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Endocrine Flashcards

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1
Q

What hormones does the thyroid gland produce

A

3 hormones → T3, T4, calcitonin

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2
Q

What does calcitonin do

A

↓ serum calcium (ca+) by taking calcium OUT of the blood and pushing it back into the BONE

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3
Q

What do you need to make hormones

A

Iodine (dietary iodine)

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4
Q

What do the thyroid hormones do

A

Give US energy!

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5
Q

What is hyperthyroidism

A

Too much energy (graves disease)
* too much thyroid hormone

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6
Q

S&S of hyperthyroidism

A
  • Nervous and irritable
  • ↓ attention span
  • ↑ appetite
  • ↓ weight
  • sweaty /hot
  • exopthalamos (bulging eyes)
  • fast GI
    *↑BP and ↑ pulse
  • arrhythmia/palpitations
  • thyroid size enlarges
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7
Q

How is hyperthyroidism diagnosed

A

*↑ T4 level
* ↓ TSH
* thyroid scan
** client must D/C any iodine containing meds 1 WEEK PRIOR to thyroid scan
* ultrasound/MRI/CT

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8
Q

How is hyperthyroidism treated

A
  1. Anti-thyroids: Methimazole (Tapazole), propylthiouracil (PTU)
  2. Iodine compounds: Potassium Iodine (SSKI & Lugols solution)
  3. Beta blockers - supportive therapy: Propanolol (Inderal)
  4. Radioactive iodine therapy (1 dose)
  5. Surgery
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9
Q

What anti-arrhythmic drugcontains high levelsof iodine and may affect thyroid function

A

Amiodlarone (Cordarone)

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10
Q

Anti-thyroid meds: Methimazole (Tapazole), Propylthiouracil (PTU)

A
  • Stops the thyroid from making thyroid hormones
    ** used pre-op to STUN the thyroid (helps ↓ bleeding)
  • want client to become euthyroid (eu= normal)
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11
Q

What do iodine compounds like potassium iodine (SSKI & Lugals solution) do

A

• ↓ the size and vascularity of the gland
** all endocrine glands are VERY VASCULAR
** give in milk or juice and use a straw (stain teeth)

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12
Q

How do beta blockers (Propanolol (Inderal)) help hyperthyroidism

A

• ↓ myocardial contractility
• ↓ cardiac output possible
• ↓HR & BP
• ↓ anxiety
• ↓ cardiac output possible

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13
Q

Who should NEVER be given a beta blocker

A

Asthmatics or diabetics

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14
Q

Radioactive iodine therapy (1 dose):

A

• Given PO (liquid or tablet form)
** rule out pregnancy 1st
• destroys thyroid cells → may cause hypothyroidism
• follow radioactive precautions
** stay away from BABIES for 1 WEEK
**don’t KISS anyone for 1 WEEK
** watch for THYROID STORM (thyrotoxicosis & thyrotoxic crisis)
* possible rebound effect of post-radioactive iodine

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15
Q

What is a thyroid storm (thyrotoxicosis and thyrotoxic crisis)

A

Hyperthyroidism x100

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16
Q

Surgical treatment of hyperthyroidism →thyroïdectomy (partial/complete)

A

• assess for recurrent laryngeal nerve damage by listening for HOARSENESS
•Could lead to vocal cord PARALYSIS
** when there’s paralysis of BOTH vocal cords airway OBSTRUCTION WILL OCCUR which req. IMMEDIATE TRACH → trach set at bedside
• put personal items near client
• teach client how to support their neck
* raise HOB to ↓ edema
* nutrition (pre & post-op): ↑ calorie needs

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17
Q

Thyroidectomy(partial/complete) post op priority

A

HEMORRHAGE → check for BLEEDING at INCISION site & BEHIND NECK
*** report feelings of PRESSURE

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18
Q

Trash set at bedside:

A
  • Swelling
  • recurrent laryngeal nerve damage (vocal cord paralysis)
    ** hypocalcemia → assess for parathyroid removal
    **s&s → NOT sedated
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19
Q

Hypothyroidism:

A

Too little thyroid hormone/energy

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20
Q

S&S of hypothyroidism

A
  • No energy
  • fatigue
  • no expression
  • speech slurred
  • ↑ weight
  • slow GI
  • cold
  • amenorrhea

• you may have a totally immobile client

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21
Q

How is hypothyroidism diagnosed

A

↓ thyroxine (T4)
↑TSH
• opposite labs of thyroid
• blood test for TSH is most commonly used

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22
Q

How is hypothyroidism treated

A
  • Levothyroxine (Synthroid), Liothyronine (Cytomel)
  • take on an EMPTY STOMACH
  • people with hypothyroid tend to have coronary artery disease (CAD)
    ***** WORRY about MI (heart attack)
    ** must take meds for FOREVER/rest of their lives
    *↑ energy when starting meds
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23
Q

What is Hashimoto’s disease

A

*When the immune system attacks the thyroid
( diff than hypo. Bc hypo is underactive/inadequate production)
* inflammation of the thyroid caused a leak which a hormones (hyperthyroid) → over time inflammation stops from thyroid producing enough hormones (hypo.)
* disease usually results in ↓ hormones production (hypo.)

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24
Q

Parathyroids secrete what….

A

Parathyroid hormone (PTH)

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25
Q

What does (PTH) parathyroid hormone do?

A

Makes you PULL calcium from the BONE and place it into the BLOOD
** this ↑ serum calcium levels

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26
Q

Too much PTH=
Not enough PTH=

A

Too much =↑ serum calcium levels
Too little = ↓ serum calcium levels

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27
Q

PTH and Ca+ have a direct relationship

A

↑PTH = ↑ Ca

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28
Q

Parathyroid problems

A
  1. Hyperparathyroidism = hypercalcemia=hypophosphatemia
  2. Hypoparathyroidism = hypocalcemia = hyperphosphatemia
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29
Q

S&S of hyperparathyroidism (hypercalcemia=hypophosphatemia)

A

Too much PTH
• serum calcium is ↑, serum phosphorus is ↓
** calcium and phosphorus have an INVERSE RELATIONSHIP
** client will appear SEDATED (hypercalcemia)

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30
Q

How is hyperparathyroidism treated?

A
  • Partial parathyroïdectomy → when 2 parathyroids are taken out
    ** ↓PTH secretion
    **     monitor for HYPOCALCEMIA & RIGID MUSCLES
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31
Q

S&S of hypoparathyroidism =hypocalcemia = hyperphosphatemia

A
  • Not enough PTH
    ↓ serum calcium & ↑serum phosphorus
    **    NOT SEDATED
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32
Q

How is hypoparathyroidism treated

A

*IV calcium
* phosphorus binding drugs

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33
Q

What are the adrenal glands for

A

Need them to be able to handle stress

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34
Q

2 parts of the adrenal glands

A

Adrenal medulla and adrenal cortex

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35
Q

What hormones does the adrenal medulla produce

A

Epi & Nor-epi

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36
Q

Adrenal medulla problem:

A

Pheochromocytoma→ benign tumors thatsecrete epi and nor epi(hormones) in bonuses
*** tend to be familial → screen the family

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37
Q

Pheochromocytoma S&S

A

*↑ BP
* ↑HR
* palpitations
* flushing/ extremely diaphoretic
*H/A

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38
Q

How is pheochromocytoma diagnosed

A

•Catecholamine levels: VMA (vanillymandelic acid test) or metanephrine (MN) test
MN test is the most commonly used and is ALTERED BY CAFFEINE
** foods that alter the VMA test → anything with vanilla in it, Vit. B, fruit juices & bananas
• a 24 hr urine specimen is done to screen for ↑levels of epi & nor-epi (AKA catecholamines)
*THROW away 1st void
**KEEP the LAST void
• any activities that ↑ epi & nor-epi should be avoided (no stress)

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39
Q

Pheochromocytoma treatment

A

Surgery to remove tumors

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40
Q

What should you AVOID doing in a client with pheochromocytoma

A

Palpating the abdomen → causes a sudden release of catecholamines & severe HTN

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41
Q

What hormones does the adrenal cortex produce

A

Glucocorticoids, mineralocorticoids and sex hormones

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42
Q

Adrenal cortex

A

Even though the body secrets steroids normally the adverse effects are more pronounced when the client is receiving oral or IV steroids

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43
Q

Glucocorticoids

A
  • Change your mood → depressed, psychotic, euphoric, insomnia
  • alters defense mechanisms →immunosurpressed →high infection risk
  • help BREAKDOWN FATS&PROTEIN
    **INHIBITS INSULIN →HYPERGLYCEMIC (monitor glucose)
    ** helps regulate glucose metabolism
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44
Q

Mineralcorticoids (aldosterone)

A
  • Makes you RETAIN sodium (Na+) & water
  • makes you LOSE potassium (K+)
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45
Q

Sex hormones

A

testosterone, estrogen and progesterone

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46
Q

Hirsutism, acne, irregular periods are caused by….

A

Too many sex hormones

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47
Q

Decreased axillary/pubic hair, ↓ libido

A

Not enough sex hormones

48
Q

Adrenocorticotropin hormones (ACTH)

A

**Stimulate CORTISOL production
* cortisol is a hormone of adrenal cortex
* ↑ACTH = ↑ cortisol levels
** too many steroids = hypercorticolism (same words )

49
Q

Where are adrenocorticotropin hormones (ACTH) made

A

***Made in the PITUITARY

50
Q

What is hypercortisolism

A

Same thing as too many steroids

51
Q

Problems with the adrenal cortex

A
  1. Not enough steroids
  2. Shock
  3. Hyperkalemia (high potassium)
  4. hypoglycemia
52
Q

What is Addison disease aka

A

Adrenocortical insuffiency - not enough steroids

53
Q

Addison disease patho:

A

Not enough glucocorticoids,mineral corticoids or sex hormones

54
Q

S&S of Addison’s disease

A
  • Extreme fatigue
  • N/V
  • diarrhea
  • hypotension (low bp)
  • anorexia/weight loss
  • confusion
  • vitiligo → white patchy area of depigmented skin
  • hyperpigmentation - bronzing color of skin
  • ↓ sodium (Na+);↑potassium (K+) and hypoglycemia
55
Q

Treatment of Addison’s disease

A
  • Combat shock (losing sodium and water)
  • ↑ sodium in diet
  • processed fruit juice/broths ( ↑ in sodium)
    *I&O and daily weights
  • if losing sodium and water the BP WILL ↓ (less vol. Less pressure)
  • losing weight
  • fluid vol. Deficit
56
Q

What meds are given to treat addiSon’s disease

A

•Corticosteroids → given 2x/day in split doses
*** take 2/3 dose in morning; 1/3 dose at night
• fludrocortisone acetate → synthetic aldosterone
• prednisone (Winpred), hydrocortisone (Cortef), cortisone →all corticosteroids

57
Q

Med precautions for addiSon’s disease

A
  • Daily weights and blood pressure MUST be monitored
    ** keep weight within 2-3 lbs (1-2kgs) (+ or -)normal weight
    REPORT weight gain >5lbs/week(2kgs)
    MONITOR for blood pressure changes
58
Q

Severe hypotension and vascular collapse = _____________

A

Addisonian crisis

59
Q

What can cause an addisonian crisis

A

Infections, emotional stress, physical exertion or stopping steroids abruptly

60
Q

What causes cushings disease

A

Too many steroids (gluco corticoids, sex hormones, mineral corticoids)

61
Q

Signs and symptoms of too many glucocorticoids

A

• Growth arrest
• thin extremities/skin (lipolysis
• ↑ risk of infection
• hyperglycemia
• psychosis to depression
• moon faced (fat redistribution;lipogenesis)
• buffalo hump (fat redistribution)

62
Q

Too many sex hormones causes what:

A
  • Oily skin/acne
  • women with male traits (facial hair, deep voice, etc.)
63
Q

Too many mineralcorticoids cause what?

A
  • High BP
  • chronic heart failure (CHF)
  • weight gain
  • fluid volume excess (FVE)
    *** too many mineralcorticoids (aldosterone) makes serum potassium (K+) ↓
64
Q

If you did a 24hr urine screen on A client with suspected Cushings what would come back

A

↑ cortisol levels

65
Q

Urine screen for long term term steroids

A
  • Glucose and ketones altered
66
Q

Cushings treatment

A
  • Adrenalectomy (removal of one or both adrenal glands)(unilateral or bilateral)
    *** bilateral= life time replacement
    *QUIET environment
  • avoid infection
  • pre-treatment diet: ↑ potassium (K+) ↑ protein ↑ calcium (Ca+); ↓ sodium (Na+)
    ***STEROIDS ↓ serum calcium (Ca+) by excreting through GI tract
    **AVOID exposure to infections
67
Q

Two types of diabetes

A
  1. Type l→ insulin DEPENDENT →auto-immune response or idiopathic causing beta cell destruction →clients have LITTLE TO NO INSULIN
  2. Type 2 →insulin RESISTANT →clients don’t have enough insulin or good insulin
68
Q

What type of diabetes is usually found by accident

A

Type 2

69
Q

What type of diabetes is usually diagnosed in childhood

A

Type l

70
Q

What type of diabetes appears abruptly despite years of beta(pancreatic) cell destruction

A

Type I

71
Q

What type of diabetes requires clients to be evaluated for metabolic syndrome

A

Type 2
(Metabolic syndrome aka syndrome X)

72
Q

Type _______ diabetics CANNOT have ORAL ANTIDIABETICS

A

Type I

73
Q

What are the 3 P’s and what type of diabetes

A
  • Polyria (excessive urination)
  • polydipsia (excessive thirst)
  • polyphagia (excessive hunger)

ALL SIGNS OF TYPE 1

74
Q

Type I classification

A
  • Little or no insulin
  • usually diagnosed in childhood
  • causes: autoimmune response
  • first sign may be DKA
  • appears abruptly despite years of beta cell destruction
    *3P’s → polyuria, polyphagia, polydipsia
75
Q

Normal blood glucose

A

70-99 mg/dL (3.9 - 5.5mmol/l) → normal without diabetes

76
Q

Blood glucose with diabetes

A

<140 mg/dL (7.8 mmol/l)
80-130mg/dL (4.4-7.2 mmol/L)

77
Q

Type 1 diabetes patho:

A
  • You need INSULIN to carry glucose out of the blood and into the cell… since there’s no insulin the glucose builds up in the BLOOD, the blood becomes HYPERTONIC and pulls fluid into the vascular space…the kidneys filter excess glucose and fluids (POLYURIA & POLYDIPSIA) the cells are STARVING so they start breaking down PROTEIN and FAT for energy (polyphagia)… when you break down fat you get KETONES (acid) now the client is ACIDOTIC (metabolic) → KUSSMAUL RESPIRATIONS (compensation)
78
Q

Signs and symptoms of type l diabetes

A
  • Polyuria → excessive urination
  • polydipsia → excessive thirst
  • polyphagia → excessive hunger
    *POLYURIA think SHOCK 1st
    *3P’s = HYPERGLYCEMIA
79
Q

How is type 1 diabetes treated

A

ALWAYS NEED INSULIN
**NO ORAL hypoglycemia agents

80
Q

Type 2 patho:

A
  • Clients don’t have enough INSULIN or they insulin they have is INADEQUATE
  • clients are usually OVERWEIGHT
  • can’t make enough insulin to keep up with the glucose load client is taking in
    *NOT as abrupt as type 1
    *usually FOUND BY ACCIDENT (wounds won’t heal, repeated vaginal infections, etc.)
  • evaluate for METABOLIC SYNDROME (syndrome X)
81
Q

Features of metabolic syndrome (MUST HAVE 3 OR MORE)

A
  • Waist circumference:
    >40 in. (101.6 cm) for MALES
    >35 in. (88.9 cm) for FEMALES
  • triglycerides
    >150 mg/dL (1.60 mmol/L)
    *HDL
    < 40 mg/dL (1.036 mmol/L) for MALES
    < 50 mg/dL (1.2295 mmol/L) for FEMALES
    *BP
    > 130/85
    *FBS
    >100 mg/dL (5.5 mmol/L)
82
Q

Metabolic syndrome is known to ↑ risk level for dev. Of what

A

Type 2 diabetes and cardiovascular disease

83
Q

How is metabolic syndrome treated

A
  • Start with diet and exercise → then add oral agents
    ** some clients may require insulin
84
Q

What type of diabetes resembles type 2

A

Gestational

85
Q

Gestational diabetes

A
  • Resembles type 2
  • mom needs 2-3X more insulin than normal
    *1st visit screening - if mom has RISK factors
    screen ALL MOMS at 24-48 WEEKS gestation**
86
Q

What complications can a baby have from the mom having gestational diabetes

A
  • ↑ birth weight
  • hypoglycemia
87
Q

General treatment of diabetes (type 1 and 2)

A

A. Diet: majority of calories should come from COMPLEX CARBS, then FATS, LASTLY PROTEIN
carbs: 45% of diet
**fats: 30-40% of diet
**proteins: 15-20% of diet
• why WORRY about CARBS→ SUGAR destroys VESSELS just like FAT
•HIGH FIBER SLOWS DOWN GLUCOSE ABSORPTION in the intestines → ELIMINATES the SHARP RISE/FALLL in blood sugar
B. Exercise:
• wait until blood sugar normalizes to begin exercise
• to prevent hypoglycemia → EAT PRIOR
•exercise when blood sugar is HIGHEST
• exercise SAME TIME & SAME AMOUNT DAILY
C. Meds:
• prescribed for type 2
• oral or subcutaneous admin.
• improves how the body PRODUCES INSULIN and how the body USES INSULIN & GLUCOSE
• most widely used ORAL anti-diabetic is METFORMIN (GLUCOPHAGE)
**1st choice for most clients
** may be used for weight control in type 2
*** some clients with pre-diabetes

88
Q

Vascular damage is caused by…

A

Extremes in blood sugar

89
Q

Metformin (glucophage)

A
  • Favorite bc it ↓ glucose production and enhances how glucose enters the cell
    *** does NOT stimulate the release of more INSULIN so NO HYPOGLYCEMIA with this med.
  • hypoglycemia destroys vessels?
    *may be prescribed in COMBO
  • if metformin is not controlling blood glucose levels, another anti-diabetic will be prescribed possibly GLARGINE (Lantus)
90
Q

What is the most common method of daily dosing

A

Basal bonus dosing

91
Q

What is a combination of long acting and rapid acting insulin

A
  • Long acting → given 1x/day
  • rapid → given through out the day, before meals, in divided doses and it covers the food eaten at meals
    ***SNACKS ARE NOT REQ. But client MUST EAT when dosing the rapid, so have food available
92
Q

When should clients eat

A

When insulin is at its peak → blood sugar is at its lowest
* always monitor a client on insulin for hypoglycemia

93
Q

Client teaching for diabetes

A

** glucosated hemoglobin (HbA1C) : BLOOD TEST; gives an AVERAGE blood sugar for the past 3-4 months
** blood sugar INCREASES when STRESSED OR SICK →a normal pancreas can handle these fluctuation
** an ↑ in blood sugar when sick or stressed is NORMAL →helps to fight infections/stress

94
Q

_________________ = DKA (diabetic ketoacidosis)

A

ILLNESS = DKA

95
Q

Hemoglobin A1C goal

A

Greater than or equal to 6.5% is DIAGNOSTIC for diabetes
**<7% is the DIABETIC GOAL

96
Q

Normal HgbA1C

A

Less than or equal to 5.7%

97
Q

What med should be held 48 hr pre and post-op

A

Metformin- ↑ risk of lactic acidosis

98
Q

What is the initial dose of insulin based on

A

Clients weight
* average adult dose is 0.4-1 unit/kg/day
* dose adjusted until the blood sugar is normal and there is NO MORE GLUCOSE OR KETONES in the urine

99
Q

Insulin times

A
  • Rapid → onset: 15 mins; peak: 1 hour; duration: 2 to 4hrs
  • regular/short → onset: 30min; peak:2-3 hours; duration: 3-6 hours
  • intermediate → onset: 2-4 hours; peak: 4-12 hours; duration: 12 to 18 hours
  • long acting →onset: 2 hours; peak: NONE; duration: up to 24 hours
  • ultra long acting → onset: 6 hours; peak: none; duration: 36 hrs or longer
100
Q

What type of insulin is clear vs cloudy

A

Regular (clear), NPH (cloudy)
*draw up CLEAR 1st

101
Q

What type of insulinis clear and can’tbe mixed with any otherinsulin or given IV

A
102
Q

What is the insulin standard

A

Regular (rapid may also be given IV)
* plan based on clients lifestyle and activity
* goal → keep the before meal glucose near normal at 80 - 130mg/dl

103
Q

Insulin infusion pumps

A
  • Alternative to daily injections
    ***ONLY RAPID ACTING insulin is used in INFUSION PUMPS
    *obtain. BETTER CONTROL recieving a basallevel of insulin from the pump and bonuses of additional insulin as needed with meals or high blood sugar
104
Q

What type of insulin is used in infusion pumps

A

Only RAPID acting
***OBTAINS BETTER CONTROL - receiving a basal level of insulin from the pump and boloses of additional insulin as needed with meals or ↑ in blood sugar

105
Q

What is the standard insulin that can be given in IV fluids or as an IV ‘ infusion

A

REGULAR INSULIN

106
Q

What is the ONLY INSULIN that can be given via SUBCUTANEOUS INSULIN INFUSION PUMP

A

Rapid acting insulin

107
Q

Small computerized devices worn by the client that can provide BOTH, a CONTINUOUS (basal) dosing of rapid acting insulin and on demand (BOLUS) dosing

A

Insulin infusion pumps

108
Q

Signs and symptoms of hypoglycemia

A
  • Cold and clammy
  • confusion
  • shakey
    *H/A
  • nervousness
  • nausea
  • ↑ pulse
  • hunger
109
Q

If hypoglycemic…

A

Eat simple carbs
* snacks should be 15g of carbs
* glucose absorption delayed in foods with lots fat
*15-15-15 rule

110
Q

15-15-15 rule

A
  • Eat 15 g carbs
  • wait 15 min.
  • take blood sugar
  • repeat as needed
111
Q

Once the blood sugar is up

A

Complex Carbs and protein (PB crackers)
* if unconscious, likely hypoglycemia
**D50W ( hard to push, if you have A choice you need a LARGE BORE IV
** injectable glucagon (Glucagen) → used when there’s NO IV access; given IM

112
Q

Hypoglycemia prevention

A

I. Eat
2. Take insulin regularly
3. Know S&S of hypoglycemia
4. Check blood glucose regularly

113
Q

Hypoglycemia is blood glucose of ______ or less

A

70 or less

114
Q

Complications of diabetes

A

A. Diabetic ketoacidosis (DKA) TYPE 1
* anything that ↑blood sugar can throw the client into DKA (illness, infection, skipping insulin)
*may be the 1ST SIGN OF DIABETES
*have all the usual S&S of type 1
B. Hyperosmolar hyperglycemic non-ketosis (HHNK) or hyperglycemia hyperosmolar state (HHS) TYPE 2
*looks likeDKA but NO ACIDOSIS
making JUST ENOUGH insulin so they aren’t breaking down FAT
**no ketones, acidosis, kussmaul resp.
C. Vascular problems - will dev. POOR CIRCULATION EVERYWHERE due to vessel damage (sugar irritated—decreased blood flow) 1. Diabetic retinopathy 2. Nephropathy
D. Neuropathy
1. Sexual problems - impotence/ ↓ sensation
2. Foot/leg problems- pain/parenthesis/numbness
3. Neurogenic bladder….spontaneous emptying/doesn’t empty properly → incontinence or may not empty at all → retention
4. Gastroparesis-stomach emptying is delayed so there’s an ↑risk for aspiration
E. ↑ risk of infection

115
Q

Diabetic ketoacidosis patho:

A
  • Absent or inadequate insulin → blood sugar sky rockets → polyuria, polyphagia, polydipsia → FAT BREAKDOWN (acidosis) → kussmaul resp. (Trying to compensate by blowing off co2) → more acidic = more LOC ↓
116
Q

DKA treatment

A
  • Find the cause
    HOURLY blood sugar and K+ levels
    ****ECG
    **    HOURLY U/O
    ABG’s
    ****IV INSULIN → insulin LOWERS blood sugar and potassium (K+) levels → DRIVES them OUT of the VASCULAR SPACE & into the cell
    **    IV FLUIDS…POLYURIA CAUSES SHOCK → start with NS…. Then when blood sugar gets down to about 250-300mg/dL…SWITCH to D5W to prevent hypoglycemia
  • anticipate that the PCP will want to ADD POTASSIUM (K+) to the IV SOLUTION at some point

Nclex Cards (4 decks)

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