Metabolic and Endocrine Flashcards
Key Functions of the Metabolic System
- governs the chemical and physical changes that take place in the body.
- Metabolism includes breakdown of body’s complex organic compound – generates energy for body processes and synthesis of complex substances that form tissues and organs.
- Catabolism – organic compounds are broken down
- Anabolism – combines simple molecules for tissue growth
Key Functions of the Endocrine System
- Endocrine glands that secrete hormones that travel through the body to specific target cells.
- Hormones bind selectively to specific receptor sites on the surface of receptor cells.
- Endocrine and Nervous system work in conjunction to maintain homeostasis (can work together or alone)
- They regulate: metabolism, response to stress, sexual reproduction, blood pressure, and water and salt balance
What are the glands of the endocrine system
Hypothalamus
Pituitary Gland
Thyroid Gland
Parathyroid Glands
Adrenal Glands
Pancreas
Ovaries
Testes
Hypothalamus (as an endocrine gland)
*regulation of ANS
- Body temp, appetite, sweating, thirst, sexual behavior, rage, fear, BP, sleep)
- And other endocrine functions
*does this by its impact on the pituitary gland
Pituitary Gland
- Beneath the hypothalamus
- 2 parts: adenohypophysis (anterior) & neurohypophysis (posterior)
- Considered the most important part of the endocrine system. (the “master gland”)
- Secretes endorphins that act on the nervous system and reduce a person’s sensitivity to pain.
- Controls ovulation and works as a catalyst for testes and ovaries to create sex hormones
Thyroid Gland
- Produces thyroxine and triiodothyronine.
- Act to control rate at which cells burn the fuel from food
- Increase in thyroxine increases the rate of the chemical reactions within the body.
Parathyroid Glands
- Posterior surface of the thyroid’s lateral lobes
- Produces parathyroid hormone.
- Functions as an antagonist to calcitonin and important for maintenance of normal blood levels of calcium and phosphate.
- Parathyroid hormone increases the reabsorption of calcium and phosphate from bones to the blood.
- Stimulated by hypocalcemia
- Inhibited by hypercalcemia
- Normal clotting, neuromuscular excitability, and cell membrane permeability are depend on normal calcium.
Adrenal Glands
- Located on top of kidney
- Produces corticosteroids –
- Regulates water and sodium balance
- Body’s response to stress
- Immune system
- Sexual development and function
- Metabolism
- Adrenal medulla produces epinephrine that increases HR and BP when there is stress
Pancreas
- LUQ of abdomen
- Includes endocrine and exocrine glands
- Islets of Langerhans are the hormone-producing cells of the pancreas
- Alpha cell produce glucagon
- Beta cells produce insulin
Hormones Function, regulation, and secretion (Table on pg 524-525)
Aerobic metabolism:
The ATP producing metabolic processes that are dependent on oxygen transported via the circulatory system.
Aerobic metabolic functions typically provide energy for low intensity and/or longer duration activities.
Anabolism:
The metabolic process in which simple molecules (e.g., nucleic acids, polysaccharides, amino acids) are combined to create the complex molecules (e.g., proteins) needed for tissue and organ growth.
Anaerobic metabolism:
Metabolic functions that do not require the presence of oxygen and produce energy for high intensity, shorter duration activities.
Adenosine triphosphate (ATP):
The molecular unit within the body which transports the chemical compounds used for cellular metabolism.
Catabolism:
The metabolic process in which complex materials (e.g., proteins, lipids) are broken down in the body for the purpose of creating and releasing heat and energy.
DNA (deoxyribonucleic acid):
A double helix molecule that contains the genes that provide the blueprint for all of the structures and functions of a living being.
Metabolism:
The physical and chemical processes of cells burning fuel to produce and use energy. Examples include digestion, elimination of waste, breathing, thermoregulation, muscular contraction, brain function, and circulation.
Mitochondria:
The part of the cell that is responsible for energy production. The mitochondria are also responsible for converting nutrients into energy and other specialized tasks.
Osteopenia:
A condition presenting with low bone mass that is not severe enough to qualify as osteoporosis. Individuals with osteopenia may not have actual bone loss, but a naturally lower bone density than established norms.
Osteopetrosis:
A group of conditions characterized by impaired osteoclast function which causes bone to become thickened but fragile. Osteopetrosis is an inherited condition that can vary widely in symptoms and severity.
ph:
A measure of the hydrogen ion concentration in body fluid.
Addison’s Disease
- Adrenal dysfunction that presents with hypofunction of the adrenal cortex. (adrenal insufficiency)- Considered primary insufficiency
- Decreased production of both cortisol (glucocorticoid) and aldosterone (mineralocorticoid).
*Etiology
- When the adrenal cortex produces insufficient cortisol and aldosterone hormones
- autoimmune, infection, neoplasm, or hemorrhage
- Signs and symptoms
- Widespread metabolic dysfunction secondary to cortisol deficiency as well as fluid and electrolyte imbalances secondary to aldosterone dysfunction.
- Hyperpigmentation (typically 1st symptom to present) aka bronze skin
- Hypoglycemia
- susceptible to infections
- personality changes
- Hypotension
- Weakness, fatigue, myalgias
- Anorexia
- Weight loss
- dehydration
- Diarrhea
- If left untreated this condition will result in shock and possible death.
- Treatment - Treatment primarily consists of long-term pharmacological intervention using synthetic corticosteroids and mineralocorticoids.
- Pt implications:
- slow progression of exercise and monitor vital signs
- Fall risk 2* to hypoglycemia and OH
- most common in females 30-50 y/o
Adrenal Crisis
Significant N/V
Confusion
Cyanotic
Abdominal symptoms: abdominal distention, pain, and tenderness
Cushing’s Syndrome
- Adrenal dysfunction that presents with hyperfunction of the adrenal gland, allowing for excessive amounts of cortisol (glucocorticoid) production.
*Etiology
- Pituitary gland produces excessive adreno-corticotropic hormone (ACTH) with subsequent hypercortisolism.
- Most common etiology is pituitary or adrenal gland tumor
- Or could also be excess of corticosteroid medication
- Females’ 25-40 y/o most common
- Signs and symptoms
- Evolve over years and can include:
- Persistent hyperglycemia,
- HTN
- OP
- Growth failure,
- Truncal obesity,
- Purple abdominal striae,
- “moon shaped face,”
- “buffalo hump” posteriorly at the base of the neck aka dorsocervical fat pad
- weakness,
- slender limbs
- acne,
- thinning of skin-straie
- Hair loss
- Bruise easily
- male gynecomastia.
- Mental changes can include depression, poor concentration, and memory loss.
- Treatment - Treatment may include pharmacological intervention to block the production of the hormones, radiation therapy, chemotherapy or surgery.
- PT implications:
- Caution 2* to impaired wound healing/bruise easily
- Closely monitor resistance exercises for m pain or increased weakness
- Slow progressive WB and precautions with mobilization 2* to OP.
- FYI Cushing’s disease is due to a pituitary tumor that results in the same stuff as above.
DM (Type 1)
- Pancreas fails to produce enough or any insulin. * Normally diagnosed in childhood, but can occur at any age.
- AKA It is also known as insulin-dependent diabetes or juvenile diabetes.
- Requires subcutaneous insulin
*Etiology
- The exact cause is unknown, but genetic predisposition in combination with exposure to a viral or environmental trigger is believed to cause an immune reaction that damages the pancreas with subsequent failure in secretion of endogenous insulin.
- Signs and symptoms - rapid onset of symptoms:
- polyphagia,
- weight loss,
- ketoacidosis,
- polyuria,
- polydipsia,
- blurred vision,
- dehydration,
- fatigue.
Treatment -
- exogenous insulin injections that are required to maintain proper glucose blood levels and avoid complications.
- Proper nutritional management is also required for blood glucose control. Insulin pumps may be indicated for continuous administration of insulin.
- Presently, there is no cure for type 1 DM and as a result, the goal is to control the regulation of blood glucose levels (Fig. 7-5).
To diagnosis DM1 & DM2
- Asymptomatic pts: >126mg/dl of two different fasting plasma glucose (fasting = no caloric intake for 8 hrs)
- Symptomatic pt: a random (casual) glucose of 200 mg/dl
- 2 hours postload glucose > or = to 200 mg/dL during oral glucose tolerance test
- A1c test - diabetes = greater or equal to 6.5%
A1c
measure average blood glucose for past 2-3 months
- Normal <5.7%
- Prediabetes 5.7%-6.4%
- Diabetic > or equal to 6.5%
Complications of DM1
hypoglycemia/hyperglycemia
diabetic ketoacidosis
increased risk of infecitons
cardiovascular and peripheral vascular disease
retinopathy
nephropathy
impotence
acceleration of atherosclerosis
major cause of blindness in adults 20-74 y/o
Leading cause of non-traumatic LE amputation and end-stage renal disease
DM (Type 2)
- Over the age of 45 (however increase in children diagnosed due to childhood obesity)
- Typically retains the ability to produce some endogenous insulin. (but can eventually loose all ability)
- alteration in the metabolism of glucose.
- Excess body fat interferes with body’s ability to metabolize insulin correctly
- Etiology - Array of dysfunctions resulting from the combination of resistance to insulin action and inadequate insulin secretion. This disorder is characterized by hyperglycemia when the body cannot properly respond to insulin.
- Obesity is found to contribute to this condition by increasing insulin resistance.
- Signs and symptoms -
- Relatively the same as with type 1, however, ketoacidosis does not occur since insulin is still typically produced.
- polydipsia, polyuria, blurred vision, delayed healing and frequent infections
- Treatment - Treatment of type 2 diabetes includes blood glucose control through diet, exercise, oral medications or insulin injections when necessary.
Gout
- complex form of arthritis from abnormally high uric acid levels
- needle like crystals form and accumulate causing joint inflammation and swelling.
- Most common in males
- Joints affected: great toe, knee, and ankle
Acute
* single joint
* signs of inflammation (pain, redness, swelling, warmth)
* Pain (throbbing, crushing, or excruciating)
* Rapid progression that eases over time (night pain)
Chronic
* multiple joints
* less intense symptoms
* initially may be unrecognized due to the symptoms attributed from arthritis
* Firm, lumpy deposits of uric acide form under the skin
Increases risk:
* obesity, kidney disease, DM or diabetes insipidus, leukemia, and sickle cell anemia
Graves Disease
- Most specific cause of hyperthyroidism.
- Women over age 20 (occurs in men as well and can affect any age group).
- Etiology - Caused by an autoimmune disease in which certain antibodies produced by the immune system stimulate the thyroid gland causing it to become overactive.
- Signs and symptoms -
- Symptoms are consistent with hyperthyroid presentation.
- Classic signs of Graves’ disease:
- Mild enlargement of the thyroid gland (goiter),
- Heat intolerance
- Nervousness
- Weight loss,
- Tremor
- Palpitations
- Weakness
- Frequent bowel movement
- Cardio: DOE, palpitations, tachy, arrhythmias
- Cognitive: anxiety, mental fatigue, and difficulty concentration
- Treatment - Management includes pharmacological intervention and/or removal of the thyroid gland using radiation or surgical intervention.
Hyperparathyroidism
- Excessive levels of hormone production by the parathyroid gland that leads to hypercalcemia (in blood/urine) impacts multiple systems
- Leads to disruption of calcium, phosphate, and bone metabolism.
- Females age >60 y/o
- Symptoms:
- renal stones and kidney damage
- muscle wasting,
- bone deformity,
- myopathy.
- bone decalcification-pain/pathologic fx
- weakness/fatigue
- Joint hypermobility
- CNS: memory, depression, personality changes
- Acute treatment:
- 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.
- Implication to PT: Bone pain (in spine), risk for fx, care with joint mobs, proper hydration and monitor for fatigue
Hypoparathyroidism
- hypo-secretion or low-level production of parathyroid hormone by the parathyroid gland causing hypocalcemia (in blood/urine).
- Symptoms:
- Muscle weakness, pain, and tetany
- Trousseau sign (carpal spasm)
- Chovostek sign (facial spasm)
- Cardiac arrhythmias
- hypocalcemia,
- Seizures
- cognitive defects
- short stature
- Shortened 4th and 5th metacarpals
- Treatment
- Acute hypoparathyroidism requires rapid elevation in serum calcium levels through intravenous calcium.
- Long-term treatment includes pharmacological management and dietary modifications
- Pt implications:
- Acute: Life threatening; immediate emergency care
- Chronic: Hyperventilation may worsen tetany; focus on breathing during exercise
- Cardiac complications may occur; careful monitoring of vital signs
Hyperpituitarism
- Excessive secretion of one or more hormones under the pituitary gland’s control (frequently growth hormone that produces acromegaly in adults).
- Disorders and symptoms are dependent on the hormone that are affected.
- Some disorders include gigantism or acromegaly, hirsutism, galactorrhea (abnormal lactation in males or females), amenorrhea, infertility, and impotence.
- Treatment is hormone and site dependent and can include tumor resection, surgery, radiation therapy, and hormone suppression or replacement (if gland becomes dysfunctional after treatment).
Hypopituitarism
- Decreased or absent hormonal secretion from the anterior pituitary gland.
- Rare disorder and symptoms are dependent on the age of the affected person and deficit hormones.
- Typical disorders may include short stature (dwarfism), delayed growth and puberty, sexual and reproductive disorders, and diabetes insipidus.
- Treatment is also based on the deficit hormones and usually includes pharmacological replacement therapy.
Hyperthyroidism
The thyroid is the metabolic regulator….This is increased so all metabolic functions are increased
- Excessive levels of thyroid hormones (T3 & T4) in the bloodstream.
- Females 20-40
- Typically Graves disease
- Symptoms:
- increase in nervousness,
- excessive sweating,
- fatigue
- palpitations
- hyperreflexia
- tremor
- weight loss,
- increase in blood pressure,
- exophthalmos,
- myopathy,
- chronic periarthritis,
- enlarged thyroid gland.
- atrial fibrillation, CHF, and MI
*Treatment may include pharmacological intervention, radioactive iodine, and surgery.
- PT implications: exercise intolerance and reduced exercise capacity.
-Thyrotoxicosis can aggravate a preexisting heart disease
Hypothyroidism
- Decreased levels of thyroid hormones (T3&T4) in the bloodstream, slowing metabolic processes within the body (so think everything slower).
- Symptoms
- fatigue,
- weakness,
- anorexia
- decreased heart rate,
- weight gain,
- constipation,
- delayed puberty,
- retarded growth and development.
- decreased absorption of food and glucose
- hair loss
- Anemia
- Carpal tunnel syndrome
- FMS
- Depression
- If chronic: forgetfulness, myxedema (excessive swelling of the body), coma/death
- Common causes of hypothyroidism are Hashimoto’s thyroiditis or an underdeveloped thyroid gland.
- Treatment includes oral thyroid hormone replacement therapy.
- PT implications: exercise intolerance with fatigue, weakness, myalgias, and risk of rhabdo if excessiv progression of exercise
- After long-term meds at risk for psudo-gout, osteoporosis, and A-fib
Hypogonadism (male)
- Primary hypogonadism is defined as a deficiency of testosterone secondary to failure of the testes to respond to FSH and LH (produced by the pituitary and hypothalamus).
- The most common cause of primary hypogonadism is Klinefelter’s syndrome.
- Secondary hypogonadism occurs when there is a failure of the hypothalamus or pituitary to produce the hormones that will subsequently stimulate the production of testosterone.
- If a male experiences this prior to puberty:
- sparse body hair,
- underdevelopment of skeletal muscles,
- long arms and legs secondary to a delay in the closure of the epiphyseal growth plates.
- Adult-onset testosterone deficiency
- decreased libido,
- erectile dysfunction,
- infertility,
- decreased cognitive skills,
- mood changes,
- sleep disturbances.
- Treatment includes hormone replacement pharmacological intervention.
Hypogonadism (Female)
- Primary hypogonadism results if the gonad does not produce the amount of sex steroid sufficient to suppress secretion of LH and FSH at normal levels.
- The most common cause of primary hypogonadism 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.
- If a female experiences this prior to puberty symptoms will include:
- gonadal dysgenesis,
- short stature,
- failure to progress through puberty or primary amenorrhea,
- premature gonadal failure.
- postpubescent females,
- secondary amenorrhea is the primary symptom.
- Treatment includes hormone replacement pharmacological intervention.
Metabolic Acidosis
- Accumulation of acids due to an acid gain or bicarbonate loss.
- pH drops below 7.35.
- Etiology - Metabolic acidosis commonly occurs with conditions such as renal failure, lactic acidosis, starvation, diabetic or alcoholic ketoacidosis, severe diarrhea or poisoning by certain toxins.
- Signs and symptoms - Symptoms include
- compensatory hyperventilation, (to induce respiratory alkalosis)
- vomiting,
- diarrhea,
- headache,
- weakness and malaise,
- hyperkalemia,
- cardiac arrhythmias.
- confusion
- lethargy
- tinnitus
- If left untreated the continued increase in acid can induce coma and eventual death.
- Treatment - Treatment includes managing the underlying cause, correcting any coexisting electrolyte imbalances, and administering sodium bicarbonate.
Metabolic Alkalosis
- Increase in bicarbonate accumulation or an abnormal loss of acids.
- pH rises above 7.45.
- Etiology - Commonly occurs when there has been continuous vomiting, ingestion of antacids or other alkaline substances or diuretic therapy. It may also be associated with hypokalemia or nasogastric suctioning.
- Signs and symptoms -
- nausea,
- diarrhea,
- prolonged vomiting,
- confusion,
- muscle fasciculations,
- muscle cramping,
- neuromuscular hyperexcitability,
- convulsions,
- paresthesias,
- hypoventilation.
- If left untreated the patient can become comatose, experience seizures, and respiratory paralysis.
- Treatment - The most important interventions include managing the underlying cause, correcting coexisting electrolyte imbalances, and administering potassium chloride to the patient.
Mitochondrial Disorder
- Over 100 different forms of mitochondrial disease and each produces a different spectrum of disability and clinical manifestations.
- Etiology - Mitochondrial disorders result from genetically inherited or spontaneous mutations in the DNA that lead to impaired function of proteins found within the mitochondria.
- Signs and symptoms - Symptoms vary depending on the type of mitochondrial disorder, however, can include:
- loss of muscle coordination,
- muscle weakness,
- visual and hearing problems,
- learning disabilities,
- heart,
- liver,
- kidney disease,
- respiratory, neurological, and gastrointestinal disorders, and dementia.
- Treatment - These diagnoses are relatively new and treatment is as varied as the symptomatology and presentation of the disease.
- Treatment is aimed at alleviating the current symptoms and slowing the progression of the disease process.
Osteomalacia
- Metabolic condition where bones become soft secondary to a calcium, phosphorus, or Vitamin D deficiency.
*Adequate bone matrix, however, there is insufficient calcification of the matrix due to the deficiency. - Etiology -
- Calcium is typically lost secondary to inadequate intestinal absorption
- Phosphorus is lost secondary to an increase in renal excretion.
- A deficiency in vitamin D will also cause osteomalacia.
- Signs and symptoms - vague presentation of
- aching,
- fatigue,
- weight loss.
- Myopathy and sensory polyneuropathy
- periarticular tenderness and pain,
- thoracic kyphosis deformity,
- bowing of the lower extremities.
- The patient may also struggle to perform transfers and assume a standing position.
- Treatment - Specific intervention will focus on the underlying etiology. Increased nutrition is recommended and pharmacological intervention may include vitamin D or phosphate supplements.
Osteoporosis
- Metabolic condition that presents with a decrease in bone mass that subsequently increases the risk of fracture.
- Primarily affects trabecular and cortical bone where the rate of bone resorption accelerates while the rate of bone formation declines.
- Declining osteoblast function coupled with the loss of calcium and phosphate salts will cause the bones to become brittle.
- Etiology -
- Primary osteoporosis can include idiopathic, post-menopausal or involutional (senile) osteoporosis.
- Secondary osteoporosis can occur as a result of another primary condition or with use of certain medications.
- Signs and symptoms -
- compression and other bone fractures,
- low thoracic or lumbar pain,
- loss of lumbar lordosis,
- deformities such as kyphosis,
- decrease in height,
- dowager’s hump
- postural changes.
- Treatment - Management of primary osteoporosis includes vitamin and pharmacological intervention, proper nutrition, assistive and adaptive device prescription, and patient education. Surgical intervention may be required for fracture stabilization.
- PT for WB activities. Aquatic therapy will assist with conditioning however shouldn’t replace WB activities
Paget’s Disease
- Metabolic condition characterized by heightened osteoclast activity.
- Excessive bone formation lacks true structural integrity.
- Bone appears enlarged, but lacks strength due to the high turnover of bone secondary to abnormal osteoclastic proliferation.
- Etiology - This disease has a genetic component as well as geographical incidence, and most commonly affects patients over 50 years of age.
- Signs and symptoms -
- MSK pain accompanied by bony deformities (kyphosis, coxa varus, bowing of the long bones, vertebral compression).
- Skull, clavicle, pelvis, femur, spine and tibia are common sites that will exhibit bony changes.
- Advanced progression of the disease include continued pain, headache, vertigo, hearing loss, mental deterioration, fatigue, increased cardiac output, and heart failure (secondary to an increased cardiac output).
- Treatment - Management relies heavily on pharmacological intervention using bisphosphonates in order to inhibit bone resorption and improve the quality of the involved bone.
- Exercise, weight control, and cardiac fitness are all key components in a program to maintain strength and motion.
Phenylketonuria (PKU)
- Autosomal recessive inherited trait characterized by intellectual disability and behavioral and cognitive issues
- Characterized by elevated of serum phenylalanine >6 mg/dl due to a deficiency of phenylalanine hydroxylase
- Symptoms include intellectual disability, gait disturbances, hyperactivity, psychoses, abnormal body odor, and light colored features than family members
- most common in Caucasian populations.
- If left untreated, severe intellectual disability will occur.
- Treatment - Phenylketonuria is treated through dietary restriction of phenylalanine throughout the person’s lifetime. Adequate prevention will avoid all manifestations of the disease.
