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ADULT 2 EXAM 2 > ENDOCRINE > Flashcards

ENDOCRINE Flashcards

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1
Q

What are Antithyroid drugs

A

slows thyroid down, doesn’t destroy thyroid.

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2
Q

What are the two antithyroid drugs used to treat hyperthyroidism

A

Propylthiouracil
methimazole

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3
Q

What drug shrinks/destroys thyroid in preparation for removal

A

Iodine (high levels IV)

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4
Q

What drug decreases the function of the thyroid (possibly permanently). Why would you use it?

A

Radioactive iodine
Hyperthyroidism Tx
Used for non-pregnant clients

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5
Q

What secondary sx of hyperthyroidism is most concerning and how should you control it?

A

Tachycardia

Beta blockers

If pt becomes too tachycardic they can become hypotensive and enter thyrotoxicosis (elevated levels of thyroid hormones (T3 and T4) in the bloodstream, leading to a hypermetabolic state in the body)

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6
Q

What do you need to do BEFORE a thyroidectomy?

A

Thyroid must be shrunken/prepped before (antithyroid drugs, beta blockers, iodine)

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7
Q

What are the post-op risks of a thyroidectomy?

A

Can result in postoperative hypothyroidism

Can have postoperative swelling (swelling might compromise airway). Might need additional O2 support

Hemorrhage

HYPOCALCEMIA (r/t accidental damage to parathyroid gland)

May become easily OVERSTIMULATED by thyroid hormone replacement therapy (synthetic T3/4) so you need to watch for increased HR, BP, anxiety, etc.

Hoarseness is expected for 3-4 days after surgery

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8
Q

A pt with HYPERTHYROIDISM is acutely experiencing high fever, extreme tachycardia, angina, agitation, restlessness. What might they be experiencing?

A

Thyrotoxicosis: Thyroid crisis (storm)

Thyrotoxicosis refers to a condition characterized by elevated levels of thyroid hormones (T3 and T4) in the bloodstream, leading to a hypermetabolic state in the body

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9
Q

What drugs can cause hypothyroidism as a side effect

A

amiodarone, lithium

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10
Q

What is the expected calcium level for patients with hyper/hypothyroidism?

A

Hyperthyroidism can lead to elevated calcium levels (hypercalcemia). This happens because the increased metabolic activity associated with excess thyroid hormones can stimulate bone resorption, releasing calcium into the bloodstream.

Hypothyroidism may result in lower calcium levels (hypocalcemia) in some cases. The reduced metabolic activity can lead to a decreased release of calcium from bones, and the parathyroid hormone activity may also be affected, impacting calcium balance.

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11
Q

What medications do you give a patient who is newly diagnosed with hypothyroidism?

A

If the pt is acutely ill, start with Liotrix (a combination of T3 and T4, quickly relieves issue) then slowly replace with levothyroxine (Synthroid) based on client response/labs over the span of 4-6 weeks.

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12
Q

A Myxedema coma happens when

A

metabolism is so slowed from hypothyroidism that people can enter a Coma, hypothermia, respiratory collapse, cardiovascular collapse (potentially cardiac arrest)

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13
Q

DKA is characterized by a triad of:

A

Hyperglycemia: Elevated blood glucose levels.

Ketosis: The presence of ketones in the blood and urine.

Acidosis: Metabolic acidosis, indicated by low blood pH and low bicarbonate levels

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14
Q

DKA is mostly seen in patients with…

A

type 1 diabetes

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15
Q

What can cause someone with diabetes to go into DKA?

A

eating disorder

lots of physical activity

getting off of oral contraceptives

infection

failure of insulin pump/delivery device

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16
Q

What is the difference between DKA and Hyperglycemic hyperosmolar syndrome (HHS)

A

DKA:
Ketones present in urine and serum
DKA glucose high (350+) but lower than HHS
Type 1 diabetes complication

HHS:
Glucose (600+)
Type 2 diabetes complication

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17
Q

How can you tell someone has been in DKA for a while?

A

elevated lactate

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18
Q

How do you stabilize someone in DKA?

A
  1. fluid replace with LR, then slowly start dextrose to avoid hypoglycemic episode
  2. IV push insulin, start insulin drip, titrate insulin up/down per hourly BG check
  3. Bicarb if ABG indicates severe acidosis
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19
Q

What are some clinical manifestations of HHS (Hyperglycemic hyperosmolar syndrome)?

A

Tachycardia w/ orthostatic hypotension

Sunken eyes

Lethargy

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20
Q

What will the ADH values for Central vs. Nephrogenic Diabetes Insipidus be

A

Central: hypothalamus is not making ADH or pit gland not releasing, so ADH is not in serum to transport to kidneys. ADH value will be LOW

Nephrogenic: brain (pit/hypothalamus) IS releasing ADH but kidneys are damaged and can’t receive signal. ADH value will be NORM/HIGH

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21
Q

What can cause Nephrogenic Diabetes Insipidus

A

Hypercalcemia: chronic causes kidney damage

Severe, persistent hypokalemia: chronic causes kidney damage

Pyelonephritis

Renal disease

Lithium toxicity

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22
Q

What can cause Central Diabetes Insipidus

A

Vascular disease affecting hypothalamus or pituitary

Traumatic head injury

Surgery in the area close to hypothalamus or pituitary

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23
Q

How do you test the difference between DI (Diabetes Insipidus) and SIADH (Syndrome of Inappropriate Anti-Diuretic Hormone excretion)

A

Water deprivation test:
take pt’s weight
no water allowed and measure hourly urine output
If pt produces a significant amount of urine, DI
If pt doesn’t produce urine, consider SIADH

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24
Q

How do you test the difference between Central DI (Diabetes Insipidus) and Nephrogenic DI (Diabetes Insipidus)

A

Vasopressin test:
See pt’s SG of urine
Give pt synthetic ADH (vasopressin)
If SG of urine increases, its Central b/c you didn’t have ADH in your system
If SG in urine stays the same, its Nephrogenic

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25
How do you treat Central DI (Diabetes Insipidus)
With vasopressin/DDAVP (antidiuretic hormone) Also Carbamazepine—Anticonvulsant that helps the posterior pituitary release ADH
26
How do you treat Nephrogenic DI (Diabetes Insipidus)
To reduce urine output: NSAIDS: diclofenac, meloxicam, celecoxib, ibuprofen Thiazide diuretics: Hydrochlorothiazide To increase renal sensitivity: Indomethacin Replace fluids: PO preferred hypo/isotonic fluid replacement
27
Why does a Nephrogenic DI (Diabetes Insipidus) patient need to be on a Low sodium diet when they're severely dehydrated?
we expect hypernatremia (high Na, so much so that it can cause seizures) and that's why we treat with hypotonic solutions
28
What is the difference between DI (Diabetes Insipidus) and SIADH (Syndrome of Inappropriate Anti-Diuretic Hormone excretion)
DI: due to lack of or inability to respond to vasopressin excrete large volumes of dilute urine quickly dehydrated hypernatremia SIADH: excessive secretion of vasopressin despite normal or low plasma osmolarity water retention, causing decreased urine output and dilution of blood hyponatremia
29
Name symptoms that indicate immediate intervention with SIADH
JVD (indc Increased intrathoracic pressure), PERIPHERAL EDEMA (starting to affect right heart), severe HYPONETREMIA (indc INCREASED INTRACRANIAL PRESSURE/BRAIN HERNIATION)
30
Name some Medications that can cause secretion of more ADH
Carbamazepine Cyclophosphamide SSRIs CAN CAUSE SIADH
31
LUNG TUMORS HAVE ECTOPIC CELL THAT CREATE THEIR OWN ____.
ADH
32
How do you treat SIADH
Induces nephrogenic DI: Demeclocycline—antibiotic Lithium Diuretics: Furosemide ADH receptor antagonists: -Vaptan (ex: Tolvaptan, Conivaptan Fluid Restriction
33
What is Central pontine myelinolysis
rapid change in sodium levels in the body causes demyelination of the brainstem (NOT FROM DISEASE PROCESS, FROM BAD MED INTERVENTIONS)
34
What is Cushing's Syndrome (not disease)
The manifestation of symptoms that result from hypersecretion of cortisol Not to be confused with Cushing disease which is tied specifically presence of a pituitary tumor that secretes excess ACTH
35
What is responsible for the production and release of glucocorticoids, mineralocorticoids, and androgens
The cortex (outer layer) of the adrenal gland
36
What is a Glucocorticoid
—play role in metabolism as well as inflammation (example is cortisol)
37
What is a Mineralocorticoid
—Maintain sodium/potassium balance (example is aldosterone)
38
Describe the role of the hypothalamus, pit gland, and adrenal cortex in the release of cortisol
Hypothalamus releases Corticotropin-Releasing Hormone [CRH] which travels to Anterior pituitary releases Adrenocorticotropic hormone (ACTH) which travels to Cortex of adrenal glands releases cortisol
39
What is the difference between ACTH dependent and ACTH independent Cushings Syndrome
ACTH dependent: tumor on lung/pit gland causes significant increase in ACTH which stimulates adrenal cortex to release a ton of cortisol ACTH independent: Something is wrong with the adrenal gland (hyperplasia/tumor) itself which causes it to release a ton of cortisol without ACTH stimulation
40
The administration of high doses of corticosteroids can cause what issue
Cushings Syndrome Exogenous Corticosteroids: When corticosteroids are administered in high doses (such as for treating autoimmune diseases, inflammation, or certain cancers), they mimic the effects of cortisol produced by the adrenal glands. Negative Feedback: Corticosteroids exert negative feedback on the hypothalamus and pituitary gland. This reduces the secretion of adrenocorticotropic hormone (ACTH) from the pituitary, which normally stimulates the adrenal glands to produce cortisol. Adrenal Suppression: Over time, the adrenal glands may become less responsive or even atrophy due to the lack of ACTH stimulation. When corticosteroid administration is stopped or reduced, the body may not immediately resume normal cortisol production, leading to potential adrenal insufficiency.
41
What medication can cause an upregulation of the adrenal glands
Chemotherapy
42
What will the ACTH and cortisol labs look like for ACTH dependent and ACTH independent Cushings Syndrome
ACTH dependent: high ACTH, high cortisol ACTH independent: low ACTH, high cortisol
43
Describe what someone with Cushings might be like
Tired, red, MOON FACED dude with a BUFFALO HUMP, boobs, acne, and purple stretch marks. Thin skin with lots of bruises. Broken bones. GERD. Look like a ball with thin extremities. Kind like a diabetic: hyperglycemia, lots of peeing, high risk for infection/impaired healing
44
Describe the labs for someone with Cushings might be like
Serum cortisol (elevated) Urine cortisol (elevated) ACTH levels (depends on dependent/independent) Potassium (low) Calcium (low) Glucose (elevated) Sodium (elevated) Lymphocytes (low) Salivary cortisol levels (elevated)
45
How do you treat ACTH independent (issues with adrenal gland) Cushings
Treatment for ACTH Aminoglutethimide—decreases adrenal hormone synthesis Ketoconazole—antifungal that will inhibit adrenal hormones at high doses Mitotane—suppresses adrenal cortex
46
How do you treat the secondary effects of Cushings
Low K Spironolactone—diuretic that will get rid of excess fluid while also retaining potassium (fluid from hyperaldosteronism)
47
How do you treat ACTH dependent (issues with pit gland) Cushings
Hypophysectomy (removal of pit gland): After surgery it is important to monitor for CSF leaks (drainage that is clear in middle and has a “halo” is CSF = HALO test) Patient should not blow nose, use a straw, or do anything that will raise ICP Shouldn’t strain to have a BM long-term hormone replacement if pit gland had to be completely removed
48
What should you watch out for with a patient with Cushings
Monitor I&O (hyperglycemia causes increased UO) Assess for s/s hypervolemia (fluid from hyperaldosteronism) Minimize exposure to pathogens (increased risk for infection) Monitor for s/s skin breakdown (too much causes collagen issue (less skin elasticity/thin skin, stretch marks)
49
What are some complications commonly experienced by patients with Cushings
Perforation of the viscera—caused by weakened stomach lining due to increased cortisol Pathologic bone fractures—due to hypocalcemia Adrenal crisis—can occur with abrupt withdrawal of steroids
50
What is the difference between Cushings and Addisons
Cushings is too much cortisol, Addisons is too little cortisol
51
What is Addisons
Issue with hypothalamus(tertiary)/pit gland(secondary) so that ACTH isn't getting to adrenal cortex (LOW ACTH AND LOW aldosterone, cortisol, androgens, and estrogens) OR (Primary) Adrenal cortex itself isn't working so all aldosterone, cortisol, androgens, and estrogens aren't being excreted (HIGH ACTH AND LOW aldosterone, cortisol, androgens, and estrogens)
52
How can sepsis cause Addisons
adrenal glands have one small artery for perfusion each. hypotension stops perfusion to glands
53
What does a person with Addison's look like
tired old lady with a bad bronze tan, mustache, and low energy. She faints when she stands up and craves salt. She's dehydrated and has a dry, cracked smile. She is always tachycardic and has dysrhythmias, but is other wise slow, cold, and tired. Even though she's hypoglycemic don't give her a banana because her potassium is high.
54
How does Addison's affect renal labs? (Creatine, GFR)
elevated creatinine low GFR (r/t hypovolemia)
55
How does Addison's affect electrolytes (K, Na, and Ca)?
increased K, decreased Na, increased Ca
56
How do you test whether a patient's Addisons is primary or secondary/tertiary?
Adrenocorticotropic hormone (ACTH) stimulation test Baseline Measurements: Measure the baseline cortisol level in the morning (usually between 8:00 AM and 9:00 AM). ACTH Administration: Administer a synthetic form of ACTH (e.g., cosyntropin) intravenously or intramuscularly. Post-Administration Measurements: Measure cortisol levels again after 30 minutes and 60 minutes. Normal Response: In healthy individuals, cortisol levels should rise significantly (typically > 20 mcg/dL) after ACTH administration. Primary Adrenal Insufficiency: ACTH Levels: High (due to the lack of feedback inhibition from cortisol). Cortisol Response: Poor or no increase in cortisol levels after ACTH administration. The adrenal glands are unable to respond because they are damaged. Secondary/tertiary would show no increase in cortisol because adrenal gland is healthy and knows not to turn ACTH into cortisol. Cortisol levels would be normal.
57
How do you treat Addison's
Give Mineralocorticoids(maintain Na/K balance)/Glucocorticoids(metabolism) Fluids to replace lost volume in Addisonian crisis (NS and 5% dextrose) Manage hypoglycemia (eating, D5) Regimen for hyperkalemia INSULIN (stimulates the Na+/K+ ATPase pump in cell membranes. This pump transports potassium into cells while bringing sodium out of cells. The administration of insulin thus encourages cells, particularly muscle and liver cells, to take up more potassium.) CALCIUM (does not lower potassium levels but protects the heart.)
58
What kind of diet does a patient with Addison's need to be on?
Increased sodium diet Avoid alcohol or caffeine
59
Why do Addisons pts become hypoglycemic
increased sensitivity to insulin with decreased corticoids
60
Why do potassium levels increase with addisons
In Addison's disease, the adrenal glands fail to produce sufficient aldosterone. Aldosterone is a hormone that helps regulate sodium and potassium levels in the body. It promotes sodium reabsorption and potassium excretion in the kidneys. When there isn't any aldosterone, sodium is lost and potassium is retained

ADULT 2 EXAM 2 (4 decks)

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