Ati Gastrointestinal Unit 6 Rn Care Of Clients W/endocrine Disorders

Front 1

Hypothroidism?

Back 1

-condition in which there is an INADEQUATE amt of circulating thyroid hormones (T3 & T4)
-DECREASE in metabolic rate affects all body systems

Front 2

Primary Hypothyroidism?

Back 2

--most common
-caused by disease or loss of thyroid gland
-EX: iodine deficiency, surgical removal of thyroid gland

Front 3

Secondary Hypothyroidism?

Back 3

--failure of Anteriod Pit. Gland to stimulate gland
-or failure of targe tissues to respond to the thryoid hormones (pituratry tumors)

Front 4

Teritary Hypothyroidism?

Back 4

-failure of hypothalamus to proude thyroid releasing factor

Front 5

Hyptothroyroidism is calssied by?

Back 5

-AGE OF ONSET

Front 6

Cretinism

Back 6

-state of severe hytothryoidsm found in fants
0don't rpdoude normal amts of thyroid hormones
-skelttal maturation and CNS decolpment altered = growth retardation of phycial growth & mental growth or both

Front 7

Juveinile hypothyroidism?

Back 7

-caued by chronic automimunie thyroididtis
-affectgs: growth & sexual maturation of child
-treatment can reverse most cases of disease

Front 8

Disorder of hypothyroidism is most prevelant in?

Back 8

-Women
-Persons age 40 - 50

Front 9

What is LOW during hypothyroidism?

Back 9

-T3 and T4
-

Front 10

Serum thyroid-stimulaation hormone (TSH) is?

Back 10

-Level is ELEVATED w/Primary Hypothyroidism
-Level is DECREASED w/Secondary hypothyroidism

Front 11

what is elevated during Thyrotropin-releasing hormone (TRH) stimulation test?

Back 11

-Basal
-presence of early hypothyroidism

Front 12

During hypothyroidsm Free thyroxing indexx (FTI) and thyroxing (T4) levels are?

Back 12

-DECREASED

Front 13

What do skull X-rays, CT scans, and MRI's do for hypothyroidsm?

Back 13

-Locate pituitary or hypothalmic lesions that may be underlying cause of hypothyroidism

Front 14

Radioisotope (131 I ) scan and uptake for hypothyroidism will be?

Back 14

-less than 10% in 24hr period
-2ndary hypothyroidism intake INCREASES w/admin of exogenous TSH

Front 15

What will a ECG look like for hypothyroidism?

Back 15

-SINUS Bradycardia
-flat or inverted T-waves

Front 16

Hypothyroidsm Serum Cholesterol will be?

Back 16

-ELEVATED

Front 17

CBC of hypothyroidism will show?

Back 17

-Anemia

Front 18

Early Symptoms of Hypothyroidsm are?

Back 18

-weakeness and fatigue
-intolerance to cold
-decreased bowel motility
-weight gain
Joint or muscle pain
-Brittle, thinning hair
-Pale Skin
-Depression

Front 19

Late symptoms of hypothyroidism are?

Back 19

-Slow thought processes and speech
-Thickening of skin
-Thinning eyebrows
-dry flaky skin
-swelling in hands and feet
-decreased cardiac output
-ineffective breathing pattern
-activity intolerance
-imbalanced nutrition: more than body requirements
-risk factor for constipation
-deceased acuity of taste and smell
-hoarse, raspy speech
-abnormal menstrual periods and decreased libido

Front 20

What drus are CONTRAINDICATED for hypothyroidism?

Back 20

-Barbiturate
-Sedatives
-CNS depressants!!!!

Front 21

What is most frequently admined for Thyroid hormone therapy? [Hypothyroidism]

Back 21

-Levothyroxine(Synthroid)

Front 22

What should the PT be monitored for during thyroid hormone therapy for Hypothyroidism?

Back 22

-risk for cardiac compliactions
-Monitor: for cardio comprimise (palpiations, cehst pain, SOB, rapid heart rate)
-usually occurs during early therapy

Front 23

How does thyroid hormone therapy begin? [Hypothyroidism]

Back 23

-SLOWLY
-dosage Increases every 2 - 3 weeks
-Treatment considered LIFELONG

Front 24

S/S of hyperthyroidism with overmedication from Thyroid hormone therapy include?

Back 24

-irritability
-termors
-tachycardia
-palpitations
-heat intolerance

Front 25

For Hypothyroidism what should be increased gradually?

Back 25

-client's activity level
-provide frequent rest periods to avoid fatigue
-Decreasemyocardial oxygen demand

Front 26

For Hypothyroidism, what shoudl be applied to the client's legs?

Back 26

-Antiembolism stockins
-elevate PT's legs to assist venous return

Front 27

For Hypothyroidism, what should be encouraged to precent pumonary complications?

Back 27

-Cough and deep breathe deeply

Front 28

For Hypothyroidism, what type of diet should be encouraged?

Back 28

-HIGH BULK, LOW Calorie diet
-encourage exercise to promote weight loss
-Admin: laxatives and stool softners as needed

Front 29

For Hypothyroidism, if person is in bed rest what should you do?

Back 29

-Turn and reposition every 2 hr
-Use alochol free skin care products and emollient lotion after bathing

Front 30

For Hypothyroidism patients with decreased cold tolerance should be taken care of how?

Back 30

-extra clothing and blankets
-Dress client in layers
-adjust room temp
-encourage warm liquids if possible
-Caution against electric blankets and heating devices b/c combo of vasodilation, decreased sensation, decreased alertness may result in unrecognized burns

Front 31

Myxedma Coma

Back 31

-life threatening condition occurs when hypothyroidism is UNTREATED
-when strressor such as infection affects individual with hypothyroidism

Front 32

What do PT's with Myxedma Coma experince?

Back 32

-Decreaed respirations
-PaCO2 lvls may rise
-Decreased cardiac output
-Worsening cerebral hypoxia
-Stupor
-Hypothermia
-Bradycardia
-Hypotension

Front 33

RN responses to Myxedma Coma?

Back 33

-Maintain ariway patency
-Maint cirucalion: IV flurid replacment
-Continuous ECG monitoiring
-Monitor ABG (arterial blood gases) - detects hypotxia and metabolic acidosis
-Warm cleitn w/blankets
-Monitor body temp until stable
-Replacy thryoid hormone by admin large IV levothyroxine(Synthroid) as ordered
-Monitor VS b/c radid correctoin of MC can ause advers Cardiac effects
-Wigh daily and montior I&O, with treament Urine output will increase body weight decrease
-Provide supplemental glucoses as needed
-check of rinfections: wound,

Front 34

The Thyroid gland produces what three hormones?

Back 34

--T4 (thyroxine)
-T3 (triiodothyronine)
-Thyrocalcionin (calcitonin)

Front 35

What regulates T3 and T4 secretion?

Back 35

-Anterior Pit. Gland though (-) feebback mechanism

Front 36

What happens when T3 and T4 are decreased?

Back 36

-TSH is relased by Anterior Pit. Gland
-stimulates gland to secrete MORE homrones until normal lvl released

Front 37

How does T3 and T4 affect all body systems?

Back 37

-Regulate overall body metabolism, energy production, fluid & electrolyte balances, controlling tissue use of fats, proteins and carbohydrates

Front 38

What does calcitonin inhibit?

Back 38

-Mobilization of Ca+ from bone and reduces blood Ca+ levels

Front 39

Hypterthyroidism?

Back 39

-caussed by Excessive circulation thyroid hormones
-Affecte enire body
-causes exaggerate state of normal body functios

Front 40

What can hyperthyroidism produce?

Back 40

-Hyper metabolic state

Front 41

Causes of Hypterthyroidism?

Back 41

-action of immunboglobulins on thyroid hormones

Front 42

Graves disease:

Back 42

-most common cause of HyperT
--automimmune mimic TSH lead to hypersectretion of thyroid hormones

Front 43

Hyperthyroidism Serum TSH test?

Back 43

-DECREASED

Front 44

Hyperthyroidism Free thyroxine index (FTI) & T4?

Back 44

-ELEVATED

Front 45

Hyperthyroidism Thyrotropin-releasing hormone (TRH) stimulation test?

Back 45

-failure of expected rise in TSH

Front 46

Hyperthyroidism radioiodine (131 I ) and thyroid scan

Back 46

-clarifies size of gland and detect presence of hot or cold nodules

Front 47

For Hyperthyroidism why would a medication history be necessary to determine use of Iodines?

Back 47

-Contrast median and OC cause falsely ELEVATED serum TSH lvls
-Severe illness, malnutrition use of aspirin, corticosteroids and phenytoin Na_ cause false decrease in serum TSH lvls

Front 48

S/S of Hyperthyroidism?

Back 48

-Nervoussness, irriability, emotianl lability decreased attention span
-weakeness, easy fatibability, exercise intolerance
-Heat intolerance
-Weight change (usually loss);
-increased appetite
-Insomnia (interrupted sleep)
-Frequent stools (diarrhea)
-Mensstural irregulatirites, increased libido
-Warm, sweaty flushed skin w?velverly smooth texture
-Tremor, hyperknesias, hyperflexia
-Vision changes, expohthalmos, treaterace eye lids, staring gaze
-Hair loss
-Goiter
-Bruits over the thyroid gland
-Elevated systolic BP, widened pulse pressure, S3 heart sound

Front 49

For Hyperthyroidism Antithyroid medications?
Propplthiouracil(PTU)
Methiimazol(Tpazole)

Back 49

-blocks thyroid hormone synthesis

Front 50

For Hyperthyroidism Antithyroid medications?
Beta-Adrengergic blockers

Back 50

-Treats sympathetic nervous systems effects (tachycardia, palpiations)

Front 51

For Hyperthyroidism Antithyroid medications?
Iodine containing meds

Back 51

-inhibit release of stored thyroid hormone and retard hormone synthesis
-Use of these meds is CONTRAINDICATED in pregnancy

Front 52

What should PT's receiving antithyroid meds for Hyperthyroidism be monitored for?

Back 52

-Hypothyroidism, occurs with OVERMEDICATION

Front 53

If PT is unresponsive to antithroid meds what should be done?

Back 53

-Prepare PT for total/subtotal thyroidectomy or has airway obstruction goiter

Front 54

What should be monitored during anitthyroid med therapy?

Back 54

-Vital Signs
-Hemodyanmic parameters for sings of HF

Front 55

What should be provided for a patient with exopthalmos (hyperthyroidism)?

Back 55

-Eye protection(patches, eye lubricant, taping eyelids closed)

Front 56

Thyroid Storm [Thyrotoxic crisis}?

Back 56

-large amts of thrydoid hromones into bloodstream
-causes greater increased body metabolism
-this is a MED emergency w/high mortality rate

Front 57

Thyroid Storm precipiating factors?

Back 57

-Inefection, anemia, trauma, emotional stress = all increase demond on body metabolism
-Can occur with subtoal thyroidectome b/c manipulaion of gland during surgery

Front 58

Thyroid Storm symptoms?

Back 58

-hyperthermia, hypertension, delirium, vomiting, abdominal pain, tachdysrhthmias

Front 59

RN response to Thyroid Storm?

Back 59

-Maintain patent airway
-Montor for dyshrthmias
-Admin ASA (acetominophen) to decrease temp DONT USE ASPRIN
-Cool sponge baths: or ice packs to client's axilla an graoin to decrease fever
-Admin Propylthiouracil (PTU) : to prevent synthesis & release of thyroid hormones
-Admin Propanol (inderal) to block sympathetic nervous system effects
-Admin IV fluids
-Admin Sodium Iodine 1 hr after admin of PTU
-Admin small doses of Insulin to control hyperglcemia
-Admin supplemental O2

Front 60

Thyroidectomy?

Back 60

-surgical removal of part/all of thyroid gland

Front 61

Thyroidectomy?

Back 61

-performed for treatment of hyperthyroidism when drug therapy FAILS, & radiaion contraindicated
-used to correct diffuse goiter & thyroid cancer

Front 62

LIfelong thyroid replacement therapy is required for?

Back 62

-client who has total thyroidectomy

Front 63

Steps taken before thyroidectomy?

Back 63

-4 - 6 weeks before surgery pt placed on PTU or methimazol(tapazole)
-client should receive IODINE 10 - 14 weeks before
-Helps reduce size of gland & prevent excess bleeding
-Propanol (inderal) may be given to block adrengeric effects

Front 64

Why is it important to collect serum thyroid hormones before a thyroidectomy?

Back 64

-Determination to check for Euthyroidism preoperatively

Front 65

ECG before thyroidectomy?

Back 65

-To evaluate cardiac status

Front 66

Complications of Thyroidectomy include?

Back 66

-Hemorrhage: surgical dressing and incision need to be assessed for excessive drainage and bleeding
-Tell PT to avoid neck flexion or extension - avoids pressure on suture line
-Suport head and neck with pillow/sandbags
-Thyroid storm (tachycardia, diaphoreses, increase BP, anxiety)
-Airway Obstruction: trach tray kept near client at ALL times
-Bed in HIGH fowler's postion to decrease edema and swelling of neck
-Hypocalcemia and tetany (due to damage of parathyroid glands)
-Monitor for signs of hypocalcemia (tingle of fingers and toes, carpopedal spams and convulsions)
-have Calcium gluconate available
-maintain seizure precautions
-Nerve Damage
-led to vocal cord paralysis and vocal disturbances
-PT will be able to speak rarely and to rst voice for several days, should also expect it to be hoarse
-Monitor clients ability to speak
-Asses client' voice tone and quality pre/post op

Front 67

Diabetes Insipiduse

Back 67

-results from deficiency of ADH hormone

Front 68

Antidiuretic Hormone (ADH)?

Back 68

-Also known as vasopressin
-Secreted by posterior lobe of Pituitary gland (neurohpophysis)

Front 69

What does DECREASED adh do?

Back 69

-reduces ability of distal and collection renal tubules in kideny to concentrate urine
-results in EXcessive diluted urination, excessive thirst, excessive fluid intake

Front 70

What is Neurogenic diabetes insipidus?

Back 70

-Known as Primary or Central-
-caused by: defect in hypothalamus or Pit. Gland as in trauma, irradiation, or cranial surgery

Front 71

What is Nephrogenic diabetes insipidus?

Back 71

-Inherited
-renal tubules do not respond to ADH

Front 72

What is drug-induced diabetes insipidus?

Back 72

-From certain medications

Front 73

Urine Chemistry for Diabetes Insipidus will be?

Back 73

-think DILUTE
-Decreased specific grav. ( < 1.005)
-Decreased urine osmalit (50 - 200 mOsm/kg)
-Decreased Urine pH
-Decreased urine Na+ & K+
As urine vol. INCREASES, Osmoalty DECREASES

Front 74

Serum Chemistry for Diabetes Insipidus will be?

Back 74

-Think CONCENTRATED
-Increased serum Osmality
-Increased serum Na+ and K+
-as serum volume INCREASES, serum osmality DECREASES

Front 75

Diabetes insipidus Radioimmunoassay will have?

Back 75

-Decreased ADH

Front 76

Water deprivation test for diabetes insipidus?

Back 76

-Simplest and most reliable test
-inablilty of kidneys to concentrate urine despite increased plasma osmolaity and low plasma vasopression level

Front 77

Vasopression test for diabetes insipidus?

Back 77

-subQ injection of vasopression produces output with increaesd urine specific gravity if client has CENTRAL diabetes
-Helps diffrentiate between Central and Nephrogenic diabetes

Front 78

S/S of diabetes insipidus?

Back 78

-Polyuria (abrupt onset of exsessive urine)
-Urinary output of 5 to 20L/day of dilute urine
-Polydipsia (excessive thirst, consumption of 4 to 30L/day)
-Nocturia
-Fatigue
-Dehydration: EV by: exterme thirst, weight loss, muscle weakness, headache, tachycardia, hypotension, poor skin turgor, dry mucous membranes, constipation, dizziness

Front 79

What can untreated diabetes insipidus produce?

Back 79

-Hypovolemia, hyperosmality, circulatory collapse, unconsciousness, and CNS damage

Front 80

Meds for Diabetes Insipdius?
ADH replacment agent?

Back 80

-Desmopression acetate (DDAVP)
-Aquaeous Vasopressin (Pitression) admined intranasally, orally or parentreally

Front 81

Meds for Diabetes Insipdius?
ADH stimulant

Back 81

-Carbamzepine (Tegretol)

Front 82

Why should Vasopression be given caustiously for a PT with CAD & diabetes insipdius?

Back 82

-Med causes vasoconstriction

Front 83

What shoud you tell a DI patient the reason for lifelong vasopressin therapy?

Back 83

-Daily weight, and importance of reporting weight gain, polyuria and polydipsia to primary care provider

Front 84

SIADH?

Back 84

-Syndrome of inappopriate ADH
-excessive release of ASD [vasopressin]

Front 85

[SIADH ] Excess ADH ?

Back 85

-leads to renal absorption of water an disruptions of angiotension mech
-causes renal exreciotn of sodium leading to water intoxication, cellular edema, and dillutional hyponatermia,
-Fluid shifts within compartments caused decreased serum osmality

Front 86

What conditions stimulate the hyptothamlus to hypersecrete ADH?

Back 86

-Malignant tumors( commosn cause is oat-cell lung cancer)
-increasing intrathoracic pressure
-head injury
-Meningitis
-Cardiovascular accident
-Meds (alcohol, lithium carbonate, phenytoin)
-Trauma
-Pain
-Stress

Front 87

[SIADH] Urine Chemistry?

Back 87

-Think CONCENTRATED
-Increased urine Na+
-Increased urine osmolaity
-urine vol. DECREASES, urine osmolality INCREASES

Front 88

[SIADH] blood chemistry?

Back 88

-Think DILUTE
-Decreased serum Na+ (110mEq/L)
-Decreased osmolality (< than 270 mEq/L)
-As serum vol increases, serum osomlality decreaess

Front 89

[SIADH] Radioimmunoassay will show?

Back 89

-Increased ADH

Front 90

Early symtpoms for SIADH?

Back 90

-Headache, weakeness, anorexias, muscle cramps, weight gain (w/o edema b/c wat not Na+ is retatined)
-

Front 91

For SIADH as serum Na+ decreased the patient will?

Back 91

-experience personality changes, hostility, sluggish deep tendon reflexes, nausea, vomiting, diarrhea, and oliguria
-experience confusion, lethargy, Cheynes-Stokes respirations

Front 92

For SIADH as serum Na+ is extremly decreased patient will?

Back 92

-seizures, cooma, death may occur

Front 93

SIADH?

Back 93

-Syndrome of inappopriate ADH
-excessive release of ASD [vasopressin]

Front 94

[SIADH ] Excess ADH ?

Back 94

-leads to renal absorption of water an disruptions of angiotension mech
-causes renal exreciotn of sodium leading to water intoxication, cellular edema, and dillutional hyponatermia,
-Fluid shifts within compartments caused decreased serum osmality

Front 95

What conditions stimulate the hyptothamlus to hypersecrete ADH?

Back 95

-Malignant tumors( commosn cause is oat-cell lung cancer)
-increasing intrathoracic pressure
-head injury
-Meningitis
-Cardiovascular accident
-Meds (alcohol, lithium carbonate, phenytoin)
-Trauma
-Pain
-Stress

Front 96

[SIADH] Urine Chemistry?

Back 96

-Think CONCENTRATED
-Increased urine Na+
-Increased urine osmolaity
-urine vol. DECREASES, urine osmolality INCREASES

Front 97

[SIADH] blood chemistry?

Back 97

-Think DILUTE
-Decreased serum Na+ (110mEq/L)
-Decreased osmolality (< than 270 mEq/L)
-As serum vol increases, serum osomlality decreaess

Front 98

[SIADH] Radioimmunoassay will show?

Back 98

-Increased ADH

Front 99

Early symtpoms for SIADH?

Back 99

-Headache, weakeness, anorexias, muscle cramps, weight gain (w/o edema b/c wat not Na+ is retatined)
-

Front 100

For SIADH as serum Na+ decreased the patient will?

Back 100

-experience personality changes, hostility, sluggish deep tendon reflexes, nausea, vomiting, diarrhea, and oliguria
-experience confusion, lethargy, Cheynes-Stokes respirations

Front 101

For SIADH as serum Na+ is extremly decreased patient will?

Back 101

-seizures, cooma, death may occur

Front 102

[SIADH] Restrict Oral fluids to?

Back 102

-500 - 1000mL ro prevent further hemodiluation
-privide oral hysteopine as well as ice chips, lozenges or hard candy and scheduled water intake

Front 103

[SIADH] Monitor VS for?

Back 103

-Increased BP, tachycardia, and hypothermia

Front 104

Cushing's disease/Syndrome?

Back 104

-characterized by adrenal glands hyperfunction excess production of glucocoritocid coritsol

Front 105

What do high levels of corisold reduce?

Back 105

-Lymphocyte activity which creates immunosuppression

Front 106

What is endogenous causes of Cushing's disease include?

Back 106

-Adrenal hyperplasia
-Adrenocoritcal neoplasm
-Pituitary neoplasm that secreated adrennocoricopropic horomone (ACTH)
-Carincoma: lung, GI tract, pancreas (these tumors can secrete ACTH)
-

Front 107

When does Cushing's disease usually occur?

Back 107

-in women between 25 - 40 years old

Front 108

What is endogenous causes of Cushing's disease therapeutic uses of glucocoricoids for?

Back 108

-Chronic fibrosis
-Allergies
-Cancer chemotherapy
-Organ transplantation
-Autoimmune disorders
-Asthma

Front 109

[Cushing's Syndrome/Disease]
Dexamethasone suppression test

Back 109

-24hr urine collection reveal suppression of cortisol exertion in clients' w/o cushing's
-Nonsuppriession of coritsol excretion = Cushing's
-

Front 110

[Cushing's Syndrome/Disease]
Diagnostic for Serum Na+, K+, glucose

Back 110

-Serum Na+ lvl = INCREASED
-Serum K+ & Ca+ = DECREASED
-Serum glucose lvl = INCREASED

Front 111

[Cushing's Syndrome/Disease]
Urine corisol levels?

Back 111

-Elevated lvls of free coritsol

Front 112

Therapeutic procedures for engodneous hyptercorisolism include?

Back 112

-Surgical removal of Pit. or Adr. Gland (depending on cause)
Hypophysectomy: Intervene for risk ass. with cranial surgery
-Adrenlaectomy: intervene for risks assoc. with flank or abdominal surgery. provide glucocoritcoid replacement as needed
Chemothearpy w/cytotoxic agents: Monitor AE example thrombocytopenia
Radiation Therapy: Intervene for skin and alopecia effects

Front 113

S/S of [Cushing's Syndrome/Disease]

Back 113

-Decreased immune fucntion
-Decreased inflammatory resonse
-HTN (Na+ and H20 retention)
-Changes in fat distrubution: moon face, truncal obestity, fat collection on back of next (buffalo hump)
-Emotional lability
-Fractures (osteoporosis)
-Impaired glucose tolerance
-Hirsutism
-Bruising and petechiae (fragile blood vessels)
-Muscle wasting

Front 114

Addison's disease:

Back 114

-adrenocortical insufficieny
-caused by damge or dysufntion of adrenal cortex

Front 115

What does the adrenal cortex produce?

Back 115

-Mineralcoricoids, Gluccoritcoids, Sex hormones

Front 116

Mineralcorticoids:
[Addison's disease]

Back 116

-Aldosterone: Increases na absorption, causes K+ secretion

Front 117

Glucocoricoids:
[Addison's disease]

Back 117

-Corisole -affects glucose, protein and fat metabolism and body's resonse to stress and body's immune function

Front 118

Sex hormones:
[Addison's disease]

Back 118

-ANdrogens and Estrogen

Front 119

Production of what is diminshed in Addison's disease?

Back 119

-Mineralcoritcoids and glucocoritcoids, resulting in decreased aldosterone and cortisol

Front 120

Adrenal Crisis:
[Addison's disease]

Back 120

-also knowsn as acute adrenal insufficency
-is a MED emergency

Front 121

Majority causes of [Addison's disease]

Back 121

-Idopahtics autoimmune dysfunction
-Tuberculosis

Front 122

Adrenal crises [Addison's disease] caused by

Back 122

-acute chronic insufficiency due to:
-sepsis
-trauma
-stress
-adrenal hemmorrhage
-steroid withdrawal

Front 123

Diagnostic procedures and expected findings for [Addison's disease]:
Serum electrolytes?

Back 123

-increased K+ & Ca+, decreased Na+,

Front 124

Diagnostic procedures and expected findings for [Addison's disease]:
BUN, Creatinine?

Back 124

-Increased

Front 125

Diagnostic procedures and expected findings for [Addison's disease]:
ECG?

Back 125

-Dysrhythmias

Front 126

Diagnostic procedures and expected findings for [Addison's disease]:
Serum glocuose and cortisol?

Back 126

-Decreased

Front 127

Diagnostic procedures and expected findings for [Addison's disease]:
ACTH

Back 127

-ACTH infused and cortisol lvl measured
-Plasma cortisol lvls don't rise

Front 128

S/S [Addison's disease]:

Back 128

-Hyperpigmentation
-Weakness and fatigue
-Nausea and vomiting
-Dizziness w/orthostatic hypotension
-Dehydration
-Hyponatremia
-Hyperkalemia
-Hypoglycemia
-Hypercalcemia

Front 129

Pheochromocytoma

Back 129

-tumor of the adrenal gland
-rare tumor
-about 10% of pheochromocytomas are malignant

Front 130

Pheochromocytoma produced and stored?

Back 130

-catecholamines, such as epinephrine and norepinephrine
-excess epi and nonepi, produce sympathetic nervous system effects

Front 131

Preciptating factors of a catecholamine surge by peochromoocytome in a PT may be?

Back 131

-Anesthesia
-Opiates and opiate antagonists (ex: naloxone)
-Dopamine antagonist (droperidol, phenothizines)
-Drugs that inhibit catecholamie reputake (TCA)
-Childbirth
-Radograhic contrast media
-Foods high in tyramine (wine, aged cheese)

Front 132

Diagnostic tests for Pheochromocytoma:
Vanillymandelic acid testing (VMA)

Back 132

-24 hour urine collection for catecholamines, metanephrine, and VMA
-Normal: 2 - 7mg/24hr
-High levels @ rest indicate pheochromocytoma

Front 133

Diabetes mellitus is characterized by?

Back 133

-Chronic hyperglycemia due to problems w/insulin secregoin or effectiveness of endogenous insulin

Front 134

Diabetes mellitus is a contributing factor to?

Back 134

-Cardiovascular disease, hypertension, renal failure, blindness, and stroke
-Due to impact on larg and small blood vessels

Front 135

Hallmark symptoms assoc. with Diabetes Mellitus? 3P's!

Back 135

-Polyuria
-Polydipsia
-Polyphagia

Front 136

Normal Range for Diabetes mellitus

Back 136

-70 - 120 mg/dL

Front 137

Type 1 diabetes characterized by?

Back 137

-autoimmune disorder characterized by beta cell destruction
-Occurs genetically suspectiple ppl before the age of 30

Front 138

Type 2 diabetes characterized by?

Back 138

-development of resistance to endogenous insulin
-occurs frequently in individuals with family disposition who are Obese and over the age of 40

Front 139

Hallmark risk factors for development of insulin resistance include?

Back 139

-Obesity, physical inactivity, high triglycerides (.250 mg/dL) and hypertension

Front 140

Secondary causes of diabetes mellitus include?

Back 140

-Pancreatitis
-Cushing's syndrome

Front 141

Iatrogenic causes of diabetes mellitus include?

Back 141

-Glucocorticoid usage

Front 142

Diagnostic criteria for diabetes mellitus two findings (separate days) of one of the following:

Back 142

-Sym. of diabets + casual plams glucose concentration of greater than 200mg/dL (w/o regard to time since last meal)

-Fasting blood glucose greater than 126 mg/dL (8 hr fasting)
-Two-hour glocse greater than 200mg/dL with an oral glucose tolerance test (10 - 12 hr fasting)

Front 143

Fasting blood glucose

Back 143

-Ensure pt has fasted for 8 hr period prior to blood draw
-Antibidabetic meds should be postponed

Front 144

Pre-meal glucose:

Back 144

-Target is 90 - 130 mg/dL
-

Front 145

Oral glucose tolerance test:

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-Instruct client to consume balnced diet for 3 days prior to test
-Than instruct client to fast for 10 - 12 hrs prior to test
-Fasting blood glucose drawn at start of test
-Client than instructed to consume specified amt of glucose
-Blood glucose levels than taken every 30 min for 2 hrs
-Client must be assessed for hyperglycemia throughout procedure

Front 146

Glycosylated hemoglobin (HbA1c)

Back 146

-Target is 4 - 6%
-best indicator of average blood glucose level for past 120 days

Front 147

S/S of Type 1 Diabetes:

Back 147

-Polyurida, Polydipsia, Polyphagia
-weight loss
-fatigue
-Increased frequency of infections
-Rapid onset
-controlled by exogenous insulin

Front 148

S/S of Type 2 Diabetes:

Back 148

-Polyurida, Polydipsia, Polyphagia
-Obesity
-fatigue
-Increased frequency of infections
-Gradual onset
-controlled by oral antidiabetic meds and insulin

Front 149

S/S by Glucose alteration:
Hypoglycemia

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- ( < 50mg/dL)
-Cool, clammy skin
-Diaphoresis
-Anxiety, irritability, confusion, blurred vision
-Hunger
-General weakness, seizures, (severe hypoglycemia)

Front 150

S/S by Glucose alteration:
Hyperglycemia

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- ( > 250mg/dL)
-Hot, dry skin
- Absence of diaphoresis
-Alert to coma (varies)
-N/V, abdominal pain (w/ketoacidosis)
-Rapid deep respirations (acetone/frutiy odor due to ketones)

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Appropriate Assessments for PT with diabetes mellitus include?

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-Blood glucose lvls
-I & O, weight
-Skin integerity and healing status of wounds
-Sensory alterations (tingling, numbness)
-Condition of feet and foot care practices
Dietary practices
-Exercise patterns
-Client's self montior of blood glucose skill profeicency
-Client's self med admin proficiency
-Pain levels

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Instructions for proper foot care for patient with diabetes mellitus?

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-Insepect feet daily wash with warm water & mild soap
-Pat feet dry, especially between toes
-Use mild foot powder (powder with cornstartch) on sweaty feet
-Don't use commercial remedies to remove calluses or corns
-Cut toenails even with rounded contour of toes; don't cut corners
-Best time to cut nails = after shower/bath
-Cusult podiatrist for trimming thick, malformed toenails
-Avoid open-toed, open heel shoes. Leather shoes are perferred over plastic ones. Wear slippers with traction. Never go barefoot. Shake shoes upside down before putting them on
-Wear clean abosorbent socks or stockings
-Don't apply exernal heat to warm feet. wear socks for warmth
-avoid extensive periods of sitting, standing, and avoid crossing legs

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Nutritional Management for a patient with diabetes mellitus?

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-Count grams of carbohydrates consume (Dosage of insulin determined by this consumption; 1 unit/15 g carbohydrates)
-Restric calories and increased physical activity for clients that are obese
-Include fiber in diet to increase carbohydrate metabolism and help control cholesterol levels
-use artificial sweetners
-Use fat replacers within guidelines

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Rapid-Acting (Humalog, Lispro)
Onset:
Peak:
Duration:
Administer:

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Onset: < 15 mins
Peak:0.5 - 1.5 hr
Duration: 2 - 6 hr
Administer: 5 - 15 min ac

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Intermediate-Acting (Lente)
Onset:
Peak:
Duration:

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Onset: 3 -4 hrs
Peak:4 - 12 hrs
Duration: 12 - 20 hrs

Front 156

Short-Acting (Humulin R, Regular)
Onset:
Peak:
Duration:
Administer:

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Onset: 30 - 60 min
Peak: 2 - 3 hrs
Duration: 3 - 10 hrs
Administer: 30 min ac

Front 157

Intermediate-acting: Humulin N, NPH, 70/30, 70/25)
Onset:
Peak:
Duration:
Administer:

Back 157

Onset: 2 - 4 hrs
Peak: 4 - 10 hrs
Duration: 10 - 18 hrs

Front 158

Long-acting: Ultralente
Onset:
Peak:
Duration:

Back 158

Onset: 6 - 10 hrs
Peak: 8 - 20 hrs
Duration: 18 - 24 hr

Front 159

Long Acting: Lantus
Peak:
Duration:

Back 159

Peak: none
Duration: 24 hrs

Front 160

Why is it important to rotate injection site for pt with diabetes mellitus?

Back 160

-prevents liphohypertrophy

Front 161

How to inject insulin for patient with diabetes mellitus?

Back 161

-90 degree angle for obese patient
-45 degree angle for thin patient
-Aspiration of blood not necessary

Front 162

How to mix rapid or short acting insulin with long acting insulin?

Back 162

-1st draw up shorter acting insulin into syringe
-Than draw up longer acting insulin

Front 163

Diabetic ketoacidosis (DKA):

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-acute, life threatening condition
-characterized by hyperglycemia (> 300mg/dL)
-results in breakdown of body fat for energy and accumulation of ketones in blood and urine
-Onset = rapid
-Moratly rate 1 - 10%

Front 164

Hyperglycemic-hyperosmolar nonketotic syndrome (HHNS)

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-acute, life thretening condiong
-characterized by profound hyperglycemia (>600 mg/dL)

Front 165

DKA & HHNS both result in sever hyperglycemia from:

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-lack of sufficient insulin (new onset diabetes, lack of compliance of diabetes plan)
-increased need for insulin (stress, illness, infection, surgery, trauma)

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DKS more common in:

Back 166

-individuals with type 1 diabetes mellitus

Front 167

HHNS more common in?

Back 167

-older adult clients and individuals with untreated or undiagnosed type 2 diabetes mellitus

Front 168

Diagnostic Procedures: DKA
Serum Glucose lvls

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- > 300 mg/dL

Front 169

Diagnostic Procedures: DKA
Serum Electrolytes

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-Na+ increased due to water loss
-K+ initally low due to diuresis, may increase due to acidosis

Front 170

Diagnostic Procedures: DKA
Serum Renal studies

Back 170

-BUN & Cretinine: Increased seocndary to dehydration

Front 171

Diagnostic Procedures: DKA
Ketone Levels

Back 171

-Serum and Urine: both present

Front 172

Diagnostic Procedures: DKA
Serum Osmolarity

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-High

Front 173

Diagnostic Procedures: DKA
Serum pH (ABG)

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-Metabolic acidosis with respiratory compensation (Kussmaul respirations)

Front 174

Diagnostic Procedures: HHNS
Serum pH (ABG)

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-Absence of acidosis

Front 175

Diagnostic Procedures: HHNS
Serum osmolarity

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-very high

Front 176

Diagnostic Procedures: HHNS
Ketone levels

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-Serum & Urine: Both absent

Front 177

Diagnostic Procedures: HHNS
Serum Renal studies:

Back 177

-BUN and Creatinine: Increased secondary to dehydration

Front 178

Diagnostic Procedures: HHNS
Serum electrolytes

Back 178

-Na+ increased due to water loss
-K+ initially low due to diuresis

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Diagnostic Procedures: HHNS
Serum glucose levels

Back 179

- ( > 600 mg/dL)