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Pathophysiology & Pharmacology > Endocrine System Diseases > Flashcards

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
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2
Q

Endocrine Glands: Pituitary Gland

A
  • Attached to the base of the hypothalamus.
  • Regulates growth, reproduction,
    metabolism and fluid balance.
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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.
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4
Q

Hyperthyroidism

A
  • Excessive thyroid gland activity
  • Cause
    ~ Hyper Functioning Tumor
    ~ Autoimmune Response
    > Antibodies stimulate TSH receptors
    • Grave’s Disease
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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
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6
Q

Hyperthyroidism: Treatment

A
  • Removal of Thyroid = Leads to hypothyroidism
  • Drugs to suppress thyroid activity = Leads to hypothyroidism
  • Radioactive iodine treatment.
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7
Q

Hypothyroidism

A
  • Diminished thyroid gland activity
  • Cause
    ~ Thyroidectomy
    ~ Radioactive lodine
    ~ Autoimmune Response
    > Thyroid Cell Destruction
    > Hashimoto’s Thyroiditis
    ~ lodine Deficiency
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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
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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

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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
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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
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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
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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.
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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
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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
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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
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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.
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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.

Pathophysiology & Pharmacology (20 decks)

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