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DPT 724 Pathophysiology > Lecture 11: Endocrine and Metabolic Systems > Flashcards

Lecture 11: Endocrine and Metabolic Systems Flashcards

1
Q

Endocrine System

A
  • composed of various glands, cell clusters, and hormones
  • regulates and integrates a body’s metabolic activities and homeostasis
  • hormones have slower onset than neural effect, but maintain longer duration of action
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2
Q

Hypothalamus

A
  • secretes releasing hormones
  • main integrative center for endocrine and ANS
  • helps control some endocrine glands by neural and hormonal pathways
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3
Q

Anterior Pituitary Gland

A
  • hypothalamic hormones stimulate anterior pituitary to release 4 tropic hormones: ACTH, TSH, LH, FSH
  • also release effector hormones: HGH and prolactin
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4
Q

Adrenocorticotropic Hormone (ACTH/Corticotropin)

A
  • stimulates adrenal cortex causing secretion of corticosteroids
  • often produced in response to biological stress
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5
Q

Thyroid-Stimulating Hormone (TSH/Thyrotropin)

A

-controls how quickly the body burns energy, makes proteins, and how sensitive body should be to other hormones

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6
Q

Luteinizing Hormone (LH/Lutropin)

A
  • female: acute rise of LH (LH surge) triggers ovulation

- male: stimulates production of testosterone

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7
Q

Follicle-Stimulating Hormone (FSH)

A

-similar functions as LH

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8
Q

Human Growth Hormone (HGH/Somatotropin)

A
  • affects most body tissues by increasing protein synthesis and fat mobilization and by decreasing carbohydrate utilization
  • stimulates and controls rate of skeletal and visceral growth
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9
Q

Prolactin (Lactotropin)

A
  • stimulates growth of breast tissue and milk production

- will increase with variety of stressful stimuli

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10
Q

Posterior Pituitary

A
  • neural stimulation results in secretion of two effector hormone
  • hormones produced in hypothalamus but stored in posterior pituitary: ADH and oxytocin
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11
Q

Oxytocin

A

-stimulates contraction of uterus during labor and milk secretion

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12
Q

Negative Feedback System

A
  • regulates endocrine system
  • inhibits hormone overproduction allowing for self correction
  • simple and complex
  • simple: when level of one substance regulates secretion of hormones
  • complex: when hypothalamus receives feedback from target glands, feedback occurs through hypothalamic-pituitary-target organ axis
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13
Q

Example of Simple Loop

A
  • low serum calcium level stimulates parathyroid gland to release parathyroid hormone
  • PTH in turn promotes resorption of calcium
  • high serum calcium level inhibits it
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14
Q

Example of Complex Loop

A
  • injury or stress cause secretion of hypothalamic corticotropin-releasing hormone (CRH) which causes pituitary to release ACTH which stimulates adrenal (target organ) cortisol secretion
  • subsequently a rise in serum cortisol inhibits ACTH by decreasing CRH secretion
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15
Q

Dysfunction

A
  • pathology results as result of dysfunction of releasing, tropic, or effector hormones or when defects occur in…
  • gland, release of trophic or effector hormones, hormone transport, or target tissue
  • result is abnormal hormone concentrations in blood
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16
Q

Adrenal Glands

A
  • upper part of kidneys
  • produce steroids, amines, epinephrine and norepinephrine (last two are catecholamines)
  • adrenal cortex is outer layer: mineralocorticoids (aldosterone) and glucocorticoids (cortisol) and sex steroids (adrenal androgens and estrogens)
  • adrenal medulla is inner portion: aggregate of nervous tissue; produces catecholamines which induce fight/fight causing vasoconstriction, marked dilation of bronchioles, increased BP, blood glucose level, and HR
17
Q

Cortisol

A
  • stimulation of gluconeogenesis (glycogen from non-CHO sources): occurs in liver in response to low CHO intake or starvation
  • breakdown of increased protein and mobilization of FFA
  • suppression of immune response (inhibits T-cells)
  • assistance with stress response
  • assistance with maintenance of BP
  • prolonged secretion can lead to significant physiological complications (cushing’s disease)
18
Q

Pancreas (Islets of Langerhans)

A
  • produces glucagon from alpha cells: releases stored glucose from liver to increase blood glucose level
  • produces insulin from beta cells: decrease blood glucose levels)
  • delta cells produce somatostatin: believed to regulate release of insulin and glucagon
19
Q

Insulin

A
  • facilitates glucose transport into cells
  • promotes glucose storage
  • stimulates protein synthesis
  • enhances free fatty acid uptake and storage
  • normal blood glucose is less than 100 mg/dl
20
Q

Thyroid

A
  • located in anterior neck
  • secretes iodine-containing hormones: thyroxin (T4) and triiodothyronine (T3): necessary for normal growth and development and regulates basal metabolism; increases metabolic activity and protein synthesis
  • calcitonin: acts to reduce blood calcium (opposes effects of PTH)
21
Q

Parathyroid

A
  • 4 parathyroid glands behind thyroid
  • secrete parathyroid hormone (PTH): regulates calcium and phosphate metabolism; controls bone formation
  • hyperparathyroidism/hypoparathyroidism causes hypercalcemia/hypocalcemia
  • hyposecretion PTH: decreases in serum calcium levels that can lead to tetany and seizures
  • hypersecretion PTH: increases serum calcium levels that can lead to cardiac arrhythmias, muscle and bone weakness, and renal calculi
22
Q

Addison’s Disease

A
  • adrenal insufficiency (hypofunction): decreased production of cortisol and aldosterone leading to increased sodium secretion, dehydration, and hypotension
  • can be classified as either primary or secondary and can progress into adrenal crisis
  • relatively uncommon
  • primary: originates within adrenal glands; decreased mineralocorticoid, glucocorticoid, and androgen secretion
  • secondary: caused by disorder outside gland (pituitary tumor with corticotropin deficiency) aldosterone may be unaffected
  • patho:
  • primary > 90% of both adrenal glands destroyed usually as result of autoimmune process; may also result from neoplasms and infections; leads to increased glucocorticoid production
  • secondary hypopituitarism (decreased corticotropin secretion); removal of nonendocrine corticotropin-secreting tumor; disorders in hypothalamic pituitary function that decrease corticotropin production
  • CM: confusion, fatigue, GI disturbances and weight loss, nausea and vomiting, hyperkalemia, hyperpigmentation, hypoglycemia, hyponatremia, hypotension, weakness, craving salty food; pt. skin is deep bronze in primary d/t high levels of corticotropin
  • dx: measure corticotropin levels (high is primary, low is secondary)
  • tx: lifelong corticosteroid replacement (hydrocortisone)
  • addisonian crisis: critical deficiency of mineralocorticoids and glucocorticoids
23
Q

Cushing’s Syndrome

A
  • cluster of physical abnormalities that occur when adrenal glands secrete excess glucocorticoids (too much cortisol in system)
  • primary: disease of adrenal cortex
  • secondary: hyperfunction of corticotropin-secreting cells of anterior pituitary
  • tertiary: hypothalamic dysfunction or injury
  • patho: ~70% results from excess corticotropin leading to hyperplasia of adrenal cortex; overproduction may stem from pituitary hypersecretion, corticotropin-producing tumor in another organ, administration of synthetic glucocorticoids; 30% results from cortisol-secreting adrenal tumor; administration of steroids can also lead to this
  • CM: weight gain, muscle weakness, fatigue, buffalo hump, thinning extremities with muscle wasting, thin skin, thinning scalp hair, moon face and ruddy complexion, hirsutism (unwanted hair growth in women), truncal obesity, broad purple striae, bruising, impaired wound healing
  • dx: ACTH levels, radiologic evaluation to look for pituitary or adrenal tumor
  • tx: radiation, drug therapy or surgery
24
Q

Diabetes Mellitus

A
  • body doesn’t produce or properly use insulin leading to hyperglycemia, enhanced lipolysis, and protein catabolism
  • occurs in primarily 2 forms
  • also secondary forms caused by pancreatic disease, pregnancy, hormonal or genetic problems, and certain drugs or chemicals
  • insulin deficiency blocks tissues’ access to essential nutrients
  • type 1: beta cells destroyed or suppressed; require exogenous insulin
  • type 2: endogenous insulin production but difficulty with effective insulin actin; resistance to insulin action in target tissues (receptor insensitivity(; abnormal insulin secretion; obesity causes some degree of insulin resistance
25
Q

Type 2 Pathogenesis

A
  • glucose in general circulation not taken up or removed by tissues and continues to accumulate in blood
  • new glucose not deposited in liver, so it synthesizes more glucose and releases it into general circulation, making situation worse
  • kidney excretes excess glucose –> glycosuria (acts as osmotic diuretic and causes excretion and increased amounts of water); results in extreme thirst and water consumption (polydipsia)
  • protein catabolism increases
  • ketone formation: leads to formation of breakdown products called ketones which are excreted in lungs and kidneys; produce hydrogen ions causing pH to fall leading to metabolic acidosis, increases osmotic diuresis
26
Q

Clinical Manifestations and Medical Management for Diabetes

A
  • type 1: polyuria, polydipsia, weight loss with polyphagia, increased ketone levels in urine, lethargy,fruity odor to breath, glycosuria
  • type 2: visual blurring, polyuria, polydipsia, fatigue, neuropathic complications, infections, and polyphagia
  • chronic complications: CVD, PVD, retinopathy, nephropathy, dermopathy, neuropathy
  • dx: symptoms of diabetes plus a random blood glucose level of more than 200 mg/dL; fasting plasma glucose greater than or equal to 126 mg/dL on at least 2 occasions; 2 hour postload glucose greater than or equal to 200 mg/dL during oral glucose tolerance test
  • tx: manage blood glucose, usually can be controlled with diet, exercise, and oral meds
27
Q

SIFTT Diabetes and Exercise

A
  • muscle activity improves skeletal muscle glucose transport
  • program should have all elements of fitness
  • exercise improves glycemic control in people with DM2 but not DM1
  • insulin should not be injected into muscles or at sites close to areas involved in exercise within one hour of exercise
  • in DM2 exercise can improve insulin sensitivity and reduce insulin resistance
  • do not exercise if glucose levels at or near 300 mg/dL (can release stored glycogen)
  • therapy sessions scheduled to avoid peak insulin times
28
Q

Hyperglycemia

A
  • can lead to diabetic ketoacidosis
  • triad of hyperglycemia, acidosis, and ketosis
  • any condition that increases insulin deficit is a cause
  • patho: insufficient or absent levels of circulating insulin; without insulin CHO cannot be used for energy so cells convert fats into glycerol and fatty acids for energy: fatty acids can’t be metabolized as quickly as they’re released so they accumulate in liver where they’re converted into ketones, which accumulate in blood and urine and cause acidosis
  • CM: mild nausea to coma, thirst, polyuria, weakness, hot dry skin, fruity (acetone) breath
29
Q

Hypoglycemia

A
  • symptomatic when blood glucose drops below 70 mg/dL
  • can be caused by overdose of insulin, late or skipped meals, and overexertion in exercise
  • provide CHO immediately
30
Q

Hyperparathyroidism

A
  • overactivity of one or more parathyroid glands –> excess production of PTH
  • disrupts calcium and phosphate bone metabolism
  • results in hypercalcemia
  • patho:
  • primary: hyperfunction of parathyroid glands themselves where there is oversecretion of PTH
  • secondary: due to physiological secretion of PTH by parathyroid glands in response to hypocalcemia
  • most common causes are vitamin D deficiency and chronic renal failure
  • PTH not regulated by pituitary or hypothalamus
  • over secretion causes increased osteoclastic activity
  • CM: skeletal, articular and neuromuscular manifestations: chronic low back pain, easy fracturing, marked muscle weakness and atrophy esp in lungs, arthritis
  • postoperative care following parathyroidectomy: early ambulation essential to expose bones to WB pressures to speed up re-calcification
31
Q

Hypoparathyroidism

A
  • hyposecretion or hypofunction of PTH causing hypocalcemia
  • autoimmune or d/t trauma to parathyroid glands with thyroidectomy
  • CM: neuromuscular irritability-cramping and twitching of muscles
  • need intravenous calcium
32
Q

Hyperpituitarism

A
  • oversecretion of pituitary hormones especially GH
  • typically caused by benign adenoma
  • CM: gigantism-develops in children before epiphyses of bones close, acromegaly-develops after closure of epiphyses, cushing’s-oversecretion of ACTH
  • distinct features of acromegaly: prominent forehead, hands, knuckles, orbital fissures, affects face, jaw, hands, and feet most obviously
33
Q

Hypopituitarism

A
  • GH deficiency common

- CM: dwarfism

34
Q

Goiter

A
  • thyroid disorder
  • enlargement of thyroid gland not caused by inflammation or neoplasm
  • nontoxic goiter
  • most common in females (increased demand for thyroid hormones)
  • endemic: caused by lack of iodine in diet
  • sporadic: ingestion of certain drugs or food that decrease T4 production
  • toxic goiter arises from long-standing nontoxic goiter and occurs in elderly people
  • patho: nontoxic occurs when thyroid gland can’t secrete enough thyroid hormone to meet metabolic needs so mass increases to compensate
  • CM: irregular enlargement of thyroid gland; respiratory distress and dysphagia from compression of trachea and esophagus
  • MM: diet and medication
35
Q

Hyperthyroidism

A
  • overproduction of thyroid hormone; generalized elevation of body metabolism
  • CM: graves’ disease: autoimmune which increases T4 production; affects women more; classic symptoms-mild goiter, nervousness, heat intolerance, weight loss, exophthalmos (protrusion of eyes)
  • rx: meds, radioactive iodine, sx
36
Q

Hypothyroidism

A
  • deficiency of thyroid hormone that results in generalized slow body metabolism
  • common in women and those with down syndrome
  • primary: disorder of thyroid gland
  • secondary: failure to stimulate normal thyroid function (pituitary may fail to produce TSH or hypothalamus may fail to produce TSH-releasing hormone; this form may progress to myxedema coma, medical emergency: significantly decreased respirations, stuporous and hypothermic
  • severe hypothyroidism or myxedema: characterized by thickening of facial features
  • CM: energy loss, forgetfulness, fatigue, sensitivity to cold, unexplained weight gain, constipation; progresses to anorexia, neuromuscular symptoms, joint stiffness, and muscle cramping; goiter: may be result of lack of iodine, inflammation, or tumors
  • rx: synthetic thyroid hormone preparations
37
Q

Metabolic Syndrome

A
  • cluster of conditions characterized by abdominal obesity, high blood glucose level, insulin resistance, high blood cholesterol and triglyceride levels, HTN
  • more than 22% of people in US demonstrate 3+ characteristics, meeting requirements
  • patho: excess quantity and force of insulin causes damage to lining of arteries, promotes fat storage deposits, and prevents fat breakdown-leads to diabetes, blood clots, and coronary events
  • CM:
  • abdominal obesity:waist > 40 in in men > 35 in women
  • elevated TG: < 150 mg/dL or higher
  • reduced HDL: < 40 mg/dL in men < 50 mg/dL in women
  • HTN: 130/85 or higher d/t history of HTN
  • elevated fasting blood glucose level: 100 mg/dL or higher
  • increases person’s risk of heart disease and stroke

DPT 724 Pathophysiology (18 decks)

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