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Phcol 401 > Quiz #6 Material > Flashcards

Quiz #6 Material Flashcards

1
Q

Thyroid

A
  • Composed of two lobes that flank the pharynx and esophagus
  • Contains numerous follicles, composed of epithelial follicle cells and colloid
  • Largest true endocrine gland
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2
Q

Thyroid hormones control:

A
  • The body’s basal metabolic rate
  • The overall metabolism of protein, fat, and carbohydrates
  • The sensitivity to catecholamines
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3
Q

Thyroid Hormones

A
  • Triiodothyronine (T3) and thyroxine (T4) are synthesized from thyroglobulin
    • 660 kDa protein with ~120 tyrosines
  • The major form of thyroid hormone in the blood is T4
    • T4:T3 is ~20:1
    • T4 has a longer half-life
    • T3 is 5-10x more potent
    • 25% of T4 is converted to T3 in peripheral tissues
      • Mainly the liver and kidney
  • Decarboxylation and deiodination of T3 and T4 produce thyronamine (T0a) and iodothyronamine (T1a)
    • Their physiological roles are not completely understood
    • Have generally opposing roles to T3 and T4
    • May also function as neuromodulators
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4
Q

Thyroid hormone synthesis

A
  • The thyroid can store many weeks worth of thyroid hormone (cupled to thyroglobulin)
  • If no dietary idoine is available for this period, thyroid hormone secretion will be maintained.
  1. Iodine ion comes into thyroid follicle cell via Na/I symporter and then leaves into follicle colloid via pendrin channel
  2. Thyroglobulin is made and then secreted via exocytosis into the follicle colloid
  3. Thyroid peroxidase (TPO) causes the oxidation of Iodine ion.
  4. Thyroglobulin is then iodinated and conjugated
  5. New molecule is taken into thyroid follicular cell via endocytosis
  6. Proteolysis causes molecule to split into T3 and T4, which is then secreted
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5
Q

Thyroid stimulating hormone

A
  • Acts directly on follicular cells
  • Increases
    • Iodide transport into follicular cells
    • Production of thyroglobulin
    • Iodination of thyroglobulin
    • Endocytosis of iodinated thyroglobulin from the colloid into follicular cells
    • Proteolysis of iodinated thyroglobulin
    • Exocytosis into the capillaries
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6
Q

Physiological roles of thyroid hormone (think heart and lungs)

A
  • Cardiovascular system
    • Increase heart rate
    • Increase force of cardiac contractions
    • Increase stroke volume
    • Increase cardiac output
    • Increase catecholamine receptors
  • Respiratory system
    • Inrease resting respiratory rate
    • Increase minute ventilation
    • Increase ventilatory response to hypercapnia and hypoxia
  • Oxygen-carrying capacity
    • Increase red blood cell mass
    • Increase oxygen dissocation from hemoglobin
  • Oxygen consumption
    • Increase mitochondrial size, number and enzymes
    • Increase plasma membrane Na-K ATPase activity
    • Increase futile thermogenic energy cycles
    • Decrease superoxide dismutase activity
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7
Q

Physiological roles of thyroid hormone (others)

A
  • Renal system
    • Increase blood flow
    • Increase glomerular filtration rate
  • Reproductive system
    • Required for normal follicular development and ovulation
    • Required for normal maintenance of pregnancy
    • Required for normal spermatogenesis
  • Growth and tissue development
    • Increases growth and maturation of bone
    • Increases tooth development and eruption
    • Increases growth and maturation of epidermis, hari follicles, and nails
    • Increases rate and force of skeletal muscle contractions
  • Nervous system
    • Critical for central nervous system development
    • Enhances wakefulness and alertness
    • Enhances memory and learning capacity
    • Increases speed and amplitude of peripheral nerve reflexes
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8
Q

TR-RXR heterodimer action

A
  • No ligand, no expression
  • With ligand, activation of gene expression
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9
Q

4 different thyroid hormone receptors

A
  • Tα1 and Tα2 are splice variants of the THRA gene
  • Tβ1 and Tβ2 are splice variants of the THRB gene
  • Tα1, Tβ1 and Tβ2 generally activate transcription when T3 binds (except in pituatary, TRβ2 is a transcriptional activator until T3 binds then it inhibits)
  • Tα2 does not bind T3/T4 and therefore inhibits
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10
Q

Feedback control in the HPT axis

A
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11
Q

Thyroid hormone circulation

A
  • ~99.98% of T4 is bounds to 3 serum proteins
    • 75% thyroid-binding globulin (TBG)
    • 15-20% thyroid-binding prealbumin (TBPA or transthyretin)
    • 5-10% albumin
  • 0.02% of T4 in serum is free
  • 0.4% of total T3 in serum is free
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12
Q

Regulation of T4 metabolism

A
  • Activation (β adrenergic)
    • Deiodination (peripheral dehalogenases in liver/kidneys)
    • T3
  • Inactivation (glucocorticoids)
    • Deiodination (peripheral dehalogenases in liver/kidneys)
    • Reverse T3
      • Inhibits T3 production
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13
Q

Hypothyroidism

A
  • Primary
    • Cretinism
      • Hypothyroidism during childhood
      • Retarted growth, sluggish movements, mental deficiencies
    • Myxedema
      • Hypothyroidism during adulthood
      • ~5% of the adult population
    • Simple Goiter
      • Iodine deficency
      • High TSH causes thyroid hypertrophy
    • Hashimoto’s syndrome
      • Autoimmune
    • Iatrogenic
      • Often following treatment of hyperthyroidism
  • Secondary
    • Pituitary disease
    • Hypothalamic diease
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14
Q

Hyperthyroidism

A
  • Grave’s Disease
    • Autoimmune
    • Usually in 3rd decade, 8:1 women
    • Diffuse thryoid enlargement, wide staring gaze, lid lag, protuberant eyes, hyperpigmentation, high body temp, jittery
  • Excess endogenous thryoid hormone
    • After treatment of hypothyroidism
  • Thyroid cancers
    • Produces excess thyroid hormone
  • Acute hyperthyroidism
    • Causes often unknown
    • Muscle fatigue, weakness, weight loss, sweating, heat intolerance
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15
Q

Hypothyrodisim treatment

A
  • Iodine supplementation
  • Synthetic T4 (Synthroid or equivalent)
    • T3 is more active and acts faster but is more toxic
    • T4 is less susceptible for feedback regulation
    • Goal is to normalize TSH serum concentrations
    • Always check for angina and perform an ECG
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16
Q

Hyperthyroidism Treatments

A
  • Thioamide drugs (TPO inhibitors)
    • PTU, propylthiouracil
    • MMI, methimazole (Tapazole)
    • Disadvantages
      • Short half lives (1.5 hours for PTU)
      • Can inhibit dehalogenase
      • Slow acting
      • Potential side effects; agranulocutosis, aplastic anemia, liver damage
  • 131I
    • Advantages
      • Short path length of radiation and local concentration makes it safe and effetive
      • Excreted rapidly
    • Disadvantages
      • Cannot be used long term (cancer risk)
      • Can lead to delayed hypothyroidism
      • Cannot be used during pregnancy
  • Surgery
    • Partial (adenoma) or complete (Grave’s disease) thyroidectomy
    • For patients allergic to thioamides or resistant to 131I treatment
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17
Q

Multiple hormones influence eating

A
  • Ghrelin
    • Made in response to an empty stomach
  • PYY
    • Made in response to food entering the small intestine
  • Insulin
    • Made in response to rising blood glucose levels
  • Leptin
    • Made in response to increasing fat stores
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18
Q

Cyclic secretion of apetite hormones

A
  • Grehlin peaks at meals
  • Insulin peaks post-prandial
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19
Q

Leptin

A
  • Discovered in 1994 as a gene mutated in obese mice that arose in Jackson Labs in the 50s
  • Secreted by fats cells and circulating plasma levels of leptin correlate with fat stores
  • Production depends on the number and size of adipocytes
  • Obese people have high leptin levels
  • Leptin levels do not appreciably rise after overfeeding
  • Leptin levels do decrease rapidly with food restriction, suggesting it may be a signal to control fuel metabolism during fasting and starvation
  • Adminstration of leptin during a fast prevents the starvation response (decreased thyroid and gonadal hormones, increased glucocorticcoids, decreased body temp, increased eating)
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20
Q

Leptin Action

A
  • Binds POMC neurons (anorexigenic neurons)
    • Induces production of α-melanocyte-stimulating hormone (α-MSH)
    • α-MSH suppresses appetite by signaling a “stop eating” signal
  • Leptin binds NPY neurons (orexigenic neurons)
    • Relieves inhibtion of POMC neurons
    • Prevents triggering of “start eating” signal
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21
Q

Leptin injection a treatment for obesity?

A
  • Obese patient show elevated blood leptin concentrations
    • Leptin production is a function of fat cell abundance and size
  • In most cases, leptin injections have no weight-reduing effects
  • Obses patients have developed a resistance to the leptin signal
  • Congential leptin deficency and leptin receptor dificency have been reported
    • Leptin administration does help
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22
Q

Adiponectin

A
  • Secreted by adipocytes in response to high fat reserves
  • Stimulates AMP-dependent protein kinase (AMPK)
    • Increases fatty acid uptake by myocytes
    • Increases the rate of fatty acid oxidation
    • Slows fatty acid synthesis in the liver
    • Slows gluconeogenesis in the liver
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23
Q

Adiponectin and Type II Diabetes Drugs

A
  • Obese of type II diabetes patients show reduced levels of adiponectin
  • Thiazolidinediones used to treat type II diabetes elevate expression of adiponectin
  • Thiazolidinedione bind PPAR: peroxisome proliferator-activated receptors
  • These normally bind fatty acids or fatty acid derivatives
  • Regulate genes involved in fatty acid metabolism including PEP carboxykinase, a regulated step in glyconeogenesis, and adiponectin
24
Q

Leptin and Insulin

A
  • Insulin and leptin work in similar ways to regulate appetite
  • Insulin brain levels reflect visceral fat
  • Leptin levels reflect subutaneous fat
25
Q

Ghrelin

A
  • Discovered in 1999 as the first circulating hunger hormone
  • Secreted by P/D1 cells of the stomach and epsilon cells of the pancreas
  • Levels increase before meals and decrease after meals
  • Ghrelin and synthetic ghrelin mimetics increase food intake and increase fat mass
  • Ghrelin levels in obese individuals are lower than lean individuals, except in teh case of Prader-Willi syndrome-induced obesity
  • Studies in 2004 found that ghrelin levels during the day were similar in lean and obese people, but during sleep were higher in thin people
  • This suggests obese people may have a problem in the circadian regulation of ghrelin
  • In normal people, shortened sleep cycles produce more ghrelin and less leptin, thus increasing appetite and food intake
26
Q

Ghrelin Action

A
  • Ghrelin binds NPY neurons
    • Inhibits POMC neurons and production of α-MSH
    • Increases appetite by sending the “start eating” signal
    • Leptin and insulin sensitive
  • NPY neurons also produce Agouti-related protein (AgRP)
    • One of the most potent and long-lived appetite stimulators
    • Blocks the “stop eating” signal
27
Q

Other GI hormones induce satiety

A
  • CCK (cholecystokinin)
    • Released from the small intestine in response to nutrients
    • Produces a satiety signal by stimulating vagal afferents to the brain
  • PYY
    • Released from the intestine in proportion to meal size
    • A satiety signal
  • GLP-1
    • A satiety signal
  • Obestatin
    • Product of the ghrelin gene by differential peptide processing
    • Decreases feeding
28
Q

Serotonin and Satiety

A
  • Serotonin increases short-term satiety signals associated with the consumption of a meal
  • Decreases
    • urge to eat high-calorie food
    • consumption of fat
    • intensity of hunger
    • size of meals
    • number of snacks
    • bingeing
  • Serotonin inhibits NPY/AgRP neurons and activated POMC neurons
29
Q

Sibutramine (Reductil, Meridia)

A
  • Mechanism: inhibits serotonin reuptake in the CNS
  • Has anorectic and thermogenic effects
  • Side effects: insomnia, constipation, increase heart rate, slight hypertension
  • Effective in causing ~5-10% weight loss, increase HDL (good cholesterol) and decreased triglycerides
  • Casuses a reduction in diabetes, improved glycemic control
  • As of 10/8/10, Abbot labs withdrew sibutramine from the US due to FDA concerns of efficacy couple with increased cardiovascular events and stroke
30
Q

Lorcaserin (Belviq)

A
  • Belviq was approved in June 2012
  • Lorcaserin is a serotonin receptor agonist
  • Thought to increase satiety signals
31
Q

Orlistat (Xenical, Alli)

A
  • MOA: specific gastric and pancreatic lipase inhibtor
    • Prevents fat absorption
    • Up to 30% of dietary fat will be excreted
    • Drug is not absorbed
  • To be used in conjunction with reduced-calorie diet
  • Side effects: GI problems (only if excess fat in diet), slight reducing in fat-soluable vitamin levels
  • Weight loss is modest, ~3% over placebo
  • Total LDL and cholesterol decrease, glycemic control improved
32
Q

Phentermine

A
  • Phentermine is a component of the infamous Fen-Phen which is off the market because of cardiac toxcity-heart valve disease
  • Norepinephrine and dopamine reuptake inhibitor
  • Causes hypertension, insomnia
  • Short term appetite suppression, but not very effective by itself
  • Qsymia recenetly approved by FDA is a combination of phentermine and topiramate
33
Q

Chronic GI disorders

A
  • GERD
  • Peptic ulcer disease (PUD)
  • Inflammatory Bowel Diseases
    • Crohn’s
    • Ulcerative coltitis
    • Coeliac disease
34
Q

Gastric acid secretion

A
  • Acid production
    • Stomach lumen in acididc
    • pH 2-3
    • Isotonic HCl solution
    • Acid converts inactive pepsinogen to active pepsin
    • Acid denatures proteins
  • Mucus production
    • Mucosal cells secrete mucus and bicarbonate
    • pH gradient across the mucosa
    • Alcohol affects the mucosa
35
Q

GERD

A
  • Backflow of acids into the esophagus
    • Scarring can occur
    • 10-20% population affected
  • Triggers
    • Food (fatty, alcohol, caffeine)
    • Smoking
    • Obesity
    • Pregnancy
  • Symptoms
    • Heartburn, major
    • Difficulty swallowing
    • Chest pain
  • Complications
    • Esophogeal erosions
    • Esophogeal ulcer
    • Esophageal stricture
36
Q

Barrett’s Esophagus

A
  • ~10% of patients, normal esophageal epithelium is replaced with abnormal (Barrett’s) epithelium
  • This is linked to cancer of the esophagus
    • Needs monitoring to make sure it doesn’t become malignant
37
Q

Peptic Ulcer Disease (PUD)

A
  • Benign
    • Normal secretic of gastric acid
    • Mucosal barrier is weak
  • Malignant
    • Excessive secretion of gastric acid
    • Normal mucosal barrier is overwhelmed
  • Causes
    • H. pylori (85% of cases)
      • Bacteria attach to epithelial cells
      • Can’t be washed out
      • Damage mucosa be secreting enzymes/toxins
      • Also elicit destructive immune response
    • NSAIDs (10%) of cases
      • Irritate stomach lining
      • Inhibit prostaglandin synthesis
    • Other (<5% of cases)
      • Benign pancreatic tumor secretions
      • Unknown causes
38
Q

Treatment goals for GERD and PUD

A
  • Neutralize stomach pH
  • Decrease gastric acid secretion
  • Decrease H. pylori infection
  • Provide mucosal protecion
  • Promote mucosal healing
  • Lifestyle changes
39
Q

Treatments for GERD and PUD

A
  • Antacids
  • H2 Receptor blockers
  • PPI
  • Mucosal protection
  • Anti-microbial agents
40
Q

Regulation of Acid production

A
41
Q

Antacids

A
  • Weak bases
  • Efficacy depends on
    • Rate of dissolution
    • Solubility in water
    • Rate of reaction
    • Often combined for better efficacy
  • Treats symptoms, not underlying condition
    • Typically taken 5-7 times per day
42
Q

Histamine H2 receptor antagonists

A
  • Histamine stimualtes acid production by parietal cells
    • Activate histamine H2 receptors
    • Increase proton pump activity
  • Histamine H2 receptor antagonists
    • Drugs of choice during 70-90’s
    • Modifications of histamine structure
    • Cimedtidine, Famotidine, Ranitidine, Nizatidine
43
Q

Histamine H2 Receptor Antagonists: Details

A
  • Highly selective
    • No effects at histamine H1, H3, or H4 receptors
  • Long acting
    • 6-12 hours of duration, 1-2 times per day
  • Inhibit 60-70% of gastric acid secretion in 24 hour period
  • Rank order of potency
    • famotidine>nizatidine=ranitidine>cimetidine
  • Side effects (<3% of patients)
    • Diarrhea
    • Fatigue
    • Headache
    • Myalgias
44
Q

PPI

A
  • Irreversible inhibit the PP in parietal cells
  • Inactive at neutral pH, but activated in the acidic stomach
  • Omeprazole, Lansopraxole, Esomeprazole, Rabeprazole
45
Q

PPI: details

A
  • Long acting
    • Acid production reduced for 24-48 hours
    • Once a day
  • Inhibit 90-98% of gastric acid secretion in 24 hours period
  • Similar efficacies across compounds
    • Effective in 80-90% of patients
  • Minimal side effects (<5% of patients)
    • Diarrhea
    • Headache
    • Abdominal pain
    • Reduced vitamin B12, Ca2+, iron, zinc absorption
  • Current drug of choice
46
Q

Mucosal protective agents

A
  • Potentiate endogenous mucosal repair and defense mechanisms
  • Misoprostol
    • Prostaglandin E1 analog
    • Endogenous PGs stimulate mucus and bicarbonate production
    • Activates PGE3 and PGE4 receptors on parietal cells
    • Counters histamine effects
    • Often used with NSAIDS that inhibit endogenous PG synthesis
  • Suralfate (Carafate)
    • Sucrose sulfate-aluminum salt
    • Requires an acid pH to activate
    • Forms complex gels with mucus to improve the mucosal barrier
    • Not absorbed, local and effective
    • Can bind with drugs and interfere with absorption
    • Generally free of side effects
47
Q

Peptic Ulcer therapies; Antibiotics

A
  • Disrupt the cell wall of H. pylori
    • Bismuth
    • Amoxicillin
  • Disrupt protein synthesis in H. pylori
    • Clarithromycin
    • Tetracycline
  • Disrupt nucleic acid synthesis in H. pylori
    • Metronidazole
    • Often used due to bacterial resistance or intolerance to amoxicillin and tetracycline
  • Standard treatment regimen is often a combination therapy
    • Omprazole, bismuth, tetracycline, and metronidazole
48
Q

Inflammatory Bowel Disease

A
  • Crohn’s Disease
    • Patchy inflammation
    • May affect any part of GI tract
    • Symptoms:
      • Abdominal pain
      • Diarrhea
      • Weight loss
      • Intestinal obstruction
  • Ulcerative colitis
    • Diffuse inflammation
    • Limited to the colon
    • Symptoms:
      • Abdominal pain
      • Diarrhea
      • Weight loss
      • Intestinal obstruction
49
Q

Causes of IBD

A
  • Gut microbiota is altered in affected individuals
    • 30-50% reduced biodiversity in commensalism bacteria
    • More likely to have been prescribed antibiotics 2-5 years before onset
  • Genetics may be a factor
    • 163 IBD susceptibility loci have been identified
    • Many genes involved in cytokine production, lymphocyte activation, response to bacterial infection
    • Account for an 8-13% variance in Crohn’s disease
    • Account for a 4-7% variance in ulcerative colitis
50
Q

Coeliac Disease

A
  • Autoimmune disease
    • ~1 in 140 are affected in US
    • Reaction to gliadin (a gluten protein)
    • Symptoms:
      • Pain and GI discomfort
      • Weight loss
      • Anemia
      • Fatigue
  • Genetic cause
    • Nearly all patients have a mutant allele in HLA-DQ1 or HLA-DQ8
    • HLA-DQ is part of the MHC class II antigen-presenting receptor
    • Mutant forms bind gliadin peptides more tightly
    • Increased activation of lymphocytes and heightened immune reaction
  • Treatment
    • Lifelong GF diet
51
Q

IBD Treatements

A
  • Treatment
    • Current goal is to resolve acute episodes and prolong remission
    • Individualized to each patient
  • Drug choice and administration route depends on many factors
    • Type, distribution, and severity of the patient’s disease
    • Patient history
    • Patient preferences
  • Therapies
    • Aminosalicylates
    • Corticosteroids
    • Thiopurines
    • Methotrexate
    • Cyclosporin
    • Infliximab or adalimumab
    • Surgery to remove a protion of the intestine
    • Fecal transplant
52
Q

Aminosalicylates treatment of IBD

A
  • Derivative of salicylic acid
    • Anti-inflammatory
    • Poorly absorbed so acts locally in the GI
    • Oral and rectal preparations
    • Used in active disease
    • Used to maintain remission
  • Aminosalicylates
    • Mesalazine (5-aminosalycilic acid, 5-ASA)
    • Sulfasalazine (a sulfapyridine form of 5-ASA)
    • Balsalazide (prodrug from of 5-ASA)
    • Olsalazine (5-ASA dimer cleaved in colon)
  • Adverse effects
    • 10-45% patients can have nausea, headache, epigastric pain, diarrhea, pancreatitis, blood disorder, lung disorder, and myo/pericarditis
    • Caution with renal impairment, pregnancy and breast feeding
53
Q

Corticosteroid treatment of IBD

A
  • Used for moderate to severe relapses
  • Prednisone is typically used
  • Adverse effects (typical for corticosteroids)
    • Acne
    • Moon face
    • Sleep disturbances
    • Dyspepsia
    • Glucose intolerance
    • Osteoporosis
    • Myopathy
    • Glaucoma and cataract formation
54
Q

IBD treatments: Thiopurines

A
  • Mode of action
    • Inhibitors of ribonucleotide synthesis
    • Can induce T-cell apoptosis
    • Used to manage active and chronic disease
    • Allows discontinuation of steroids (steroid sparing)
  • Thiopurines
    • Thioguanine
    • Mercaptopurine
    • Azathioprine
  • Adverse effects
    • Leukopenia
    • Flu-like symptoms after 2-3 weeks
    • Liver and pancreas toxicity
    • ~30% of patients do not respond properly to treatment
    • Genetic variation in thiopurine S-methyltransferase (TPMT) is associated with adverse effects if standard doses are used
55
Q

IBD treatments: methotrexate

A
  • MOA:
    • Inhibits dihydrofolate reductase: converts dihydrofolate into tetrahydrofolate
    • Tetrahydrofolate is essential for purine and thymidylate synthesis
    • Important for cell proliferation and cell growth
    • Likely prevents cytokine and eicosanoid production
    • Used in active or relapsing disease that is refractory/intolerant to thiopurines
  • Adverse effects
    • Blood in urine or stools
    • Nausea or vomiting
    • Diarrhea
    • Hair loss
    • Hepatotoxicity
    • Skin complications (acne, rash, itching)
56
Q

IBD treatments: Cyclosporin

A
  • MOA:
    • Binds to cyclophilin
    • This inhibits calcineurin function
    • Calcineruin is important for production of IL-2 and cytokines
    • Used to manage active and chronic disease
    • Steroid sparing
  • Adverse effects
    • Gingical hyperplasia
    • Convulsions
    • Peptic ulcers
    • Pancreatitis
    • Fever
    • Vomiting
    • Diarrhea
    • High blood pressure
    • Nephrotoxicity
    • Hepatotoxcity
57
Q

IBD treatments: infliximab adalimumab

A
  • MOA
    • Monoclonal Ab against tumor necrosis factor alpha (TNF-α)
    • TNF-α is a cytokine involved in systemic inflammation
    • Very potent anti-inflammatory effects
    • Must be given as an IV infusion
    • Used for severe disease refractory/intolerant to steroids or immunosuppressive agents
    • Remicade (infliximab), Humira (adalimumab)
  • Adverse effects
    • Infusion reactions
    • Sepsis
    • Serious blood disorders that can become fatal
    • Increased risk of infection
    • Increased risk of acquiring or reactivating tuberculosis
    • Psoriasis
    • Liver injury
    • Lymphoma and solid tissue cancers

Phcol 401 (10 decks)

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