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MedSurg > Endocrine Disorders > Flashcards

Endocrine Disorders Flashcards

1
Q

Hypothyroidism

A

Autoimmune disease
- Hashimoto’s thyroidism –> primary hypothyroidism

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2
Q

Hypothyroid clinical manifesatations

A
  • Hypometabolic state
  • Goiter: enlarged thyroid gland
  • Skin & edema changes
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3
Q

Hypothyroid clinical manifestations - hypometabolic state

A
  • Decreased energy
  • Increased sleep
  • Fatigue
  • Weight gain
  • Decreased appetite
  • Susceptibility to cold temps
  • Constipation
  • Cardiac: decreased contractility, cardiac output and heart rate
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4
Q

Hypothyroid clinical manifestations - skin & edema changes

A
  • Periorbital edema
  • Facial puffiness
  • Dry and coarse skin d/t lack of sweating
  • Dry and coarse hair, which is thin and fragile
  • Cardiac: pericardial effusion
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5
Q

Lab changes in primary hypothyroidism

A
  • Increased TSH
  • Decrease T3 and T4
    ** Due to feedback to the anterior pituitary and hypothalamus, TSH increases because of low T3 and T4
  • Antithyroid Antibodies (in suspected Hashimoto’s disease)
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6
Q

Levothyroxine

A
  • Take in the AM at the same time every day

Safety Issues:
- Patients with CVD - increase dose with caution as Levothyroxine (Synthroid) increases HR and contractility → can cause angina or CHF

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7
Q

*Hypothyroid complications

A

Myxedema coma
- Resp: hypoxia, hypoventilation leading to CO2 retention
- Cardiac: bradycardia, hypotension
- Fluid & electrolyte imbalance: hypoglycemia, hyponatremia, significant hypothermia

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8
Q

What kinds of meds do you need to be careful with myxedema coma?

A

Slow metabolism of medications warranting extreme caution
- Sedatives
- Hypnotics
- Narcotics

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9
Q

*Hypothyroidism risks for hypocalcemia secondary to ?

A

Parathyroid disruption, post thyroidectomy as the parathyroid tissue may be damaged
- Labs & Physical Assessment - Chvostek’s and Trousseau signs

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10
Q

Hypothyroidism nursing assess

A
  • VS & O2 Sat: decreased everything
  • Daily weights
  • Skin: dry, no sweat, deposit of metabolites under skin, edema
  • GI: decreased bowel sound, abd distention, constipation
  • Hypocalcemia
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11
Q

Hypothyroidism nursing intervention

A
  • Thyroid replacement therapy: mimic normal circadian rhythms regarding metabolism (taken at the same time daily in the AM), caution if dose is increased in patient with CVD
  • Cautiously administer narcotics, sedatives, and opiates
  • Warming Blankets PRN: warm slowly to avoid vasodilation and hypotension
  • Turning, Repositioning, Skin Care
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12
Q

Hypothyroidism pt teaching

A
  • Educate pt w CVD regarding interaction between levothyroxine (synthroid) and cardiac physiology – report sympts & monitor HR
  • Levothyroxine education → increased HR, timing of dose, side effects increased doese
  • S/S of hypo and hyperthyroidism
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13
Q

*Hyperthyroidism: primary vs secondary

A

Primary:
- Grave’s dz: autoimmune, most common cause
- Thyroid nodules: toxic multinodular goiter, toxic nodule
- Thyroiditis: inflamm of thyroid, autoimmune or other
- Exogenous thyroid hormone, ectopic thyroid tiss

Secondary:
- TSH secreting pituitary adenoma

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14
Q

*Hyperthyroidism clinical manifestations

A
  • Hypermetabolic state
  • Goiter: hyperplasia d/t TSH stimulation
  • Exophthalmos: eyeball protrusion, visual changes
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15
Q

Hyperthyroidism clinical manifestations - hypermetabolic state

A
  • Increased HR, heart sounds, dysrhythmias
  • Thyroid bruit d/t increased blood flow
  • Heat intolerance
  • Increased appetite
  • Weight loss
  • Fatigue
  • Nervousness
  • Insomnia
  • Light to absent menses
  • Hair loss
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16
Q

Lab changes in primary hyperthyroidism

A
  • Decreased TSH
  • Increased T3 and T4
    *D/t feedback to anterior pituitary and hypothalamus, TSH decrease bc of high T3 and T4
  • Anti-TSH antibodies (in suspected Grave’s dz)
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17
Q

Postoperative thyroidectomy risks

A
  • Hypoparathyroidism: removal of all parathyroid tissue
  • Laryngeal nerve damage affects swallowing and voice
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18
Q

Post thyroidectomy monitoring and care

A
  • *Airway Compromise: assess breathing, secretions
  • Hemorrhage: assess bandages, neutral head position
  • Hypocalcemia: assess tetany (periodic muscle spasms) r/t parathyroid
  • Laryngeal Nerve Damage: hourly voice checks
  • Semi-Fowler’s position for ease of breathing and aspiration prevention

At bedside:
- Tracheostomy tray (d/t swelling and laryngospasm)
- Suction
- Supplemental oxygen

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19
Q

Hyperthyroidism nursing assess

A
  • VS and O2 sat: increased everything
  • I&O: insensible fluid loss, weight loss, protein consumpt
  • Eyes and vision: exophthalmos
  • Goiter
  • Sz: hyponatremia, elevated temp
  • *Thyroid hormone lvls: increased T3, free T4, TSH
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20
Q

*Hyperthyroidism nursing intervention

A
  • Administer antithyroid med as ordered: assess for SE, low WBC, lithium SE
  • Administer iodine prep
  • Administer beta blockers
  • Implement cooling measures
  • Administer eye lubricants to minimize complications of incomplete eyelid closure d/t exophthalmos
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21
Q

Hyperthyroidism pt teaching

A
  • Dz process
  • Antithyroid meds: timing of daily dose, importance of consistent dosing
  • Nutrition: high calorie intake to minimize weight loss
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22
Q

Hypoparathyroidism idiopathic (autoimmune) v. acquired

A

Idiopathic (unknown):
- Autoimmune screen for antiparathyroid hormone antibodies (seen in DM and adrenal insufficiency)

Acquired:
- Removal of parathyroid glands during thyroidectomy (most common)

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23
Q

Hypoparathyroidism

A

Mainly hypocalcemia

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24
Q

Hypoparathyroidism clinical manifestations

A
  • Decreased Ca level
  • Numbness and tingling around the mouth, hands, feet
  • Severe muscle cramps
  • Spasms of the hands and feet
  • Tetany

2 spec assess:
- Chvostek’s sign: facial twitch when stroke along
- Trousseau’s sign: spasm of hand and wrist after upper arm compress w BP cuff

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25
Q

*Hypoparathyroidism lab anormalities

A
  • Low Ca++ levels
  • High Phos levels
  • Low serum PTH levels
  • Serum Mg lvls – hypomagnesia could be cause of hypoparathyroidism
  • Serum albumin levels bc majority of Ca is protein bound – if low albumin, low Ca, draw ionized (free) Ca
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26
Q

Hypoparathyroidism treatment

A

Focus on raising serum calcium levels, monitoring Ca++ levels

Acute:
- IV Ca initially w Ca gluconate, Ca Cl
- Follow up with oral calcium and vitamin D
- Patients with cardiac disease history: slow IV to minimize hypotension and bradycardia

Chronic:
- Oral Ca & vitamin D

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27
Q

Hypoparathyroidism nursing assess

A
  • VS: hypotension d/t decreased cardiac contractility
  • Cardiac monitoring: cardiac dysrhythmias, cardiac automaticity
  • Neuromuscular activity: muscle weakness, twitching, cramps, aches, balance problems, numbness, tingling
  • Lab values: ionized Ca in setting of low albumin lvls, hypomagnesia as cause of hypoparathyroidism, alkaline pH increase Ca binding to protein (decreased ionized Ca)
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28
Q

Hypoparathyroidism nursing intervention

A
  • Administer calcium replacements (oral and IV)
  • Monitor EKG
  • Administer Vitamin D
  • Safety due to neuromuscular instability
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29
Q

Hypoparathyroidism pt teaching

A
  • Medication regimen: lifelong calcium supplementation
  • Eat foods high in calcium and low in phosphorous
  • Signs of hypocalcemia and hypercalcemia
30
Q

*Primary hyperparathyroidism

A

Parathyroid gland makes too much parathyroid hormone
- *Parathyroid adenoma – benign tumor = 85% of hyperparathyroidism cases

31
Q

*Hyperparathyroidism clinical manifestations

A
  • *Neuro: lethargy, confusion, fatigue, musc weakness
  • *Cardiac: shortened ST segment resulting in prolonged PR interval & shortened QT interval
  • *Bone: bone demineralization
  • *Abd: increased gastric secretion in stomach assoc w PUD
  • GU/GI: polyuria, anorexia, constipation
  • Some asymptomatic
32
Q

Hyperparathyroidism treatment

A

Lower Ca levels by giving fluids
- Severe: IV fluids of NS to prevent renal stones
- *AVOID thiazine diuretics –> increase Ca reabsorp in kidney

33
Q

Risk of hyperparathyroidism

A

Kidney stones

34
Q

Hyperparathyroidism nursing assess

A

*Labs & cardiac monitoring
- Serum calcium levels (HIGH) d/t high levels of PTH release calcium from bone and increase renal and intestinal absorption leading to high Ca++
- Serum phosphorus levels (LOW) → PTH Increases renal excretion of phosphorus
- Acid-base status → acid pH decreases Ca++ binding to protein and elevates ionized calcium

35
Q

*Hyperparathyroidism nursing interventions

A
  • Increase fluid intake to 3L a day
  • Administer furosemide (lasix) as ordered
  • Administer oral phosphates as ordered
  • Strain urine for renal caliculi
36
Q

Hyperparathyroidism pt teaching

A
  • Signs of hypocalciumia and hypercalcemia
  • Low calcium diet
  • Increase fluids and fiber to decrease complications of constipation
37
Q

*Type I DM

A

Autoimmune destruction of beta cells

Genetic triggers:
- Family w Type 1 DM
- Family w autoimmune dz: thyroid, celiac, Addison’s dz

Environmental triggers:
- Viruses: mumps, rubella, coxsackle B4
- Toxic chemicals
- Exposure to cow’s milk w bovine antibodies
- Cytotoxins

38
Q

*Type I DM clinical manifestations

A
  • Polyuria
  • Polydipsia
  • Polyphagia (feeling of extreme, insatiable hunger) = lack of insulin prevents glucose mov to cells
  • Fatigue
  • Weight loss
39
Q

Tests to diagnose Type I/II DM

A
  • HgbA1c
  • Fasting blood glucose
  • 2 hour postprandial (after meals)
  • Glucose tolerance test (OGTT)
  • Random blood glucose
40
Q

Why is treatment of SQ insulin (basal/bolus) most effective in diabetes?

A
  • Basal: long-acting
  • Bolus: short-acting, mealtimes
  • Basal insulin is given 1-2 times/day: long-acting insulin & intermediate-acting insulin
  • Mimic the healthy pancrease response to BG levels throughout the day: basal insulin levels thruout day, sharp increases at mealtime
41
Q

SQ insulin as DM treatment

A
  • Basal insulin is given 1-2 times/day: long-acting insulin & intermediate-acting insulin

Mealtime insulin for incoming carbs:
- Short-acting insulin
- Rapid-acting insulin: prandial insulin (aka nutritional insulin), sliding scale correctional insulin (aka supplemental insulin) → compensates for BG elevation, determined immediately before meal by CBG level
- Prandial and correctional insulin are given together at the same time before eating

42
Q

What is glycemic control?

A

Maintenance of BG within normal range

43
Q

What is goal of diabetes tx?

A

Maximize glycemic control to prevent complications of hyperglycemia

44
Q

Insulin SQ injection sites

A

Abdomen, upper arm, thigh, lower back, hips, or buttocks

45
Q

Syringe considerations of insulin

A
  • Match syringe size to insulin concentration: U-100 concentration to U-100 syringe
  • Coordinate syringe size to dose for more accurate administration: small doses use a 0.3 mL syringe to measure a more accurate amount
  • Insulin pens: dial exact dosage, eliminates measuring errors
  • Continuous SQ insulin pumps and continuous glucose monitoring: pump for basal and bolus insulin, better glycemic control (pump makes auto adjustments to BG levels), delivery of more precise dosage, convenience, $$$ embarassing + skin issues
46
Q

Methods to assess blood glucose

A
  • Self monitoring
  • Continuous glucose monitoring, - Hemoglobin A1c monitoring
47
Q

*Type I DM nursing assess

A

VS:
- Hypotension and tachy → FVD related to osmotic diuresis in hyperglycemia
- Tachypnea → Kussmaul breathing, fruity breath
odor → DKA

  • I&O: increased urine output
  • Carbohydrate intake at meals
  • Serum Glucose: increased glucose, decreased d/t insulin given w/o PO intake, etc.
  • Potassium levels: decreased d/t increased vol loss, increased d/t shift of H and K in intracellular space in metabolic acidosis
48
Q

Type I DM nursing interventions

A
  • POC- CBG testing
  • Administer insulin as ordered
  • Administer isotonic IV fluids as ordered
  • Administer meds to manage electrolyte abnormalities (if hyperkalmeia, eliminate w Kayexalate)
  • Cardiac monitoring r/t potassium
49
Q

Type I DM pt teaching

A
  • Signs of hypoglycemia/hyperglycemia
  • SQ insulin administration
  • Med education
  • Regular BG monitor via finger sticks or alternate site testing
  • Healthy lifestyle: diet, exercise
50
Q

Diabetic ketoacidosis

A

Body breaks down fats which releases fatty acids –> metabolic acidosis

51
Q

*DKA clinical manifestations

A
  • Initial: polyuria, polydipsia, polyphagia
  • 1st: hyperkalemia (K leaves cell to maintain balance)
  • 2nd: hypokalemia (excess K excreted thru kidney)
  • Hyponatremia d/t increased serum osmolality
    *Cardiac monitoring
52
Q

*DKA treatment

A
  • Fluids with isotonic (0.9%) normal saline
  • Correct electrolyte imbalances, especially hypoK prior to insulin admin
  • Insulin administration (IV)
53
Q

Untreated DKA clinical manifestations

A
  • Hypotensive and Tachycardic (Hypovolemia)
  • Rapid, deep respirations (Kussmaul Respirations) compensation to raise pH by blowing off CO2 due to metabolic acidosis,
  • Breath smells fruity due to ketone bodies
  • Nausea and vomiting
  • Lethargy and coma
54
Q

*Why should you correct ELECTROLYTES BEFORE INSULIN in DKA?

A

Prevent insulin from exacerbating the hypokalemia by pushing K+ into the cell

55
Q

Hypoglycemia

A

BG < 65 mg/dL

56
Q

Causes of hypoglycemia

A
  • Excess dose of SQ insulin
  • Excess dose of oral agents stimulating insulin release (eg Type 2 DM)
  • Reduced insulin clearance (eg renal dz)

Situations:
- Decreased nutritional intake
- Increased metabolism of glucose thru exercise
- Alc blunting release of glucose from liver

57
Q

*Initial S&S of hypoglycemia

A

associated with SNS triggering and hormonal release:
glucagon, epinephrine, and norepinephrine
Anxiety
Hunger
Palpitations
Circumoral paresthesia
Sweating
Shakiness
Irritability

58
Q

Progressive/untreated sympts of hypoglycemia

A

*NEUROLOGIC
Difficulty thinking
Dizziness
Fatigue
Sleepiness
Slurred speech
Weakness/lack of coordination
Untreated → Seizures and/or Coma
Hypoglycemia Unawareness → No hypoglycemia symptoms associated with SNS triggering
Do not experience symptoms until BG is low enough to affect the CNS.

59
Q

Hypoglycemia treatment

A

-if conscious - give po glucose
-D50 if unconscious
-IM glucagon if no IV access

60
Q

Type II DM

A

Peripheral tiss become resistant to insulin

61
Q

*Type II DM risk factors

A
  • Obesity
  • Sedentary
  • Genetics
62
Q

*S&S of Type II DM

A
  • Polyuria, Polydipsia, Polyphagia
  • Fatigue
  • Poor wound healing
  • CVD***
  • Visual disturbances***
  • Renal insufficiency***
  • Recurring infection (e.g., yeast infection)
  • slower onset than type I DM

** = result from micro- and macrovascular sequelae of long-term hyperglycemia

63
Q

Type II DM medical management

A

oral meds (metformin) and lifestyle management, the role of insulin

Pharmacological interventions:
Increase insulin production
Lower insulin resistance
Slow carb absorption
Lower BG

64
Q

Type II DM self-management

A

BG monitoring, diet, weight control, exercise, psychosocial care

65
Q

Type II DM nursing assess

A
  • VS: decreased BP, increased HR (FVD), temp
  • Cap refill in LE
  • Skin assessment esp wounds
  • I&O: increased urine output, osmosis diuresis secondary to hypoglycemia
  • WBC count
  • Spot urine for microalbuminuria (microvasc dz of kidney d/t DM/HTN)
66
Q

Macrovascular complications DM

A

CVD, Carotids

67
Q

Microvascular complications DM

A

Eyes, gums, kidneys, peripheral vascular dz

68
Q

*Neurological complications DM

A
  • Impaired sensation in feet
  • ANS impairment leading to gastroparesis (paralysis of stomach) and erectile dysfunction
69
Q

Type II DM nursing intervention

A
  • BG monitoring before meals and at bedtimes
  • Administer oral diabetes meds
  • Administer insulin: basal, preprandial, correctional
  • Administer isotonic IV fluids
  • Administer abx as ordered
  • Wound care if ordered
70
Q

*Type II DM pt teaching

A
  • Meds
  • Regular BG checks via finger sticks or CGM
  • Healthy lifestyle
  • Diabetic wound care: wash feet daily, dry thoroughly, do not soak feet , careful of hot water, use creams & lotions, avoid injury, be careful cutting nails, properly fitting footwear

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