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Endocrine Flashcards

1
Q

Clinical uses of endocrine drugs

A
  • hormone replacement
  • diagnosis of endocrine disorders
  • treatment of excessive endocrine function
  • exploitation of beneficial hormone effects
  • uses of hormones to alter normal endocrine fx
  • uses of hormones for non-endocrine disease
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2
Q

hormone replacement Rx

A
  • diabetes and hypothyroidism
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3
Q

treatment of excessive endocrine function

A

use negative feedback to inhibit secretion/release

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4
Q

exploitation of beneficial hormone effects:

A

prednisolone: 4x anti-inflammatory, < Na retention
Giving hormone to exploit beneficial effects

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5
Q

Uses of hormones to alter normal endocrine fx

A
  • contraceptives: progesterone inhibits LH and FSH
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6
Q

Use of hormones for non-endocrine disease

A

Cancer treatment such as anti-estrogens (tamoxifen)

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7
Q

Examples of Receptor Mechanisms

A
  • Either work in the nucleus or work in the periphery
  • Periphery are more superficial in their effect and faster acting
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8
Q

Pituitary Hormones (anterior lobe)

A
  • Growth Hormone: tissue growth and development
  • Luteinizing hormone: Female ovulation, increase estrogen and progesterone; male increase spermatogenesis
  • Follicle stimulating hormone: Female increase follicular development and estrogen; male increase spermatogenesis
  • Thyroid stimulating hormone: synthesis of T3 and T4
  • Adrenocorticotropic hormone: increase adrenal cortisol production
  • Prolaction: lactation
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9
Q

Andrenocorticosteroids

A
  • produced in adrenal gland
  • adrogens and testosterone (anabolic steroids)
  • glucocorticosteroids
  • mineralocorticosteroids
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10
Q

Androgens and testosterone

A
  • secondary sexual characteristics
  • Androgen, androstenedione, nandrolone
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11
Q

Glucocorticoids

A
  • function is to regulate glucose metabolism and combat stress
  • cortisol and corticosterone
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12
Q

Mineralocorticosteroids

A
  • Function: water and electrolyte balance
  • Aldosterone
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13
Q

Where is cortisol produced?

A

Fasiculata of the adrenal gland

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14
Q

Physiologic dose

A

same concentration as hormone
is normally found in the body

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15
Q

Pharmacological dose

A
  • use higher dose to exploit effect
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16
Q

See steroid synthesis on slide 8

A
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17
Q

steroid synthesis facts

A
  1. there is a common pathway up to cholesterol
  2. 4 branching pathways lead to three classes of steroids
  3. many similarities in structure: cortisol differs from aldosterone by 1 OH and 1 COH group
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18
Q

glucocorticoids in normal function

A
  • primary glucocorticoid: cortisol
    (hydrocortisone)
  • cortisol is under control of ACTH
  • ACTH is under control of CRH
  • hypothalamus controls release of CRH
  • Circadian rhythm release
  • peak around 8 am
  • low point around 1 to 4 am
  • need this to wake up
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19
Q

Actions of glucocorticoids

A
  • Released during stress: physical (ie. trauma) or
    psychological stress (anxiety)
  • Alter cellular “protein expression” by altering
    transcription of certain genes
  • Glucose, protein & lipid metabolism effects:
  • Anti-inflammatory effect * Immunosupression
  • Sodium and H2O reabsorption
  • CNS changes (mood and behavior changes)
  • Alter composition of blood & muscle
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20
Q

Metabolic effects of cortisol

A
  • Muscle: decrease glucose uptake, increase protein break down –> amino acids –> liver
  • Fat Cells: decrease glucose uptake, increase fat breakdown –> free fatty acids –> liver
  • once in the liver, there is gluconeogenesis —> glucose goes to blood and body
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21
Q

Effects on Glucose, Protein & Lipid Metabolism

A
  • Paradoxical Effect: increased blood glucose,
    while at the same time increase glycogen
    storage (in Liver)
  • Accomplishes by enhancing catabolism:
    – Stored fat → free fatty acids
    – Muscle protein→ free amino acids
  • Elevation in BG occurs at expense of muscle
    – This accounts for one of the major side effects of
    corticosteroids: muscle wasting
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22
Q

Anti-inflammatory Effects of glucocorticoids

A
  • Attenuate pain, erythema, swelling & tenderness by multiple cellular actions, But takes 3-5 days
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23
Q

How do glucocorticoids decrease inflammation

A

1)-Inhibit eicosanoid synthesis (proinflamatory
substances like prostaglandins & leukotrienes) through lipocortins (inhibit eicosanoid synthesis by action on phospholipid substrates)
2) Inhibition of cellular inflammatory response:
-block chemotaxsis, -inhibit release of inflammatory mediators (interlukins, TNF, etc.)
3) stabilize WBC lysosomal membranes
4) decrease vascular permeability & inhibit histamin

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24
Q

Glucocorticoid Effects on other systems

A
  • Inhibit “hypersensitivity” reactions
  • Increases kidney reabsorption of Na+ & H2O
    – impaired ability to excrete water load
  • “Personality” or mood changes
  • impaired skeletal & cardiac muscle function (too little or too much harmful
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25
Q

How do glucocorticoids inhibit hypersensitivity reactions

A

decrease in chemotaxis, decrease “killing ability” of T and B cells, and decrease activation of T & B cells secondary to decrease in mediators (interlukins and TNF)

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26
Q

Therapeutic uses of glucocorticoids for anti-inflammatory effects:

A

Injection (into joints, tendons, bursa, etc…)
Topical & transdermal: Phonophoresis (US) and Iontophoresis (E-stim)
Systemic (SLE, MS, RA, scleroderma, etc…)

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27
Q

in terms of hormone replacement therapy, cortisol is given for:

A
  • Addisons disease (primary adrenal insufficiency)
  • secondary adrenal insufficiency (decrease ACTH or CRF)
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28
Q

Indications for glucocorticoids

A
  • allergic reactions
  • collagen disorders
  • dermatological disorders
  • hematological and GI disorders
  • non-rheumatic inflammation
  • neoplastic disease
  • respiratory disorders
    -rheumatic disorders
  • neurological conditions
  • ophthalmic disorders
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29
Q

most common drugs for iontophoresis

A

dexamethasone and lidocaine

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30
Q

What is Cushing’s syndrome?

A

chronic over-production of glucocorticoids

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31
Q

what are the symptoms of Cushing’s syndrome

A

– “moon face”
– centripetal obesity
– bone and connective tissue damage
– muscle wasting especially of limbs
– behavioral changes (mood swings)
– Hyperglycemia and type II DM
- Buffalo Hump

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32
Q

Side Effects of Glucocorticoids

A
  • Adrenocortical Suppression: negative feedback on the hypothalamic/pituitary axis suppresses CRH production
    – even after a single systemic dose, or after topical administration if given over large area (in child)
  • Drug-induced Cushings Syndrome:
    • Round face, fat deposition on trunk, muscle wasting, hypertension, osteoporosis, hyperglycemia
    • Connective Tissue destruction
    • Peptic ulcer, growth retardation in children, immunosupression, glaucoma, mood changes & psychosis, Na and water reabsorption
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33
Q

Why is the pancreas unique?

A

It is both an endocrine and exocrine gland.

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34
Q

What do acinar cells make?

A

powerful digestive enzymes

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35
Q

What does Islet of Langerhans contain?

A

alpha cells: make glucagon
beta cells: make insulin

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36
Q

What are the 3 peptide hormones

A
  • insulin
  • glucagon
  • glucagon like peptide (GLP)
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37
Q

What does insulin do?

A

decreases BG, facilitates glycogen synthesis
and anabolism and acts as trophic hormone on muscle & other tissues

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38
Q

What does glucagon do?

A

increases blood glucose (antagonizes insulin)

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39
Q

What does glucagon like peptide do

A
  • causes production of glucagon and insulin
  • also called incretin
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40
Q

what is glucagon-like peptide secreted in response to?

A

feeding

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41
Q

characteristics of GLP

A

– Very short half-life (<2 min) secondary to degraded by dipeptidyl peptidase-4 (DP-4)
– GLP-1 promotes glucose-dependent insulin
secretion by increasing insulin-sensitivity in beta-cells
– Decreases glucagon secretion
– Inhibits gastric emptying in the stomach.
– Promotes satiety in brain to decrease hunger
– Promotes insulin sensitivity in peripheral tissue

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42
Q

Why is GLP good?

A
  • insulin tends to make you hungry
  • GLP can break that cycle of hungriness to help you lose weight
43
Q

Insulin action on skeletal muscles

A
  • Insulin causes GLUT proteins to function
  • These GLUT proteins are responsible for transporting glucose out of the blood
  • Located on skeletal & cardiac muscle, adipose GLUTs tissue and live
44
Q

What is normal blood glucose?

A

80-90 mg/ml of blood

45
Q

what happens with a severe drop in blood glucose?

A
  • hypoglycemia
  • can cause death/coma
46
Q

what happens with chronically elevated blood glucose

A
  • hyperglycemia
  • causes pathologic neural, immune, and cardiovascular changes
47
Q

How does insulin work?

A
  • negative feedback
  • increase in BG stimulates insulin release from beta-cells via glucose receptors
    – decrease in BG inhibits insulin release
    – Insulin is high after a meal and gradually decrease
48
Q

how does glucagon work?

A
  • negative feedback
  • decrease in BG stimulates release, increase in BG inhibits release
    – glucagon is highest in PREparandial state (before a meal)
49
Q

How does GLP-1 work?

A

with insulin and glucagon to regulate blood glucose, satiety, and insulin action

50
Q

What is type 1 diabetes caused by?

A
  • insulin deficiency: usually due to auto-immune mechanism (10%)
  • beta cells are destroyed and there is little or no insulin
  • blood insulin is markedly reduced
51
Q

What is type II diabetes cause by?

A
  • alterations in insulin receptors (90%)
  • receptors are down regulated in response to increased blood glucose
  • blood insulin is typically normal or increased
52
Q

Signs, symptoms, and effects of DM - Hyperglycemia

A

– Glucosurea (spilling of glucose into urine)
– Dehydration: glucose takes H2O w/ it in urine
– Electrolyte imbalance
– Metabolic shift: decreased intracellular glucose causes fat and protein catabolism
– Ketoacidosis: decrease pH secondary to ketone bodies and free fatty acids in blood
– Glycosolation of vascular & neural structures
– Atherosclerosis and ischemic heart disease

53
Q

T2DM Management

A
  • Lifestyle!
  • Self-monitoring
  • Weight management
  • Activity
  • Nutrition
  • Education
54
Q

2 Types of insulin:

A
  • Insulin Preps: basic differences in length of action
  • rapid acting (short half life): given when BG is hard to control (such as in “brittle diabetic”)
    – check BG and give insulin often
  • long acting (long half life) given when BG is stable
55
Q

How are insulin preps given?

A

injected secondary to insulin broken down in the GI tract

56
Q

What is the best type of insulin? Producing fewest side effects?

A

Human (recombinant)

57
Q

Insulin Administration

A
  • Given “subcutaneously” secondary to must be
    absorbed slowly
  • In emergency (diabetic coma) given IV, but unless BG is extremely high, if given IV hypoglycemia and death may result
58
Q

Considerations for self administration:

A

– adequate refrigeration and storage
– sterility of the needle and injection site
– accurate measurement of the dose (insulin needle)
– rotation of the site (thigh, abdomen, arm etc)

59
Q

Dietary considerations in insulin dosing

A
  • need to monitor BG to accurately determine when dose is given
    – increase dose if given before a meal
    – decrease if no meal planned for a while
60
Q

Exercise considerations in insulin dosing

A
  • dramatically affects BG: so plan for exercise
    or PT by adjusting dose down
    – pts often need something to boost BG during exercise or PT if insulin dose not adjusted
61
Q

Is implantable-insulin delivery better than self injection?

A
  • no
  • there is still a continued need for hour-hour or day-day adjustments
62
Q

Goal of insulin:

A

maintain BG as close to normal as possible, with minimal fluctuation

63
Q

Intensive Insulin treatment

A
  • pt carefully monitors BG (4 or more x/day and gives frequent (3-4x/day) small doses)
  • Requires more cooperation, compliance and
    motivation by patient
  • Long term studies show this strategy has the
    best outcome (decreased complications)
64
Q

Side Effects of Insulin: Hypoglycemia

A

decrease in BG below 80 mg/ ml
– HA, tachycardia, fatigue, anxiety or nervousness, hunger, diaphoresis, confusion
– symptoms become progressively worse w/ decreasing BG
– severe hypoglycemia: LOC, coma, death

65
Q

How does insulin act with exercise

A
  • synergistically to decrease BG
  • a 30-35% or > decrease in insulin dose required if exercise is intense
66
Q

How can you recover from hypoglycemia

A

20 g of D-glucose IV or comparable amount orally
will temporally restore BG
– orange juice or some other beverage w/ fructose

67
Q

Side Effects of Insulin: Allergic Reaction

A

to non-recomninant human insulin:
– rash, anaphylactic reaction, etc

68
Q

Smoggy Effect or “rebound”

A

An increase in BG due to antibodies to insulin
- Causes a decrease in the effectiveness and “insulin resistance” to that particular type.
– Most often due to non-human insulin
– Need to switch brand or go to Humalin (recombinant)

69
Q

What patients are oral hypoglycemics used for?

A

Pts with T2DM

70
Q

How do oral hypoglycemics work?

A
  • These drugs can both increase insulin release from the pancreas and increase sensitivity of peripheral tissues to insulin
  • Effective in about 1/2 of patients w/ INDDM
    – can sometimes eliminate need for insulin
  • Especially useful when combined with dieting
71
Q

Most oral hypoglycemics are ….

A

Sulfonylureas

72
Q

What is Glucovance?

A

a new combo drug that mixes Glyburide and
Metformin together:
– Have complementary mechanisms of action to improve glycemic control in patients with T2DM

73
Q

How does Glucovance work?

A
  • Glyburide lowers BG by stimulating the release of insulin from the pancreas
  • Metformin improves glucose tolerance in T2DM by decreasing hepatic glucose production, decreasing intestinal absorption of glucose and increasing insulin sensitivity of peripheral tissues
74
Q

Concerns with Rosiglitazone (Avandia):

A
  • 50% more weight gain than similar medications
  • 2 X risk of fluid retention
  • Elevate the risk of bone fractures
  • Heart problems (46% increase risk of MI)
  • GlaxoSmithKline, the maker of Avandia, says the
    analysis included too few long-term studies to
    produce reliable results
    ** has black box warning
75
Q

Other Agents used to treat hypo and hyperglycemia

A

Cyclosporin: used in the early treatment of pts w/
type 1: inhibits autoimmune reaction against the beta- cells of the pancreas (blocks production of anti-bodies)
* Glucagon: used to Rx hypoglycemia-induced coma

76
Q

New Agents for Treating Diabetic Complications: Microangiopathy, neuropathy, nephropathy, retinopathy

A
  • Aldose Reductase Inhibitors
  • Anti-advanced glycation end-product drugs
  • Free-Radical scavengers
  • Visoactive Agents
  • Growth Factor Inhibitors
  • Growth Factors themselves
77
Q

Aldose Reductase Inhibitors (ARI’s):

A
  • inhibit an enzyme in the microvasculature and in neurons that is responsible for converting glucose to sorbitol
78
Q

Anti-advanced glycation end-product drugs:

A

– AGE’s on long lived proteins (like Hb) inhibit protein function

79
Q

Free Radical Scavengers

A

combat the oxidative stress generated by reaction of sugars with proteins in DM
– Probocol, Vit E, glutathione, butylated hydroxytoluene and other

80
Q

Vasoactive Agents

A

these are designed to prevent the peripheral nerve ischemia in DM: potent locally
acting vasodilators
- Anyone with T1 OR T2 should be on one of these

81
Q

What is paramount for patients with both T1 and T2DM

A

Nutrition

82
Q

Nutrition: Type 1

A

watching carbohydrate and saturated fat
is important in minimizing complications
- minimize simple sugars; fiber is good to prolong breakdown of food

83
Q

Nutrition: Type 2

A

total caloric intake as well as carbohydrate and saturated fat are important

84
Q

Exercise for T2DM

A
  • especially critical
    – facilitates wt loss (decrease amount of tissue requiring insulin), increased glucose uptake (independent of insulin), decreased CV and neurologic complication
85
Q

PT and Pharmacological management

A
  • Treat the underlying problem through non-pharmacological menas
  • Awareness of metabolic derangement (ketoacidosis and hypoglycemia.. keep D-glucose tablets, OJ, or snack handy)
  • reinforce compliance
86
Q

Thyroid hormone:

A

regulates metabolism and works synergistically with other hormones to promote growth and development

87
Q

What works together to regulate blood calcium and bone mineralization

A

parathyroid hormone, calcitonin, and vitamin D

88
Q

2 Hormone from the Thyroid Gland:

A
  1. Thyroxin - T4 (back up)
  2. Triiodothyronine (T3)
    ** most physiological effects are due to T3
89
Q

See regulation slide 50

A
90
Q

Production of T3 and T4

A

-Thyroid gland takes up Iodine from the blood
- Iodine is combined with Thyroglobin in the thyroid follicle producing Iodothyroglobin
- Iodothyroglobin then is broken down into T3 and T4 and released into blood stream

91
Q

Goiter

A

a build up of thyroglobin in the follicles secondary to lack of Iodine (enlarged thyroid gland)

92
Q

How a goiter forms:

A
  • If Iodine is not present in the diet, then thyroglobin cannot be converted to iodothyroglobin and T3 & T4.
  • Thyroglobin builds up and causes swelling of thyroid
93
Q

Effects of Thyroid hormone

A
  • Plays direct role (stimulating metabolism) but also plays a “permissive” role, allowing other hormones such as androgen and growth hormone to work
  • Thermogenesis
  • Growth and Development
  • CV effect
  • Metabolic effect
94
Q

Thermogenesis effect of thyroid hormone

A

T3 and T4 increase metabolic rate to increase heat production

95
Q

Growth and development effect of Thyroid hormone

A

T3 stimulated the release and facilitates the effects of growth hormone on skeletal and cardiac muscle, nervous, and skeletal systems

96
Q

CV effects of thyroid hormone

A

increases HR and contractility causing greater CO
- also sensitizes heart to NE and epi

97
Q

Metabolic effect of thyroid hormone

A

increased cellular metabolism

98
Q

Hyperthyroidism

A
  • Graves disease
  • sweating, hot all the time, tachycardia, body temp increased, nervous, shaky, increased CO
99
Q

Hypothyroidism

A
  • primary or secondary
  • mental slowing, cold all the time, body temp drops, wound healing, metabolism slowed, myxedema, bradycardia
100
Q

Treatment of hyperthyroidism consists of either

A

1) surgical removal of the thyroid gland if surgery is performed secondary to thyroid tumor, them often RT or radioactive I is given for follow up.
2) radioactive Iodine, which destroys the gland

101
Q

See parathyroid hormone regulation slide 56

A
102
Q

Metabolic Bone diseases

A
  • Hypoparathyroidism: impaired bone resorption and hyocalcemia
  • Hyperparathyroidism: excessive resorption and hypercalcemia
  • Osteoporosis
  • Rickets: Vitamin D deficiency
  • Osteomalacia: adult Rickets
  • Paget Disease: excessive bone formation, ineffective remodeling, abnormalities
  • Renal Osteodystrophy: chronic renal failure, excessive bone resorption
103
Q

Concerns for Rehab Patients

A
  • Be alert for over-medication with thyroid drugs:
    – generally, symptoms of over-medication with thyroid supplementation are similar to hyperthyroidism
    – generally, symptoms of under-medication with thyroid supplementation are similar to hypothyroidism
  • Don’t over tax CV system in patients w/ either
    hypo or hyperthyroidism
104
Q

What can drugs to treat osteoporosis have?

A

serious, life threatening toxic effects so be alert for the early side effects

Pharm (12 decks)

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