Endocrine System Diseases Flashcards
1
Q
Endocrine System Overview
A
- Made up of glands that secrete hormones into the blood stream.
~ Hormones are chemical messengers
secreted from one site and have
actions elsewhere in the body.
~ Because hormones circulate in blood,
they potentially have contact with all
cells.
> A hormone usually affects only a
limited number of cells because
the only those cells have receptors
for the hormone.
~ Diseases and disorders of the
endocrine system usually occur when
too little or too much of a hormone is
produced
2
Q
Endocrine Glands: Pituitary Gland
A
- Attached to the base of the hypothalamus.
- Regulates growth, reproduction,
metabolism and fluid balance.
3
Q
Endocrine Glands: Thyroid and Parathyroid Glands
A
- Thyroid Gland
~ Located in the anterior, upper neck
region.
~ Regulates metabolism and bone
maintenance. - Parathyroid Glands
~ Located in the posterior portion of the
thyroid.
~ Regulates calcium and phosphate
balance.
4
Q
Hyperthyroidism
A
- Excessive thyroid gland activity
- Cause
~ Hyper Functioning Tumor
~ Autoimmune Response
> Antibodies stimulate TSH receptors
• Grave’s Disease
5
Q
Hyperthyroidism: S&S
A
- Tachycardia
- Tremor
- Hypertension
- Nervousness
- Weight Loss/Gain
~ Burning calories more due to
increased metabolism = weight loss
or weight gain due to increased
hunger - Exophthalmoses
~ Inflammation of muscles that move
the eyes and soft tissues behind the
eye. - Toxic Goiter
~ Thyroid is overly stimulated
6
Q
Hyperthyroidism: Treatment
A
- Removal of Thyroid = Leads to hypothyroidism
- Drugs to suppress thyroid activity = Leads to hypothyroidism
- Radioactive iodine treatment.
7
Q
Hypothyroidism
A
- Diminished thyroid gland activity
- Cause
~ Thyroidectomy
~ Radioactive lodine
~ Autoimmune Response
> Thyroid Cell Destruction
> Hashimoto’s Thyroiditis
~ lodine Deficiency
8
Q
Hypothyroidism: S&S and Treatment
A
- Bradycardia
- Fatigue
- Constipation
- Cool, Dry Skin
- Hair Loss
- Brittle Nails
- Weight Gain
- Nontoxic Goiter
~ Thyroid is overly stimulated due to
inadequate hormone levels - Treatment
~ Administer thyroid hormone
9
Q
What is the cause of osteoporosis in the RED-S triad?
A
Energy/caloric deficit or low calcium in diet that causes the body to get it from somewhere else
10
Q
Regulation of Bone Density
A
- Bone structure is made up of calcium and phosphorous crystals embedded in a framework of interlocking protein fibers.
- Bone density is dependent on balance of calcium levels in the blood and tissues
~ Bone density is dependent on balance
of calcium levels in the blood and the
tissues.
~ Calcium has many uses and will be
drawn from the bone to be used in
more important functions.
> Muscle Contraction
> Nerve Impulse Transmission
> Blood Clotting
11
Q
Regulation of Bone Density: Decreased Ca Levels
A
- Fall in blood calcium levels triggers the release of Parathyroid Hormone (PTH) from the parathyroid glands
~ Triggers the kidneys to retain more
calcium
~ Triggers intestines to absorb calcium.
~ Triggers bone to release calcium.
> Osteoclasts are activated and
osteoblasts are inhibited - If all three triggers go in too long = osteoporosis
12
Q
Regulation of Bone Density: Increased Ca Levels
A
- Rise in blood calcium levels triggers the release of calcitonin (CT) from the Thyroid gland
~ Triggers the kidneys to excrete more
calcium.
~ Decreases calcium absorption in the
intestine.
~ Triggers bone to absorb calcium.
> Osteoclasts are inhibited and
osteoblasts are activated
13
Q
Regulation of Glucose
A
- Body always using carbs (glucose), fats (FFA) and protein (AA) for energy.
- % of energy source used depends on activity and stores.
~ Glucose is needed by CNS for energy
regardless of activity so glucose level
in the blood is very tightly regulated.
14
Q
Regulation of Glucose: Insulin
A
- Produced by the beta cells of the pancreas.
- Released in reaction to increased glucose levels in the blood.
~ Stimulates cells to take up glucose
15
Q
Additional Functions of Insulin
A
- Carbohydrates
~ Increases rate of glycolysis.
~ Increases rate of glycogen synthesis.
~ Decreases rate of glycogen
breakdown. - Fat
~ Decreases lipid catabolism.
~ Stimulates lipid anabolism.
~ Decreases fatty acid metabolism in
muscle and liver. - Protein
~ Decreases protein catabolism.
~ Increases protein anabolism.
~ Increases transport of amino acids
into tissues - In general, insulin is anabolic = builds
16
Q
Regulation of Glucose: Glucagon
A
- Produced by alpha cells of the pancreas.
- Released in reaction to decreased glucose levels in the blood.
~ Stimulates breakdown of glycogen and
release of glucose from the liver and
muscles
17
Q
Type 1/Insulin Dependent Diabetes Mellitus: Cause and Result
A
- Cause
~ Body doesn’t produce or produces low
levels of insulin - Result
~ Cells do not take in the glucose
necessary for cell function.
18
Q
Type 1/Insulin Dependent Diabetes Mellitus: S&S and Management
A
- S&S
~ Polyuria
~ Polydipsia
~ Weight Loss
~ Fatigue
> Glucose is in blood and can’t be
used for energy - Management
~ Balanced Diet: special attention to
carbs/sugars.
~ Exercise: Increases insulin sensitivity.
~ Monitor Blood Glucose Levels Prior to
Exercise (normal is 70-110 mg/dl)
• <100 mg/d| - Ingest carbohydrate
snack or administer glucagon to
increase glucose level.
• >240 mg/d - Test for ketones in
urine - if present, insulin
administered, and medical
referral made.
19
Q
Insulin Shock: Cause and Result
A
- Cause
~ Too much insulin relative to the
circulating glucose (hypoglycemia) - Result
~ Blood glucose levels drop below
normal levels.
~ Fluid lost to tissues decreasing O2
delivery to body. - Can result in death due to lack of O2
20
Q
Insulin Shock: S&S
A
- Rapid Onset
- Dizziness
- Tachycardia
- Sweating
- Palpitations
- Hunger
- Nervousness
- Headache
• Intense Hunger
• Pale, Cold, Clammy Skin
• LOC
21
Q
Insulin Shock: Management
A
- If conscious, able to swallow, and follow directions
~ Administer 10-15g of carbohydrate:
> 4-8 glucose tablets
~ Recheck glucose levels after 15.
~ Administer another dose of
carbohydrate if levels remain low.
~ Activate EMS if levels do not return to
normal after second round.
~ Provide snack if glucose levels
normalize. - If unconscious or unable to swallow or follow directions -
~ Activate EMS
~ Administer Glucagon (frees up
glucose)
~ Administer carbohydrate if patient
becomes conscious, able to swallow
and follow directions.
22
Q
Diabetic Coma: Cause and Result
A
- Cause
~ Too much circulating glucose, did not
take enough insulin (Hyperglycemia) - Result
~ Body utilizes abnormally high amount
of fat for energy.
~ Body produces excess ketones leading
to ketoacidosis. - Can cause death due to pH imbalance
23
Q
Diabetic Coma: S&S
A
- Slower Onset
- Fatigue
- Sleepiness
- Loss of Appetite
- Polyuria
- Polydipsia
- Confusion
- Fruity/Acetone Breath
- Kussmaul Breathing
~ Abnormally deep, rapid ventilation. - LOC
24
Q
Diabetic Coma: Management
A
- If conscious, able to swallow, and follow directions -
~ Give non-carbohydrate fluids. (water
not Gatorade or juice)
~ Administer Insulin - If unconscious or unable to swallow or follow directions -
~ Activate EMS
25
Q
Type 2 Diabetes/Non Insulin Dependent Diabetes Mellitus
A
- Sensitivity to insulin is diminished
- Exact mechanism is not clear.
~ insulin binds to receptor, but has
diminished effect.
~ Malfunction in the signaling
mechanism for glucose transport
proteins to present themselves.
26
Q
Type 2 Diabetes/Non Insulin Dependent Diabetes Mellitus: Prevention/Management
A
- Exercise
- Diet Modifications (less sugar)
- Insulin?
~ Will only help temporarily
27
Q
Receptor/Drug Interaction
A
- Each cell has receptors that are necessary to proper functioning of that specific cell.
- Reaction to Changes in Chemical Concentration
~ Increase or decrease the number of
receptors to adapt to the environment
> Add more receptors when
chemical levels are low.
> Decrease receptors when chemical
levels are high. (Tolerance)
~ Increase or decrease the sensitivity of
a receptor.
28
Q
Drugs for Type 2 Diabetes: Insulin Secretagogues
A
Bind to beta cells causing increased insulin release
29
Q
Drugs for Type 2 Diabetes: Insulin Secretagogues Adverse Effects
A
- Hypoglycemia (too much insulin)
- Weight Gain (Anabolism)
30
Q
Drugs for Type 2 Diabetes: Biguanides
A
- Metformin
- Mechanism
~ Inhibits gluconeogenisis in the liver
(inhibits glucose production)
~ Increases insulin receptor activity.
~ Increases glucose transport protein
presentation.
~ Opposes action of glucagon.
~ Decreases glucose absorption.
31
Q
Drugs for Type 2 Diabetes: Biguanides Adverse Effects
A
- Less likely to cause hypoglycemia.
~ Does not affect insulin levels. - Gl Tract
~ Nausea
~ Diarrhea
~ Vomiting
~ Metallic Taste
~ Lactic Acidosis (Rare)
> Drops pH = bad
> Lactate is a substrate for
gluconeogenesis
32
Q
Drugs for Type 2 Diabetes: Insulin Sensitizers
A
- Increases insulin receptor activity
~ Preserves beta cells in the pancreas
33
Q
Drugs for Type 2 Diabetes: Insulin Sensitizers Adverse Effects
A
- Liver Toxicity
- Increased risk of MI.
- Increased risk of fracture especially in women.
34
Q
Drugs for Type 2 Diabetes: Alpha Glucosidase Inhibitors
A
- Alpha glucosidase is an enzyme in the small intestine that breaks carbohydrates down into glucose, galactose, and fructose
- Mechanism
~ Inhibits enzyme so less carbohydrates
can be converted to simple sugars and
absorbed into blood
> Taken immediately before a meal
35
Q
Drugs for Type 2 Diabetes: Alpha Glucosidase Inhibitors Adverse Effects
A
- Undigested carbohydrates move
to the large intestine and are used by bacteria.
~ Flatulence
~ Diarrhea
36
Q
Drugs for Type 2 Diabetes: DPP-4 Inhibitors
A
- Incretin is released from the small intestine when glucose is present.
~ Causes beta cells to release insulin. - DPP-4 Inactivates Incretin
~ Mechanism
> Drug inhibits DPP-4 so incretin can
act more fully on the beta cells
• Insulin release
37
Q
Drugs for Type 2 Diabetes: DPP-4 Inhibitors Adverse Effects
A
- Hypoglycemia
- Infection
~ DPP-4 is important in immune
function
38
Q
Drugs for Type 2 Diabetes: Incretin Like Compounds
A
- Mimic action of incretin
~ Causes beta cells to release more
insulin
39
Q
Drugs for Type 2 Diabetes: Incretin Like Compounds Adverse Effects
A
- Hypoglycemia
~ Only dug that increases insulin levels - Nausea
- Vomiting
- Diarrhea
40
Q
Drugs for Type 2 Diabetes: Sodium-Glucose Contransporter-2 (SGLT2) Inhibitors
A
- SGLT2 is a transporter protein in the kidney that is responsible for glucose reabsorption.
- When SGLT2 is inhibited glucose is excreted through kidney/urine
41
Q
Drugs for Type 2 Diabetes: SGLT2 Inhibitors Adverse Effects
A
- Increased risk of leg and foot amputation.
~ Double the risk!
~ Maybe due to low blood volume/
dehydration.
> Makes effects of peripheral
vascular disease worse.
> Decreases blood flow/oxygen
delivery. - Decreased Bone Density/Increased Bone Fracture Risk
- Serious Urinary Tract Infection
~ Due to high glucose in the urine
> Bacteria use glucose for energy
~ Causes necrosis of genitalia - Ketoacidosis
~ Body using more fat for energy
metabolism
> Ketones are a product of fat
metabolism
42
Q
Diabetes Insipidus
A
- Inadequate secretion of ADH from pituitary gland leads to decreased fluid reabsorption in the kidney
- May also be due to inability of kidneys to respond to ADH
- Measure to blood glucose to determine this vs. diabetes
43
Q
Diabetes Insipidus: Cause, S&S, & Management
A
- Cause
~ Idiopathic
~ Tumor or infection that affects the
hypothalamus or pituitary. - Signs and Symptoms
~ Polyuria
~ Polydipsia
~ Normal blood Glucose Levels - Management
~ ADH Replacement
~ Drugs to make kidney more responsive
to ADH.
