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Pathophysiology and Pharmacology > Endocrine Problems > Flashcards

Endocrine Problems Flashcards

1
Q

Diabetes Insipidus (DI)

A

Deficiency of production or secretion of ADH or with decreased renal response to ADH d/t injury to neurohypophyseal system

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2
Q

3 types of Diabetes Insipidus (DI)

A
  1. Central 2. Nephrogenic: 3. Primary
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3
Q

Central Diabetes Insipidus

A

(Neurogenic): interference in ADH synthesis or release (brain tumor, head trauma, brain injury, CNS infection)

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4
Q

Nephrogenic Diabetes Insipidus

A

inadequate renal response to ADH (in the setting of N ADH levels) (drug therapy esp. lithium, renal damage or hereditary renal disease)

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5
Q

Primary Diabetes Insipidus

A

(aka psychogenic): excessive water intake (lesion in thirst center, psychological disorder)

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6
Q

Clinical Manifestations (Central and Nephrogenic) of diabetes insipidus

A

◦ Polydipsia, polyuria (5-20 L/day) with very low specific gravity and low urine osmolality (dilute urine) ◦ Serum osmolality is elevated d/t hypernatremia caused by pure water loss from kidneys ◦ Patients compensate by drinking water ◦ May be fatigue from nocturia, may have generalized weakness ◦ If PO intake cannot keep up with urinary losses – hypovolemia results (weight loss, constipation, poor tissues turgor, hypotension, tachycardia, hypovolemic shock) ◦ CNS manifestations – irritability, mental dullness, coma ◦ Primary DI – overhydration and hypervolemia (vs. the dehydration and hypovolemia)

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7
Q

Diagnostic studies of Diabetes Insipidus

A

◦ ID cause – Hx and PE, water deprivation test

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8
Q

Thyroid Function

A

regulates energy, metabolism, growth and development

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9
Q

Thyroid Hormones

A

thyroxine (T3) and triiodothyronine (T3)

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10
Q

Thyroid Disorders

A

enlargement benign and malignant nodule, inflammation, hyper and hypo function

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11
Q

Goitre

A

Enlargement of the thyroid gland; may be associated with hyperthyroidism, hypothyroidism, or normal thyroid function.

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12
Q

Most common cause of goitre

A

Lack of iodine

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13
Q

Treatment of goitre

A

thyroid hormones, surgical removal for large goitres

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14
Q

Nodules

A

palpable deformity, increased incidence with age

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15
Q

Malignant nodules

A

Thyroid CA – most common endocrine CA

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16
Q

Thyroiditis

A

An inflammation of the thyroid gland that may cause hyperthyroid or hypothyroid manifestations.

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17
Q

Causes of thyroiditis

A
  1. Viral (subacute granulomatous thyroiditis), bacterial/fungal infection (acute thyroiditis) – abrupt onset painful (T3 T4 high then decrease; TSH low then increases) 2. Chronic autoimmune thyroiditis (Hashimoto’s thyroiditis) - can lead to hypothyroidism; thyroid tissues replaced by lymphocytes and fibrous tissue – most common cause of goitorus hypothyroidism (T3 T4 low, TSH high, antithyroid antibodies present) 3. Silent thyroiditis (T3 T4 high then decrease; TSH low then increases; RAIU decreased) 4. Postpartum thyroiditis
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18
Q

Hyperthyroidism

A

A clinical syndrome characterized by a sustained increase in synthesis and release of thyroid hormones by the thyroid gland

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19
Q

Thyrotoxicosis

A

A hypermetabolic state caused by excessive circulating levels of thyroxine, triiodothyronine, or both.

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20
Q

Grave’s Disease

A

An autoimmune disease of unknown origin, marked by diffuse thyroid enlargement and excessive thyroid hormone secretion. ◦ Develop antibodies that attach to TSH receptors and stimulate the thyroid to produce T3 and/or T4 – cause manifestations/thyrotoxicosis ◦ Disease pattern characterized by exacerbations and remissions and may progress to destruction of thyroid tissue (causes hypothyroidism)

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21
Q

Clinical Manifestations of Grave’s Disease

A

◦ Related to effects/amount of excess hormones ◦ Palpable or visualized goiter – may be able to auscultate bruit d/t increased blood supply ◦ Exophthalmos - protrusion of eyeballs d/t impaired venous drainage – edema, fate deposits ◦ See Table 51-6 p. 1405 for additional manifestations of thyroid hyperfunction

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22
Q

Complication of Grave’s disease

A

Thyrotoxic Crisis ‘Thyroid Storm’ – rare – intensified manifestations of hyperthyroid – medical emergency – can be induced by stressors (trauma, infection, surgery); heart and nervous tissue more sensitive to epinephrine and norepinephrine

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23
Q

Diagnostic Studies of Grave’s disease

A

◦ Labs – decreased TSH, elevated free T4(free: unbound to protein – only free T4 is biologically available) ◦ RAIU demonstrated increased and more diffuse uptake than other forms of thyroiditis

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24
Q

Goal of treatment of Grave’s disease

A

block effects of excessive hormones and stop their oversecretion

25
Q

Medications used to treat Grave’s disease

A

ØAntithyroid Drugs ØIodine - high dose, (with antithyroid drugs) – inhibits synthesis of T3 and T4, blocs release of hormones, decreased vascularity of thyroid gland; for use during thyroid storm or prior to surgery ØBeta Blockers: (with antithyroid drugs) symptoms relief – decreased HR, BP

26
Q

Radioactive Iodine Therapy for Grave’s disease

A

treatment of choice (unless pregnant) – damages or destroys thyroid tissue, limiting hormone secretion; high incidence of post treatment hypothyroidism

27
Q

Subtotal Thyroidectomy for Grave’s disease

A

surgical removal; if goiter large and/or compression of trachea, or no response to other therapies

28
Q

Hypothyroidism

A

Insufficient circulation of thyroid hormones resulting in a hypometabolic state.

29
Q

2 types of hypothyroidism

A

Primary and Secondary

30
Q

Primary Hypothyroidism

A

destruction of thyroid tissue, defective hormone synthesis

31
Q

Secondary hypothyroidism

A

pituitary disease with decreased secretion of TSH or hypothalamic dysfunction with decreased secretion of TRH

32
Q

Causes of hypothyroidism

A

• May be transient, related to thyroiditis, or from discontinuation of thyroid hormone therapy • Worldwide – iodine deficiency is the most common cause • Canada - adult atrophy of thyroid gland (end result of Hashimoto’s thyroiditis an Grave’s disease); also as a result of treatment for hyperthyroidism – surgical removal, or radioactive iodine therapy; drugs – Amiodarone, Lithium

33
Q

Clinical Manifestations of hypothyroidism

A

Vary depending on severity and duration of deficiency ◦ Insidious and non-specific slowing of body processes ◦ Onset is slow ◦ Fatigue, lethargy, impaired memory, depression, slowed speech, decreased initiative and concentration ◦ Decreased CO and contractility, decreased exercise tolerance and SOBOE ◦ Anemia, easy bruising, increased lipids and triglycerides ◦ Constipation, cold intolerance, dry skin, hair loss, brittle nails ◦ Menstrual abnormalities – menorrhagia, anovulation, fertility issues ◦ See Table 51-6 p. 1405 for additional manifestations of thyroid hypofunction

34
Q

Myxedema

A

The characteristic facies of severe, longstanding hypothyroidism (i.e., puffiness, periorbital edema, and masklike affect) caused by an accumulation of hydrophilic mucopolysaccharides in the dermis and other tissues. ◦ Severe longstanding hypothyroidism ◦ Accumulation of hydrophilic polysaccharides in the tissues ◦ Characterize facies- periorbital edema, puffiness, masklike effect

35
Q

Myxedema coma

A

The progression of the mental sluggishness, drowsiness, and lethargy of hypothyroidism to a notable impairment of consciousness or coma that is a medical emergency.

36
Q

Diagnostic studies of hypothyroidism

A

Labs: TSH and free T4 (correlated with Hx and PE); increased TSH = defect in thyroid, decreased TSH – defect in pituitary or hypothalamus

37
Q

Goal of treatment of hypothyroidism

A

restoration of erythroid state

38
Q

Hormone replacement therapy of hypothyroidism

A

levothyroxine – doses adjusted based on TSH value

39
Q

Acromegaly

A

A condition caused by excessive secretion of growth hormone and characterized by an overgrowth of the bones and soft tissue

40
Q

Acromegaly in children (Gigantism)

A

over growth of bones and soft tissues (epiphyses open) Gigantism

41
Q

Acromegaly in adults

A

thickening of bones and soft tissues (epiphyses closed) rare Acromegaly

42
Q

What usually causes acromegaly

A

Usually caused by benign pituitary tumor (adenoma)

43
Q

Clinical manifestations of acromegaly

A

◦ Slow onset, 3rd-4th decade ◦ enlarged hands and feet with associated joint pain, potential arthritis; enlargement of bones and soft tissues of face and head; ◦ Dysphasia d/t enlarged tongue ◦ Voice deepened d/t hypertrophy of the vocal cords ◦ Sleep apnea d/t narrowed airway ◦ Skin thick, leathery, oily ◦ Peripheral neuropathy and muscle weakness ◦ Menstrual disturbances ◦ Colon CA and polyps ◦ Enlarged pituitary – pressure on surrounding structures – can impact vision, headaches ◦ Mobilizes free fatty acids – atherosclerosis ◦ GH antagonizes insulin – hyperglycemia – DM ◦ Cardiomegaly, ventricular hypertrophy, angina, HTN

44
Q

Drugs used to treat acromegaly

A
  • somatropin analogue (decreases GH levels) - dopamine agonists (suppress GH secretion) - GH receptor agonist ( directly blocked GH action)
45
Q

Prolactinoma

A

Prolactin secreting adenoma– most frequently occurring pituitary tumor

46
Q

Prolactinoma manifestations in women

A

ovulatory and menstrual abnormalities, decreased libido, hirsutism

47
Q

Prolactinoma manifestations in men

A

ED, decreased libido and sperm density

48
Q

Visual problems in prolactinoma due to:

A

tumor pressure

49
Q

Prolactinoma therapies

A

drug therapy (dopamine agonists); surgery, radiation (last resort)

50
Q

Hypopituitarism

A

A rare disorder that involves a decrease in one or more of the pituitary hormones. Ant Pit (ACTH, TSH, FSH, LH, GH, prolactin; Post Pit (ADH, Oxytocin)

51
Q

Hormones of the pituitary gland

A

Ant Pit (ACTH, TSH, FSH, LH, GH, prolactin; Post Pit (ADH, Oxytocin)

52
Q

Causes of Hypopituitarism

A

autoimmune disorders, infections, pituitary infarction (Sheehan’s syndrome), trauma, radiation, surgery

53
Q

Hypopituitarism diagnostics

A

Labs to measure hormone levels; CT/MRI

54
Q

Hypopituitarism treatment

A

directed at cause, hormone replacement therapy

55
Q

Syndrome of inappropriate antidiuretic hormone (SIADH)

A

a condition characterized by fluid retention, serum hypo-osmolality, dilutional hyponatremia, hypochloremia, and concentrated urine in the presence of normal or increased intravascular volume; results from an abnormal production or sustained secretion of antidiuretic hormone despite normal or low plasma osmolarity.

56
Q

Clinical Manifestations of SIADH

A

◦ Dependent on severity ◦ S & S hyponatremia ( cramps, muscle weakness, vomiting, abdominal cramps, muscle twitching, seizures) ◦ Low urinary output and increased body weight ◦ Decreases serum Na and plasma osmolality levels – cerebral edema, headache, seizure, coma

57
Q

SIADH Diagnostic Studies

A

◦ Urine and serum osmolality (increased urine specific gravity, decrease serum osmolality), ◦ Serum Na level (< 134 mmol/L)

58
Q

Collaborative care of SIADH

A

◦ Treatment is directed at cause and based on severity ◦ Goal – restore normal fluid volume and osmolality ◦ Fluid restriction 800-1000mL/24H (mild symptoms, Na > 125 mmol/L) ◦ Hypertonic IV saline carefully, gentle diuresis(severe, neuro S&S, Na <120 mmol/L ) ◦ Chronic – fluid restriction, medications ◦ See Table 51-2 for Nursing Assessment/Management of SIADH

59
Q

Collaborative care in Diabetes Insipidus

A

◦ Based on cause, restoration of fluid and hormonal replacement ◦ Acute DI – hypotonic saline to replace urine output ◦ Hormone replacement – Desmopressin (analogue of ADH) , PO, IV, nasal spray

Pathophysiology and Pharmacology (17 decks)

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