Endocrine Disorders Flashcards
1
Q
Hypothyroidism
A
Autoimmune disease
- Hashimoto’s thyroidism –> primary hypothyroidism
2
Q
Hypothyroid clinical manifesatations
A
- Hypometabolic state
- Goiter: enlarged thyroid gland
- Skin & edema changes
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
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
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)
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
7
Q
*Hypothyroid complications
A
Myxedema coma
- Resp: hypoxia, hypoventilation leading to CO2 retention
- Cardiac: bradycardia, hypotension
- Fluid & electrolyte imbalance: hypoglycemia, hyponatremia, significant hypothermia
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
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
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
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
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
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
14
Q
*Hyperthyroidism clinical manifestations
A
- Hypermetabolic state
- Goiter: hyperplasia d/t TSH stimulation
- Exophthalmos: eyeball protrusion, visual changes
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
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)
17
Q
Postoperative thyroidectomy risks
A
- Hypoparathyroidism: removal of all parathyroid tissue
- Laryngeal nerve damage affects swallowing and voice
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
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
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
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
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)
23
Q
Hypoparathyroidism
A
Mainly hypocalcemia
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
25
*Hypoparathyroidism lab anormalities
- 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
26
Hypoparathyroidism treatment
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
27
Hypoparathyroidism nursing assess
- 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)
28
Hypoparathyroidism nursing intervention
- Administer calcium replacements (oral and IV)
- Monitor EKG
- Administer Vitamin D
- Safety due to neuromuscular instability
29
Hypoparathyroidism pt teaching
- Medication regimen: lifelong calcium supplementation
- Eat foods high in calcium and low in phosphorous
- Signs of hypocalcemia and hypercalcemia
30
*Primary hyperparathyroidism
Parathyroid gland makes too much parathyroid hormone
- *Parathyroid adenoma -- benign tumor = 85% of hyperparathyroidism cases
31
*Hyperparathyroidism clinical manifestations
- *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
Hyperparathyroidism treatment
Lower Ca levels by giving fluids
- Severe: IV fluids of NS to prevent renal stones
- *AVOID thiazine diuretics --> increase Ca reabsorp in kidney
33
Risk of hyperparathyroidism
Kidney stones
34
Hyperparathyroidism nursing assess
*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
*Hyperparathyroidism nursing interventions
- Increase fluid intake to 3L a day
- Administer furosemide (lasix) as ordered
- Administer oral phosphates as ordered
- Strain urine for renal caliculi
36
Hyperparathyroidism pt teaching
- Signs of hypocalciumia and hypercalcemia
- Low calcium diet
- Increase fluids and fiber to decrease complications of constipation
37
*Type I DM
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
*Type I DM clinical manifestations
- Polyuria
- Polydipsia
- Polyphagia (feeling of extreme, insatiable hunger) = lack of insulin prevents glucose mov to cells
- Fatigue
- Weight loss
39
Tests to diagnose Type I/II DM
- HgbA1c
- Fasting blood glucose
- 2 hour postprandial (after meals)
- Glucose tolerance test (OGTT)
- Random blood glucose
40
Why is treatment of SQ insulin (basal/bolus) most effective in diabetes?
- 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
SQ insulin as DM treatment
- 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
What is glycemic control?
Maintenance of BG within normal range
43
What is goal of diabetes tx?
Maximize glycemic control to prevent complications of hyperglycemia
44
Insulin SQ injection sites
Abdomen, upper arm, thigh, lower back, hips, or buttocks
45
Syringe considerations of insulin
- 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
Methods to assess blood glucose
- Self monitoring
- Continuous glucose monitoring, - Hemoglobin A1c monitoring
47
*Type I DM nursing assess
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
Type I DM nursing interventions
- 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
Type I DM pt teaching
- Signs of hypoglycemia/hyperglycemia
- SQ insulin administration
- Med education
- Regular BG monitor via finger sticks or alternate site testing
- Healthy lifestyle: diet, exercise
50
Diabetic ketoacidosis
Body breaks down fats which releases fatty acids --> metabolic acidosis
51
*DKA clinical manifestations
- 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
*DKA treatment
- Fluids with isotonic (0.9%) normal saline
- Correct electrolyte imbalances, especially hypoK prior to insulin admin
- Insulin administration (IV)
53
Untreated DKA clinical manifestations
- 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
*Why should you correct ELECTROLYTES BEFORE INSULIN in DKA?
Prevent insulin from exacerbating the hypokalemia by pushing K+ into the cell
55
Hypoglycemia
BG < 65 mg/dL
56
Causes of hypoglycemia
- 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
*Initial S&S of hypoglycemia
associated with SNS triggering and hormonal release:
glucagon, epinephrine, and norepinephrine
Anxiety
Hunger
Palpitations
Circumoral paresthesia
Sweating
Shakiness
Irritability
58
Progressive/untreated sympts of hypoglycemia
*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
Hypoglycemia treatment
-if conscious - give po glucose
-D50 if unconscious
-IM glucagon if no IV access
60
Type II DM
Peripheral tiss become resistant to insulin
61
*Type II DM risk factors
- Obesity
- Sedentary
- Genetics
62
*S&S of Type II DM
- 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
Type II DM medical management
oral meds (metformin) and lifestyle management, the role of insulin
Pharmacological interventions:
Increase insulin production
Lower insulin resistance
Slow carb absorption
Lower BG
64
Type II DM self-management
BG monitoring, diet, weight control, exercise, psychosocial care
65
Type II DM nursing assess
- 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
Macrovascular complications DM
CVD, Carotids
67
Microvascular complications DM
Eyes, gums, kidneys, peripheral vascular dz
68
*Neurological complications DM
- Impaired sensation in feet
- ANS impairment leading to gastroparesis (paralysis of stomach) and erectile dysfunction
69
Type II DM nursing intervention
- 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
*Type II DM pt teaching
- 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
