Unit 6 Endocrine System Flashcards

1
Q

What are the categories of endocrine function disturbance?

A

Hypofunction: underproduction of hormone
Causes

  • Congenital defects
  • Disruption in blood flow, infection, inflammation, autoimmune responses, or neoplastic growth
  • Decline in function with aging
  • Atrophy as the result of drug therapy or unknown reasons
  • Receptor defects

Hyperfunction: excessive hormone production
Causes

  • Excessive stimulation and hyperplasia of the endocrine gland
  • Hormone-producing tumor of the gland
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2
Q

What are the categories of endocrine function disturbance?

A
  • Primary disorders: Originate in the target gland responsible for producing the hormone
  • Secondary disorders: The target gland is essentially normal, but its function is altered by defective levels of stimulating hormones or releasing factors from the pituitary system.
  • Tertiary disorders
    Result from hypothalamic dysfunction
    Both the pituitary and target organ are under stimulated.
    uncommon
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3
Q

What hormones are secreted by the Hypothalamus?

A

Seven tropic hormones are produced in the hypothalamus:

  • TRH– Thyrotropin Releasing Hormone, This hormone will affect the anterior pituitary which will then affect thyroid gland activity
  • PRH– Prolactin Releasing Hormone, PIH– Prolactin Release-Inhibiting Hormone, These two hormones will affect the secretion of prolactin from the anterior pituitary
  • CRH– Corticotropin Releasing Hormone, This hormone affects ACTH release from the anterior pituitary
  • GnRH– Gonadotropin Releasing Hormone, This hormone will affect the anterior pituitary which will then affect the gonadal release of sex hormones
  • GHRH– Growth Hormone Releasing Hormone,
  • SS– Somatostatin

These two hormones both affect secretion of growth hormone by the anterior pituitary

Note that all of these seven hormones are tropic hormones. Even the last one, SS, used to be called GHIH for growth hormone release-inhibiting hormone. Every single one of these hormones exerts an effect directly upon the anterior pituitary.

  • *
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4
Q

What hormones are secreted by Anterior pituitary gland?

A

The anterior pituitary secretes four tropic hormones and two regular hormones:

  • TSH– thyroid stimulating hormone, This hormone influences thyroid gland secretion of hormones.
  • ACTH– adrenocorticotropic hormone, Do you see the “tropic” in its name? Good! It works on the adrenal cortex (adrenocortico-).
  • LH– luteinizing hormone
  • FSH– follicle stimulating hormone, These last two together are often termed “gonadotropins” because they exert a tropic hormone effect on the gonads, influencing gonadal secretion of sex hormones.
  • PRL– prolactin
  • GH– growth hormone
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5
Q

What hormones are secreted by the Posterior pituitiary gland?

A

Two Hormones are Produced in the Hypothalamus for Posterior Pituitary Secretion

The hypothalamus makes two additional hormones:  OT (oxytocin) and ADH (antidiuretic hormone).  The hypothalamus does NOT secrete these hormones, however.  Instead, the neurons that make the hormones transport the hormones to their axonal terminals.  These axonal terminals are located in the posterior pituitary.

I edited the image from above and put it here to highlight this function.  Can you imagine that one of the three neurons shown here makes OT?   The other two, let's say, make ADH.  After the cell bodies of these neurons make the hormones, they get transported down their axons to be released from their axonal terminals.

The axonal terminals simply release the hormones into the blood, rather than onto a postsynaptic neuron.  It's that easy.  And this is how the hormones OT and ADH are released by the posterior pituitary into the blood.

Take a look through the PowerPoint presentation and your textbook to get a feel for what these hormones do.  Oxytocin is the same hormone that is injected into a woman to induce labor, but it also has some other functions.  ADH may require a bit more explanation...

ADH is involved in water retention in your body.  ADH signals the kidneys to not allow any excess water leave the body.  How does the hypothalamus know when we need to retain water?  There are sensory neurons detecting visceral things, as well as sensory neurons that detect our obvious senses like touch and vision.   Some visceral sensory neurons detect blood gas levels, others detect changing concentrations of fluids; the ones of this second type are called osmoreceptors (do you recognize "osmo-" from osmosis, another term about water?).   If our blood starts getting to concentrated, we have to retain some more water to dilute it back out.  The osmoreceptors signal the hypothalamus to secrete ADH, and our goal is accomplished.
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6
Q

What hormones are produced by the thyroid?

A
  • triiodothyronine (T3) and
  • thyroxine (T4),

are tyrosine-based hormones produced by the thyroid gland that are primarily responsible for regulation of metabolism.

Iodine is necessary for the production of T3 and T4. A deficiency of iodine leads to decreased production of T3 and T4, enlarges the thyroid tissue and will cause the disease known as goitre.

The major form of thyroid hormone in the blood is thyroxine (T4), which has a longer half-life than T3. The ratio of T4 to T3 released into the blood is roughly 20 to 1. T4 is converted to the active T3 (three to four times more potent than T4) within cells

http://postimg.org/image/ugjsepwx9/

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7
Q

What are the effects of T3 and T4?

A
  • Increases cardiac output
  • Increases heart rate
  • Increases ventilation rate
  • Increases basal metabolic rate
  • Potentiates the effects of catecholamines (i.e. increases sympathetic activity)
  • Potentiates brain development
  • Thickens endometrium in females
  • increase metabolism of proteins and carbohydrates
  • promotes cell growth in the nervous system
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8
Q

How is the function of the thyroid controlled?

A
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9
Q

What are the most important function of thyroid hormone?

A
  • Increases metabolism and protein synthesis
  • Influences growth and development in children
    • Mental development and attainment of sexual maturity
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10
Q

Describe hypothyroidism

A

Hypothyroidism (http://postimg.org/image/ypbp1y6f5/)

  • Decreased metabolic rate
  • Accumulation of hydrophilic mucopolysaccharide substance (myxedema) in the connective tissues
  • Elevated serum cholesterol

Causes

  • Congenital
    • Lack of thyroid gland
    • Anti-thyroid drugs from mother
  • Acquired
    • Thyroidectomy
    • Goitrogenic agents
    • Hashimoto thyroiditis - an autoimmune disease in which the thyroid gland is attacked by a variety of cell- and antibody-mediated immune processes

Manifestations

  • Mental and physical sluggishness
  • Myxedema
  • Somnolence
  • Decreased cardiac output, bradycardia
  • Constipation
  • Decreased appetite
  • Hypoventilation
  • Cold intolerance
  • Coarse, dry skin and hair
  • Weight gain
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11
Q

Describe hyperthyroidism.

A

http://postimg.org/image/ypbp1y6f5/

  • Increased metabolic rate and oxygen consumption
  • Increased use of metabolic fuels
  • Increased sympathetic nervous system responsiveness

Causes

  • Multi-nodular goitre
  • Adenoma of the thyroid gland
  • Grave’s disease - is an autoimmune disease. It most commonly affects the thyroid, frequently causing it to enlarge to twice its size or more (goiter), become overactive, with related hyperthyroid symptoms such as increased heartbeat, muscle weakness, disturbed sleep, and irritability. It can also affect the eyes, causing bulging eyes (exophthalmos). It affects other systems of the body, including the skin, heart, circulation and nervous system.

Manifestations

  • Restlessness, irritability, anxiety
  • Wakefulness
  • Increased cardiac output
  • Tachycardia and palpitations
  • Diarrhea, increased appetite
  • Dyspnea
  • Heat intolerance, increased sweating
  • Thin and silky skin and hair
  • Weight loss
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12
Q

What is a thyroid storm?

A

Extreme, life threatening form of thyrotoxicosis

Predisposing factors:

  • Manipulation of hyperactive thyroid gland
  • Ketoacidosis
  • Severe infection

Manifestation:

  • Very high fever
  • Extreme cardiovascular effects
    • Tachycardia, congestive failure, and angina
  • Severe CNS effects
    • Agitation, restlessness, and delirium
  • High mortality rate
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13
Q

What hormones are produced why the adrenal cortex?

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14
Q

What are the funtions of glucocorticoids (cortisol)?

A
  • antagonistic to insulin
  • protein catabolism
  • lipolysis
  • immune suppression
  • antiinflammatory

http://postimg.org/image/4n6xn4ftj/

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15
Q

What is the name of a disease associated with glucocorticoid excess?

A

Cushing’s syndrome describes the signs and symptoms associated with prolonged exposure to inappropriately high levels of the hormone cortisol. This can be caused by taking glucocorticoid drugs, or diseases that result in excess cortisol, adrenocorticotropic hormone (ACTH), or CRH levels.

Etiology

Cushing’s disease refers to a pituitary-dependent cause of Cushing’s syndrome: a tumor (adenoma) in the pituitary gland produces large amounts of ACTH, causing the adrenal glands to produce elevated levels of cortisol. It is the most common non-iatrogenic cause of Cushing’s syndrome, responsible for 70% of cases excluding glucocorticoid related cases.[2][3]

Pathophysiology

  • Strictly, Cushing’s syndrome refers to excess cortisol of any etiology (as Syndrome means a group of symptoms).
  • One of the causes of Cushing’s syndrome is a cortisol secreting adenoma in the cortex of the adrenal gland (primary hypercortisolism/hypercorticism).
  • The adenoma causes cortisol levels in the blood to be very high, and negative feedback on the pituitary from the high cortisol levels causes ACTH levels to be very low.
  • On the other hand, Cushing’s disease refers only to hypercortisolism secondary to excess production of ACTH from a corticotroph pituitary adenoma (secondary hypercortisolism/hypercorticism) or due to excess production of hypothalamus CRH (Corticotropin releasing hormone) (tertiary hypercortisolism/hypercorticism).
  • This causes the blood ACTH levels to be elevated along with cortisol from the adrenal gland.
  • The ACTH levels remain high because the tumor is unresponsive to negative feedback from high cortisol levels.
  • Cushing’s Syndrome was also the first autoimmune disease identified in humans.[18]

Manifestations

  • Extreme weight gain (truncal obesity)
  • Skin striations
  • Moon face
  • Buffalo hump
  • Immune suppression
  • Water retention/edema
  • Diabetes mellitus

Other

  • Moodiness, irritability, or depression
  • Muscle and bone weakness
  • Osteoporosis
  • Hypertension
  • Sleep disturbances
  • Menstrual disorders such as amenorrhea in women and decreased fertility in men
  • Hirsutism
  • Baldness
  • Hypercholesterolemia
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16
Q

Describe the pancrease and substances it produces

A
  • Pancreas (5 inches long) consists of head, body & tail
  • Cells (99%) in acini produce digestive enzymes
  • Endocrine cells in pancreatic islets produce hormones
    • Alpha cells (20%) produce glucagon
    • Beta cells (70%) produce insulin
    • Delta cells (5%) produce somatostatin
  • somatostatin turns off alpha and beta cells and allows insulin or glucagon to function without being impacted by an antagonist

http://postimg.org/image/tmmdrbmjb/

17
Q

Describe the events that occr during high blood glucose levels and during low blood glucose levels to restore glucose levels to normal. (test question)

18
Q

What is the affect of chronic stress on blood glucose levels?

A
  • Stress has a role in humans as a method of reacting to difficult and possibly dangerous situations. The “fight or flight” response when one perceives a threat helps the body exert energy to fight or run away to live another day.
  • This response is noticeable when the adrenal glands release epinephrine, causing the blood vessels to constrict and heart rate to increase.
  • In addition, cortisol is another hormone that is released under stress and its purpose is to raise the glucose level in the blood. Glucose is the main energy source for human cells and its increase during time of stress is for the purpose of having energy readily available for over active cells.[8]
  • The release of these hormones is intended to be temporary. If someone is under stress for long periods of time they may have adverse health effects later on, such as hypertension and increased risk of cardiovascular disease.[9]
19
Q

What hormones affect glucose, protein and fats in the body?

A
  • Insulin
  • Glucagon
  • Catecholamine
  • Growth hormone
  • Glucocorticoids (cortisol)
20
Q

Explain the action of each of these on glucose, fats and proteins in the body.

  • Insulin
  • Glucagon
  • Catecholamine
  • Growth hormone
  • Glucocorticoids (cortisol)
A

Insulin

  • Anabolic in nature
  • Promotes glucose uptake by target cells and provides for glucose storage as glycogen
  • Prevents fat and glycogen breakdown
  • Inhibits gluconeogenesis and increases protein synthesis

Glucagon

  • Catabolic in nature
  • Increases transport of amino acids into hepatic cells
  • Increases breakdown of proteins into amino acids for use in gluconeogenesis
  • Increases conversion of amino acids into glucose precursors

Catecholamines

  • Epinephrine and norepinephrine
  • Help to maintain blood glucose levels during periods of stress
  • Antagonists to insulin

Growth hormone

  • Increases protein synthesis in all cells of the body, mobilizes fatty acids from adipose tissue, and antagonizes the effects of insulin
  • hyperglycemia?

Glucocorticoids

  • Critical to survival during periods of fasting and starvation
  • Stimulate gluconeogenesis by the liver
  • Antagonist to insulin
21
Q

Describe hormonal control of glucose, fat and protein metabolism in fed and fasting states.

A

In the fed state:

  • glucose is the primary energy source
  • insulin secreted
  • diffusion of glucose into adipose and muscle tissue
  • utilized in glycogen synthesis

In the fasting state:

  • glucose is produced by glycogenolysis and gluconeogenesis
  • primary source of energy to muscle tissue is FFA
  • for neural tissue – glucose
  • Counterregulatory hormones in the fasting state:
  1. Corticosteroids
  2. growth hormone
  3. Catecholamines
22
Q

What is diabetes mellitus and what is its etiology?

A

Disorder of carbohydrate, protein, and fat metabolism
Results from an imbalance between insulin availability and insulin need

Can represent:

  • An absolute insulin deficiency
  • Impaired release of insulin by the pancreatic beta cells
  • Inadequate or defective insulin receptors
  • Production of inactive insulin or insulin that is destroyed before it can carry out its action

Types (Etiology)

  • Type 1 results from:
    • Loss of beta cell function
    • An absolute insulin deficiency
  • Type 2 results from:
    • Impaired ability of the tissues to use insulin
    • A relative lack of insulin or impaired release of insulin in relation to blood glucose levels
23
Q

What are the type 1 subdivision and their etiology?

A

Type 1A (evidence of autoimmune issue; common at 10-14 yrs buy can be as young as 2yrs)

  • Immune-mediated diabetes

Type 1B (often have issues with ketoacidosis)

  • Idiopathic diabetes
24
Q

What is the pathogenesis of type 1a and type 1b

A

type 1a

  • Genetic predisposition (diabetogenic genes)
  • A hypothetical triggering event involving an environmental agent that incites an immune response
  • Immunologically mediated beta cell destruction

type 1b

  • Those cases of beta cell destruction in which no evidence of autoimmunity is present
  • Only a small number of people with type 1 diabetes fall into this category; most are of African or Asian descent.
  • Type 1B diabetes is strongly inherited.
  • People with the disorder have episodic ketoacidosis
25
Q

What Metabolic Abnormalities Contribute
to Hyperglycemia in Type 2 Diabetes

A

Etiology - no exact cause but stronig relationship to genetic/family history, age (middle-aged and older), obesity

  • Impaired beta cell function and insulin secretion
  • Peripheral insulin resistance
  • Increased hepatic glucose production
  • Cell can also become resistant to action by insulin

**More common that type 1

26
Q

What are major causes of secondary diabetes mellitus?

A

Secondary DM is associated with a disorder that casuses dibetes.

Pancreatic diseases

  • pancreatitis
  • cystic fibrosis
  • neoplasms

Endocrine disorders

  • Cushing’s syndrome
  • Hyperthyroidism – Grave’s disease
  • Acromegaly
27
Q

What other types of diabetes are there?

A

Gestational Diabetes (high risk of type II DM later)

  • 20wks to 42 days past birth is defined period for g. diabetes
  • 2 – 5% of pregnancies
  • Family history
  • Obese
  • Advanced maternal age
  • multiparity

MODY (maturity-onset diabetes of the young
< 25 years of age; type II)

  • increased FFA stimulates beta cells (excessive and chronic)  beta cell failure
  • Recent finding – monogenetic defects in beta cell function

LADA (latent autoimmune diabetes of adults; type I)

  • no CM until >35yrs
  • no remission
  • insulin dependent
28
Q

What is the pathophysiology of diabetes mellitus?

A
  • lack of insulin
  • glucose cannot enter cells
  • increase in glucose concentration in blood stream
  • glucose will be excreted in urine (causing increased infection of bladder and vulva)
  • increased osmotice pressure increases the amount of urine produced (causing dehydration)
  • loss of water and salts produces tachycardia and hypotension
  • glucose levels are not controlled

http://postimg.org/image/3x7peb34b/

29
Q

What are the manifestations of diabetes millietis?

A

Type 1 – rapid onset of signs and symptoms
Type 2 - no symptoms or gradual onset

  • 3 polys
    • polyuria (osmotic diuresis)
    • polydipsia
    • polyphagia
  • Glycosuria
  • Hyperglycemia
  • Signs of dehydration
30
Q

What are the criteria for diagnosing DM?

A

Test Results

http://postimg.org/image/rkkbt4sf7/

Criteria for diagnosis

http://postimg.org/image/v1ojy2o4h/

Classification of DM based on OGTT

  • IFG – impaired fasting glucose
  • IOGTT – impaired oral glucose tolerance test
  • They are pre-diabetic states
31
Q

What tests are used to screen for diabetes? (test question)

A

Glycated hemoglobin (A1C) test. This blood test indicates your average blood sugar level for the past two to three months. It measures the percentage of blood sugar attached to hemoglobin, the oxygen-carrying protein in red blood cells. The higher your blood sugar levels, the more hemoglobin you’ll have with sugar attached. An A1C level of 6.5 percent or higher on two separate tests indicates that you have diabetes. (6% is max, 6-7% prediabetes, and >7% is uncontrolled diabetes)

Random blood sugar test. A blood sample will be taken at a random time. Regardless of when you last ate, a random blood sugar level of 200 milligrams per deciliter (mg/dL) — 11.1 millimoles per liter (mmol/L) — or higher suggests diabetes.

Fasting blood sugar test. A blood sample will be taken after an overnight fast. A fasting blood sugar level between 100 and 125 mg/dL (5.6 and 6.9 mmol/L) is considered prediabetes. If it’s 126 mg/dL (7 mmol/L) or higher on two separate tests, you’ll be diagnosed with diabetes.

Oral glucose tolerance test. A blood sample will be taken after you fast for at least eight hours or overnight. Then you’ll drink a sugary solution, and your blood sugar level will be measured again after two hours. A blood sugar level less than 140 mg/dL (7.8 mmol/L) is normal. A blood sugar level from 140 to 199 mg/dL (7.8 to 11 mmol/L) is considered prediabetes. This is sometimes referred to as impaired glucose tolerance.

32
Q

Using the following graph, if you had a patient with X, and Y blood glucose levels at time T1 and T2 what would be your diagnosis? (test question)

http://postimg.org/image/zavw3xmvt/

A
33
Q

What are the acute complications of DM?

A

Diabetic Ketoacidosis

  • Excessive ketone bodies in the blood
  • Lack of insulin – decreased glucose entry into the cells
  • leads to mobilization of fatty acids

Hyperosmolar Hyperglycemic State

  • Common in elderly, severe uncontrolled Diabetes
  • Most common in Type II Diabetes
  • Hyperglycemia and osmotic diuresis leads to dehydration and high serum osmolality

Hypoglycemia - Occurs from excess insulin due to:

  • error in dose
  • failure to eat
  • increased exercise
  • change in insulin site
34
Q

What is the Somogyi effect and Dawn Phenomenon?

A

Somogyi effect

  • A cycle of insulin-induced post-hypoglycemic episodes
  • this results in the production of NE and E by the body to try and increase the blood sugar levels
  • but this can cause hyperglycemia if person also ingests to much glucose to counter act
  • can be a result of too much insulin or long acting insulin
  • can be misdiagnosed as insulin resistance

Dawn Phenomenon

  • Increased level of fasting glucose or insulin requirements or both between 5:00 am – 9:00 am without antecedent hypoglycemia
  • due to diurnal rhythm of hormones
  • causes hypoglycemia
35
Q

What are chonic complications of DM?

A

Three Complications

I. Disorders of circulation

  • Macrovascular complications
  1. Coronary artery
  2. Cerebral artery
  3. Peripheral artery – skin ulcers, foot ulcers
  • Small vessel disease (Diabetic microangiopathy)
  1. Increased capillary permeability – edema
  2. Enlarged pores in kidney – nephropathy
  3. Retinal vessels - retinopathy

II. Neuropathies

  • Ischemia and demyelinization – leading to tingling, numbness, burning sensation
  • Autonomic neuropathy
    • * Defects in autonomic nervous system response – e,g, postural hypotension, sexual dysfunction

III. Infections

  • impaired wound healings
  • impaired immune system – susceptible to Tuberculosis (TB) and urinary tract infections (UTI)
  • increased fetal death rate
36
Q

What are four theories that explain chronic complications of DM?

A

Theories of pathogenesis

1) Polyol pathway

  • glucose sorbitol fructose
  • sorbitol is osmotically active and alter cell function

2) Formation of advanced Glycation end products
* produce structural defects in the basement membrane
3) Problems with tissue oxygenation
* Hb A1c increase the hemoglobin’s affinity for oxygen —less oxygen unloading for tissues
4) Protein kinase C

  • is an intracellular signaling molecules that can regulate vascular functions
  • levels are increased in DM —can produce vascular damage
37
Q

Explain how diabetic nephropathies form.