Unit 6 Endocrine System Flashcards by Honey-Marie de la Giroday

What are the categories of endocrine function disturbance?

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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What are the categories of endocrine function disturbance?

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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What hormones are secreted by the Hypothalamus?

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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What hormones are secreted by Anterior pituitary gland?

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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What hormones are secreted by the Posterior pituitiary gland?

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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What hormones are produced by the thyroid?

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

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What are the effects of T3 and T4?

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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How is the function of the thyroid controlled?

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What are the most important function of thyroid hormone?

Increases metabolism and protein synthesis
Influences growth and development in children
- Mental development and attainment of sexual maturity

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Describe hypothyroidism

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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Describe hyperthyroidism.

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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What is a thyroid storm?

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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What hormones are produced why the adrenal cortex?

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What are the funtions of glucocorticoids (cortisol)?

antagonistic to insulin
protein catabolism
lipolysis
immune suppression
antiinflammatory

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

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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Describe the pancrease and substances it produces

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

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

Glucose and insulin secretion

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Insulin

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

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]

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

Insulin
Glucagon
Catecholamine
Growth hormone
Glucocorticoids (cortisol)

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

Insulin
Glucagon
Catecholamine
Growth hormone
Glucocorticoids (cortisol)

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

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

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:

Corticosteroids
growth hormone
Catecholamines

What is diabetes mellitus and what is its etiology?

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

What are the type 1 subdivision and their etiology?

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

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

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

What Metabolic Abnormalities Contribute to Hyperglycemia in Type 2 Diabetes

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

What are major causes of secondary diabetes mellitus?

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

What other types of diabetes are there?

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

What is the pathophysiology of diabetes mellitus?

* 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/](http://postimg.org/image/3x7peb34b/)

What are the manifestations of diabetes millietis?

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

What are the criteria for diagnosing DM?

Test Results [http://postimg.org/image/rkkbt4sf7/](http://postimg.org/image/rkkbt4sf7/) Criteria for diagnosis [http://postimg.org/image/v1ojy2o4h/](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

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

**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.

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/](http://postimg.org/image/zavw3xmvt/)

What are the acute complications of DM?

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

What is the Somogyi effect and Dawn Phenomenon?

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

What are chonic complications of DM?

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

What are four theories that explain chronic complications of DM?

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

Explain how diabetic nephropathies form.

[http://postimg.org/image/w6ic0e5ut/](http://postimg.org/image/w6ic0e5ut/)