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NPTE Prep > Metabolic and Endocrine Pathologies > Flashcards

Metabolic and Endocrine Pathologies Flashcards

1
Q

Addisons Disease

A
  • adrenal dysfunction that presents with hypofunction of the adrenal cortex
  • decreased production of both cortisol and aldosterone

Etiology: when adrenal cortex produces insufficient cortisol and aldosterone hormones

s/s: widespread metabolic dysfunction, fluid and electrolyte imbalance, hypotension, weakness, anorexia, weight loss, altered pigmentation; if left untreated, can result in shock and death

treatment: long-term pharmacological intervention using synthetic corticosteroid and mineralocorticoids

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2
Q

Cushings syndrome

A
  • adrenal dysfunction that presents with hyperfunction of the adrenal glands, allowing excessive amounts of cortisol production
    etiology: when the pituitary gland produces excessive adrenocorticotropic hormone with subsequent hypercortisolism

s/s: persistent hyperglycemia, growth failure, truncal obesity, purple abdominal striae, moon shaped face, buffalo hump, weakness, acne, hypertension, male gynecomastia, depression, poor concentration, memory loss

treatment: pharmacological intervention to block the production of the hormones, radiation, chemotherapy, surgery

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3
Q

DM I vs DM 2

A

DM I

  • onset: usually less than 25 years of age
  • abrupt onset
  • 5-10% of all cases
  • etiology: destruction of islets of langerhans cells secondary to possible autoimmune or viral causative factor
  • insulin production: very little or none
  • ketoacidosis can occur and polyphagia, weight loss, polyuria, polydipsia, blurred vision, dehydration, and fatigue
  • treatment: insulin injections, exercise, diet

DM 2

  • onset: usually older than 45 ears of age
  • gradual onset
  • 90-95% of all cases
  • etiology: resistance at insulin receptor sites usually secondary to obesity; ethnic prevalence
  • insulin production: variable
  • ketoacidosis will rarely occur
  • treatment: weight loss, oral insulin, exercise, and diet
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4
Q

diabetes testing

A

fasting plasma glucose: 8 hours after last intake of food or drink; positive if blood glucose level is >125 mg/dL (normal is <100)

oral glucose tolerance test: taken two hours after ingestion of sugary drink; positive if blood glucose level is 200 mg/dL (normal is <140)

A1c testing: based on attachment of glucose to hemoglobin that measures average blood glucose level over last few months; positive if A1c level is 6.5% or greater (normal is <5.7)

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5
Q

Graves Disease

A
  • most specific cause of hyperthyroidism
  • most common in women over age 20 but can occur in any gender or age

etiology: caused by an autoimmune disease in which certain antibodies produced by the immune system stimulate the thyroid gland causing it to become overactive

s/s: consistent with hyperthyroidism; mild enlargement of thyroid gland (goiter), heat intolerance, nervousness, weight loss, tremor, and palpitations

treatment: pharmacological interventions; removal of thyroid gland using radiation or surgical interventions

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6
Q

hyperparathyroidism

A
  • occurs due to excessive levels of hormone production by the parathyroid gland that leads to disruption of calcium, phosphate, and bone metabolism
  • symptoms may include renal stones and kidney damage, depression, memory loss, muscle wasting, bone deformity, and myopathy
  • acute treatment may include pharmacological intervention that produces an immediate lowering of serum calcium using diuretics or antiresorptive medications
  • surgical intervention is usually required to remove the diseased parathyroid gland
  • pharmacological intervention may be used prior to surgery or for long term management
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7
Q

hypoparathyroidism

A
  • occurs due to hyposecretion or low-level production of parathyroid hormone by the parathyroid gland
  • symptoms may include hypocalcemia, neurological symptoms such as seizures, cognitive defects, short stature, tetany, muscle pain, and cramps
  • acute treatment requires rapid elevation in serum calcium levels through intravenous calcium
  • long term treatment includes pharmacological management and dietary modification
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8
Q

hyper vs hypo parathyroidism

A

hypo

  • decreased bone resorption
  • hypocalcemia
  • elevated serum phosphate levels
  • shortened 4th and 5th metacarpals (pseudohypoparathyroidism)
  • compromised breathing due to intercostal muscle and diaphragm spasms
  • cardiac arrhythmias and potential heart failure
  • increased neuromuscular activity that can result in tetany

hyper

  • increased bone resorption
  • hypercalcemia
  • decreased serum phosphate levels
  • osteitis fibrosa, subperiosteal resorption, arthritis, bone deformity
  • nephrocalcinosis, renal hypertension, and significant renal damage
  • gout
  • decreased neuromuscular irritability
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9
Q

hyperpituitarism

A
  • occurs when there is an excessive secretion of one or more hormones under the pituitary glands control
  • disorders and symptoms depend on the hormones affected
  • can include gigantism, acromegaly, hirsutism, galactorrhea, amenorrhea, infertility, and impotence
  • treatment is hormone and site dependent, can include tumor resection, surgery, radiation therapy and hormone suppression/replacement
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10
Q

hypopituitarism

A
  • there is a decreased or absent hormonal secretion from the anterior pituitary gland
  • rare disorder
  • typical disorders and symptoms include dwarfism, delayed growth and puberty, sexual anti reproductive disorders, and diabetes insipidus
  • treatment is also based on deficit hormones and usually includes pharmacological replacement therapy
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11
Q

hyperthyroidism

A
  • excessive levels of thyroid hormones in the bloodstream
  • symptoms can include an increase in nervousness, excessive sweating, weight loss, increase in blood pressure, exophthalmos, myopathy, chronic periarthritis, and an enlarged thyroid gland
  • treatment may include pharmacological intervention, radioactive iodine, and surgery
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12
Q

hypothyroidism

A
  • decreased levels of thyroid hormone in the blood stream, slowing metabolic processes within the body
  • symptoms include fatigue, weakness, decreased heart rate, weight gain, constipation, delayed puberty, and retarded growth and development
  • common causes include hashimotos thyroiditis or an underdeveloped thyroid glan
  • treatment includes oral thyroid hormone replacement therapy
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13
Q

hypo vs hyper thyroidism

A

hypo

  • depression, anxiety, increased lethargy, fatigue, headache, slowed speech, slowed mental function, impaired short-term memory
  • proximal muscles weakness, carpal tunnel syndrome, trigger points, myalgia, increased bone density, cold intolerance, paresthesias
  • dyspnea, bradycardia, CHF, respiratory muscle weakness, decreased peripheral circulation, angina, increase in cholesterol
  • anorexia, constipation, weight gain, decreased absorption of food and glucose
  • infertility, irregular menstrual cycle, increased menstrual bleeding

hyper

  • tremors, hyperkinesis, nervousness, increased DTR’s, emotional lability, insomnia, weakness, atrophy
  • chronic periarthritis, heat intolerance, flushed skin, hyperpigmentation, increased hair loss
  • tachycardia, palpitations, increased respiratory rate, increase in blood pressure, arrhythmias
  • hypermetabolism, increased appetite, increased peristalsis, nausea, vomiting, diarrhea, dysphagia
  • polyuria, infertility, increased first trimester miscarriage, amenorrhea
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14
Q

male hypogonadism

A
  • primary is defined as a deficiency of testosterone secondary to failure of the testes to respond to FSH and LH
  • most common cause of primary is Klinefelters syndrome
  • secondary occurs when there is a failure of the hypothalamus or pituitary to produce the hormones that will stimulate the production of testosterone
  • occurs before puberty: symptoms will include sparse body hair, underdevelopment of skeletal muscles, and long arms and legs secondary to a delay in the closure of the epiphyseal growth plates
  • adult onset will present with a decreased libido, erectile dysfunction, infertility, decreased cognitive skills, mood changes, and sleep disturbances
  • treatment includes hormone replacement pharmacological intervention
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15
Q

female hypogonadism

A
  • primary results if the gonad does not produces the amount of sex steroid sufficient to suppress secretion of LH and FSH at normal levels
  • the most common cause of primary is Turner syndrome
  • secondary hypogonadism occurs when there is a failure of the hypothalamus or pituitary to produce the hormones that subsequently stimulate the production of estrogen
  • pre puberty symptoms will include gonadal dysgenesis, a short stature, failure to progress through puberty or primary amenorrhea, and premature gonadal failure
  • adult onset symptoms include secondary amenorrhea
  • treatment includes hormone replacement pharmacological intervention
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16
Q

metabolic acidosis

A
  • when there is an accumulation of acids due to an acid gain or bicarbonate loss, pH drops below 7.35
    etiology: renal failure, lactic acidosis, starvation, diabetic or alcoholic ketoacidosis, severe diarrhea, or poisoning by certain toxins

s/s: compensatory hyperventilation, vomiting, diarrhea, headache, weakness, and malaise, hyperkalemia, and cardiac arrhythmias. Untreated can lead to coma and death

treatment: managing underlying cause, correcting any coexisting electrolyte imbalance, and administering sodium bicarbonate

17
Q

metabolic alkalosis

A
  • when there is an increase in bicarbonate accumulation or an abnormal loss of acids, pH rises above 7.45
    etiology: when there has been continuous vomiting, ingestion of antacids, or other alkaline substances or diuretic therapy . May also be associated with hypokalemia or nasogastic suctioning

s/s: nausea, diarrhea, prolonged vomiting, confusion, muscle fasiculations, muscle cramping, neuromuscular hyperexcitability, convulsions, parethesias, hypoventilation. If left untreated, patient can experience seizures, and respiratory paralysis

treatment: managing underlying cause, correcting coexisting electrolyte imbalances, and administering potassium chloride to the patient

18
Q

osteomalacia

A
  • where bones become soft secondary to calcium or phosphorus deficiency. there is adequate bone matrix, but insufficient calcification of the matrix
    etiology: calcium is lost secondary to inadequate intestinal absorption and the phosphorus is lost secondary to an increase in renal excretion. Deficiency in vitamin D will also cause this

s/s: aching, fatigue and weight loss, myopathy and sensory polyneuropathy, periarticular tenderness and pain, thoracic kyphosis, and bowing of lower extremities, difficulty performing transfers and standing

treatment: focus on underlying etiology. Increased nutrition and pharmacological intervention may include vitamin D or phosphate supplements

19
Q

osteoporosis

A
  • decrease in bone mass that subsequently increases the risk of fracture
  • primarily affects trabecular and cortical bone where the rate of resorption accelerates while the rate of bone formation declines
  • declining osteoblast function coupled with loss of calcium and phosphate salts will cause bones to be brittle

etiology: primary can include idiopathic, post menopausal, or involutional. Secondary can occur as a result of another primary condition or with use of certain medications

s/s: compression and bone fractures, thoracic or lumbar pain, loss of lumbar lordosis, deformities such as kyphosis, decrease in height, dowagers hump, and postural changes

treatment: vitamins and pharmacological treatment, proper nutrition, assistive devices, patient education, surgical intervention

20
Q

Pagets disease

A
  • heightened osteoclast activity
  • lacks true structural integrity
  • bone appears large but lacks strength due to the high turnover of bone secondary to abnormal osteoclastic proliferation

etiology: genetic component as well as geographical incidence, most commonly affects patients over 50 years old

s/s: msk pain and bony deformities, continued pain, headache, vertigo, hearing loss, mental deterioration, fatigue, increased cardiac output, heart failure

treatment: pharmacological intervention using bisphosphonates in order to inhibit bone resorption and improve quality of involved bone, exercise, weight control, and cardiac fitness are key

21
Q

phenylketouria

A
  • consists of intellectual disability as well as behavioral and cognitive issues secondary to an elevation of phenylalanine hydroxylase
  • normally, excessive phenylalanine is converted to tyrosine by phenylalanine hydroxylase
  • the brain is the primary organ that becomes affected
  • children in the united states are tested at birth for PKU and levels greater than 6 of phenylalanine require treatment

etiology: autosomal recessive inherited trait and is most common in caucasian populations

s/s: appear shortly after birth; gait disturbances, hyperactivity, psychoses, abnormal body order, display features that are lighter when compared to other family members

treatment: dietary restriction of phenylalanine throughout the person’s lifetime

22
Q

tay-sachs disease

A
  • absence of deficiency of hexosaminidase A
  • this produces an accumulation of gangliosides within the brain

etiology: autosomal recessive inherited trait in Jewish population

s/s at approximately 6 mo, the child will start to miss developmental milestones and will continue to deteriorate in motor and cognitive skills; usually will die by age 5

treatment: no effective treatment

23
Q

wilsons disease

A
  • a rare inherited disorder that can occur in anyone
  • appears in people under 40 and symptoms can develop in children between 4-6

etiology: autosomal recessive inherited trait that produces a defect in the bodys ability to metabolize copper

s/s: appear between 4-6, include kayser-fleischer rings surrounding the iris secondary to copper deposits; degenerative changes in the brain, hepatitis, cirrhosis, athetoid movements, ataxic gait patterns

treatment: continual pharmacological intervention using vitamin B6 and D-penicillamine as both promote the excretion of excess copper from the body . treatment should also focus on prevention of hepatic disease

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