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PHCOL 401 > Quiz #6 (11/20-11/30) > Flashcards

Quiz #6 (11/20-11/30) Flashcards

1
Q

thyroid hormone

A
  1. Triiodothyronine (T3) and thyroxine (T4) are synthesized from thyroglobulin
  2. T4 is the major form of thyroid hormone in the blood
  3. T0a and T1a: produced by decarboxylation and deiodination of T3 and T4. Physiological roles are not known but generally oppose T3 and T4
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2
Q

Thyroid synthesis

A
  1. Thyroid hormone can be stored in the thyroid for many weeks
  2. Na/I symporter brings I- into the thyroid follicular cell. I- diffuses out the other side of the cell into the follicle colloid.
  3. Thyroid peroxidase (TPO) oxidizes I- to I0 which can now be conjugated to the protein.
  4. The conjugated protein is endocytosed back into the cell and then out into the blood stream
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3
Q

TSH function

A

acts directly on follicular cells to increase iodide transport into follicular cells, production of thryroglobulin, iodination of thyroglobulin, endocytosis of iodinated thyroglobulin from the colloid into follicular cells, proteolysis of thryoid thyroglobulin and exocytosis into the capillaries

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4
Q

TSH: effects on Cardiovascular system

A

: increases heart rate, force of contraction, stroke volume, cardiac output, catecholamine receptors

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5
Q

TSH Effects on respiratory system:

A

increases resting respiratory rate, minute ventilation and ventilatory response to hypercapnia and hypoxia

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6
Q

TSH effects on oxygen-carrying capacity

A

increases red blood cell mass, and oxygen dissociation from hemoglobin

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7
Q

TSH effects on renal system

A

increases blood flow and GFR

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8
Q

TSH effects on the reproductive system

A

Required for normal follicular development and ovulation, maintenance of pregnancy, and spermatogenesis

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9
Q

TSH Effects on growth and tissue development

A

increases growth and maturation of bone, tooth development, growth of epidermis, hair follicles and nails and rate and force of skeletal muscle contraction

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10
Q

TSH effects on the nervous system

A

critical for CNS development, enhances wakefulness, alertness, memory and learning capacity, increases speed and amplitude of peripheral nerve reflexes

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11
Q

TSH MOA

A

TR-RXR heterodimer that is always present on DNA in the nucleus. When the ligand is bound, activation of gene expression occurs.

T-alpha -1 and T-beta-1 & 2 generally activate transcription when T3 binds

T-alpha-2 does not bind T3 or T4 and therefore inhibits transcription

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12
Q

TSH Regulation

A
  1. TRH is released from the hypothalamus which acts on the anterior pituitary to release TSH. TSH acts on the thyroid to release T3 and T4 which acts on nearly every organ.
  2. T3 and T4 negatively feedback on the anterior pituitary and the hypothalamus
  3. Estrogen, low body temps and carbs positively feedback on the hypothalamus
  4. GH, GHIH, cortisol and stress negatively feedback on the hypothalamus
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13
Q

TSH Circulation

A

Almost all of T4 is bound to serum proteins, less than 0.02% is free. About 0.4% of T3 is free in serum

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14
Q

TSH Metabolism

A

deiodination through peripheral dehalogenases in the liver and kidneys

Activation: T4 –> T3 by beta-adrenergic

Inactivation: glucocorticoids convert T4 to Reverse T3, which inhibits T3 production.

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15
Q

5 Primary Hypothyroidism disorders

A
  1. Cretinism: during childhood. Causes retarded growth, sluggish movements, mental deficiencies
  2. Myxedema; during adulthood. Occurs in about 5% of the population
  3. Simple goiter: iodine deficiency, high TSH causes thyroid hypertrophy
  4. Hashimoto’s syndrome: autoimmune
  5. Iatrogenic: often following treatment of hyperthyroidism
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16
Q

Secondary hypothyroidism disorder

A

pituitary disease or hypothalamic disease

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17
Q

Hypothyroidism treatment

A
  1. Iodine supplementation
  2. Synthetic T4: T3 is more active and faster but also more toxic. T4 is less susceptible to feedback regulation. Goal is to normalize TSH
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18
Q

4 hyperthyroidism disorders

A
  1. Graves Disease: autoimmune usually in 30 year old women. Causes diffuse thyroid enlargement, wide staring gaze, lid lag, protuberant eyes, hyperpigmentation, high body temp and jittery
  2. Excess endogenous thyroid hormone: after treatment of hypothyroidism
  3. Thyroid cancers: produce excess thyroid hormone
  4. Acute hyperthyroidism: causes often unknown, muscle fatigue, weakness, weight loss, sweating, heat intolerance
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19
Q

Hyperthyroidism treatment

A
  1. Thioamide drugs: TPO inhibitors. Examples are PTU (propylthiouracil) and methimazole
  2. 131-I: local radiation
  3. Surgery: partial or complete thyroidectomy
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20
Q

Ghrelin function

A
  1. made in response to an empty stomach. Increasing levels prior to eating and decreased levels after meals
  2. Secreted by P/D1 cells of the stomach and epsilon cells of the pancreas
  3. Levels are lower in obese patients than in lean individuals. Levels during the day are similar but during sleep levels are higher in lean people
  4. In shortened sleep cycles, people produce more ghrelin and less leptin thus increasing appetite and food intake
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21
Q

Ghrelin MOA

A

binds NPY neurons to inhibit POMC neurons and thus production of alpha-MSH, increasing the appetite by sending the “start eating” signal. Also produce Agouti-related protein (AgRP) which is the most potent and long-lived appetite stimulators to block the “stop eating” signal

22
Q

Leptin Functions

A
  1. made in response to increasing fat stores
  2. Secreted by fat cells, and production depends on the number and size of adipocytes.
  3. Levels decrease with food restriction suggesting it may be a signal to control fuel metabolism during fasting and starvation.
  4. Administration of leptin during a fast prevents the starvation response
  5. Levels reflect subcutaneous fat
23
Q

Leptin MOA

A

binds POMC neurons (anorexigenic neurons) to increase production of alpha-MSH which suppresses appetite by signaling a “stop eating” signal. Leptin binds NPY neurons (orexigenic neurons) to relieve inhibition of POMC neurons and prevent triggering of the “start eating” signal

24
Q

Leptin injections for obesity

A

obese patients have elevated blood leptin concentrations. Leptin injections have no weight-reducing effects and obese patients have developed resistance to the leptin signal

25
Q

Adiponectin

A
  1. Secreted by adipocytes in response to high fat reserves
  2. Stimulates AMP-dependent protein kinase (AMPK) to increase fatty acid uptake by myocytes, rate of fatty acid oxidation, slows fatty acid synthesis in the liver and slows gluconeogenesis in the liver.
  3. Elevated expression with thiazolidinediones which bind PPAR (peroxisome proliferator-activated receptors). PPAR normally binds fatty acids and regulates genes involved in fatty acid metabolism
26
Q

GI hormones to induce satiety (5)

A
  1. CCK: cholecystokinin. released from small intestine to produce a satiety signal
  2. PYY: released from the intestine in proportion to meal size to produce a satiety signal
  3. GLP-1: produces satiety signal
  4. Obestatin: product of the ghrelin gene to decrease feeding
  5. Serotonin: Increases short-term satiety signals by inhibiting NPY/AgRP neurons and activating POMC neurons. Decreases need to eat.
27
Q

treatment for obesity: Sibutramine

A

: Reductil, Meridia.

MOA: inhibits serotonin reuptake in the CNS with anorectic and thermaogenic effects

Side effects: insomnia, constipation, increased heart rate, hypertension

About 5-10% weight loss and a reduction in diabetes
Withdrawn from US

28
Q

Treatment for obesity: Lorcaserin

A

Belviq. Serotonin receptor antagonist, increase satiety signal

29
Q

Treatment for obesity: Orlistat

A

Xenical or Alli. Specific gastric and pancreatic lipase inhibitor used in combination with reduced-calorie diets. Side effects are GI problems and weight loss is modest (3%)

30
Q

Treatment for obesity: Phentermine

A

component of Fen-Phen which is off the market. Is a NE and DA reuptake inhibitor. Side effect is hypertension and insomnia. Not effective as a single treatment . Qsymia is the combination of phentermine and topiramate and was just approved.

31
Q

Acid and mucus production and function

A
  1. Acid Production: bicarbonate is produced through carbonic anhydrase and is transported into the plasma. This facilitates the movement of Cl ions into the cell and powers the Cl/K/H+ transport out into the lumen.
  2. Acid function: converts inactive persinogen to active pepsin and denatures proteins
  3. Mucus production: mucus protects stomach lining, also pump out bicarbonate to neutralize acid
32
Q

GERD causes, symptoms, triggers, complications

A

Caused by the backflow of stomach acid into the esophagus.

Triggers: food (fatty food, alcohol, caffeine), smoking, obesity, pregnancy

Symptoms: heartburn, difficulty swallowing, chest pain

Complications: esophageal erosions, ulcer or stricture

33
Q

Barrett’s esophagus

A

Linked to cancer of the esophagus

Normal esophageal epithelium is replaced with abnormal (Barrett’s) epithelium

34
Q

Types of PUD

A

Benign: normal secretion of gastric acid but mucosal barrier is weak

Malignant: excessive secretion of gastric acid, normal mucosal barrier is overwhelmed

35
Q

PUD causes

A
  1. Helicobacter pylori (85% of cases): damage mucosa by secreting enzymes and elicits a destructive immune response
  2. NSAIDS (10% of cases): irritate stomach lining by inhibiting prostaglandin synthesis
  3. Other (5% of cases): benign pancreatic tumor secretions, unknown causes
36
Q

Treatment goals for GERD and PUD

A

Goals: neutralize stomach pH, decrease gastric acid secretion, decrease H.pylori infections, provide mucosal protection and healing, and lifestyle changes

37
Q

Treatment PUD or GERD: antacids-weak bases

A

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.

38
Q

Treatment GERD and PUD: H2 receptor antagonists

A

MOA: histamine stimulates acid production by parietal cells act to increase activity of proton pump

Cimetidine (Tagamet), Famotidine (Pepcid), Ranitidine (Zantac), Nizatidine (Axid). Potency: famotidine > nizatidine = ranitidine > cimetidine

Highly selective to H2 receptor.

Long acting, side effects include diarrhea, fatigue, headache and myalgias.

39
Q

Treatment for GERD and PUD: PPIs

A

MOA: irreversibly inhibit proton pump in parietal cells. PPIs are inactive and are only activated in the acidic stomach

Drugs: Omeprazole (Prilosec), Lansoprazole (Prevacid), Esomeprazole (Nexium) and Rabeprazole. similar efficacy across compounds

Long acting (24-48 hours), side effects include diarrhea, HA, abdominal pain and reduced vitamin absorption

40
Q

GERD treatment: Mucosal protective agents

A

Misoprostol (Cytotec): endogenous PGs stimulate mucus and bicarbonate production, often used with NSAIDS that inhibit endogenous PG synthesis

Sucralfate (Carafate): improves mucosal barrier, not absorbed and only works locally. Interferes with absorption of other medications.

41
Q

PUD treatment

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. Used if tolerance developed

Standard Therapy: Omeprazole, bismuth, metronidazole, tetracycline

42
Q

Two types of IBD

A
  1. Crohn’s disease
    Patchy inflammation, may affect an part of the GI tract
    Symptoms: abdominal pain, diarrhea, weight loss, intestinal obstruction
  2. Ulcerative colitis
    diffuse inflammation limited to colon
    Symptoms: abdominal pain, diarrhea, weight loss, intestinal obstruction
43
Q

IBD causes

A

gut microbiota is altered in affected individuals and genetics may be a factor

44
Q

Coeliac disease

A

Coeliac disease: autoimmune disease

Reaction to gliadin, a gluten protein

Symptoms: pain and discomfort in the GI, weight loss, anemia, fatigue

Genetic cause with mutant allele in HLA-DQ2 or HLA-DQ8

Treatment: lifelong gluten-free diet

45
Q

Treatment IBD: Aminosalicylates

A

derivatives of salicylic acids. Anti-inflammatory effects but act locally in GI. Used to maintain remission. Common adverse effects are nausea, HA, GI pain, diarrhea. Caution in renal impairment, pregnancy and breast feeding

46
Q

Treatment IBD: corticosteroids

A

used for moderate to severe relapses. Prednisone is typically the one used. Adverse effects are typical for corticosteroids and include acne, moon face, sleep disturbances, dyspepsia, glucose intolerance, osteoporosis, myopathy and glaucoma.

47
Q

Treatment of IBD: Thiopurines

A

Used to manage active and chronic disease and is steroid sparing (allows dx of steroids). Adverse effects include leukopenia, flu-like symptoms, liver and pancreas toxicity. About 30% of patients will not respond to this therapy. TPMT polymorphism

48
Q

Treatment of IBD: methotrexate

A

Used in active or relapsing disease that is refractory/intolerant to thiopurines. Adverse effects include blood in urine or stools, N/V/D, hair loss, hepatotoxicity, skin complications

49
Q

Treatment of IBD: Cyclosporin

A

Used to manage active and chronic disease and is steroid sparing. Reduces production of cytokines. Adverse effects include gingival hyperplasia, convulsions, peptic ulcers, pancreatitis, fever, V/D, Hypertension, nephro and hepatic toxicity

50
Q

Treatment of IBD: Infliximab (Remicade), adalimumab (Humira)

A

: Against TNF-alpha that have extremely important anti-inflammatory effects. Used for severe disease refractory/intolerant to steroids or immunosuppressive agents. Adverse effects include infusion reactions, sepsis, serious blood disorders, increased risk of infection or tuberculosis, psoriasis, liver injury, lymphoma and solid tissue cancers

51
Q

Functions of thyroid hormone

A

Thyroid Hormones control the body’s basal metabolic rate, overall metabolism of protein, fat and carbohydrates and the sensitivity to catecholamines

PHCOL 401 (9 decks)

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