Pathophysiology, Chp. 16 - The Endocrine System

Promotes the transport of glucose into the cells, thereby decreasing blood sugar.

The pancreas

Can either increase or decrease blood sugar. It makes sure it never gets too low. Antagonistic to insulin.

- tumor

- excretion by liver of kidney is impaired

- congenital condition

- antagonistic hormone production is increased (^glucagon)

- congenital defect

- atrophy, surgical removal of gland

- malnutrition

The possibility of malignancy.

Checks serum hormone levels.

daily levels of hormones.

replacement therapy. Ex. insulin to treat DM

- meds

- surgery

- radiation

- chemotherapy for tumors

An autoimmune response causing a destruction of the pancreatic beta cells (secretes insulin), leading to a dependency and deficit on insulin.

DM I: juvenile, insulin dependent, more severe, lifelong

DM II: milder, can be reversed through diet, older people, just a decreased effectiveness of insulin

The hormone might have turned into a different shape (lock & key) and thus can't properly fit. The body then can't properly use it or it may get a form of resistance to it.

Insulin Dependent Diabetes Mellitus (Type I)

Type II

Noninsulin-dependent diabetes mellitus (Type II)

decreased production of insulin and/or increased resistance by body cells to insulin.

Type I: common acute onset in children and adolescents

Type II: slow, insidious and usually in those older than 50

- diet

- ^ body's use of glucose (exercise)

- stimulating beta cells to produce more insulin

1. Decreased transport of and use of glucose (insulin brings glucose to the cells, when there's a deficit not as much sugar will be going into the cells).

2. As a result glucose will remain in the blood and thus blood glucose levels rise (hyperglycemia).

3. The excess glucose spills into the urine (glucosuria).

4. Glucose in the urine exerts osmotic pressure (pulls in lots of fluid), resulting in a large volume of urine being excreted (polyuria).

5. Large fluid loss from hyperglycemia pulls water from the cells, resulting in dehydration.

6. Dehydration causes thirst (polydipsia).

7. Lack of nutrients (ex. glucose) entering the cells stimulates appetite (polyphagia).

8. Diabetic ketoacidosis (DKA): Lack of glucose in cells results in catabolism (breakdown) of fats and proteins instead to compensate. This leads to excessive amounts of fatty acids and their metabolites, known as ketones or ketoacids to appear in the blood.

9. As dehydration continues, the excretion of acids by the kidneys decreases resulting in decompensated metabolic acidosis (DKA) or a diabetic coma.

A) People with Type I typically have had it since they were young. Thus, have been in an insulin deficit for a prolonged period of time. As a result, if not being properly treated, the body begins to break down fats and proteins to compensate for the lack of glucose in the cells. An excess of ketones, the byproduct of fats, then are released into the blood. With an excess of ketones in the blood, the body becomes more acidic, thus ketoacidosis.

B) With ketones appearing in the blood, the kidneys then filter the blood to create urine. In the process they also bring the ketones into the urine to be excreted, thus their presence.

- hunger and fatigue

- thirst (from dehydration)

- polyuria (+ large volumes of urine)

- dry mouth (from dehydration)

- itchy skin

- blurred vision

Remember the three Ps!

weight loss.

weight gain.

- polyuria

- polydipsia

- polyphagia

The three P's.

a type of oral medication to treat DM type II. It increases insulin secretion, thus lowering blood glucose levels.

Because sugars can damage and destroy blood vessels. Meaning the longer you have an abnormal amount, the more damage they can do to your vessels.

excess of insulin, which causes a deficit of glucose in the blood.

- following strenuous exercise

- dosage error

- vomiting (thus not properly absorbing nutrients)

- skipping a meal after taking insulin (now there's an imbalance of insulin compared to glucose in the body, since the meal you should've taken would have compensated for the insulin you took, without it there will be an excess of insulin)

Affects the neurological function:

- poor concentration

- slurred speech

- lack of coordination and staggering gait

Affects the SNS:

- increased pulse

- pale, moist skin

- anxiety and tremors

Loss of consciousness, seizures, and death.

- If conscious, immediately give sweet fruit, juice, honey, candy or sugar.

- If unconscious, IV glucose 50%, nothing by mouth.

- insulin

- fluid

- sodium bicarbonate

Signs are related to dehydration:

- thirst

- dry, rough oral mucosa

- warm, dry skin

- oliguria (indicates that compensation mechanisms to conserve fluid in the body are taking place)

Ketoacidosis signs:

- rapid, deep respirations (Kussmaul respirations)

- acetone breath

- lethargy (indicating depression of the CNS from acidosis and decreased blood flow)

Metabolic acidosis signs:

- decreased serum bicarb levels

- serum pH falls

- loss of consciousness

A state of uncontrolled DM, especially in patients with DM II. Usually indicated by severe hyperglycemia and dehydration.

1. High blood sugar

2. Beta cells of pancreas increase secretion of insulin

3. Insulin promotes transport of glucose into cells

4. Blood sugar decreases/becomes low

5. Alpha cells secrete glucagon (prevents glucose levels from dropping too much)

6. Gluconeogenesis (trasforming non-carbohydrates into glucose) in the liver

DM results in abnormal carbohydrate, protein and fat metabolism.

Obesity

- variations in diet and alcohol use

- change in physical activity

- infection (destruction of vessels, area becomes more prone to infections)

- vomiting (loss of glucose through emesis)

- increased incidence of atherosclerosis

- Microangiopathy - due to an obstruction or rupture of small capillaries and arteries --> tissue necrosis and loss of function

- retinopathy --> leading cause of blindness

- chronic renal failure --> degeneration in glomeruli of kidney

- neuropathy and loss of function

- infections, common and severe

- cataracts (from abnormal metabolism of glucose)

It releases calcium into the blood from the bone.

Hypoparathyroidism is a deficit or lack of function of the parathyroid. This may be caused by a congenital lack of the glands, surgery or radiation in the neck area.

Leads to hypocalcemia:

- weak cardiac muscle contractions (cardiac muscles rely on the calcium in the blood for contractions).

- increases the excitability of nerves, leading to spontaneous skeletal muscle contractions (tetany).

Hyperparathyroidism is caused by an excess function of the parathyroid glands. This may be caused by a tumor, paraneoplastic syndrome.

Leads to hyperglycemia:

- forceful cardiac contractions

- osteoporosis

- increased predisposition to kidney stones

Adenomas, which can have two types of manifestations:

1. Effect from its mass in the brain - ^ pressure in the skull --> ^ headaches, seizures, drowsiness, visual deficits

2. Effect on hormone secretion - excess or decrease release of hormones

A deficit in growth hormone production and release. A person who has pituitary dwarfism still has normal proportions and intelligence.

An excess of GH prior to puberty resulting in a large stature.

A result of excess GH in adults, likely from an adenoma. The bones become broader and heavier, soft tissue grow (hand and feet) a thicker skull and changes in facial features.

- polyuria, resulting in large amounts of dilute urine

- thirst

ADH

False; this is because diabetes insipidus is not due to a lack of insulin, but rather a deficit in ADH.

Inappropriate ADH syndrome:

- retention of fluid

- mental confusion

- irritability

Symptoms are similar to sever hyponatremia

- thyroxine (T4)

- triiodothyronine (T3)

An enlargement of the thyroid gland as a result of low iodine levels, which synthesizes T4 and T3. To compensate, the gland undergoes hyperplasia and hypertrophy. It can compress the esophagus interfering with swallowing, or it can cause pressure on the trachea.

Foods which contain elements that block the synthesis of T3 and T4. This can induce a goiter through the regular compensation method if taken in excess.

It's a hyperthyroid condition from a hyperactivity of the gland. This can produce a large nodular gland.

A hyperthyroid condition, usually occurring in women over 30. This is related to an autoimmune factor.

Signs and symptoms:

- ^ body temp.

- hyper metabolism

- sweating

- insomnia

- reduced BMI

The presence of protruding, staring eyes and decreased blink and eye movements. It's from increased tissue mass in the orbit pushing the eyeball forward.

- radioactive iodine

- surgical removal of thyroid tissue

- anti-thyroid drugs

Hashimoto thyroiditis: autoimmune disorder.

Myxedema: refers to nonpitting edema of the face and thick tongue. Myxedema coma can result in hypotension, hypoglycemia, and loss of consciousness.

Cretinism: a congenital disorder. Where the thyroid gland is nonfunctional or absent. Results in short stature and severe cognitive deficits.

- goiter

- intolerance to cold

- ^BMI

- lethargy and fatigue

- decreased appetite

A benign tumor of the adrenal medulla that secretes epinephrine, norepinephrine and other substances. Produces headache, heart palpitations, sweating, intermittent anxiety which are all related to blood pressure.

- excess levels of glucocorticoids

- adrenal adenoma

- pituitary adenoma

- ectopic carcinoma

- iatrogenic conditions

- substance abuse

- round face

- heavy trunk

- thin limbs

- thin hair

- osteoporosis

- gluconeogenesis and insulin resistance --> DM

- decreased blood glucose levels

- poor stress response

- fatigue

- low bp

- weight loss and decreased appetite

- hyperpigmentation

- frequent infections

Addison disease is a result of a deficit in corticosteroids, whereas cushing syndrome is a result of having too much of it.