early signs of crisis and because fluid and electrolytes must be replaced, patients should notify their physicians if these symptoms occur.

162
Q

When caring for a patient with primary hyperaldosteronism, the nurse would question which drug?

a. Lasix
b. amiloride (Midamor)
c. Aldactone
d. aminoglutethimide (Cytadren)

A

A. Lasix; hyperaldosteronism retains too much sodium and water and excretes potassium. Lasix is a potassium-wasting diuretic that would increase the potassium deficiency. Aminoglutethimide blocks aldosterone synthesis. amiloride is a potassium-sparing diuretic and Aldactone blocks mineralocorticoid receptors in the kidney, increasing the excretion of sodium and water but retaining potassium.

Adult Health (18 decks)

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