Chapter 31 ENDOCRINE Flashcards

1
Q

Differentiate primary, secondary, and tertiary endocrine disorders.

A

Primary - originate in the target gland responsible for producing the hormone.

Secondary disorders - target gland is normal but function is altered by defective levels of stimulating hormones or releasing hormones from the pituitary system

Tertiary - hypothalamic dysfunction

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2
Q

Discuss the effects of pituitary tumors

A
  • usually benign
  • adenoma most common type
  • adenoma can be divided into nonfunctional and functional tumors that secrete pituitary hormones
  • usually endocrine abnormalities related specifically to functional adenomas and local mass effects of the expanding tumor
  • intracranial pressure, headache, nausea, vomiting. seizures, hemorrhage.
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3
Q

Describe the clinical features and causes of hypopituitarism.

A

CAUSES
-Congential
Benign tumor compressing pituitary gland
Radiation

MANIFESTATION
-loss of GH, LH, FSH, TSH, and ACTH, and PROLACTIN.

-ACTH deficiency leads to weakness, nausea, anorexia, fever, and postural hypotension

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4
Q

Compare the causes and effects of three types of childhood growth hormone deficiency.

A

IDIOPATHIC SHORT STATURE

  • unknown cause
  • > 2 standard deviation below normal mean height for age, sex and population

PSYCHOSOCIAL DWARFISM
-emotional deprivation

GH deficiency
-lack of GHRH
-lack somatotropes
decreased birth length and growth

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5
Q

Discuss the result of growth hormone deficiency in adults.

A
  • present in childhood or adulthood turmor
  • somatopause: GH decline with age

MANIFESTATION

  • decrease in lean body mass and increase in fat mass (hyperlipidemia)
  • reduce exercise tolerance
  • decreased bone density

CVS: central adiposity, insulin resistance.

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6
Q

Compare growth hormone excesses in children and adults.

A

GH EXCESS IN CHILDREN

-Gigantism
Rare, due to adenoma
Prior to puberty
Epiphyses of long bone aren’t fused

Manifestations
Excessive skeletal growth

Recognized early and treated

ACROMEGALY
Adenoma secreting GH, often benign
After puberty when epiphyses has fused

Small bone growth
Fingers, hands, toes, jaw, forehead
Kyphosis, arthralgia, degenerative arthritis

Soft tissue/cartilage growth
Nose, larynx, respiratory tract
Deep voice, risk of bronchitis, sleep apnea
Paresthesis (nerve compression)

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7
Q

Explain the condition known as precocious puberty

A
  • Early activation of hypothalamus, pituitary and gonadal hormones causing early emergence of secondary sexual characteristics and fertility
  • girls <9

CAUSES
-Idiopathic
CNS tumor
Gonadal, adrenal, hypothalamic disorder

TREATMENT
-long acting GnRH agonist

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8
Q

Describe the hypothalamic-pituitary-thyroid feedback system.

A

thyrotropin-releasing hormone (TRH), in the hypothalamus, controls the release of TSH from the anterior pituitary gland. TSH then stimulates the thyroid to produce thyroid hormones. Increased levels of thyroid hormone act in the feedback inhibition of TRH or TSH.

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9
Q

Describe tests in the diagnosis and management of thyroid disorders

A
  • diagnosis of hypothyroidism is based on history, physical examination, and lab test.
  • low serum T4 and elevated TSH levels
  • hypo is treated by replacement therapy of T3 and T4
  • hyper is treated with reducing the level of thyroid hormone. Surgical or drugs
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10
Q

Relate the functions of thyroid hormone to hypothyroidism and hyperthyroidism

A

-abnormal thyroid hormone or deficient TSH secretion in hypothyroidism

  • high level of circulating thyroid hormones in tissue
  • thyroid hormone may heighten the sensitivity of the body to the catecholamines.
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11
Q

Describe the causes of primary versus secondary hypothyroidism

A

CAUSE of PRIMARY

  • thyroidectomy
  • radiotherapy with iondine
  • iondine deficiency
  • HASHIMOTO
  • CRETINISM
CAUSE OF SECONDARY
*-Infection
Inflammation
Infiltration
Hemorrhage
Tumor

-impaired pituitary function
In rare instances, usually due to a tumor, the pituitary gland will fail to produce thyrotropin (TSH), the hormone that stimulates the thyroid to produce its hormones. In such cases, the thyroid gland withers. When this happens, secondary hypothyroidism occurs.

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12
Q

Describe Hashimoto’s thyroidosis

A
Most common hypothyroidism
Autoimmune
Lymphocytic infiltration of thyroid gland
Women more than men
Manifestation
Goiter
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13
Q

Describe Cretinism

A

-Congenital
Appear normal at birth d/t Mom’s hormones
1st sign: prolongation of physiologic jaundice
If treated, minimal symptoms

If untreated
Enlarged tongue: hoarse cry, difficulty feeding
Enlarged abdomen, umbilical hernia
Sluggishness, mental retardation
Impaired physical growth
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14
Q

Causes, manifestations and treatment of myxedematous coma

A
  • cold exposure
  • severe hypothyroidism
  • Non-pitting mucous type of edema d/t accumulation of mucopolysaccharide substance throughout connective tissue
  • unable to metabolize sedatives, analgesics, and drugs which leads to coma
MANIFESTATION
-life-threatening
Resp: CO2 retention, hypoxemia
CVS/Renal: Fluid/electrolyte imbalance
CNS: Hypothermia

TREATMENT
-support cardiorespiratory status, hyponatremia, hypoglycemia and thyroid replacement therapy

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15
Q

Causes, manifestations and treatment of thyroid storm

A
-rare, risk is hyperthyroidism
CAUSE
-infection
-diabetic ketoacidosis
-physical or emotional trauma
-thyroid stimulation during surgery

MANIFESTATION

  • high fever
  • tachycardia, angina, heart failure
  • agitation, restlessness, and delirium

TREATMENT

  • beta blocker
  • meds to decrease circulating TH
  • surgical removal
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16
Q

Describe the function of the adrenal cortical hormones and their feedback regulation

A

-stress exerts its effects on cortisol release through the HPA system and corticotropin-releasing hormone (CRH), which controls the releae of ACTH from the anterior pituitary gland. Increased cortisol level incite a negavtive feedback inhibition of ACTH elease

17
Q

Describe functions and consequences of altered adrenal cortical hormones resulting in Addison disease (i.e., adrenal insufficiency)

A

Addison Disease
90% destruction of gland

Causes
Autoimmune (most common)
Tuberculosis, metastasis, fungal (all rare)

MANIFESTATION
-Loss of aldosterone
Loss of Na+, Cl-, H2O via kidneys
Retention of potassium
Dehydration, hypotension, hypovolemic shock
Weakness, fatigue
Loss of glucocorticoids
Hypoglycemia
Decreased immunity, fever
Anorexia, lethargy, weakness, N+V, weight loss
Hyperpigmentation (d/t elevated ACTH) (bronze hand)

Treatment
Lifetime mineralocorticoid replacement

ACUTE ADRENAL CRISIS
-Addison disease + stress
Slow or fast onset
N+ V, weakness
Hypotension, dehydration, vascular collapse
Hemorrhage d/t septicemia, trauma, anticoagulants, thrombosis, metastasis

18
Q

Compare the functions and consequences of altered adrenal cortical hormones Cushing syndrome (i.e., cortisol excess).

A
Cushing Syndrome
Results from:
Excess production of ACTH by pituitary tumor
Adrenal tumor, benign or malignant
Non-pituitary ACTH secreting tumor
Small cell carcinoma of lung

MANIFESTATION
-Altered fat metabolism
Scapular fat pads (buffalo hump)
Moon face, protruding abdomen

Muscle protein breakdown
Weakness

Bone protein breakdown
Osteoporosis, compression fractures
renal calculi

Integument
Parchment skin, purple striae
Altered cortisol
Poor immunity

Altered glucose metabolism
20% develop DM
Hypokalemia, hypernatremia
Increased androgens 
Hirsutism(exxcessive body hair, mild acne, menstrual irregularities
Emotional instability
19
Q

Describe causes of Secondary Adrenal Cortical Insufficiency

A
Causes
Hypopituitarism
Removal of pituitary
Hypothalamic defect
Rapid withdrawal of glucocorticoids
they suppress HPA system for days/weeks